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THE FEDERATION OF EUROPEAN


COMPANION ANIMAL
VETERINARY ASSOCIATIONS

SOCIET CULTURALE ITALIANA


VETERINARI PER
ANIMALI DA COMPAGNIA

55

55

55

5 55

555

4 CONGRESSO

FECAVA SCIVAC
EUROPEO

BOLOGNA

18-21

GIUGNO

PROGRAMMA DEFINITIVO
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Ter 15

1998

Con il patrocinio di

Facolt di Veterinaria dellUniversit di Bologna


FNOVI, Federazione Nazionale Ordini Veterinari Italiani
Provincia di Bologna
Comune di Bologna
Ambiente, Sviluppo Sostenibile, Politiche Giovanili,
Protezione Civile
Comune di Bologna
Politiche Sociali, Sanit e Sicurezza
In collaborazione con
A.I.V.P.A Associazione Italiana Veterinari Piccoli Animali

Circolo Veterinario Bolognese

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5

THE FEDERATION OF EUROPEAN COMPANION


ANIMAL VETERINARY ASSOCIATIONS

SCIVAC

SOCIET CULTURALE ITALIANA VETERINARI


PER ANIMALI DA COMPAGNIA

PALAZZO

TRECCHI

26100

CREMONA

TEL. 0372 460440 FAX 0372 457091 - email: info.scivac@softeam.it

THE

FEDERATION OF EUROPEAN COMPANION


ANIMAL VETERINARY ASSOCIATIONS

Caro Collega,
sono veramente onorato di presentare il 4 Congresso Europeo della FECAVA che si
terr a Bologna dal 18 al 21 Giugno 1998. Limportanza di questo evento assume molteplici significati. Innanzitutto viene riconosciuta alla Medicina Veterinaria Italiana la crescita compiuta in questi anni che lha portata a qualificarsi a livello europeo in una posizione di tutto rispetto. Contemporaneamente, laver affidato a SCIVAC lorganizzazione congressuale
testimonia il ruolo che la nostra Associazione ha assunto nellambito FECAVA, e questo ci rende giustamente orgogliosi.
Queste le cifre del 4 Congresso FECAVA che dimostrano di quale portata sar questo congresso: un pre-congress day con otto gruppi specialistici, dodici ore di discussione interattiva di casi
clinici, tre giorni interi con un programma scientifico eccellente, sei sale con relazioni in contemporanea, relazioni dal livello base a quello avanzato, undici relazioni sullo stato dellarte dei vari settori
della clinica e della chirurgia, oltre quaranta relatori invitati, tredici argomenti trattati. In quattro giorni
verranno trattati argomenti che spazieranno dalla clinica alla chirurgia, dalla medicina felina a quella degli animali esotici, dalla cardiologia alloftalmologia senza tralasciare alcun argomento che possa
interessare la clinica degli animali da compagnia. I relatori invitati sono stati selezionati tra i migliori
dEuropa e degli Stati Uniti, con la presenza di un buon gruppo di Colleghi italiani.
A questo congresso si sono completamente dedicati una Commissione Scientifica di altissimo livello, che ha lavoratto per oltre due anni al programma, e uno staff tecnico che render levento unico
per la sua organizzazione. Ritengo quindi di poter dire che per molto tempo sar difficile avere unaltra occasione di questa portata per fare il punto sui traguardi e sulle nuove indicazioni terapeutiche
nella clinica degli animali da compagnia.
La sede congressuale sar la meravigliosa citt di Bologna, ricca di storia e di tradizione. Sita in una
delle pi belle regioni dItalia la citt far certamente da degna cornice ad un evento cos importante.
Mi preme ringraziare fin dora il Consiglio Direttivo della FECAVA che ha voluto accordarci la sua
fiducia, dando mandato a SCIVAC di organizzare questo congresso. Devo inoltre un doveroso ringraziamento al Consiglio Direttivo e alla Commissione Scientifica della SCIVAC per il lavoro svolto ed infine a tutti gli Sponsor che hanno voluto sostenere questa importante iniziativa.
In attesa di incontrarTi a Bologna Ti porgo i pi cordiali saluti.
Carlo Scotti
Presidente SCIVAC

scivac

Presidente
CARLO SCOTTI

Presidente Senior
GIORGIO ROMANELLI

SOCIET CULTURALE ITALIANA VETERINARI


Vice Presidente
PIERMARIO PIGA

Segretario
UGO LOTTI

PER

Tesoriere
GILDO BARONI

ANIMALI

DA

Consigliere
MARCO CALDIN

COMPAGNIA
Consigliere
MATTEO SPALLAROSSA

Uffici: Palazzo Trecchi - 26100 Cremona - Tel. O (0372) 460440 - Telefax (0372) 457091 - E MAIL: info.scivac@softeam.it - Partita I.V.A. 00861330199

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5

ANIMAL VETERINARY ASSOCIATIONS

THE FEDERATION OF EUROPEAN COMPANION

________ FECAVA _______

Cari Colleghi,
a nome dei componenti del Direttivo della Federazione Europea delle Associazioni
Veterinarie per Animali da Compagnia, ho il piacere di invitarvi al 4 Congresso
Europeo FECAVA SCIVAC che si terr in una delle pi belle citt dEuropa: Bologna.
LAssociazione organizzatrice, la SCIVAC - Societ Culturale Italiana Veterinari per
Animali da Compagnia - il cui numero di iscritti il pi alto fra tutte le Societ aderenti alla FECAVA - vi offre lopportunit di prendere parte ad un evento unico per la vostra crescita professionale che unisce laggiornamento scientifico allesperienza di una delle aree storico-geografiche che
pi hanno concorso alla formazione della civilt moderna occidentale.
La decisione del Direttivo FECAVA di aderire unanimemente e con entusiasmo alla proposta
della SCIVAC di organizzare il 4 Congresso Europeo e di eleggere Bologna a sede congressuale
ha un particolare significato.
Abbiamo cos voluto onorare la SCIVAC, Associazione fondatrice della Federazione attivamente impegnata a sostenerne i progetti e le iniziative, e rendere omaggio alla straordinaria bellezza della citt di Bologna, alla sua felice collocazione geografica e al contributo che ha saputo
dare allo sviluppo della vita artistica, culturale e spirituale dEuropa.
Nessun altro Continente pu paragonare il proprio passato a quello lunghissimo e affascinante che lEuropa ha conosciuto, sia per gli aspetti culturali e scientifici che per il sentimento damicizia maturato fra le sue popolazioni. LEuropa da sempre la pietra di paragone di ogni progresso dellumanit.
sulla base di questa concezione e di questorgoglio europeisti che qualche anno fa nata la
nostra Federazione. Allora, nessuno avrebbe potuto immaginare limpatto e linfluenza che la
FECAVA avrebbe ottenuto sulla professione veterinaria per animali da compagnia.
La nascita della FECAVA stata ufficialmente sancita il 12 maggio 1990, alla presenza di tredici Associazioni fondatrici; adesso, la FECAVA conta ventisei societ aderenti, per un totale di
circa venticinquemila soci effettivi e dieci Societ Specialistiche veterinarie europee, in qualit di
membri associati.
I congressi europei fino ad ora realizzati si sono rivelati tra i principali eventi scientifici
dEuropa. Anche in questa occasione, stata rispettata la consuetudine di mantenere il programma scientifico ad alti livelli di qualit e successo come nei precedenti congressi europei e quindi
offrire ai partecipanti conoscenze consolidate, aggiornamenti ed elementi di valutazione critica
degli stessi, nellintento di promuovere lo scambio e il confronto culturale.
Lottimo programma scientifico, linvitante programma sociale e la citt di Bologna, con la sua
storia e i suoi paesaggi mirabili, sono elementi ideali combinati con la tradizionale ospitalit italiana, i vini e la cucina dItalia. Sar felice di vedervi numerosi, da tutti i Paesi dEuropa, e sono certo
che ricorderete questa occasione come degna e importante.
Dr. Ben Albalas
Presidente FECAVA

RELATORIALCONG
DAVID AUCOIN
DVM, Dip ACVCP
Vets Choice
Santa Monica, California
USA

MARCO CALDIN
Med Vet
Libero Professionista,
Padova

ELLEN BJERKAS
DVM, PhD, Dipl ECVO
Dept of SA Clin Sciences
Norwegian College of
Vet Med
NORVEGIA

MARIO CANIATTI
DVM
Universit di Milano
Istituto di Anatomia
Patologica Veterinaria

CLAUDIO BROVIDA
Med Vet
Libero Professionista,
Torino

DIDIER CARLOTTI
DVM, Dipl ECVD
Les Places Sainte Eulalie
FRANCIA

LEONARDO BRUNETTI
Med Vet
Libero Professionista,
Pistoia

DANIELE COTTO
Med Vet
Libero Professionista, Torino

PAOLO BURACCO
Med Vet
Universit di Torino
Dipartimento di Patologia
Animale

GUILLERMO COUTO
DVM, Dipl ACVIM
The Ohio State University
Columbus, Ohio
USA

CLAUDIO BUSSADORI
Med Vet, Dipl ECVIM
Libero Professionista,
Milano
6

GRESSO
LORENZO CROSTA
Med Vet
Libero Professionista,
Milano

STEPHEN DIVERS
Bsc, C Biol, M.I. Biol,
B.Vet. Med, MRCVS
Exotic Animal Center, Essex
GRAN BRETAGNA

BERNARD F. FELDMAN
DVM, PhD, Dipl ACVIM
College of Vet Medicine
Blacksburg, Virginia - USA
LUIS FERRER
DVM, Dipl ECVD
Universitat Autonoma de
Barcelona - Barcelona
SPAGNA
ANTONIO FERRETTI
Med Vet, Dipl ECVS
Libero Professionista,
Milano

CORINNE FOURNEL-FLEURY
DVM, PhD
Ecole Nat Vet de Lyon
Marcy lEtoile - FRANCIA
TOMMASO FURLANELLO
Med Vet

Libero Professionista,
Padova

ADOLFO GUANDALINI
Med Vet
Libero Professionista,
Roma

HERMAN A. W. HAZEWINKEL
DVM, PhD, Dipl ECVS
State University of Utrecht
OLANDA
DOMINIQUE HERIPRET
DVM, Dipl ECVD
Clinique Veterinaire Fregis
Arcueil - Paris - FRANCIA

RICHARD LeCOUTEUR
VMD, PhD, Dipl ACVIM
University of California
Davis, California - USA

CHRISTOPHE LOMBARD
DVM, Dipl ACVIM,
Dipl ECVIM
Universitat Bern
SVIZZERA
GEORGE LUBAS
Med Vet
7
Universit di Pisa, Istituto di Pat

RELATORIALCONG
GIUSEPPE MOSCONI
Med Vet,
Libero Professionista,
Ozzano Emilia

Speciale e Clin Med


Veterinaria
LUCA MECHELLI
Med Vet
Universit di Perugia
Istituto di Anatomia
Patologica

GERT NIEBAUER
Med Vet, PhD,
MS, Dipl ECVS
Libero Professionista,
Orbetello

DENNY MEYER
DVM, Dipl ACVP,
Dipl ACVIM
Boulder, Colorado - USA

CLAUDIO PERUCCIO
Med Vet, Dipl ECVO
Universit di Torino
Dipartimento di Patologia
Animale

AR MICHELL
Dsc, MRCVS
Animal Health Trust
Newmarket Suffolk
GRAN BRETAGNA

S.M. PETERSEN-JONES
DVO, Dipl ECVO, MRCVS
University of Cambridge
Cambridge
GRAN BRETAGNA

MASSIMO MILLEFANTI
Med Vet
Libero Professionista, Milano

STEFANO PIZZIRANI
Med Vet, Dipl ECVS
Libero Professionista,
Firenze

PIERRE M. MONTAVON
DVM
Veterinar-Chirurgische
Klinik der Universitat Zurich
SVIZZERA

AD RIJNBERK
DVM PhD
University of Utrecht
OLANDA

GRESSO
GIORGIO ROMANELLI
Med Vet, Dipl ECVS
Libero Professionista,
Milano

MATTEO TOMMASINI
Med Vet, Dipl ECVS
Libero Professionista,
Roma

GIANLUCA ROVESTI
Med Vet, Dipl ECVS
Libero Professionista,
Reggio Emilia

ALDO VEZZONI
Med Vet, Dipl ECVS
Libero Professionista,
Cremona

ROBERTO SANTILLI
Med Vet
Libero Professionista,
Milano

FRANK VERSTRAETE
DVM, Dipl AVDC,
Dipl ECVS
University of California
Davis, California, USA

KARSTEN SCHOBER
DVM
University of Leipzig
GERMANIA

C. VON WERTHERN
DVM, Dipl ECVS
Veterinar-Chirurgische Klinik
der Universitat Zurich
SVIZZERA

PETER W. SCOTT
Msc, BVSc, FRCVS
Zoo & Aquatic Vet Group
Winchester
GRAN BRETAGNA

SIMON WHEELER
BVSc, PhD, Dipl ECVN
The Royal Veterinary College
University of London
GRAN BRETAGNA

DANIEL D. SMEAK
DVM, Dipl ACVS
The Ohio State University
Columbus, Ohio
USA

RICHARD A.S. WHITE


PhD, DVR, FRCVS, Dipl
ACVS, Dipl ECVS
University of Cambridge
GRAN BRETAGNA
9

SEMINARI PRE-C
S

8,30

A
R

L
E

A
G

D
S

I
T R

SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

HOLIDAY INN 250

ESFM
MEDICINA FELINA

SIDEV
DERMATOLOGIA

ESVO - ECVO - SOVI


OFTALMOLOGIA

ESCG
GASTROENTEROLOGIA

Approccio diagnostico
alle malattie cutanee su
base autoimmune nel
cane e nel gatto (30)
Dominique Heripret (F)

PALPEBRE E TERZA PALPEBRA


Tecnica di cantoplastica laterale per la
correzione della macro fessura palpebrale nel cane - P. Bedford (UK)

Tecniche per il
trattamento dei tumori colorettali nel cane:
valutazione critica (30)
R.A.S. White (UK)

9,30 Alterazioni ematiche


(1a parte)
Neutropenia e
piressia nel gatto (60)

Gioved Mattina 18 Giugno 1998

10,00

Pemfigo e pemfigoide
nel cane e nel gatto
(1a parte)
(30)

Guillermo Couto (USA) e


Bernard Feldman (USA)
10,30

Luis Ferrer (E)

11,00 Alterazioni ematiche


(2a parte)
Il gatto anemico:
modalit pratiche di
valutazione (60)

Pemfigo e pemfigoide
nel cane e nel gatto
(2a parte)
(30)

Luis Ferrer (E)


11,30

Guillermo Couto (USA) e


Bernard Feldman (USA)

Lupus discoideo e
lupus sistemico (60)

Aspetto ultrasonografico e con


Risonanza Magnetica dell'adenite eosinofilica della ghiandola della nittitante in
un cane - S.M. Turner (UK)

Prolasso ed iperplasia della ghiandola


della membrana nel coniglio
P. Boydell (UK)

ORBITA
Un caso di miosite eosinofilica unilaterale in un cane - M. Bandini (I)

Fisiopatologia della
ritenzione degli acidi
biliari (30)

D. Meyer (USA)

CORNEA
Un caso di ulcera bilaterale simmetrica
e stagionale cortico-responsiva in un
coniglio nano - P. Anfray, C. Bonetti (I)
Individuazione con microscopio elettronico a trasmissione di particelle citoplasmatiche simil-virali nelle cornee e congiuntive di cani con panno (cheratite
superficiale cronica - Uberreiter)
F. Rapp (A)
Cheratoplastica lamellare per la cura del
sequestro corneale nel gatto
M.T. Pena Gimenez (E)
Uso di collanti tissutali per la cura dell'erosione corneale cronica nel gatto
A.C. Leber (D)
Applicazioni cliniche di lembi tarso-congiuntivali isolati nel cane e nel gatto:
risultati in 40 casi - N. D'Anna (I)

L Helicobacter
gastrico nel cane
e nel gatto (30)

G.Cattoli (I)
Telediagnostica,
telechirurgia e
teleinsegnamento
(30)
J. Uson (E)
R

12,00
Discussione (30)

12,30

Alterazioni ematiche
(3a parte)
Il gatto anemico:
approccio terapeutico
pratico (60)

Altre malattie cutanee


immunomediate
(1a parte) (30)

Luis Ferrer (E)

TERAPIA
Penetrazione corneale, congiuntivale e
intraoculare dell'acido fusidico per uso
topico nel cane - G. J. McLellan (UK)

Dominique Heripret (F)

Guillermo Couto (USA) e


Bernard Feldman (USA)
13,00

GLAUCOMA
La crioterapia per la cura del glaucoma.
Risultati con l'azoto liquido - B. Clerc (F)
Glaucoma secondario a difetti oculari
multipli in un Gatto Inglese a pelo corto
R. Elks (UK)
Displasia del legamento pettinato nel
Siberian Husky. Studio clinico, biometrico e istopatologico
G. Chaudieu (F)

18

CONGRESSUALI
E S S O
O N E

8,30

SALA AZZURRA 150

SALA BIANCA 200

IEWG
ORTOPEDIA

SIMESC
ESVC
MEDICINA SPORTIVA CARDIOLOGIA

INTRODUCTION
Fisiopatologia
Who is IEWG? What are the aims of the
dellallenamento (15)
IEWG?
Dominique Grandjean (F)
Flckiger (Zurich - CH)

Diagnostic accurracy
of high resolution radiography and
arthroscopy
of elbows in growing dogs
Kramers (Zurich - CH)

Tecniche di allenamento
(1a parte) (25)
Dominique Grandjean (F)

PATHOPHYSIOLOGY OF ED
Pathophysiology of bony changes in
the dysplastic elbow joint
Poulos (Davis - USA)
Role of nutrition on the skeletal development
Hazewinkel/Nap (Utrecht/Eindhoven - NL)
EPIDEMIOLOGY/PREVENTION
CONCEPTS
Incidence of developmental articular
malformation in the Labrador Retriever
Wind (Davis - USA)
Effect of breed animal selection on the
incidence of ED in German Shepherd
dogs
Lavelle (Melbourne - AUS)
Prevalence and incidence of ED in a
colony of Labrador Retrievers
Lang/Ohlert (Bern - Switzerland)
open
Swenson (Uppsala - Sweden)
Predictability of FCPM in Dutch
Labrador Retrievers and Bernese
Mountain dogs
Ubbink (Utrecht - The Netherlands)
Breed value estimation in the dog.
Impact on the incidence of heritable
diseases
Beuing (Giessen - Germany)
PREVENTION CONCEPTS (continued)
The German ED prevention protocol;
preliminary results in selected breeds
Tellhelm (Giessen - Germany)
The British ED protocol
Pead (London - England)
Incidence of canine ED in Italy and clinical approach by veterinary profession
Mortellaro (Milano - Italy)
The WSAVA Hereditary Defects
Committee: Current activities and goals
Hedhammar/Bedford (Sweden/London)

Anestesia degli uccelli


da gabbia e da voliera
(60)

L.P. Tilley (USA)

Tecniche di allenamento
(2a parte) (20)
Dominique Grandjean (F)

Peter Scott (UK)

Fisioterapia e riabilitazione nel


cane sportivo (20)

Recenti acquisizioni
nei risultati clinici dellimpiego degli ACE inibitori in medicina per
piccoli animali (40)
J.L. Pouchelon (F)

Problemi ortopedici di
metacarpo, metatarso e falangi
nel cane sportivo (20)
Alessandro Piras (I) e Brian Jones
(IRL)

Aggiornamenti in tema
di patologie valvolari
acquisite nel cane (40)
J. Haggstrom (S)

Trattamento delle fratture delle


ossa lunghe nel cane atleta (20)

Problemi riproduttivi nei cani


sportivi (20)
Giovanni Majolino (I)

Le pi frequenti malattie virali dei pappagalli


(50)
Claudio Peccati (I)

10,30
11,00

11,30

Tecniche diagnostiche
impiegabili in medicina
aviare (50)
Peter Scott (UK)

11,50
12,00

Difetti del setto interventricolare nel cane


(40)
G. DAgnolo (I)
12,30
Indagine sulla flora residen- 12,40
te nelle prime vie respiratorie degli psittacidi (20)

Linseminazione artificiale con


seme fresco e congelato: che
cosa c di nuovo (20)
Stefano Romagnoli (I)

9,30

10,00

Incongruenze articolari del gomito: un problema emergente nelle


razze sportive (15)

*
Hills

Gruppo di Studio
ANIMALI ESOTICI

Il prontuario
farmaceutico
cardiologico Tilley
per il veterinario
pratico (60)

DIAGNOSIS OF ELBOW DYSPLASIA (ED)


Radiographic technique and film interpretation for ED screening
Lang (Bern - CH)

SALA SMERALDO 100

SALA BLU 150

Sandra De Oliveira (UK)

E
13,00

19

4 C O N G R E S S O F E C AVA S C I VA C

N G R
A Z I

Gioved Mattina 18 Giugno 1998

SEMINARI PRE-C
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

HOLIDAY INN 250

ESFM
MEDICINA FELINA

SIDEV
DERMATOLOGIA

ESVO - ECVO - SOVI


OFTALMOLOGIA

ESCG
GASTROENTEROLOGIA

14,00 Biochimica
clinica felina:
i gatti non sono cani
piccoli da un punto di
vista biochimico !!! (60)

Altre malattie cutanee


immunomediate
(2a parte) (30)

LENTE
Controllo del diabete del cane e cataratta
diabetica
D. Salgado ( CH)

Luis Ferrer (E)

UVEA
Uveite pigmentaria nel Golden Retriever:
43 casi
J.S. Sapienza (USA)

Il trattamento endoscopico nella palliazione dei tumori gastrointestinali nelluomo (30)


E. Meroni (I)

14,30

Diagnosi clinica
differenziale delle
patologie cutanee
autoimmuni (45)

Denny Meyer (USA)

Sindrome uveodermatologica in un cane


V.J. Babo (BRA)
L'uveite felina: riscontri sierologici e clinici in 44 casi
M. Roze (F)

Il linfoma
gastrointestinale del
cane e del gatto (30)

G.Couto (USA)

Gioved Pomeriggio 18 Giugno 1998

15,00

Alterazioni vestibolari
nel gatto (60)

15,15

Dominique Heripret (F)

Valutazione immunoistochimica della


risposta immune in un caso di uveite
ricorrente nel cavallo
L. Mertel (I)

Diagnosi istologica
differenziale delle
patologie cutanee
autoimmuni (45)

RETINA
La retina normale nella Phoca vitulina,
riscontri elettroretinografici e morfologici
E. Bjerkas (N)

Approccio nutrizionale al paziente


gastrectomizzato e\o
enterectomizzato (30)
B. Stanley (USA)
Discussione (30)

Aspetti elettroretinografici dell'onda d nel


gatto normale e distrofico
B. Ekesten (S)

Rick LeCouteur (USA)


Luis Ferrer (E)
16,00

16,30 Patologie spinali nel


gatto (60)

OTTICA E TECNICHE DIAGNOSTICHE


Risultati della cheratometria e della
schiascopia pre e post operatoria in 1000
cani di razze diverse - W. Neumann (D)

Protocolli terapeutici
(e nuove terapie) delle
malattie cutanee
autoimmuni (60)

Studio biometrico dell'occhio del cane


mediante ultrasonografia - S. Schoofs (B)
Indagine ultrasonografica dei nervi ottici
in cani colpiti da cecit improvvisa
P. Boydell (UK)

Rick LeCouteur (USA)

Fabbisogno dietetico
nel cane con patologia epatica (30)

H. Meyer (NL)
Discussione (30)

ANIMALI ESOTICI
Anomalie dello sviluppo oculare in una
tigre del Bengala - T. Grimes (UK)

Dominique Heripret (F)

Tonometria negli erbivori selvatici


R. Ofri (ISR)

17,30
Disordini
neuromuscolari nel
gatto (60)

Discussione (60)

OCULOPATIE EREDITARIE
Oculopatie ereditarie: il punto di vista
Italiano - C. Peruccio (I)
Oculopatie ereditarie: risultati preliminari
in alcune razze in Italia
E. Barbasso (I)
Per le presunte malattie oculari ereditarie: note sulle procedure adottate
dall'ECVO (relazione del Comitato
Malattie Genetiche dell'ECVO)
F.C. Stades (NL)

18,30 Rick LeCouteur (USA)

20

CONGRESSUALI

SALA AZZURRA 150

SALA BIANCA 200

IEWG
ORTOPEDIA

SIMESC
ESVC
MEDICINA SPORTIVA CARDIOLOGIA

TREATMENT
Arthroscopic approach in dogs
with ED
Meyer-Lindenberg, Hannover (D)
Results of ulna ostectomy
as a treatment for UAP
Vezzoni (Cremona - I)

Doping nel cane sportivo: vecchi


e nuovi concetti (20)
Dominique Grandjean (F)

SALA SMERALDO 100

SALA BLU 150

Rottura LCA: diagnosi,


ricostruzione e follow-up (30)
Immunoprofilassi
dallevamento:
organizzazione di un
programma vaccinale (20)
Swanneke D. Hendriks (NL)

Gruppo di Studio
ANIMALI ESOTICI

Ipertensione: diagnosi e Tecniche


trattamento (40)
anestesiologiche e
L.P. Tilley (USA)
patologie
chirurgiche nei rettili
(60)

14,00

14,30
Aggiornamenti in tema
di cardiomiopatia
dilatativa nel cane (40)
M. Borgarelli (I)

Distocie dei rettili (60)

Rottura del gastrocnemio nei


cani da caccia e da corsa (20)
Gianluca Rovesti (I)

15,15

Stress ossidativo indotto dallesercizio nel cane


sportivo e conseguenze sui fabbisogni nutrizionali di sostanze
anti-ossidanti (30)

Nuovi concetti nel


trattamento della
cardiomiopatia
dilatativa del cane e
terapie alternative (40)
C. Amberger (CH)

Comunicazioni libere

Discussion of the
seminar films

Integrazione
nutrizionale ergogenica nel
cane atleta (15)
D. Grandjean (F)

Workshop di
ecocardiografia (90)
C. Bussadori (I) e
C. Lombard (CH)

*
Hills
La zoppia di spalla nel cane
atleta: diagnosi e trattamento (15)
M. Olivieri (I)

Miopatia dei muscoli gracile e


semitendinoso (15)
A. Piras (I)

Tecniche diagnostiche
impiegabili nei rettili
(50)
Stephen Divers (UK)

16,00
16,30

17,00

17,20
Utilizzo della miscela
anestetica ZKX in pic17,30
coli animali esotici e
selvatici (20)
Amerio Croce (I)
Le pi comuni
patologie dei ricci: un
problema veramente
spinoso (50)
Rosanna Trossarello (I)

Patologie articolari degenerative:


un aggiornamento (15)

Impiego del Benazepril


nel gatto: farmacocinetica ed efficacia nel trattamento della cardiomiopatia dilatativa (30)
C. Amberger (CH) e
J.N. King (UK)

Alterazioni
muscolo-tendinee nel cane
atleta (15)
A. Piras (I) e B. Jones (IRL)

Annual General
Meeting of the IEWG

Giuseppe Visigalli (I)

18,30

21

4 C O N G R E S S O F E C AVA S C I VA C

15,00
Film Reading Seminar
Participants are encouraged to
interpret some 2 dozens elbow
cases, which then will be discussed with Dr. Alida Wind, former
Small Animal staff surgeon at the
University of California Veterinary
Medical Teaching Hospital.
Participant may also bring their
own ED cases along for discussion
(if time permits)

Gioved Pomeriggio 18 Giugno 1998

Stephen Divers (UK)

PROGRAMMASCI
S

8,30

A
R

L
E

A
G

D
S

I
T R

SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

EMATOLOGIA
Chairman: Marco Caldin

ORTOPEDIA
Chairman: Gildo Baroni

OFTALMOLOGIA
Chairman: Claudio Peruccio

Formazioni ossee
patologiche (60)
Segni clinici e radiologici,
eziologia, trattamento e prognosi
delle patologie caratterizzate da
formazioni ossee: panosteite,
osteodistrofia ipertrofia, ecc.

RELAZIONE SULLO STATO


DELLARTE
Recenti acquisizioni
nellinterpretazione della GPRA
Atrofia retinica generalizzata
progressiva (60)

9,30 Interpretazione della conta


cellulare ematica:
Prima parte
Lemogramma completo
(60)

Venerd Mattina 19 Giugno 1998

Bernard Feldman (USA)


10,30

H.A.W. Hazewinkel (NL)

EMATOLOGIA
Chairman: Marco Caldin

Simon Petersen-Jones (UK)

ORTOPEDIA
Chairman: Antonio Ferretti

Bernard Feldman (USA)

Il ruolo della nutrizione nelle


patologie ortopediche (60)
Linfluenza del contenuto
energetico, proteico, minerale e
vitaminico nella dieta sullo
sviluppo scheletrico e
sullaccrescimento

RELAZIONE SULLO STATO


DELLARTE
La cataratta nel cane:
eziologia, evoluzione
e riscontri clinici (60)

H.A.W. Hazewinkel (NL)

11,00 Interpretazione della conta cellulare ematica: Seconda parte


RELAZIONE SULLO STATO
DELLARTE
Procedure diagnostiche speciali
in ematologia (40)

OFTALMOLOGIA
Chairman: Stefano Pizzirani

Ellen Bjerkas (N)

Approccio clinico allanemia


(50)

12,00

Anemia nel cane giovane (30)

George Lubas (I)


13,00

Interpretazione clinica delle


emorragie oculari (60)

Aldo Vezzoni (I)

Bernard Feldman (USA)

Diagnosi precoce di displasia


dellanca (60)
Elementi clinici e radiografici che
permettono una diagnosi precoce
di displasia dellanca in funzione
della selezione cinofila e delle
scelte terapeutiche pi opportune

Claudio Peruccio (I)

Livello di Aggiornamento

Livello Avanzato

22

Relazione sullo Stato de

ellArte
S

Sessione Specialistica
O

23
Sessione Interattiva
M

13,00

Induzione dellestro nella gatta con


cabergolina: studi preliminari
Daniele Zambelli (I)

Displasia follicolare (60)

Safety trial in bitches with tablets containing oestriol (Incurin)


S. Hendriks (NL)

12,00

RIPRODUZIONE
Chairmen: Matteo Spallarossa (I)
e Patrizia Ponzio (I)

Medicina durgenza degli


uccelli (60)

Patologie infiammatorie dei follicoli piliferi (60)

Efficacia luteolitica ed effetti


collaterali dellalfaprostol,
un analogo sintetico della
prostaglandina F2alfa, nella cagna:
risultati preliminari
Sandra Annarella (I)

11,00

10,30

4 C O N G R E S S O F E C AVA S C I VA C

Patologie cutanee degli uccelli:


un incubo per il veterinario
pratico (60)

DERMATOLOGIA
Sessione specialistica
Chairman: Chiara Tieghi (I)

Venerd Mattina 19 Giugno 1998

Luca Mechelli (I)

?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I
M0@@M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I?@4I?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I4I
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I
?M0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4I
?Y0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4VI?
M(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'
Y0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4V?
?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
?MY(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V?
(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'I
gh?Y0@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@4V
ghY(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V?
fh?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
fh?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3N?
fhH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
eh?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
ehY(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V?
h?Y(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
h?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3
h(@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@'V
g?YH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N?
g?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3
gH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N?
g5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3?
f?H@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N
f?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3N?
fH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
f@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N
e?H5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3?
e?5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3
e?@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@N?
eH@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
e5@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@3?
e@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@?
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g?1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7
g?X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
hL@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7J?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
h?1)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
h?X@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
ehX)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W?
eh?X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@ @@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
fhL@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
fh?1@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@7J?
@@
fh?X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
ghX)6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
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gh?X?K)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&O2WW?
@@@@
X)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W?
?XX6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2W?
)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&W
K)@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@&
?X6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2WO?
?K?K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O2O
6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?K?K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O2O
6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
K6@@K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O?@2O?
@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@
?K6@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@@2O

Peter Scott (UK)

Luis Ferrer (E)

Trattamento con finasteride in cani


affetti da patologie prostatiche
Daniele Zambelli (I)
Treatment of urinary incontinence in
the bitch: clinical trail with tablets containing oestrol (Incurin)
S. Hendriks (NL)

Lorenzo Crosta (I)

Interruzione di gravidanza nella cagna


mediante somministrazione endovaginale di PGF2 alfa
Mario Cinone (I)
Induzione dellestro nella cagna con un
analogo del GnRH
Stefano Belluzzi (I)

MEDICINA PER ANIMALI ESOTICI


Chairman: Massimo Millefanti

Peter Scott (UK)


Alimentazione e patologie
nutrizionali degli uccelli (60)

9,30

MEDICINA PER ANIMALI ESOTICI


Chairman: Lorenzo Crosta

SALA BIANCA 200

N G R
A Z I

SALA BLU 120

SALA AZZURRA 100

E S S O
O N E

8,30

IENTIFICO

PROGRAMMASCI
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

EMATOLOGIA
Chairman:
George Lubas

ORTOPEDIA
Chairman:
Carlo Maria Mortellaro

OFTALMOLOGIA
Chairman:
Claudio Peruccio

Displasia del gomito:


eziologia, epidemiologia,
genetica, segni clinici, segni
radiologici, diagnosi e
approccio terapeutico (120)

Approccio alla cecit


improvvisa (60)

14,30 RELAZIONE SULLO STATO


DELLARTE
Coagulopatie nel cane e nel
gatto (60)

Venerd Pomeriggio 19 Giugno 1998

Marco Caldin (I)

Simon Petersen-Jones (UK)

15,30 Daccordo: una coagulopatia!


Ma non potrebbe essere
Ehrilichiosi? (60)

Guillermo Couto (USA)


16,30

Mancata unione del processo anconeo e frammentazione del processo coronoideo mediale, osteocondrosi e
incongruit articolari del gomito: fattori eziologici e metodi di controllo. Una procedura guidata per il veterinario
pratico per arrivare alla diagnosi. Indicazioni terapeutiche, vantaggi e svantaggi dei trattamenti chirurgici pi
comunemente impiegati.

H.A.W. Hazewinkel (NL)

ENDOCRINOLOGIA
Chairman:
Alessandra Fondati

Segni oculari di patologie


sistemiche nel cane (60)

Ellen Bjerkas (N)

ORTOPEDIA
Chairman:
Aldo Vezzoni

17,00 RELAZIONE SULLO STATO


DELLARTE
Approccio diagnostico e
terapeutico allipotiroidismo
(60)
A.D. Rijnberk (NL)

Nuove tecniche e nuovi materiali in


ortopedia (120)

OFTALMOLOGIA
Chairman:
Antonella Vercelli
Masse oculari pigmentate e
non pigmentate (60)

Fissatore esterno tubolare, PC-FIX, mini-placca


maxillofacciale Trattamento chirurgico alternativo
nellartrosi dellanca del cane (15) Tenotomia dellileopsoas, neurectomia della capsula articolare,
miectomia del pettineo Protesi totale danca non
cementata (20) Dagli studi sperimentali allimpiego clinico

Adolfo Guandalini (I)

*
Hills

18,00
RELAZIONE
SULLO STATO DELLARTE
Approccio diagnostico
e terapeutico
alliperadrenocorticismo (60)
A.D. Rijnberk (NL)

Descrizione di una modifica della tecnica di


Slocum per il trattamento non convenzionale della
rottura del legamento crociato anteriore nel cane
(25) Trattamento della lussazione rotulea nel
cane e nel gatto (30) Cranializzazione della tuberosit tibiale per il ripristino della biomeccanica
articolare

Pierre Montavon (CH) e


Cornelius Von Werthern (CH)

Manifestazioni oculari del


complesso eosinofilico del
gatto (60)

Stefano Pizzirani (I)

19,00 Interruzione
19,30

C E R I M O N I A
20,30

Livello di Aggiornamento

Livello Avanzato

24

S A L A
E
D A P E R T U R
Q U A
F E T

R
D

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

MEDICINA PER
ANIMALI ESOTICI
Chairman:
Peter Scott

NEUROLOGIA
Sessione interattiva
Chairmen: Massimo Baroni e
Tommaso Furlanello

MALATTIE INFETTIVE
Chairman:
Alessandra Fondati (I)

Trattamento chirurgico delle


pi comuni patologie delle
tartarughe (60)

Il grande dibattito:
vantaggi e svantaggi nelluso
dei corticosteroidi nelle
patologie spinali del cane (60)

Mielopatia degenerativa del


Pastore Tedesco: una patologia
controversa difficile da
diagnosticare e da trattare (60)

Rick LeCouteur (USA)


e Simon Wheeler (UK)

15,30

Efficacy of a high titre MLV against CDV in


puppies with maternal antibodies
J.G.H.E Bergman (NL)
Canine leptospirosis, do we use proper vaccination programmes? - D. Salgado (E)
Un caso clinico di Febbre delle Montagne
Rocciose in un cane del nord est dellItalia
Tommaso Furlanello (I)

16,30

MEDICINA PER
ANIMALI ESOTICI
Chairman:
Leonardo Brunetti

TECNICHE DIAGNOSTICHE
MINI-INVASIVE
Sessione interattiva
Chairman: Stefano Romussi

MEDICINA FELINA
Chairmen: Stefano Bo (I) e
Hans Lutz (CH)

Anestesia e chirurgia dei pesci


ornamentali (50)

Metodiche mini-invasive per


lapproccio diagnostico alle
principali patologie addominali
Una discussione interattiva basata
su casi clinici con lausilio della
valutazione citologica (120)

Attempts to cure feline leukemia virus


infection with biologic response modifier
treatment
Karin Hartmann (D)

17,00

Peter Scott (UK)

Efficacia della marbofloxacina iniettabile nel


trattamento delle infezioni delle vie urinarie
distali nel cane - Claudio Brovida (I)

Pi comuni malattie virali,


batteriche e parassitarie dei
pesci ornamentali (50)

Mario Caniatti (I)


e Roberto Santilli (I)

ellArte

Effect of recombinant human granulocyte


colony-stimulating factor on hematopoiesis
in neutropenic cats caused by different
diseases
Manuela Kuffer-Frank (D)

18,00

19,00

E U R O P A
A
E
C O N C E R T O

P O
B E

Comparative studies of the efficacy of two


leukemia virus vaccines
Hans Lutz (CH)
Serum bile acids and feline trypsin-like
immunoreactivity after exogenous pancreatic
stimulation with ceruletid in normal cats
Thomas Spillmann (D)
Adenocarcinoma of a labial minor salivary
gland in a cats
Dimitrios Tontis (GR)
Monitoraggio ecografico di morte fetale nel
gatto: caso clinico
Iacopo Vannozzi (I)

Massimo Millefanti (I)


Recenti acquisizioni nellimpiego
dei glucani come integrazione
nutrizionale nei pesci ornamentali (20)
Giuseppe Mosconi (I)

R T I C O
N V E N U

19,30

L I R I C O
20,30

Sessione Specialistica

Sessione Interattiva

25

4 C O N G R E S S O F E C AVA S C I VA C

Treatment of canine leishmaniosis with


Amphtotericin B (Fungizone): four years
later - Jacques Lamothe (F)

Venerd Pomeriggio 19 Giugno 1998

Rick LeCouteur (USA)


e Simon Wheeler (UK)

Stephen Divers (UK)

14,30

A new drug for the teatment of canine leishmaniosis: Amphotericin B lipid complex
(Abelcet) - Jacques Lamothe (F)

Leonardo Brunetti (I)

RELAZIONE SULLO STATO


DELLARTE
Trattamento demergenza e
stabilizzazione medica dei rettili (60)

Protective effect of an insecticidal spray


against Phlebotomus perniciosus , a vector
of leishmaniasis - Frederic Ascher (F)

PROGRAMMASCI
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

ONCOLOGIA
Chairman:
Claudio Capurro

EPATOLOGIA
Chairman:
Marco Caldin

OFTALMOLOGIA
Chairman:
Alberto Crotti

Recenti applicazioni e
interpretazioni degli esami
epatici (60)

Segni oculari di patologie


sistemiche nel gatto (60)

Denny Meyer (USA)

Ellen Bjerkas (N)

8,30 RELAZIONE SULLO STATO


DELLARTE
La chemioterapia da un punto
di vista pratico (60)
Guillermo Couto (USA)

Sabato Mattina 20 Giugno 1998

9,30

Guillermo Couto (USA)


10,30

DERMATOLOGIA
Chairman:
Antonella Vercelli

Gli effetti delle patologie


extra-epatiche sul fegato
(60)

Trattamento delle ulcere


corneali nei piccoli animali
(60)

Denny Meyer (USA)

Complicazioni della
chemioterapia ed emergenze
oncologiche (60)

Simon Petersen-Jones (UK)

EPATOLOGIA
Chairman:
Ugo Lotti

Dominique Heripret (F)

OFTALMOLOGIA
Chairman:
Adolfo Guandalini

La biopsia epatica: quando e come


eseguirla alla luce di una corretta
interpretazione del referto clinico (60)
Quando il clinico e il patologo hanno
bisogno luno dellaltro

Modificazioni oculari
nellanimale anziano
(60)

Denny Meyer (USA)

11,00 Manifestazioni dermatologiche


di patologie sistemiche
(60)

Claudio Peruccio (I)


R

12,00
Patologie cutanee da
micobatteri (60)

Novit nellapproccio
terapeutico alle patologie
del fegato (60)

Denny Meyer (USA)

Luis Ferrer (E)


13,00

Lussazioni della lente (60)

Stefano Pizzirani (I)

Livello di Aggiornamento

Livello Avanzato

26

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

DERMATOLOGIA
Chairman:
Alessandra Fondati

ORTOPEDIA
Sessione specialistica
Chairman: Piermario Piga

NEUROLOGIA
Chairman: Stefano Pizzirani (I)

Discussione clinico-patologica
di casi dermatologici (120)

Progressi nel trattamento delle


pi frequenti patologie
ortopediche
Il metodo di Ilizarov in ortopedia dei piccoli animali: dallanalisi retrospettiva alle possibilit
per il futuro (60)
Antonio Ferretti (I)
e Matteo Tommasini (I)

Atypical behaviour of a nasopharyngeal


polyp causing a vestibular syndrome in a
cat - Marco Bernardini (I)

CITOLOGIA
Chairman:
Davide De Lorenzi

Tre casi di cisti aracnoidee nel


cane: valutazione a lungo termine
del protocollo terapeutico
Stefano Romussi (I)

CHIRURGIA DEI TESSUTI MOLLI


Sessione interattiva
Chairman: Carlo Scotti

Citologia pratica per il


veterinario.
Dalla corretta preparazione
allinterpretazione dello
striscio citologico (120)

9,30

GM 1 - Gangliosidosis in Alaskan
Huskies
Andreas Moritz (CH)

Daniele Cotto (I)


e Gianluca Rovesti (I)

A case of canine central diabetes insipida caused by a chromophobe cell adenoma of the hypophysis
J.H. Duarte Correia (P)

Problemi in chirurgia toracica


(120)
Da una discussione interattiva di
casi clinici lanalisi dei principali
problemi riscontrati dal veterinario
nellesecuzione delle tecniche di
chirurgia toracica
R

10,30

CARDIOLOGIA
Chairmen: Claudio Bussadori (I)
e Chris Lombard (CH)
Electrocardiographic features of
Deerhounds - A.R. Bodey (UK)

11,00

Valutazione dellanestesia generale con


propofol in cani normali e con
compromesse funzioni cardiorespiratorie
Antonello Bufalari (I)
Clinical trial of pimobendan: a new
inotropic/vasodilator drug: Long term
survival time study: the results
D. Bruyre (B)
Correlazione tra dilatazione atriale sinistra,
peso corporeo ed insorgenza della
fibrillazione atriale nel cane
Carlo Guglielmini (I)

12,00

Clinical efficacy of the new inodilator


pimobendan, in comparison to digoxin for
the treatment of congestive heart failure in
dogs - Rainer Kleeman (D)

ellArte

Percutaneous balloon valvuloplasty in


dogs with pulmonic stenosis
M Schneider (D)

Dan Smeak (USA)


e Richard A. White (UK)

Corinne Fournel (F)

Sessione Specialistica

Sessione Interattiva

27

13,00

4 C O N G R E S S O F E C AVA S C I VA C

Vercelli/Schiavi
Noli/Fabbrini
Mechelli/Galeotti
Noli/Scarampella
Tieghi/Abramo

Neurological findings in Cocker


Spaniels with familial vitamin E deficiency and retinal pigment Epithelial
Dystrophy - Rodolfo Cappello (I)

Sabato Mattina 20 Giugno 1998

*
Hills
Fissazione con chiodo
bloccato: un nuovo metodo di
fissazione ossea nei piccoli
animali (60)

8,30

PROGRAMMASC
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

DERMATOLOGIA
Chairman:
Chiara Noli

EMATOLOGIA
Chairman:
Marco Caldin

NEUROLOGIA
Chairman:
Marco Bernardini

Linterpretazione dello striscio


ematico

Identificazione delle lesioni


neurologiche (localizzazione,
diagnostica per immagini
e altri esami)

14,30 RELAZIONE FECAVA


Patologie ungueali nei cani e
nei gatti: diagnosi e trattamento
(60)

Alterazioni morfologiche dei


globuli rossi e dei globuli
bianchi (120)

Prima parte:
Lesioni cerebrali (40)

Sabato Pomeriggio 20 Giugno 1998

Didier Carlotti (F)

15,30

*
Hills
Approccio diagnostico
allalopecia nel cane e nel gatto
(60)

Dominique Heripret (F)


16,30

Seconda parte:
Lesioni del midollo spinale (40)
Terza parte:
Lesioni a livello
neuromuscolare (40)
Rick LeCouteur (USA)
e Simon Wheeler (UK)

Bernard Feldman (USA)

DERMATOLOGIA
Chairman:
Alessandra Fondati
17,00 Reazioni cutanee da farmaco
(60)

MEDICINA INTERNA
Chairman:
Tommaso Furlanello
Febbre di origine sconosciuta
(60)

NEUROLOGIA
Chairman:
Donatella Lotti
Diagnosi e trattamento
dellepilessia nel cane e nel
gatto (60)

Guillermo Couto (USA)


Luis Ferrer (E)
Simon Wheeler (UK)
18,00
Prurito cronico nel cane e nel
gatto e impiego di farmaci
antiprurito (60)

Dominique Heripret (F)

Trattamento clinico
e chirurgico del paziente
con trauma spinale (60)
Infezioni recidivanti nel cane
(60)

Guillermo Couto (USA)

Rick LeCouteur (USA)

19,00

Livello di Aggiornamento

Livello Avanzato

28

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

UROLOGIA E
NEFROLOGIA
Chairman:
Claudio Brovida

CHIRURGIA DEI TESSUTI MOLLI


Sessione interattiva
Chairman:
Carlo Maria Mortellaro

ONCOLOGIA
Chairmen: Giorgio Romanelli (I)
e Claudio Capurro (I)

Utilit dellultrasonografia nella


diagnosi delle malattie delle
vie urinarie nel cane e nel
gatto (60)

Approccio al paziente con


patologie delle prime vie
respiratorie (120)

Su un caso di pseudocisti pancreatica


associata a carcinoma acinoso, pancreatite cronica e steatite multifocale necrotizzante in un gatto.
Andrea Boari (I)

14,30

Parametri istologici di prognosi nei tumori


mammari maligni della gatta
Cinzia Benazzi (I)

Claudio Bussadori (I)

A.R. Michell (UK)

Micrometastasi linfonodali nei tumori


mammari maligni della cagna
Giuseppe Sarli (I)
Valutazione dellerogazione locale di
cisplatino in un modello di carcinoma
mammario murino
Emanuela Morello (I)

Richard A. White (UK)

UROLOGIA E
NEFROLOGIA
Chairman:
Fabio Vigan

CHIRURGIA DEI TESSUTI MOLLI


Sessione interattiva
Chairman:
Giorgio Romanelli

Insufficienza renale acuta:


dallemergenza alla
stabilizzazione del paziente
(60)

Claudio Brovida (I)

Chirurgia plastica ricostruttiva


(120)
I concetti pratici per una corretta
applicazione dei principi della
chirurgia plastica ricostruttiva
dallanalisi di casi clinici

Pericardiectomia toracoscopica per il


trattamento della pericardite effusiva
recidivante: prime esperienze in due
casi - Fabio Acocella (I)

A.R. Michell (UK)

ellArte

17,00

Evaluation of Valtrac biofragmentable


anastomosis ring on thoracal esophagus in the dog - T. Nmeth (H)
Systemic response of blood inflow
occlusion to the liver in dogs
Jani Pecar (SI)

Trattamento della contrattura in flessione


del carpo mediante la tecnica di Ilizarov:
4 casi - Gianluca Rovesti (I)
Bone defects in dogs treated by a new
tissue transplantation
Nenad Sesic (Croatia)

Dan Smeak (USA)

18,00

Clinicopathological features of multiple


cartilaginous exostosis in three littermate dogs - M. Novales (E)

Approccio terapeutico alle


patologie renali (60)

16,30

CHIRURGIA E ORTOPEDIA
Chairmen: Carlo Scotti (I) e
Aldo Vezzoni (I)

Medial approach for Total Hip


Replacement in Dogs: an experimental
study - Z. Diszegi (H)

15,30

Sessione Specialistica

19,00

Sessione Interattiva

29

4 C O N G R E S S O F E C AVA S C I VA C

Parametri istologici di prognosi nei tumori


mammari maligni della cagna
Marco Galeotti (I)

Tecniche diagnostiche
impiegabili per il
riconoscimento precoce delle
patologie renali (60)

Sabato Pomeriggio 20 Giugno 1998

Integrazione dei parametri clinici ed istologici nella prognosi dei tumori mammari
maligni della cagna e della gatta
Ombretta Capitani (I)

PROGRAMMASCI
SALA EUROPA 900

SALA ITALIA 350

SALA TOPAZIO 300

CHIRURGIA DEI TESSUTI MOLLI


Chairman:
Massimo Gualtieri

CARDIOLOGIA
Chairman:
Gino DAgnolo

NEUROLOGIA
Chairman:
Marco Bernardini

Tachicardia sopraventricolare
nel cane (60)

Patologie discali cervicali:


approccio diagnostico e
modalit di trattamento (60)

8,30 Concetti attuali nel trattamento


della peritonite (60)

Simon Wheeler (UK)


Dan Smeak (USA)

Domenica Mattina 21 Giugno 1998

9,30
RELAZIONE SULLO STATO
DELLARTE
Trattamento chirurgico delle
lesioni retto-anali, anali,
perianali e perineali (60)

CHIRURGIA DEI TESSUTI MOLLI


Chairman:
Carlo Maria Mortellaro

Patologie discali
toraco-lombari: diagnosi e
trattamento (60)

Stefano Pizzirani (I)

12,00

Richard A. White (UK)

CARDIOLOGIA
Chairman:
Claudio Bussadori

NEUROLOGIA
Chairman:
Massimo Baroni

Considerazioni terapeutiche
sulla cardiomiopatia dilatativa
del cane (60)

Patologie lombo-sacrali (60)

Karsten E. Schober (D)

Rick LeCouteur (USA)

Cardiomegalia nel gatto: cosa


fare dopo la diagnosi (60)

11,00 Approccio chirurgico alle patologie dellorecchio esterno e


dellorecchio medio (120)

13,00

Istruzioni per un approccio


ragionato alle extrasistoli
sullECG (60)

Cristophe Lombard (CH)

Gert Niebauer (A)


10,30

Karsten E. Schober (D)

La Sindrome di Wobbler:
considerazioni sul
trattamento (60)

Cristophe Lombard (CH)

Livello di Aggiornamento

Simon Wheeler (UK)

Livello Avanzato

30

Relazione sullo Stato de

IENTIFICO
SALA BIANCA 200

SALA BLU 120

SALA AZZURRA 100

ODONTOSTOMATOLOGIA
Chairman:
Dea Bonello

CITOLOGIA
Sessione specialistica
Chairman: Mario Caniatti

MEDICINA INTERNA
Chairmen: Tommaso Furlanello (I)
e A.R. Michell (UK)

Urgenze in odontostomatologia (60)

Citologia linfonodale:
quadri normali, infiammatori e
neoplastici (120)

Un caso di discinesia ciliare primaria


nel cane - Davide De Lorenzi (I)
Analysis of morbidity of dogs in the
region of the city Kosice, Slovakia
during 1995-1997 - M. Kozak (SK)

Frank Verstraete (B)

Preliminary results on the use of


cabergoline, a prolactin inhibitor, for
the control of mammary tumors in
the bitch before surgery
J. Verstegen (B)

Corinne Fournel (F)

ODONTOSTOMATOLOGIA
Chairman:
Simon Kleinjan
La radiologia come strumento
diagnostico delle patologie del
cavo orale (60)

ellArte

Incidence of atopic diseases


in dogs in Slovakia
Pavol Chandoga (SK)

10,30

Granulomatosi linfomatoide cutanea


primaria in un cane
Leonardo Della Salda (I)

Sessione Specialistica

12,00

Efficacy of terbinafine against


dermatophytosis in cats an open randomized blind study
(preliminary results)
R. Wagner (A)

Guillermo Couto (USA)

11,00

Efficacia delle permetrine CIS:


Trans 25/75 microincapsulate
nella terapia delle otoacariasi
in cani e gatti
Fabrizio Fabbrini (I)

Le leucemie (60)

Linfomi extranodali nel cane e


nel gatto (60)

Tavola rotonda su casi clinici


Etica, limiti e compromessi nel
trattamento delle malocclusioni (60)

DERMATOLOGIA
Chairmen:
Alessandra Fondati (I) e
Luca Mechelli (I)

Guillermo Couto (USA)

Dea Bonello (I), Thomas Eriksen


(DAN), Peter Fahrenkrug (D),
Frank Verstraete (B),
Aldo Vezzoni (I)

ONCOLOGIA
Sessione specialistica
Chairman:
Claudio Capurro

Frank Verstraete (B)

*
Hills

9,30

Prolactin and antiprolactinic drugs in


dogs and cats: relative efficacy and
mode of action of the veterinary available drugs - J. Verstegen (B)

Aggiornamenti in odontoiatria
felina (60)

Sessione Interattiva

31

13,00

4 C O N G R E S S O F E C AVA S C I VA C

Diagnosi di glomerulopatia nel cane:


valutazione qualitativa della proteinuria - Paola Scarpa (I)

*
Hills

Domenica Mattina 21 Giugno 1998

Comparative diagnostic imaging of


the pelvic cavity in dogs
Dieter Malleczek (A)

Frank Verstraete (B)

8,30

PROGRAMMASC
SALA ITALIA 350

SALA TOPAZIO 300

CHIRURGIA DEI TESSUTI MOLLI


Chairmen:
Carlo Maria Mortellaro
e Matteo Tommasini

Domenica Pomeriggio 21 Giugno 1998

SALA EUROPA 900

CARDIOLOGIA
Chairman:
Michele Borgarelli

NEUROLOGIA
Chairman:
Stefano Pizzirani

Meccanismi patogenetici e
trattamento delle patologie
pericardiche (60)

Neoplasie del Sistema


Nervoso Centrale (60)

14,30 RELAZIONE SULLO STATO


DELLARTE
Concetti attuali nel trattamento
della dilatazione-torsione di
stomaco nel cane (60)
Dan Smeak (USA)

Claudio Bussadori (I)


Rick LeCouteur (USA)

15,30
Polipi auricolari, otite media e
sinusite nel gatto (60)
Esperienze e metodi personali di
trattamento di queste frequenti
patologie chirurgiche del gatto

Dan Smeak (USA)


16,30

Ipertensione nel cane (60)


Una patologia difficile
da riconoscere e trattare

A. R. Michell (UK)

RELAZIONE SULLO STATO


DELLARTE
Aggiornamenti in chirurgia
spinale (60)

Simon Wheeler (UK)

S A L A
C E R I M O N I A
D I
C H I U S U R A
A R R I V E D E R C I
A
L

17,00

T E R M I N E

D E L

INCONTRA
Durante il Congresso, saranno organizzate sessioni di
approfondimento con i relatori, durante le quali i partecipanti potranno porre domande ai relatori.
Sar cos possibile approfondire un argomento o prolungare una discussione in un contesto rilassato ed informa-

Livello di Aggiornamento

Livello Avanzato

32

Relazione sullo Stato de

IENTIFICO
SALA AZZURRA 100

FARMACOTERAPIA
Chairman:
Enrico Febbo

ONCOLOGIA
Sessione interattiva
Chairmen: Claudio Capurro e
Richard A. White

ODONTOSTOMATOLOGIA
Chairmen: Dea Bonello (I) e
Frank Verstraete (USA)

Farmacoterapia pratica: dove possiamo arrivare con un uso pi ragionato dei farmaci a nostra disposizione?

Discussione interattiva da casi


clinici di oncologia
Questo un caso trattabile o
no? (120)
Da una discussione tra i relatori e
luditorio le linee guida pratiche
per un corretto approccio
terapeutico al paziente oncologico

Dalla farmacocinetica
allapplicazione clinica (40)
David Aucoin (USA)

Sialadenitis and salivary gland infarction in cats and dogs


Mahmut Sozmen (UK)

15,30

Utilizzo di una corona tipo Richmond per


la ricostruzione del canino inferiore in
un cane di razza Boxer
Paolo Squarzoni (I)
Estrazione di un canino superiore paratopico in un cane
Enrico Stefanelli (I)

Paolo Buracco (I)


e Giorgio Romanelli (I)

E U R O P A
E
C O C K T A I L
D I
L I O N E
N E L
1 9 9 9

14,30

Risultati del trattamento di 56 tumori


del cavo orale nel cane
Emanuela Morello (I)

Criteri di utilizzo dei punti di fulcro per gli


elevatori durante le estrazioni dentali nel
cane - Paolo Squarzoni (I)

Trattamento antibiotico
empirico nelle malattie infettive
del cane e del gatto (40)
David Aucoin (USA)
Recenti acquisizioni in tema di
trattamento con corticosteroidi (40)
Tommaso Furlanello (I)

Valutazione radiologica dei tumori


maligni non odontogenici del cavo
orale del cane - Dea Bonello (I)

16,30

C O M M I A T O :
! ! !
17,00

C O N G R E S S O

IL RELATORE

ellArte

le. Lelenco dei relatori e gli orari delle sessioni saranno inseriti nella cartella congressuale ed affissi presso gli stand dei main sponsor, grazie al cui sostegno la partecipazione alle sessioni gratuita anche se limitata ad un numero massimo di 15
partecipanti per sessione. Le iscrizioni avranno luogo presso la segreteria
Congressuale fino ad esaurimento dei posti disponibili.

Sessione Specialistica

Sessione Interattiva

33

4 C O N G R E S S O F E C AVA S C I VA C

SALA BLU 120

Domenica Pomeriggio 21 Giugno 1998

SALA BIANCA 200

COMMISSIONESC
COMMISSIONE SCIENTIFICA
Presidente

GIORGIO ROMANELLI
STEFANO BO
DEA BONELLO
CLAUDIO BUSSADORI
ALESSANDRA FONDATI
TOMMASO FURLANELLO
SIMON KLEINJAN
MASSIMO MILLEFANTI
CLAUDIO PERUCCIO
STEFANO PIZZIRANI
ALDO VEZZONI

Coordinatore Congressuale FULVIO STANGA


Segreteria Congressuale

Med Vet,
Med Vet
Med Vet
Med Vet,
Med Vet
Med Vet
DVM
Med Vet
Med Vet,
Med Vet,
Med Vet,

DECVS

DECVIM-CA

DECVO
DECVS
DECVS

Med Vet

LUDOVICA BELLINGERI

DIRETTIVI
Consiglio Direttivo
SCIVAC in carica

CARLO SCOTTI
GIORGIO ROMANELLI
PIERMARIO PIGA
UGO LOTTI
GILDO BARONI
MARCO CALDIN
MATTEO SPALLAROSSA

Presidente
Past President
Vice Presidente
Segretario
Tesoriere
Consigliere
Consigliere

Direttivo FECAVA
in carica

BEN ALBALAS
MARC BUCHET
RAY L. BUTCHER
SIMON KLEINJAN

Presidente
Vice Presidente
Segretario
Tesoriere

58

I componenti dei Consigli Direttivi della FECAVA


e della SCIVAC ringraziano le aziende che attraverso
la sponsorizzazione hanno sostenuto la realizzazione
del Programma Scientifico e del Programma Sociale
di questo Congresso.
Grazie al loro contributo si sono potute contenere
le quote di iscrizione congressuale.

MAIN SPONSORS

MAJOR SPONSORS

*
Hills

Animal Health

4th European FECAVA SCIVAC Congress

SPEAKERS CURRICULAE VITAE


DAVID AUCOIN
DVM, Dipl ACVCP
Dr. David Aucoin graduated in 1980 at the Michigan State
University. He then attended an Internship in Medicine and
Surgery in 1981 until 1983 at the Animal Medical Center of
New York. In 1985 he attended a Fellowship at the Cornell
University Medical College in Clinical Pharmacology. In
1984-85 he became Associate Staff Professor at the Animal
Medical Center in New York then Visiting Assistant Professor
at the North Carolina State University Raleigh from 1985 to
1990. From 1990 to 1992 he was Associate Research Professor at the same University. He is a Diplomate of the American College of Veterinary Clinical Pharmacology since 1992
and Board Qualified of the American College of Veterinary
Internal Medicine

ELLEN BJERKAS
DVM, PhD, Dipl ECVO
Graduated from the Norwegian College of Veterinary medicine in 1972. Associate Professor at the Norwegian College of
Veterinary Medicine. Head of the outpatient clinic and the
ophthalmology section.
1991: PhD degree. Thesis: Inherited eye diseases among dogs
in Norway. Founding member of the Norwegian panel for diagnosing inherited eye diseases. ECVO Diplomate.

CLAUDIO BROVIDA
Med Vet
Graduated in Veterinary Medicine at the University of Turin
in 1974. He has always been a small animal private practitioner with main interest in urology/nephrology and respiratory tract. He has spent long periods of updating in veterinary
medicine in Great Britain, Holland and USA. Author of articles on national and international scientific reviews and
speaker at veterinary conferences. He has been President of
AIVPA, President of the Organising Committee of the 7th
WSAVA Congress held in Rome in 1992. Currently he is vice
President of WSAVA.

LEONARDO BRUNETTI
Med Vet
Graduated in Veterinary Medicine at the University of Pisa in
1982. His interest has always been on Exotic Animals and he
has spent many years carrying out researches in numerous

zoos in Italy and abroad. He has attended the Italian edition


of a book on anaesthetics on wild animals and is author of scientific papers on exotic animals. For many years he has been
co-ordinator of the SCIVAC Exotic Animal Study Group.

PAOLO BURACCO
Med Vet
Graduated in Veterinary Medicine at the University of Turin
in 1981. In 1987/88 he was Visiting Professor at the School
of Veterinary Medicine of the Purdue University (Indiana,
USA) in the Comparative Oncology Group. Since November
1992 he is Associate Professor of Semiotics Surgery at the
University of Turin. He has been speaker at numerous national and international meetings on veterinary oncology and his
main interests are on early diagnosis of primitive animal tumours, of their metastasis and of the most effective treatments. He therefore studies mainly skeletal, oral, endonasal,
endothoracic and cutaneous neoplasias. He is author of 89 papers, including congress communications and papers published on national and international veterinary journals.

CLAUDIO BUSSADORI
Med Vet, Dipl ECVIM
Graduated in Veterinary Medicine at the University of Milan
in 1982. He is a private practitioner and consultant in cardiology and has carried out numerous cardiological researches for the Universities of Turin and Parma where he has also
been lecturer. His main researches are on lung and systemic
hypertension, treatment of congenital cardiopathies, experimental echocardiography and cardiac tumours. He is a Diplomate of the European College of Internal Medicine (ECVIM)
and since 1990 he is Study Director of international research programmes on the use of cardiovascular drugs in veterinary cardiology.

MARCO CALDIN
Med Vet
Graduated in Veterinary Medicine at the University of
Bologna with a thesis on Instrumental Diagnosis in Small
Animal Cardiology. He has been the co-ordinator of SCIVAC Study Group on Imaging Diagnostics from 1988 to
1990. He has been speaker at numerous meetings, practical
courses and seminars as well as lecturer at the University of
Pisa and University of Padova. He has also been SCIVAC
Board member and co-ordinator of SCIVAC Study Group on

Internal Medicine. He is a private practitioner in Padova at the


San Marco Veterinary Clinic.

MARIO CANIATTI
Med Vet
Graduated in Veterinary Medicine at the University of Milan.
In 1990-1994 he worked at the University of Milan in the department of Veterinary Pathologic Anatomy
and Avian
Pathology. In 1994 he became researcher at the University of
Milan. From September 1988 to March 1989 he carried out a
research work at the University of California (Davis) at the
Department of Pathology on immunoistochemicals of cutaneous neoplasias in the dog with Professor Peter F. Moore. In
April/May 1989 he stayed at the University of Barcelona for
a research work on immunistochemicals of cutaneous tumours.
His current research work is on diagnostic cytology, comparative pathology of cutaneous neoplasias of linphoproliferative
diseases. He has published over 40 scientific articles on Italian and international scientific journals.

DIDIER CARLOTTI
DVM, Dipl ECVD
Dr. Didier Carlotti graduated from Toulouse University in
1977 and has been a private practitioner in Carbon Blanc, near
Bordeaux, Aquitaine, France since 1979. He has been a full
member of the AAVD since 1985 and was the President of
the French Small Animal Dermatology Study Group
(GEDAC) from 1985 to 1991. The GEDAC is a specialised
group of the French Small Animal Veterinary Association
(CNVSPA), of which he was the representative at WSAVA
since 1985 and Vice-President since April 1989 until April
1993. He is currently the General Secretary of CNVSPA. He
was also the Chairman of the Federation of European Companion Animal Veterinary Associations (FECAVA) from May
1990 to June 1995. He is a founder Member and Past President (1988-1990) of the European Society of Veterinary Dermatology (ESVD). He is a Diplomate (and currently the honorary secretary) of the European College of Veterinary Dermatology (ECVD). He has published about 50 papers and has
given numerous lectures in the field of Veterinary Dermatology.

GUILLERMO COUTO
DVM, Dipl ACVIM
Graduated from Buenos Aires University in 1976. From 1976
to 1981 he was Assistant Professor at the Department of
Pathology of the same University. He attended a Residency on
Clinical Oncology at the University of California, Davis from
1981 to 1983 and for the following 5 years he was Assistant
Professor at the Ohio State University Department of Veterinary Clinical Sciences. He then became Associate Professor
at the same University and from 1995 he is Professor at the
Department of Veterinary Clinical Sciences of the Ohio State

4th European FECAVA SCIVAC Congress

University.
Moreover he is Charter Diplomate of the American College of
Veterinary Internal Medicine, Specialty of Veterinary Medical
Oncology, co-editor of Essentials of Small Animal Internal
Medicine, Editor in Chief of the Journal of Veterinary Internal
Medicine and has over 150 scientific publications in the areas
of oncology, haematology and immunology.
He was President of the Veterinary Cancer Society from 1990
to 1992.

LORENZO CROSTA
Med Vet
Graduated in Veterinary Medicine at the University of Milan
in 1989 with a thesis on avian diseases. He is member of the
Association of Avian Veterinarians and has attended various stages in avian clinics abroad.
Author of papers at international avian meetings and organiser of practical courses and seminars for SCIVAC and for the
University of Milan. His current interest is exclusively in
avian medicine with a particular interest in problems linked to
breeding in captivity. The preferred species are parrots, eagles
and ostriches. He is one of the founders of Clinica Veterinaria Fiera, a private practice in Milan.

STEPHEN J. DIVERS
BSc (Hons), BVetMed, CBiol, MIBiol, MRCVS
Dr. Stephen Divers achieved a bachelor of Veterinary Medicine degree (BVetMed) at the Royal Veterinary College, University of London in 1994 with a distinction in the exotic animal elective. He has been lecturer on MSc degree course in
Wild Animal Medicine at the London Zoo and lecturer on the
final year elective at the Royal veterinary College (small animals, reptile pharmacology, reptile therapeutics and reptile
anaesthesia). Dr. Divers has been speaker at numerous national and International Meetings and is author of over 50 articles mainly on reptile medicine.

BERNARD F. FELDMAN
DVM, PhD, Dipl ACVIM
Dr. Bernard F. Feldman is currently Professor of Veterinary
Clinical Haematology and Biochemistry at the Virginia
Maryland Regional College of Veterinary Medicine (VMRCVM). He is formerly Professor of Veterinary Clinical
Pathology at the University of California at Davis. Dr. Feldman has received numerous teaching and research awards, has
published 3 books and over 250 articles. He has been on the
faculty at the Veterinary College of the University of Utrecht,
The Netherlands, and the Royal Veterinary College in Copenhagen, Denmark. He was recently nominated as Outstanding
Alumnus (1997) of the University of California at Davis,
School of Veterinary Medicine. Currently he is Chief of Laboratory Diagnostics Services and Director of the Clinical
Pathology Laboratory at the VMRCVMs Veterinary Medical
Teaching Hospital. Dr. Feldman is President of the American

4th European FECAVA SCIVAC Congress

Society for Veterinary Clinical Pathology and on the Board of


Directors of the Veterinary laboratory Association.

LUIS FERRER
DVM, PhD, Dipl ECVD
Graduated in Veterinary Medicine in 1981 in the Veterinary
School of Zaragoza (Spain) and obtained the PhD in 1984 in
the Veterinary School of Hannover (Germany). Since 1984 he
is Professor of Pathology and Dermatology in the Veterinary
School of Barcelona (Spain). His major research lines are dermopathology, canine leishmaniosis and the role of mast cells
in canine allergic dermatitis.

ANTONIO FERRETTI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Milan
in 1979. He is a private practitioner and has always carried out
researches on small animal surgery especially Orthopaedics
and Traumatology. In 1982 he began studying the Ilizarov
Method and the year after he started its application. In 1988
and 1991 he spent time with Prof. G.A Ilizarov at the Orthopaedic and Traumatological Institute of Kurgan in Siberia
to deepen the knowledge on his method. Since 1993 he is a
Diplomate of the European College of Veterinary Surgeons
and is SCIVAC co-ordinator of the orthopaedics study group.
He is currently a veterinary surgeon in a private practice near
Milan.

speaker at numerous SCIVAC national meetings and seminars on internal medicine which represents his scientific and
professional interest. He has been instructor at SCIVAC Practical Courses on Laboratory Diagnostics and Problem Oriented Clinical Approach. He is co-author of SCIVAC Therapeutical Manual. He is author of numerous scientific papers and
has been speaker also at international meetings. He has been
lecturer in Infectious Diseases in the Dog and Cat at the University of Padova in the years 1996-1997.

ADOLFO GUANDALINI
Med Vet
Graduated in Veterinary Medicine in 1998 with honours at
the University of Perugia. In 1990/1991 he attends an Internship in Veterinary Ophthalmology at the National Veterinary
School of Lyon. In 1993 he is Visiting Assistant Professor at
the College of Veterinary Medicine, Ophthalmology Department of the University of Florida. From 1991 to 1997 he attends externships at: Animal Eye Associates (Chicago, Illinois), Animal Ophthalmology Clinic (Dallas, Texas), Ohio
State University, Sacramento Animal Medical Group (Sacramento, California), Veterinary Ophthalmology Services (Warwick, Rhode Island), University of North Carolina at Chapel
Hill. He is author and co-author of various scientific paper on
veterinary ophthalmology . Since 1993 he is Board member of
SOVI (Italian Association of Veterinary Ophthalmology). He
has been Board member for abroad of AIVPA in 1993/1996.

HERMAN A. W. HAZEWINKEL
DVM, PhD, Dipl ECVS
CORINNE FOURNEL-FLEURY
DVM, PhD
In 1978-1980 she was Resident in Internal Medicine and in
1981 to 1986 she has been Assistant Professor in Internal
Medicine and in 1991 she became Professor. 1993 she became
Chief Internal Medicine Service/Domestic carnivores at the
National School of Veterinary Medicine Lyon, France. She
has had an intense clinical laboratory activity starting in 1988
with the creation and direction of the Immunopathology - Cytology - Haematology Diagnostic and Research Laboratory
and in the same year achieved the specialised studies certificate in immunology and immunopathology. In 1989 she specialised in General Haematology and in 1990 in Cellular Biology Methods and achieved a Masters in Immunology and
haematology biological sciences. Her PhD in 1996 was on
Morphological and Phenotypical characterisation of canine
lymph node lymphoid cells. Application to the study of canine
non-Hodgkin lymphomas.

TOMMASO FURLANELLO
Med Vet
Graduated in Veterinary Medicine at the University of
Bologna in 1991. He is a small animal private practitioner at
the Clinica Veterinaria San Marco. Since 1992 he has been

Graduated in 1976 at Utrecht University. After working in private practice he joined the Universitys Department of veterinary Sciences in Companion Animals. Responsible for education and treatment of referred orthopaedic patients, he became interested in nutritional and hormonal related skeletal
diseases. He is member of AO-Vet, Diplomate of the European College of Veterinary Surgeons, Board member of the
European Society for Veterinary Orthopaedics and Traumathology, and chaired the organisation of the annual congress of
the European Society for Veterinary and Comparative nutrition.

DOMINIQUE HERIPRET
DVM, Dipl ECVD
Dr. Heripret graduated from the Vet School of Maisons Alfort
in 1981, he then completed a PhD on Use of skin-tests in the
diagnosis of FAD: about 169 cases. From 1987 to 1994 he
worked at the referral practice Clinique Fregis in France
where he was in charge of the internal medicine service mainly of dermatology and endocrinology. In 1990 he was Member of the scientific comity of GEDAC (French Dermatology
Group) and in 1991 he was secretary of the same group. In
1992 he was Board member (Treasurer) of the ESVD and in
1996 he became Diplomate of the European College of Vet-

erinary Dermatology. He has done more than 75 presentations and his main interests include Endocrinology, Non
steroid antipruritic drugs and hypersensitivity in dermatology.

RICHARD LeCOUTEUR
BVSc, VMD, PhD, Dipl ACVIM (Neurology), Dipl
ECVN
Rick graduated from the University of Sydney in Australia
in January 1975. After a year in private small animal practice in Sydney, he completed an Internship and Residency in
Surgery at the University of Guelph in Canada in 1976-78.
He then completed a Residency in Neurology and Neurosurgery at the University of California Davis from 1978 to
1980. From July 1980 through January 1984, Rick completed a PhD in Comparative Pathology at the University of California in Davis. The area of Study was spinal Cord Injury.
From 1984 to June 1988 he was on faculty at Colorado State
University, where he was an Assistant Professor and then
Associate Professor until 1989. In September 1989 he returned to Australia to establish a Specialty Practice in Neurology and Neurosurgery in Sydney. In January 1995 he returned to the USA to assume the position of Professor in
Neurology and Neurosurgery at the University of California
at Davis.
he is Diplomate of the American College of Veterinary Internal Medicine (Neurology) and a Diplomate of the European College of Veterinary Neurology. He is currently President of the ACVIM Specialty in Neurology.

CHRISTOPHE LOMBARD
DVM, Dipl ACVIM, Dipl ECVIM
Dr. Christophe Lombard graduated in 1971 at the University of Zurich Switzerland. From 1972 to 1974 he attended a
Residency in Physiology at the University of Zurich - College of Veterinary Medicine - from 1975 to 1977 a Residency in cardiology at the University of Pennsylvania, Philadelphia followed by a Residency of another two years in Internal Medicine at the same University. He then started in 1978
his career as Assistant and Associate Professor of Medicine
and Cardiology at the College of Veterinary Medicine of the
University of Florida Gainesville until 1991. Since 1991 and
presently he is Professor of Medicine at the College of Veterinary Medicine at the University of Bern/Switzerland. His
special interests cover clinical cardiovascular medicine especially echocardiography. The Specialty Boards he is currently in are ACVIM and ECVIM-CA. He has currently 67
scientific publications and bookchapters in various professional journals.

GEORGE LUBAS
Med Vet
Graduated in Veterinary Medicine at the University of Pisa
in 1975 where he also specialised in Small Animal Diseases
in 1977.

4th European FECAVA SCIVAC Congress

In 1979 he became Assistant Professor and since 1983 he is


Associate Professor of Comparative Haematology at the
University of Pisa. Since 1985 he is also Professor of Genetics in the Specialisation Section of the University of Pisa.
He is author and co-author of about 150 papers on immunohaematology and clinical haematology in the dog, cat ,
horse and cattle. He has been speaker at numerous veterinary
conferences, meetings, seminars and practical courses on the
above topics.

LUCA MECHELLI
Med Vet
Graduated in Veterinary Medicine at the University of Pisa
in 1981. In 1982-83 he was Resident at the Institute of Veterinary Medicine, University of Perugia and in 1984-85 Veterinary Pathologist at the Ministry of Health in Rome. In the
years 1986-90 he was an instructor pathologist at the Institute of Veterinary Medicine of the University of Perugia and
since 1991 he is teaching general pathology at the Institute
of Veterinary Medicine, University of Perugia. Author of
over 65 scientific papers and reviews on many aspects of
companion animal dermopathology and oncology.

DENNY MEYER
DVM, Dipl ACVP, Dipl ACVIM
Dr. Denny Meyer received a BS and DVM from the University of Minnesota in 1970 and 1972, respectively, followed
by an Internship and Residency in Small Animal Medicine
at the University California-Davis. While at the University
of Florida (1976-1989), he was granted tenure as an Associate Professor , served as Service Chief for both Small Animal Medicine and Clinical Pathology, achieved Diplomate
status in both the American College of Veterinary Internal
Medicine and the American College of Veterinary Pathologists. This was followed by a career in industry; Associate
Director of Veterinary Affairs-Hills Pet Products and Director of Clinical Pathology and safety Pharmacology-Smith
Kline Beecham Pharmaceuticals (appointments in both the
US and UK). Upon return to academia at the Colorado State
University as Professor of Pathology, he served as Service
Chief-Clinical Pathology and was awarded the Carl J. Norden Distinguished Teaching Award which complemented six
prior teaching awards at the University of Florida. Currently he is a Senior Clinical Pathologist at IDEXX Veterinary
Services/California Veterinary Diagnostics. In addition to
more than 70 scientific papers and book chapters, he is an
author of Veterinary Laboratory Medicine-Interpretation and
Diagnosis and is a co-author on Strombecks Small Animal
Gastroenterology, 3rd edition. He has given more than 100
invited lectures. He has served as President of the Comparative Gastroenterology Society and established the Veterinary Liver Study Group. He recently completed terms as Associate Editor of the Journal of Veterinary Internal Medicine
and member of the editorial Board-Veterinary pathology
Journal. His clinical and investigative interests are haematology, cytopathology, hepatic histopathology, and the

4th European FECAVA SCIVAC Congress

pathophysiology of hepatic disease.

nicians (C.E.F.A., IRECOOP, ITTIOCONSULT, AIVPA,


SCIVAC etc.).

A R MICHELL
DSc, MRCVS

GERT NIEBAUER
Med Vet, PhD, MS, Dipl ECVS

Professor Michell has recently joined the AHT from the Royal Veterinary College (University of London) where he was
Professor of Applied Physiology & Comparative Medicine.
He is a former President of the Association of Veterinary
Teachers & Research workers and a current member of the
Council of the British Veterinary Association and the Royal
College of Veterinary Surgeons. He received the Blaine
Award from the BSAVA in 1991 and shared the George Fleming Prize in 1992. His main interests are the physiology and
clinical disturbances of fluids, electrolytes and acid-base balance and the links between renal disease, salt intake and hypertension.

Gert Niebauer has been professor of Surgery at the Small Aninmal Department of the Pennsylvania University at Philadelphia. He is author of numerous scientific publications and
various chapters of Surgery texts including the latest edition
of the Slatter. He is Diplomate of the European College of
Veterinary Surgeons of which he is also Chairman of the Credentials Committee.

MASSIMO MILLEFANTI
Med Vet
Graduated in Veterinary Medicine at the University of Milan
in 1982. He is a private practitioner near Milan. His main interests have always been on Exotic Animals especially on rodents, reptiles and fishes. In 1987 he helped with the birth of
SCIVAC Study Group of Medicine and Surgery of Exotic
Animals of which he is currently the co-ordinator since 1995.
He has been speaker at meetings, seminars and practical
courses and has written articles for journals, a book on iguanas and one on diseases of ornamental fishes. He has also
been invited to TV shows and radio broadcasts.

PIERRE MONTAVON
DVM
Prof. Pierre Montavon graduated at the University of Zurich
and then attended a Residency from 1979 to 1985 at the Ohio
State University Department of Clinical Sciences were he
then became Assistant Professor. In 1985 he entered The University of Zurich as Assistant and then as Lecturer and since
1994 he is Professor at the Surgery Clinic of the University of
Zurich. Since 1980 he has been instructor at the AO Vet
Courses in Davos, Waldenburg, Courcheval , Cremona,
Columbus and Zurich. He is currently author of over 30 original articles published in National and International Journals.

GIUSEPPE MOSCONI
Med Vet
Graduated in Veterinary Medicine at the University of
Bologna in 1978 and in 1979 started working as fish pathologist at the EUROAQUARIUM of Bologna where he is currently brand manager. He attended two intensive courses
(1981-1983) at the University of Hobenheim of Stuttgart on
ornamental fish pathology. He has been speaker at numerous
post-degree courses for veterinarians, biologists and fish tech-

CLAUDIO PERUCCIO
Med Vet, Dipl ECVO
Graduated in Veterinary Medicine at the University of Turin
in 1970 with honours. Specialised in small animal diseases in
1974 at the University of Milan with the highest marks discussing a thesis on surgery of cataract in the dog. Since 1974
he is employed at the University of Turin at first as Researcher
then as Associate Professor. His main interest is small animal
veterinary and comparative ophthalmology. Since 1987 is Adjunct Associate Professor at the Department of Clinical Medicine, College of Veterinary Medicine, University of Illinois,
USA. Since 1993 he is a Diplomate of the European College
of Veterinary Ophthalmologists of which currently he is Vice
President. Speaker at numerous national and international
meetings and author of 130 papers and numerous text books.
Secretary, Vice-President and President of AIVPA in the years
1978-1984; Secretary, Vice-President, President and PastPresident of ISVO (International Society of Veterinary Ophthalmology) from 1980 to 1994; President of SOVI (Italian
Society of Veterinary Ophthalmology affiliated to SCIVAC)
since 1989; he has been Vice-President of SINVET. He has
been in SCIVAC Board and has been director of numerous
national and international veterinary journals.

SIMON M. PETERSEN - JONES


DVetMed, DVO, Dipl ECVO, MRCVS
He completed his undergraduate and ophthalmology residency training at the Royal Veterinary College, London and was
awarded a Doctorate of Veterinary Medicine in 1990. He
holds Ophthalmology specialist qualifications from the Royal
College of Veterinary Ophthalmologists. From 1998 to 1994
he was a lecturer in Veterinary Ophthalmology at the Royal
(Dick) School of Veterinary Studies, Edinburgh. Currently he
is conducting a research into the molecular genetics of generalised progressive retinal atrophy at the Veterinary University
of Cambridge. Additionally he is the current Chief Panellist of
the British Veterinary Association/Kennel Club Eye Scheme
and also runs a private ophthalmology referral service.
In 1994 he was awarded the BSAVA Simon Award for outstanding contributions in the field of veterinary surgery and
also a Pfizer Academic Award for young British research scientists. He is a co-editor of the successful BSAVA Manual of

Small Animal Ophthalmology.

STEFANO PIZZIRANI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Pisa
in 1979. In July 1993 he became a Diplomate of the European College of Veterinary Surgeons. Founder in 1984 of
SCIVAC where he has been Board Member (1985-86),
Vice-President ( 86-87), President (87-89), President senior
(89-91). He has spent various periods of updating in neurology at the Veterinary Teaching Hospital of the Colorado
State University; in ophthalmology at the Cornell University of the State of New York and in small animal surgery at
the North Carolina State University. His main interests are
in ophthalmology, neurology and small animal surgery. He
has been speaker in more that 50 occasions at national and
international meetings and seminars on ophthalmology, neurology, orthopaedic surgery and leishmaniosis. he is author
and co-author of articles, manuals and is co-translator of the
Handbook of Small Animal Orthopaedics and fracture
treatment.

ADAM RIJNBERK
DVM, PhD
Ad Rijnberk graduated from the Faculty of Veterinary Medicine of Utrecht University in 1962. In 1971 he completed a
thesis entitled Iodine metabolism and thyroid disease in the
dog. In 1973 he became reader and in 1976 professor of
companion animal medicine at Utrecht University. Over the
years his research interests have concentrated on endocrine
diseases in dogs and cats, with currently some emphasis on
the pathophysiology of the pituitary-adreno-cortical axis and
of growth hormone release at pituitary and extra-pituitary
sites.
Ad Rijnberk is Diplomate of the European College of Veterinary Internal Medicine-Companion Animals. In 1986 he was
awarded the Walter Frei Preis of the University of Zurich and
in 1993 he received the Scientific Achievement Award at the
18th World Congress of the World Small Animal Veterinary
Association.

4th European FECAVA SCIVAC Congress

has spent various periods at the University of Cambridge


(UK), North Carolina (USA) and Purdue-Indiana (USA).

GIANLUCA ROVESTI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Parma
in 1982. Since 1983 he has been working in a private practice
for dogs and cats where he is mainly involved in surgery, with
a particular interest in orthopaedics, neurology and ophthalmology. In 1992 he spent time at the Colorado State University in the Small Animal Surgery Department, in 1993 at the
University of Zurich - Surgery Session of the Kantonales Tierspital and in 1997 at the North Carolina State University
Small Animal Surgery, Veterinary Teaching Hospital. He has
been speaker and instructor at SCIVAC AO/ASIF Courses,
at the SCIVAC Course on Total Hip Replacement in the Dog
with Prof. Bardet and Prof. Matis held in January 1997, speaker at SCIVAC Course on Surgery of Limb Distal Extremities
with Prof. Jon Dee. He is a Diplomate of the European College of Veterinary Surgeons since June 1997.

ROBERTO SANTILLI
Med Vet
Graduated in Veterinary Medicine at the University of Milan
in 1990. In 1991 he attended a specialisation course on small
animal cardiology at the University of Turin and then started his updating periods in small animal cardiology at the
North Carolina State University, Ohio State University, University of California (Davis) and Cornell University. He is a
private practitioner in a small animal veterinary clinic near
Milan. he is an instructor at SCIVAC practical courses on
small animal cardiology and abdominal ultrasonography. Author of articles on ultrasonography and echocardiography.
His main research is on feline cardiomiopathies and has presented at an annual congress of the European Society of Veterinary Internal Medicine the results of a study on the diastolic
functions in feline cardiomiopathies through the doppler
method.

KARSTEN E. SCHOBER
DVM
GIORGIO ROMANELLI
Med Vet, Dipl ECVS
Graduated in Veterinary Medicine at the University of Milan
in 1981. Immediately after the graduation he carries out a
research on experimental surgery on the transplantation of
the heart and of the pancreas. He is a small animal private
practitioner in Milan and his main interests are on general
and orthopaedic surgery and surgical and medical oncology.
He is a Diplomate of the European College of Veterinary
Surgeons since 1993 and has been SCIVAC President in
1993-1995 and is currently Chairman of the SCIVAC Scientific Committee.
Speaker at about 40 national and international meetings. He

Graduated at the Leipzig University in 1990 with a degree


thesis on Acid-base disorders in venous blood and erythrocytic hemolysate in dogs. From 1990 to 1991 he was scientific
assistant (Intern) at the small animal clinic of the University
of Leipzig and from 1991 to 1994 he was research student
(Resident) at the same University. He then won a grant Award
from the above mentioned university and went to attend a
clinical work at the Virginia Tech, Virginia Maryland Regional College of Veterinary Medicine, Small Animal Clinic,
Blacksburg USA. He then won another grant award of 12
months from the German Academic Exchange Service in
Bonn for postdoctoral scientific and clinical work on cardiology at the University of Edinburgh. From 1995 he is assistant

4th European FECAVA SCIVAC Congress

at the Small Animal Clinic, Faculty of Veterinary Medicine,


University of Leipzig.
He is author of several scientific publications and has been
speaker in numerous veterinary congresses.
His non professional interests are ornithology, music and art.

PETER W. SCOTT
MSc, BVSc, FRCVS
Peter W. Scott is a veterinarian with a special interest in
birds, fish, reptiles and amphibians. He is recognised by the
Royal College of Veterinary Surgeons as a Specialist in both
Zoo & Wildlife Medicine and Fish Health & Production
and in 1997 became Fellow of the RCVS in Psittacine Medicine.
Since doing field work in Kenya for his MSc, he has worked
with exotic species for 20 years. Since 1984 this has been
full time and now as the principal of the Zoo and Aquatic
Veterinary Group he works with many professional and keen
amateur aviculturists, plus many fish keepers and fish farms.
He is a member of the Association of Avian Veterinarians,
an ex-President of the British Veterinary Zoological Society
and Veterinary Adviser to several companies. He is the author of four books (on Axolotls, dogs, livebearing fishes, and
the latest The Complete Aquarium), an editor of three conference proceedings and a contributor to many other books
including four BSAVA Manuals related to exotic pets, Genus
Amazona, and Lories and Lorikeets. He established VETARK PROFESSIONAL, an animal health company dealing especially with exotic species, and also VETGEN EUROPE to provide diagnostic DNA probe technology to veterinarians.

DANIEL D. SMEAK,
DVM, Dipl ACVS
Graduated with Honours at the Michigan State University,
College of Veterinary Medicine in 1979. He then attended a
Small Animal Rotating Internship at the Colorado State University in 1980 and a Residency in Small Animal Surgery at
the Ohio State University College of Veterinary Medicine in
1983. He became Assistant Professor in Surgery at the Ohio
State University in 1984 and Professor in 1989. Since 1995
he is Professor of Surgery at the Ohio State University and
Chief of the Small Animal Surgery Section until 1997.
As far as publications are concerned he has 61 Peer reviewed articles authored, he is Co-editor of the book Disease Mechanisms in Small Animal Surgery, he is section editor of the Manual of Small Animal Practice and has 18
Book Chapters Authored.

FRANK J.M. VERSTRAETE


DrMedVet, BVSc, MMedVet, FAVD, Dipl AVDC, Dipl
ECVS
Frank Verstraete graduated as a veterinarian at the University of Gent (Belgium) in 1980. He pursued his graduate stud-

ies at the University of Pretoria (South Africa) where he


completed a residency in small animal surgery and became
board- certified in surgery in 1985. At Pretoria University
he started a Dental Clinic in 1982, which proved to be most
successful, and in 1988 he was appointed Associate Professor of Surgery and Head of the Small Animal Surgery Section.
Since the end of 1994, he is Chief of the Dentistry Service
at the School of Veterinary medicine of the University of
California at Davis. His main research interests are comparative dentistry and oral pathology.
He is charter fellow of the Academy for Veterinary Dentistry, a Diplomate of the American Veterinary Dental College (and current Secretary) and a Diplomate of the European College of Veterinary Surgeons. He is also a member of
the Organising Committee of the European Veterinary Dental College.

ALDO VEZZONI
Med Vet, SCMPA, Dipl. ECVS
Born in 1947 in the province of Cremona, North Italy, married with Franca in 1972, two sons, Dario 21 years old and
Luca 18 yeras old.
Degree in Veterinary Medicine in 1975, Veterinary School of
the University of Milan, with maximum score cum laude.
Specialisation degree in Small Animal Medicine in 1978,
Veterinary School of the University of Milan, with maximum score cum laude.
In 1976 starts his veterinary practice in Cremona where he is
still working with other two colleagues.
President of the Italian Small Animal Veterinary Association
(SCIVAC) in 1989-1991, member of its Board from 1984 to
1993, its national representative in FECAVA from 1989 to
1994, Chairman of its Scientific Committee from 1987 to
1993, Chairman of its Publication Committee from 1993.
Secretary of the European Society of Veterinary Orthopaedics and Traumatology (ESVOT) from 1993.
Board Certified by the European College of Veterinary Surgeon in 1993 in Cambridge, and Chairman of its PR Committee from 1994 to 1996.
Chairman of the Scientific Committe of the two Italian Scientific Meetings on Canine Heartworm Disease in 1988 and
in 1993.
Member of the Board of the Italian Federation of Veterinary
Orders (FNOVI) from 1994 to 1997 and its Secretary from
1997.
President of the Veterinary Order of the Province of Cremona since 1997.
Speaker in several national and international meetings on
parasitology (heartworm), orthopaedics, surgery and dentistry.
Editor and co-Author in 1987 of a book on canine heartworm disease La filariosi cardiopolmonare; co-Author in
1991 of Small Animal Drug Formulary, 2nd edition in
1995; italian editor of the following american books: 1990
Brinker, Piermattei and Flo Handbook of Small Animal
Orthopedics and Fracture Treatment , 1995 S.J.Plunkett
Emergency procedures for the small animal veterinarian,

10

1996 W.R.Fenner Quick reference to Veterinary Medicine,


1996 G.T.Wilkinson &R.C.Harvey Color atlas of small animal dermatology, 1998 S.I.Bistner & R.B.Ford Kirk and
Bistners Handbook of veterinary procedures & emergency
treatment.
Author of several papers on scientific journals on heartworm
disease and on small animal surgery and orthopaedics.

SIMON WHEELER,
BVSc, PhD, CertVR, Dipl ECVN, MRCVS
Graduated from the University of Bristol in 1981, Simon J.
Wheeler was appointed House Surgeon at the Glasgow University Veterinary School. Following a year in general practice in Wales, he was appointed Clinical/Research Assistant
in neurology at the Veterinary Royal College. He received a
Veterinary Research Training Scholarship from the Horserace
Betting Levy Board and a Grant from the BSAVA Clinical
Studies Trust Fund to pursue his interest in neurological disorders, particularly peripheral nerve and spinal conditions.
He was awarded PhD by the University of London in 1988.
From 1988-1992 he was assistant Professor of Neurology at
the College of Veterinary Medicine, North Carolina State
University. Currently he is Senior Lecturer in Neurology and
Director of Clinical Training at the Department of Small Animal Medicine and Surgery, The Royal Veterinary College. He
is President of the European Society of Veterinary Neurology
. He is editor of the BSAVA s Manual of Small Animal Neurology, co-author of Small Animal Spinal Disorders: Diagnosis and Surgery and of Self Assessment Colour Review of
Small Animal Neurology. He has published research and continuing education articles and textbook chapters in the USA
and Great Britain.

RICHARD A.S. WHITE


BVetMed, PhD, DVR, Dipl ACVS, Dipl ECVS, FRCVS
Dr. Dick White is a Lecturer in Small Animal Soft Tissue
Surgery at the University of Cambridge. He is a graduate of
the Royal Veterinary College in London, gaining his doctorate
in small animal oncology from the University of Cambridge.
His areas of expertise covers all aspects of soft tissue surgery
but his particular interests and publications include oncology
surgery, wound management and reconstructive surgery,
surgery of the upper airways and surgery of the head and
neck.
He is a Diplomate of the American College of Veterinary Surgeons and the European College of Veterinary Surgeons and
an RCVS recognised Specialist in Small Animal Surgery.
Dick White was a member of the founding committee and
Past President of the European College of Veterinary Surgeons.

4th European FECAVA SCIVAC Congress

13

SCIVAC EXOTIC ANIMALS STUDY GROUP

Anaesthesia and surgical conditions of reptiles


Stephen John Divers
BSc (Hons) - C Biol. MI Biol - B Vet Med - MRCVS
The Exotic Animal Centre - Essex - United Kingdom

Summary
Veterinarians are increasingly been asked to perform
surgery on non-domesticated animals. The surgical procedures themselves are often not complicated but successful
anaesthesia remains the greatest concern. This paper introduces the clinician to reptile anaesthesia and surgery, highlighting the importance of pre-anaesthetic stabilisation and
fluid therapy, suitable environment, monitoring and safe
drug regimes. Reptile surgery is discussed using common reproductive disease (dystocia) as examples in snakes, lizards
and chelonia.

Starvation. Putrefaction of undigested foods is a hazard


of ectothermic anaesthesia and therefore fasting for 24-96
hours is recommended. Larger species, particularly the boas
and pythons should be starved for 7-14 days to enable full
digestion of their large meals.
Pre-existing disease. Metabolic disturbances, cachexia,
chronic infections etc must be considered prior to any anaesthetic induction.
Handling. Reptiles should be handled as little as possible
to prevent bruising and trauma. During induction, skilled
staff and correct handling techniques are essential to minimise stress.

Introduction

INDUCTION AND INJECTION SITES

Anaesthesia and sedation permit surgery, but sedation


and chemical restraint are equally important to facilitate
handling, clinical examination and investigation (e.g. blood
sampling, endoscopy, radiography etc) of animals that may
be dangerous. The requirements of anaesthesia are restraint,
muscle relaxation, analgesia, and uncomplicated recovery.

Induction can be achieved using an injectable agent or an


inhalational agent via a mask or induction chamber. Intravenous injection sites for reptiles vary from those commonly
employed in mammals. Preferred reptile venepuncture sites:
SnakesVentral tail vein, caudal to cloaca; The needle is angled
at 45-90 (craniodorsal) and placed in the ventral mid line
in-between paired caudal scales. A 5/8-1 21-25 g needle is
advanced, avoiding the hemipenes of males, while maintaining a slight negative pressure. If the needle hits a vertebral body withdraw slightly and redirect. Avoid the
hemipenes of males.
Cardiocentesis; The snake is restrained in dorsal recumbency and the heart located at a point 22-33% from the snout
to the vent. The heart is palpated and immobilised using the
thumb and forefinger and a 23-25 g 5/8-11/2 needle is advanced at 45 in a craniodorsal direction into the apex of the
beating ventricle. Blood often enters with each heart beat.
LizardsVentral tail vein; A 5/8-1 21-25 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect.
Ventral abdominal; A 5/8-1 23-25 g needle is advanced
in the ventral mid line in a craniodorsal direction. The vein
lies just below the abdominal musculature and it is difficult
to apply post-sampling pressure which makes haemorrhage
a concern.
Tortoises, turtles and terrapins-

ANAESTHETIC CONSIDERATIONS1,2,3
Body weight. It is vital that an accurate body weight is
recorded for drug calculation and assessment of hydration
and fluid deficits.
Premedication. Atropine is considered unnecessary as
salivary secretions are insignificant during surgery, however
low-dose ketamine can be used as pre-anaesthetic sedative.
Temperature. Reptiles are ectothermic and it is important
that they are maintained at their species-specific preferred
body temperature at all times i.e. pre-induction, at induction,
during maintenance and recovery.
Fluid therapy. Dehydration (reduced skin elasticity,
sunken eyes, elevated packed cell volume) must be corrected prior to induction and monitored after surgery, especially
when recovery is prolonged. Bathing tortoises in warm water for several hours may be sufficient, but intracoelomic fluids (e.g. Hartmanns, lactated Ringers) at a rate of 15-35
ml/kg/24 hours can be easily administered to most species,
even chelonia. In cases of moderate to severe dehydration,
intravenous or intraosseous fluid therapy is to be recommended.

PRE-CONGRESS DAY MEETINGS

4th European FECAVA SCIVAC Congress

14

Dorsal tail vein; A 5/8 21-25 g needle is angled at 45-90


and placed, as cranial as possible, in the dorsal mid line of
the tail. The needle is advanced while maintaining a slight
negative pressure. If the needle hits a vertebral body, withdraw slightly and redirect. The exact position, size and even
presence of this vessel may vary between species.
Right jugular; A 5/8 23-25 g needle is positioned lateral
at the level of the tympanic scale, and directed caudally midway down the neck. It is important to maintain post-sampling pressure to avoid haematoma formation.
Subcarapacial vein; The head is pushed inside the
coelomic cavity and a needle (bent to 60-75) is inserted in
the mid line just caudal to where the skin of the neck attaches to the cranial rim of the carapace. Advance the 5/8-1 2325 g needle in a dorsal direction and maintain slight negative
pressure. It is important to maintain post-sampling pressure
to avoid haematoma formation.
There are a variety of other venepuncture sites including
the brachial plexus and femoral plexus, however they usually provide smaller samples which are more often contaminated by lymphatic fluid.
CrocodiliansVentral tail vein; A 1-3 18-23g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Larger crocodilians
(over 1.5 m in length) may require chemical restraint using
a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with neostigmine), and it may be necessary to use large spinal needles (3-8) to reach the vein.
Supravertebral vein; A 1-2 20-23 g needle is inserted at
90o in the mid line just caudal to the occiput. The needle is
advanced to just dorsal to the spinal cord, while maintaining
a slight negative pressure. Larger crocodilians (over 1.5 m)
may require chemical restaint using a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with
neostigmine).
Intramuscular injections can be given into the epaxial
muscles of snakes and proximal forelimb muscles of chelonia, lizards and crocodilians.

INHALATIONAL ANAESTHESIA
Inhalational anaesthesia can be induced via a face mask
(e.g. iguanas and other large lizards) or by conscious intubation (e.g. snakes). Endotracheal intubation is recommended
in all species. Open, semi-closed and closed circuits (Ayres
T-piece, Bain Co-axil) can be used giving considerations to
circuit resistance and animal size. Assisted ventilation (IPPV)
is often required and therefore artificial ventilation, either
manual or mechanical should be available. Anaesthetic
chambers can be used for the induction of small or venomous
species, but beware that prolonged breath holding can occur.
Intubation using a standard uncuffed endotracheal tube is
preferable but often not possible. A dog urinary catheter cut
down to size makes a suitable ET tube for many species, and
even the smallest specimen can be intubated using an intravenous catheter.

4th European FECAVA SCIVAC Congress

MONITORING ANAESTHESIA
ECG machines can be utilised in reptiles to monitor cardiac function. The heartbeat of snakes is visible ventrally
about a third of the way caudal to the head while the heart
beat of many lizards can be seen within the axillae.
Reflexes and muscle tone diminish as the depth of anaesthesia increases. Muscle relaxation progresses in an anterior
to posterior direction. The righting reflex is lost during the later stages of anaesthesia but this may not represent a surgical
plane. Loss of the corneal reflex is a good indicator of deep
anaesthesia, except in the snake and certain gecko lizards
which possess a spectacle covering the cornea. In snakes the
tongue withdrawal reflex and the ventral muscle reflex can be
used to good effect, while the deep pain withdrawal reflex of
the tail or foot can be used in lizards and chelonia. The authors preferred method of monitoring is pulse oximetry which
provides information on peripheral pulse and pulse strength,
and possibly an indication of blood oxygen saturation.

POST-OPERATIVE CARE
Post-operative recovery requires maintenance at the animals preferred body temperature. Respiration must be
monitored during recovery, especially following the use of
ketamine, halothane or methoxyflurane. Respiratory stimulants can be used to reduce post-operative observation, e.g.
doxapram (Dopram, Willows Francis) at 0.25 ml/kg i/v, i/o.
Recovery is considered to have occurred when the righting
and pedal reflexes have returned.
Hydration status should be assessed and it is good practice to give i/c, i/v, i/o or oral fluids up to 35 ml/kg/24 hours.
Antibiotics may also be indicated but until the culture
and sensitivity results are obtained, broad spectrum antibiotic cover can be provided using enrofloxacin (Baytril 2.5%,
Bayer) at 10 mg/kg i/m, i/o, po q 24 hrs or ceftazidime (Fortum 500 mg, Glaxo) at 40 mg/kg i/m i/v, i/o q 72 hrs.

SURGICAL PROCEDURES5,6,7,8
A wide range of surgical and medical procedures are now
commonly performed thanks to the safer, modern anaesthetics;
jugular cut-down and catheter placement in snakes, cardiac catheterisation in snakes, pharyngostomy tube placement, lung catheterisation and pulmonary lavage, joint
lavage/aspiration, abscess removal, tumour removal, wound
debridement, fracture repair, limb/tail amputation, enucleation, hemilaminectomy in large lizards, exploratory coeliotomy, cystotomy, enterectomy, enterotomy, pneumotomy,
biopsy, endoscopy (diagnostic, biopsy and sexing), rib removal in snakes, bone marrow aspiration in lizards and chelonia, prolapse repair, penis amputation, etc etc.
In general, the surgical techniques are similar to those established for mammals, however certain anatomical differences peculiar to reptiles must be considered by the surgeon
prior to operating. As an example reproductive disease (dystocia) and their surgical treatments will be described.7,8

15

Injectable anaesthetic and immobilisation regimes for reptiles


DRUG

DOSAGE

COMMENTS
CHELONIANS

Ketamine HCl

20-60mg/kg s/c, i/m

Useful and safe. Doses less than 50mg/kg produce tranquillisation, while doses
above 50mg/kg produce anaesthesia. Recovery time proportional to dose, often
several hours. Ketamine (50mg/kg) and xylazine (10mg/kg) combination has
been recommended. C/I - debilitated or dehydrated reptiles, hepatic or renal
dysfunction.

Alphaxalone/ alphadolone

6-9mg/kg i/v 9-15mg/kg i/m Rapid, predictable response if given i/v with intubation possible within three
mins. I/m route less predictable, induction is slower at 25-40 mins. Anaesthesia
lasts 15-35 mins, recovery 1.5-4 hours.

Propofol

14-15mg/kg i/v

Rapid, smooth induction, minimal accumulation, 20 mins anaesthesia, rapid recovery. AUTHORS AGENT OF CHOICE

Succinylcholine*

0.25-1.5mg/kg i/m

Very effective at facilitating E/T intubation and diagnostic procedures. Paralysis lasts 20 mins, recovery takes 45 mins.

Tiletamine HCl and Zolazepam HCl 10-20mg/kg i/m

Most suitable for sedation to facilitate E/T intubation. Zolazepam incorporated


to reduce convulsions and improve muscle relaxation. Not yet available in UK.

Etorphine

0.3-2.75mg/kg i/m

Used in terrapins up to 5mg/kg.

Ketamine HCl

20-100mg/kg s/c, i/m

Same as for chelonians

Alphaxalone/ alphadolone

6-9mg/kg i/v 9-15mg/kg i/m Same as for chelonians

Propofol

10-15mg/kg i/v

LIZARDS

Same as for chelonians. AUTHORS AGENT OF CHOICE

Tiletamine HCl and Zolazepam HCl 30mg/kg i/m

Produces mild to moderate plane of surgical anaesthesia with rapid induction


time, recovery may be prolonged. Particularly suited to iguanas. Not readily
available in UK.
SNAKES

Metomidate*

10-20mg/kg i/m

Very useful sedative to facilitate blood sampling, radiography, intravenous injections. Rapid onset with heavy sedation after 15 mins. Safely used on a daily
basis for cleaning, debriding wounds.

Propofol

10-12mg/kg i/v

Same as chelonians. AUTHORS AGENT OF CHOICE

Ketamine HCl

20-130mg/kg s/c, i/m

Rapid induction, prolonged recovery. May need to IPPV at higher doses, lower
dose for pre-anaesthetic sedation.

Alphaxalone/ alphadolone

6-9mg/kg i/v 9-15mg/kg i/m Same as chelonians

Tiletamine HCl and Zolazepam HCl 10-20mg/kg i/m

Same as chelonians. Fatalities at 55mg/kg

Methohexital sodium

Induction and recovery times rapid, concentration should not exceed 0.5%.

5-15mg/kg i/m, s/c

CROCODILIANS
Propofol

10-15mg/kg i/v

Same as for chelonians. AUTHORS AGENT OF CHOICE FOR SMALL


SPECIMENS

Succinylcholine*

0.4-1mg/kg i/m

Rapid onset of paralysis in American alligators, recovery in 45-90 mins.

Gallamine triethiodide*

0.6-4mg/kg i/m

Good in Nile crocodiles, unsafe in American alligators at 1mg/kg. Reverse with


0.05mg/kg neostigmine i/m and 0.02mg/kg atropine i/m. AUTHORS AGENT
OF CHOICE FOR LARGE SPECIMENS

Ketamine HCl and Xylazine HCl

20mg/kg i/m 1mg/kg i/m

Good in Nile crocodiles, ketamine given 30 min after xylazine, anaesthesia lasts
50 mins, recovery in 4 hours.

Etorphine

0.3-2.75mg/kg i/m

10-30 mins induction, 45-100 mins of analgesia hence combine with muscle
relaxant.

*Provides no analgesia - must be combines with local or general analgesia for painful procedures. It may be necessary to assist respiration, especially at higher doses
or in debilitated patients.

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4th European FECAVA SCIVAC Congress

16

4th European FECAVA SCIVAC Congress

Inhalational anaesthetic agents used in reptiles


AGENT
Methoxyflurane

INDUCTION/
MAINTENANCE

COMMENTS

3-4%/1.5-2% in oxygen

All species. Excellent relaxation and analgesia, prolonged induction and recovery times,
myocardial depressant and nephrotoxic.

Halothane

3-5%/1-3% in oxygen

All species. Rapid induction and recovery times, respiration and myocardium depressed with
respiratory and cardiac arrest occurring simultaneously, hepatotoxic, lizards more sensitive.

Isoflurane

3-5%/1-3% in oxygen

All species. Rapid induction and recovery, minimal organ toxicity, ideal for debilitated reptiles. AUTHORS AGENT OF CHOICE

Nitrous oxide

1:1 to 1:3 with oxygen

All species. May be used with volatile anaesthetics to reduce induction time and improve
muscle relaxation and analgesia.

PRE-OVULATORY OVA STASIS (POOS)


In cases where the ova enlarge but do not ovulate and remain within the ovary the term pre-ovulatory ova stasis
(POOS) is applicable. In such circumstances the presence of
the greatly enlarged ovaries severely reduces the coelomic
space available to the gastrointestinal tract resulting in prolonged anorexia particularly in saurians. In most untreated
cases affected females usually die from the secondary
changes associated with dehydration and anorexia. A diagnosis of POOS can be made by ultrasonography, laparoscopy or more commonly radiography. It is possible for
the ova to be spontaneously reabsorbed over a period of 412 weeks. However, if affected animals are completely
anorexic and becoming debilitated then further deterioration
and death can ensue before the problem resolves naturally. If
medical therapy is contemplated then intensive
nutritional/fluid support will be required for many weeks
and ova reabsorption should be monitored using radiography
or ultrasonography. In the authors experience medical management is seldom successful in lizards presented late in the
course of the disease and does not prevent recurrence the
following year. Greater success has been seen with short
term patient stabilisation using fluid therapy for 1-3 days
followed by surgery (ovariosalpingectomy). A case of follicular aspiration as a treatment for POOS has been reported.

POST-OVULATORY EGG STASIS (POES)


In cases of post-ovulatory egg stasis (POES), the eggs
(usually shelled) or foetuses are located within the shell
glands or oviducts but normal laying or birth at term fails to
occur because of the lack of a suitable nesting site (temperature, humidity, nest material, seclusion), excessive disturbance by the owner, competition for nesting sites (overcrowding), stress of transportation, metabolic disturbances
(particularly involving calcium), systemic or localised infections of the shell glands, oviducts or cloaca and obstructions
due to abnormal eggs, foetuses or cloacal prolapse. The
space occupied by the eggs/foetuses again compresses the
gastrointestinal tract and leads to secondary hypophagia or
anorexia.

If there is no indication of infection, metabolic disease or


obstruction as determined by radiography, digital palpation
and direct visualisation of the cloaca and a limited haematological and biochemical assessment, then conservative treatment should be attempted. Complications including abnormal eggs, abnormal foetuses, cloacal prolapse, suspected infection of the cloaca, shell glands or oviducts will prevent
normal laying or birth and in these, and refractory medical
cases, surgery is indicated.

SURGICAL TECHNIQUE
Once the patients hydration status has been returned to
normal (as determined by serial packed cell volume, total
protein and albumin) surgery can proceed. Preoperative antibiotics, for example 40 mg/kg ceftazidime (Fortum, 500
mg, Glaxo), IM is advisable. The rate of fluid administration
can be increased to 5 ml/kg/hour during anaesthesia, surgery
and the immediate postoperative period.
Anaesthesia is induced with 10-14 mg/kg propofol
(Rapinovet, 10 mg/ml, Mallinckrodt Veterinary), IV or IO
followed by intubation and maintenance on oxygen and 24% isoflurane. It is vital than the preferred body temperature
of the patient is maintained before, during and after surgery.
The use of a low wattage heat mat or water bed to maintain
a core preferred body temperature is recommended. The
subject is connected to an ecg or pulse oximeter (cloacal/oesophageal) and prepared for aseptic surgery. The use of plastic adhesive drapes enables better monitoring and are to be
preferred over cotton drapes. Post operative analgesics
should always be considered and the author prefers 2-4
mg/kg carprofen IM (Zenecarp, 50 mg/ml, C-Vet).

LIZARDS
A standard paramedian or mid-line coeliotomy is performed, avoiding the large, ventral, mid line venous sinus
and, often voluminous, saurian bladder. The incision may
have to extend from the xiphoid process to just cranial to the
pelvis to provide sufficient exposure. The bladder must be

identified to prevent accidental incision, and emptied by cystocentesis if necessary. In cases of POOS, the enlarged
ovaries will be immediately obvious, often resembling clusters of yellow-orange grapes. Each ovary, supplied by 4-8
ovarian vessels that branch off the aorta and renal veins, is
lifted to expose these vessels which can be clamped using hemoclips, or ligated using vicryl (3/0-5/0). Once clamped the
ovaries can be carefully dissected free and removed. The
oviducts are usually small and involuted. Theoretically it
may be possible to leave the oviducts in place but subsequent
infection is always a possibility and therefore removal is recommended. The small blood vessels can usually be sealed using radiosurgery, hemoclips or ligatures as necessary. The
oviducts should be double ligated using 3/0-5/0 vicryl as far
distally as possible, close to their insertion to the cloaca.
In cases of POES, it is the thin shell glands full of eggs
that are immediately obvious. Multiple salpingotomy incisions can be made to remove the eggs in an effort to maintain
future breeding capacity, however, surgery time is greatly extended. In most cases complete salpingectomy is recommended. The large, numerous blood vessels that supply each
oviduct must be ligated or hemoclipped. Hemoclips greatly
reduce surgery time and several vessels can often be clamped
with a single medium clip. The oviducts must be ligated close
to the cloaca and removed as described above. In these cases, the ovaries are often small lying on top of the renal veins.
Their removal is considered by some to be unnecessary as it
has been suggested that folliculogenesis requires feedback
from the shell glands. The author prefers complete ovariosalpingectomy due to the possible danger of ectopic ova in the
future. When removing inactive ovaries the ovarian vessels
are smaller and shorter and it is generally easier to clamp
these vessels with hemoclips than to ligate them. Special care
is also required not to damage the closely associated adrenal
glands. The coelomic membrane and muscle layers are
closed in a routine manner using 3/0-5/0 vicryl. The skin is
sutured using 3/0 -5/0 nylon in an everting horizontal mattress pattern. This will prevent the natural inverting tendency
of reptilian skin and prevent dysecdysis in the future. The patient is returned to a vivarium at 30-35C to recover. Postoperative antibiotics are not routinely required unless infection
was confirmed at surgery but parenteral fluid therapy remains
essential for the next 24 hours. Discharge typically occurs the
next day with a return to normal feeding within a week. Skin
sutures are removed in 6-8 weeks.

SNAKES
The procedure is similar in snakes. In general a long incision is made between the ventral and lateral scales over the
area of greatest coelomic distension. POOS is rarer in snakes
and in most cases the eggs (or foetuses) will be within the
shell glands. Dissection is continued through the muscle layer and a standard salpingotomy incision is made in the thinly walled shell gland. The eggs or foetuses can then be removed, and it may be possible to milk eggs or foetuses from
further up or further down the shell gland into the surgical
site so preventing the need for additional salpingotomies.
The shell gland incision is closed using 5/0 vicryl in a single

17

or double inverting suture pattern. Suturing may be made


easier by the administration of oxytocin or vasotocin which
causes contraction and thickening of the shell gland wall.
Skin closure is routine.
A less invasive surgical option is the aspiration of the infertile egg contents through a needle (14-20 g) which is introduced through the coelomic and shell gland walls into the
retained egg. The skin surface must be aseptically prepared
prior to this technique but there is a danger that egg contents
may leak from the egg and into the shell gland or coelomic
cavity causing an intense coelomitis. In general, the collapsed egg is voided within 12-96 hours, but this may be facilitated by the use of oxytocin, vasotocin or prostaglandins.
Ovariosalpingectomy is more difficult to perform in
snakes but is certainly possible and with practice will produce a satisfactory and permanent cure to reproductive problems in these species.

CHELONIA
Access to the reproductive tract of chelonians presents
an obvious challenge to the surgeon, notably the shell. In
those species with large inguinal fossae including the large
land tortoises and many species of terrapin and turtle, an inguinal soft tissue approach will provide sufficient access for
egg removal and prevent the need for plastronotomy. In
species with small inguinal fossae, or in those cases where
there are large numbers of retained eggs, or extensive disease that warrants complete ovariosalpingectomy, then a
transplastron approach is often indicated.
Using an oscillating sector cutter or small diameter circular saw, a plastronotomy with a bevelled edge is performed,
making sure that any functional plastron hinges are avoided.
It is important that the clinician makes the plastronotomy incision large enough to operate through as it is difficult to subsequently enlarge the incision. The bone segment is carefully lifted and dissected free from the underlying soft tissues
and placed in sterile normal saline. In chelonia there are
paired ventral abdominal veins, and the coeliotomy incision
is made between these vessels to gain access to the coelomic
cavity. Ovariosalpingectomy and salpingotomy procedures
are carried out in much the same way as previously described
for squamates, but the chelonian shell gland is often thicker
than that of lizards and snakes. The coelomic membrane is
closed in a simple continuous or interrupted pattern. The
bone segment is replaced and secured in place using autoclaved fibreglass patches and epoxy resin.

Key words
Anaesthesia, surgery, reptile, propofol, isoflurane, dystocia.

References
1.

2.

Bennett, R.A. (1996). Anaesthesia. In: Reptile Medicine and Surgery.


First edition (Ed. D. R. Mader). W.B. Saunders, Philadelphia. Pages
241-247.
Lawton, M.P.C. (1992). Anaesthesia. In: Manual of Reptiles (Eds.

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18

3.
4.
5.

4th European FECAVA SCIVAC Congress


P.H. Beynon, M.P.C. Lawton, J.E. Cooper). BSAVA, Cheltenham.
Pages 170-183.
Mader, D.L. (1996) Reptile Medicine and Surgery. WB Saunders,
Philadelphia.
Malley, A.D. (1997) Reptile anaesthesia and the practising veterinarian. In Practice 19(7):351-368.
Lawton, M.P.C. (1992). Surgery. In: Manual of Reptiles (Eds. P.H.
Beynon, M.P.C. Lawton, J.E. Cooper). BSAVA, Cheltenham. Pages
184-193.

6.

7.

8.

Bennett, A.R. and Mader, D.R. (1996). Soft tissue surgery. In: Reptile Medicine and Surgery. First edition (Ed. D. R. Mader). W.B.
Saunders, Philadelphia. Pages 287-298.
DeNardo, D. (1996). Dystocias. In: Reptile Medicine and Surgery.
First edition (Ed. D. R. Mader). W.B. Saunders, Philadelphia. Pages
370-374.
Divers, S.J. (1996). Medical and surgical treatment of pre-ovulatory
ova stasis and post-ovulatory egg stasis in oviparous lizards. ARAV
1996 Proceedings, Pages 119-123.

19

SCIVAC EXOTIC ANIMALS STUDY GROUP

Diagnostic techniques for reptiles


Stephen John Divers
BSc (Hons) - C Biol. MI Biol - B Vet Med - MRCVS
The Exotic Animal Centre - Essex - United Kingdom

Summary
Making a definitive diagnosis is the end point of a clinical journey. This may start with history taking and the clinical examination may provide a list of possible differential diagnoses. However, it is often necessary to take clinical samples, perform laboratory techniques and utilise diagnostic
imaging before a definitive answer can be found. This paper
attempts to clarify the major aspects of reptile diagnostics
from taking a history from the owner to sending a liver biopsy for histopathological confirmation of fungal hepatitis!

Introduction
The art of veterinary medicine and making that previously elusive reptile diagnosis rests upon our abilities as
clinicians to untangle the complex clinical web and piece together the pathology to determine the underlying aetiology
and clinical picture. A logical approach to reptiles will provide the veterinarian with most of the information required
to successfully diagnose and treat the majority of ailments.
When discussing diagnostic techniques it is vital that we
do not forget that a thorough history and full clinical examination are important diagnostic aids in their own right and
should be performed ahead of any other diagnostic tests.
Further investigations include haematology, serum biochemistry, parasitology, microscopy, cytology, microbiology, radiography, endoscopy, ultrasonography, MRI and CT, and
exploratory surgery.

History Taking1
Reptiles should be transported to the practice in linen or
cloth bags within styrofoam boxes, and their owners encouraged to keep and bring along their own husbandry
records. The identity of an unfamiliar species should be ascertained before arrival to permit the clinician to become familiar with the species specific husbandry requirements.
The vast majority of reptile diseases are due either directly
or indirectly to substandard husbandry and therefore a thorough review of husbandry practices, hygiene and nutrition is
essential. It is often useful when dealing with an unfamiliar
species to have a sample history which can be followed during the consultation. Exotic animals invariably require an

extended consultation period but the extra time taken to obtain a detailed history will be clinically valuable and will often provide a tentative diagnosis. Qualitative and, where
possible, quantitative changes in husbandry, food and water
consumption, faeces, urine/urates, and behaviour should be
identified. Specific changes associated with breeding and hibernation are frequently associated with disease problems
and therefore careful questioning is required. Recent additions to the reptile collection are also significant, especially
as few owners operate the recommended 3-6 month quarantine period.
Sample history form
1).reptiles name or identification.
2) species, subspecies, native locality, colour morphology.
3) date of birth, age.
4) sex.
5) duration in owners care/captivity.
6) origin (captive bred, wild caught, when imported).
7) details of source (breeder, retailer, importer).
8) enclosure/vivarium specifications:
type (arboreal, terrestrial, aquatic).
size (length x depth x height).
construction (materials, paints, sealant, internal fittings,
or purchased ready-made).
furnishings (bark, plants, floor material).
provision for vivarium ventilation (mesh, air holes).
frequency of cleaning.
detergents, disinfectants used.
9) environment: vivarium (temperate, tropical).
outdoor enclosure (grassland, wooded, overgrown).
10) heating equipment (spot lights, ceramics, heating cables, heat mats).
11) temperature control (thermostat, rheostat) and method
of recording (type and position of thermometer).
12) temperatures (daytime air, daytime basking, night
time air).
13) lighting equipment (spot lights/fluorescent strip lights).
14) lighting control (photoperiod, manual/timer).
15) humidity level (day, night and seasonal changes, method
of provision - spray, sprinkler).
16) diet (varieties and quantities).
17) feeding: amount of food normally offered/actually eaten.
frequency of feeding.
time food offered (morning, overnight etc).
changes in appetite.

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18) method of water provision (bowl, spray).


how often is water changed.
how often is the water container cleaned.
what disinfectant/detergent is used.
changes in drinking behaviour.
18) food and water vitamin/mineral supplements.
19) breeding details (recent breeding attempts including
changes of temperature, humidity, feeding and animals
groupings).
20) other specimens in same vivarium or have shared the
same vivarium within the last 6 months.
21) other specimens in same room or that have been in the
same room in the last 6 months.
22) disease history of animal in question or any in-contact
animals.
23) quarantine protocol for all new additions (length of
quarantine period, position of quarantine vivarium in relation to established collection).
24) other details of relevance.

Clinical Examination1,2
Reptiles as a group are relatively easy to evaluate and
the standard examination techniques used for domestic pets
apply equally to reptiles. Calm specimens should be observed from a distance without handling to observe demeanour, locomotion and any obvious neurological disorders. Nervous or aggressive species are best restrained using appropriate techniques, including towels and gloves, at
all times. Observation of reptiles within their vivarium or
enclosure is particularly valuable and should be performed
whenever possible.
Reptiles present no more of a zoonotic danger than domestic animals, however the risks of Salmonella sp,
Pseudomonas sp, Rickettsia sp and pentastomids (arachnid
lung parasites) does necessitate adequate hygienic precautions at all times.
All reptiles should be accurately weighed. It is also
worth taking the cloacal temperature of any reptile weighing
more than 1 kg which has not been out of the vivarium environment for more than an hour. This temperature will give
an accurate indication of a large reptiles core temperature
and consequently an indication of that of its environment.
For example, a 5 kg iguana with a cloacal temperature of
15C is unlikely to have been removed from a 30C environment within the last hour. Length is also an important measurement that should be routinely recorded. The snout-vent
length of lizards and snakes is usually recorded, while the
horizontal carapace length of chelonians is more useful, especially when combined with weight to give a weight-length
(Jacksons) ratio.
Useful equipment for the reptile consulting room
Electronic scales, 0-2000 g accurate to 1 g, 0-100 kg accurate to 0.2 kg.
Handkerchiefs, tea-towels and bath towels.
Rubber gloves, thin leather gloves, gauntlets.
Snake hooks.
Transparent plastic boxes to observe small reptiles unre-

4th European FECAVA SCIVAC Congress

strained.
Plastic or wooden spatulas.
Sexing probes.
Dedicated auroscope attachment for cloacal examination.
Assortment of plastic gags.
Focused light source, preferably flexible for transillumination.
Digital thermometer with remote probe and a range of 0-50C.
Stethoscope with swab attached to diaphragm.
A systematic examination from rostrum to tail tip is always indicated, including a thorough palpation of all accessible areas for any abnormalities. It not uncommon for a reptile to void faeces and urates during the clinical examination,
and this material should be collected for immediate laboratory investigation.
Transillumination using a powerful light source is particularly useful for visualising the internal structures of small
lizards and snakes, although care must be exercised due to
the heat produced by these appliances. A flexible endoscope
is ideal but a far cheaper alternative is the flexible light
source recently introduced by Medical Diagnostic Services.
The light source can be held against the body of small reptiles or lubricated and inserted into the oesophagus or cloaca and rectum. Transillumination enables coelomic masses
to be identified and the cardiac shadow can be located for
cardiocentesis in small specimens.
Auscultation is possible and useful in reptiles but does
require a silent consulting room. The adventitious sounds
produced between the shell or scales and the stethoscope diaphragm can be reduced by placing a dampened swab or
towel between the stethoscope and the surface of the reptile.
Intractable animals are best sedated to facilitate a safer
more thorough examination. Ketamine HCl (Vetalar, ParkeDavis; Ketaset, Willows-Francis) at 20-50 mg/kg IM can be
employed but greater care must be exercised when using this
drug in debilitated reptiles.
Snakes
Aggressive snakes should be restrained before they are
removed from their transportation bag. The head is held behind the occiput using the thumb and middle finger, while
the index finger is placed on top of the head. The larger
pythons and anacondas can exceed 6 metres and 150 kg and
are powerful and potentially dangerous. In such circumstances, a second or even third handler will be required to
support the body during the examination. It is usually safer
and more convenient to sedate a large pugnacious snake than
to struggle on and risk injury to the snake, client or staff.
Non-venomous species should be removed from their
cloth bag when an assessment of demeanour and muscle
tone will quickly become obvious. Sick snakes will usually
remain limp while healthy specimens will grip or move over
the clinicians hands and arms giving a sense of strength. A
healthy snake that is permitted to wrap a coil around the handlers wrist while the head is allowed to hang down should
be able to raise its head to the level of the tail. Head position,
body posture, cloacal tone and righting reflexes can be used
to assess neurological function.
The integument, particularly the ventral scales, should be
carefully examined for any evidence of dysecdysis (poor
shedding) and trauma. Skin tenting and ridges may indicate

cachexia or dehydration while ticks and the snake mite


(Ophionyssus natricis) may congregate in skin folds, infraorbital pits and corneal rims. The infraorbital pits (where
present) and the nostrils should be free from any discharge
or retained skin. The eyes should be clear, unless ecdysis is
imminent when a bluish haze may be present. The spectacles
covering the eyes should be smooth as any wrinkles may indicate the presence of a retained spectacle. Ocular swellings
are often due to a build up of lachrymal secretions within the
sub-spectacular space because of a blockage within the nasolachrymal duct. Such swellings may become infected resulting in abscessation.
The body should be thoroughly palpated for any abnormal masses, and their position related to that of the major organs to identify their likely significance. Depending upon
the musculature of the snake the heart and faecal masses are
often palpated and erroneously considered pathological. The
cloaca should be free from faecal staining and discharge. Examination of the cloaca can be carried out using an auroscope and digital palpation. In the large constrictors it is possible to insert a lubricated gloved hand to perform an internal cloacal and even rectal examination. The sex of the
snake can be ascertained by examination of the tail length
and probing of the hemipenes. The tail length (and the number of sub-caudal scales) is always smaller in females than
males but this method requires access to published information on tail length and scale counts unless both sexes are
available for examination. The hemipenes are entered by
placing a caudally pointing probe, either side of mid line,
just inside the caudal cloacal rim. In males the probe passes
to a depth of 6-12 subcaudal scales whereas in females the
probe enters a musk sac to a depth of only 2-4 subcaudal
scales.
Examination of the oral cavity is best left until last as
most snakes object to such manipulation. However, even before the mouth is opened the tongue should have been seen
frequently flicking in and out of the labial notch. The mouth
can be gently opened using a plastic or wooden spatula to
permit an assessment of mucous membrane colour and examination for signs of mucosal oedema, hypersalivation,
haemorrhage, necrosis and the presence of caseous exudates.
The presence of white deposits may indicate uric acid deposition due to visceral gout. The pharynx and glottis should be
examined for haemorrhage, foreign bodies and discharge. It
is important to observe the glottis during respiration in an attempt to differentiate between discharges originating from
the respiratory and gastro-intestinal tracts.
Body organ position in boas and pythons
Organ

Percentage position from snout

Heart
Lung
Air sac
Liver
Stomach
Small intestine
Cranial pole of right kidney
Caudal pole of left kidney

22-33
33-45
45-65
38-56
46-67
68-81
69-77
74-82

21

Colon

81-100

Figures relate to the percentage distance of each organ from


the snout. The total length being that from the snout to the
cloaca. The organ positions of other species of snake are
broadly similar although differences in anatomy certainly
exist between the major serpentine groups.
Lizards
Lizards vary greatly in size and temperament and therefore a variety of handling techniques are required to cover all
situations. The tegus and monitor lizards are renowned for
their powerful bites while other species, particularly the
green iguana, are much more likely to use their claws and tail
to painful effect. The main problem of handling small lizards
is restraining them before they flee from the cloth bag. In all
cases, the lizard should be transported in a securely tied cloth
bag so that the position of the lizards head can be identified
and restrained before the bag is even opened.
The large lizards are best restrained with the forelimbs
held laterally against their thorax and the limbs held laterally against the tail base. Smaller lizards can be restrained
around the pectoral girdle holding the forelimbs against the
thorax, although care is required not to impair respiratory
movements. Never grasp a lizard by the tail because many
species can perform autotomy and shed their tails in an attempt to evade a predator (or in this case clinician!). Restricting the vision of these animals is often the simplest way
to facilitate handling and a towel placed over the head will
enable the clinician to thoroughly examine the rest of the
body and limbs. A useful restraint technique for iguanid
lizards utilises the vaso-vagal response: gentle digital pressure is applied to both orbits and in many cases the lizard
will enter a state of stupor for up to 45 minutes or until a
painful stimulus is applied. This technique can be employed
to calm nervous iguanids and monitors but, more importantly, enables the mouth to be gently opened without the need
for excessive force.
The integument should be examined for parasites and evidence of trauma due to fighting, mating and burns. Lizards
tend to shed their skin in a piecemeal fashion and therefore
retained skin (often dry and brown) must be differentiated
from normal ecdysis (flexible and transparent). Classically,
dysecdysis and skin retention occurs around the digits and
tail causing ischaemic necrosis. Extensive skin folding and
tenting are indicators of cachexia and possible dehydration.
The nostrils, eyes, and tympanic scales should be clean
and free from discharges, although some iguanids excrete
salt through specialised nasal glands which is then expelled
through the nostrils. The rostrum should be examined for
trauma due to repeated escape attempts from a poorly designed vivarium. The head and limbs must be palpated for
masses which may be abscesses or fibrous periosteal reactions associated with metabolic bone disease. Lizards suffering from severe hypocalcaemia due to metabolic bone disease may exhibit periodic tremors and muscle fasiculations.
The cloaca should be free from faecal staining, while visual
and digital examination should be considered routine. The
mouth can be opened using a spatula to examine the oral
cavity as described previously. In addition, the internal ex-

PRE-CONGRESS DAY MEETINGS

4th European FECAVA SCIVAC Congress

22

tent of any rostral abrasions can be evaluated.


Many species of lizards are sexually dimorphic, although
sexing juveniles can be very difficult. Adult males tend to be
larger, more colourful, exhibit more courting (head bobbing)
and aggressive behaviours, possess paired hemipenal bulges
at the tail base and more developed femoral or pre-anal pores.
Tortoises, turtles and terrapins
The commonly presented tortoises such as the spurthighed and Hermanns (Testudo spp) are not difficult to
handle, although a persistently withdrawn head can hinder
the examination. A little patience while holding the tortoise
upside down will usually persuade a shy individual to protrude the head from the shell when the thumb and middle
finger can be placed behind the occipital condyles. The
mouth can then be opened by applying steady distractive
pressure to the maxilla and mandible, and once open the index finger can be inserted into the corner of the mouth to
prevent closure. This method enables the handler to keep the
mouth open using one hand, leaving the other free to examine the buccal cavity, remove foreign bodies, and take samples for laboratory investigation. The limbs can also be withdrawn by applying steady traction. The coelomic space within the shell is restricted and therefore, gently forcing the
hindlimbs into the shell, leads to protrusion of the forelimbs
and head, and vice versa. The more aggressive species, especially the terrapins and turtles should be held at the rear of
the carapace. Some larger species (snapping turtle, Chelydra
serpentina; soft shelled turtles, Trionyx spp) can deliver an
extremely powerful bite and so great care is required at all
times. Certain species also possess functional hinges at the
front and back of the plastron. The box tortoises are becoming increasingly common since the importation ban on
Mediterranean tortoises, and care should be exercised not to
trap a finger when the hinge closes.
The chelonian shell presents an obvious barrier to a thorough clinical examination, however much can still be
achieved in the consulting room before resorting to imaging
techniques. The head must be extended and the mouth
opened to permit a thorough buccal examination including
an assessment of the mucous membranes and tongue for
signs of stomatitis. The glottis should be examined for signs
of discharge suggestive of pneumonia. The eustachian tubes
enter the lateral walls of the pharynx and any solid deposits
in this area may indicate otitis or urate deposition. The nostrils should be clear and free from any discharge. The eyelids should be open and not obviously distended while the
eyes should be clear and bright. The tympanic scales should
be examined for any swellings indicative of ear abscessation.
The neck and limbs should be palpated for masses and
signs of skin damage, parasites and dysecdysis. The inguinal
fossae should be palpated with the chelonian held upright.
Gently rocking the animal may then enable the clinician to
palpate eggs, uroliths or other coelomic masses. The shell
should be examined for poor conformation, trauma and infection. Pyramiding or softening of the shell is often caused
by inappropriate nutrition while shell infection may present
as loosening and softening of the scutes, erythema and haemorrhages within the shell, and discharges from shell lesions.

4th European FECAVA SCIVAC Congress

Prolapses through the cloaca are obvious but it is necessary to differentiate between prolapses of the cloaca and
those of the male penis. Internal examination using digital
palpation and an auroscope or endoscope is recommended.
Male chelonians can be differentiated from females by their
longer tails and the position of their cloaca caudal to the
edge of the carapace.
A detailed history and clinical examination will usually
indicate which further investigations may be necessary to
make a definitive diagnosis. Radiography, ultrasonography,
MRI and CT, endoscopy, haematology, blood biochemistry,
microbiology, cytology and parasitology are all proven techniques that are used extensively in reptile medicine.

Haematology and biochemistry


There is now a great deal more clinicopathological data
available for many of the common pet reptile species and so
blood sampling offers a great wealth of information. Unfortunately, venepuncture is often blind in reptiles but with
practice it can be efficiently and consistently performed.
Preferred reptile venepuncture sites:
SnakesVentral tail vein, caudal to cloaca; The needle is angled
at 45-90 (craniodorsal) and placed in the ventral mid line
in-between paired caudal scales. A 5/8-1 21-25 g needle is
advanced, avoiding the hemipenes of males, while maintaining a slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Avoid the hemipenes of
males. Preferred site for larger specimens.
Cardiocentesis; The snake is restrained in dorsal recumbency and the heart located at a point 22-33% from the snout
to the vent. The heart is palpated and immobilised using the
thumb and forefinger and a 23-25g 5/8-11/2 needle is advanced at 45 in a craniodorsal direction into the apex of the
beating ventricle. Blood often enters with each heart beat.
Preferred site for smaller specimens.
LizardsVentral tail vein; A 5/8-1 21-25 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining
slight negative pressure. If the needle hits a vertebral body
withdraw slightly and redirect. Preferred site for all lizards.
Ventral abdominal; A 5/8-1 23-25 g needle is advanced
in the ventral mid line in a craniodorsal direction. The vein
lies just below the abdominal musculature and it is difficult
to apply post-sampling pressure which makes haemorrhage
a concern.
Tortoises, turtles and terrapinsDorsal tail vein; A 5/8 21-25 g needle is angled at 45-90
and placed, as cranial as possible, in the dorsal mid line of
the tail. The needle is advanced while maintaining a slight
negative pressure. If the needle hits a vertebral body, withdraw slightly and redirect. The exact position, size and even
presence of this vessel may vary between species. Preferred
site for those aggressive chelonians that possess a well de-

veloped dorsal tail vein.


Right jugular; A 5/8 23-25 g needle is positioned lateral
at the level of the tympanic scale, and directed caudally midway down the neck. It is important to maintain post-sampling pressure to avoid haematoma formation. Preferred site
for most chelonians.
Subcarapacial vein; The head is pushed inside the
coelomic cavity and a needle (bent to 60-75) is inserted in
the mid line just caudal to where the skin of the neck attaches to the cranial rim of the carapace. Advance the 5/8-1 2325 g needle in a dorsal direction and maintain slight negative
pressure. It is important to maintain post-sampling pressure
to avoid haematoma formation. Preferred site for very small
specimens.
There are a variety of other venepuncture sites including
the brachial plexus and femoral plexus, however they usually provide smaller samples which are more often contaminated by lymphatic fluid.
CrocodiliansVentral tail vein; A 1-3 18-23 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Larger crocodilians
(over 1.5 m in length) may require chemical restraint using
a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversed with neostigmine), and it may be necessary
to use large spinal needles (3-8) to reach the vein. Preferred
site for smaller specimens.
Supravertebral vein; A 1-2 20-23 g needle is inserted at
90o in the mid line just caudal to the occiput. The needle is
advanced to just dorsal to the spinal cord, while maintaining
a slight negative pressure. Preferred site for larger crocodilians (over 1.5 m) but chemical restraint using a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversed
with neostigmine) must be considered for both animal and
operator safety.

Haematology3
Some species are sensitive to EDTA as an anticoagulant
and so lithium heparin is the anticoagulant of choice. Reptiles
possess nucleated red and white blood cells and so differential cell counts must usually be performed manually using either the Eosinophil Unopipette or Toluidine blue technique.
Erythrocytes
 nucleated
 blood parasites common but not usually significant
Thrombocytes
 smaller than erythrocytes
 dense basophilic nucleus
 often found in clusters
Lymphocytes
 most common leucocyte
 variable in size and colour
 eccentric nucleus
 reactive lymphocytes are called plasma cells
Monocytes
 large in size but rare in number

23

 bluish-grey fine granular cytoplasm with vacuoles


 indented or U-shaped nucleus
Azurophils
 non-segmented nucleus
 basophilic cytoplasm with azurophilic area but without granules
 reactive azurophils may contain vacuoles, granules,
phagocytosed material
 often considered an acute inflammatory cell
Heterophils
 variable nucleus
 spiculate eosinophilic granules
 reptilian equivalent of the mammalian neutrophil
 elevated during bacterial infections and tissue necrosis
Eosinophils
 may be difficult to distinguish from heterophils
 eosinophilic granules are usually more rounded
Basophils
 small but common leucocyte
 intensely basophilic granules
 fragile cells that may disintegrate during slide processing.
Interpretation may be difficult and requires experience
so try to locate an experienced, preferably avian and exotic
haematologist. When developing an in-house haematology
service there are various normal ranges scattered throughout
the literature that can be employed, but nothing is superior
to developing your own series of normal ranges. In cases of
emergency, haematocrit (PCV) estimations and qualitative
evaluations of the buffy coat and stained blood smear may
be very useful until a full haematology can be obtained.

Biochemistry3
Various biochemical parameters and electrolytes can be
routinely used to assess organ damage and metabolic disturbance. Heparinised plasma or serum can be should be used
for most estimations. The author uses two main biochemistry profiles for reptile;
Mini-profile: Calcium, phosphorus, uric acid, AST, total
protein, albumin and globulin.
Extended profile: Calcium, phosphorus, uric acid, AST,
ALT, GGT, bile acids, cholesterol, triglycerides, CPK, glucose, total protein, albumin, globulin, sodium, chloride,
potassium.
Normal blood ranges for green iguanas (Iguana iguana).4
Biochemical parameter
Total protein g/l
Albumin g/l
Globulin g/l
Uric acid mmol/l
Alkaline phosphatase u/l
Alanine aminotransferase u/l
Aspartate aminotransferase u/l
g-Glutamyl transferase u/l
Cholesterol mmol/l
Triglycerides mmol/l
Glucose mmol/l

Normal range
50-78
21-28
25-43
70-140
50-290
5-68
5-52
0-3
2.7-8.6
0.6-7.8
9.4-16.0

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4th European FECAVA SCIVAC Congress

24

4th European FECAVA SCIVAC Congress

Calcium mmol/l
Phosphorus mmol/l

2.2-3.5
1.5-3.0

Haematological parameter

Normal range

Total red blood cell count x10^12/l


Packed cell volume l/l
Haemoglobin g/dl
MCV fl
MCH pg
MCHC g/dl
Total white blood cell count x10^9/l
Heterophils x10^9/l
Azurophils x10^9/l
Lymphocytes x10^9/l
Eosinophils x10^9/l
Monocytes x10^9/l
Basophils x10^9/l

1.0-1.9
0.25-0.38
6.0-10.0
165-305
48-78
20-38
3-10
0.35-5.2
0.0-1.7
0.5-5.5
0.0-0.3
0.0-0.1
0.0-0.5

mogenous predominant bacterial


population
Faecal floatation
- use a concentrated floatation medium and examine for helminth ova
Faecal culture
- Mixed bacterial/fungal growths are
less clinically important (even if
Gram-negative) than a heavy pure
growth of a single bacteria or fungus
Beware of pseudo parasites e.g. pollen, prey parasites etc
Urine tests;
Direct wet mount
Dip-stick tests
Specific gravity
Cytology
Microbiology

Faecal and urine examination6,7


Reptiles will often void faeces and urates during the consultation, usually all over the veterinarian who should be
grateful for this gift of clinical material. When dealing with
an anorexic reptile that may not be voiding faeces it is a simple process to perform a cloacal wash;
 insert a lubricated catheter (attached to a syringe containing warm normal saline) into the cloaca and advance into the colon
 Instil up to 1% body weight of normal saline and repeatedly flush and aspirate until a sample is obtained
Faecal tests;
Direct wet mount

- examine under x400 for flagellate


protozoa, helminth larvae and ova
Mix with eosin
- examine under x400 for encysted
amoeba
Acid-fast (ZN) stain - examine for acid fast Cryptosporidia spp
Gram-stain
- examine Gram-positive and Gramnegative bacteria. Most reptiles
possess G- bacteria, look for ho-

- examine under x400 for protozoa


(e.g. Hexamita sp)
- blood, leucocytes (glucose, protein)
- not very useful as reptile urine is
isosthenuric
- active inflammation, renal casts
- bladder urine is not sterile but
heavy pure growth may be clinically significant.

Radiography8,9
Radiography is an important tool in reptile diagnostics that
should be utilised more often. It is important to remember that
lower kV values will be required for smaller exotic species.
Adequate restraint is vital to facilitate proper positioning;
 place conscious lizard in radiolucent cloth bag or box
 place conscious snake into restraint tube
 place chelonian on a raised column to keep limbs clear
of table
 use the vaso-vagal response in larger lizards
 consider chemical restraint and anaesthesia
 use tape to secure animals in position
Standard views for various species are as follows;
Snakes: dorsoventral views of straight body (not coiled)
horizontal beam laterals of straight body
remember to use markers along body length
Lizards: dorsoventral views of whole body or particular part
horizontal beam lateral
Chelonia: dorsoventral view of whole body

Observed normal haematological and biochemical ranges used to assess dehydration and biochemical
imbalances in selected reptiles
(adapted from references 4 and 5, and the authors unpublished observations)

Green iguana

Gila monster

PCV (l/l)
TP (g/l)
Urea (mmol/l)
Creatinine (mmol/l)
Uric acid (umol/l)

25-38
50-78
0-0.7
42-80
70-140

Glucose (mmol/l)
Sodium (mmol/l)
Chloride (mmol/l)
Potassium (mmol/l)

9.4-16.0
140-183
102-125
1.3-5.2

25-30
60-85
na
na
100-1000
0
2.5-6.0
150-190
114-130
4.1

Tortoise
(Testudo sp)

Box tortoise

Boa constrictor

Rat snake

Caiman

19-40
50-75
0.25-6.70
20-150
75-200

20-38
40-50
na
na
100-200

20-32
46-80
0-1.67
0-26.5
75-250

20-30
40-70
na
na
75-250

26
50-65
na
na
175

2.6-5.2
120-158
98-128
4.0-7.0

2.0
130-149
104-108
4.6-4.7

0.6-4.0
130-152
104-124
3.0-5.7

na
130-160
125-147
4.1-5.2

4.1-6.3
139-150
109-132
3.8-7.9

horizontal beam lateral


horizontal beam anterior-posterior view

Ultrasonography8,9
Ultrasound permits the visualisation of soft tissues and
may be most useful in the chelonia. 7.5 and 10 MHz transducers with stand-off are usually better at providing good
resolution in small reptile patients. 5 and 3.5 MHz transducers can be used for larger reptiles. Copious contact gel must
be applied to the reptilian scaly skin, especially in heavily
keeled species.
In some cases a water bath may be more appropriate. Organ position will change with rotation of the reptile and
therefore (as with radiography) try and maintain the animal
in a normal body posture.
Chelonia: sector scanners can be used in the soft tissue
spaces between the carapace, plastron and limbs. The reproductive tract, heart and liver can all be assessed for major abnormalities, but identifying subtle differences in tissue structure may be more difficult.
Lizards and snakes: the ribs of snakes almost extend
along the whole body-length and will be a hindrance to ultrasound. Nevertheless, gonads, ova, eggs can be assessed
and masses can be differentiated.

25

veterinary use.

Cytology and microbiology


Cytology2
The submission of clinical material (e.g. impression
smears, skin scrapes, fine needle aspirates, lung washes,
stomach washes, faeces, urine, spinal fluid, tissue biopsies
or post mortem tissues) for microscopy, histopathology and
microbiology is often the best means of obtaining a definitive diagnosis. However, the often unique tissue structure of
reptiles does necessitate the services of a pathologist with
experience in reptile pathology. This is especially true when
submitting small biopsies obtained from endoscopy.
When time permits full histopathology is to be preferred,
but in cases of emergency cytology offers the clinician a good
second best. Cytology will usually not provide a complete diagnosis and therefore cannot replace histopathology, however
it can provide a working diagnosis while histology is pending.
Impression smears from skin lesions, fine needle aspirates,
lung wash smears, stomach wash smears etc can be stained
using Diff Quik stains and examined under a microscope.

Microbiology11
10

Endoscopy

Fibre-optic endoscopy is the diagnostic imaging and


sampling technique of choice in the authors experience. The
use of small flexible and rigid endoscopes (1-2 mm) enable
the clinician to get inside the animal and depending on the
reptiles size, permits;
visualisation of the gastro-intestinal tract via the mouth and
cloaca
visualisation of the respiratory tract via the glottis
laparoscopy
 visualisation and biopsy of kidneys
 visualisation and biopsy of liver
 visualisation and biopsy of pancreas
 visualisation and biopsy of spleen
 visualisation of the heart
 visualisation of the lungs
 visualisation of the reproductive tract
 visualisation of the bladder (where present)
 visualisation of the gastro-intestinal tract
 visualisation and biopsy of any masses, neoplasia etc
With new endoscopic operating equipment such as the
Storz endoscopic scissors, forceps and injection needle it is
also possible to debride, cut, retrieve foreign bodies, aspirate
and execute remote local injections.

MRI and ct8,9


These sophisticated imaging techniques are unlikely to
be easily accessible to most clinicians or financially unacceptable to most clients. However, the quality of the images
are excellent and some hospitals may be prepared to tolerate

Gram-negative bacteria are common (often commensal)


organisms in reptiles, but heavy pure growths of a single
predominant bacteria is often significant. Anaerobic bacteria
are often important pathogens that are simply overlooked on
routine microbiological culture. Mycotic infections also appear to be more common in reptiles than domesticated mammals. In summary request aerobic, anaerobic and fungal culture with appropriate sensitivity testing.
Viruses are becoming more clinically apparent. Aspirates
used be sent on dry swab while tissues are best transported
fresh on ice. Scanning electronmicrscopy may reveal virus
particles while virus culture and isolation is now possible in
many labs using reptile and avian cell lines.

Post mortem examination12,13,14


No clinician can save every animal. Death, however unfortunate to the animal and owner, does provide the clinician
with a huge resource for not only making an elusive diagnosis but also for learning the pathogenesis of reptile disease.
Every reptile clinician needs to familiarise themselves with
normal reptile anatomy and post mortem examination is invaluable. A systemic approach is vital and useful histopathological and microbiological information will only be obtained if the submitted tissues are fresh at sampling and
stored correctly.

Key words
Reptile, diagnostics, history, clinical examination,

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4th European FECAVA SCIVAC Congress

26

4th European FECAVA SCIVAC Congress

haematology, biochemistry, faecal examination, radiography,


ultrasonography, endoscopy, cytology, microbiology, post
mortem.

References
1.
2.

3.

4.

5.

6.

7.

8.

9.

Divers, S.J. (1996). Basic reptile husbandry, history taking and clinical
examination. In Practice 18(2): 51-65.
Jackson, O.F. and Lawton, M.P.C. (1992). Examination and diagnostic
techniques. In: Manual of Reptiles (Eds. P.H. Beynon, M.P.C. Lawton,
J.E. Cooper). BSAVA, Cheltenham. Pages 32-39.
Campbell, T.W. (1996). Clinical pathology. In: Reptile Medicine and
Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages 248257.
Divers, S.J., Redmayne, G. and Aves, E.K. (1996). Haematological and
biochemical values of 10 green iguanas (Iguana iguana). Veterinary
Record 138:203-205.
Stein, G. (1996). Hematologic and blood chemistry values in reptiles.
In: Reptile Medicine and Surgery, p473-483 (Ed. D. R. Mader). WB
Saunders, Philadelphia.
Lane, T.J. and Mader, D.R. (1996). Parasitology. In: Reptile Medicine
and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages
185-202.
Frye, F.L. (1991). Applied clinical nonhemic parasitology of reptiles.
In: Biomedical and Surgical Aspects of Captive Reptile Husbandry
(Ed. F.L. Frye, second edition). Pages 281-325.
Silverman and Janssen, D.L. (1996). Diagnostic imaging. In: Reptile
Medicine and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia.
Pages 258-264.
Rubel, A., Kuoni, W. and Frye, F.L. (1991). Radiology and imaging.
In: Biomedical and Surgical Aspects of Captive Reptile Husbandry
(Ed. F.L. Frye, second edition). Pages 185-208.

10.

11.

12.

13.
14.

Jenkins, J.R. (1996). Diagnostic and clinical techniques. In: Reptile


Medicine and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages 264-276.
Rosenthal, K. and Mader, D.R. (1996). Microbiology. In: Reptile
Medicine and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages 117-125.
Cooper, J. E. (1992). Post mortem examination. In: Manual of Reptiles (Eds. P.H. Beynon, M.P.C. Lawton, J.E. Cooper). BSAVA, Cheltenham. Pages 40-49.
Mader, D.R. (1996). Euthanasia and necropsy. In: Reptile Medicine
and Surgery (Ed. D. R. Mader). WB Saunders, Philadelphia. Pages
277-281.
Frye, F.L. (1991). Euthanasia and necropsy. In: Biomedical and Surgical Aspects of Captive Reptile Husbandry (Ed. F.L. Frye, second
edition). Pages 513-528

27

EUROPEAN SOCIETY OF FELINE MEDICINE-ESFM

Diagnostic and therapeutic approaches to neutropenia


and neutrophil dysfunction
The neutropenic and pyrexic cat

Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

OVERVIEW
Neutropenia
Neutropenia may indicate excessive tissue demand for
neutrophils, decreased production, or immune-mediated destruction. Neutropenia is as great a concern as neutrophilia
and is possibly a more serious a problem because neutrophils are the bodys first line of defense against invading
microorganisms. Neutropenia is any decrease in neutrophil
numbers below the reference interval. However, clinical
signs associated with neutropenia are seldom observed unless the neutrophil count is below 1000 per microliter and,
perhaps, less than 500 per microliter. Neutropenia is associated with infection, drugs, immune dysfunction, acquired
immunodeficiency, neoplasia, and may be idiopathic.

Fever
Temperature, like so many biologicial functions, normally displays circadian rhythmicity. In the cat, temperatures
are often lowest in the morning and highest in the afternoon.
Temperature is regulated by homeostatic mechanisms that
strike a balance between heat production and heat dissipation. Abnormal elevation in body temperature, or pyrexia,
can occur due to hyperthermia or fever. Hyperthermia is
treated with physical cooling methods whereas fever is often
treated with drugs. Fever is often a positive response and, in
most instances, is simply noted. Interleukin-1 is produced by
mononuclear phagocytes and directly acts upon the hypothalamic control center causing fever.

Fever of undetermined origin


Fever of undetermined origin (FUO) is an unusual presentation of a usual problem. FUO is caused by infection,
immune dysfunction, or neoplasia

CLINICAL AND THERAPEUTIC APPROACH


Diagnostic Evaluation of Granulocytopenia (less than
5000 cells per microliter in the dog and less than 3300 cells
per microliter in the cat).

Diagnostic evaluation should include an extensive history of current and recent (including the past 6 weeks) drug
therapy and physical examination to evaluate or estimate
splenic size.
1. Hematologic evaluation - the total white blood cell count
and differential in absolute terms with or without relative
lymphocytosis.
2. Bone marrow aspiration (and/or biopsy) is necessary
when the white cell count is persistently below 3000 cells
per microliter. This is especially needed when another cell
line is also abnormal to determine marrow cellularity or
arrest in cell maturation.
3. Screening tests for antinuclear antibodies in both systemic
lupus erythematosus or rheumatoid arthritis. Again, this is
especially required when rheumatoid arthritis is suspected
of being associated with hypersplenism.
4. Radiographic, ultrasound or cytologic examination of the
spleen to evaluate size, and potential for cellular sequestration since hypersplenism may be associated with leucopenia as well.

Neutropenia
Leucopenia is most often caused by neutropenia. Neutropenia may be the result of overwhelming inflammatory
processes which shorten circulating neutrophil survival especially when myelopoiesis -specifically neutrophil production - is ineffective, or when there is bone marrow myelosuppression. Neutropenia and toxic morphologic alterations
of neutrophils may be anticipated in Gram-negative sepsis or
endotoxemia. If mature neutrophils are fewer than immature
cell forms, this is regarded as a degenerative left shift. Degenerative left shifts may appear with both neutrophilia or
neutropenia and indicate inappropriate - deficient - bone
marrow response. Increased neutrophil margination, adherence of neutrophils to microvascular endothelium pseudoneutropenia - may result from endotoxemia or from
anaphylactic reactions. Viral infections, a wide variety of
disparate drugs and environmental toxins, and neoplasia (especially during chemotherapy) may induce severe neutropenia as well as affecting other cell lines in a similar manner.
Feline immunodeficiency virus (FIV) infection is characterized by moderate to severe leucopenia, neutropenia,
and often, lymphopenia and eosinopenia. Appropriate
myeloid activity or mild bone marrow myeloid hyperplasia

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28

with a left shift to progranulocytes often accompanies the


neutropenia. Chronic infection is characterized by intermittent neutropenia and lymphopenia. Viral infection of bone
marrow myeloid precursors may be involved with the cytopenias. Feline immunodeficiency virus induces progressive immunodeficiency, opportunistic infections, nutritional
deficiencies, as well as some forms of neoplasia. The cytopenias that develop during the symptomatic disease induced by FIV may play a significant role in these processes.
Experimental inoculation of canine parvovirus in the cat induces a decrease in total numbers of both myeloid and erythroid cells in the bone marrow.
Feline leukemia virus infection (FeLV) is a retrovirus
(oncovirus subfamily) that causes immunodeficiency and
neoplastic disease in domestic cats. The physiologic systems
affected are the hematopoietic, lymphatic, and immune systems possibly by neuroendocrine dysfunction, resulting in
immunosuppression with secondary infections and/or development of neoplastic disease. Anemia is often severe. Lymphopenia and neutropenia may be present; however neutrophils can be elevated in response to secondary infections.
Serology and bone marrow examination are indicated
among diagnostics.
Feline panleucopenia is an acute, enteric, viral infection
of cats characterized by sudden onset, depression, vomiting
and diarrhea, severe dehydration, and a high mortality caused
by feline parvovirus. The systems affected are the
hematopoietic, lymphatic, and immune systems with loss of
all white blood cells and atrophy of the thymus. Panleucopenia is the most consistent finding with total leucocyte counts
between 500 and 3000 cells per microliter. Immunoassays
and serology are the only useful diagnostics. Supportive
treatment is indicated as specific therapy is not usually successful.
Bacterial-induced myelonecrosis occurs in dogs and cats.
Reduced survival neutropenia can be caused by bacteremia (pneumonia, peritonitis, pyothorax), immune-mediated destruction, drug-induced destruction, hypersplenism
(sequestration), and paraneoplastic syndrome (the precise
mechanism is unknown).
Drug/Chemical-induced Neutropenia is often caused by
chloramphenicol or benzene ring compounds in cats - eucalyptus oil, menthol, camphor.
Mitoxanthrone is a chemotherapeutic agent which induces myelosuppression. The myelosuppression has been
successfully treated with recombinant canine granulocytecolony stimulating factor (rcG-CSF).
Administration of zidovudine (> 30 mg/kg) in cats resulted in dose dependent progressive neutropenia and anemia.
Griseofulvin administration has been associated with the
development of absolute neutropenia in cats. This is especially apparent in cats infected with FIV.
Cephalosporin administration may induce bone marrow
suppression in both dogs and cats as the result of ineffective
marrow erythropoiesis and myelopoiesis.
Other potential drugs include gold salts, thiacetarsamide, meclofenamic acid, quinidine gluconate, captopril, and penicillamine.
Recombinant canine G-CSF (2.5 ug/kg q 12 h) administration had been observed to be effective in stimulating

4th European FECAVA SCIVAC Congress

myelopoiesis in dogs.

Cyclic neutropenia
Cyclic neutropenia is an inherited disease in Grey Collies
(Grey Collie Syndrome; Cyclic Hematopoiesis) and is suspected in other canine breeds. It is characterized by recurrent
episodes of neutropenia lasting 12 to 14 days. Thrombocytopenia and anemia may accompany cyclic neutropenia. Neutrophil functions are also impaired and frequent infections are
therefore anticipated. Affected dogs given low dose rcG-CSF
continued to have neutropenic cycles but the degree of neutropenia and the clinical signs were ameliorated. Cyclic
hematopoiesis has been described in the cat as an acquired disease possibly related to feline leukemia viral infection (FeLV).

Chronic idiopathic neutropenia syndrome


Persistent neutropenia has been described in the cat that
resembles chronic idiopathic neutropenia syndrome of man.
Decreased numbers of mature granulocytic cells and colony
forming units-granulocyte macrophage (CFU-GM) have
been observed in bone marrow and in bone marrow culture
respectively.

Diagnostic evaluation of functional


granulocytic defects
Neutrophils function as phagocytes by a complex interaction of immunoglobulins, complement, and neutrophil enzymes. Total evaluation involves evaluation of patients who
exhibit an inability to handle infections.
1. Chemotaxis may be tested in agar media or in a three part
Boyden chamber.
2. Quality and quantity of immunoglobulins and complement must be determined. Quantity is determined my immunoelectrophoresis and determination of the presence of
various complement components. Quality of immunoglobulins may be tested similarly to chemotaxis in
agar media. A screening test of complement function is
the total lytic complement test.
3. The nitroblue tetrazolium dye test (NBT) is a test of nonimmune phagocytosis and measures the contribution of
peroxidase qualitatively.
4. The myeloperoxidase stain which measures the presence
of the enzyme in neutrophil cytoplasm also provides qualitative measures.

Functional defects of granulocytes


Neutrophil function involves chemotaxis, phagocytosis,
and bacterial killing. Problems with neutrophil function can
involve one or all of these functions. Chemotaxis and phagocytosis are dependent on external factors involving immune
(antibody) globulin and complement opsonins C3a, C5a, and
C567. Bacterial killing involves production of hydrogen per-

oxide intracellularly by anaerobic glycolysis and the hexose


monophosphate shunt and utilizes myeloperoxidase of granulocytic primary granules.
Diseases associated with functional defects of granulocytes are characterized by repeated bacterial or fungal infection beginning early in life or infections with otherwise lowvirulence organisms in patients with appropriate granulocyte
counts. Most involve inherited disorders of immunoglobulins, complement, or the hexose monophosphate shunt. Acquired transient deficiencies secondary to drugs are poorly
understood.
Leucocyte dysfunctions in small animals include the
Chediak-Higashi Syndrome, canine granulocytopathy, and
defective neutrophil function of the Doberman Pinscher.
Neutrophil dysfunctions may also be associated with complement or immunoglobulin deficiencies. Defective humoral
immune components include specific IgA deficiency of German Shepherds, Beagles, Shar Peis, and other breeds, IgM
deficiency of the Doberman Pinscher, C3 deficiency of the
Brittany Spaniel and possible IgG deficiency of the
Weimaraner.
The Pelger-Huet Anomaly is in inherited defect observed
in dogs and cats as well as numerous other species. Mature
neutrophils of affected individuals have nuclear hyposegmentation and, possibly, moderate dysfunction associated
with diminished migratory capabilities.
Myeloproliferative disorders - leukemias - often have associated neutrophil dysfunction and/or neutropenia. Decr-

29

reased production of neutrophils (or other hematopoietic


cells can occur from infiltrative bone marrow diseases leukemia, nonhematopoietic neoplasia metastatic to the marrow cavity, myelofibrosis or ostesclerosis, disseminated
granulomatous disease, or myelodysplasia.

Suggested reading
Gabbert NH: Cyclic neutropenia in a feline leukemia-positive cat: a case report. J Amer Animal Hosp Assoc 20:343, 1984.
Helton KA, Nesbitt GH, Caciolo PL: Griseofulvin toxicity in cats: literature
review and report of seven cases. J Amer Animal Hosp Assoc 22:453,
1986.
Latimer KS, Rowland GN, Mahaffey MB: Homozygous Pelger-Huet anomaly and chondrodysplasia in a stillborn kitten. Vet Pathol 25: 325, 1988.
Obradovitch Je, Ogilvie GK, Stadler-Morris S et al: Effect of recolmbinant
canine granuloctye colony-stimulating factor on peripheral blood
neutrophil counts in normal cats. J Vet Intern Med 7: 65, 1993.
Breitschwerdt EB, Brown TT, de Buysscher E et al: Rhinitis, pneumonia,
and defective neutrophil function in the Doberman Pinscher. Am J
Vet Res 48:1054-1062, 1987.
Withbread TJ, Batt RM, Garthwaite G: Relative deficiency of serum IgA in
the German Shepherd dog: a breed abnormality. Res Vet Sci 37:350352, 1984.
Hansen P, Clercx C, Henroteaux M et al: Neutrophil phagocyte dysfunction
in a Weimaraner with recurrent infections. J Small Animal Practice
36:128-131, 1995.
Mandell CP, Jain NC, Farver TB et al: The significance of normoblastemia
and leucoerythroblastic reaction in the dog. J Amer Animal Hosp Assoc 25, 665-672, 1989.

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4th European FECAVA SCIVAC Congress

31

EUROPEAN SOCIETY OF FELINE MEDICINE-ESFM

Feline anemia: practical investigation and management


Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Summary
Red blood cell production and its control are intrinsic to
understanding anemia. Anemia is a sign of underlying disease. Complete physical examinations are complemented by
complete hemograms. Responsive anemias are caused by hemorrhage and hemolysis. Nonresponsive anemias are more
common in the cat than are responsive anemias. The prior use
of drugs must be considered. Retroviral diseases are another
consideration. Bone marrow examination may be beneficial.
Treatment of anemia is directed against the underlying cause.

The erythroid cell system comprises the population of


circulating red blood cells (RBCs) and their nucleated precursors located in the bone marrow of normal feline adults.
A complex and not yet fully understood homeostatic mechanism (involving in part the hormone erythropoietin) operates upon marrow precursors to maintain a circulating RBC
population at a size and hemoglobin content adequate to preserve normal tissue oxygen tensions. The critical factor in
the homeostatic mechanism that regulates the production of
erythropoietin is tissue oxygen tension, not RBC number or
blood hemoglobin concentration.1-3
RBCs traditionally have been considered to be solely
oxygen-carrying and oxygen-delivering cells, functions certainly of critical importance. These cells are now being reexamined in terms of their role in physiologic defense. The surface area of RBCs is enormous - and is known to be adsorptive. The redefinition of RBC function has to do with this adsorptive capacity and the intrinsic ability of RBCs to remove
or cleanse the plasma component of blood. RBCs adsorb
many microscopic materials, which are removed by the
phagocytes of the mononuclear-phagocyte system (MPS) located primarily in the liver and spleen. The RBC membrane
is thus cleansed, and for the most part the cleansed cell is returned to the circulation. This phagocytic processing also has
an impact on the RBC in terms of its longevity (or senescence). Repeated phagocytic incursions does affect the
shape, viability, and longevity of the RBC.1,2,4,5

ANEMIA IN PERSPECTIVE
Anemia, defined as a lower than normal blood hemoglobin
(Hb) concentration or packed cell volume (PCV; hematocrit

[HCT]), occurs if RBC production is acutely or chronically insufficient to replace RBC losses, which may be caused by normal RBC senescence, accelerated RBC destruction (hemolysis), or extracorporeal blood loss (bleeding). Some examples
of anemia result from relatively uncomplicated alterations in
single factors, for example, transient anemia following an
acute hemorrhagic event in an otherwise healthy individual. In
most cases, however, the pathophysiology of anemia involves
the interplay of several disturbances in RBC homeostasis, including limitations of production as well as abnormal red cell
survival. Our first obligation is to examine these factors in a
general sense and to evaluate the significance and limitations
of the techniques for distinguishing and quantitating them.1-3

RED BLOOD CELL PRODUCTION


Basic knowledge about feline RBC production is intrinsic to understanding how the cat responds to a lowered red
cell mass (i.e., anemia). In the normal adult, RBC production is confined to the axial skeleton. When erythropoiesis
is required, the volume of active marrow may expand into
the distal long and flat bones, that is, into the fatty marrow
and at the expense of bony matrix. Under extreme and prolonged stress or when marrow is replaced by pathologic tissues, extramedullary sites such as spleen, liver, and lymph
nodes may develop foci of erythropoiesis. All of these tissues including the marrow are capable of a six- to eightfold
increase in RBC production in response to the stimulus of
anemia. Thus even under conditions of accelerated red cell
destruction, blood Hb concentration may remain nearly normal as long as the rate of destruction does not exceed the
capacity for compensatory expansion of the RBC precursor
population.6

ERYTHROPOIETIN
Erythropoietin (EPO) has a number of effects. High concentrations of EPO, in concert with granulocyte macrophage
colony-stimulating factor (GM-CSF), stimulate the erythroid progenitor to become an erythroid burst forming unit
(BFU-E), an explosive erythroid productive cell. In low concentrations EPO together with GM-CSF and interleukin 3
(IL-3) convert the BFU-E to an erythroid colony-forming
unit (CFU-E), a cell capable of producing colonies of red

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32

cell precursors. Low concentrations of EPO also convert the


CFU-E into the first recognizable RBC precursor in the bone
marrow. In addition, EPO accelerates RBC production and
maturation, internal cell Hb production, and finally modulates the movement of marrow reticulocytes into peripheral
blood reticulocytes. To summarize, EPO activates erythropoiesis, accelerates erythropoiesis, and is intrinsic to the successful delivery of RBCs to peripheral blood.2

4th European FECAVA SCIVAC Congress

aggregate reticulocytes greater than 50,000/l is evidence of


regeneration.7 Basophilic stippling, a dark bluish stippling of
some immature RBCs, is commonly found in some RBCs
released into peripheral blood in response to anemia. This
finding has no special significance insofar as the etiology of
anemia in the cat is concerned.6

FELINE HEMOGLOBIN
MORPHOLOGY OF ERYTHROPOIESIS
The process of red cell production from blast to adult RBC
takes from 4 days to 1 week. The first morphologically identifiable bone marrow erythroid precursor is the rubriblast. In
this cell is the initiation of characteristic RBC protein production (Hb and enzymes), as well as surface antigens and metabolic machinery. One of these cells can have as many as 16 to
32 progeny erythrocytes. When this cell divides giving rise to
the prorubricyte (which in turn leads to the formation of the
basophilic rubricyte) loss of replicative function and loss of
the nucleus itself begins. The basophilic rubricyte gives rise to
the polychromatophilic rubricyte, a cell in which morphologic recognition of cytoplasmic hemoglobin production is first
possible. Whether the polychromatophilic rubricyte is the last
of the dividing RBC precursors is arguable, but from it arises
the metarubricyte, in essence the nucleated RBC (nRBC) often observed in peripheral blood smears of anemic patients.
The nucleus of this cell is almost nonfunctional, and when extruded the metarubricyte becomes the earliest bone marrow
reticulocyte. Under normal circumstances bone marrow reticulocytes mature in the marrow for approximately 3 days and
then move from the extravascular hematopoietic space to the
intravascular space via the bone marrow venous sinus. Here
the cell is simply called a reticulocyte. After approximately 24
hours the reticulocyte loses its intracellular materials (which
stain with new methylene blue). The cell is now an adult RBC
destined to live approximately 80 days in a normal blood volume of about 70 ml/kg (a number different than in other common domestic animals).6
Nucleated RBCs may appear in peripheral blood of adult
cats without evidence of intensified erythropoiesis and may
be a sign of systemic stress of disease or splenic inactivity.
This finding is unique to the cat. Nucleated RBCs do acutely accompany increased reticulocyte numbers in early, active erythropoiesis. The presence of increased nRBCs without reticulocytes or in nonanemic states also suggests bone
marrow disease or cardiopulmonary dysfunction. These
cells are often observed in myeloproliferative disease.6

FELINE RETICULOCYTES
Feline RBCs retain stainable reticulum for several
weeks. Type I forms have a punctate reticulum staining and
are not counted in traditional peripheral blood reticulocyte
counts. Types II and III with dense aggregates of reticulum
and conforming to the morphologic appearance of reticulocytes of other species are counted in peripheral blood as a
gauge of erythroid response.6 A reticulocyte concentration of

Two hemoglobins, designated major and minor, in the


cat differ from other mammalian hemoglobins in that they
have the largest number (eight) of reactive sulfhydryl
groups. The physiologic occurrence of small eccentric refractile bodies (erythrocyte refractile bodies; Heinz bodies;
Schmauch bodies) indicates the unusual propensity for hemoglobin denaturation in cats. This is most probably related
to the unique structure of feline hemoglobins.6 This may also be related to the fact that cats have a unique nonsinusoidal
spleen, which does not readily remove atypical RBCs.8

ADULT FELINE RED BLOOD CELL


ANALYTES
With respect to PCV, Hb, and RBC number as well as
RBC indices, cats generally attain adult values by 4 or 5
months of age. There are significant differences between kitten and adult values, as discussed in more definitive texts on
the subject.6,9

PHYSICAL EXAMINATION
A thorough physical examination is essential in the diagnosis of feline anemia. For example, icterus can be caused
by hemolysis, cats with lymphatic diseases often have concurrent or associated anemia, and cats with petechiae and/or
ecchymoses most probably have thrombocytopenia and/or
thrombocytopathia or vasculitis.

ANEMIA AS A DIAGNOSTIC SIGN


Anemia is the result of only a few processes and when
these processes are considered, a series of diagnostic steps
may be set in motion, often revealing the underlying cause.
Iron- deficiency anemia in kittens may result from portosystemic shunts (microcytosis without evidence of RBC regeneration), all milk diets, or from external or internal parasitism: in adults parasitism would be lower on a differential
list and blood loss through ulceration or neoplasia would be
more common causes. Decreases in total protein (TP) and
the RBC indices along with decreases in serum iron (SI) and
increases in total iron-binding capacity (TIBC) would be anticipated. Anemia of inflammatory disease (AID; anemia of
chronic disease) is mild if detectable and is associated with
decreases in both SI and TIBC. Anemia associated with hemorrhage is not difficult to diagnose and is usually associated with a history of trauma.

Hemorrhagic anemia and hemolytic anemia are unique


in terms of increasing reticulocyte percentage once the bone
marrow reaches increased productive status 3 to 4 days after
the insult. Often in intravascular hemolysis or hemolysis induced by Heinz bodies, the mean corpuscular hemoglobin
concentration (MCHC) is above the reference interval.
Whenever this analyte is increased, the preceding causes
should be considered.
Hypohormone anemia, which is anemia associated with
renal disease, hypothyroidism, and hypoadrenocorticism, requires specific and incisive testing. Anemia associated with
bone marrow disease is usually accompanied by cytoses or
cytopenias in at least one other cell line.

EVALUATING LABORATORY TESTS


A complete hemogram complete with all three RBC indices (mean cell volume [MCV], hemoglobin concentration
by percentage [MCHC] and hemoglobin by weight [MCH]),
HCT, Hb, RBC number, reticulocyte and nRBC numbers,
TP, examination of RBC, white blood cell (WBC) and
platelet morphology, and a differential in absolute numbers
is the first step in solving the mystery of anemia. Regenerative anemias are those with elevated reticulocyte counts (see
above) and are indicative of hemolysis or hemorrhage. Only
when they are accompanied by large numbers of reticulocytes can nRBCs be associated with RBC regeneration.
All other forms of anemia are considered nonregenerative or hypoproliferative. When these anemias are severe,
transfusion is indicated.

33

dogs because the occurrence of natural isoantibodies is common. Approximately 70% of all type B cats have anti-A antibody in a high enough titer to cause decreased RBC survival
and acute hemolysis. As little as 5 ml of incompatible blood
is enough to cause a fatal reaction. In 35% of all type A cats
anti-B is present but usually in low titer; reaction in these animals is less frequent. Although the incidence of type B cats
in the United States is low, many purebred cats (excepting the
Siamese) such as the Cornish and Devon Rex, British shorthair, Abyssinian, and Himalayan cats have a high frequency
of B blood types. Crossmatching is strongly recommended
for all cats about to receive blood or blood products. The
presence of natural isoantibody always result in decreased
RBC survival posttransfusion. Mean RBC survival is approximately 30 days in cats of the same blood type and less
than 10 to 14 days in cats with differing blood types.10
Donor cats should be screened for red cell parasites,
heartworms and feline leukemia virus (FeLV), feline infectious peritonitis (FIP), and feline immunodeficiency virus
(FIV). At 2 week intervals 10 ml/kg can be collected. The use
of citrate-phosphate-dextrose-adenine (CPD-A1) is the recommended anticoagulant. Heparin is contraindicated as it activates platelets and antithrombin III and can result in many
unwarranted and disparate reactions including hemorrhage.
When delivering feline whole blood taken in a citrate anticoagulant care must be taken not to cause hypocalcemia,
which may be severe and even lethal. Citrate is a strong calcium chelator. Caution must also be used not to induce volume overload. Generally if less than 20% of blood volume is
delivered to a normovolemic but anemic feline patient during
an 8 hour period, volume overload does not occur. As mentioned, cats have a normal blood volume of approximately 70
ml/kg.6

BONE MARROW BIOPSY


Bone marrow aspiration or core biopsy is reserved for
any unexplained cytopenia or when neoplasia is staged.
When bone marrow examination is used to help explain cytopenia, it is imperative that the bone marrow preparations
be accompanied by a concurrent hemogram (i.e., blood
drawn at the same time as the marrow sampling). Because
normal diurnal and day-to-day variation is quite significant
and the hematologists diagnostics are always referable to
peripheral blood numbers, it is incorrect and poor science to
draw information from a bone marrow aspirate without reference to a concurrent hemogram. A core biopsy is indicated when attempts at aspiration do not yield bone marrow
particles or sufficient cells.
Bone marrow aspirate or core biopsy are helpful in the
diagnosis of myelofibrosis, myelophthisis, and myeloproliferative diseases in general. These samples may also aid in
the diagnosis of pure red cell aplasia or aplastic pancytopenia, which are often drug induced.

FELINE BLOOD GROUPS AND FELINE


TRANSFUSION MEDICINE
Three feline blood groups have been described: A, B, and
AB. The feline blood group system is different than that in

CONSIDERATIONS11
Acepromazine, Chloramphenicol, Trimethoprim Sulfa, Griseofulvin
These are drugs that can cause hemolytic anemia in the
cat or cytopenias due to bone marrow suppression. Pancytopenia commonly occurs in cats when griseofulvin is used
in the treatment of dermatomycosis.
Oxidative RBC Injury
Denaturation of feline hemoglobin and Heinz body anemia results from excessive doses of Vitamin K. In dosages
in excess of 5 mg/kg/day vitamin K results in severe Heinz
body hemolysis. Other drugs that can cause oxidative injury
are benzocaine, acetaminophen, methylene blue, and acepromazine. Onions can also cause Heinz bodies.
Severe Heinz body hemolysis can result when tiny
amounts of lidocaine are sprayed into the oral cavity before
intubation or when urinary antiseptics containing methylene
blue are used. MPS removal of these cells leads to dramatic
and severe anemia.11
Propylene Glycol in Semi-Moist Cat Foods
These materials cause Heinz bodies in cats. In cats receiving these foods red cell masses are generally lower than

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in other cats.

Retroviruses
FeLV and FIV induce a variety of bone marrow diseases
including anemia. These viruses also cause erythroid dysplasia. The peripheral blood manifestations of these viral incursions are macrocytic RBCs that are not reticulocytes and
nucleated cells that are unclassifiable. These anemias are not
regenerative, but often the MCV is elevated significantly
above the reference interval.

4th European FECAVA SCIVAC Congress

but not observed, the examiner should place the ethylene diamine tetracetate (EDTA) anticoagulated blood in the refrigerator for 8 to 10 hours and look for autoagglutination on the
test tube walls or hemolysis in plasma.
Doxycycline is the drug of choice in treating hemobartonellosis in cats and it has the advantage of once a day dos-

Table 1. Effects of erythropoietin


Direct activation of stem cells and erythroid precursors

Immune-Mediated Hemolysis
Positive direct antiglobulin test (DAT; direct Coombs
test), albeit useful in detecting immune-mediated hemolysis,
is positive when there is a detectable concentration of immunoglobulin on the red cell surface for any reason.4,5 For
example, hemobartonellosis can cause a positive DAT, which
will remain so until this organism is cleared from the body.10
In treating immune-mediated hemolytic anemia (IHA) in
the cat, prednisone at 2 to 4 mg/lb (in contrast to the dog in
which low dosage glucocorticoid is successful), is administered every 12 hours. In confirmed cases of IHA in the cat,
chlorambucil, which is not expensive and has few side reactions, has also been reported to be successful as a second
drug. Chlorambucil comes in 2 mg tablets; typically, cats receive 2 to 3 tablets of chlorambucil once every other week.
It is an excellent immunosuppressive agent. Azathioprine is
not recommended as an immunosuppressive agent in the cat.

Increased erythroid precursor hemoglobin production


Decreased bone marrow erythroid maturation time
Increased (earlier) release of bone marrow reticulocytes

Table 2. Classification of anemia


Nonregenerative, hypoproliferative anemia
Iron deficiency
Anemia of inflammatory disease
Early stages of hemolysis and hemorrhage
Hypoendocrine diseases
Bone marrow disease

RBC Morphologic Changes


There are numerous morphologic changes in RBCs that
are diagnostically helpful. Unfortunately, spherocytes are
difficult to recognize in feline blood smears. Schistocytes,
(fragmented RBCs) are recognized in disseminated intravascular coagulation (DIC). Leptocytes and acanthocytes,
which are suggestive of hepatic diseases in other domestic
species are rare in the cat. Basophilic stippling, although
rare, may be associated with lead toxicity.
Howell-Jolly bodies (remnants of nuclear materials), are
observed when erythropoiesis is active and suggest bone
marrow activity in the erythroid cell line. Often Howell-Jolly bodies are associated with increased reticulocyte numbers
in a new methylene blue stain or with polychromasia in a
Wrights stained smear. Heinz bodies (sometimes described
as signet ring cells) are evidence of hemoglobin denaturation and may involve certain drugs as has been described.
They may also be seen in anorectic cats that are not receiving vitamin B complex in their diets.
Although not common, autoagglutination is indicative of
immune-mediated hemolytic processes, most probably involving immunuoglobulin M or some forms of immunoglobulin G.
Hemobartonellosis
The DAT is often positive in cats with hemobartonellosis. This disease is always secondary to another physiologically stressing event, and an infectious etiology must be
considered. Most commonly these are viral- or bacterial-induced primary processes. If hemobartonellosis is suspected

Regenerative, hyperproliferative anemia


Hemolytic disease: after 3-4 days
Acute hemorrhage: after 3-4 days

Table 3. Feline hematologic reference intervals


Analyte

Interval

Hemoglobin
Hematocrit
Red blood cells
MCV
MCHC
MCH
Reticulocytes
White blood cells
Neutrophils
Band neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Platelets
Total protein
Fibrinogen

6.9 - 9.6 nmol Hb(Fe)/L


33 - 46 L/L
7.55 - 10.87 (1012/L)
38.2 - 48.0 fL
19.7 - 22.5 nmol/L
0.81 - 1.02 fmol
0.2% - 1.6%
5.7 - 16.3% 109/L
2,500 - 12,500/l
0 - 300/l
1,500 - 7,000/l
0 - 800/l
0 - 1,500/l
Rare
140 - 500 x 109/L
6.0 - 8.0 g/dL
0.1 - 0.3 mg/dL

*Modified from deBruijne JJ, Feldman BF: Referentiewaarden van laboratoriumonderzoek bij hond en kat. Analyse 38:11, 248 - 252, 1983.

ing. Tetracycline generally suppresses the feline appetite and


sometimes induced fever. Hypersalivation and vomiting are
other feline tetracycline reactions.
Total Protein, Total Bilirubin, Urine Bilirubin
In cats hemorrhaging is associated with decreases in total plasma or serum proteins accompanying the decreases
observed in red cell mass whereas hemolysis is characterized by normal to increased total proteins. Increases are often artifactual and are caused by the amount of hemolysis or
red cell membrane debris in the plasma or serum. Cats with
hemolysis often have increases in both total bilirubin and
urine bilirubin. Cats that are hemorrhaging would not have
increases in these analytes.

35

ic renal disease. Dosage is 100 to 150 units/kg subcutaneously every 2 to 3 days. As it is a human recombinant
product, about one fourth to one third of cats receiving this
hormone will produce antibodies against it in 6 to 8 weeks.
Care must be taken against overzealous use of this product,
which can lead to as polycythemia with severe to fatal results. As the Hct reaches the reference level, the interval
dosage of erythropoietin is reduced to every fourth of fifth
day. The underlying renal disease is unaffected, but the quality of life is markedly improved.12

References
1.

Zinc
The ingestion of zinc containing pennies and the resultant intravascular hemolysis is seen more often in dogs than
cats. Nevertheless, many of the cat carriers have zinc containing materials in the carrier locks or clamps. Stressed or
angry cats that chew on these could be subject to severe intravascular hemolysis.
Insulin
Cats that are being aggressively treated with insulin for
diabetes mellitus have reduced serum phosphate content, often to a concentration incompatible with RBC integrity.
When intracellular phosphorus is reduced, the adenosine
triphosphate ion and water exchanges are also reduced,
causing spherocytosis and intravascular hemolysis.

2.
3.
4.

5.

6.
7.
8.
9.

Erythropoietin as a Therapeutic Agent


Erythropoietin (Epogen[TM] - Amgen) is used almost
exclusively in treating anemia associated with feline chron-

10.

Rifkind RA, Bank A, Marks PA, Nossel HL: Fundamentals of Hematology, Chicago, Year Book Medical Publishers, 1976, pp 7 - 24.
Schrier S: Hemopoiesis and red blood cell function. Scientific Am
Med 5(1): 1-8, 1988.
Hillman RS, Finch CA: Red Cell Manual, ed 5, Philadelphia, FA
Davis Company, 1985, pp 33 - 55.
Jones DRE, Gruffyd-Jones TJ, Stokes CR, et al: Investigation into
factors influencing the performance of the canine antiglobulin test.
Res Vet Sci 48:53 - 58, 1990.
Jones DRE, Stokes CR, Gruffyd-Jones TJ, et al: An enzyme-linked
antiglobulin test for the detection of erythrocyte-bound antibodies in
canine autoimmune haemolytic anemia. Vet Immunol Immunopathol,
16:11-21, 1987.
Jain NC: Schalms Veterinary Hematology, ed 4 Philadelphia, Lea &
Febiger, 1986, pp 126 - 139.
Kociba GJ: Feline anemia, in Kirk RW (ed): Current Veterinary Therapy X, Philadelphia, WB Saunders Co, 1989, pp 425 - 429.
Weiss L, Blue J: Anatomy of the spleen, in Lichtman MA (ed): Hematology and Oncology. New York, Grune & Stratton, 1980, pp 49 - 53.
Mackey L: Haematology of the cat, in Archer RK, Jeffcott LB (eds):
Comparative Clinical Haematology. Oxford, Blackwell Scientific
Publications, 1977, pp 441 - 482.
Giger U: Feline blood groups and incompatibility reactions. Proceedings of the 8th ACVIM Forum, Washington, DC, 1990, pp 319 - 321

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ITALIAN SOCIETY OF VETERINARY DERMATOLOGY - SIDEV

.D.

Diagnostic approach to canine and feline autoimmune


skin diseases
Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Auto-immune skin diseases are rare dermatoses (less


than 1% of canine dermatoses). Even if the clinical presentation of these dermatoses is often suggestive, the suspicion
must be established only after a good differential diagnosis,
elimination of frequent other dermatoses by routine diagnostic procedures (mainly pyoderma, dermatophytosis, demodicosis), and the final diagnosis must be established
based on compatible history, clinical aspect and histolopathological findings. Direct immunofluorescence or
immuno-histochemical testing may also be helpful but these
procedures have relatively poor diagnostic sensitivity and
specificity

A - Classification (Suter M - Olivry T)


1) Autoimmune diseases with cutaneous
target
Autoimmune disease with keratinocyte surface molecules
as targets:
- Pemphigus foliaceus (PF): far most frequent autoimmune
skin disease in the dog. It is a crusting and scaling dermatitis starting bilaterally symmetrical at the face and/or
paws, sometimes spreading as a general disease. Antigen:
Desmoglein 1
- Pemphigus erythematosus: it is a variation of PF. A linear
deposition of immunoglobulins at the basement membrane (in addition to the keratinocyte membrane fluorescence) as seen on immunopathological staining is the difference with PF.
- Pemphigus vulgaris (PV): it is the most severe form but is
very rare. Oral and mucocutaneous junctions lesions (with
ulcerations) are seen.
Antigen: Desmoglein 3 (in man).
- Panepidermal Pustular Pemphigus: it has been recently described based on the location of the lesions within the stratified squamous epithelium.
- Paraneoplastic Pemphigus: frequently described in human
medecine
Pathogenesis of Pemphigus (Suter MM): binding of autoantibody to desmosomal cadherin adhesion molecules
(Desmoglein 1 or 3) - Activation of keratinocytes - Disruption of intercellular adhesion.
Autoimmune diseases with basement membrane targets:
- Bullous Pemphigoid (BP): it resembles PV with blisters

and ulceration in the oral cavity and at the mucocutaneous


junctions. Histopathology: subepidermal cleft formation
within the lamina lucida.
Antigen: BPAG II (collagen XVII)
Pathogenesis: autoantibody binding to collagen XVII Cytokine production by keratinocytes - Attraction of
eosinophils and neutrophils - Cytokine and protease secretion - Lesion formation.
- Acquired Epidermolysis bullosa: a case of suspected collagen type VII subepidermal bullous dermatosis as been described (Olivry)
- Linear IgA dermatosis of Dachshund
Miscellaneous:
- Alopecia areata: in man, hair keratines are antibodies target, but in the dog, it seems that trichohyalin may be the
target.
- Vitiligo and uveo-dermatologic syndrome (VKH-like syndrome) are autoimmune diseases of pigmentation. Antimelanocytes antibodies have been described in vitiligo.

2) Autoimmune diseases with circulating


auto-antibodies non specific of cutaneous
antigens
- Systemic Lupus Erythematosus: it is an autoimmune disease with cutaneous immuncomplex deposition. It is a systemic disease.
- Chronic Discoid Lupus Erythematosus: in classical cases,
depigmentation and ulceration of the nose and planum
nasale. There is no circulating auto-antibodies.
- Vasculitis: they may be related to various antigens (infectious, neoplastic, drug induced, vaccination, chemical).
Pathogenesis of vasculitis involves type III hypersensitivity.
- Cold Agglutinin disease

B - Biopsy site selection (Gross TL)


Pustular autoimmune dermatitis: because of the fragile and
transient nature of primary lesions (pustules, vesicopustules),
early lesions should be obtained. If no pustules are available,
crusted lesions or sites directly adjacent to early pustules
should be sampled. Crusted lesions should be procured carefully and the veterinary pathology service should be instruct-

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ed to include any dissociated crusts in the slide preparation.


If a low number of pustules or vesicles or bullae are present, they should be removed carefully, preferably by excisional biopsy.
Non bullous autoimmune skin diseases:
- Discoid Lupus: recent sites of depigmentation, with partial
lost of pigment, are optimal sites for skin biopsy. Traumatized lesions or lesions with severe crusting, ulceration or
scarring should be avoided. Lips, dorsal muzzle and
planum nasale are the best sites for skin biopsy.
- Systemic Lupus: erythematous areas adjacent to ulcers are
the best sites since an intact epidermis is necessary to yield
diagnostic results.
- VKH-like syndrome: areas of depigmentation, erythema
and scaling are beneficial sites. Lips and dorsal muzzle are
preferred sites. Secondary infected or self-traumatized lesions should be avoided.
General considerations:
- multiple biopsies should be taken
- samples should be selected from the most representative
lesions of the suspected disease
- excision biopsy should be prefered in bullous diseases
- if possible, biopsy specimens should be taken when the animal is not under the effects of glucocorticoid or immunosuppressive therapy
- dermatopathologic examination should be performed by a
veterinary pathologist.

C - Direct immunofluorescence (DIF)


and Immunohistochemical testing (IHT)
DIF and IHT are methods used to detect the presence of
abnormal antibody or immune complex deposition on tissue

4th European FECAVA SCIVAC Congress

specimens. In human medecine, these procedures are considered highly valuable for many of the immune-mediated
dermatoses. however, their value in veterinary medecine is
considerably less. There are many false negative (glucocorticoid treatment, low quality of biopsy site selection, small
biopsy, technical problems) and many false positive (intercellular and basement membrane zone deposition of immunoglobulins or complement can be detected in a wide variety of chronical inflammatory dermatoses, and are physiologicaly found in footpads and planum nasale). For exemple,
DIF is positive in 100% of cases of sarcoptic mange, 73% of
superficial chronical pyoderma, 67% of dermatophytosis,
50% of Demodicosis.
Results of immunopathologic testing can never be appropriately interpreted in the absence of histopathologic
findings.
For DIF, biopsy site selection is the same as for
histopathological examination but biopsy specimens should
be snap-frozen or placed in Michels fixative. IHT is performed on formalin-fixed, routinely processed tissues (immunoperoxidase methods) or on frozen sections. Generally,
biopsy specimens should be selected from areas not secondarily infected and representing the earliest lesion typical for
that disease. Planum nasale (dogs and cats) or footpads
(dogs) should not be sampled or should be interpreted with
great caution.
Intercellular intraepidermic autoantibody deposits: Pemphigus (95% IgG in Pemphigus foliaceus).
Linear dermo-epidermal autoantibody deposit: Bullous
Pemphigoid, Discoid and Systemic Lupus, Linear IgA dermatosis of Dachshund
Because of the high incidence of false positive, DIF or
IHT are of low interest, except in the differential diagnosis
between Bullous Pemphigoid and Epidermolysis bullosa,
and in the differential diagnosis of interface dermatitis.

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.D.

Discoid and systemic lupus erythematosus


Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Systemic and Discoid Lupus Erythematosus are dermatosis associated with circulating auto-antibodies, non specific of cutaneous antigens.

A - SYSTEMIC LUPUS ERYTHEMATOSUS


SLE is a circulating immune complex disease characterized by multisystemic involvment and the presence of a
wide variety of autoantibodies.

1) Etiology
Although the etiology of Lupus is unknown, most reports
emphasize the interaction of various factors:
- a genetic predisposition
- hormonal factors
- viral factors
- inducing drugs
- UV light
Genetic predisposition: it has been proven in man (familial
studies, relationship with MHC, ...), in mice (NZB et NZW,
SWAN, ...) and in dogs (Manathos family, German shepherd, Lyon Vet School, France). When crossing infected
dogs, 70% of second generation dogs are ill, 15% are ANA
positive but healthy and 15% are ANA negative and healthy.
This crossings have been able to demonstrate a positive
relationship between Ag DLA-A7 (Dog Leukocyte Antigen
= DLA) and SLE, and a negative relationship between Ag
DLA-A1, DLA-B5 and SLE.
Actual research in human and in dogs are looking for the
gene involved in SLE transmission. A close relationship between SLE and TcR gene (Lymphocyte T - antigen receptor)
seems to exist in human.
Hormonal factors: in human, there is a strong predilection of
young women before 40 years old (90%); in dogs results show
no sexual predisposition or male predisposition (50-68%).
Androgens may increase suppressive T lymphocytes activity (and be protective) and oestrogens may induce abnormalities of antigen presentation.
Hormonal treatments (androgens or anti-oestrogens) in
human have given various (desappointing) results
Viral factors: C-type viruses have been involved. The SP
104 virus (retrovirus) has been found to contain an antigen
that cross-reacts with an antigen present on the surfaces of

circulating lymphocytes of humans and dogs with SLE. But


the mere presence of such a virus is not sufficient to provoke
the expression of clinical disease.
A study has shown a higher incidence of SLE in owners
of dogs with SLE; this result has not been confirmed by other studies.
Inducing drugs: drug-induced SLE is a well recognized
syndrome in human (hydralazine, procainamide, methyldopa, penicillins, tetracycline, griseofulvin, sulfonamides,
...). Experimental dogs treated with hydralazine developed a
similar syndrome to SLE. In a dog, SLE appears after a routine vaccination, and in hyperthyroid cats, SLE has been described after giving propylthiouracil.
For the moment, in animals, it is better to name it SLE
like drug reaction than drug induced SLE.
UV light: in dogs, cutaneous lesions are mostly localized
on the face, suggesting an action of UV light, which may
change cutaneous nuclear antigens.
Actually, SLE occurs in the presence of a disturbed immune system in a genetically susceptible host, and with various favourable environmental factors (viral, UV).

2) Pathogenesis
In human and animals, most lesions are due to type III
hypersensitivity reactions. Antibodies (IgG) are formed secondarily to increased circulating antigens (mainly nuclear
antigens). Circulating soluble Ag-Ac immune complexes are
set down along epithelial and vascular basement membrane
zones inducing complement activation which induces neutrophiles chemotactism. Lysosomial enzymes and free radicals create local lesions.
In SLE, deposition of immune complexes in joints, muscles, renal glomerules, CNS, ... is responsible of problem in
the affected organ.

3) Immunological abnormalities
Various and numerous auto-antibodies are produced in
SLE.
antinuclear antibodies (ANA).
- Total ANA: they are present in 97-100% of SLE , but their
presence is not specific for SLE. For exemple, dogs with
Leishmaniasis would present frequent positive ANA.

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There is a wide variety of ANA depending on the target


(nuclear antigen): anti native DNA, anti-histones, antiENA, ...
- Anti native DNA antibodies: Antibodies against DNA
(double chain) are quite characteristic of the human disease
(80%), but in dogs their presence is very rare (< 5%). This
is the main difference between canine and human SLE.
- Anti-histones antibodies: in human, anti-histones antibodies are frequently reported(30-70%) but mainly in drug induced SLE; anti-H1, anti-H2B, anti-H3 are frequent. In
dogs, they are frequently reported too (55-65%) but have
been found in non lupoid dogs; moreover, antiH3, anti-H4
et anti-H2A are frequent.
- anti-ENA antibody (ENA = Extractable Nuclear Antigens):
these antigens come mainly from nucleoplasmic constituants and for a small part of them from chromatin molecules. Positive anti-ENA is an other difference between
dogs and human; in dogs anti-type I (20%) and anti-type II
(9%) are found but not in human, anti-Sm is found occasionaly in dogs (16%) but frequently in human (70%).
Moreover, other known anti-ENA in human (anti-SSA and
anti-SSB) are not found in dogs.
- other nuclear antibodies: non histone proteins like HGM
(High Mobility Group) type I and II have been seen in canine SLE.
Important facts in canine SLE:
- high frequency and elevated titer of ANA
- rarely or no anti-nDNA
- anti-type I and anti-Sm highly diagnostic
other auto-antibodies
Auto-immune response in SLE is not exclusively directed
against nuclear antigens. Other antibodies have been found:
- seric auto-antibodies
* rhumatoid factors: low title in canine SLE
* anti erythrocyte antibodies, detected by Coombs test,
but hemolytic anemia is only a criteria of SLE (2030%) and each AIHA with positive Coombs test is not
linked to SLE.
- fixed antibodies
* on skin biopsies, detected by direct immunfluorescence (IFD)
* on renal biopsies (in case of glomerulonephritis), detected by IFD
other abnormalities
- lymphocytic abnormalities: in dogs, some recent works
show
* lymphopenia
* decrease of peripherical population of CD8+ T cells
and increase in CD4+
* decrease suppressive activity of T cells
* increase in CD5+ when there is no activity of the disease
- NK cells, Ag presentating cells, cytokines: no study in canine SLE

4th European FECAVA SCIVAC Congress

* localized CLE
* generalized CLE
* oral LE
* lupus panniculitis
- LE-non specific skin disease
* vasculitis
* vesicobullous lesions
Systemic LE (SLE)
- SLE without CLE
- SLE with CLE

5) Epidemiology and history


Male dogs seem overrepresented (different from human
condition) in some studies (70%) but equallly in others (51%).
Medium class of age is 5 years old (6 months to 14 years
old) but we have to consider the moment when symptoms began or when diagnostic was made because SLE is a slow evoluting disease (episodic evolution), worsening with time. SLE
begins in young adults and may be very severe at 5 years.
Breed predilection: German shepherd, Belgium shepherd, Shetland sheepdogs, collies, beagles, ...

6) Clinical presentation
SLE is evoluting subacutely or more often chronically
with episodic attacks and remission periods. Symptoms are
numerous but non erosive polyarthritis (76-90%), proteinuria (50-65%) and cutaneous lesions (54-65%) are the principles figures. All these symptoms are not present at the
same time but more often successively.
lameness: non erosive polyarthritis (no radiologic signs),
beginning intervertebraly with difficulties to stand up and
jump, amyotrophy of lombo-dorsal muscles. Then carpus
and tarsus are involved with turning lameness. At the
end of evolution, temporo-mandibular joint is sytematicaly
involved.
skin lesions: they are often erythematosus and seborrheic
in nature and commonly involve the face, ears and limbs.
Erythema is also frequent in less hairy areas. Mucocutaneous ulceration or erosion and nasal depigmentation are
also seen. The butterfly pattern often referred to in human medecine, is common to many canine dermatosis.
Chronic ulcerative stomatitis may be the only cutaneous manifestation.
others: glomerulonephritis with proteinuria (50-65%), hemolytic anemia (10-20%), thrombocytopenia (< 5%) and
purpura, spleen and lymp nodes enlargment, central neurologic symptoms, pleural and pericardic inflammation
(10%).

7) Diagnosis
4) New classification (T Olivry)
LE related skin disease:
- LE specific skin disease (Cutaneous LE = CLE): acute or
chronic

Diagnosis is based upon ARA (American Academy of


Rhumatology) criterions:
1) facial erythema (butterfly appearance)
2) disoid lupus

3)
4)
5)
6)
7)
8)
9)

UV sensitivity
oral ulcerations
polyarthritis
pleural or pericardic inflammation
renal troubles (proteinuria)
neurologic disturbances
haematological disturbances: hemolytic anemia, leucopenia, lymphopenia, thrombocytopenia
10) immunological abnormalities: LE cells, anti-nDNA
Ab, anti-Sm Ab
11) ANA positive
Suspect SLE: 2 positive criterions.
Possible SLE: 3 positive criterions or polyarthritis +
ANA positive.
SLE: 4 positive criterions.
This list of criterions is a human one and not perfectly
adapted to canine SLE:
- criterion 11 is an obligation because there is no SLE without positive ANA (97-100%);
- anti-nDNA create many false ANA positive in human, but
these Antibodies do not exist in dogs;
- transposition from human to dogs of criterion 1 (butterfly
appearence), 3 and 8 , is difficult;
- episodic hyperthermia is very frequent in dogs and is a
missing criterion;
- anti-type I is very specific of canine SLE;
- Leishmaniasis should be excluded before just thinking of
SLE (be careful, there are many cases of canine Leishmaniasis with positive ANA).
It seems better to interpret ARA criterions in this way:
- positive ANA is mandatory (with exclusion of Leishmaniasis) with high titer
+ 3 criterions: diagnostic
+ 2 criterions: possible SLE; perform analysis of ANA (anti-type I or anti-Sm highly suggestive of canine SLE)
An other classification of criterions has been proposed by
Halliwell (1989) with major and minor symptoms . Definitive diagnosis is made with: positive ANA + 3 majors
symptoms or positive ANA + 2 major symptoms + 2 minor
symptoms:
- major symptoms
* non infectious polyarthritis
* compatible skin lesions with characteristic histopathology
* hemolytic anemia
* severe thrombocytopenia
* glomerulonephritis and proteinuria
* neutropenia
* polymyositis
- minor symptoms
* hyperthermia with unknown origin
* CNS symptoms
* pleural inflammation
Cutaneous histopathology: avoid ulcers and erosions for
biopsy site selection; intact erythematous epidermis adjacent to ulcers may yield diagnostic results.
Histopathology reveals:
* patchy, mild to moderate vacuolar degeneration of the
basal cell layer
* colloid (Civatte) body formation is a consistent finding
but may be rare

41

* lichenoid mixed inflammatory dermal infiltrate


* pigmentary incontinence
Indirect immunofluorescence of skin biopsies (Michels
medium) reveals: deposition of granular and irregular deposits of immunoglobulin (usually IgG) and complement
at the dermal-epidermal junction. One must be aware that
similar but normal IgM deposits are found in normal canine and feline nose and footpath.
ANA: high title is required (> 1/256), but ANA are not
specific of SLE because they are found in other diseases
(Leishmaniasis).

8) Treatment: (see therapeutic protocols)


Prednisolone 2 mg/kg/day tapered slowly after clinical
remission + levamisole 2-5 mg/kg each other day (max 150
mg/day) 4 months. Heamatological control after 10 days
(neutropenia).
Results: 57% in remission for months or year(s) (no
longer than 3 years) without treatment.
Other treatments (mainly if severe side effects of glucocorticoids): azathioprine 2 mg/kg/day, cyclophosphamide 50
mg/m2 four days a week, vincristine if severe thrombocytopenia (0,7 mg/m2 once a week).
Prognosis is always guarded, especially when renal lesions are severe.

B - DISCOID LUPUS ERYTHEMATOSUS


DLE is a cutaneous form of SLE without involvment of
internal organ. It has been described in human, dogs, cats,
horses, seals.
epidemiology: there is no real age predilection but must
animals presenting this dermatoses are young adults.
Breed predilection: Collie, German shepherd, Siberian
Husky, Shetland Collie.
clinical signs are mostly localized on the face, the nose,
and periocular areas. Oral and pinnae lesions are very rare.
Podal lesions are seen.
Lesions: hypopigmentation, erythema, scales, erosion, ulceration, crusts.
diagnosis
- histopathology: best sites for skin biopsy are areas of early
depigmentation with partial loss of pigment; traumatized
lesions or lesions with severe crusting or ulceration should
be avoided. Histopathology reveals:same lesions as SLE
with less severe basal cell vacuolisation.
- immunofluorescence: see SLE
- ANA are negative and there is no haematological or biochemical abnormalities
treatment
- mild cases: sun screen, vitamin E, avoid sun exposure, topical glucocorticoid
- more severe cases: glucocorticoids until remission (1-2
mg/kg/day), then nicotinamide-tetracycline
- very severe cases or refractory cases (large ulcerations,
spontaneous bleeding, pain): glucocorticoids and immunosuppressive drugs

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ITALIAN SOCIETY OF VETERINARY DERMATOLOGY - SIDEV

.D.

Clinical differential diagnosis of autoimmune


skin diseases
Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Clinical aspects and localizations of auto-immune skin


diseases (AISD) are common with a great number of other
dermatosis.
Because of the low incidence of this diseases, we must
always rule out other more common dermatosis before
thinking to AISD.
Clinical differential diagnosis depends on the lesions
(crust, ulcerations, erosions, depigmentation, pustules) and
on their localizations (facial, podal, generalized).

FACIAL DERMATOSIS
Virtually any skin disease may affect the face, but AISD
are often symmetrical, involving periocular areas, lips, nose
and pinnae. Pruritus is generally mild but secondary pyoderma or Malassezia dermatitis may be pruritic.
* If pruritus is present:
- atopic dermatitis: erythema, lesions of self trauma, often
secondary pyoderma and crusts
- food allergy: erythema, secondary pyoderma, erosions or
ulcerations in cats
- contact allergy or irritation: erythema, macules, papules,
rarely erosions (plastic dish contact allergy)
- eosinophilic furonculosis of the face: papules, pustules
- eosinophilic granuloma complex (cats)
- sarcoptic mange (dogs)
- pyoderma
- mucocutaneous pyoderma
- demodicosis with secondary pyoderma
- dermatophytosis: some dermatophytes may creat an autoimmune like dermatosis (M persicolor)
- Malassezia dermatitis
- Mucocutaneous Candidiasis
- Juvenile cellulitis of the adult dog
- Zinc responsive dermatitis
- Drug reaction
* If pruritus is absent or mild:
- Leishmaniasis
- Nasal hyperkeratosis
- Superficial necrolytic dermatitis
- Neoplasia (cutaneous lymphoma, mycosis fungoides)
- Vitiligo

- Demodicosis
- Dermatophytosis
- Dermatomyositis
- VKH-like syndrome
* Facial dermatosis which may affect the planum nasale
- Vitiligo
- VKH-like dermatosis
- Nasal hyperkeratosis
- Dermatophytosis
- Drug eruption
- Leishmaniasis
- Neoplasia

PODODERMATITIS
- Pyoderma
- Demodicosis
- Dermatophytosis
- Malassezia dermatitis, Candida dermatitis
- Peladora and hookworm infestations
- Leishmaniasis
- Hypersensitivities (atopic dermatitis, food allergy, contact
allergy)
- Superficial necrolytic dermatitis
- Irritant contact dermatitis
- Trauma
- Zinc responsive dermatitis
- Digital hyperkeratosis
- Sterile pyogranuloma
- Neoplasia (squamous cell carcinoma, metastasis of pulmonary adenocarcinoma in cats)
- Plasma cell pododermatitis (cats)

LESIONS OF THE NAILS AND NAILBED


- Dermatophytosis
- Candidiasis
- Leishmaniasis
- Superficial necrolytic dermatitis
- Lupoid onychodystrophy
- Drug eruption

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PUSTULES AND CRUSTING PAPULES


- Primary or secondary pyoderma
- Sarcoptic mange and other ectoparasitic infections
- Hypersensitivity

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- Drug eruption
- Contact irritant dermatitis
- Sub corneal pustular dermatosis
- Sterile eosinophilic pustular dermatitis
- AISD

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Therapeutic protocols of autoimmune skin diseases


Dominique Heripret
Dr Vet, CES DV, Dip ECVD
Private Practitioner, Arcueil, Paris - France

Management of autoimmune skin diseases requires


changing, varying or adjusting the immune response by
pharmacological therapy. Suppressing the immune response
is often easy to do, however, controlling the degree of immunosuppression can be difficult.
Prior to use an immunosuppressive drug, there are important pretreatment considerations:
- ensure that the diagnosis is correct
- ensure that there is no contraindication to immunosuppressive treatment
- control secondary pyoderma, Malassezia dermatitis
- precribe the less toxic drug as possible
- avoid predisposing factors (UV, some drugs, ...)
Selection of an immunosuppressive treatment and then
control of the disease on a long term basis is individual and
the main rule is: dont do worse with the treatment that the
disease would do alone.
The goals of immunosuppressive treatment are:
- decrease production of autoantibody
- decrease or suppress activation of cytotoxic lymphocytes
- suppress the migration or activation of inflammatory cells

tolone) are indicated when lesions are small or well circumscribed (Discoid lupus erythematosus). Owners have
to wear glothes. Unsing topicals q12h the first week, q24h
the second week and q48h the third week is recommended
to avoid systemic side effects or localized reactions (atrophy).
dosages: induction with prednisolone/prednisone 2-4
mg/kg/day for dogs, 4-6 mg/kg/day for cats; if there is no
change in 10 days, increase the dosage by 30%. Use maintenance therapy when the lesions regress: decrease frequency of administration to every other day (same dosage)
and the step down doses 20-30% every two to four weeks
(depending on the speed of regression speed of lesions). If
regression of lesions is complete and quick, it is possible to
try to stop treatment after a few months (4-6 months); otherwise, look for the lower efficious dosage to control lesions with minimum side effects (0,5-1 mg/kg AD).
side effects: iatrogenic Cushings disease, polyuria polydipsia, steroid hepatopathy, feline skin fragility syndrome,
gastric ulceration, secondary infections (ITU, pyoderma),
diabetes mellitus.

A - DRUGS

2) Alkylating drugs: cyclophosphamide


and chlorambucil

1) Glucocorticoids:
Glucocorticoids (GC) represent the first choice treatment
of most autoimmune skin diseases.
mechanism of action: paralyze Fc receptors on
macrophages, suppress immunoglobulin production (high
doses), suppress leukocyte accumulation at inflammatory
site, decrease lymphoblastogenesis, decrease abnormal auto-antibodies production, decrease neutrophils function.
compounds:
- prednisolone and prednisone, methyl-prednisolone (1,6
mg/kg/day for dogs): may be used on alternate day basis
- methyl-prednisolone succinate: used for pulse therapy
(10-30 mg/kg IV 3 consecutive days)
- dexamethasone (0,25-0,75 mg/kg/day), triamcinolone
(0,2-0,7 mg/kg/day): may be more effective in cats but
cannot be used on an alternate day basis
- injectable methyl-prednisolone acetate: is only indicated in
cats unwilling to accept oral medications
- topical therapy: the potency of topical GC can be geared to
the severity of lesions. High power GC (clobetasol, flucor-

mechanism of action: interaction with DNA of cells under


divison: they replace an hydrogene by an alkyl group which
create a wrong lecture or DNA breaking. They affect induction and effector phases of immune response, suppress antibody formation and production, affect neutrophil and
macrophage function. They act slower than GC (10 days).
drugs:
- cyclophosphamide 50 mg/m2/day, po, 4 consecutive days
each week; during maintenance therapy with GC, every
other day cyclophosphamide may be used. Treatment of
more than 2 months must be prescribed with great caution
(sterile hemorrhagic cystitis).
- chlorambucil (0,1-0,2 mg/kg/day po for cats, 2-6
mg/m2/day initially then q 48h for dogs). Chlorambucils
action is slower (4 weeks) than cyclophosphamides one
(10 days).
indications: Cyclophosphamide is indicated mostly in
dogs, in severe or non-responsive AID. Chlorambucil is
excellent for cats requiring cytotoxic drugs in combination
with glucocorticoid.

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4th European FECAVA SCIVAC Congress

46

side effects: bone marrow suppression with neutropenia,


sterile hemorrhagic cystitis (cyclophosphamide but not
chlorambucil), gastroenteritis, anorexia, alopecia.

3) Thiopurines: azathioprine
and 6-mercaptopurine
Azathioprine is metabolized in the liver to 6-mercaptopurine.
mechanism of action: these drugs are antimetabolites
which inhibit enzymes contribuating to the synthesis of
puric basis and so interfering with DNA and RNA synthesis. They are active on rapidly developping cells, affecting
mainly the effector phase of immune response and are
more effective in modifying T lymphocyte responses.
dosage: 50 mg/m2 or 2 mg/kg/day in association with GC
during the induction phase (4 weeks minimum) and then
on an alternate day basis with GC. After a few months,
some dogs would only require azathioprine.
side effects: azathioprine is CONTRAINDICATED IN
CATS. There is a very strong bone morrow suppression,
leading to death in a few weeks. In dogs, azathioprine is
very well tolerated. Platelet count must be checked every 2
or 3 months.

4) Gold salts: chrysotherapy


mechanism of action: inhibition of chemotaxis, suppression of autoantibody formation, inhibition of complement
activation, inhibition of phagocytosis.
Drugs:
- aurothioglucose: 1 mg/kg IM q7days for induction then
q30days as maintenance therapy. Test doses of 0,25 and
then 0,5 mg/kg are recommended on weeks 1 and 2 respectively.
- auranofin: 0,05-0,2 mg/kg q12h for induction
Side effects: cutaneous drug eruption, thrombocytopenia

5) Cyclosporin
This is a very potent immune suppressor.
mechanism of action: inhibition of IL2 and gamma-interferon production, inhibition of cytotoxic T cells, decreased
production of sensitized cytotoxic T cells.
dosage: 5-10 mg/kg/day po
side effects: gastroenteritis, gingival hyperplasia, surinfections, ...
This drug is very expensive and has been reported to be
rather unsuccessful for autoimmune skin diseases treatment
(Rosenkrantz 1989).

6) Others
Tetracycline/niacinamide: this treatment seems to be interesting in Discoid Lupus Erythematosus (25-64% positive
results).

4th European FECAVA SCIVAC Congress

Dosages for dogs less than 10 kg: 250 mg tetracycline


and 250 mg niacinamide po, tid for induction. For dogs
greater than 10 kg: 500 mg tetracycline and 500 mg niacinamide po, tid for induction. For maintenance therapy, doses are decresed incrementally. Side effects are minimal (occasional vomiting).
Methotrexate: it is a competitive enzyme inhibitor of folic
acid reductase. Used in SLE in human medecine (0,5-0,8
mg/kg IV q7-14 days or 2,5 mg/m2 po q 48h). Side effects
include leukopenia, vomiting, renal tubular necrosis with
high doses.
Heparin: it has been used in one case of Pemphigus vulgaire
(Olivry, Hripret) with GC at a dose of 100 UI/kg/day SC.
Heparin seems to inhibit proteases involved in acantholysis.
Vitamin E: mechanism of action is unknown but its efficacy may be related to anti-oxydant properties (stabilization
of lysozomial membrans against effects of free radicals
and superoxides ions). Used in DLE and PE with GC (200400 mg/kg/j or 400-800 UI bid po).
Vitamin E is a relatively benign drug that may reduce the
need for other therapy. Some authors have found vitamin
E to be rarely effective by itself.
Levamisole: it seems to have immunostimulating properties (not in normal dogs but in immunodepressed dogs) by
increasing production of T Helper lymphocytes. Used in
SLE in conjonction with GC: 2-3 mg/kg every other day.
Sulphones (dapsone): mechanism of action: inhibition of
lysosomial enzymes and prostaglandines synthesis. It has
been used in Pemphigus cases (1 mg/kg bid or tid) with
some good results (less than 50%) and in immune complexing vasculitis. Side effects include: anemia, neutropenia, thrombocytopenia, hepatotoxicity, gastrointestinale
disorders.
Antimalarial drugs: quinacrine, chloroquine, hydroxychloroquine have been use in the treatment of DLE in humans but they have not been evaluated in dogs.
Sun avoidance: sun screen or dog kept indoor between 10
am and 5 pm.

B - TREATMENT OF AUTO-IMMUNE
DERMATOSIS
1) Superficial Pemphigus (PF and PE)
Treatment should be individualized depending on severity and extension of lesions.
Secondary pyoderma should be treated (empirical selection of agents effective against coagulase positive Staphylococcus).
Crusts have to be removed, lesions have to be cleaned
(often under general anesthesia).
Systemic glucocorticoids is the treatment of choice
(prednisone 2 mg/kg/day in dogs, 4-5 mg/kg/day in cats). If
the response to GC is good, the dose is tappered on an alternate day basis as previously described.
If the response is poor (recheck after 10-15 days of treatment), a cytotoxic drug may be added for at least one month
(delay of activity of these drugs): azathioprine (dogs only),
chlorambucil (cats). When lesions regress, GC are slowly

stopped and azathioprine or chlorambucil given 3 then 2


then 1 time a week.
If the response is still weak or if undesirable side effects
develop (polyuria polydipsia), alternate GC (dexamethasone, triamcinolone) may be tried.
Some individuals may be cured after more than 4 months
of treatment, others should be treated all their life long.
In PE, sun avoidance is indicated; nicotinamide-tetracycline may be used too.
If drugs were given previously to diagnosis (antibiotics,
antifungal therapy, ...), they have to be stopped in case of
drug induced Pemphigus like reaction.
NB - The benefit of association between GC and cytotoxic drugs is not realy proven in auto-immune skin diseases.

47

quires long term therapy. Ocular examination is recommended every 4 months even though the cutaneous component is controlled.

7) Disoid lupus erythematosus


This is a cutaneous disease with a rather good prognosis.
GC must be used carefuly.
In mild cases, when lesions are localized and superficial,
topical therapy (high power GC at the beginning, then low
power GC) + sun avoidance or sunscreen are prescribed.
When ulcrations or spontaneous bleedings are present, GC
are prescribed until remission, then niacinamide + tetracycline are indicated. Vitamin E may be added.
Spontaneous total remission have been described.

2) Deep Pemphigus (PV)


Treatment must be very potent because PV is a life
threatening condition. GC have to be associated to cytotoxic drug at the beginning of treatment (cyclophosphamide).
Antibiotic treatment is important because lesions are deep
and sepsis is always possible. Pronostic is guarded and total
remission very rare. If GC and cyclophosphamide fail, heparin may be tried.

8) Systemic lupus erythematosus


Treatment should be individualized but initial treatment
of choice is large doses of systemic GC. Some cases respond
to the only GC therapy but most dogs need a combined therapy with levamisole and cytotoxic drugs.
Prognosis is poor: Over 40% of the dogs are dead within 1 year after the diagnosis is made.

3) Bullous Pemphigoide (BP)


9) Vasculitis
In human medecine, relationship between internal diseases (neoplasia) and PB has been proven in a majority of
cases. Complete work up is indicated (haematological, biochemical, radiographs, ...). Previous drugs should be stopped
(PB like drug reactions). Otherwise the treatment is the same
as in PV.

Prognosis and treatment depend on the underlying problem, affected organs and disease severity. All previous treatments should be stopped at the time of diagnosis.

Conclusion
4) Alopecia aerata
No treatment; lesions may regress in a few months.

Therapy of auto-immune skin diseases have to follow


two rules:
- treatment should not been worse than the disease
- treatment should be individualized, depending on the precise diagnosis of the disease, the animal and the owner

5) Vitiligo
No treatment; lesions are only cosmetic ones.

6) VKH-like syndrome
(uveo-dermatologic syndrome)
Treatment should be aggressive because of the possibility of blindess; moreover, cutaneous lesions may be reversible if therapy is started early in the disease progress:
GC + cyclophosphamide, topical ocular treatment (ocular
topical dexamethasone 0,1% or prednisolone 1% qid + mydriatic/cycloplegic like 1% atropine quid at the beginning).
Prognosis is guarded. Control of the disease usually re-

Readings
HALLIWELL (REW), GORMAN (NT) - Anti-inflammatory drugs, immunosuppressive agents, and immunomodulators. In Veterinary Clinical Immunology, Halliwell and Gorman, WB Saunders Co, Philadelphia, 1989, 493-507.
KUMMEL (BA) - Medical treatment of canine Pemphigus-Pemphigoid. In
Kirks Current Vet Therapy XII, Bonagura and Kirk, WB Saunders
Co, Philadelphia, 1995, 636-638.
SCOTT (DW), MILLER (WH), GRIFFIN (CE) - Immunologic skin diseases. In Muller & Kirks Small Animal Dermatology V, WB Saunders Co, Philadelphia, 1995, 484-626.
ROSENKRANTZ (WS) - Management of immune mdeiated disorders. In
Manual of Small Animal Dermatology, Harvey Locke P Ed, BSAVA,
1993, 270-275.

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SCIVAC EXOTIC ANIMALS STUDY GROUP

Survey of the resident flora of the upper respiratory


tract in psittacine birds and its antimicrobial sensitivity
S.O.T.S. Jesus
DVM, MSc
Dept. of Pathology and Infectious Diseases, Royal Veterinary College, University of London

To try to clarify the hypothesis that the resident flora of


the upper respiratory tract of psittacine birds can behave as
opportunstic pathogens, this project was set out to study, by
means of a survey, its resident flora and compare it with that
of birds with upper respiratory infections.
Swabs were taken from the choanal slit of nineteen
healthy psittacines and four birds with upper respiratory disease - three with sinusitis and one with an unspecified upper
respiratory pathology. The isolation and identification of
bacteria and fungi was accomplished by standard microbiological methods and the use of commercial identification
systems.
A total of 44 isolates were recovered from the choanae of
the 23 psittacines sampled. Twenty six precent of the isolates
recovered from the choanal slits of healthy birds were grampositive bacteria, 62% gram-negative and 12% fungi. From
sick birds, 60% of the isolates were bacterial and 40% fungal. Fifty eight percent of the healthy birds yielded more
than one isolate, whereas in sick birds 75% had more than
one isolate.

Among other organisms, Streptococcus spp., Staphylococcus spp., Alcaligenes sp., Klebsiella pneumoniae pneumoniae, K. oxytoca, Pasteurella spp., Pseudomonas alcaligenes, P. stutzeri and Xanthomonas maltophila, all considered to be potential pathogens to the respiratory tract, were
isolated from the choanal slits of healthy birds, suggesting
that these animals can harbour in their upper respiratory tract
microorganisms which can behave as opportunistic
pathogens.
From the choanal slits of sick animals the following potential organisms were isolated: Streptococcus sp., Staphylococcus sp., Escherichia coli, Klebsiella pneumoniae pneumoniae, K. oxytoca, Proteus mirabilis, Candida albicans
and Aspergillus flavus. All of them have been reported to be
associated with upper respiratory disease under certain circumstances.
The sensitivity testing showed the drugs of choice, for
gram-positive and gram-negative organisms, to be, in decreasing order: gentamicin, amikacin, enrofloxacin, tetracycline, ticarcillin, kanamycin and sulfamethoxazole+trimethoprim.

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EUROPEAN SOCIETY OF FELINE MEDICINE - ESFM

Feline vestibular disorders


Richard A. LeCouteur
VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN
Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

Summary
Vestibular disorders produce varying degrees of loss of
equilibrium, causing imbalance and ataxia. Strength is not
lost and therefore paresis is not observed. Most commonly
the disturbance is unilateral and the clinical signs are those
of asymmetrical ataxia without the loss of strength. Unilateral vestibular signs may result from either central (brain
stem) or peripheral (labyrinth) disease. It is important to
differentiate central from peripheral disease, because of the
difference in treatment and prognosis. Signs of vestibular
disease include falling, rolling, head tilt, circling, nystagmus, positional strabismus, and asymmetrical ataxia. Hearing disorders are often associated with vestibular dysfunction (and vice versa) as the auditory and vestibular systems
are closely associated anatomically.

tympanic cavity of cats and dogs. In dogs the tympanic cavity is composed of a small dorsal epitympanic recess and a
large ventral tympanic bulla. The auditory ossicles are located in the middle portion of the tympanic cavity of dogs. The
feline tympanic cavity is divided into two compartments by
a thin, bony septum that arises along the cranial aspect of the
bulla and curves to attach to the mid-point of the lateral wall.
The majority of the lateral wall of the smaller craniolateral
compartment is formed by the tympanic membrane. These
compartments communicate through a narrow fissure on the
caudomedial aspect of the bony septum. Near this fissure the
sympathetic nerves form a plexus on a structure called the
promontory. Because of their location, these sympathetic
nerves are easily traumatized during surgical curettage of the
feline middle ear, resulting in a Horners syndrome.

Receptors - General information


INTRODUCTION
The vestibular system has 2 main functions: (1) to maintain the visual image by stabilizing the eyes in space during
head movements; the stabilization is performed utilizing
phasic or tonic vestibulo-ocular reflexes; and (2) to stabilize
the position of the head in space - thus ensuring that the position of the body is stable. The stabilization is performed
utilizing phasic or tonic vestibulospinal reflexes.

ANATOMICAL CONSIDERATIONS

Two sets of mechanoreceptors are involved in vestibular


function: (1) a set responsive to angular (rotational) acceleration (or deceleration); these receptors are located in the
membranous semicircular canals; and (2) a set responsive to
linear acceleration (or deceleration) and gravity. These receptors are found at 2 locations, one in the utriculus and one
in the sacculus. The mechanoreceptor generates a receptor
potential that results in the development of a generator potential in the primary afferent fibre. The cell bodies of the
primary afferent fibers are bipolar cells located in the
vestibular ganglion. The primary afferent fibers comprise
the vestibular part of the vestibulocochlear (VIIIth) nerve.

Gross anatomy
The ear is composed of three parts: (1) the inner ear,
which consists of a membranous and bony labyrinth, and
which functions for hearing and balance, (2) the middle ear,
which comprises the tympanic cavity, and communicates
with the nasopharynx by means of the auditory tube (eustachian tube), and (3) the external ear, formed by the auditory meatus and a short canal.
The middle and external ears are separated by the tympanic membrane, and the opening of the horiziontal canal into the middle ear is called the external acoustic meatus. The
theree auditory ossicles (stapes, malleus, and incus) connect
the tympanic membrane to the inner ear.
There are important diferences between the air-filled

Receptors for angular acceleration


These receptors are located in the petrous portion of the
temporal bone. The vestibular organ consists of interconnecting canals in the bone called bony (or osseous)
labyrinths, and a single large cavity within the bone to which
all canals connect, called the vestibule. Within the bony
labyrinths are fluid-filled membranous tubes called the
membranous labyrinths. These membranous labyrinths contain a fluid called endolymph. Surrounding the membranous
labyrinths, filling the osseous labyrinths, is a fluid called
perilymph. Three membranous semicircular canals form the
mechanism for detection of angular (or rotational) accelera-

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tion. These 3 canals join the utriculus located in the osseous


vestibule. On each membranous semicircular canal is an enlargement called the ampulla. Running transversely across
each ampulla is a connective tissue crest with receptor cells
(hair cells) on its surface - called the crista ampullaris. The
receptor cells have cilia protruding from them in stepwise
gradations of length. The largest cilium is called the kinocilium and the rest are called stereocilia. The cilia project into
a gelatinous substance called the cupula. The cupula extends
across the entire ampulla. Endolymph does not flow past the
cupula. The hair cells produce receptor potentials, that give
rise to generator potentials, that produce action potentials in
the vestibular portion of the vestibulocochlear nerve. The
vestibular fibers show a tonic discharge even at rest.
When the head is rotated, the inertia of the endolymph
places a shear force on the cupula. This bends the cilia. If the
shear on the cupula bends the stereocilia towards the kinocilium, the tonic nerve impulse rate from all of the nerve fibers
supplying that crista is changed from a tonic to a phasic response. If the rotation is slight, the resting tonic rate is
quickly resumed. If the rotation is a sustained movement, the
friction of the endolymph on the walls of the membranous
labyrinth results in acceleration of the movement of the endolymph until the velocity of the endolymph equals the rotational velocity of the head; thus the shear exerted on the
cupula is removed. The tonic firing rate is then resumed as
though the head were not rotating. If the head rotation is
stopped, the momentum of the endolymph places a shearing
force on the cupula in the opposite direction. This bends the
kinocilium towards the stereocilia and this inhibits the generation of nerve impulses. As soon as the friction of the endolymph on the walls slows down the movement of the endolymph, the cupula returns to the non-rotational position
and the tonic rate of discharge is resumed. If the rotation of
the head is in the opposite direction so that the kinocilium is
first displaced towards the stereocilia, the tonic rate of discharge will be first inhibited and then accelerated at the end
of head rotation.
There are 3 semicircular canals on each side of the head
- a rostral, a caudal and a lateral. Each pair of semicircular
canals works in a push-pull arrangement. When the rate of
discharge from the crista on one side is increased, the rate of
discharge from the opposite crista is decreased. Note that the
hair cells are excited only when acceleration (velocity is increasing) or deceleration (velocity is decreasing) of the endolymph is occurring.

Receptors for linear acceleration and


gravity
These receptors are located in raised areas called the
macula utriculus in the utriculus, and the macula sacculus in
the saccule. The cilia of hair cells project into a gelatinous
mass in which small granules, called otoliths (or otoconia)
are embedded. The mass and its contents are together called
the otolithic membrane. The macula in the utricle is horizontal, and the macula in the saccule is vertically orientated,
when the head is upright.
If the head is tilted to one side or the other, the force of

4th European FECAVA SCIVAC Congress

gravity slightly displaces the otolithic membrane towards


the tilted side. This places shearing forces on the cilia. If the
head tilt is such that the movement of the otolithic membrane forces the stereocilia toward the kinocilium, then an
increase in the tonic rate of discharge results. If it is in the
opposite direction, a decrease in the tonic rate of discharge
results. These discharges continue for as long as the pull of
gravity displaces the otolithic membrane. For this reason,
these receptors are often referred to as statolithic organs.
The maculae respond to linear acceleration because the
otolithic membrane has an inertia during acceleration of the
linear movement of the head. If acceleration does not continue (i.e. velocity remains constant), the otolithic membrane returns to its resting position, and the frequency returns to the resting rate. During deceleration of the head, the
otolithic membrane has momentum; thus, a shearing force is
exerted on the hair cells until the momentum ceases.
In linear acceleration, acceleration (or deceleration) is
necessary to alter activity in the vestibular fibers. Velocity
(movement of the head at a constant speed) will not stimulate the maculae. There is no push-pull effect from left and
right maculae as occurs relative to the semicircular canals.

Central vestibular connections


Primary afferent fibers from the crista of the semicircular canals and the maculae directly terminate in 2 central
nervous system (CNS) sites: (1) cerebellar cortex of the flocculonodular lobe of the cerebellum; (2) 4 vestibular nuclei
(rostral, medial, lateral, caudal). Primary afferent fibers from
the crista ampullaris of the semicircular canals (angular acceleration) terminate in rostral, medial, and caudal nuclei.
Primary afferent fibers from the macula (linear acceleration
and gravity) terminate mostly in the lateral vestibular nuclei.

Central pathways and reflex connections


of the vestibular nuclei
These connections descend via the lateral vestibulospinal
tract to lower motor neurons of neck muscles, and muscles
of thoracic and pelvic limbs; they descend via the medial
vestibulospinal tract to the neck muscles and ascend to motor nuclei of the eye muscles via the medial longitudinal fasciculus. Other pathways include connections to the cerebellum via the caudal cerebellar peduncle, to the reticular formation, to the ventrobasilar nucleus of the thalamus, to the
post-sigmoid gyrus of the cerebral cortex, for conscious processing of vestibular inputs (vestibulothalamic pathway) and
to the hypothalamus via the medial longitudinal fasciculus.

Lateral vestibulospinal tract


This is an important tract for posture and locomotion.
Cells of origin of this pathway are located in the lateral
vestibular nucleus (Dieters nucleus). The cells in this nucleus are organized topographically. Afferents to the lateral
vestibular nucleus include: (1) macula (gravity and linear ac-

celeration - tonic input); (2) crista cells of rostral semicircular canal (tonic input); (3) cerebellar nuclei (tonic input); and
(4) collaterals from ascending pathways, particularly muscle
spindles and Golgi tendon organs.
All fibers of the lateral vestibulospinal tract produce EPSPs at their synapses. This tract establishes monosynaptic
connections with lower motor neurons innervating neck,
back, thoracic and pelvic limb antigravity muscles (mostly
extensors). It is the largest (and thus the fastest) of all the descending pathways. It also has facilitatory polysynaptic connections with other extensors and inhibitory polysynaptic
connections with flexors. It modulates segmental reflexes
and it is an ipsilateral tract.

Medial vestibulospinal tract


This pathway originates from the medial and caudal
vestibular nuclei, with some fibers coming from the lateral
vestibular nucleus. It descends in the medial longitudinal
fasciculus. Afferent inputs to this pathway mainly come
from the semicircular canals (angular acceleration), cerebellar nuclei (tonic input) and the cerebellar cortex (tonic input
- inhibitory).
Terminations of the medial vestibulospinal tract include
monosynaptic inhibition of ipsilateral and contralateral lower motor neurons (LMNs) to extensor muscles of the neck
and to some back muscles, and monosynaptic excitation of
contralateral LMNs supplying extensors of the neck.

Ascending vestibular fibers


Fibers from all vestibular nuclei synapse with LMNs of
the III, IV, and VI cranial nerves. Some are crossed and some
uncrossed. They all ascend via the medial longitudinal fasciculus. These fibers are involved in the vestibulo-ocular reflexes, such as compensatory rolling of the eyes when the
head is moved. Vestibular fibers also go to the flocculonodular lobe of the cerebellum.

Reticular formation
There are numerous projections from vestibular nuclei
into the ascending and descending reticular formation. Some
of these descending reticular projections are involved in the
vomiting and cardiovascular reactions that may occur in
vestibular disturbances.

CLINICAL SIGNS OF VESTIBULAR


DISEASE
Vestibular disease produces varying degrees of loss of
equilibrium causing imbalance and ataxia. Strength is not interfered with, and therefore paresis is not observed. As a
rule, the disturbance is unilateral or asymmetrical, and the
signs are those of an asymmetrical ataxia with preservation
of strength.

53

Unilateral vestibular signs may result from either central (brain stem) or peripheral (labyrinth) disease. It is important to differentiate central from peripheral disease because of the differences in treatment and prognosis. Signs
of vestibular disease include: falling, rolling, tilting of the
head, circling, nystagmus, positional strabismus (deviation
of one eye in some head positions), and an asymmetrical
ataxia.

Nystagmus
The sign of disturbed vestibular input to the neurons that
innervate extra-ocular eye muscles is abnormal nystagmus.
Nystagmus probably occurs at some time during all types of
vestibular disease. Nystagmus is an involuntary rhythmic
oscillation of the eyeball, that nearly always affects both
eyes equally. Typically, nystagmus consists of a slow phase
in one direction and a fast phase in the other.
n cats, oscillations of the head that are synchronous with
the nystagmus will frequently be seen. It is customary to describe nystagmus clinically in terms of the fast phase, despite the fact that in most cases the slow phase will be directed towards the affected side. Nystagmus tends to occur
early in the course of peripheral vestibular disease, and to
disappear later, which means that nystagmus may not be obvious at the time of clinical examination in all acts with
vestibular disease.
Nystagmus may be induced in normal animals, where it
may be termed physiological nystagmus. For example, it occurs with normal turning of the head from side to side, or up
and down (vestibular in origin), or when watching the passing scenery from a railway carriage (visual in origin). Also,
it occurs normally after rotation, and is then called post-rotational nystagmus. If nystagmus occurs when the head is
still, and there is no rotation or movement of the surroundings, it is called spontaneous nystagmus. Spontaneous nystagmus is usually pathological in origin. Spontaneous nystagmus may be horizontal, rotatory, or vertical in direction.
If nystagmus occurs only when the head is placed in an unusual position (e.g. laterally or dorsally), it is known as positional nystagmus.
Nystagmus that consists of eye movements of the same
velocity in each direction is termed pendulous nystagmus,
and is not of vestibular origin. Pendulous nystagmus is usually associated with visual deficits.
Caloric testing consists of irrigation of the external ear
canals with warm or cold water. This sets up currents in the
endolymph, stimulating nystagmus and head tilt. It is difficult to interpret the results of this test in an animal already
showing clinical signs of vestibular disease. The test may
have some value in demonstrating whether or not the
labyrinth or VIIIth nerve is functional, since a complete absence of response to caloric stimulation usually indicates total loss of receptor function or nerve function. Nystagmus in
an inappropriate direction, and dissociated (disconjugate)
nystagmus, are abnormal responses to caloric testing, and
suggest a lesion of the vestibular nuclei or of the medial longitudinal fasciculus.

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4th European FECAVA SCIVAC Congress

Abnormal posture and ataxia

Central vestibular disease

Loss of co-ordination between head, trunk, and limbs, results in loss of balance. This is reflected in a head tilt, with
the more ventral ear directed towards the side of the vestibular disturbance. The trunk may fall, or even roll, towards the
side of the lesion. The trunk may be flexed laterally, with the
concavity directed towards the side of the lesion. The animal
may tend to circle towards the side of the lesion. These are
usually circles with a small radius. It may be possible to elicit mild hypertonia and hyperreflexia in the limbs on the side
of the body opposite to a vestibular system lesion.
An animal will often fall when attempting to shake its
head. Vision will assist an animal to compensate for a
vestibular system deficit. Blindfolding an animal with a
vestibular lesion will accentuate the clinical signs.

Any signs of brainstem disease in association with


vestibular signs indicate that central involvement is present.
The most frequent differentiating feature is a deficit in postural reactions, as central vestibular lesions most often result
in paresis or loss of conscious proprioception. Alterations in
mental status, or deficits in Vth or VIth cranial nerves, are
also indicative of central disease. Nystagmus may be a key
to differentiating central from peripheral disease. Nystagmus occurs in most central syndromes, and appears to be a
permanent deficit. It is a positional nystagmus; therefore it
may be present in some head positions (with respect to gravity), but not in others. Also the nystagmus may vary in direction with change in head position. Vertical nystagmus in
any head position is most consistent with central vestibular
disease.

Postural reactions - Strabismus


When the head is extended in a tonic neck reaction, the
eyeballs should remain in the center of the palpebral fissure
in dogs and cats. This often fails to occur on the side of a
unilateral vestibular disturbance, and results in a ventrally
deviated eyeball. Occasionally, in vestibular disease, an eyeball is noticed to deviate ventrally or ventrolaterally without
extension of the head and neck. This appears as a LMN strabismus, and can be corrected by moving the head into a different position or by inducing the patient to move its eyeballs to gaze in different directions. This is referred to as
vestibular strabismus. The ventrally deviated eyeball is on
the side of the vestibular lesion. Occasionally, the opposite
eyeball will appear to be deviated dorsally.

Peripheral vestibular disease


Peripheral lesions involve the middle and inner ear. Middle ear (bulla ossea) lesions usually produce head tilt (ipsilateral to the lesion) only, in the absence of other signs. Horizontal or rotatory nystagmus may be seen occasionally. Inner ear disease, which actually involves the receptors and
vestibular nerve within the petrosal bone, usually produces
other signs in addition to the ipsilateral head tilt - falling,
rolling, circling, nystagmus, positional strabismus, asymmetrical ataxia.
Horners syndrome (miosis, ptosis, enophthalmos) of the
ipsilateral eye may be present with either middle or inner ear
disease in dogs and cats, because the sympathetic trunk
passes through the middle ear in close proximity to the petrosal bone. The facial nerve may be affected in inner ear disease, as it courses through the petrosal bone in contact with
the vestibulocochlear nerve.
The primary characteristics of unilateral peripheral
vestibular disease are: asymmetrical ataxia without deficits
in postural reactions, and a horizontal or rotatory nystagmus
that does not change in direction with different head positions. The fast phase of the nystagmus is directed away from
the affected side.

Paradoxical central vestibular syndrome


Unilateral lesions of the peripheral vestibular system
produce a head tilt towards the side of the lesion. With few
exceptions, the same occurs with lesions of the central components of the vestibular system. Exceptions to this rule are
therefore termed paradoxical. Some unilateral lesions of
the central vestibular pathways, especially unilateral involvement of the flocculonodular lobe of the cerebellum or
the supramedullary part of the caudal cerebellar peduncle,
produce a head tilt and ataxia directed toward the side opposite to the lesion, and a nystagmus with the fast component
towards the side of the lesion. Such lesions are usually
space-occupying lesions. Usually these lesions will produce
postural reaction deficits or additional cranial nerve abnormalities on the affected side, which aid in determining on
which side a lesion is located.

Bilateral vestibular disease


Bilateral peripheral vestibular disease with complete loss
of function is characterized by symmetrical ataxia and loss
of balance of either side, with strength preserved. There is
no postural asymmetry. A characteristic side-toside head
movement often accompanies these signs. Abnormal nystagmus is not observed, and with bilateral destruction of the receptor organs, normal vestibular nystagmus cannot be elicited by head movement or caloric testing.

DISEASES OF THE VESTIBULAR SYSTEM


PERIPHERAL VESTIBULAR DISEASES
Otitis Media-Interna (or Labyrinthitis)
Etiology & Pathogenesis. Labyrinthitis refers to inflammation of the inner ear that results in dysfunction of the membranous labyrinths. This disorder is almost always an extension of otitis externa. Retrograde infection may occur via the
auditory tubes. Another source of infection of middle ear
structures is hematogenous spread. Medial extension of mid-

dle ear infection to involve meninges is not uncommon in


cats.
The majority of infections are caused by bacteria, including Staphylococcus spp., Streptococcus spp., Proteus
spp., Pseudomonas spp., Enterococcus spp. and Escherichia
coli. Occasionally, yeast infection (e.g. Pityrosporon spp.
and Candida spp.) is observed. Rarely, fungal infection may
be confined to the middle ear (e.g.. Cryptococcus sp.). Foreign bodies such as grass awns may initiate inflammation
and predispose to secondary bacterial infection.
Cinical Findings. Varying degrees of vestibular dysfunction accompany otitis media-interna or labyrinthitis. Ipsilateral head tilt, nystagmus (usually rotatory), and ataxia are almost always present. Circling, falling, and rolling, may be
seen in more severely affected animals. Ipsilateral facial
paresis/paralysis and Horners syndrome may occur. Because the facial nerve contains the parasympathetic preganglionic neurons that modulate lacrimal gland secretion, animals with labyrinthitis may have decreased tear production
and develop ipsilateral keratoconjunctivitis sicca. Ipsilateral
hemifacial spasms, resulting from irritation of the facial
nerve, have been reported in dogs in association with otitis
media. Deafness, resulting from involvement of the cochlear
nerve, may accompany otitis interna.
Diagnosis. The diagnosis may be confirmed by otoscopic examination and skull radiography. Otoscopy may reveal
otitis externa, and evidence of erosion or rupture of the tympanic membrane. Fluid in the middle ear may produce discoloration or bulging of the tympanic membrane. Inflammatory exudate or fluid should be submitted for culture and sensitivity testing. Fluid may be obtained by either aspiration or
myringotomy. Radiographic examination of the temporal
bones may reveal fluid within the tympanic cavity, or osteitis,
sclerosis, or erosion of the tympanic bulla. Computed tomography (CT) images are more sensitive in outlining these
alterations. Magnetic resonance imaging (MRI) is useful
when central extension of otitis media/interna is suspected.
Myringotomy procedure: Myringotomy is a surgical
puncture of the tympanic membrane to relieve pressure or to
obtain samples for analysis. The procedure should be completed under general anesthesia. Positioning - lateral recumbency, with affected ear uppermost, or if fluid is difficult to
obtain, there may be an advantage in having the affected ear
on the down (lowermost) side. The tympanic membrane consists of a loose dorsal section (pars flaccida) and a larger more
rigid ventral portion (pars tensa). Whereas the pars flaccida is
pink or white and contains small branching blood vessels, the
pars tensa is tough, glistening, pearly gray, and often striated.
The ear canal should be gently flushed with dilute (1:10)
aqueous povidone-iodine solution several times until the ear
canal is clear of debris. A myringotomy is then done using a
20-gauge or 22-gauge spinal needle. The use of a needle permits both collection of fluid for cytology and culture, and introduction of a small volume of sterile saline (0.2-0.4 ml) for
lavage of the middle ear cavity when a fluid sample is not abtained following aspiration through the needle. The needle
should penetrate the tympanic membrane in the ventral and
caudal aspect of the pars tensa, in order to avoid the bony ossicles. Some authors recommend the routine flushing of the
middle ear cavity with dilute povidoneiodine after fluid for

55

cytologic examination and culture has been withdrawn, followed by a saline flushing and introduction of a broad spectrum antibiotic. This author recommends a gentle flushing
with saline only after a myringotomy procedure, followed by
the use of systemic broad spectrum antibiotic therapy.
Treatment. The prognosis is usually favorable with prolonged oral antibiotic therapy, where selection is based on
culture and sensitivity studies. Some authors recommend the
use of repeated ear cleanings and irrigation, and topical antibiotic therapy, in cases of otitis media/interna. This author
recommends these procedures for otitis externa associated
with otitis media/interna only when the tympanic membrane
is intact. In addition, the use of topical therapies should be
avoided for four or five days following myringotomy. Cats
with concurrent mite infestation should be treated with a
topical miticide. In more chronic cases, surgical drainage of
the middle ear cavity may be required by means of lateral or
ventral bulla osteotomy.

Idiopathic peripheral vestibular disease


Etiology & Pathogenesis. This is an acute vestibular syndrome of unknown etiology of cats of all ages. A similar
condition occurs in older dogs. There is no evidence of inflammatory disease in affected animals. Some affected cats
have had a concomitant or recent upper respiratory tract infection, suggesting that previous viral infection may directly (due to seeding of virus in the inner ear) or indirectly (because of altered antigenicity) cause inflammation of the
vestibular sensing apparatus. Pathological or immunological
confirmation of this hypothesis is lacking, however. In one
study of 75 affected cats, 80% were diagnosed in the months
of July and August, suggesting an environmental factor may
be involved, however none was identified.
The syndrome in cats has been compared to Mnires
disease of humans, a disorder characterized by recurrent
bouts of vertigo, nystagmus and tinnitus. Abnormal flow of
endolymph within the membranous labyrinth apparently
contributes to the pathogenesis of Mnires disease in humans, and an increased concentration of potassium ions
within the perilymph (separating the bony and membranous
labyrinths) may also have a role. Considering that, unlike
Mnires disease of humans, the feline syndrome spontaneously resolves and generally does not reoccur, it is not
clear whether these factors have a role in the development of
the problem in cats.
Clinical Findings. A breed or sex predilection does not
exist for feline idiopathic peripheral vestibular disease. The
median age of affected cats is approximately four years.
Both cats and dogs exhibit signs of peripheral vestibular involvement. The signs of vestibular dysfunction usually are
unilateral, however occasionally bilateral signs may be seen
in affected cats. In addition to neurological deficits of peripheral vestibular disease, some affected cats may have
vomiting or anorexia. The signs appear suddenly, and often
result in severe dysfunction and inability to stand and walk.
In a few days the affected animals tend to stabilize and improvement continues for 4-6 weeks. Residual deficits such
as mild head tilt may persist, and blindfolding or darkness

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4th European FECAVA SCIVAC Congress

will cause a re-occurrence of signs well after apparent recovery has occurred.
Diagnosis. A diagnosis of idiopathic feline peripheral
vestibular disease is made by excluding other causes. There
is not a definitive antemortem or postmortem finding. It is
important to distinguish this idiopathic benign disorder,
which resolves spontaneously without therapy, from otitis
media-interna, which requires vigorous therapy, and may
produce recurrent or persistent signs. The idiopathic disease
is characterized by a peracute onset of head tilt, asymmetrical ataxia, and horizontal or rotatory nystagmus, in the absence of facial paresis, Horners syndrome, or signs of CNS
involvement. An absence of otitis externa, normal tympanic
membranes, and normal radiographs of the temporal bones,
further support this diagnosis.
Treatment. While the cause of this idiopathic disorder remains undetermined, prognosis for spontaneous recovery is
good, however, recovery may require 4-6 weeks. Re-occurrence may be seen, especially in dogs, either on the same
side or the opposite side. There is no evidence that treatment
of any type alters the course of the disease. Cats with concurrent otitis externa or otitis media/interna should be treated for these problems as previously described. Antiemetics
may be considered in cats that vomit.

following retraction of the soft palate.


Diagnosis. Polyps should be suspected in cats with appropriate clinical signs, particularly in young cats. Most
polyps can be visualized with a thorough otoscopic or pharyngeal examination. Opacitiy of the tympanic cavity, associated with sclerosis of the tympanic bulla, may be seen on
plain skull radiographs. Computed tomography provides
precise information regarding location and extent of polyps.
Bony lysis is rarely seen in association with nasopharyngeal
polyps. Cerebrospinal fluid analysis may be abnormal in
cats with extension of inflammation to brain or meninges.
Excised polyps are variable in size, red in color, and of
smooth appearance. Many have a stalk or pedicle of attachment. Microspcopically, there is a central core of well-vascularized fibrous tissue that is covered by epithelium (varying from stratified squamous to pseudostratified columnar
cells). Glands composed of goblet cells may be seen within
the fibrous tissue. There may also be an infiltration of a
mixed population of inflammatory cells within the polyp.
Treatment. Many polyps in the external ear, or in a nasopharyngeal location, may be removed by means of gentle
traction, thus avulsing the stalk from its attachment. Bulla
osteotomy with curettage has been advocated to remove
residual polyps from within the tympanic cavity.

Nasopharyngeal polyps

Neoplasia

Etiology & Pathogensis. Inflammatory or nasopharyngeal polyps are benign masses that may be located in the nasophaarynx, auditory tube, and/or the tympanic cavity.
Rarely the polyp may rupture the tympanic membrane and
protrude into the external ear canal. Polyps consist of wellvascularized fibrous tissue lined by epithelium. The site of
origin of the polyps has not been determined. It has been
speculated that some polyps may arise subsequently to otitis
externa or otitis media, however otitis media appears to frequently be a complication of auditory tube obstruction by
the polyp, rather than an initiating factor. Vestibular dysfunction follows extension of otitis media into the labyrinth
(otitis interna). Occasionally there may be further extension
of infection into the brain, resulting in central vestibular
signs and brainstem dysfunction. In one published report,
calici virus was isolated from one of three young cats affected in a household. Another report suggested a congenital
origin, as two young cats affected with polyps were siblings.
Clinical Findings. The majority of cats affected with
polyps are less than two years of age at the time of initial
clinical signs (age range 2 months to 15 years). There is no
apparent breed or sex predilection. Clinical signs in affected
cats vary widely, depending on the location of the polyp or
polyps. Polyps originating within the auditory tube or middle ear cavity may interfere with drainage of middle ear secretions, resulting in signs of otitis externa and/or middle ear
involvement and subsequent otitis interna and signs of peripheral vetsibular disease. Polyps may be seen by means of
otoscopic examination. Cats with a polyp or polyps in a nasopharyngeal location have signs of upper respiratory compromise (coughing, dyspnea, sneezing, stertorous respiration). Polyps in a nasopharyngeal location usually are seen

Neoplasms that involve the temporal bone may produce


peripheral vestibular disease, often in association with facial
paralysis or paresis. Fibrosarcoma, osteosarcoma, chondrosarcoma, and squamous cell carcinoma have been reported. Squamous cell carcinoma and ceruminous gland adenocarcinoma may involve adjacent soft tissues. It has been reported that squamous cell carcinoma is the most frequently
occurring tumor affecting the middle ear of cats, whereas
papillary adenomas and extension of adnexal or ceruminous
gland tumors appear to be more common in dogs in this location. Rarely, middle ear tumors may extend directly into
brainstem. Neurofibroma or lymphoma of the vestibulocochlear nerve usually cause signs of unilateral vestibular
disturbance prior to signs associated with compression of
brainstem.

Congenital vestibular syndromes


Signs of peripheral vestibular disease, usually in the absence of deafness, have been observed in several breeds of
dog (including English cocker spaniels, German shepherd
dogs, and Tibetan terriers), and in cats (Siamese and
Burmese kittens). Severe head tilt, circling, and falling or
rolling, may be noted from birth to 4 months of age. Nystagmus is rarely present. The cause is undetermined. Pathological lesions have not been demonstrated. Prognosis is
guarded, as clinical signs may regress completely, re-occur,
or remain static. There is no effective treatment.
Congenital pendular nystagmus has been recognized in
Siamese cats. The head may oscillate synchronously with
the nystagmus. Signs of vestibular dysfunction are not ap-

parent, and lesions of the visual pathways are responsible for


this syndrome.

Toxicity
Prolonged therapy with aminoglycoside antibiotics may
result in degeneration of the labyrinth receptors of the
vestibular or auditory systems, or both. Vestibular dysfunction may be fully or partially reversible, however hearing
may be permantly affected. In the southeastern U.S.A., acute
peripheral vestibular signs may follow ingestion by cats of
the tail of the blue-tail lizard.

Trauma
Cranial trauma may result in signs of peripheral vestibular disease secondary to fractures of the temporal bone or
tympanic bulla. Facial paralysis may accompany petrosal
bone injury.

CENTRAL VESTIBULAR DISEASES


Any cause of meningo-encephalitis may result in involvement of central vestibular structures. The vestibular
deficits may occur alone, or with signs indicating involvement of other areas, such as spinal cord, cerebellum, or cerebrum. Reported causes in cats include feline infectious peritonitis, toxoplasmosis, and cryptococcosis. Aberrant parasitic migration may produce severe signs of vestibular disturbance. Neoplasms of the cerebellomedullary angle affect
the vestibular system. Neoplasms may be located at the surface of the parenchyma (e.g. meningioma, neurofibroma,
choroid plexus papilloma or malignant lymphoma), or may
be located within the parenchyma (e.g. astrocytoma or lymphoma). Neoplasms at these locations occur in cats of all
ages. Thiamine deficiency may produce a mild vestibular
ataxia as the earliest sign of degeneration.

57

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59

EUROPEAN SOCIETY OF FELINE MEDICINE - ESFM

Feline spinal cord disorders


Richard A. LeCouteur
VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN
Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

Summary
The spinal cord may be divided into four major longitudinal divisions. These divisions are : 1) cervical (C1 to C5);
2) cervical enlargement ( C6 to T2); 3) thoracolumbar ( T3
to L3); 4) lumbar enlargement (L4 to Cd5). Diseases of each
of these regions results in a combination of neurological
signs that is specific for the region involved. Recognition of a
characteristic group of clinical signs is essential in the accurate localization of the spinal cord lesion. This lecture will
review the clinical signs in cats associated with spinal cord
disease and localization of the lesion to a particular level of
the spinal cord. The lecture will also review the congenital,
degenerative, metabolic, infectious, parasitic, traumatic,
vascular, and idiopathic causes of feline spinal cord disorders.

INTRODUCTION
Motor, sensory, reflex and sphincter abnormalities may
be used to determine the location of a lesion within one of
four major longitudinal divisions of the spinal cord. The divisions are cervical (C1 to C5 spinal cord segments), cervical enlargement (C6 to T2), thoracolumbar (T3 to L3), and
lumbar enlargement (L4 to Cd5). It is essential to remember
that these divisions refer to spinal cord segments, not vertebrae, and that spinal cord segments do not correspond exactly with vertebrae of the same number. Some variations
may be encountered due to slight differences between animals in segments that form cervical or lumbar enlargements.
A disorder of each of the four regions of the spinal cord
results in a combination of neurologic signs that is specific
for the region involved. Recognition of a characteristic
group of clinical signs therefore allows accurate localization
of a spinal cord lesion. The presence of neurological deficits
indicative of involvement of more than one region of the
spinal cord is highly suggestive of multifocal or disseminated spinal cord disease.
The functional differences between upper motor neurons (UMNs) and lower motor neurons (LMNs) may be
used to localize lesions to one of the functional regions of
the spinal cord.
Cell bodies of spinal cord LMNs are located in the spinal
cord gray matter. Their axons leave the spinal cord via the
ventral nerve roots to become part of a peripheral nerve, and

to terminate on a muscle. The LMNs of the thoracic limb


have their cell bodies in C6 to T2 spinal cord segments that
form the cervical enlargement, while LMNs of the pelvic
limb arise from the L4 through S1 spinal cord segments of
the lumbar enlargement. Anal and urethral sphincter LMNs
originate from S1 through S3 spinal cord segments. Signs of
LMN dysfunction, which in diseases affecting the spinal
cord reflect damage to the spinal cord segment(s) from
which LMNs originate, are: depression or loss of voluntary
motor activity, normal or depressed segmental spinal reflexes, depression or loss of muscle tone, and rapid, severe atrophy of an affected muscle due to denervation.
Upper motor neurons arise from cell bodies located in
the brain. Their axons form descending pathways of the
spinal cord, and terminate on interneurons that in turn
synapse with LMNs. Lesions affecting UMNs result in
UMN signs. These UMN signs result from an increase in the
excitatory state of LMNs. Upper motor neuron signs include: depression or loss of voluntary motor activity, normal
or exaggerated segmental spinal reflexes, appearance of abnormal spinal reflexes (e.g., crossed extensor reflex), increased muscle tone, and muscle atrophy due to disuse.
Unilateral signs resulting from spinal cord disease are
unusual, however signs frequently are asymmetrical. In the
majority of cases, a lesion resulting in asymmetrical signs
will be located on the side of greater motor and sensory
deficit.

CERVICAL (C1 to C5)


Fatal respiratory paralysis resulting from interruption of
descending respiratory motor pathways or damage to motor
neurons of the phrenic nerve (C5 to C7 spinal cord segments) occurs in a complete transverse myelopathy. Lesions
that are less than complete may not affect respiration, and in
such cases other signs may be detectable.
Ataxia and paresis of all four limbs usually are seen.
Tetraplegia rarely is seen, as lesions of sufficient severity to
cause tetraplegia also produce respiratory paralysis. Hemiparesis occasionally may be present in association with a
cervical lesion. Lesions of the cervical spinal cord may result in paraparesis with minimal neurologic deficits in thoracic limbs. The reasons for this are poorly understood.
Spinal reflexes and muscle tone are intact in all limbs,
and may be normal or exaggerated. Muscle atrophy general-

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60

ly is not present, however disuse atrophy may develop in


cases that have a chronic course. Anal reflexes are intact and
anal tone usually is normal.
Bladder dysfunction may occur with normal or increased
urinary sphincter tone, and loss of voluntary control of micturition. Reflex dyssynergia may also be seen. Although voluntary control of defecation may be lost, reflex defecation
will occur when faeces are present in the rectum.
Horners syndrome (ptosis, miosis, and enophthalmos)
rarely may be present in an animal with a severe destructive,
cervical lesion.
Conscious proprioception and other postural reactions
usually are depressed or absent in all limbs. It should be remembered that complete loss of conscious proprioception
may be present without detectable loss of pain perception.
Cervical hyperesthesia (spasms, apparent pain on palpation, cervical rigidity, and abnormal neck posture) may be
seen in some animals with cervical myelopathy. Occasionally an animal may hold a thoracic limb in a partially flexed
position, a posture that may be consistent with C1 to C5
nerve root or spinal nerve entrapment (root signature), although this posture is seen more commonly with a disorder
of the cervical enlargement.
Disorders that affect the cervical region of the spinal
cord must be differentiated from brain lesions that result in
tetraparesis. This may be accomplished by doing a complete
neurological examination, however occasionally this distinction may be difficult. In most circumstances a cervical
lesion does not result in neurological deficits attributable to
involvement of the medulla oblongata, however, there are
several notable exceptions to this rule. Positional strabismus
resulting from loss of the vertebral joint proprioceptive input
to the attitudinal reflexes, may be seen in association with a
cranial cervical lesion (C1 to C3 spinal cord segments). A
cranial cervical lesion may also cause facial hypesthesia as a
result of involvement of the spinal nucleus and tract of the
trigeminal nerve. Cranial cervical trauma often results in
clinical signs referable to injury of the caudal brain stem
(head tilt, pharyngeal paresis, facial paresis) or cerebellum.
The Schiff-Sherrington sign (syndrome or phenomenon)
consists of hypertonicity of thoracic limb muscles and hyperextension of the neck, and is seen in association with
spinal cord lesions caudal to the cervical enlargement. It is
essential to differentiate this sign from thoracic limb hypertonicity caused by a cervical lesion, or an injury rostral to the
foramen magnum.

CERVICAL ENLARGEMENT (C6 to T2)


Ataxia and paresis of all four limbs usually are present.
Occasionally paresis of thoracic limbs and paralysis of
pelvic limbs may be seen. Spinal reflexes and muscle tone
may be normal or depressed in thoracic limbs, and normal
or exaggerated in pelvic limbs. The nature of thoracic limb
reflex alterations depends on the exact craniocaudal location of a lesion within this region. Muscle atrophy often is
severe in thoracic limbs. Panniculus reflex may be depressed or absent unilaterally or bilaterally due to interruption of the LMNs involved in this reflex (C8 and T1 spinal

4th European FECAVA SCIVAC Congress

cord segments).
Should bladder dysfunction occur it is similar to that observed with a lesion in the cervical region, with loss of voluntary control of urination. Anal reflexes and anal tone most
often are normal although voluntary control of defecation
may be absent.
Unilateral Horners syndrome commonly is observed
with a spinal cord lesion of the cervical enlargement, particularly a lesion involving T1 to T3 spinal cord segments or
nerve roots.
Conscious proprioception and other postural reactions
usually are depressed in all four limbs. Alterations in these
functions may be more pronounced in the pelvic limbs than
in thoracic limbs. Occasionally conscious proprioception
will be absent only in a thoracic and pelvic limb on the
same side.
Severe depression or loss of pain perception rarely are
seen in association with a lesion of the cervical enlargement,
except in intrinsic myelopathies (e.g., ischemic myelopathy). Hyperesthesia at the level of a lesion of the cervical enlargement, thoracic limb lameness, or apparent neck pain
may be present.

THORACOLUMBAR (T3 to L3)


The majority of spinal cord lesions of dogs or cats occurs
in this region. Typically thoracic limb gait is normal, and
paresis and ataxia, or paralysis, are seen in pelvic limbs.
Thoracic limb spinal reflexes are normal. Pelvic limb spinal
reflexes and muscle tone are normal to exaggerated, depending on the severity of the lesion. Muscle atrophy is not
seen in thoracic limbs. Pelvic limb muscle atrophy, if present, is the result of disuse and is seen in animals with a severe, chronic lesion.
Anal reflexes and anal tone usually are normal or exaggerated. Voluntary control of defecation may be lost. Reflex
defecation will occur when the rectum is filled with faeces,
however may not be at an appropriate time or place. Degree
of bladder dysfunction varies depending on the severity of a
spinal cord lesion. There may be loss of voluntary control of
urination, detrusor muscle areflexia with normal or increased urinary sphincter tone, or reflex dyssynergia where
initiation of voiding occurs and is stopped by involuntary
contraction of the urethral sphincter. The bladder may be
manually expressed in some animals, and not in others, due
to increased tone of the urinary bladder sphincter. This is often referred to as an UMN bladder. Although overflow
incontinence may occur with lesions of the spinal cord in
this region secondary to overfilling of the bladder, detrusor
muscle tone and urinary sphincter tone are present, distinguishing this type of incontinence from that due to lesions of
the lumbar enlargement and cauda equina (LMN bladder).
Conscious proprioception and other postural reactions
are normal in the thoracic limbs, and depressed or absent in
the pelvic limbs.
Pain perception is normal in the thoracic limbs and may
be normal, depressed or absent in the pelvic limbs. Panniculus reflex may be reduced or absent caudal to a lesion. In the
lumbar region the panniculus reflex may be present in le-

sions caudal to L3 due to the pattern of cutaneous innervation of lumbar spinal nerves. There may be an area of hyperesthesia at the level of a lesion.
The Schiff-Sherrington sign may be seen with a lesion in
this region. Usually it is an indication of an acute and severe
spinal cord lesion, although such a lesion may be reversible.

LUMBAR ENLARGEMENT (L4 to Cd5)


and CAUDA EQUINA
Involvement of this region by a pathological process results in varying degrees of pelvic limb paresis and ataxia, or
paralysis, and is often accompanied by dysfunction of bladder, and paresis or paralysis of anal sphincter and tail. Thoracic limb function is normal.
Pelvic limb reflexes and muscle tone are reduced or absent. Muscle atrophy often is present in pelvic limbs. Conscious proprioception and other postural reactions are reduced or absent in pelvic limbs.
Anal tone and anal reflexes are reduced or absent. The
rectum and colon may become distended with feces, and fecal incontinence, with continual leakage of feces, often is
seen. Constipation may result from the inability to void feces. Paresis or paralysis of the urethral sphincters and detrusor muscle result in overfilling of the bladder and overflow incontinence. Affected animals have a large residual
volume of urine in the bladder, and the bladder is easily expressed manually.
The Schiff-Sherrington sign occasionally may be seen
with an acute lesion affecting this region of the spinal cord.
The term cauda equina is used to describe the lumbar,
sacral, and caudal nerve roots and spinal nerves as they extend caudally from the caudal tip (conus medullaris) of the
spinal cord within the vertebral canal. Lesions that affect
cauda equina result in clinical signs that are indistinguishable from lesions that affect the spinal cord segments from
which the nerves of the cauda equina arise (L6 to Cd5).

ALPHABETICAL LISTING OF FELINE


SPINAL CORD DISORDERS
Bacterial or Fungal meningomyelitis
Etiology and Pathogenesis. Bacterial or fungal meningitis and/or myelitis occur infrequently in cats. Several routes
of infection exist. Direct implantation of organisms may occur following a bite wound, spinal puncture, or surgery, or
may accompany migration of a foreign body such as a grass
awn. Extension may occur from a focus of infection such as
a paravertebral infection or diskospondylitis. Infection may
also result from hematogenous spread of systemic infection
such as endocarditis. As clinical signs produced by bacterial
or fungal agents depend more on the neural structures affected than on the agent responsible, these agents are discussed together.
Meningitis may be accompanied by infection of the underlying parenchyma of the spinal cord (myelitis). Meningitis and/or myelitis may be focal, multifocal, or disseminated

61

in distribution and are frequently accompanied by meningoencephalitis. Pathologically, meningitis is characterized


by infiltration of inflammatory cells into the leptomeninges.
Inflammation may occur throughout the entire subarachnoid
space of the brain and spinal cord. Myelitis is characterized
by necrosis and infiltration of inflammatory cells within
spinal cord parenchyma.
Bacteria that have been isolated from cats with meningitis and myelitis include Pasteurella multocida, Actinomyces
viscosus, Fusobacterium sp, Eubacterium sp and Bacteroides sp.
The most common fungi that infect the CNS of cats are
Cryptococcus neoformans, Blastomyces dermatitidis, and
Cladosporium bantianum. Cryptococcus neoformans is
found ubiquitously and frequently causes infection in immunosuppressed animals. Cryptococcosis is more common
in cats than dogs and infection may result from extension of
nasal infection through the cribriform plate. Blastomyces infections are found in certain geographic areas in the United
States and in such cases the CNS is infected by hematogenous spread.
Focal epidural infections have been reported to occur,
generally as a result of migrating grass awns or penetrating
wounds. Proliferation of inflammatory tissue may result in
an extradural space-occupying lesion causing spinal cord
compression and clinical signs of a transverse myelopathy.
Abscessation may occur within the spinal cord and may
have the radiographic appearance of an intramedullary mass.
Clinical Findings. Clinical signs of meningitis include
apparent spinal pain, hyperesthesia, and cervical or thoracolumbar rigidity, occasionally manifest as a sawhorse
posture. Irritation of the numerous nerve endings in the
meninges results in reflex muscle spasms when affected animals are stimulated. Fever is intermittent and is more likely to occur in association with concurrent bacteremia or disseminated fungal infection. Fever may occur in association
with primary CNS infections due to presence of leukocytic
pyrogens in the CSF or in the hypothalamic circulation.
Neurologic deficits are indicative of associated myelitis
or radiculitis, and abnormalities depend on the location and
extent of infection. Focal myelitis may result in signs of
transverse
myelopathy.
Disseminated
bacterial
meningomyelitis often is associated with meningoencephalitis, and clinical signs usually are acute and rapidly progressive. Focal bacterial meningitis and/or myelitis and fungal
meningomyelitis may be associated with development of
more slowly progressive clinical signs.
Paraparesis and pelvic limb ataxia are common presenting signs in cats with cryptococcal meningitis and/or
myelitis. Progressive paralysis of a single pelvic limb has
been reported in two cats with cryptococcal infection of the
lumbar spinal cord. Cats with CNS cryptococcal infections
may show an acute onset of clinical signs despite chronic destruction of nervous tissue.
Clinical signs of bacterial or fungal meningitis and
myelitis are indistinguishable from other causes of meningitis and myelitis in cats. Causes include CNS toxoplasmosis,
FIP meningomyelitis, intervertebral disk protrusion (especially in the cervical spine), spinal fracture, diskospondylitis, polymyositis, and polyarthritis.

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Diagnosis. A diagnosis of bacterial or fungal meningitis


and/or myelitis is made on the basis of results of CSF analysis, and isolation of a causative organism by culture of CSF.
Clinical signs may reflect meningeal irritation or myelopathy that may be indistinguishable from signs caused by other noninfectious myelopathies such as intervertebral disk
disease. Presence of fever or abnormal hemogram cannot be
relied upon for diagnosis of meningitis/myelitis, as neither
may be present in affected animals.
Bacterial or fungal meningitis has been reported to result
in moderate to severe CSF pleocytosis. More than 5000
white blood cells/ill may be present in some cases. Polymorphonuclear (PMN) cells predominate. Mixed mononuclear and PMN pleocytosis occurs with fungal meningitis,
and eosinophils may be present, especially in cases of cryptococcal meningitis. The CSF appears turbid if the cell count
is greater than 500 white blood cells/ill. In our experience,
disseminated bacterial meningomyelitis is rarely recognized
antemortem in dogs or cats. Focal bacterial epidural,
meningeal, or parenchymal infections more commonly occur. Cerebrospinal fluid findings in affected animals reflect
the degree of leptomeningeal or ependymal involvement,
and the CSF white blood cell count may be normal or only
slightly elevated (less than 50 white blood cells/u1).
Cerebrospinal fluid protein is usually moderately to
markedly elevated due to increased capillary permeability
and leakage of serum proteins into the CSF, and probably also due to local production of immunoglobulins. If CSF protein content is high, fibrin clots may develop. Cerebrospinal
fluid pressure is usually normal but occasionally is elevated,
especially in animals with cryptococcal meningitis. Hemorrhage into the CSF may occur; a red or pink supernatant is
indicative of recent hemorrhage. Xanthochromia develops if
more than 48 hours have elapsed following hemorrhage.
Cerebrospinal fluid glucose content may be decreased (CSF
glucose is normally 60 to 80 per cent of a simultaneously determined plasma glucose concentration) as a result of glucose utilization by microorganisms and possibly by PMN
leukocytes. However, low CSF glucose concentration is not
a consistent finding in animals with bacterial meningitis.
Bacteria or fungal organisms may be identified by
Grams stain or acridine orange stain of sedimented or centrifuged CSF. Cryptococcal organisms often are observed in
cell preparations of CSF and can be identified by staining
with Wrights stain or Grams stain, or using a wet mount
preparation with India ink.
Cerebrospinal fluid from all animals with CSF abnormalities consistent with meningitis should be submitted for
both aerobic and anaerobic bacterial culture, and antibiotic
sensitivity testing of any cultured bacterial isolates. Because
of the prevalence of anaerobic bacteria in CNS infections of
cats, anaerobic culturesare essential when bacterial meningitis is suspected. Cerebrospinal fluid fungal culture may also
be done. Negative CSF cultures are common, even in those
animals in which bacteria or fungal organisms can be identified in CSF. Culturing the sediment of centrifuged CSF, or
filtering CSF and culturing the filter, may increase the likelihood of obtaining a positive CSF culture. Causative organisms may be isolated from blood cultures of animals that are
bacteremic or have systemic fungal infection. It is recom-

4th European FECAVA SCIVAC Congress

mended that a large volume of CSF, preferably 2 or 3 ml, be


collected for bacterial and/or fungal culture. If a delay in
processing of a CSF sample is anticipated, CSF can be aseptically inoculated into a blood culture bottle for submission
to a diagnostic laboratory.
Serology may also be useful in diagnosis of CNS fungal
infections. The titer of antibody-coated latex agglutination
to cryptococcal (capsular) antigen may be useful in the diagnosis of cryptococcal meningitis and in assessing the response to therapy. The latex cryptococcal agglutination titer
(LCAT) is more sensitive than the indirect fluorescent antibody test and can be used on CSF. However, animals with
localized CNS infection may have a negative titer.
Focal epidural inflammatory lesions may appear as an
extradural mass on myelography. Chronic focal meningitis
may result in obstruction of CSF flow and blockage of contrast material on myelography due to arachnoid adhesions.
Treatment.
Bacterial Infections. In treating bacterial meningitis and/or
myelitis it is desirable to use an antimicrobial that is specific
for the causative organism, and that crosses the blood-brain
barrier (or blood-spinal cord barrier) in therapeutic concentrations, in order that drug concentrations may be maintained after the acute phase of inflammation has subsided. The bloodbrain, blood-spinal cord, and blood-CSF barriers are most permeable to antimicrobials with high lipid solubility, low ionization potential, and low protein binding affinity.
Antibiotics may be administered to animals with suspected bacterial meningitis prior to obtaining results of culture and sensitivity testing. Selection should be based on
tentative organism identification (by Grams stain or acridine orange stain) from CSF, the suspected source of infection, and the ability of an antibiotic to reach effective tissue
concentrations in CNS.
High-dose intravenous therapy with a bactericidal drug
should be used when possible, although many bactericidal
drugs penetrate poorly into the CSF. Penicillin and penicillin derivatives in high doses have been recommended for
the treatment of CNS infections caused by gram-positive
cocci (e.g., penicillin G 5000-10,000 units IV every 6 hours
for at least 7 days). Oxacillin may be used for the treatment
of meningitis caused by penicillin-resistant strains of
Staphylococcus.
Most cephalosporins penetrate poorly into the CNS. Several third-generation cephalosporins (e.g., cefotaxime) reach
effective CNS concentrations and are considered the drugs
best suited for treatment of gramnegative meningitis. Firstand second-generation cephalosporins do not reach effective
CSF concentrations, and should not be used in treatment of
CNS infections. The cephalosporins largely have replaced
the aminoglycosides, which penetrate poorly into the CNS.
Metronidazole is useful for treatment of most anaerobic
infections, is bactericidal, and diffuses well into all tissues
including the CNS. Metronidazole has had an increasing
role in the therapy of brain abscesses of humans. Metronidazole is used in combination with high doses of penicillin
when aerobes are present. Toxicity (central vestibular signs
and cerebellar dysfunction) has been reported in dogs treated with metronidazole.
Chloramphenicol reaches higher CSF concentrations

than most other antibiotics; however, it is bacteriostatic, and


many strains of Staphylococcus have been shown to be resistant to this drug. Chloramphenicol may be given at a
dosage of 20 mg/lb IV four times a day or 25 mg/lb orally
three times a day in dogs, and 5 to 10 mg/lb/day divided
twice a day in cats. Adverse effects of chloramphenicol include gastroenteritis in dogs and cats, and bone marrow depression in cats. Because of the high frequency of adverse
effects, and as bactericidal drugs are preferred for treatment
of CNS infections, use of chloramphenicol is restricted to infections caused by susceptible organisms that are resistant to
other agents.
Most sulfonamides penetrate effectively into the CSF.
Sulfadiazine (which is less protein-bound than other sulfonamides) penetrates into the CSF and nervous tissue better
than sulfamethoxazole and is effective if given orally. Data
are not available regarding the concentration of trimethoprim in CSF of dogs; however, CSF concentrations may be
as high as 35 per cent of serum concentrations in other
species. Trimethoprim-sulfadiazine combinations usually
are bactericidal in action, and are effective for treatment of
some bacterial CNS infections.
In general, tetracycline, a broad-spectrum bacteriostatic
drug, only reaches effective CNS concentrations when
meninges are inflamed. However, newer tetracyclines
(minocycline, doxycycline) penetrate the CNS better than
tetracycline and have better activity against anaerobes and
some aerobic organisms.
Intrathecal administration of antibiotics has been used in
humans. Although possible for use in dogs, multiple CSF
punctures, each requiring anesthesia, are needed. Some drugs
are toxic when directly introduced into the CNS (e.g., penicillin may cause seizures), and drugs may not diffuse freely
through CSF especially if there is a blockage of CSF flow.
Treatment with antibiotics should be started as soon as
possible after submission of CSF for culture. After results of
culture and sensitivity are known, therapy may be altered.
Treatment is continued for 2 to 4 weeks; however, treatment
for longer periods is often necessary and relapses are possible. It is also important to identify possible sources of infection outside the CNS (endocarditis, diskospondylitis, paravertebral abscess). Localized spinal cord or meningeal infections that are well encapsulated may be resistant to antibiotic therapy. Surgical exploration is indicated if focal
meningeal or epidural infection refractory to medical therapy is suspected.
Use of corticosteroids in cases of bacterial meningitis
and myelitis is controversial. Corticosteroids may decrease
inflammation and thereby decrease the resulting spinal cord
and nerve root damage; however, such treatment may also
decrease host defense mechanisms, and in turn may result
in worsening of clinical signs and in a higher incidence of
relapse.
Prognosis in cases of bacterial meningitis and myelitis
depends both on the ability to eliminate the causative organism, and on the extent of neurologic deficits. Neurologic
deficits occurring as a result of spinal cord or nerve root inflammation may be permanent.
Fungal Infections. Fungal infection of the CNS of cats is
extremely difficult to eliminate. The disease is often multi-

63

systemic, and is seldom recognized in the early stages of


CNS involvement.
Amphotericin B is frequently used to treat systemic fungal infections, although it is poorly absorbed into the CSF
and nervous tissue. Intrathecal administration of amphotericin B has been recommended, especially in animals with
Coccidioides immitis meningitis, but may result in arachnoiditis and cranial nerve toxicity.
Combinations of drugs have been recommended. Amphotericin B, ketoconazole (poor CNS penetration), and
flucytosine (good CNS penetration) are the main agents
used. Rifampin has been used to enhance amphotericin B activity. Combined treatment with amphotericin B and 5- fluorocytosine (SFU) has been recommended for use in cases
of cryptococcosis. Long-term, high-dose ketoconazole therapy is reported to be effective for treatment of cryptococcosis in cats.
Because of the difficulty in obtaining therapeutic concentrations of antifungal agents within nervous tissue, the
prognosis for CNS mycotic infections is poor. In the future,
newer generation imidazoles (e.g., fluconazole, itraconazole) that are currently under investigation may be efficacious for treatment of fungal infections of the CNS.

Congenital vertebral anomalies


Etiology and Pathogenesis. Congenital anomalies frequently occur in the vertebral column of cats; however, the
majority of such anomalies are not clinically significant. If a
vertebral anomaly causes instability or deformity of the vertebral canal, spinal cord compression and associated clinical
signs may result.
Clinical Findings. Clinical signs related to anomalous
vertebrae are not present in the majority of affected animals.
In most animals in which clinical signs develop, trauma to
the spinal cord has occurred secondary to vertebral instability or progressive deformity with growth. Block vertebrae
and butterfly vertebrae most often are stable and rarely are
associated with clinical signs of spinal cord dysfunction.
Hemivertebrae are more often associated with neurologic dysfunction than are other vertebral anomalies. Hemivertebrae may result in vertebral instability and/or narrowing of
the spinal canal, especially in the dorsoventral plane, owing
to moderate to severe angulation of the spine, which can result in spinal cord compression or intermittent trauma to the
spinal cord. Clinical signs produced depend on the location
of the anomaly and usually reflect a progressive or intermittent transverse myelopathy.
Diagnosis. Diagnosis of a vertebral anomaly is made by
means of radiographs of the vertebral column. Radiographically, hemivertebrae and adjacent vertebrae appear to be
formed of normal bone, and disk spaces are usually well
formed or widened. Vertebral bodies appear to have a portion absent and do not appear to be compressed. Adjacent
vertebrae frequently have an altered shape that conforms to
the defect found in the congenitally affected segment. Vertebral end- plates are smooth and of normal thickness. In most
cases, myelography is necessary to determine the presence
of spinal cord compression resulting from a congenital

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anomaly.
Treatment. Vertebral anomalies resulting in spinal cord
compression and instability of the vertebral column may be
treated by means of surgical decompression and stabilization.
It is important to determine that a congenital anomaly is the
cause of an animals myelopathy by ensuring that the clinical
signs are consistent with the observed abnormality. Caution
must be exercised in completing surgery on an animal with a
vertebral anomaly, and prognosis must be guarded. Animals
may have more than one spinal abnormality, and vertebral
anomalies may be associated with congenital spinal cord
anomalies that are not amenable to surgical treatment.

Degenerative myelopathy
Etiology and Pathogenesis. Degenerative myelopathy
has been described in a 6-year-old cat. Histologic examination of spinal cord confirmed diffuse demyelination and
marked astrocytosis in white matter. The etiology of the
myelopathy was not determined; however, the cat was FeLV
positive, and the possibility of virus-induced myelopathy
was considered. Retroviruses have been associated with the
development of chronic progressive myelopathy in humans.
In light of this information, all cats with progressive
myelopathy should be tested for both FeLV and FIV.

Diskospondylitis (spondylitis, vertebral


osteomyelitis)
Etiology and Pathogenesis. Diskospondylitis has been
reported to occur in cats. Bacterial or fungal infection of the
intervertebral disks and adjacent vertebral bodies
(diskospondylitis), or of only the vertebral bodies (spondylitis), may result in extradural spinal cord or cauda equina
compression due to extension of granulation tissue and bony
proliferation within the vertebral canal, or due to pathologic
fracture or luxation of an infected vertebra or vertebrae.
Hematogenous spread of bacteria or fungi is probably the
most common cause of diskospondylitis. Sources of infection include bacterial endocarditis and sites of dental extraction. Urinary tract infections have been implicated as a primary focus of infection. Retrograde flow in the vertebral
veins has been suggested as a possible route of infection to
the vertebral column.
Affected intervertebral disks may have evidence of degeneration (collapsed disk space, spondylosis deformans) or
trauma (traumatic disk protrusion, vertebral luxation). Prior
disease or injury to the disk has been suggested as a factor in
the pathogenesis of diskospondylitis.
Clinical Findings. Diskospondylitis may occur at any
level of the vertebral column, and multiple lesions may be
seen. Diskospondylitis occurs more commonly in thoracic
and lumbar spine than in cervical spine. The lumbosacral
disk space frequently is involved. Clinical findings depend
on the location of the affected vertebra or vertebrae. The
most common clinical signs are weight loss, anorexia, depression, fever, reluctance to run or jump, and apparent
spinal pain (which may be severe). Hyperesthesia may be

4th European FECAVA SCIVAC Congress

present only over the site of the lesion or may be poorly localized, especially with involvement of multiple sites.
Diagnosis. Diagnosis may be difficult, as clinical signs
often are nonspecific. Diskospondylitis should always be
considered in an animal with fever of unknown origin. Clinical signs commonly are present for several weeks or months
before a diagnosis of diskospondylitis is made.
Neurologic deficits associated with spinal cord or cauda
equina compression may be present, and may reflect either a
transverse or a multifocal myelopathy. Neurologic deficits
associated with a transverse myelopathy (T3-L3) occur most
commonly and include paraparesis, decreased conscious
proprioception, exaggerated spinal reflexes, and much less
commonly, paraplegia. Cervical lesions most commonly
cause only apparent cervical pain, and lumbosacral lesions
may cause neurologic deficits due to compression of nerves
of the cauda equine.
Affected animals may have a normal or elevated peripheral white blood cell count. Typical radiographic findings are
destruction of the bony end-plates adjacent to an infected
disk, collapse of the intervertebral disk, and varying degrees
of new bone production. Early lesions may consist only of
lytic areas in affected vertebral endplates. More advanced lesions show a mixture of bone Iysis and extensive new bone
production, with osteophytes bridging adjacent vertebrae
containing a central destructive focus. Affected vertebral
bodies may be shortened, and bony proliferation may result
in fusion of one or more vertebrae. Dogs with paravertebral
grass seed migration may have radiographic abnormalities
suggestive of paravertebral abscess formation and periosteal
bone formation on the ventral aspect of vertebral bodies. This
occurs most frequently in the cranial lumbar region.
Collection of CSF is indicated in animals with neurologic deficits. Cerebrospinal fluid may be normal, or may have
an increased protein content in cases in which
diskospondylitis lesions cause extradural compression of
spinal cord or result in meningitis and/or myelitis. The CSF
white blood cell count may be normal, or may be elevated,
with an increase in PMN neutrophils in CSF from animals
with meningitis or myelltls.
Myelography is indicated in animals with neurologic
deficits indicative of spinal cord compression and is mandatory in cases in which decompressive surgery is considered.
Myelographic findings usually indicate extradural compression, which results from extension of granulation tissue and
bony proliferation within the spinal canal. Clinical signs do
not always correlate well with the degree of compression
seen on myelography, and depend on factors such as rate and
duration of compression as well as degree of compression.
Aerobic, anaerobic, and fungal cultures of blood and
urine should be done prior to treatment in an attempt to isolate causative organisms.
Surgical biopsy may be indicated in affected dogs in
which a causative organism is not isolated from blood or
urine, and/or animals that are unresponsive to treatment with
broadspectrum antibiotics.
Treatment. Treatment consists of long-term use of an antimicrobial that is effective against the causative organism(s)
determined by results of blood and/or urine cultures. If an
organism is not cultured, cats without severe neurologic

deficits may be treated empirically, assuming infection with


the most common organism isolated from animals with
diskospondylitis (coagulase-positive Staphylococcus sp).
Antibiotics that are most effective for this purpose are
cephalosporins, or (beta- lactamase resistant penicillins such
as oxacillin and cloxacillin. A trimethoprim/sulfonamide
combination or chloramphenicol is less effective but is less
expensive, and may be effective in some cases.
Clinical signs may recur if the infection is not completely eliminated prior to cessation of antibiotic therapy, and repeated cultures of blood and urine and ongoing treatment
with an appropriate antibiotic may be necessary. Treatment
is continued for at least 6 weeks, and vertebral radiographs
are done every 2 to 3 weeks to monitor progression/ regression of a lesion. Antibiotic administration may be necessary
for up to 6 months before radiographic evidence of resolution of lesions is seen. Obtaining radiographs to monitor response to therapy is important also to monitor for development of new lesions.
Clinical improvement in animals with diskospondylitis
(resolution of fever, improved appetite, reduction of apparent spinal pain) should be seen within 2 weeks of starting antibiotic therapy. If clinical improvement is not seen, treatment should be reevaluated. Antibiotic therapy should be reviewed, and surgical biopsy of a lesion may be considered.
Use of analgesics and restriction of exercise during the first
weeks of treatment may be helpful.
Prognosis for animals with diskospondylitis depends on
the ability to eliminate the causative organism(s) and on the
degree of neurologic dysfunction. Animals with severe neurologic deficits have a guarded to poor prognosis.

Feline infectious peritonitis (meningitis


and myelitis)
Etiology and Pathogenesis. Pyogranulomatous meningitis and myelitis may occur in cats with FIP. Feline infectious
peritonitis results from a coronavirus infection and is most
commonly seen in younger cats between 6 months and 5
years of age. Infected cats may also have concurrent FeLV
infection. Meningeal and spinal cord lesions are probably
the result of immune complex-mediated vasculitis. Involvement of the CNS is more frequently observed in the noneffusive (dry) form than in the effusive (wet) form of FIP.
Multifocal and diffuse involvement of the CNS is common,
and a consistent clinical course is not associated with FIP.
Clinical Findings. Feline infectious peritonitis may result
in focal, multifocal, or diffuse involvement of the spinal cord,
brain, and meninges, and clinical signs reflect the location of
these lesions. Leptomeningitis with infiltration of spinal
nerve roots has also been reported. The most commonly recognized neurologic signs are pelvic limb ataxia, hyperesthesia (especially over the back), and generalized ataxia.
Affected animals usually manifest other clinical signs indicative of disseminated disease such as persistent fever
(frequently greater than 105 F), weight loss, enlarged kidneys, chorioretinitis, panophthalmitis, or anterior uveitis.
Diagnosis. Diagnosis is made on the basis of clinical
signs, clinical pathology (blood, CSF), and serology. Hema-

65

tologic changes include neutrophilia, Iymphopenia, and elevated serum fibrinogen and gamma globulins. Cerebrospinal
fluid usually is abnormal with an elevated white blood cell
count and protein level. The differential CSF white blood
cell count is variable but PMN cells, Iymphocytes, and
monocytes usually are present. Polymorphonuclear cells
may be the predominant cell type in CSF. Protein concentration may be very high (greater than 2000 mg/dl), and CSF
may be viscous and may clot. This should be taken into consideration when a CSF puncture is performed, as fluid may
flow into the needle very slowly.
Results of cytologic examination of CSF depend on the
degree of meningeal involvement. Meningeal inflammation
may be extensive, and CSF in these cases is generally highly abnormal. In the presence of focal or parenchymal inflammation, CSF may be normal.
Cats with FIP generally have a high antibody titer. Presence of a positive antibody titer is not diagnostic of FIP, but
in the presence of clinical signs, hypergammaglobulinemia
and abnormal CSF findings consistent with FIP, a positive
antibody titer is highly suggestive of FIP infection. Similarly, a low antibody titer does not rule out FIP. The differential
diagnosis list for CNS FIP includes toxoplasmosis, cryptococcosis, and lymphosarcoma.
Treatment. Prognosis for cats with FIP of the CNS is
poor. The FeLV status of cats suspected to have FIP should
be determined prior to commencing treatment, as the prognosis for cats with both viruses is hopeless. The most effective treatment protocols combine high levels of corticosteroids (prednisolone, I to 2 mg/lb orally once daily in the
evening), cytotoxic drugs (either cyclophosphamide, 1 mg/lb
orally once daily for 4 consecutive days of each week, or
melphalan, 1 mg orally every third day) and broad-spectrum
antibiotics (ampicillin, 10 mg/lb orally q8h), together with
maintenance of nutrient intake and electrolyte balance. Cats
receiving cytotoxic drugs should be routinely monitored for
evidence of kidney dysfunction or bone marrow suppression.
If a positive response to therapy is seen, treatment should be
continued for at least 3 months. Cats with neurologic disease
associated with FIP usually respond poorly to treatment.

Feline polioencephalomyelitis (feline


non-suppurative meningencephalomyelitis)
Etiology and Pathogenesis. Feline polioencephalomyelitis is a chronic, slowly progressive encephalomyelitis of unknown etiology described in immature
and mature cats. Histopathologically, the disease is characterized by neuronal degeneration and perivascular cuffing by
mononuclear cells. Demyelination and axonal loss are most
conspicuous in the ventral and lateral columns of the spinal
cord and most severe in the thoracic spinal cord segments.
Lymphocytic meningitis, neuronophagia, and glial nodules
also have been described, and lesions may be found in the
cerebral cortex, diencephalon, midbrain, and medullary nuclei.
The pathogenesis of the disease is unknown. A viral etiology is suspected on the basis of the histopathologic changes,
although a specific viral agent has not been isolated The

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chronic clinical course, distribution of lesions, and lack of inclusions distinguish this disease from rabies, pseudorabies,
and FIP. Feline panleukopenia virus, FeLV, and arboviruses
have been suggested as possible agents in the pathogenesis of
lesions. Further virologic and serologic tests are needed to determine the role of viral infection in the pathogenesis of this
disorder. It has been proposed in a recent study that a tickborne virus may be the causative agent in Sweden.
Clinical Findings. Clinical signs include ataxia, paraparesis, tetraparesis, hypermetria, head tremors, and localized hyperesthesia. Spinal reflexes, pupillary light reflexes,
and postural reactions may be normal or depressed. Two animals have been described as having episodes of hallucinations, clawing, hissing, and biting at imaginary objects during sleep. These seizures preceded other clinical signs by
more than 2 years in one cat. Clinical signs usually are indicative of multifocal CNS disease but may be suggestive of
focal transverse myelopathy in the thoracolumbar region or
lumbar enlargement. Clinical signs are slowly progressive
over several months.
Diagnosis. Antemortem diagnosis is difficult and is
made by ruling out other multifocal CNS diseases. Two affected cats have been reported to be leukopenic, and one affected cat had an elevated CSF protein concentration (40
Treatment. Treatment of affected cats has not been reported.

Hypervitaminosis A of cats
Etiology and Pathogenesis. Hypervitaminosis A in cats
is characterized by extensive confluent exostosis that is most
prominent in the cervical and thoracic spine. It is caused by
a chronic excess of dietary vitamin A and is usually a result
of feeding a diet consisting largely of liver. Exostosis may
extend to involve the entire spine, ribs, and pelvic and thoracic limbs with complete fusion of the spine and joints.
Compression of spinal nerve roots or nerves may occur if
new bone formation extends into intervertebral foramina.
Clinical Findings. Clinical signs in affected cats include
apparent cervical pain and rigidity, thoracic limb lameness,
ataxia, reluctance to move, paralysis, and hyperesthesia or
anesthesia of the skin of the neck and forelimbs. The three
most proximal diarthrodial joints of the cervical spine are
almost always first affected. Osseous lesions develop insidiously, and clinical disease usually is advanced in cats older
than 2 years of age before significant clinical features are
recognized.
Diagnosis. Radiographic evidence of extensive exostosis
of the cervical vertebral column and a history of excessive dietary intake of vitamin A or liver are necessary for diagnosis.
Treatment. Reduction of dietary intake of vitamin A prevents the development of further exostosis, however it may
be difficult to persuade affected cats to eat anything other
than liver.

Intervertebral disk disease


Etiology and Pathogenesis. Degenerative disk disease

occurs in cats, although the incidence of clinical signs associated with disk protrusion is low compared to that in dogs.
Degenerative changes and distribution of disk protrusions
are similar to type II disk protrusions in nonchondrodystrophoid dogs. Clinical signs seen usually are indicative of a
slowly progressive transverse cervical or thoracolumbar
myelopathy. Type I disk extrusion associated with calcification of intervertebral disks and an acute onset of neurologic
deficits have been reported in cats. Diagnosis and treatment
are similar to that described for dogs.
Clinical Findings. Clinical signs seen with intervertebral
disk disease vary, depending on whether type I or type II
disk herniation is present, the location of the lesion, and
severity of the spinal cord lesion. Clinical signs seen in association with type I disk extrusion include apparent pain
and/or motor and/or sensory deficits.
Clinical signs associated with type II disk protrusion
generally are slowly progressive over a period of months,
but may develop acutely over days in some animals. Neurologic deficits usually are indicative of a cervical or thoracolumbar myelopathy. Paraparesis or tetraparesis, depending on the site of the lesion, is the most common clinical
finding, and deficits may be asymmetric. In the cervical
spine, type II protrusions most commonly occur in caudal
cervical disks. In some cases, caudal cervical type II disk
protrusion may be part of the spectrum of abnormalities associated with cervical spondylomyelopathy. Apparent neck
or back pain may or may not be a feature of type II disk protrusion.
Diagnosis. The differential diagnosis in animals with
type II disk protrusion includes other causes of progressive
transverse myelopathy, the most likely being neoplasia or
degenerative myelopathy. Spinal radiographs and, in almost
all cases, CSF analysis and myelography are necessary to
confirm a diagnosis of disk extrusion or protrusion. General
anesthesia is required to achieve the precise positioning
needed to obtain radiographs of diagnostic value. Foam
wedges or sandbags are usually needed to align the vertebral
column parallel to the table top for lateral projections. Care
must be taken, however, in anesthetizing and positioning animals that have acute type I disk extrusions, as further extrusion of disk material and further spinal cord compression
may occur with manipulation and movement of the spine.
Type II disk protrusion may be associated with narrowing of the disk space, osteophyte production, and end-plate
sclerosis. Calcification of disk material rarely is seen in association with type II disk protrusion. In some animals with
type I or type II disk herniation obvious abnormalities are
not seen on noncontrast vertebral radiographs.
Myelography is almost always necessary to confirm that
disk material has herniated into the spinal canal resulting in
spinal cord compression. Myelography is most important in
determining the site (or sites) of disk herniation and in lateralization of disk material within the spinal canal prior to surgical decompression. Myelography is necessary for diagnosis in most cases of type II disk protrusion in order to distinguish disk protrusion from other causes of slowly progressive transverse myelopathy, such as spinal neoplasia and degenerative myelopathy.
Cerebrospinal fluid should be collected and analyzed pri-

or to myelography to rule out inflammatory or infectious


disease of the spinal cord and/or meninges. Clinical signs in
animals with GME, distemper myelitis, FIP, spinal lymphoma, and other disorders may mimic those of cervical or
thoracolumbar disk disease. The characteristic myelographic findings in both type I and type II disk herniation into the
spinal canal are extradural compression of the spinal cord
with displacement of the spinal cord and narrowing of the
subarachnoid space on lateral and/or ventrodorsal views, depending on the location of the compressive mass. Type II,
and most type I, disk herniations result in a ventral or ventrolateral epidural mass that causes dorsal displacement of
the spinal cord.
Treatment. Type I Disk- Extrusion. The appropriate treatment for animals with type I disk extrusion depends on the
animals neurologic status. Each animal should be evaluated
individually. Medical treatment directed at decreasing spinal
cord edema may be appropriate for animals with apparent
pain only or animals that have mild neurologic deficits but
are ambulatory and have not had previous clinical signs associated with disk disease. These animals should be strictly
confined to a small area such as a hospital cage or a quiet
place away from other pets for at least 2 weeks. Very cautious use of analgesics or anti-inflammatory agents occasionally may be indicated; however, strict confinement followed by a period of restricted exercise is imperative.
Surgical decompression of the spinal cord and removal
of disk material from the spinal canal should be considered
in animals with neurologic deficits such as paresis or paralysis with deep pain perception intact. Surgical decompression should be done as soon as possible to prevent further
spinal cord damage incurred as a result of sustained compression or further extrusion of disk material. In addition, if
surgery is delayed 2 to 3 weeks, disk material hardens and
becomes adherent to dura mater, and becomes difficult or
impossible to remove from the spinal canal.
Regardless of whether medical or surgical treatment is
instituted, animals that are paretic or paralyzed require intensive nursing care. Neurologic improvement may take
weeks or months and this requires owner cooperation and
enthusiasm regarding care and physical therapy. Manual expression, intermittent catheterization, and /or indwelling
catheterization of the bladder are often required to ensure
emptying of the bladder. Weekly urinalysis, especially in animals that do not have voluntary control of micturition, is
important in monitoring for urinary tract infection. It is also
important to keep animals well padded, clean, and dry to
prevent formation of pressure sores, and to ensure that
caloric and water intake is adequate.
Type 11 Disk Protrusion. Treatment with corticosteroids
may result in neurologic improvement for variable periods
of time in animals with type II disk protrusion. However,
corticosteroid therapy is not curative. The reason for this improvement is not clear as intramedullary hemorrhage and
edema seen in cases of acute spinal cord injury are not a feature of chronic spinal cord compression.

Ischemic myelopathy due


to fibrocartilaginous embolism

67

Etiology and Pathogenesis. Fibrocartilaginous embolism


and ischemic myelopathy have been reported in a cat Ischemic myelopathy results from ischemic necrosis of spinal
cord gray and white matter associated with fibrocartilaginous emboli that occlude arteries and/or veins of the leptomeninges and spinal cord parenchyma. This disease is
characterized by an acute onset of neurologic deficits and is
generally nonprogressive after several hours.
The substance occluding spinal cord arteries and veins
has histologic and histochemical properties similar to fibrocartilage of intervertebral disks and is presumed to originate
from the nucleus pulposus of an intervertebral disk. Pathogenesis of the fibrocartilaginous embolism is not known.
Clinical Findings. Ischemic myelopathy is characterized by an acute onset of neurologic deficits that may be
severe. Clinical signs may progress over several hours but
are generally not progressive after 12 hours. Affected animals usually do not have a history or evidence of trauma
but may have a history of exercise prior to the onset of clinical signs. Apparent pain usually is not present at the time
of examination or during the course of the disease, although dogs are often reported to cry out at the onset of
clinical signs.
Diagnosis. Ischemic myelopathy should be suspected in
any cat with an acute onset of nonprogressive neurologic
deficits that are not associated with apparent spinal pain, especially if deficits are asymmetric or indicate that at least
several spinal cord segments are involved. A diagnosis is
made by ruling out other causes of myelopathy. Spinal radiographs are normal. Cerebrospinal fluid may be normal or
may have an elevated protein concentration as a result of
leakage of protein through damaged vascular endothelium.
The white blood cell count of CSF may be normal or may be
mildly increased in the early stages, probably as a result of
an inflammatory response triggered by spinal cord ischemia.
Xanthochromia may be present 48 hours or more after a subarachnoid hemorrhage. Appearance on a myelogram usually
is normal, although mild intramedullary swelling as a result
of spinal cord edema may be seen for as long as 24 hours after the onset of clinical signs .
Treatment. Corticosteroids (as recommended for spinal
trauma) may be given initially to reduce any secondary
spinal cord edema; however, after several days, edema usually is resolved. Good nursing care is essential in recumbent
animals to prevent pressure sores, urinary tract infections,
and contracture of denervated muscles. Prognosis depends
on the severity of an animals neurologic deficits. Animals
that retain pain perception in affected limbs and tail usually
regain neurologic function, although recovery may take several weeks to months and LMN signs may persist (muscle
atrophy and/or paresis). Animals with absent pain perception
for 24 hours are likely to have irreversible spinal cord damage and have a poor prognosis for return of function in affected limb or limbs. Many animals show improvement
within 2 weeks of onset of signs, unless extensive gray matter destruction has occurred.
Clinical improvement seen in the first 2 weeks may be
accounted for by resolution of edema and hemorrhage, and
establishment of collateral circulation to areas that were is-

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chemic but not necrotic. Later clinical improvement is


proably due to compensation by remaining spinal cord neurons.

Mucopolysaccharidosis
Etiology and Pathogenesis. The mucopolysaccharidoses
are a group of genetic diseases that result from defects in the
metabolism of glycosaminoglycans. Two subclasses have
been recognized in cats, and paraparesis associated with
spinal cord compression has been reported in Siamese cats
with mucopolysaccharidosis VI (MPS VI). Mucopolysaccharidosis VI is the result of a deficiency of the lysosomal
enzyme arylsulfatase B and, in addition to causing characteristic physical deformities, can result in skeletal changes,
including fusion of the cervical vertebrae, variable fusion of
thoracic and lumbar vertebrae, bony proliferation and bony
protrusion into the vertebral canal in the thoracic and lumbar
spine causing compression of the spinal cord, and bony proliferation in the intervertebral foramina causing nerve root
compression. Bony proliferative changes and associated
spinal cord compression occur prior to, or at the time of, epiphyseal closure (about 9 months of age) and are probably
nonprogressive after this time. Mucopolysaccharidosis VI is
an inherited abnormality and has an autosomal recessive
mode of inheritance.
Mucopolysaccharidosis I due to a deficiency in alpha-Liduronidase has been reported in a domestic shorthaired cat.
The clinical features were similar to MPS VI, but bony proliferative changes and associated spinal cord compression
were not found. Although vacuolar changes were observed
in neurons of brain and cervical spinal cord, presumably as
a result of storage of glycosaminoglycans, neurologic
deficits were not found clinically. Mucopolysaccharidosis I
probably has an autosomal recessive mode of inheritance.
Clinical Findings. The characteristic physical findings in
cases of MPS VI are small head, flat broad face, widely
spaced eyes, corneal clouding, small ears, depressed bridge
of the nose, large forepaws, and concave deformity of the
sternum. Affected kittens are smaller than normal littermates, and physical deformities are noticeable by 8 weeks of
age. Neurologic deficits due to skeletal changes and spinal
cord compression are seen between 4 and 7 months of age
and progress over 2 to 4 weeks. Neurologic findings are indicative of a transverse myelopathy between T3 and L3, and
include absent conscious proprioception, normal to exaggerated pelvic limb reflexes, and decreased pain perception in
the pelvic limbs. The thoracic limb gait may be normal or affected cats may have a crouching posture. Spinal reflexes in
the thoracic limbs are normal.
Diagnosis. Radiographs of the spine show vertebral fusion and bony protrusions into the spinal canal and intervertebral foramina of the thoracolumbar spine. However, bony
proliferation is not an indication of neurologic dysfunction.
Myelography is necessary to demonstrate spinal cord compression. Subarachnoid CSF puncture may be difficult due
to proliferative changes around the vertebrae. MPS VI can
be confirmed by measurement of arylsulfatase B activity in
leukocytes.

Treatment. As skeletal changes are nonprogressive after


about 9 months of age, decompressive surgery may result in
improvement in neurologic signs. However, spinal cord
compression may be present at more than one site. The underlying lysosomal enzyme deficit is not amenable to treatment at present. Bone marrow transplantation is being investigated as a possible therapy for MPS VI.

Neoplasia
Etiology and Pathogenesis. The spinal cord may be a site
of primary or metastatic neoplasia, or may be compressed or
invaded by primary or metastatic tumors arising from the
vertebrae and surrounding tissues. Primary neural tumors include astrocytoma, glioma, ependymoma, neuroepithelioma,
malignant nerve sheath neoplasm (schwannoma, neurofibroma, neurofibrosarcoma), meningioma, meningeal sarcoma,
and reticulum cell sarcoma.Tumors of spinal nerves that extend into the spinal canal or spinal nerve roots may cause extradural or intradural compression of the spinal cord. These
tumors may also invade the spinal cord parenchyma. Lymphosarcoma may also involve peripheral nerves and extend
along spinal nerves and nerve roots into the spinal canal, resulting in clinical signs of spinal cord disease.
Meningeal sarcomatosis is a rare condition characterized
by diffuse infiltration of the leptomeninges by neoplastic
mesenchymal cells. In one reported case in a dog, clinical
signs were lameness, reluctance to sit, apparent spinal pain,
seizures, and urinary incontinence.
The spinal cord may also be compressed by tumors originating from surrounding structures. Most commonly these
tumors arise from bone, cartilage, fibrous tissue, and blood
vessels of vertebrae, and less commonly from the hemopoietic elements of bone and tissue outside the vertebral column
including muscle, fat, and paraganglia. Secondary tumors
result from hematogenous or Iymphatic spread of tumor emboli and include hemangiosarcoma, lymphosarcoma, mammary adenocarcinoma, pulmonary carcinoma, prostatic carcinoma, and malignant melanoma.
Epidural Iymphosarcoma is the most commonly occurring spinal tumor in cats. Primary intramedullary tumors
rarely occur in cats. Etiology of vertebral and spinal cord tumors is unknown. Lymphosarcoma in cats may be associated with FeLV or FIV infection; however, not all cats with
spinal Iymphosarcoma test positive for FeLV or FIV.
Clinical Findings. Clinical signs depend on the location
of the tumor. Tumors may involve more than one spinal cord
segment and more than one spinal tumor may be present, resulting in multifocal signs. However, most animals present
with clinical signs referable to a transverse myelopathy. Tumors may occur anywhere within the spinal cord or spinal
canal and usually result in progressive neurologic deficits.
The duration of clinical signs may vary considerably (from
one week to one year in one study). Animals may present
with the following signs: an acute onset of severe neurologic deficits associated with pathologic fracture of a vertebra,
resulting in spinal cord compression; epidural, subarachnoid, or intramedullary hemorrhage; or spinal cord ischemia
associated with tumor expansion. Neurologic deficits are

usually bilateral but may be asymmetric.


Tumors of nerves of the brachial plexus initially cause
progressive LMN signs in the ipsilateral thoracic limb, including muscle atrophy and paresis. The affected limb is often painful on palpation or movement; cutaneous sensation
generally remains intact. If the tumor extends into the spinal
canal, UMN signs to the pelvic limbs may become apparent.
Tumors of the nerves of the cauda equine or lumbosacral
plexus, with extension into the spinal canal, may cause unilateral or bilateral LMN signs in the pelvic limbs, tail, perineum, urinary bladder, and anal sphincter.
Apparent pain is a common finding associated with extradural and intradural tumors. Apparent pain may be intractable, especially in animals with a tumor affecting spinal
nerve roots. This may be due to stretching or inflammation
of the meninges surrounding the expanding tumor. In general, however, extradural, intraduralextramedullary, and intramedullary tumors cannot be distinguished on the basis of
clinical findings.
Diagnosis. A tentative diagnosis of spinal tumor can be
made on the basis of radiographic, CSF, and myelographic
findings. Definitive diagnosis can only be made after biopsy
of a suspected lesion.
Radiography. Bone lysis with a cortical break is the most
common radiographic finding in animals with vertebral tumors. Other radiographic findings include destruction of
vertebral end-plates, collapse of an adjacent disk space, collapse and shortening of a vertebral body, pathologic fracture,
bone sclerosis and bony production, cystlike expansile lesions, or adjacent soft tissue masses.
Vertebral lesions may also occur with spread of tumors
from surrounding soft tissues into the vertebrae. Bone tumors are not always easily detected by means of radiography, owing to inconsistent vertebral shape, overlying rib and
soft tissue shadows, and improper patient positioning. Other
diseases, such as bacterial or fungal diskospondylitis,
spondylitis, or vertebral osteomyelitis, must be considered in
the differential diagnosis of vertebral tumors.
Expanding tumors within the spinal canal may result in
widening of the vertebral canal and loss of bone density due
to ischemia and necrosis of overlying bone. Similarly, tumors of spinal nerves extending into the spinal canal may
cause widening of intervertebral foramina.
Cerebrospinal fluid analysis. Cerebrospinal fluid may be
normal or may have an increased protein concentration
and/or white blood cell count. A mild to moderate increase
in CSF white blood cell count may occur in animals with tumors arising from or invading the leptomeninges. Polymorphonuclear cells may predominate, probably as a result of
meningeal inflammation and necrosis. Tumor cells rarely are
found in CSF, except in CSF from animals with lymphosarcoma, in which abnormal lymphocytes are often present in
association with meningeal infiltration. Collection of CSF
from the lumbar subarachnoid space may yield more cells
than cisternal collection, owing to probable caudal flow of
CSF in animals. Inability to demonstrate tumor cells in CSF
may be the result of the methods used to analyze CSF. The
use of cell concentrating techniques that yield a greater percentage of cells present in CSF may result in the preservation of more neoplastic cells. Xanthochromia, suggesting

69

previous subarachnoid hemorrhage, occasionally is present.


Cerebrospinal fluid protein concentration may be increased
due to abnormal permeability of blood-spinal cord or bloodmeningeal barrier, as a result of extradural compression or
meningeal or parenchymal tumor infiltration.
Myelography. Myelography may be helpful in differentiating intramedullary, intradural-extramedullary, and extradural tumors. Cisternal and lumbar injection of contrast
material may be necessary to outline both the cranial and
caudal extent of a tumor. It is important to obtain survey radiographs of the entire vertebral column prior to and after injection of contrast, as more than one tumor may be present
and the neurologic deficits of one tumor may mask those
produced by another. Several radiographic views (at least
lateral and ventrodorsal) are necessary to determine whether
a tumor is intramedullary, intradural-extramedullary, or extradural. Tumors may have a mixed myelographic appearance, with extradural, intradural, and/or intramedullary components (e.g., nerve root tumors, meningioma, and spinal
cord blastoma).
Other Diagnostic Tests. As many spinal tumors are secondary tumors and primary vertebral tumors commonly
metastasize, careful attention should be directed toward
eliminating the presence of other tumors by performing a
thorough physical examination, survey thoracic and abdominal radiographic examinations, rectal examination, complete blood count, and other diagnostic tests as necessary.
For example, animals with Iymphosarcoma may show abnormal circulating lymphocytes and/or hypercalcemia, and
animals with plasma cell myeloma may show aplastic anemia, myelophthisis, hypercalcemia, elevated serum protein,
monoclonal gammopathy on serum electrophoresis, and/or
Bence Jones proteinuria.
Both CT and MRI aid in exact determination of location
and extent of spinal tumors. Use of these advanced imaging
modalities aids in precise surgical planning and radiation
therapy planning.
Biopsy. Biopsy of suspected lesions is necessary to differentiate neoplasms from other vertebral and spinal cord
abnormalities and to determine histologic type. An open
surgical technique is most often used to obtain an adequate
specimen of most spinal tumors; however, in the future, fluoroscopy- or CT-guided needle biopsy techniques will become available for use in dogs and cats.
Treatment. The majority of vertebral tumors are not surgically resectable, owing to the malignant characteristics of
the tumor and the decreased stability of the vertebral column
that may result from extensive surgery. Surgical decompression of the spinal cord and debulking of tumor mass may be
palliative in some cases. Some tumors within the spinal
canal are surgically resectable, including some tumors that
appear intramedullary on myelography, such as spinal cord
blastoma.
There is not a direct relationship between tumor size and
rate of progression or severity of clinical signs. The spinal
cord is able to compensate for pressure applied gradually,
and animals with spinal tumors may remain ambulatory despite having little normal spinal cord tissue remaining. Compression applied to the spinal cord rapidly, such as may occur with a pathologic fracture, may cause severe and irre-

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versible spinal cord damage.


Corticosteroids may decrease spinal cord edema associated with spinal cord tumors and result in clinical improvement for a variable period of time. Radiation therapy and
chemotherapy may be helpful in animals with spinal lymphosarcoma. Most chemotherapeutic agents do not cross the
blood-spinal cord or blood-CSF barrier in concentrations to
eliminate tumor cells in the meninges or spinal cord. Several chemotherapeutic agents, including methotrexate and cytosine arabinoside, may be given intrathecally and have been
used in the treatment of meningeal lymphosarcoma and
leukemic meningitis. Complications of intrathecal use of
chemotherapeutic agents include arachnoiditis and seizures.
Chemotherapy may be helpful in the treatment of plasma
cell myeloma.
Chemotherapy and radiotherapy have not been used in
the treatment of a sufficient number of primary spinal cord,
nerve root, and meningeal tumors to assess results; however, initial experience suggests that further use of radiation
therapy is warranted. Various chemotherapeutic regimens
have been used in the treatment of various bone tumors and
tumors that metastasize to bone, generally with poor results.
Chemotherapy regimens in the future may offer more hope
in the treatment of vertebral tumors. In general, the prognosis for animals with nonresectable spinal tumors is poor.

Osteochondromatosis
(multiple cartilaginous exostoses)
Etiology and Pathogenesis. A skeletal osteochondroma
is a cartilage-capped exostosis arising from the surface of a
bone formed by endochondral ossification. An animal with a
monostotic lesion has a solitary osteochondroma. Polystotic
skeletal involvement is called osteochondromatosis (synonyms: multiple cartilaginous exostoses, hereditary multiple
exostoses , multiple osteochondromatosis , diaphyseal aclasis, dyschondroplasia, and hereditary deforming chondrodysplasia). There are consistent differences between cats
and dogs regarding age of onset of lesions, patterns of skeletal involvement, and pathogenesis.
The incidence of feline osteochondromatosis is unknown. Feline osteochondromatosis is characterized by an
initial appearance of lesions in the skeleton of mature cats (2
to 4 years of age). Growth of the lesions is progressive. The
disease has no apparent sex or breed predilection in cats, and
a hereditary pattern has not been demonstrated in cats. Malignant transformation to osteosarcoma has been reported to
occur in an osteochondroma of a cervical vertebra in a cat.
The incidence of osteochondromatosis in dogs remains
undetermined. The disease is frequently demonstrated in the
skeleton of dogs radiographed for unrelated reasons. Onset
of clinical disease is usually in dogs less than 18 months of
age. Onset in mature dogs is infrequently recognized. A
hereditary basis has been indicated in dogs, although a sex
or breed predilection is not apparent. Continued growth or
reactivation of growth of exostoses in dogs is suggestive of
neoplastic transformation.
The etiology of canine osteochondromatosis is unknown.
The current view regarding pathogenesis of feline osteo-

4th European FECAVA SCIVAC Congress

chondromatosis is that the disease is virus-related, and probably virus-induced. The random distribution of lesions is
compatible with a hematogenous distribution of a virus. The
virus may be FeLV, feline fibrosarcoma virus acting in an
atypical manner, or another member of the feline retrovirus
family.
Clinical Findings. Osteochondromatosis may occur anywhere in the vertebral column but most commonly is found
in the thoracic and lumbar spine. The disease may result in
spinal cord compression and clinical signs indicative of a
progressive transverse myelopathy between T3 and L3.
Neurologic deficits are often asymmetric.
Diagnosis. Radiographically, vertebral lesions tend to be
circular and smooth, with sclerotic borders. Lesions are usually multiple and may be cystic or proliferative, with an increased radiodensity. Myelography is necessary to demonstrate associated spinal cord compression. Extension of exostoses into the spinal canal results in extradural compression of the spinal cord. Surgical biopsy is necessary to differentiate osteochondromatosis from benign bone tumors
(osteomas), neoplastic lesions, or infectious processes.
Treatment. Treatment of canine osteochondromatosis affecting the vertebral column is unnecessary unless a lesion
results in clinical sequelae. An osteochondroma should be
removed if it impinges on spinal cord, or if malignant transformation is suspected. Surgical excision of cartilaginous
exostoses and spinal cord decompression are the recommended treatments for lesions causing spinal cord compression and neurologic deficits. Intraoperative spinal stabilization may be indicated following lesion removal. The prognosis for dogs that have stopped growing is good; however,
the prognosis for animals that are still growing is guarded, as
lesions may continue to expand and subsequently result in
spinal cord compression.
Treatment of feline osteochondromatosis is complicated
by the association with FeLV and the progressive nature of
lesions in cats. It seems that at best the surgical removal of a
lesion may provide only temporary relief to a cat, because of
the tendency for excised lesions to recur and for new lesions
to develop.

Protozoal myelitis
Etiology and Pathogenesis. Toxoplasma gondii infection
may cause a focal or disseminated myelopathy in cats. Animals are infected after ingesting meat containing toxoplasma
bradyzoites and/or tachyzoites, after ingesting cat feces containing sporulated oocysts, or by transplacental or congenital infection. The infective organism is spread hematogenously to most organs of the body, including the CNS. The
incidence of disease associated with Toxoplasma gondii is
thought to be low; however, opportunistic infection in immunosuppressed animals may be more widespread than previously reported. Immaturity and concurrent CD virus infection may result in an increased susceptibility of dogs to toxoplasmosis. In dogs with systemic toxoplasmosis, the incidence of CNS involvement is high. In cats, concurrent infection with FeLV or FIV or administration of corticosteroids may predispose to the development of clinical signs

of toxoplasmosis through immunosuppression and reactivation of latent infection.


Pathologically, CNS toxoplasmosis lesions are characterized by diffuse perivascular cuffing, infiltration of tissues
by inflammatory cells (predominantly mononuclear cells),
hemorrhage, necrosis, edema, and neuronal degeneration.
Granulomatous reactions may be seen. Encysted or free
forms of Toxoplasma gondii may be present. Observed tissue reactions may occur as a result of cell rupture, immune
complex deposition, delayed hypersensitivity reaction, or
degeneration of toxoplasma cysts.
Clinical Findings. Affected animals usually have clinical
signs of progressive multifocal or disseminated CNS disease. Clinical signs indicating a focal transverse or diffuse
myelopathy only may be seen initially. Neurologic deficits
depend on site of involvement and may be UMN or LMN. If
lower motor neurons are involved, denervation may result in
severe muscle atrophy.
Animals with CNS toxoplasmosis may or may not have
other clinical signs indicative of systemic infection (fever,
Iymphadenopathy, pneumonia, apparent muscle pain, gastrointestinal tract disease, iritis, or chorioretinitis).
Diagnosis. Antemortem confirmation of CNS toxoplasmosis in dogs or cats is extremely difficult. Results of routine hematologic and biochemical tests may be abnormal in
cats or dogs with acute systemic toxoplasmosis; however,
such results reflect only the organ systems involved and are
not specific for toxoplasmosis. Cerebrospinal fluid may be
normal, or may have an elevated white blood cell count with
a mixed mononuclear pleocytosis, and an elevated protein
concentration. Xanthochromia may be present if subarachnoid hemorrhage has occurred. Radiography of the thorax or
abdomen of animals with acute disease may demonstrate effusion, pneumonia, or abdominal masses.
Toxoplasma organisms may be identified in cytologic
preparations of thoracic or peritoneal effusions, or in biopsies of Iymph node or muscle examined by conventional
histopathologic techniques, or by other methods such as immunoperoxidase staining. It is difficult, however, to be certain of the association between clinical disease and demonstration of organisms.
Numerous serologic tests have been used in the diagnosis of toxoplasmosis. Serologic testing for antibody (immunoglobulin G or IgG) is of limited use for determining active infection, unless paired titers done 2 to 3 weeks apart
demonstrate a fourfold increase. Certainly, a negative titer
does not rule out a diagnosis of toxoplasmosis. Currently it
is recommended that for serologic diagnosis of toxoplasmosis in dogs or cats a single serum sample should be submitted for immunoglobulins G and M (IgG and IgM) determinations, and for calculation of levels of circulating antigen to
Toxoplasma gondii. Further, in cats suspected of having toxoplasmosis, both FeLV and FIV titers should be determined.
Fecal examination for oocysts is the most practical
method for determining the public health risk of a cat suspected to have toxoplasmosis. Oocysts are shed in feces of infected cats for only a short time (5 days to 2 weeks postinfection).
Treatment. Several antibacterial agents have been recommended for treatment of toxoplasmosis and neosporosis in

71

dogs and cats. Available drugs are effective in CNS tissues


only against actively proliferating forms of the organism, and
are not active against encysted forms, which are dependent
on host humoral and cell-mediated immune responses for
eradication. Clindamycin is currently recommended for treatment of systemic infection of dogs or cats. Oral therapy at a
total daily dosage of 12 mg/lb (25 mg/kg) divided ql2h appears effective in cats, whereas a daily dose of 5 to 18 mg/lb
(10 to 40 mg/kg) divided q6h or q8h should be effective in
dogs. Therapy should be continued for 2 to 4 weeks. The effectiveness of clindamycin in penetrating CNS tissues of
dogs or cats has not been determined, and it is therefore recommended that sulfadiazine or triple-sulfas be given orally at
a daily dosage of 50 mg/lb divided ql2h for CNS toxoplasmosis. Addition of pyrimethamine at a daily dosage of 0.25
to 0.5 mg/lb permits reduction of the sulfadiazine dosage by
half. Hematologic monitoring for bone marrow suppression
is essential for cats placed on this therapeutic regimen.
The public health risk posed by a cat with active Toxoplasma gondii infection must be considered prior to and during treatment for toxoplasmosis.

Sacrocaudal dysgenesis in manx cats


Etiology and Pathogenesis. Manx cats have varying degrees of taillessness associated with sacral and/or caudal
vertebral deformities. Some tailless cats have a normal
sacrum, spinal cord, and cauda equina. Others show varying
dysgenesis or agenesis of the sacral and/or caudal vertebrae
that may be associated with spine bifida and/or malformations of the terminal spinal cord and/or cauda equina. Spinal
cord malformations include absence or partial development
of sacral and caudal spinal cord segments or cauda equina,
myelodysplasia, meningocele, meningomyelocele, diastematomyelia of sacral segments (duplication), myeloschisis
(cleft within the spinal cord), syringomyelia in the lumbar
and sacral spinal cord segments, shortening of the spinal
cord, and subcutaneous cyst formation. These spinal cord
and cauda equina malformations are associated with variable
neurologic deficits.
Sacrocaudal dysgenesis is inherited as an autosomal
dominant trait and may be lethal in some homozygote cats.
Sacrocaudal dysgenesis and associated malformations have
been recognized in most breeds of cats, many not of true
Manx breeding. Sacrocaudal agenesis in a Maltese kitten has
been reported.
Clinical Findings. Clinical signs are variable depending
on the degree of spinal cord and cauda equina malformation
and include paraparesis, paraplegia, megacolon, atonic bladder, absent anal and urinary bladder sphincter tone, absent
anal reflex, urinary and fecal incontinence, and perineal
analgesia. Affected cats often walk plantigrade in the pelvic
limbs with a bunny-hopping gait. Vertebral abnormalities
may be palpable in the lumbosacral region, and in some cats
a meningocele, congenital or the result of necrosis of the
overlying skin, may exit through the skin and drain CSF.
Clinical signs usually are evident soon after birth and
may remain static or may be progressive. Worsening of neurologic deficits may be due to progressive syringomyelia in

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the lumbar and sacral spinal cord.


Diagnosis. Diagnosis is made on the basis of clinical
findings and radiographic findings indicative of dysgenesis
or agenesis of the sacral and caudal vertebrae. Myelography
may demonstrate meningocele or attachment of spinal cord
to subcutaneous tissues in the lumbosacral region. The degree of spinal deformity does not always correspond with the
degree of neurologic impairment. Clinical findings are the
most important factors to consider in determining prognosis.
Treatment. Prognosis for severely affected cats is hopeless and treatment is not available. Cats with urinary and fecal incontinence may be managed with manual bladder expression and fecal softening agents; however, recurrent urinary tract infection, megacolon, and chronic constipation are
common problems. Meningocele in cats with minimal neurologic deficits may be surgically correctable. Many tailless
cats do not have neurologic deficits, and sacral and caudal
deformities often are an incidental radiographic finding.

Spina bifida
Etiology and Pathgogenesis. Spina bifida is a term used
to describe a group of developmental defects characterized
by failure of fusion of the vertebral arches with or without
protrusion or dysplasia of the spinal cord, meninges, or
both. It has been described in cats. Malformations have
been variously named spine bifida occulta, cystica, manifesta and operta, depending on whether vertebral arch only,
vertebral arch and spinal cord, and/or meningeal abnormalities are present.
Anomalies of the vertebral arch and spinal cord are influenced by the development of the neural tube. Normally an
area of embryonic ectoderm thickens along the dorsal midline to form the neural plate. The neural plate subsequently
folds (forming the neural groove and then the neural tube
that separates from the ectoderm and develops into the
spinal cord) and is surrounded by the sclerotomic masses
that form the vertebrae.
Spina bifida is a midline cleft in one or more vertebral
arches. The cleft may consist of only nonfusion of the dorsal
spinous processes, or most of the vertebral arch of one or
several adjacent vertebrae may be absent. The spinal cord
and meninges may be normal (spine bifida occulta) or may
be abnormal and there may be protrusion of the meninges
and/or spinal cord through the vertebral defect. Spina bifida
may be caused by nonfusion of the two halves of the primordial vertebral arch due to failure of the neural tube to
close as the result of overgrowth of the cells of the neural
tube, or may be due to cleft formation in the neural tube after closure. It has been suggested that after formation of the
neural tube, clefts split its dorsal wall and a neuroschistic
bleb encroaches on the somites and prevents fusion of the
vertebral arches. If the neuroschistic bleb is retained, defects
of the spinal cord occur. Healing of the bleb may also occur
and result in spine bifida occulta (vertebral arch defect without concomitant spinal cord abnormalities).
Myelodysplasia consisting of hydromyelia, syringomyelia, anomalies of the dorsal septum, anomalies of
the central gray matter, abnormal position of the central gray

4th European FECAVA SCIVAC Congress

matter, anomalies of the dorsal and ventral horns, and


myeloschisis (cleft in the dorsal part of the spinal cord) may
occur in association with spine bifida. The most severe defects involve myelorachischisis, with superficial location of
the neuroectoderm that is continuous with the skin. Myelorachischisis may be due to failure of the formation of the
neural tube or rupture of the neuroschistic bleb after neural
tube closure. Spina bifida with myelorachischisis has been
reported to occur in dogs and cats.
Etiology of spine bifida is unknown and probably multifactorial with genetic and environmental components. Nutritional factors may have a role in the neural tube defects.
Spina bifida can be induced in the offspring of laboratory
animals by exposing pregnant females to a variety of chemical or environmental toxins.
Clinical Findings. Spina bifida is usually an incidental
radiographic finding; however, if associated with spinal cord
malformations, it may result in clinical signs of spinal cord
or cauda equina dysfunction. Large dorsal arch defects are
most often associated with spinal cord abnormalities. There
is a high incidence of spine bifida in English bulldogs. Spina
bifida may occur anywhere in the spinal column but occurs
most commonly in the caudal lumbar spine where clinical
signs are indicative of a transverse myelopathy from L4 to
S3 spinal cord segments (pelvic limb ataxia or paresis, complete paraplegia, fecal and urinary incontinence, decreased
or absent anal and urinary bladder sphincter tone, perineal
analgesia, and decreased spinal reflexes in the pelvic limbs).
Clinical signs usually become evident when affected animals start to walk.
Spina bifida also has been reported in the thoracic spine
of a dog and may be associated with other spinal deformities
such as scoliosis. Other associated anomalies include dimpling of the skin or streaming (abnormal direction) of the
haircoat over the affected region or a palpable abnormality
in the spinal column. Meningoceles may cause necrosis of
the overlying skin and drainage of CSF. Meningoceles may
be present in the absence of clinical signs associated with
spinal cord malformation.
Diagnosis. Absence of the vertebral arch or failure of fusion of the dorsal spinous processes in one or more vertebrae
may be evident on plain radiographs. Myelography may
demonstrate meningocele.
Treatment. Treatment is not effective for affected animals with clinical signs of spinal cord malformation.
Meningocele may be amenable to surgery if neurologic abnormalities are not evident. Treatment is not necessary for
animals with vertebral defects in the absence of spinal cord
dysfunction (spine bifida occulta).

Spinal cord trauma


Etiology and Pathogenesis. Acute spinal cord injuries of
dogs or cats result most commonly from direct physical trauma such as missile injury or vertebral fracture or luxation.
Also, spinal cord trauma is the underlying cause of neurologic signs in numerous myelopathies (e.g., intervertebral
disk protrusion or extrusion). Chronic spinal cord compression usually is seen in association with chronic progressive

diseases such as neoplasia or type II disk protrusion.


Following injury, the spinal cord may undergo sustained
compression, distraction, or both. The severity of a spinal
cord injury, as determined by the eventual degree and quality of recovery, is related to three factors: the velocity with
which the compressive force is applied, the degree of compression (transverse deformation), and the duration of the
compression. The relative roles of these factors in determining the severity of a spinal cord injury have yet to be determined.
An understanding of differences between acute and
chronic spinal cord injury is essential for effective management and determination of prognosis in cats or dogs with
spinal trauma. Extensive experimental work has been done
in order to elucidate the mechanisms involved in the production of lesions following spinal cord trauma, and results
of such research provide information that is essential for effective therapy of spinal injuries.
Acute Spinal Cord Injury. It has long been recognized
that blunt traumatic injury to the spinal cord causes neurologic deficits through both direct and indirect mechanisms.
The direct effects are due to immediate disruption of neural
pathways in spinal gray or white matter produced by the
trauma. These effects have also been termed immediate
effects and have been considered by most investigators not
to be amenable to therapy. Indirect effects develop during
the first few hours following injury, and result in delayed
secondary injury to the spinal cord. The mechanisms of this
secondary process remain largely undetermined, however, it
is likely that they result in part from release of endogenous
pathophysiologic factors in response to the initial trauma. It
has been hypothesized that such factors produce injury by
reducing spinal cord blood flow or by altering the local
metabolic environment within injured spinal cord tissue.
The secondary damage has been considered potentially reversible through the use of either physical (e.g., hypothermia) or pharmacologic interventions.
Trauma to the spinal cord triggers a progressive series of
autodestructive events that lead to varying degrees of tissue
necrosis, depending on the severity of the injury. Pathologic
changes that occur in traumatized spinal cord tissue include
petechial hemorrhages that progress to hemorrhagic necrosis, lipid peroxidation, lipid hydroxylation with subsequent
prostaglandin and leukotriene (eicosanoid) formation, loss
of calcium ions from the extracellular space and loss of
potassium ions from the intracellular space, ischemia with
consequent decline in tissue oxygen tension and energy
metabolites and development of lactic acidosis, and inflammation and neuronophagia by PMN leukocytes.
In spite of extensive investigation, the mechanisms responsible for the initiation and propagation of these pathophysiologic and biochemical events remain undetected. Recent evidence suggests, however, that the overall initiator of
this autodestructive cascade of events is mechanical deformation of any type (i.e., impact or compression injury), and
that the primary sites of injury are the cellular and subcellular membranes of glia, neurons, and vascular endothelial
cells. Lipid peroxidation and activation of membrane lipases, with release of fatty acids leading to production of
eicosanoids, are the earliest mechanically stimulated bio-

73

chemical events described at the present time.


The sequence of pathologic alterations that occurs following spinal cord injury has been reviewed by several authors.
Within 5 minutes of injury postcapillary venules become congested. This is followed by opening of endothelial gap junctions here and at the capillary level, resulting in diapedesis of
red blood cells and extravasation of fluid proteins and electrolytes through the leaky vasculature. Within 30 minutes
of injury, microscopic hemorrhages appear in the central gray
matter, and coalesce over the following several hours (central
hemorrhagic necrosis). Vacuolization develops within endothelial cells, indicating a profound ischemic or hypoxic insult, which subsequently leads to coagulative necrosis of the
neuronal population. Adjacent white matter is relatively less
severely affected; however, periaxonal swelling and retraction balls may be observed. These events may lead to autodissolution of the spinal cord within 24 hours, even in the
absence of ongoing mechanical compression.
A special feature of spinal cord injury is progressive hemorrhagic myelomalacia. This condition occurs following
spinal cord trauma and appears to be a progression of central
hemorrhagic necrosis and edema to areas of the spinal cord
not directly involved in the initiating injury.
Chronic Spinal Cord Compression. It has been shown
experimentally that when slow compression of the spinal
cord is compared to dynamic (or rapid) compression of an
equal amount, the extent of spinal cord dysfunction is determined by the contact velocity of compression. The major
pathologic substrate for neural dysfunction after slow balloon compression is thought to be physical injury to the
neural membranes, irrespective of blood flow changes, and
the ability of that membrane to recover appears to be related
to rapidity and duration of compression. Clinical observations support the conclusion that spinal cord conduction is
resistant to slow compression. Further, it has been demonstrated that levels of compression that do not have an effect
when applied slowly cause an immediate loss of conduction
through the injured site when applied rapidly.
Chronic spinal cord compression results either from a
slowly developing lesion (e.g., neoplasia), or from an acute
compression that is sustained. In contrast to acute spinal
cord injury, chronic compression affects white matter more
severely than it affects gray matter. Hemorrhage and edema,
the major findings of acute trauma, are not significant in
chronic compression. Characteristic lesions are degeneration
of myelin, focal areas of malacia, vacuolization, and loss of
white matter axons. Mechanical deformation is likely to be
the major factor in pathogenesis of these lesions; however,
ischemia and venous obstruction also may be important considerations.
Clinical Findings. Acute Spinal Cord Injury. Dogs or
cats with a spinal injury frequently have serious injuries to
other organ systems. A primary concern is to balance the relative urgency of non-neurologic injuries (hemorrhage,
shock, airway obstruction, or limb fractures) and the need
for early treatment of spinal cord injury.
A complete neurologic examination is done to localize
the site(s) of injury and to determine severity. Careful palpation of the vertebral column may aid in identification of a
vertebral fracture or luxation. Administration of tranquiliz-

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ers or analgesic drugs should be delayed until completion of


the neurologic examination, as such medications may alter
an animals responses. A neurologic examination should be
done with care to prevent further injury resulting from excessive movement of a vertebral instability.
Several aspects of the neurologic examination are of special importance in assessment of a dog or cat with a spinal
cord injury. Recognition of the Schiff-Sherrington sign is
important. Following trauma, this sign must be differentiated from other postures associated with cranial injury (e.g.
decerebrate rigidity or decerebellate posture). Both deep and
cutaneous pain perception should be assessed, as results of
these tests are important in determining prognosis. It should
be remembered that vertebral column injuries may be multiple, and that a neurologic examination may not indicate
presence of a second lesion.
Chronic Spinal Cord Compression. Clinical signs of
chronic spinal cord compression may progress over weeks
or months, or may be seen to occur acutely. Acute onset of
neurologic signs with chronic spinal cord compression frequently is seen in association with such disorders as spinal
neoplasia or type II disk protrusion. Sudden onset of signs
may accompany pathologic fracture of a vertebra, and
spinal cord hemorrhage or infarction. In some cases sudden
decompensation of chronically compressed spinal cord may
occur in the absence of pathologic changes. In these cases it
is assumed that compensatory mechanisms within the spinal
cord are exhausted, and that sudden decompensation has
occurred.
Diagnosis. Acute Spinal Cord Injury. Results of a neurologic examination are used to determine the site and severity of a spinal injury. Radiographs of the entire spinal column should be done. Two radiographic views are essential.
Ventrodorsal views may be accomplished by means of a horizontal beam. Evoked spinal cord potential testing may be of
use in determining location and severity of a spinal cord lesion in animals following trauma.
The objectives of radiographic examination of an animal
following acute spinal trauma are the following: precise determination of location and extent of a lesion, demonstration
of multiple lesions that may not be apparent on the basis of
a neurologic examination, and assessment of the need for
surgical therapy and determination of the most appropriate
surgical procedure to be used. Accurate interpretation of radiographs depends on a knowledge of results of a neurologic examination.
We recommend that a myelogram be completed in animals that have sustained spinal trauma. Results of a myelogram may determine the extent of spinal cord swelling resulting from concussion in animals without evidence of a
spinal fracture or luxation, and may confirm that surgical decompression by means of laminectomy is not necessary in
animals with a fracture that is evident on plain radiographs.
In the diagnosis of intervertebral disk disease a myelogram
is considered essential prior to surgery.
Chronic Spinal Cord Compression. Methods for diagnosis of chronic spinal cord compression are the same as for
acute spinal cord injury. A myelogram is considered essential in all such cases.
Treatment. Management of an animal with spinal trauma

4th European FECAVA SCIVAC Congress

follows a list of priorities, with the focus of treatment being


prevention of secondary spinal cord damage that occurs after the initial injury. Immediate treatment of nonneural injuries is limited to those problems that are life-threatening,
such as shock or hemorrhage.
Acute Spinal Cord Injury. Treatment of acute spinal
cord trauma should always be instituted as soon as possible
following injury. The specific objectives of therapy are the
following: relief of edema, control of intra- or extramedullary hemorrhage, relief of spinal cord compression,
and, in cases of vertebral fracture/luxation, removal of bone
fragments from the spinal canal and stabilization of the vertebral column. Treatment of acute spinal cord trauma may be
medical, surgical, or a combination of both.
Based on experimental findings in a large number of experimental models in animals, a variety of medical treatments have been advocated for the treatment of acute spinal
cord injury. Recently, interest has focused on the use of antioxidants and free radical scavengers. Unfortunately, the
role of these numerous therapies in the management of a dog
or cat with a spinal injury remains to be determined. The
large number of suggested therapies underlines the fact that
the mechanisms responsible for delayed secondary effects in
the injured spinal cord are incompletely understood.
Corticosteroids are routinely and widely used in the
treatment of acute spinal cord injury. Despite a positive clinical impression that corticosteroids have beneficial effects,
their use is controversial. Some studies have failed to
demonstrate significant improvement of neurologic recovery in association with corticosteroid administration. The
use of low or high doses of corticosteroids in the treatment
of spinal trauma also has yielded conflicting results.
Use of high doses of corticosteroids may result in complications leading to increased morbidity and mortality (e.g.,
gastrointestinal bleeding, pancreatitis, colonic perforation);
therefore, low-dose regimens are recommended. Dexamethasone sodium phosphate should be given at an initial
dosage of 0.25 to I mg/lb IV, and may be repeated at a dose
of 0.1 mg/lb q6h or q8h. Immediate post-trauma administration of methylprednisolone sodium succinate (60 mg/lb divided q8h) has been demonstrated to be effective in preserving feline spinal cord tissue following injury.
A decision regarding surgical therapy must be made as
soon as non-neural injuries have been treated and medical
management has been instituted. Ideally, this is within 2
hours of injury. Indications for surgery following spinal cord
injury are the following: moderate to severe paresis, or
paralysis, associated with myelographic evidence of spinal
cord compression; progressive worsening of neurologic
signs despite adequate medical therapy; and luxation or fracture of the vertebral column, in association with distraction,
malalignment, instability, or myelographic evidence of
spinal cord compression. Any animal with sustained compression of the spinal cord following injury, regardless of the
cause, must be considered a candidate for surgical decompression of the spinal cord. In general, it is best to initiate
surgical therapy in any animal in which there is uncertainty
regarding the indications for surgical versus medical therapy. Neurosurgical procedures require specialized knowledge
and equipment, and prompt referral to a qualified surgeon

may be indicated.
The major objectives of surgical management of spinal
trauma are decompression of sustained spinal cord compression and realignment and stabilization of vertebrae if necessary. Surgical decompression by means of laminectomy is
beneficial when there is myelographic evidence of extradural spinal cord compression. Laminectomy alone is not sufficient for decompression in most cases, and the compressing
mass (e.g., disk material, hematoma, bone fragments) should
be removed when possible. In cases in which spinal cord
swelling is the major source of compression, or in which
there is discoloration of the spinal cord, durotomy or myelotomy may be combined with laminectomy.
The most effective methods for alignment and stabilization of the vertebral column require surgical exposure and
can therefore be done at the time of decompression. Satisfactory methods of external fixation of spinal fractures do
not exist. Methods of surgical fixation have been reviewed
by several authors. Use of polymethyl methacrylate and
Steinmann pin fixation for the majority of spinal fractures or
luxations is favored by these authors. Surgical management
of spinal cord injury of animals provides the best opportunity for rapid and complete recovery in animals with sustained
compression or instability, and facilitates postinjury care, as
the risk of further injury resulting from movement of an unstable vertebral column is minimized. However, conservative management, including strict confinement for 4 to 6
weeks, may be efficacious in animals with minimal neurologic deficits and without myelographic evidence of sustained spinal cord compression or vertebral displacement or
instability.
Regardless of the type of stabilization used, strict confinement is recommended for 2 weeks after surgery. Potential complications encountered in dogs or cats with a spinal
injury include development of a urinary tract infection or
pressure sores. Careful attention to nursing care is essential
regardless of the type of therapy.
Prognosis for an animal with an acute spinal cord injury
depends on numerous factors; however, results of a neurologic examination should be the main determinant. Assessment of pain perception is essential for accurate prognosis.
Perception of a painful stimulus must be differentiated from
reflex activity that is mediated at the level of the spinal cord.
Owners of affected animals should be made aware at the
outset of therapy of factors such as prognosis, expense involved, expected time from treatment to recovery, and the
need for prolonged physical therapy in most cases. Following a severe spinal injury, an animal may require many
months to recover, and residual neurologic deficits may persist.
Chronic Spinal Cord Compression. The approach to
treatment of chronic spinal cord compression is different
from that for acute spinal cord injury. As previously stated,
hemorrhage and edema usually are not prominent factors in
chronic compression. Therefore medical management by
means of corticosteroids would not be expected to be efficacious; however, many animals with chronic spinal cord compression improve clinically following corticosteroid administration. The reason for such a response is undetermined;
however, it may be due to effects of corticosteroids at the

75

membrane level resulting in improved conduction in remaining axons. Occasionally, animals may be maintained
for months or years by means of corticosteroid therapy
alone.
Surgical decompression of the spinal cord should be approached with caution in animals with chronic spinal cord
compression. Pathologic alterations within the spinal cord
may be irreversible, in which case the most that may be
achieved is to arrest progression of neurologic deficits. In
some cases compensation for the irreplaceable loss of neural tissue may occur. Neurologic status may be worsened by
surgical decompression, even with meticulous surgical technique. Such deterioration may be the result of reactive hyperemia that follows decompression, which in turn results in
vascular protein leakage in the affected spinal cord segment.
However, surgical decompression should be considered in
most animals that have neurologic deficits associated with
chronic spinal cord compression.

Syryngomyelia and hydromyelia


Etiology and Pathogenesis. A distinction cannot be
made clinically between syringomyelia (cavitation of the
spinal cord) and hydromyelia (dilation of the central
canal). Syringomyelia may occur secondary to hydromyelia (communicating syringomyelia) or may not
communicate with the central canal (noncommunicating
syringomyelia). Syringomyelia may be associated with
spinal cord tumors, myelitis, meningitis, and spinal cord
trauma. The cause of syringomyelia is not known, but the
condition may result from venous obstruction or distention,
or may be due to mechanical disruption or shearing of
spinal cord tissue planes.
Hydromyelia with or without syringomyelia may be associated with congenital malformations such as myelodysplasia; meningomyelocele or hydrocephalus; or lesions resulting in obstruction of CSF flow into the spinal subarachnoid space at the foremen magnum such as chronic arachnoiditis, trauma, congenital malformations, and vascular
malformations; or it may be idiopathic. Hydromyelia and syringomyelia in these animals probably results from intracranial and spinal cord venous or arterial pressure changes and
associated CSF pressure changes.
Syringomyelia in Weimaraner dogs with myelodysplasia may be the result of progressive hydromyelia, abnormalities in the central canal, or abnormal vascular patterns
in local areas of the spinal cord leading to low-grade ischemia, degeneration, rarefaction, and cavitation in the
spinal cord.
Regardless of the cause, cavitation can be progressive,
probably along planes of structural weakness such as the
gray matter of the dorsal horns, and subsequent necrosis and
edema of spinal cord parenchyma around such a cavitation
(or dilated central canal) can result in the onset and progression of clinical signs.
Clinical Findings. Clinical signs depend on the location
of the lesion and whether or not other spinal cord lesions are
present. Clinical findings include progressive spinal deformity (scoliosis, torticollis), LMN or UMN signs, depending

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on location, and apparent spinal pain. Clinical signs may be


acute or may be progressive over weeks to several years. In
Weimaraner dogs with myelodysplasia, clinical signs do not
appear to be progressive.
Diagnosis. Myelography may show obstruction of the
flow of CSF at the foremen magnum if hydromyelia or syringomyelia is due to chronic arachnoiditis or arachnoid adhesions. Cisternal puncture for the collection of CSF is contraindicated in these animals owing to likely inadvertent
puncture of the spinal cord. Lumbar CSF may show evidence
of chronic inflammation. Myelography in other cases may be
normal or may show intramedullary swelling of the spinal
cord. Computed tomography of the spinal cord may be useful in the diagnosis of cavitary lesions of the spinal cord.
Treatment. Treatment in dogs has not been reported. Surgical drainage of cavitary lesions in humans has resulted in
improvement in some cases.

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77

EUROPEAN SOCIETY OF FELINE MEDICINE - ESFM

Feline neuromuscular disorders


Richard A. LeCouteur
VMD, BVSc, PhD, Dipl ACVIM (Neurology), Dipl ECVN
Professor of Neurology and Neurosurgery
Department of Surgical & Radiological Sciences - School of Veterinary Medicine
University of California, Davis, California - USA

Summary
Neuromuscular diseases are generally classified according to the disease location, that is disease involving 1) peripheral nerves, 2) neuromuscular junctions, or 3) muscle.
Feline neuromuscular diseases produce signs of lower motor neuron disease, however significant variation in clinical
signs may occur depending on the location of the lesion. Hyporeflexia, hypotonia, ataxia, and proprioceptive positioning deficits are most characteristic of feline peripheral nerve
disease. Some primary muscle diseases may be characterized by muscle hypertrophy rather than atrophy, and neuromuscular junction disorders result in a variety of clinical
signs, that range from flaccid paralysis to exercise-induced
weakness. Diagnosis of feline neuromuscular diseases requires a complete neurological examination, minimum data
base, electrophysiological evaluation, and muscle/nerve
biopsies.

INTRODUCTION
Feline neuromuscular diseases may be classified according to their location as (1) those involving peripheral nerves
and/or nerve roots, (2) those involving the neuromuscular
junction, and (3) those that involve muscle. Each of these
neuromuscular diseases will produce lower motor neuron
(LMN) disease, however significant variation in clinical
signs may occur. Peripheral nerve and muscle diseases result
in varying degrees of paresis, muscle atrophy, hyporeflexia,
and hypotonia. Hyporeflexia, hypotonia, ataxia and proprioceptive positioning deficits are most characteristic of peripheral nerve disease. Some primary muscle disorders may
be characterised by muscle hypertrophy rather than atrophy.
Neuromuscular junction disorders (junctionopathies) result in a variety of clinical signs, that range from flaccid
paralysis to exercise-induced weakness.
Cervical ventroflexion is a dramatic sign of generalised
neuromuscular weakness in cats.The chin usually rests near
the thoracic inlet, with the eyes positioned dorsally to maintain a straight-ahead gaze. Other common physical examination findings are a slight protrusion of the dorsal aspects
of the scapulae when weight is placed on thoracic limbs, and
a stiff thoracic limb gait. A crouched, wide-based stance is
often seen in pelvic limbs. Possible causes to consider for
this posture are: subacute or chronic organophosphate toxic-

ity, potassium-depletion myopathy, thiamine-responsive


neuromuscular weakness, hyperthyroidism, immune-mediated (idiopathic) polymyositis, myasthenia gravis, polyneuropathy, hypernatraemic polymyopathy, ammonium chloride toxicity, hereditary myopathies (Burmese, Devon rex),
hypocalcaemia, and portosystemic encephalopathy.
Megaoesophagus has rarely been reported in cats, although a predisposition has been noted in Siamese and
Siamese-related breeds. In most cats the cause of acquired
megaoesophagus is unknown; however, the condition has
been associated with several systemic neuromuscular disorders, such as myasthenia gravis, botulism, polymyositis,
polyradiculoneuritis, tick paralysis, lead toxicosis, feline
muscular
dystrophy-like
conditions,
laryngeal
paralysis/polyneuropathy complex, and glycogen storage
diseases.
Diagnosis of feline neuromuscular diseases requires a
complete neurological examination, minimum data base
(full blood count, serum biochemistry panel, urinalysis, thoracic radiographs), electrophysiological evaluation, and
muscle/nerve biopsies.

NEURONOPATHIES
Feline Dysautonomia
Feline dysautonomia (Key-Gaskell syndrome) is a generalised disorder of autonomic ganglia recognised in cats in
the United Kingdom in 1981, and more recently in other
countries. There is no age or breed predilection for this disease. The disorder is a neuronal disorder; however, clinical
signs relate more to autonomic dysfunction, and are largely
gastrointestinal in nature. The most common signs are depression, anorexia, constipation, dry external nares and oral
mucosa, reduced tear production, regurgitation, protrusion
of the membrana nictitans, mydriasis, and bradycardia.
These signs usually occur acutely, but may progress insidiously over a week or more.

Tetanus
Although cats are supposedly resistant to the effects of
the Clostridium tetani exotoxin, several cases of tetanus have
been reported in this species. The toxin interferes with re-

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lease of neurotransmitters from inhibitory interneurons in the


spinal cord. Local tetanus has been reported in cats, where
the disease is characterised by tonic rigidity of a single limb.

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first noted in cats at 8-10 weeks of age. Affected cats fell frequently and had a tendency to stand and walk on their hocks,
which they held in an adducted position. The gait was characterised by a slight hypermetria in all limbs and there was
progressive pelvic limb ataxia.

INHERITED POLYNEUROPATHIES
Sphingomyelinase-deficiency polyneuropathy

ACQUIRED POLYNEUROPATHIES

Niemann-Pick disease (NPD) is an autosomal-recessive


lysosomal-storage disease characterised by a deficiency of
sphingomyelinase. A NPD-associated primary polyneuropathy has been described in 3 Siamese cats (25 months of
age). Neurological signs included a progressive tetraparesis
and ataxia, a plantigrade/palmigrade stance, fine generalised tremors, and hypo- or areflexia. Hepatosplenomegaly
was also present in affected cats. This disease is progressive
and fatal.

Diabetic polyneuropathy
A distal polyneuropathy has been reported in cats with uncontrolled or poorly controlled diabetes mellitus. Neurological abnormalities include a plantigrade stance, progressive
paraparesis, muscle atrophy, and patellar hyporeflexia. The
cause of this polyneuropathy is incompletely understood.

Ischemic neuromyopathy
Hyperchylomicronemia-associated
neuropathy
Inherited primary hyperchylomicronemia is a suspected
autosomal-recessive disease characterised by fasting hyperlipemia, lipemia retinalis, and peripheral neuropathy. Clinical signs are usually not seen prior to 8 months of age. Compression by lipid granulomas of peripheral, cranial, and sympathetic nerves, especially at the level of the intervertebral
foramina, results in neurological signs. Resolution of neurological signs and decrease in blood-lipid levels occurs following 2-3 months of dietary management.

Hyperoxaluric peripheral neuropathy


Primary hyperoxaluria is a suspected autosomal-recessive disease of domestic short-hair cats in Great Britain.
Acute renal failure, in cats between 5 and 9 months of age,
results from renal tubular deposition of oxalate crystals. Severe generalised LMN weakness accompanies the renal failure. Weakness is attributed to accumulation of neurofilaments in ventral nerve roots, proximal axons, and intramuscular nerves. All reported cats died before 12 months of age.
The pathogenesis of peripheral nerve lesions is unknown.

Hypertrophic polyneuropathy
Hypertrophic polyneuropathy has been described in 2
unrelated 12-month-old cats. Affected cats had intention
tremors, decreased postural reactions, hyporeflexia, and
mild sensory loss.

Birman cat distal polyneuropathy


A degenerative polyneuropathy has been reported in several litters of Birman cats bred from the same parents. A recessive mode of inheritance is suspected. Clinical signs were

Ischemic neuromyopathy occurs in cats with cardiomyopathy, subsequent to thrombosis of the caudal aorta or its
principal branches. The ischemic injury to both muscle and
peripheral nerve is produced by collateralcirculation vasoconstriction induced by substances such as serotonin and
thromboxane A2 released by platelets trapped in the
thrombus.

Trauma
Brachial plexus avulsion produced by severe thoracic
limb abduction with secondary stretching or tearing of nerve
roots is a commonly occurring peripheral nerve injury of
cats. Sacroiliac fracture/dislocation, sacral fracture, or caudal vertebral fracture/luxation may result in damage to the
sixth and seventh lumbar and first 2 sacral nerve roots.
Mononeuropathies of radial nerve and sciatic nerve occur in
cats following mechanical blows, gunshot wounds, fractures, pressure and stretching.

Neoplasia
Feline malignant lymphoma, often associated with
FeLV-infection, may involve nerve roots or peripheral
nerves. Other primary peripheral nerve neoplasms are rarely
seen in cats.

Toxic neuropathies
Drug-induced neuropathies are not well defined in dogs
and cats. It is likely that as chemotherapeutic treatment of
neoplasia becomes more aggressive, more drug-induced neuropathies will be recognised (e.g. vincristine). A delayed neurotoxicity may occur in cats days or weeks after minimal exposure to organophosphates. Lesions are associated with distal degeneration of motor nerves that begins in the periphery
(dying-back axonopathy). Peripheral neuropathy may occur

sporadically with spontaneous lead-poisoning. Megaesophagus and partial laryngeal paralysis, believed to be due to leadassociated neuropathy, have been reported in a cat.

79

The association of acquired myasthenia gravis and thymoma


in cats is a good example of a paraneoplastic junctionopathy.

INHERITED MYOPATHIES
Laryngeal paralysis
Muscular dystrophy
Acute laryngeal paralysis was diagnosed in 3 cats with
signs of upper airway obstruction, including dysphonia, absence of purring, and progressive inspiratory dyspnea. Varying degrees of paralysis of vocal folds and arytenoid cartilages were noted. One cat was positive for FeLV. Underlying responsible mechanisms were not defined.

Miscellaneous peripheral polyneuropathies


Single case reports exist of a variety of peripheral neuropathies in cats. These include: 2 cats with histologicallyconfirmed inflammatory polyneuropathy (a chronic relapsing polyradiculoneuritis) and an acute polyneuritis, an idiopathic chronic relapsing polyneuropathy responsive to immunosuppressive glucocorticoid therapy and an acute
brachial plexus neuropathy with a suspected relationship to
a previous vaccination. It is reasonable to expect that there
will be future reports regarding FeLV and FIV infections and
their association with neuromuscular diseases of cats, particularly polyneuropathies. Paraneoplastic neuropathies and
radiation-induced neuropathies of cats are likely to be reported in the future.

JUNCTIONOPATHIES
Myasthenia gravis
Myasthenia gravis is a condition that results from either
a congenital or an acquired reduction of acetylcholine receptors of neuromuscular junctions. Both forms have been
reported to occur in cats. Two of the acquired cases were associated with thymoma, and another with a cystic thymus.
Acquired myasthenia gravis has been reported frequently in
Abyssinians and Somalis (closely related to Abyssinians),
which may suggest a possible association with the major histocompatibility complex, as in humans. The most consistent
signs in cats include tremors, initial stiffness with progression to generalised weakness on exercise, cervical ventroflexion, dysphagia, dysphonia, ptyalism, facial weakness,
and dyspnea. Overt megaesophagus or esophageal hypomotility is common.

Miscellaneous Junctionopathies
Abnormalities in neuromuscular junction function may
also result from tick paralysis, administration of certain
drugs, selected toxins, or from envenomation. Botulism has
not been reported as a clinical entity in cats, however, it may
be produced experimentally in cats. Paraneoplastic junctionopathies are likely to be reported in cats in the future.

Muscular dystrophy-like disorders of cats have been reported in the Netherlands and the U.S.A. To date all affected cats have been males, which suggests an X-linked inheritance. Clinical signs may first be seen in cats at 5-6 months
of age, and include generalised skeletal muscle hypertrophy,
excessive salivation, reduced exercise tolerance, stiff gait
and bunny-hopping when running, difficulty in jumping,
adducted hocks, cervical rigidity, vomiting/regurgitation,
and partial protrusion of the tongue.

Hereditary myopathy of devon rex cats


This is a congenital myopathy of Devon rex cats. Characteristic clinical signs, including ventroflexion of the head
and neck, protrusion of the scapulae, and esophageal weakness, all reflect dysfunction of striated muscle, while skeletal muscle pathology is suggestive of a muscular dystrophy.

Nemaline myopathy
A suspected inherited myopathy has been described in 5
related cats between 6-18 months of age, with an onset of reluctance to walk and a forced, rapid, abrupt, hypermetric
gait. Other signs included muscle tremors, hyporeflexia, and
muscle atrophy which was more pronounced in proximal
limb musculature. This myopathy is characterised by large
but variable numbers of nemaline rods within myofibres.

Myositis ossificans
Generalised ossifying myositis, a non-neoplastic form of
heterotopic ossification affecting skeletal muscle and fibrous
connective tissue, has been described in 2 young cats with a
history of progressive weakness, stiffness, difficulty in
jumping, decreased range of limb motion, and pain on
forced movement.

Miscellaneous inherited myopathies


Glycogen storage diseases (or glycogenoses) are rare
disorders of cats. Deficient activity of one of the enzymes involved in glycogen degradation or synthesis results in inadequate glycogen utilisation, and in glycogen accumulation
within various tissues, including muscle. There are several
reports of glycogenoses in cats. Glycogen storage disease
Type IV has been reported in 3 young related Norwegian
forest cats.

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ACQUIRED MYOPATHIES

Potassium-depletion polymyopathy

Infectious polymyositis

This acute feline polymyopathy, resulting from a severe


total body potassium depletion, is usually secondary to a reduced potassium intake and increases in the fractional excretion of potassium in urine (due to renal dysfunction).
Clinical signs include muscle weakness, cervical ventroflexion, stiff and stilted gait, and muscle pain. A similar syndrome with a suspected hereditary basis has been reported to
occur in Burmese cats.

Infectious myositis may occur in association with bacterial infection, migrating parasites, or protozoan disease.
Whilst cats are the only definitive hosts for Toxoplasma
gondii (and a majority of cats may have serum antibodies to
this organism) muscle involvement is not an outstanding
feature of Toxoplasma infection of cats.
Experimental inoculation of cats with the protozoan
Neospora caninum may produce fatal, necrotising encephalomyelitis, polymyositis, pneumonia and hepatitis.
Naturally-occurring feline neosporosis has not been reported to date.

Immune-mediated (or Idiopathic)


polymyositis
Polymyositis occurs sporadically in cats, occasionally in
association with thymoma. Inflammatory infiltrates are predominantly mononuclear with small lymphocytes and
macrophages. Neutrophils are seen infrequently. Eosinophils
are rarely seen.
Clinical signs are characterised by a persistent cervical
ventroflexion, appendicular weakness, painful muscles, and
exercise intolerance.
Serum levels of creatine kinase and aldolase are elevated.
A report of polymyositis in a cat in association with myasthenia gravis and thymoma further supports an immune-mediated aetiology.

Miscellaneous myopathies
There are a number of case reports of muscle-related diseases of cats. Descriptions include: nutritional myopathy
secondary to vitamin E deficiency myositis secondary to
Clostridium chauvoei and Clostridium septicum infections
fibrotic myopathy of the semitendinosus muscle and quadriceps contracture secondary to trauma. Episodic weakness
and signs of depression have been noted in young domestic
short-hair cats (less than 1 year of age) with hypernatraemia
secondary to hypodypsia. The most common clinical sign of
hypernatraemic myopathy is ventral flexion of the neck.
Causes of hypodypsia include lesions of the hypothalamus,
and mechanical inability to swallow - a potentially serious
complication of hypertrophic feline muscular dystrophy.
The association between myositis and malignant neoplasia
(paraneoplastic myopathy) is likely to be reported in the future. Myopathies in cats may occur in association with FeLV
or FIV infections (e.g. FeLV-associated immunosuppression
may enable encystment of Sarcocystis spp. in muscle).

81

EUROPEAN SOCIETY OF COMPARATIVE GASTROENTEROLOGY

The pathophysiology of retained bile acids


Denny Meyer
DVM, Dipl ACVIM, Dipl ACVP
NeXstar Pharmaceuticals, Boulder, Colorado - USA

Summary
Bile acids of mammals and birds are amphipathic
steroids (hydroxy cholanoic acids) containing monoanionic
side chain and hydroxyl groups in various numbers and positions resulting in a variety of individual bile acids in different species. They are planar molecules with hydrophilic
groups on one side and the hydrophobic steroidal part of the
molecule projecting on the opposite. This arrangement facilitates micellar formation and permits them to act as biological detergents for the solubilization of lipids in bile and
aid in the digestion and absorption of fats in the intestine;
physiologically good news. These same physiochemical
properties also enable bile acids to solubilize biological
membranes when left in prolonged contact resulting in cytotoxicity; pathologically bad news.

Cytotoxicity of retained bile acids


Prolonged retention of bile has been shown to be associated with a variety of deleterious subcellular events within
the hepatocyte (damage to mitochondria, endoplasmic reticulum, Golgi apparatus) which exacerbate intrahepatic injury.
Recently, this ultrastructural toxicity has been attributed to
selected bile acids. The more hydrophobic ones, defined by
their HPLC migration, have the greatest potential to cause
injury. The dihydroxy bile acids, chenodeoxycholic acid and
deoxycholic acid can attain high serum and intrahepatic concentration secondary to cholestasis. In vivo and in vitro studies have shown that these bile acids can cause hepatocelluar
dysfunction and necrosis at concentrations attained in prolonged cholestasis. Hepatocytes are at greatest risk of bile
acid-induced injury due to their function of concentrating
the bile acids prior to secretion through the canalicular membrane. By analogy, the liver can be considered to treat bile
acids as sticks of dynamite with burning fuses of varied
length. There is no harm if they are efficiently eliminated.
However, the longer they are retained within hepatic tissue
the greater the risk of injury.
One bile acid, ursodeoxycholic acid, has been shown not
only to be devoid of cytotoxicity but actually protected hepatocytes from the toxic effects of the other bile acids. It is
being used in numerous clinical studies for the management
of chronic liver disease in human beings. There are a variety
of proposed mechanisms its beneficial effects. The contem-

porary areas of investigation are: (1) hypercholeresis, (2) direct cellular protection against the more hydrophobic bile
acids or their displacement from the enterohepatic circulation, (3) antioxidant effect, and (4) immunomodulation. As
mentioned previously, bile acids provide the predominant
driving force for bile flow (choleresis). Unconjugated ursodeoxycholic acid has been shown to actually cause hypercholeresis, amplified bile flow compared to the physiologic
effects of other bile acids. This is thought to be related to its
ability to enhance biliary [HCO3] and excretion via a hypothetical mechanism referred to as cholehepatic recycling.
The displacement of cytotoxic bile acids from the enterohepatic circulation would theoretically decrease the prolonged exposure of hepatocytes to their high concentrations.
The high concentration of orally administered ursodeoxycholic acid has been shown to effectively compete with chenodeoxycholic acid and deoxycholic acid for ileal absorption,
thereby displacing them from the enterohepatic circulation.
In the canine patient treated with ursodeoxycholic acid, serial determinations of the serum bile acid profiles with HPLC
demonstrated a remarkable increase in the ursodeoxycholic
acid concentration and a decrease in the chenodeoxycholic
acid and deoxycholic acid concentrations. Ursodeoxycholic
acid may afford direct hepatocellular protection by partitioning into the lipid-rich membrane and excluding the cytotoxic hydrophobic bile acids. In vitro studies with ursodeoxycholic acid in rats have found a moderate to marked
reduction of substances produced as a consequence of oxidative injury suggesting a potent antioxidant effect.
The beneficial effects associated with ursodeoxycholic
acid in certain chronic liver diseases may be related to immunomodulation. Cytokines appear to be involved in the initiation, modulation and/or perpetuation of the immune responses in the liver. Ursodeoxycholic acid has been shown to
reduce the aberrant major histocompatibility complex class I
expression on hepatocytes in human beings with primary biliary cirrhosis and other studies have shown suppression of interleukin-2, interleukin-4 and interferon-g using test systems
which employed mononuclear cells from the peripheral
blood of human beings with primary biliary cirrhosis.
In summary, the determination of the total serum bile
acid concentration provides an index of hepatobiliary function and assesses the integrity of the portal circulation. Beyond their use as a diagnostic test, recent research has
demonstrated that there are good and bad bile acids.
Prolonged retention of certain endogenous bile acids appears

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to amplify intrahepatic pathology while others, notably ursodeoxycholic acid, appear to offer a novel alternative in the
management of chronic liver disease without adverse sideeffects. Ursodeoxycholic acid clearly generates excitement
with its potential multifaceted beneficial modes of action in
the management of the complex pathophysiologic alterations associated with the diseased hepatobiliary microenvironment known as chronic liver disease.

Table 1. The enterohepatic circulation of bile acids


The primary bile acids (cholic acid and chenodeoxycholic acid) are
synthesized and conjugated by the hepatocyte > excreted by the
canalicular membrane into the biliary system > carried to the intestinal tract > participate in the emulsification of lipids for absorption > move to the ileum during which time bacteria dehydroxylate a portion of the primary bile acids forming secondary
bile acids (cholic acid to deoxycholic acid and chenodeoxycholic
acid to lithocholic acid) > reabsorbed into the portal circulation
> carried to the liver and removed by the hepatocyte for recycling. Hepatocellular excretion of bile acids into the biliary system
is the primary driving force for bile flow; termed bile acid-dependent flow.

Supplemental reading
Hoffman AF: Pharmacology of ursodeoxycholic acid, an enterohepatic
drug. Scand J Gastroenterol 1994;29:S1-S15.
Meyer DJ, Thompson MB, Senior DF: Use of ursodeoxycholic acid in a
dog with chronic hepatitis: Effects on serum hepatic tests and endogenous bile acid composition. J Vet Intern Med 1997;11:195-197.

83

SCIVAC EXOTIC ANIMALS STUDY GROUP

Anaesthesia of pet birds


Peter W. Scott
Msc, BVSc, FRCVS
RCVS Specialist in Zoo & Wildlife Medicine and Fish Health & Production
Zoo & Aquatic Veterinary Group, Winchester - United Kingdom

Summary
Anaesthesia of birds with isoflurane has become a safe
and routine procedure in practices whether or not they consider themselves avian practices. It is important to gain an
understanding of the unique anatomy and physiology of the
avian respiratory tract to appreciate the value of particular
circuits, or to contemplate the use of intubation or air sac
tubes. As with any species the aims of anaesthesia should be
to provide a smooth, reliable induction with adequate restraint, muscle relaxation, and analgesia, followed by a fast,
complete and uneventful recovery (Lawton 1996 a&b). This
paper will discuss the options available for the more conventional companion species.

Introduction
Anaesthesia of birds with isoflurane has become a safe
and routine procedure in practices whether or not they consider themselves avian practices. It is important to gain an
understanding of the unique anatomy and physiology of the
avian respiratory tract to appreciate the value of particular
circuits, or to contemplate the use of intubation or air sac
tubes. As with any species the aims of anaesthesia should be
to provide a smooth, reliable induction with adequate restraint, muscle relaxation, and analgesia, followed by a fast,
complete and uneventful recovery (Lawton 1996 a&b). This
paper will concentrate on the more conventional companion
species, Heard (1997a) provides a wider review introducing
the literature covering other species.

Anatomy & physiology


Birds do not have a functional diaphragm, they draw air
into the lungs by a cranio-ventral movement of the ribs to
expand the lungs and air sacs. Because of the importance of
the ribs in this process it is vital not to restrict their movement during handling (or by wrapping tightly for recovery.
The trachea is made up of complete interlocking cartilaginous rings (ossified in some species). Because of this
when using endotracheal tubes, plain tubes are generally
preferred to avoid damaging the trachea.
Most birds have nine air sacs associated with the lungs,
paired cervical, single clavicular, and paired cranial thoracic,

caudal thoracic and abdominals, depending on species some


of these pneumatise bones. Total volume of the respiratory
tract is of the order of 100-200 ml/kg body weight (as compared to 45 ml/kg in the dog), with only approximately 12%
of this being lung. The air sacs are functionally grouped, the
anterior group (cervical, clavicular and anterior thoracic),
and the posterior group (caudal thoracic and abdominal).
The avian lung is fixed in place and does not move appreciably during breathing, air is cycled through the system
of air sacs and lung by active inspiration and expiration. The
lung is divided in the vast majority of birds into paleopulmo
and neopulmo, the relative proportions varying between
species (penguins and emu have no neopulmo). There are no
alveoli, they are replaced with a system of parabronchi, leading to infundibulae and air capillaries. Gaseous exchange primarily occurs in the air capillaries of the paleopulmonic area.
The air flow appears to be unidirectional in the paleopulmo
and bi-directional in the neopulmo. Details of air flow
through the avian lung and air sacs has been the subject of
debate and may vary with activity and between species. The
existence of anatomic valves is in doubt, there do however
seem to be aerodynamic flow controls dependent on the
anatomy. There is a very efficient exchange system operating
in birds, due to a high gas exchange surface-to-volume ratio
and the use of a countercurrent system of opposing air flow
through air capillaries and blood flow. This makes induction
and recovery when using gaseous agents very rapid. James et
al (1976) suggest that avian lungs can be considered 10X
more effective than mammalian lungs. Birds are extremely
sensitive to CO2 levels, to the extent that they will become
apnoeic if the blood becomes depleted of CO2. The CO2 is
carried in blood as plasma HCO2, and in the lungs carbonic
anhydrase in the red cells splits the HCO2, into H+ and CO2.
The CO2 has no direct effect on oxygen/haemoglobin binding
although the released H+ exerts and influence through the
Bohr effect ( a rise in H+ leads to reduction in O2 affinity). A
rise in tissue temperature also decreases the O2 affinity of the
haemoglobin. The net effect of both effects is that active tissue, respiring and producing CO2, warmer than the lungs encourages the release of oxygen from the haemoglobin.
It is suggested that a deeply anaesthetised bird may not
generate sufficient muscular movement to pump air around
this circuit. This may be particularly acute in species with a
large pectoral muscle mass. Sinn (1994) advises the routine
use of gentle positive pressure ventilation (20-40/minute at
15 mmHg) to overcome any potential hypocapnoea and

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maintain adequate oxygenation. Air is drawn in during inspiration and is divided between the paleopulmo and the
caudal air sacs via the neopulmo. Air leaving the paleopulmo enters the anterior air sacs. During expiration the caudal
air sacs empty via the neopulmo into the paleopulmo. Air
leaves the paleopulmo mixing with spent air from the anterior air sacs, this air is expired. Duncker,H.R. (1971).

lection, radiography, fluid administration, endoscopy or


bandaging. The type of assessment used for these short procedures is normally limited to the taking of a history and a
physical examination.
Prior to a prolonged anaesthetic it may be advisable to
consider any or all of the following: PCV, WBC & differential, TP, AST, LDH, UA, bile acids, grams stains of faeces
and choana, platelets, clotting time and bile acids. Other
tests may be indicated in particular cases. Liver dysfunction
is not uncommon, and its presence would make the use of
most injectable agents, plus halothane and methoxyflurane
contraindicated. Patients which are toxic due to egg retention may require stabilisation for a day or two prior to
surgery. Obese pet birds are serious anaesthetic risks and prior to elective procedures a diet is indicated. Suspect Aspergillus cases can be pre-oxygenated before induction.

Fluid therapy
There are good grounds in assuming birds suffering from
trauma or disease are dehydrated, often in the region of 10%,
maintenance requires 50 ml/kg/day ie. 5% body weight.
Lactated ringers i/v or i/osseous are recommended. 5% dextrose is regarded as inappropriate by Phalen et al (1997) who
suggests that it may cause serious electrolyte imbalances.
Sinn (1994) suggests that subcutaneous or oral fluids are not
as effective at restoring circulating volume.

Duncker, H.R. (1971)

Pre-anaesthetic

Fasting

Mammalian-type pre-anaesthetic drugs are not normally


used in birds, atropine is contra-indicated in avian patients
because it thickens respiratory mucus and increases the heart
rate. In general a pre-anaesthetic evaluation is important to
assess whether supportive treatment is indicated prior to embarking on an intervention. Isoflurane anaesthesia is however often used simply as an aid to restraint to minimise the
stress associated with minor procedures such as blood col-

In general terms it is usually advisable to fast the bird


long enough to empty the gastrointestinal tract, in small
birds this may be 3-6 hours and in large birds overnight. Always check the crop before inducing anaesthesia, passive regurgitation may block the larynx. Special care is needed if
the crop contains food, anaesthetise with the patient upright,
block the choana with a swab while the crop is emptied,
clean the area and intubate.

Volatile anaesthetics
BLOOD GAS
PARTITION
COEFF AT 37OC

PHYSIOLOGICAL
ASPECTS

Halothane

2.3

15-20% metabolised

Poor muscle relaxation and analgesia. Causes bradycardia,


sensitises the heart to catecholamines. Respiratory and cardiac
arrest tend to happen together.

Isoflurane

1.4
low solubility makes
induction & recovery
very rapid

0.3% metabolised
MAC (1.5-2%)

Good muscle relaxation and analgesia. Less respiratory and


cardiac depression than halothane, if problems then respiratory
arrest usually precedes cardiac arrest.
Rapid induction and recovery.

0.68
quick induction etc

MAC (2-3%)

Potentially expensive, similar to isoflurane, good control over


planes of anaesthesia.

12.0

50% metabolised,
hang-over

Sevoflurane
Methoxyflurane

Lawton 1997, Heard 1997b, Greenacre 1997.

GENERAL COMMENTS

Organ toxicity, highly blood soluble so long induction


and recovery.

85

Commonly used agents


Isoflurane has achieved pre-eminence as the anaesthetic
of choice for birds, it has revolutionised avian medicine,
making much more possible. It is much safer than halothane
and the data is now so good that it would be difficult to defend the continued use of halothane in birds.
A relatively high flow rate needs to be maintained, it
should be a minimum of three times the normal minute volume. ie. approximately 3 ml/g bodyweight. (an African grey
weighing 350 g needs 1.1 litres/ minute. As a rule of thumb

2 lpm is sufficient for birds of up to amazon parrot size,


macaws need 3-4 lpm.
The normal system used for all but the shortest procedures is to intubate and use a Mini-Ayres or Bethune T-piece
system, this then allows scavenging of waste gas or ventilation should a problem occur. Cooks Veterinary Products
manufacture specialist endotracheal tubes.
Nitrous oxude is still used by some veterinarians for its
analgesic properties, it reputedly accumulates within the air
sacs and should only be used during induction, usually at
50/50 with oxygen and never more than 80%.

Injectable anaesthetics
DOSE RATE

COMMENTS

Alphaxalone/alphadalone

5-10 mg/kg i/v


36 mg/kg i/m, i/p

Alphaxalone/alphadalone is a relatively good


anaesthetic agent but with a transient apnoea following intravenous administration, the preferred route due to the large
volumes required. This can be alarming and, when compared
to other anaesthetic agents, is a major disadvantage. Despite
this, there is a wide safety margin but only a short chain of
action (Mandelker, 1987).

Ketamine

20-50 mg/kg s/c, i/m, i/p

Used in birds since 1972 (Mandelker, 1972). It is a good sedative but a poor anaesthetic, with poor muscle relaxation and
little analgesia. The dose rate of ketamine is inversely
proportional to the body size (Boever and Wright, 1975).
Ketamine is eliminated by the kidneys in birds, as it is in
mammals.

Ketamine with diazepam


or midazolam

25mg/kg ketamine + 1-2 mg/kg


diazepam or 0.2mg/kg
midozolam s/c, i/m

The addition of diazepam/midazolam produce better


relaxation than ketamine alone.

Ketamine with medetomidine

1.5-2mg/kg ketamine +
60-85 mg/kg medetomidine
(reversed with atipamazole Antisedan,
250-380 g/kg i/m)

Medetomidine has sedative and analgesic properties, but


it also has hypotensive, bradycardic, and hypothermic
effects. Medetomidine and ketamine combination
provides deep sedation and good muscle relaxation with no
arrhythmias or respiratory depression (Jalanka, 1989).
This combination is particularly good in waterfowl.

Ketamine with xylazine

Various combinations;
30-40mg/kg K+ 0.5-1.0mg/kg X
or 4.4/kg K + 2.2mg/kg X
(xylazine is reversed with yohimbine
HCl, 0.1-0.2mg/kg i/v, or atipamezole
250-380 g/kg i/m)

Once reversal agents became available the use of higher


doses of xylazine and correspondingly lower doses of
ketamine were possible. Ketamine/medetomidine is
considered a better combination, although xylazine is
cheaper. Unreversed there is prolonged recovery and post
operative depression that can result in birds being unable to
feed or drink.

Propofol

1.33mg/kg i/v

Dose dependent cardio-vascular and respiratory depression,


low therapeutic index in pigeons and chickens. Metabolised
and eliminated too quickly to be of any major use in birds.
Potential use only in larger birds in good health, when
respiratory support is available but mask induction is
considered inappropriate.

Xylazine

1-20 mg/kg i/m, i/v


(Reversed with yohimbine HCl,
0.1-0.2mg/kg i/v, or atipamezole
250-380 g/kg i/m)

Xylazine by itself is unreliable, causes bradycardia and A/V


block, and can cause serious respiratory depression
(Mandelker, 1987).

Refs: Lawton 1997, Heard 1997b

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Injectable agents still have a place, especially in the


field. For use where isoflurane is not available this author
would use ketamine/xylazine or ketamine/medetomidine in
preference to inducing with halothane and oxygen.

Analgesics
Work on pigeons suggests both kappa and mu receptors
are active in pain perception, but that they are kappa dominated (76%).
Analgesics have not yet been thoroughly studied in avian
species but butorphanol certainly appears useful.

mask first. In an respiratory-emergency situation oxygen can


be given by mask whilst the tube is placed under restraint
rather than anaesthesia. A large gauge tube (French gauge
14) is used, Cook Veterinary Products actually make a tube
specifically for the purpose. Positive pressure ventilation is
usually required because the CO2 falls below the level which
stimulates breathing, and apnoea results. Birds begin breathing spontaneously one the CO2 levels rise after the oxygen
flow ceases. It is possible if necessary to leave the air sac
tube in situ in cases where a respiratory obstruction is still a
potential problem.

Monitoring
Injectable anaesthetics
DOSE RATE

COMMENTS

buprenorphine

0.02mg/kg i/m

Opiate analgesic which can cause


some respiratory depression, not
very effective in birds even at
higher doses
Butorphanol
1-2mg/kg i/m
Appeared effective in African
greys and cockatoos but not amazons.
Has been used in parakeets
Carprofen
5-10mg/kg s/c Very effective analgesic which
can be used in conjunction with
buprenorphine to have a synergistic effect in cases of severe pain
Flunixin meglumine 1-10 mg/kg i/m Has been used but carprofen is
considered more effective
Ketoprofen
5-10 mg/kg i/m Better than flunixin but not as
good as carprofen
Meloxicam
200g/kg p.o
Effective and useful for long term
use
Lawton 1997, Paul-Murphy 1997, Bauck 1990, Malley (pers comm).

Maintenance
Birds are less efficient than mammals at retaining body
heat, during anaesthesia they cool rapidly so special care is
needed. Phalen et al (1997) showed the importance of heat
supplementation during surgery. Hypothermic birds become
acidotic. A warm room >23oC is advisable, the anaesthetic
gases themselves are cold and also have a cooling effect on
the patient. Sparing use of skin disinfection minimises the
cooling effect on the skin. Heater water circulating pads are
useful or my preference is the Vetbed type materials on a
reptile heater pad in a warm room > 25oC.

A safe anaesthetic is one which is appropriately monitored, even isoflurane which is considered extremely safe
should be treated with respect.
Suitable reflexes for monitoring are the palpebral,
corneal, cere, toe pinch and wing twitch. As is expected,
these slow and eventually are abolished. The toe, cere and
wing reflexes disappear at a medium plane of anaesthesia,
while the corneal reflex remains into deep anaesthesia. Jaw
tone and leg withdrawal can also be assessed, they are reduced in a medium plane of anaesthesia, jaw tone is also
rather difficult/dangerous to assess in a parrot being masked.
Electronic respiratory monitors are available but only
when using intubation. My own experience suggests that
the probes are not sufficiently sensitive to use via a mask.
I suggest anyone contemplating purchase of monitoring
equipment should arrange to test it in the way they wish to
use it before they buy it. Changes in pattern (becoming
more rapid) are indicative of recovery, or that the bird is
feeling pain. Normal respiratory rates have been reported
as budgerigars 55-75/min, larger parrots 10-20, and 2-20
for ostrich.
Doppler probes can be a relatively simple means of at
least ensuring that there is still a pulse.
Heart rate monitors can be useful to assess changes in
rate or especially when xylazine is used to detect possible
A/V block. Monitors need to have a wide range of sensitivities, budgerigars may have an average of 600 bpm, and ostriches 60 bpm Lawton (1996a) cites painful interventions in
a cockatiel resulting in a rise from 300 to 700 bpm.
Pulse oximetry is becoming an extremely valuable tool
with probes on the wing web or tongue, cloacal probes are
also being developed. Validation of the equipment is not yet
complete, although there is a lot of interest. Readings below
80% are considered life threatening, most birds will maintain 80-85% when self ventilating hence the advice to use
gentle positive pressure ventilation (Sinn 1994).

Air sac intubation


Emergency respiratory arrest
This route has proved useful if surgery on the head and
neck is contemplated, or if the patient is suffering from an
obstructive problem of the airway. The normal site is just behind the ribs on the left side, in the same position used for
endoscopic sexing. Routinely a bird would be induced by

Disconnect the bird from the anaesthetic.


Press the chest 40-50 x per minute, ensuring that the legs
are free to move.
Intubate or fit an air sac tube and IPPV through tube.

References
BAUCK, L. (1990) Analgesics in avian medicine. In: Proceedings of the
Association of Avian Veterinarians Annual Conference, 1990. AAV,
Lake Worth.
BOEVER, W.J. and WRIGHT, W. (1975). Use of ketamine for restraint and
anesthesia of birds. Veterinary Medicine/Small Animal Clinician 70,
86.
DUNCKER, H.R. (1971) The lung air sac system of birds. A contribution
to the functional anatomy of the respiratory apparatus. Ergeb. Anat.
Entwicklungsgesch 45 (6) 1.
JAMES, A.E., HUTCHINGS, G., BUSH, M., NATARANJAN, T.K., and
BURNS, B. 91976). How birds breathe: correlation of radiographic
with anatomical and pathological studies. Journal of American Radiological Society 17, 77.
GREENACRE,C.B. (1997) Comparison of sevoflurane to isoflurane in
Psittaciformes. In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV, Lake Worth.
HEARD, D.J. (1997a) Anesthesia and analgesia In: Avian Medicine and
Surgery. (Eds R.B.Altman, S.L.Clubb, G.M.Dorrestein & K.E.Quesenberry. W.B.Saunders, Philadelphia.
HEARD, D.J. (1997b) Avian anesthesia: Present and Future Trends In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV, Lake Worth.
KING, A.S. & McLelland, J. (1984). Birds, their structure and function. 2nd
ed. Baillire Tindall, London.

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MCLELLAND, J. (1989) Anatomy of the lungs and air sacs. In Form and
Function in Birds. Vol 4 (eds. A.S.King and J.McLelland). Academic
Press, London.
LAWTON, M.P.C. (1996a) Anaesthesia. In Manual of Psittacine Birds.
(eds.P.H.Beynon, N.A.Forbes and M.P.C.Lawton). BSAVA, Cheltenham.
LAWTON, M.P.C. (1996b) Anaesthesia. In Manual of Raptors, Pigeons and
Waterfowl. (eds.P.H.Beynon, N.A.Forbes and N.Harcourt-Brown).
BSAVA, Cheltenham.
LAWTON, M.P.C. (1997). Anaesthesia. In: Core Day Proceedings of the
4th Conference of the European Committee of the Association of
Avian Veterinarians. EAAV,1997. London.
MANDELKER, L. (1972) Ketamine hydrochloride as an anaesthetic for
parakeets. Veterinary Medicine/Small Animal Clinician 67, 55.
MANDELKER, L. (1987) Anesthesia and surgery. In Companion Bird
Medicine (Ed. E.W.Burr) Iowa State University Press, Ames.
PAUL-MURPHY, J. (1997) Evaluation of analgesic properties of butorphanol and buprenorphine for the psittacine bird. In: Proceedings of
the Association of Avian Veterinarians Annual Conference,
Reno.1997. AAV, Lake Worth.
PHALEN, D.N., LAU, M.T. & Filippich, L.J. (1997) Considerations for
safely maintaining the avian patient under prolonged anesthesia. In:
Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV, Lake Worth.
SINN, L.C. (1994) Anaesthesiology. in Avian Medicine: Principles and application. (eds.B.W.Ritchie, G.J.Harrison, and L.R.Harrison).
Wingers, Lake Worth.

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89

SCIVAC EXOTIC ANIMALS STUDY GROUP

Diagnostic techniques for birds


Peter W. Scott
Msc, BVSc, FRCVS
RCVS Specialist in Zoo & Wildlife Medicine and Fish Health & Production
Zoo & Aquatic Veterinary Group, Winchester - United Kingdom

Summary
Avian medicine has developed rapidly in the last 10
years, improved analytical techniques have improved the
applications for blood biochemistry. DNA techniques have
been applied for the determination of sex, and then for various diagnostics. Improvements in anaesthesia have lead to
the extension of endoscopic sexing into the taking of endoscopically guided biopsy samples.

In avian medicine laboratory workups are extremely


valuable in diagnosis. Much is best sent to specialist laboratories since bird blood is significantly different - not least the
nucleated erythrocytes! Avian haematology requires specialist training and a good throughput to produce consistent and
meaningful results. In-house testing has a major role for referral practices where quick results are valuable in stabilising patients while specialist lab tests are in the post. Appropriate samples should be taken, if necessary speak to the
lab while you still have the patient! Lane (1992a) has covered some of the problems of sampling. Spenser (1994) and
Carpenter (1996) are recommended).

is found running down the middle of the neck, in psittacines


there is usually a featherless apterylae over it making visualisation fairly simple. In small birds it is often the only vein
large enough for venipuncture. This is my preferred route.

Blood tests
Haematology
Haematology is a very valuable tool in avian medicine,
blood can be collected into heparin and EDTA. Microtainers
are preferred since the larger tubes contain too much EDTA
which may cause cell lysis. EDTA should not be used with
corvids, ratites, cranes, penguins or kookaburras as it causes
erythrocyte lysis.
A blood smear should be made at the time of collection
for a differential leucocyte count using blood which has not
been exposed to any anticoagulant.
Making full use of avian haematology really calls for experienced technicians and clinicians. Stress haemograms occur but vary between species. In cockatiels, african greys,
cockatoos and macaws the stress haemogram is heterophilic,
whilst in amazons it appears lymphocytic.
Summary of changes

Blood sampling
Blood can be collected from the brachial/cutaneous ulnar
vein (running across the ventral surface of the humero-radial joint - under the wing) in many species including pigeons,
raptors and waterfowl. The vessel is quite small and mobile
and blood collection will often result in haematoma formation. It is often necessary to pluck the site and poor restraint
may result in wing damage.
The metatarsal vein is often used in waterfowl and
ratites, although some avian veterinarians like the site for
routine use in a wide range of species. The vessel is on the
medial aspect of the intertarsal joint, venipuncture is usually carried out proximal to the joint, first plucking a few
feathers. If the vein is accessed through the scaled area the
bleeding may be difficult to stop. Exponents of the brachial
and metatarsal routes suggest not drawing blood with the syringe plunger, rather let the blood flow by capillary action.
Avian blood clots slowly so blocked needles are rarely a
problem.
The right jugular vein is a larger less mobile vessel and

CELL TYPE

COMMENTS

Heterophils

Band cells - rise in severe inflammatory disease


such as clamydiosis toxic heterophils - especially
in chronic equilibrated disease degranulated seen in low grade or chronic conditions

Eosinophils

These are rare, seen with Giardia in cockatiels,


and with worms in other species

Basophils

Rare, some in respiratory infections

Lymphocytes

Large - cf. monocytes, small predominant cell


type in amazons

Monocytes

Chronic illness esp. Chlamydia, lead poisoning,


Aspergillosis

Serology
At present there are not many useful serological tests for
birds in Europe. In the USA there are now tests for poly-

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4th European FECAVA SCIVAC Congress

90

4th European FECAVA SCIVAC Congress

omavirus, Pachecos disease, Aspergillus, chlamydia. There


are a number of chlamydia serology tests available. In UK
PMV serology is available. Serum iron assays can be useful
in toucans.
Biochemistry
Biochemistry tests are widely available and can be extremely valuable. In-house systems such as VetTest 8008 can

be used, even though some doubt has been cast on the validity of the results but their great value is that results are
available quickly. Plasma or serum can be used, gel-separation tubes are very useful to prevent haemolysis when samples must be sent to distant laboratories.
Specialised PCR / DNA tests
Sex determination by DNA probe single drop of blood

TEST

COMMENTS

ALT

Although useful for assessment of liver disease in mammals this is of no value in avian work.

AST / SGOT

Used as an indicator of liver damage, although it is non-specific sources of AST are liver, skeletal and cardiac muscle.
When it is elevated by hepatocellular damage and eventually returns to normal this does not indicate that liver function has
returned to normal. Bile acids may give a better prognostic measure for liver function.

Bile acids

Birds excrete biliverdin, not bilirubin (they lack bilirubin reductase), so bilirubin measurements are meaningless.
Unconjugated biliverdin does not accumulate in tissues, discolouration of avian plasma (or skin) is more likely to be due
to carotenoids than pathological changes). Samples should be tested within 24 hours. Post-prandial levels are higher than
pre-prandial since they are reabsorbed after eating

Calcium

This is an important parameter to measure in many birds. Low levels can be associated with breeding failure, egg binding
or fractures. Never collect samples into EDTA.

Cholesterol

This can be a useful measure in cases of hepatic lipidosis, hypothyroidism, atherosclerosis and in assessing obese birds on
high fat diets.

Creatinine

Not considered to be a useful test in birds. Has been seen to rise associated with high protein foods.

CK / CPK

This is found in all muscle tissue and c an be found at high values associated with activity, fights, fits etc. Rough technique
in capture and blood sampling can result in elevation. It is useful in helping to interpret raised AST levels, ie a raised AST
with normal CPK is strongly indicative of liver damage.

GLDH

This is fairly liver specific (within the hepatocyte mitochondria), there is reported to be some present in kidney.

LDH

This is non-specific, found in liver, muscle, kidney and erythrocytes. Limited value, prone to elevation due to haemolysis.

Phosphorus

In theory an elevation can be associated with renal failure, but in practice changes are not seen very often.

Protein

Changes in albumin and globulin levels are not well documented in birds, although direct parallels have been drawn with
mammalian results. Dry chemistry systems are said to be unreliable for measurement of avian albumin.

Triglycerides

These can be a useful indicator in investigating egg related peritonitis, elevations will also be seen during starvation.

Urea

Birds manufacture very little urea and it is not a useful test, elevations may occur with pre-renal dehydration.

Uric acid

Used as a guide to renal function, but is not absolute. It is synthesised in the liver and excreted by the medullary nephrons
independent of urine flow rate, dehydration etc. Raised uric acid levels do not indicate dehydration, they rise when renal
function is reduced to less than 30% of normal. A rise is seen with prolonged fasting 48-72 hours due to catabolism.

TEST

COMMENTS

Sex determination

Can be carried out on blood samples or feathers.

Parrot Circovirus
(Psittacine Beak & Feather Disease)

Infected birds appear to remain viraemic (except for a small number which appear to eliminate the
virus) and so blood samples will provide suitable target DNA in the majority of cases. Clinical cases
are often immunosuppressed so feather pulp should be included since such cases can be negative on
blood test. Feather pulp or 1 drop of blood in the collection vial. Fixed material or paraffin embedded tissues can also be used.

Avian Polyomavirus
(Budgerigar Fledgling Disease)

This test can only detect virus from birds which are actively shedding the virus, birds do not remain
viraemic. In the clinical situation this is particularly likely at times of stress such as moulting or
breeding, or following transportation. Cloacal swabs or faeces from live birds appear to be the most
reliable sample for detection of this virus. Fixed material or paraffin embedded tissues. Or fresh liver, spleen or kidney tissue from post mortems in collection medium. Blood samples have been rather
unreliable until recently but improved molecular techniques are now showing that these might well
be suitable for carrier detection.

Chlamydiosis / Psittacosis

This test can detect organisms when even very few are being shed, developments in molecular
echniques are making this suitable for examining blood.

required. PCR diagnostics for PBFD and Polyomavirus.


It is recommended that before any samples are sent veterinarians should speak to the laboratory and ensure that the
collection materials are appropriate. Special media may be
required.

Faecal tests
There is a lot of useful evidence in a simple examination
of the droppings in the cage. A normal dropping will contain a coiled, semi-solid faecal component, a white/creamy
urate component and some liquid urine. Diet will influence
faecal colour and consistency considerably, seed diets usually produce compact, green faeces, formulated diets tend to
produce bulkier brown coloured faeces. Items such as beetroot, blueberries and pomegranate will also cause alarming
changes. Apparent haematuria is a feature of lead (or other
heavy metal) poisoning in amazon parrots. This topic has
been reviewed by Bauck 1995. Consistent discolouration
green or yellow discolouration of urine or urates is cause for
concern and investigation.
Microbiology
In-house microbiology in my opinion is often of very
limited value, in my experience few practice laboratories do
it thoroughly enough, cutting corners with media ranges to
keep costs down. Lane (1992b) gives a review of techniques
for the practice laboratory.
Gram stains
Although referred to often as faecal gram stains it is
more useful to look at cloacal smears, these can be useful at
a basic level for assessing levels of yeasts, presence of
megabacteria or the gram positive/gram negative (GP/GN
ratio). Small passerines usually have no gram negative organisms present while psittacines have very few. In general
megabacteria will be seen if clinically significant, the organism is difficult to find in carriers. Microbiological culture is
suggested on birds with more than 10% gram negative organisms, observations by Brown (1996) suggest poor correlation between staining and culture. Choanal smears are also examined by grams stains, there are often more gram negative organisms in choanal than cloacal samples.

Endoscopy
Direct visualisation of organs is an extremely useful
technique, the 2.7mm rigid endoscope used routinely for
surgical sexing of birds can be utilised in a range of approaches. Taylor and Harrison 1997 have produced a superb
reference work on CD-ROM showing anatomy and surgical
approaches for all of the organs. This also covers the necessary approaches for endoscopically guided biopsy.

Biopsy
Crop biopsy has proved a useful means of obtaining a diagnosis in cases of proventricular dilatation (Doolen, 1994).

91

Endoscopic guided biopsy techniques have become popular and the Stortz system has been designed specially for
the purpose. Hunter and Taylor (1992) describe a technique
for lung biopsy, they stress that this is not a routine procedure but one which is valuable in cases where a diagnosis
cannot be made otherwise. Renal biopsy has also been investigated (Murray & Taylor,1997) since renal disease is difficult to assess by blood sampling techniques, this is a more
routine procedure than lung biopsy, most haemorrhage is
minor and self limiting.
Specialist Laboratories
DNA sexing, PBFD, Polyomavirus and Chlamydia PCR
tests.
University Diagnostics Ltd, South Bank Technopark, 90
London Rd, London, SE1 6LN.
Tel: 0171-401-9898, fax: 0171-928-9297

References
BAUCK, L. (1995) Abnormal droppings and their workup. In: Proceedings
of the Association of Avian Veterinarians Annual Conference.1995.
AAV, Lake Worth.
Carpenter, J.W. (1996) Ed. Avian and exotic parasitology. In. Seminars in
Avian and Exotic Pet Medicine. 5, (2).
DOOLEN, M. (1994) Crop biopsy - a low risk diagnosis for neuropathic
gastric dilatation. In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1994. AAV, Lake Worth.
GRIMES,J.E. (1993) Interpretation of avian host Chlamydial titers using
various serologic methods. In. Seminars in Avian and Exotic Pet
Medicine. 2, (4).
HUNTER, D.B., & TAYLOR, M. (1992) Lung biopsy as a diagnostic technique in avian medicine. In: Proceedings of the Association of Avian
Veterinarians Annual Conference, New Orleans.1992. AAV, Lake
Worth.
JOYNER, K.L. (1991) The use of gram stain results in avian medicine. In:
Proceedings of the Association of Avian Veterinarians Annual Conference, Chicago.1991. AAV, Lake Worth.
LANE, R.A., (1992a). Microbiology practical tips. In: Proceedings of the
Association of Avian Veterinarians Annual Conference. New Orleans.1992. AAV, Lake Worth.
LANE, R.A., (1992b). Sampling procedures: Dos & Donts. In: Proceedings of the Association of Avian Veterinarians Annual Conference.
New Orleans.1992. AAV, Lake Worth.
MURRAY, M.J., & TAYLOR, M. (1997). The use of endoscopy and endoscopic biopsy as aids in the diagnosis. In: Proceedings of the Association of Avian Veterinarians Annual Conference, Reno.1997. AAV,
Lake Worth.
Niagro, F.D., Ritchie, B.W., Latimer, K.S., Lukert, P.D., Steffens, W.L., and
Pesti, D. (1990) Polymerase chain reaction detection of PBFD virus
and BFD virus in suspect birds. In Proceedings of the Annual Conference of the Association of Avian Veterinarians. Phoenix: 25-37,
1990.
SCOTT, P.W. (1993). DNA Technology: Practical applications for the avian
veterinarian. in Proceedings of the 1993 European Conference on
Avian Medicine & Surgery. Utrecht, Netherlands. European Committee of the Association of Avian Veterinarians. 178-190.
SPENSER, E.L. (1994) Ed. Clinical Pathology: Blood testing. In. Seminars
in Avian and Exotic Pet Medicine. 3, (1).
TAYLOR, M., & HARRISON, G.J. (1997). Diagnostic Application of
Avian Endoscopy. Wingers Publishing Multimedia Series, Lake
Worth, Florida.
WORELL, A. (1991) Serum iron levels in Ramphastids. In: Proceedings of
the Association of Avian Veterinarians Annual Conference, Chicago.1991. AAV, Lake Worth.

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95

From pharmacokinetics clinical application


Empirical antibiotic treatment in infections diseases
David Aucoin

Summary
Avoiding antimicrobial failure involves initially ensuring
that the patient has treatable infection. Antimicrobial selection can be based on probabilities and input from flexible
labeling guidelines. A clinician who is familiar with the efficacy of each antimicrobial can avoid therapeutic failure and
use therapy as a diagnostic tool.

Treatment failure can be regarding in two different


lights. On one hand, true antimicrobial failure results from
using an inappropriate agent, incorrect dosage and or duration of treatment. However, a much greater reason for failure, is absence of a treatable infectious pathogen. Our perchance to use antibiotics frequently in situations where antibiotics have no efficacy or in situations where infectious
pathogens are not even present leads to our greatest failures.
Even though most patients receiving antibiotics get better
during treatment, it is this inappropriate use of antibiotics
that has lead many lay people to call for greater restrictions
on antimicrobial use, especially in animals.
This paper will address the specific issues regarding
true antimicrobial failure in a patient with treatable infectious disease as well as address more social issues regarding appropriate antimicrobial use and avoiding misuse on
antimicrobial.

Patient selection
The presence of an antimicrobial responsive infectious
disease is usually readily apparent. Localizing signs, history
and a good physical examination are often sufficient. Fever
has been the most frequent indication for antimicrobial use,
however, there is little indication that most fevers seen in the
dog or cat are caused by bacterial or rickettsial infections.

Moreover, most fevers associated with upper respiratory


or gastrointestinal infection sin the cat are viral infections.
These common infections do not require a fever to be diagnosed but do point out that fever of unknown diagnosis is
not likely, based on more common infections, to result in a
fever. The point is most practitioners use antibiotics because
there MAY be a bacterial cause.
Herein lies the problem: If you are trying to rule out a
bacterial infection the choice of antimicrobial agent must be
based on predictable efficacy against the most probable
pathogen(s) you are trying to rule out. Terms such as broad
spectrum are of little use in this situation since spectrum
does not indicate efficacy within that spectrum. The tetracyclines have a broad spectrum of activity from bacteria, mycolplasma, rickettsiae and chlamydia.
However, their efficacy against rickettsial species is excellent while against most common gram negative bacteria
theyre fair to poor. Its appropriate using tetracyclines to
rule out an unexplained fever caused by rickettsiae but
would be inappropriate to use it to rule out any bacterial infection.
Ampicillin is a broad spectrum antimicrobial with excellent activity only against streptococci. Using it to rule out a
possible bacterial infection would be illogical. It would only eliminate a systemic streptococcal infection. A rare disease in the dog or cat. To use an antimicrobial with a higher
degree of success depends on two principals.
If an infection is readily apparent (pyoderma), then antimicrobial choice, dose and duration is important in avoiding failure. If an infection is possible but not apparent (i.e
fever of unknown origin), then an antimicrobial(s) must be
selected to rule out a wide variety of pathogens.
Again, selection, dose and especially duration of therapy is important here but very different, since the antimicrobials are being used as a diagnostic tool as well as potential
therapy.

Table 1. Presence (+) or absence (-) of fever in the presence of common infections.

Pyoderma

Otitis
Externa

Lower
UTI

Upper
Respiratory

Lower
Respiratory

Gastrointestinal

Canine

+/-

+/-

Feline

+/-

+/-

+/-

MAIN PROGRAMME

DVM, Dip ACVCP


Santa Monica, California - USA

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4th European FECAVA SCIVAC Congress

Antimicrobial selection

Antimicrobial dosing

Selection in a known infection should be based on that


antimicrobial which has a high degree of predicable efficacy
against the most common pathogens at that site.
Again, it can be appreciated that even in the most commonly infected body sites, the infection is not always bacteria and rationale antimicrobial use against these infections is
impossible.
Selecting an antimicrobic with excellent predicted efficacy against these pathogen at these sites is the first step. It
is illogical in my opinion to use an agent that usually
works only to confront that owner again after failure to then
prescribe an agent that will work.
Treatment failure is very costly to the owner, the pet and
to your practice.
Table 3. Is based solely on in vitro efficacy and does not
take into account costs, toxicity, ease of use or in vivo factors which may favor one family vs. another.

The advent of flexible label dosing in the USA has finally made antimicrobial use more rational. Antimicrobial activity may be over a wide concentration range. Enrofloxacin is
effective against most Pasteurella spp at <0.006 ug/ml while
requiring 1-2 ug/ml to have similar in vitro efficacy against
90% of P. aeruginosa. Thats a 300 fold difference in effective concentrations! It would only be logical to assume the
dose for treating pasteurellosis would be lower than treating
a Pseudomonal infection. Antimicrobial like enrofloxacin
now have flexible dosing labels, however, all antimicrobial
should be dosed according to pathogen requirements.
Frequency of dosing depends on whether an antimicrobial in vivo activity is better correlated with its peak serum
levels (Concentration dependent) or time during a dosing interval serum levels are above the inhibitory concentration
(MIC) of the pathogen (Time Dependent). B-lactams (like
amoxi-clav and cephalexin) are time dependent while
quinolones and aminoglycosides (enrofloxacin, mar-

Table 2. Most common bacterial pathogens at commonly infected sites.

Pyoderma
Canine

Staphylococci

Feline

Otitis
Externa

Lower
UTI

Upper
Respiratory

Lower
Respiratory

Proteus/
Pseudomonas

Coliforms

Not
Predictable

Coliforms

Not Usually
Bacterial

Not Usually
Bacterial

Usually
Viral

Anaerobes
Pasteurella

Not Usually
Bacterial

Pasteurella

Gastrointestinal

Table 3. Antimicrobial families with excellent predicted in vitro efficacy (> 90%) against these pathogens.
Staphylococci
Antimicrobial

Coliforms

Pseudomonas

Anaerobes

Rickettsia

Cephalosporins
Quinolones
Potentiated, Penicillins

Quinolones

Quinolones
Aminoglycosides

Metronidazole

Tetracyclines
Quinolones

Table 4. Author suggested dosing guidelines based on pathogens and maximizing in vivo activity.
Amoxicillin
clavulanate
Staphylococci
Streptococci
Pasteurella
Coliforms
Pseudomonas
Anaerobes
Rickettsiae

10-15 BID
10 BID
10-15 BID
15-30 TID

Enrofloxacin

Marbofloxacin

Cephalexin

Gentamicin

5 SID

2 SID

6 SID

5 SID
5-10 SID
10-15 SID

2 SID
2-4 SID
4-8 SID

10-15 BID
10 BID
10-15 BID
15-30 TID

10-15 BID

10-15 BID
5 SID

4 SID
6 SID
8 SID

4th European FECAVA SCIVAC Congress

Antimicrobial dosing duration


Duration of treatment is empirical and based upon how
well the patient responds. However, to short a treatment period does increase the emergence of resistant bacterial
strains and too long a treatment increases unnecessary costs
and may delay alternative treatments or diagnostics.
Acute treatments should be continued 3-5 days past clinical cure which usually respond quickly with 5-10 days of
treatment adequate. If no clinical response is noted within a
few days it is unlikely a response will be seen in after 10
days. Treating acute infections for 2-3 weeks awaiting a response is illogical and the patients needs to be reevaluated.
Chronic infections can be treated for 2- 6 weeks. Length
of treatment is designed to keep bacteria from colonizing
and replicating while local tissues heal and normal antibacterial defenses are operational. Without local healing, it will
be impossible to prevent further bacterial infections. Many
pyoderma and lower UTIs are frequently recurrent requiring
frequent treatments. I prefer pulse therapy, treating these patients for short periods but frequently.

Ruling out a treatable bacterial infection


Antimicrobial can be used as diagnostic tools. A therapeutic trial is only effective if the response to therapy gives
high probability of a yes or no answer. Selecting an antibiotic depends on the rule outs (rickettsia vs. bacteria) and the
probability of knowing which pathogen is present. A post op
patient following a bowel resection is likely to coliforms,
enterococci and anaerobes present if leakage is suspected
while a dog with an aspiration pneumonia could have any
number of potential pathogens.
Select an antimicrobial with an excellent activity rating
against the suspected pathogens administer at a dose to maximize its effect. Observe for positive changes in clinical
signs which should occur within 24 hours. If no effect is observed after 48 hours it is unlikely that he patient has treatable bacterial infection. The patient may have peritonitis or
pneumonia but antibiotics alone will not likely be efficacious. Changing antibiotics is illogical and has a high degree
of failure.
If the pathogen(s) are known, use a four quadrant approach to effectively choose agents that are effective against
all gram positive and gram negative aerobes and anaerobes.
Combining a fluoroquinolone with a potentiated penicillin
or an aminoglycoside with a penicillin are effective protocols. If no clinical response is noted within 24-36 hours, it is
highly unlikely that the patient has treatable infection and
further diagnostics are warranted.

MAIN PROGRAMME

bofloxacin and gentamicin) are concentration dependent.


Simply put, to maximize a time dependent antimicrobic you
must give it more frequently (not just higher dose) while for
a concentration depend antimicrobic increasing its dose is
more efficacious than increasing its frequency of delivery.

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99

Cataracts in dogs: etiology, development


and clinical findings
Ellen Bjerks

Summary
The definition of cataract is any light-scattering opacity
in the lens, regardless of the initial cause, but not necessarily with any demonstrable effect on vision. This definition
may also be extended to include opacities of the lens capsule. The end result of cataract formation is destruction of
lens tissue with loss of transparency, either partially or completely. Developmental cataracts initially affects cortical fibres, while nuclear cataracts are most often congenital. The
nucleus may, however, be affected in more extended developmental cataracts as well. A special form of nuclear
cataract is the pulverulent type.
Causes of primary cataract include congenital malformations, nutritional deficiencies, toxins, radiation, UV-light,
trauma, inheritance and ageing. Secondary cataracts may
be caused by systemic diseases as well as other diseases
within the eye.

Definition of cataract
The word cataract is derived from the greek word katauraktos which means waterfall.
The definition of cataract is any light-scattering opacity in
the lens, regardless of the initial cause, but not necessarily
with any demonstrable effect on vision. This definition may
also be extended to include opacities of the lens capsule1.

Development of the lens - malformations


In early embryogenesis, the optic vesicle comes in contact with the surface ectoderm, stimulating the ectoderm to
form the lens vesicle. The lens vesicle later separates from
the ectoderm. In fetal life the lens is surrounded by a plexus
of vessels, the tunica vasculosa lentis, which normally disappears shortly after the puppy is born2. Remnants of the tunica vasculosa lentis may occasionally be visible on the posterior lens capsule. The primary vitreous and tunica vasculosa lentis may also be hyperplastic, this condition is termed
PHTVL/PHPV (persistent hyperplastic tunica vasculosa
lentis/persistent hyperplastic primary vitreous). PHTVL/PHPV is seen as an inherited condition in some dog breeds, the
dobermann being most frequently affected. The changes
range from only small pigmented dots on the posterior lens

capsule, not affecting vision, to major changes of the lens including lenticonus (a bulging of the posterior lens capsule),
cataract and intralenticular hemorrhage3-5.
In front of the lens the mesodermal tissue will differentiate to form the eyelids, conjunctiva, cornea, anterior chamber and the iris. Defective differentiation of the structures
may lead to many forms of malformations, including persistent pupillary membranes (PPM) which may attach to the
anterior lens capsule and cause opacities6.
Other malformations affecting the lens include: aphakia no lens at all, microphakia7-abnormally small lens, anomalies
of the lens shape (colobomas, lenticonus and lentiglobus)8
and congenital cataract. Congenital cataract may be present in
an otherwise normal eye, or may be associated with other
malformations, most commonly microphthalmia.

Lens anatomy and physiology


The normal lens is a clear structure, the oldest part being
the nucleus. The lens is surrounded by a collagenous lens
capsule freely permeable to water, ions and other small molecules. This lens capsule forms the basement membrane of
the lens epithelium. The lens epithelial cells which cover the
anterior part of the lens are a simple layer of cells, lying side
by side, but not tied together by tight junctions. Thus,
there is no major barrier across the epithelium into the extracellular spaces between the lens fibres. This is of potential importance to the effects on the lens of drugs delivered
topically to the eye, and also to changes in the composition
of the aqueous9.
The germinative zone of the epithelium is in the periphery, at the equator, and mitoses here give rise to new rows of
cells. These differentiate into secondary lens fibres (cortical
fibres) by elongation and loss of their nucleus. The layer of
secondary lens fibres is termed the lens cortex. The cortical
fibres meet and form suture lines anteriorly and posteriorly.
The anterior suture lines form an Y, whereas at the posterior
pole they form an Y upside down.
The lens steadily grows throughout the whole life of the
animal, adding layers of cortical fibres to the already existing lens tissue. The lens can only expand to a very limited
extent, therefore the result of this growth is that the lens fibres become more densely packed with increasing age, giving the lens a blueish appearance. The increased density of
the lens is termed nuclear sclerosis and is a normal age

MAIN PROGRAMME

DVM, PhD, Dipl ECVO


Norwegian College of Veterinary Medicine - Department of Small Animal Clinical - Norway

100

change which should not be confused with cataract. True senile cataracts with loss of transparency may occur in dogs as
in other species, however.
The cortex is the most metabolic active part of the lens,
and cataractogenic factors are most likely to influence the
cortical fibres initially. In comparison, congenital abnormalities will more probably affect the nucleus which after birth
is far less metabolic active than the cortex.
The aqueous transports nutrients to the lens. Glucose is
the main source of energy, with certain amino acids providing an additional source. Glucose enters the lens by simple
diffusion and is mainly metabolized by anaerobic glycolysis. The glycolysis route is regulated by the enzyme hexokinase, which is found in a limited supply within the lens and
thus serves as a rate limiting step for glycolysis. A small
amount of glucose is also metabolized by the hexose
monophosphate shunt which also depends on hexokinase for
control rate. Excess glucose is shunted into other pathways,
mainly the sorbitol (polyol) pathway. The sorbitol pathway
converts glucose to sorbitol which is a sugar alcohol. Normally, the sobitol pathway accounts for only about 5% of the
lens metabolism. Hyperglycemia causes more glucose to enter this pathway. The accumulation of sorbitol within lens
cells causes an osmotic gradient that draws water into the
lens fibres10.

The biochemical causes of cataract


The lens fibres are normally held in a relatively dehydrated state. This is important to provide the organized structure of the lens proteins (crystallins). The normal intracellular protein structures are maintained mainly by certain essential amino acids like methionine and cysteine. Low levels of these essential amino acids may therefore lead to destruction of the protein structures and cataract formation11.
This is not a condition normally seen in dogs, but may occur
in other animal species as well as humans in the third world.
In short, it can be said that the biochemical cause of
cataract is both water entrying the cells, and the unfolding of
the regular protein structures, thus enabling the proteins to
form aggregates. Both factors may cause rupture of cell
membranes with destruction of lens fibres and production of
cellular debris. The result of these structure alterations is
scattering of light. The effect of the protein aggregates is especially of significance in cortical cataracts.
A major cause of damage to the lens is oxidative stress,
and ascorbate, vitamin C, plays an important role in protecting the lens from oxidative damage 1. This is also the reason
why vitamin C eyedrops have been tried as cataract treatment, without any effect, however. Another anti-oxidant is
glutathione which is present in high concentration in the lens
and which acts co-operatively with ascorbate. A third antioxydant which has aroused interest is vitamin E, since in vitro administration of vitamin E on lenses has been shown to
slow cataract progression12. Topical administration of vitamin E in vivo has not shown any effect, though.

4th European FECAVA SCIVAC Congress

Morphologic changes
Regardless of the initial cause of cataract formation, the
end result is destruction of lens tissue with loss of transparency, either partially or completely. When a cataract develops in previously clear mature lens fibres, there are a limited number of forms that the opacity can take. These forms
are determined by the anatomy of the lens fibres and their
arrangement within the lens, so-called fibre-based cataracts.
Thus, when fibres within a particular perinuclear cortical fibre shell are affected, a lamellar cataract is formed. When
limited groups of fibres are affected, the appeareance is that
of spokes13. This is seen for instance in the late form of developmental cataract in the Boston terrier14. If the tips of the
fibres are affected, the opacity forms the branching pattern
of the sutures as the fibre tips enter the suture lines. Such
opacities are usually subcapsular and situated at the posterior pole.
Lens vacuoles are often found in connection with
cataract and are considered to represent early changes of
lens fibres. Transient vacuoles have been reported in humans15 and may well be occurring in dogs as well. However, in dogs they will most often just represent a stage of
cataract development, indication that the cataract is progressing.
In addition to the described changes of the originally
normally developed lens fibres itself, the epithelium may
loose the ability to produce normal lens fibres. This may be
the explanation of posterior polar cataracts in dogs, and also
of radiation cataracts in humans. Abnormal fibres first appear in the posterior subcapsular region of the lens periphery, where the changes may be difficult to detect. The abnormal fibres then move axially in the direction normally
taken by the growing lens fibres. Eventually they will form
a subcapsular cataract around the posterior pole.
At a later stage of cataract development, fibrous metaplasia of epithelial cells may also occur. There may also be
proliferation of the epithelial cells, which gives rise to abnormally shaped bladder cells.
Nuclear cataracts are most often congenital, but the nucleus may also be affected in more extended developmental cataracts as well. A special form of nuclear cataract is
the pulverulent type, the name borrowed from human ophthalmology. Early changes occur early in life as small
opacities along the suture lines, just behind the fetal nucleus. At the age of 4-5 years, a ball of small opacities appear in the nucles, giving the nucleus a candy-floss appearance. The changes do not involve the whole nucleus,
the outer adult nucleus is unchanged. This type of cataract
has been described in the Norwegian buhund 16, but occurs
also in other breeds, like the German shepherd and the
Leonberger.

Description of cataract
Cataracts can be divided into primary and secondary
cataracts. Secondary cataracts occur because of other
changes within the eye. These include uveitis, glaucoma,
lens luxation and retinal degeneration. Cataract may also be

4th European FECAVA SCIVAC Congress

Description according to localization of the changes:


- nuclear cataract
- anterior/posterior polar cataract
- equatorial cataract
- cortical cataract
- complete cataract
- subcapsular cataract
- capsular cataract

Causes of cataract
Malformations (see above).
Nutritional deficiencies, not as important in dogs as in certain other animal species.
Toxins. Cataract is a common indicator in toxicity studies18. Long-term topical administration of steroids has been
proven to cause cataract in humans and in laboratory animals19. The effect in dogs is uncertain.
Radiation. UV-light is one factor causing cataracts in humans. The effect of UV-light and oxidative damage on the
dog lens has not been thoroughly studied.
Trauma. The changes in traumatic cataract depend on the
type of injury. Blunt trauma to the eye may cause complete
cataract that does not become obvious until a couple of
weeks after the accident, since the initial changes are subtle and difficult to observe. Smaller injuries, like a stab by
a cat claw through the lens capsule may result in only a focal opacity, especially if the capsule seals rapidly after the
injury and the destruction of lens fibres is limited.
Inheritance (see below).
Ageing
Secondary cataracts
Systemic diseases. These will be covered in a separate
lecture.
Other diseases within the eye.

Hereditay cataract
Hereditary cataracts are of particular importance in dogs,
and there is a long list of breeds with cataracts proven or suspected to be inherited. Despite a considerable number of affected dogs within certain breeds, establishing the modes of
inheritance has proven difficult. Evidence for autosomal recessive inheritance are convincing in the two types of
cataract in the miniature schnauzer and in cataract in the
Afghan hound. Otherwise convincing information on modes
of inheritance is lacking. There is also limited knowledge as
to what is actually inherited, that is whether it is the lens
changes per se or some initiating factor.
Criteria for classifying cataract changes as hereditary
cataracts17:
Hereditary cataract has previously been described in the
breed.
The age of appearance and the localization of the lenticular changes correspond to those described in this breed.
The cataract occurs bilaterally (there may be exceptions).
The cataract is progressive, although slowly in certain cases.
The problem arises when cataract is diagnosed in a
new breed. The advise would be not to breed the affected
animal(s). Re-examination of the dog for signs of progression of the cataract, as well as examination of littermates,
offspring and parents should be performed. Unilateral
cataracts suspected to be hereditary may also be difficult to
evaluate, and affected animals should be re-examined at a
later stage for signs of bilateral involvement. Examination of
the colsest family of the affected dog is also advised.
As the genetic lines within breeds differ from country to
country, there will be variation in the cataract incidences. Information on affected breeds and cataract incidence can be
obtained from the national eye panels for inherited eye diseases in each respective country20-21.

Secondary cataracts
Other eye diseases may cause secondary cataracts. These
diseases include uveitis, lens luxation, glaucoma and retinal
disease. The cause of cataract is the change in composition
of the aqueous, with the presence of inflammatory or other
products acting toxic to the lens. In addition, there may be a
direct effect on the lens capsule of the adherence of iris to
the lens in uveitis.
Ocular signs, including cataract, secondary to systemic
disease will be covered in a separate lecture.

Lens induced uveitis


Leakage of the smallest crystallins (d crystallins)
through the lens capsule occurs to a minor degree in normal
eyes, but the rate of leakage is increased in the presence of
cataract22. The reason for this is that breakdown of the fibre
membranes can release crystallin sub-units or proteolytic
fragments of appropriate size to leak into the aqueous. These
substances are considered foreign material by the eye and
will cause an inflammatory reaction.

MAIN PROGRAMME

associated with microphthalmia. Primary cataracts develop


in an eye otherwise normal.
Cataracts can be described according to stages of development17:
Incipient cataract describes focal opacification(s) of the
lens and/or its capsule. Vision is not impaired. This cataract
may or may not progress.
Immature cataract. The opacity is more or less diffuse, but
the fundus can still be examined. Vision may or may not be
impaired. The changes are mostly progressive.
Mature cataract. The fundus cannot be inspected, as the
opacification is complete and dense. Vision is severely impaired. If a mature cataract takes up fluid and swells it is
referred to as intumescent.
Hypermature cataract. Dissolving of the cataract may occasionally occur. The content of the lens capsule is more or
less liquefied. Lens protein can be resorbed, leading to
shrinkage of the lens with wrinkling and dimpling of the
capsule. The nucleus will dissolve to a lesser extent and
may migrate inferiorly in the capsular bag to form what is
termed a Morgagnial cataract.

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Clinical signs of lens-induced uveitis are those of a lowgrade chronic uveitis:


- red eye
- moderately lowered intraocular pressure
- moderately miotic pupil
- darkened iris
Lens-induced uveitis is treated with anti-inflammatory
therapy. The inflammation should preferably be controlled
before attempting cataract surgery.

10.

References

13.

8.

9.

11.
12.

14.
1.
2.
3.

4.

5.

6.

7.

Brown NP, Bron AJ, (1996), Lens disorders, Butterworth-Heinemann


Ltd, Oxford, 91-132.
Glaze MB, Carter JD, (1995), Veterinary Pediatrics, WB Saunders
Philadelphia 1995: 297-336.
Boev MH, van der Linde Sipman T, Stades FC, (1988), Morphogenesis of persistent hyperplastic tunica vasculosa lentis and persistent hyperplastic primary vitreous, Invest Ophthalmol Vis Sci, 29:
1076-1086.
Boev MH, Stades FC, van der Linde-Sipman, Vrensen GFJM,
(1992), Persistent hyperplastic tunica vasculosa lentis and primary
vitreous (PHTVL/PHPV) in the dog: A comparative review, Progr Vet
Comp Ophthalmol, 2: 163-172.
Leon A, Curtis R, Barnett KC, (1986), Hereditary persistent hyperplastic primary vitreous in the Staffordshire bull terrier, J Am Anim
Hosp Assoc, 22: 765-774.
Strande A, Nicolaissen B, Bjerks I, (1988), Persistent pupillary
membrane and congenital cataract in a litter of English cocker
spaniels, J Small Anim Pract, 29: 257-260.
Molleda JM, Martin E, Ginel PJ, et al, (1995), Microphakia associated with lens luxation in the cat, J Am Anim Hosp Assoc, 31: 209-212.

15.
16.
17.

18.

19.
20.
21.
22.

Narfstrm K, Dubielzig R, (1984), Posterior lenticonus, cataracts and


microphthalmia; congenital ocular defects in the cavalier king charles
spaniel, J Small Anim Pract, 25: 669-77.
Brown NP, Bron AJ, (1996), Lens disorders, Butterworth-Heinemann
Ltd, Oxford, 53-90.
Basher AW, Roberts SM, (1995), Ocular manifestations of diabetes
mellitus: diabetic cataracts in dogs, Vet Clin North Am, Small Anim
Pract 25: 661-676.
Whikehart DR, (1994), Biochemistry of the eye, Butterworth-Heinemann Ltd, Oxford, 1-30.
Kojima M, Shui YB, Murano H, Sasaki K, (1996), Inhibition of
steroid-induced cataract in rat eyes by administration of vitamin-E
ophthalmic solution, Ophthalmic Res 28: 64-71.
Brown NP, Bron AJ, (1996), Lens disorders, Butterworth-Heinemann
Ltd, Oxford, 133-160.
Curtis R, (1984), Late-onset cataract in the Boston terrier, Vet Rec,
115: 577-578.
Brown N, (1971) The visibility of transparent objects in the eye by
retro-illumination, Br J Ophthalmol 55: 517-524.
Bjerks E, Haaland M, (1995), Pulverulent nuclear cataract in the
Norwegian buhund, J Small Anim Pract, 36: 471-474.
Peiffer RL, Petersen-Jones SM, (1997), Small animal ophthalmology: a problem-oriented approach, WB Saunders, Philadelphia, 85165.
Martin CM, Christmas R, Leipold HW, (1072), Formation of temporary cataracts in dogs given a disophenol preparation, J Am Vet Med
Assoc, 161: 294-301.
Urban RC, Cotlier E, (1986), Corticosteroid-induced cataracts, Surv
Ophthalmol, 31: 102-110.
Rubin LF, (1986), Inherited eye diseases in purebred dogs, Williams
& Wilkins, Baltimore.
ACVO Genetics committee (1996), Ocular disorders presumed to be
inherited in purebred dogs.
Van der Woerdt A, Nasisse MP, Davidson MG, (1992), Lens-induced
uveitis in dogs: 151 cases (985-1990), J Am Vet Med Assoc, 201:
921-926.

4th European FECAVA SCIVAC Congress

103

Ocular signs of systemic diseases in dogs


Ellen Bjerks

Summary
Ocular change is a prominent feature of many systemic
diseases. The ocular signs may accompany changes elsewhere in the body, or may be the only present sign of systemic disease. Thus, a complete history and a thorough clinical examination of the whole animal are essential in all
dogs presented with eye disease. The age of the animal
should also be considered. Malformations, as for instance
portosystemic shunts causing hepatic encephalopathy, affect
young animals, whereas other diseases, like diabetes mellitus, usually occur in middle-aged animals.
Systemic diseases causing ocular signs may be divided into:
Infectious diseases
Immune-mediated diseases
Metabolic diseases
Diseases of the cardiovascular system
Neoplasias
Nutritional deficiencies

Ocular change is a prominent feature of many systemic


diseases. The ocular signs may accompany changes elsewhere in the body, or may be the only present sign of systemic disease. Thus, a complete history and a thorough clinical examination of the whole animal are essential in all dogs
presented with eye disease. The age of the animal should also be considered. Malformations, as for instance portosystemic shunts causing hepatic encephalopathy, affect young
animals, whereas other diseases, like diabetes mellitus, usually occur in middle-aged animals.
Systemic diseases causing ocular signs may be divided into:
Infectious diseases
Immune-mediated diseases

CAUSE OF DISEASE

Metabolic diseases
Diseases of the cardiovascular system
Neoplasias
Nutritional deficiencies
The initial ophthalmic signs of systemic disease may be
divided into two main groups: Red eyes and visual disturbance. Red eyes are caused by inflammation, either of the
extraocular or the intraocular structures. Inflammation of extraocular structures is associated with conjunctival hyperemia, while inflammation of deeper structures is also associated with episcleral hyperemia. One should always remember that the eye is highly susceptible to inflammation
which may lead to loss of vision. Thus, a correct diagnosis
both of the ocular disease as well as of the possible underlying cause is of importance. Unilateral ocular manifestations
do not exclude the presence of a systemic disease.
Some diseases may initially cause inflammation, with
later progression to blindness. In some infectious diseases
the age of the animal when infected determines the ocular
signs. Canine herpesvirus is an example of this, as puppies
infected perinatally may develop retinal dysplasia, while
adults only develop mild conjunctivitis1.
Sudden blindness may occur because of ocular change,
but one should always also remember that diseases of the
brain can cause visual disturbance. Changes in the innervation of intraocular and extraocular structures, presenting
with ocular signs, may also be a result of damage to the brain
as well as to the actual cranial nerve.
Below there is a detailed list of common and less common systemic diseases associated with ocular signs. The
most important of these diseases will be discussed in the
lecture.

OCULAR SIGNS

Infections
Virus
Canine distemper2
Infectious canine hepatitis2

Conjunctivitis, KCS, chorioretinitis, optic neuritis. The end-stage of a slowly progressing multifocal chorioretinitis may resemble PRA. Blindness may
also be associated with encephalitis.
Uveitis. Corneal edema due to endothelial damage, blue eye, is a prominent feature. This may also occur after vaccination with live hepatitis virus.
Some breeds are reported to be more susceptible than others: Afghan hound,
basset hound, Siberian husky and St.Bernard.

MAIN PROGRAMME

DVM, PhD, Dipl ECVO


Norwegian College of Veterinary Medicine - Department of Small Animal Clinical - Norway

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4th European FECAVA SCIVAC Congress

Canine herpesvirus1

Conjunctivitis, keratitis, uveitis. Usually mild signs in adults. More serious


signs including retinal dysplasia in perinatal infection.

Rabies2

Chorioretinitis, optic neuritis. Central blindness.

Bacteria
Leptospira spp.3

Episcleral injection, yellowing of the sclera due to icterus, conjunctival petechia, uveitis.

Brucella canis3

Uveitis. Ocular signs are rare.

Clostridium tetani4

Enophthalmos, protrusion of the third eyelid.

Borrelia burgdorferi5

Uveitis, chorioretinitis. Ocular signs are rare in dogs.

Sec. to systemic bacterial disease3

Uveitis, endophthalmitis. Examples of bacterial diseases: Pyometra, prostatitis, severe otitis externa.

Protozoa
Toxoplasma gondii2

Uveitis, chorioretinitis. More common in cats, but should be considered in


chorioretinitis.

Leishmania donovani5,6

Blepharitis (spectacle blepharitis) with skin surface desquamation and hair


loss. Keratoconjunctivitis, keratouveitis. Endemic disease in Southern Europe.

Babesia spp.2

Chorioretinitis. Rare.

Neospora caninum7

Uveitis, chorioretinitis.

Rickettsia
Rickettsia rickettsii8
(Rocky Mountain spotted fever)

Conjunctivitis, keratitis, uveitis, petechial (Rocky Mountain spotted fever)


retinal hemorrhage.

Ehrlichia canis9
(tropical canine pancytopenia)

Conjunctivitis, conjunctival hemorrhage, hyphema, uveitis, keratic precipitates, retinal detachment. Widespread in Europe.

Fungi and algae3


Blastomyces dermatitidis10
Cryptococcus neoformans
Histoplasma capsulatum
Coccidioides immitis
Aspergillus fumigatus11
Prototheca
Parasites
Toxocara canis12

Granulomatous uveitis and chorioretinitis Cryptococcus neoformans Systemic mycoses are more common in America than in Europe.

Visceral larvae migrans may cause choroidal granulomas, intraretinal hemorrhage and retinal necrosis. End-stage may present as generalized retinal
degeneration.

Dirofilaria immitis4

Uveitis, vitritis, larvae may be visible in the anterior chamber. Death of larvae within the eye may cause severe uveitis resulting in blindness.

Fly larvae, Cuterebra, Oestrus, Hypoderma13

Uveitis, vitritis, larvae may be visible in the anterior chamber. Occasionally


reported.

Demodex canis3

Non-pruritic blepharitis with periocular hair loss. Most common in young


animals.

Immune-mediated diseases
Uveodermatologic syndrome14

Uveitis, depigmentation of uvea. Pigment loss of the skin on eyelids, lips,


paws and occasionally elsewhere on the body as well as depigmentation of
hair in the same regions. Breed predisposition in the Akita inu, Samoyed,
Siberian husky, also reported in other breeds. Comparable with Vogt-Koyanagi-Harada syndrome in humans.

Pemphigus complex15

Ulceration of mucocutaneous areas, including eyelids. KCS.

4th European FECAVA SCIVAC Congress

105

Systemic lupus erythematosus15

Ulceration of mucocutaneous areas, including eyelids. KCS, uveitis.


Glomerulonephritis may cause hypertension (see cardiovascular diseases).

Immune-mediated thrombocytopenia15

Petechiae in conjunctiva, hyphema, retinal hemorrhage.

Atopy15

Blepharitis, conjunctivitis, chemosis

Metabolic diseases
Cataract, bilateral. Rapid development may cause swelling of the lenses and
lens induced uveitis. Diabetic retinopathy is rare in dogs.

Hypoparathyroidism (hypocalcemia)17

Linear cataract reported in a few dogs.

Hypothyroidism18

Corneal deposits, KCS, signs of hyperlipoproteinemia. Facial paralysis may


cause secondary exposure keratitis.

Hyperlipoproteinemia19

Primary or secondary. Lipemia of ocular blood vessels, corneal opacities,


lipemic aqueous.

Hyperadrenocorticism (Cushings disease)20

Sudden acquired retinal degeneration (SARD)? An association with SARD


has been found in some patients.

Ceroid lipofuscinosis (CL)21


(lysosomal storage disease)

Hereditary diseases. Deposits of lipofuscin (lysosomal storage disease) in


ganglion cells and RPE cells. Secondary retinal degeneration. CL diagnosed
in many breeds, not all of them show ocular changes. Affected English setters have normal retinas. Retinal changes described in the Tibetan terrier and
the Polish owczarek nizinny.

Other lysosomal storage diseases22

Group of hereditary storage diseases. Corneal opacities, CNS signs.

Hepatic encephalopathy (liver failure)22

Central blindness.

Ehler-Danlos syndrome23

Rare congenital disease. Corneal edema, KCS, cataract, lens luxation.

Diseases of the cardiovascular system


Hypertension24

Primary or secondary to other systemic disease, most commonly chronic renal failure. Mildest signs often not noticed: tortuosity of retinal vessels,
cotton wool spots due to ischemia of vessels in the nerve fibre layer of the
retina. More severe changes include retinal hemorrhage, retinal detachment
and edema of the optic nerve head. Dogs are most often presented with acute
loss of vision.

Coagulopathies (deficency of clotting factors)25

Conjunctival hemorhage, hyphema, retinal hemorrhage. Also see immunemediated thrombocytopenia.

Hyperviscosity syndrome26

Tumors producing plasma cells may cause monoclonal gammopathies


which lead to increased levels of plasma immunoglobulins and increased
viscosity of the blood. Distention of retinal vessels, retinal hemorrhage, retinal detachment, hyphema.

Neoplasias (metastases)
Malignant lymphoma /
malignant fibrous histiocytoma27,28

Tumor infiltration in lymphoid tissue in conjunctiva. Tumor infiltration of


uvea. Uveitis, retinal detachment, retinal hemorrhage.

Other tumors29

Metastases from other tissues. Adenocarcinomas from the mammary glands


most common.

Nutritional deficiencies
Vitamin A deficiency2

Rare in dogs. KCS, keratomalacia, retinal changes. Nyctalopia.

Riboflavin (vitamin B) deficiency2

Keratitis. (Retinal degeneration reported in fish).

MAIN PROGRAMME

Diabetes mellitus16

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Vitamin E deficiency (experimental)30

Ophthalmoscopic changes of the retina similar to central PRA. Affection


of pigment-epithelial cells.

Zinc deficiency33

Dry, scaly skin, blepharitis. Siberian husky reported to be especially susceptible. (Cataract reported in fish).

References
1.

2.
3.
4.
5.
6.

7.

8.

9.
10.

11.
12.

13.

14.

15.
16.

Albert DM, Lahav M, Carmichael LE et al, (1976), Canine herpes-induced retinal dyplasia and associated ocular anomalies, Invest Ophthalmol 15: 267-278.
Ettinger SJ, (1997), Textbook of Veterinary Intenal Medicine, 4th edition, Saunders, Philadelphia, 524-533.
Gelatt KN, (1991), Veterinary Ophthalmology, 2nd ed, Lea and
Febiger, Philadelphia, 357-395.
Morgan RV, (1992), Handbook of small animal practice, 2nd ed,
Churchill Livingstone, New York, 1119-1123.
Roze M, (1997), Les uvites, Prat Med Chir 32 (suppl): 129-147.
Gothe R, (1990), Leishmaniosen des Hundes in Deutschland: Erregerfauna und -biologie, Epidemiologie, Klinik, Pathogenese, Diagnose, Therapie und Prophylaxe, Kleintierpraxis, 36: 69-84.
Dubey JP, Koestner A, Piper RC, (1990), Repeated transplacental
transmission of Neospora caninum in dogs, J Amer Vet Med Assoc
197: 857-860.
Davidson MG, Edward BB, Nasisse MP, (1989) Ocular manifestation
in Rocky Mountain spotted fever in dogs, J Amer Vet Med Assoc,
194: 777-781.
Woody BJ, Hoskins JD, (1991) Ehrlichial diseases of dogs. Vet Clin
North Am Small Anim Pract 21: 75-98.
Bloom JD, Hamor RE, Gerding PA, (1996), Ocular blastomycosis in
dogs: 73 cases, 108 eyes (1985-1993), J Amer Vet Med Assoc, 209:
1271-1274.
Gelatt KN, Christmas CL, Samuelson DA, et al, (1991), Ocular and
systemic aspergillosis in a dog, J Am Anim Hosp Assoc, 27: 427-431.
Johnson, BW, Kirkpatrick CE, Whiteley HE et al, (1989), Retinitis
and intraocular larval migration in a group of border collies, J Am
Anim Hosp Assoc, 25: 623-629.
Gwin RM, Meredith R, Martin CL, (1984), Ophthalmomyiasis interna posterior in two dogs and a cat, J Am Anim Hosp Assoc, 20: 481486.
Murphy CJ, Bellhorn RW, Thirkill C, (1991), Anti-retinal antibodies
associated with Vogt-Koyanagi-Harada-like syndrome in a dog, J Am
Anim Hosp Assoc, 27: 399-402.
Ettinger SJ, (1989), Textbook of Veterinary Internal Medicine, 3th
edition, Saunders, Philadelphia, 2283-2327.
Basher AW, Roberts SM, (1995), Ocular manifestations of diabetes

17.
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mellitus: diabetic cataracts in dogs, Vet Clin North Am, Small Anim
Pract 25: 661-676.
Mannerfelt T, (1997), Primr hypoparathyroidism hos hund, Sv Vet T,
49: 473-478.
Crispin SM, Barnett KC, (1978, Arcus lipoides corneae secondary to
hypothyroidism in the Alsatian, J Small Anim Pract, 19: 127-142.
Crispin SM, (1993), Ocular manifestations of hyperlipoproteinaemia,
J Small Anim Pract, 34: 500-506.
van der Woerdt A, Nasisse MP, Davidson MG, (1991), Sudden acquired retinal degeneration in the dog: Clinical and laboratory findings in 36 cases, Progr Vet Comp Ophthalmol, 1:11-18.
Wrigstad A, Nilsson SEG, Dubielzig R, Narfstrm K, (1995), Neuronal ceroid lipofuscinosis in the Polish owczarek nizinni (PON) dog.
A retinal study, Doc Ophthalmol, 91: 33-47.
Oliver JE, Lorenz MD, (1993), Handbook of veterinary neurology,
Saunders, Philadelphia, 322-373.
Barnett KC, Cottrell BD, (1987), Ehler-Danlos syndrome in a dog:
ocular, cutaneous and articular abnormalities, J Small Anim Pract, 28:
941-946.
Bartges JW, Willis AM, Polzin DJ, (1996), Hypertension and renal
disease. Vet Clin North Am- Small Anim Pract, 26: 1331-1345.
Ettinger SJ, (1989), Textbook of Veterinary Intenal Medicine, 3th edition, Saunders, Philadelphia, 2246-2279.
Lane IF, Roberts SM, Lappin MR, (1993), Ocular manifestation of
vascular disease: hypertension, hyperviscosity and hyperlipidemia, J
Am Anim Hosp Assoc, 29: 28-36.
Krohne SG, Henderson NM, Richardson RC, Vestre WA, (1994),
Prevalence of ocular involvement in dogs with multicentric lymphoma: prospective evaluation of 94 cases. Prog Vet Comp Ophthalmol, 3: 152-157.
Scherlie PH, Smedes SL, Feltz T, et al, (1992), Ocular manifestation
of systemic histiocytosis in a dog, J Am Vet Med Assoc, 201: 12291232.
Dubielzig RR, (1990), Ocular neoplasia in small animals. Vet Clin
North Am. Small Anim Pract, 20: 837-849.
Riis RC, Sheffy BE, Loew E, et al, (1981), Vitamin E deficiency
retinopathy in dogs, Am J Vet Res, 42: 74-86.
Van Den Brock AHM, (1988), Diagnostic value of zinc concentrations in serum, leukocytes and hair of dogs with zinc-responsive dermatosis. Res Vet Sci, 44: 41-44.

4th European FECAVA SCIVAC Congress

107

Ocular signs of systemic diseases in cats


Ellen Bjerks

Summary
In cats, many systemic diseases show ocular manifestations. The importance of a complete work-up in cats presented with diseases of the eye or adnexa should therefore
not be under-estimated. When examining the animal, one
must determine whether there are signs of concurrent systemic disease. Conversely, if a cat is presented with a systemic disease that is frequently associated with ocular
changes, a careful examination of the eyes is necessary to
detect changes which should be treated.
Uveitis with or without chorioretinitis is one of the most
frequent and significant ophthalmic diseases in cats.The
most important causal agents are coronavirus (feline infectious peritonitis), feline leukemia virus, Toxoplasma gondii
and feline immunodeficiency virus, but other factors may also cause uveitis. The other important group of systemic diseases causing ocular changes is the infectious upper respiratory tract diseases.

In cats, many systemic diseases are associated with ocular manifestations. The importance of a complete work-up in
cats presented with diseases of the eye or adnexa should
therefore not be under-estimated. When examining the animal, one must determine whether there are signs of concurrent systemic disease. Conversely, if a cat is presented with
a systemic disease that is frequently associated with ocular
changes, a careful examination of the eyes is necessary to
detect changes which should be treated.

Uveitis
Uveitis with or without chorioretinitis is one of the most
frequent and significant ophthalmic diseases in cats. In recent reports, between 38% and 70% of the cats with uveitis
have concurrent systemic disease1. The most important
causal agents are coronavirus (feline infectious peritonitis),
feline leukemia virus, Toxoplasma gondii and feline immunodeficiency virus2,3.
Feline herpesvirus is also a suspected cause of uveitis,
since diagnostic tests (polymerase chain reaction -PCR) has
revealed herpesvirus-DNA in the aqueous of a number of
cats with so-called idiopathic uveitis.
FIP may present in a granulomatous (dry) and a produc-

tive (wet) form. The granulomatous form of FIP, which is


caused by a partial cell-mediated immune response, is most
often associated with ocular signs, and uveitis may even be
present without concurrent signs of systemic disease.
Ocular changes linked to FeLV are related to the ability
of the virus to induce immunosuppression, hematologic
changes and tumor formation4. Ocular signs include retinal
dysplasia, tumor formation, retinal hemorrhages and pupillary changes. Perinatal infection can result in retinal dysplasia, which occurs seconday to diffuse retinal inflammation.
Spontaneous retinal hemorrhage is the result of anemia-induced hypoxia of small retinal vessels followed by increased
capillary fragility and rupture of the vessels. Abnormalities
in pupil shape include spastic pupil, D-shaped pupil and reversed D-shaped pupil5. These changes probably represent
FeLV infection of the autonomic ganglia for the parasympathetic portion of the third cranial nerve which delivers one
branch to each of the two pupillary constriction muscles of
the iris.
Feline immunedeficiency virus may cause a mild uveitis
that can be aggravated by co-infection with Toxoplasma
gondii. The prevalence of toxoplasmosis has been difficult
to determine, but the demonstration that IgM titers to the organism can be found in many uveitis-affected cats has led to
heightened interest in toxoplasmosis as a cause of feline
uveitis6.

Upper respiratory tract infections


The other important group of systemic diseases causing
ocular changes is the upper respiratory tract diseases. By tradition, four infectious agents have been associated with conjuntivitis: Feline herpesvirus, Chlamydia psittaci, Calicivirus and Mycoplasma spp.
Mycoplasma is a common finding in the normal conjunctival flora of cats7. This may suggest that mycoplasma
species are rarely pathogenic unless the animal is immunosuppressed or very young.
Calicivirus-infection has also been associated with conjunctivitis. Experimental inoculation with calicivirus in cats
has not produced ocular signs as response to infection, however2. The significance of this virus in conjunctivitis may
therefore be worth further studies.
Chlamydia psittaci is a primary conjunctival pathogen in
cats, and spread to other cats within a household is not un-

MAIN PROGRAMME

DVM, PhD, Dipl ECVO


Norwegian College of Veterinary Medicine - Department of Small Animal Clinical - Norway

108

4th European FECAVA SCIVAC Congress

common8. After infection, organisms are shed for a long period of time. Although different from the human strain, there
are similarities enough for the feline strain to cause infections in humans. The zoonotic aspect should therefore be
considered when treating affected anmals. Perinatal chlamydial infection is also considered a cause of ophthalmia
neonatorum in cats.
Feline herpesvirus (FHV-1) is a very common pathogen,
studies in the USA have shown that abut 75% of the adult cat
population is seropositive. Latency is established in the
trigeminal ganglia, and a chronic carrier state develops with
intermittent virus shedding9. Recurrence is common, especially with stress or other systemic disease.
Newborn kittens may develop ophthalmia neonatorum
if infected before the eyes are opened. The infection may
also progress to affect the cornea and cause a keratitis
which may result in corneal perforation, endophthalmitis
and phthisis.
Older kittens develop a serous conjunctivitis with
chemosis and subsequent conjunctival epithelial necrosis.
Corneal changes are seen as superficial branching ulcera, socalled dendritic ulcera. These changes are often too superficial to be diagnosed by staining with fluorescein, however staining with rose-bengal may show the corneal

DISEASE

changes. Symblepharon formation (adhesion of conjunctiva


to itself or to the cornea) is not an uncommon sequela of primary FHV-1 infection. The ability of herpesvirus to produce
epithelial necrosis is presumably responsible for the symblepharon formation in young cats.
Older cats with signs of recrudescent herpesvirus-infection show only moderate signs of systemic disease. The ocular changes are often more severe than in primary infection,
however. Corneal changes are often unilateral and present as
superficial keratitis with dendritic or geographic epithelial
defects due to virus replication, or as stromal keratitis. Stromal keratitis is probably not caused by active viral replication, as virus is rarely isolated from these ulcers. The
changes of the corneal stroma may, however, be the result of
a hypersensitivity reaction to viral antigens in the stroma.
Corneal sequestration (corneal necrosis - black body) is a
non-specific response to keratitis, but FHV-1 is considered a
contributing factor in many cats. Chronic conjunctivitis may
cause keratoconjunctivitis sicca because of obstruction of
the lacrimal gland ducts.
Below there is a detailed list of both common and less
common systemic diseases which may cause ocular
changes. The most important of these diseases will be discussed in the lecture.

OCULAR SIGNS

Infectious diseases
Virus
Feline herpesvirus2

Perinatal infection: ophthalmia neonatorum. Young kittens: serous conjunctivitis, conjunctival epithelial necrosis, dendritic corneal ulcera, symblepharon. Recurrent infection: superficial or stromal keratitis, corneal sequestration, KCS, uveitis (?)

Calicivirus2

Conjunctivitis. Significance?

Coronavirus (Feline infectious peritonitis)10

Granulomatous uveitis, chorioretinitis, keratic precipitates.

Feline Leukemia virus2

Tumor cells in uvea, uveitis, retinal hemorrhage, keratic precipitates, change


in pupil shape. Retinal dysplasia in perinatal infection.

Feline immunodeficiency virus2,11

Any ocular change, serious eye changes probably due to secondary problems caused by immunosuppression.

Panleukopenia virus12

Conjunctivitis, chorioretinitis. Fetal or perinatal infection: retinal dysplasia,


optic nerve hypoplasia.

Borna disease virus (staggering disease)13

Central blindness.

Pox virus2

Blepharitis, conjunctivitis.

Bacteria

Bacteria

Mycobacterium tuberculosis14

Uveitis, chorioretinitis, retinal detachment.

Chlostridium tetani

Protrusion of third eyelid.

Chlamydia psittaci2

Conjunctivitis, chemosis. Ophthalmia neonatorum.

Mycoplasma spp.7

Conjunctivitis, chemosis. Significance?

4th European FECAVA SCIVAC Congress

109

Rickettsia
Hemobartonella felis15 (feline infectious anemia)

Anemic retinopathy, retinal hemorrhage.

Protozoa
Toxoplasma gondii16

Uveitis, chorioretinitis.

Fungi
USA. Occurs occasionally also in other parts of the world. The most common of the systemic mycoses in cats, but systemic mycoses are generally
rare in this species. Uveitis.

Histoplasma capsulatum4,18

Endemic disease in temperate and tropical regions. Uveitis.

Blastomyces dermatitidis4

America, Africa. Uveitis.

Coccidioides immitis4

America. Uveitis.

Microsporum spp.2

Blepharitis.

Parasites2
Notoedres cati

Blepharitis, pruritic.

Demodex spp.

Non-pruritic periocular hair loss.

Toxocara cati

Intraretinal hemorrhage, retinal necrosis, choroidal granulomas.

Dirofilaria immitis

Uveitis, vitritis, larvae may be visible in the anterior chamber.

Fly larvae, Cuterebra, Oestrus, Hypoderma

Uveitis, vitritis, larvae may be visible in the anterior chamber.

Thelazia californiensis

Conjunctivitis, nematodes found in conjunctiva.

Immune-mediated diseases2
Pemphigus complex

Ulceration of mucocutaneous junctions.

Allergies (especially food allergies)

Blepharitis.

Metabolic diseases
Diabetes mellitus19

Ocular manifestations are rare in cats. Cataract and diabetic retinopathy


have been reported.

Hepatic encephalopathy (liver failure)20

Central blindness.

Renal failure

See hypertension.

Hyperthyroidism

See hypertension.

Hyperparathyroidism21

Cataract.

Hyperlipemia, familial hypercholesterolemia22

Lipemia retinalis, lipemic aqueous.

Lysosomal storage diseases23

Corneal opacity, accumulation in ganglion cells, retinal lesions, central


blindness.

Chdiak-Higashi syndrome2

Color dilution, cataract.

Diseases of the cardiovascular system


Hypertension24,25

Primary or secondary to chronic renal failure or hyperthyroidism. Mildest


signs often not noticed: Tortuosity of retinal vessels, cotton wool spots

MAIN PROGRAMME

Cryptoccus neoformans4,17

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4th European FECAVA SCIVAC Congress

due to ischemia in vessels in the nerve fibre layer of the retina. More severe
changes include retinal hemorrhage, retinal detachment and edema of the
optic nerve head. Animals are most often presented with acute loss of vision.
Feline infectious anemia (Hemobartonella felis)

Retinal hemorrhage, hyphema. Also listed under infectious diseases.

Coagulation disorders2

Hyphema, conjunctival hemorrhage, retinal hemorrhage.

Hyperviscosity syndrome2

Tumors producing plasma cells may cause monoclonal gammopathies


which lead to increased levels of plasma immunoglobulins and increased
viscosity of the blood. Distention of retinal vessels, retinal hemorrhage, retinal detachment, hyphema.

Periarteritis nodosa2

Fibrinoid necrosis of small arteries, formation of granulation tissue leads to


vascular occlusion. Exudate in anterior chamber, uveitis.

Diseases of the nervous system


Dysautonomia26

Dilated pupils, KCS.

Feline spongiform encephalopathy27

Central blindness. Retinitis in other species.

Haws syndrome

Bilateral protrusion of third eyelid. Secondary to infectious diseases.

Nutritional deficiencies
Taurine deficiency28

Feline central retinal degeneration progressing to complete retinal degeneration.

Thiamin deficiency29

Mydriasis, peripapillary edema.

Arginine deficiency30

Cataract.

References
1.

2.
3.

4.
5.
6.

7.

8.
9.

10.
11.

12.
13.

Gmensky A, Lorimer D, Blanchard G, (1996), Feline uveitis: a retrospective study of 45 cases. Transactions Am Coll Vet Ophthalmol, 27:
49.
Gelatt KN, (1991), Veterinary Ophthalmology, Lea and Febiger,
Philadelphia, 529-575.
Heider HJ, Pox C, Loesenbeck G, Egberink H, (1997), Ophthalmologische Befunde im Zuzammenhang mit verschiedenen Virusinfektionen der Katze, Kleintierpraxis, 42: 887-900.
Barnett KC, Crispin SM, Feline Ophthalmology, (1998), Saunders,
London.
Gelatt KN, (1991), Veterinary Ophthalmology, Lea and Febiger,
Philadelphia, 706-743.
Chavkin MJ, Lappin M, Powell CC, Roberts SM, (1993), Seroepidemiologic and clincal observations of 93 cases of uveitis in cats, Prog
Vet and Comp Ophthalmol, 2: 29-36.
Nasisse MP, Guy JS, Stevens JB, et al, (1993), Clincal and laboratory findings in chronic conjunctivitis in cats: 91 cases (1983-1991), J
Am Vet Med Ass, 203: 834-837.
Dorin SE, Miller WW, Goodwin JK, (1993), Diagnosing and treating
chlamydial conjunctivitis in cats, Vet Med, 325-330.
Weigler, BJ, Babineau CA, Sherry B, Nasisse MP, (1997), High sensitivity polymerase chain reaction assay for active and latent feline
herpesvirus-1 infections in domestic cats, Vet Rec, 140: 335-338.
Davidson MG, Nasisse MP, English RV et al, (1991), Feline anterior
uveitis: a study of 53 cases, J Am Anim Hosp Assoc, 27: 77-83.
Loesenbeck G, Drommer W, Heider H-J, (1995), Augenbefunde bei
serologisch FIV (felines Immundefizienzvirus)-positiven Katzen,
Dtsch Tierrztl Wschr, 102: 348-351.
Percy D, Scott F, Alberts D, (1975), Retinal dysplasia due to feline
panleukopenia virus infection J Am Vet Med Assoc, 167: 935-937.
Lundgren AL, Borna disease virus infection in cats. On the etiopathogenesis of feline non-suppurative meningoencephalomyelitis (staggering disease), (1995), Academic thesis, Swedish University of
Agricultural Sciences, Uppsala.

14.
15.
16.

17.
18.
19.
20.
21.
22.
23.

24.

25.
26.
27.
28.

29.

Formston C, (1994), Retinal detachment and bovine tuberculosis in


cats, J Small Anim Pract, 35: 5-8.
VanSteenhouse JL, Millard JR, Taboada J, (1993), Feline hemobartonellosis, The Compendium, 15: 535-544.
Chavkin MJ, Lappin MR, Powell CC, et al., (1991), Seroepidemiologic and clinical observations of 93 cases of uveitis in cats, Prog Vet
Comp Ophthalmol, 2: 29-36.
Gerds-Grogan S, Dayrell-Hart B, (1997), Feline cryptococcosis: A
retrospective evaluation, J Amer Anim Hosp Assoc, 33: 118-122.
Peiffer RL, (1979), Ocular manifestations of disseminated histoplasmosis in a cat, Feline Practice, 9: 24-29.
Peiffer RL, Gelatt KN, (1974), Cataracts in the cat. Feline Pract, 4:
34-38.
Oliver JE, Lorenz MD, (1993), Handbook of veterinary neurology,
Saunders, Philadelphia, 322-373.
Stiles J, (1991), Cataracts in a kitten with nutritional secondary hyperparathyroidism, Prog Vet Comp Ophthalmol, 1: 296-298.
Crispin SM, (1993), Ocular manifestations of hyperlipoproteinaemia,
J Small Anim Pract, 34: 500-506.
Aguirre G, Stramm L, Haskins M, (1983), Feline mucopolysaccharidosis VI: general ocular and pigment epithelial pathology, Invest
Ophthalmol Vis Sci 24: 991-1007.
Stiles J, Polzin DJ, Bistner SI, (1994), The prevalence of retinopathy
in cats with systemic hypertension and chronic renal failure or hyperthyroidism, J Amer Anim Hosp Assoc, 30: 564-572.
Sansom J, Barnett KC, Dunn KA et al., (1994), Ocular disease associated with hypertension in 16 cats, J Small Anim Pract, 35: 604-611.
Blaxter A, Gruffydd-Jones TJ, (1987), Feline dysautonomia, Feline
Pract, 9: 58-61.
Gruffydd-Jones TJ, Galloway PE, Pearson GR (1991), Feline spongiform encephalopathy, J Small Anim Pract, 33: 471-476.
Sturman JA, Gargano AD, Messing JM, Imaki H, (1986), Feline maternal taurine deficiency: Effect on mother and offspring, J Nutr 116:
655-667.
Ettinger SJ, (1997), Textbook of Veterinary Intenal Medicine, 4th edition, Saunders, Philadelphia, 524-533.

4th European FECAVA SCIVAC Congress

111

Acute renal failure: from emergency to patient


stabilisation
Claudio Brovida

Summary
Acute renal failure: from emergency to patient stabilisation.
Acute ranal failure (ARF) may be recognized by an
abrupt onset of azotemia or oliguria, rapidly progressive
azotemia or sudden onset of clinical signs of uremia in a previously healty patient. Several life threatening complications
may occur in patients with ARF, they are hyperkalemia,
metabolic acidosis, severe anemia, volume depletion, sepsis.
Patients may die of the diseases process which initiated
ARF (e.g.: acute pancreatitis, sepsis, shock, hypercalcemia,
ethylen glycol intoxication) rather than from ARF or its
complications. Therefore diagnosis and initiation of specific
therapy for diseases which may have precipitated ARF
should be a high priority. The history, physical examination
and urinalysis are usually sufficient to rule out pre-renal and
post-renal causes of azotemia.
Although therapy designed to eliminate the cause(s) of
ARF will not directly result in repair of renal lesions, it will
minimize the severity and extent of renal damage. Symptomatic and supportive therapy designed to minimize deficits
and excesses in fluid, electrolyte, acid-base and nutritional
balance, will often allow life to be sustained until the body
can restore adequate renal structure and function.

Acute renal failure (ARF) is a rapid onset of azotemia


over hours to days (two weeks), or pathologic oliguria which
could not have been present for more than a few days, that
indicates rapid deterioration or loss of renal function. While
ARF may not by itself constitute an emergency, its causes
(hypovolemia, shock, urinary obstruction, sepsis, etc.) often
are life threatening. In addition, the potential for enhancing
reversibility of renal lesions and return of renal function may
be lost if therapeutic intervention is delayed. In contrast to
CFR, rapid diagnosis and initiation of therapy may greatly
enhance a favourable prognosis in ARF.
ARF may result from diverse renal diseases and injuries.
The syndrome of acute tubular necrosis (ATN) accounts for
the majority of cases. With ATN there is a rapid reduction in
GFR resulting from an ischemic or toxic renal insult. Reduced GFR is thought to result from a combination of vascular and tubular effects.
The clinical course of oliguric ATN may be characterized
by three sequential phases:

1) initiation and development,


2) maintenance,
3) diuresis (recovery).
The initiation phase begins with onset of renal injury and
continues through onset of oliguria (reduction in urine output below 0.5-1 ml/kg/hour). Glomerular filtration rate may
begin to fall immediately following the renal insult (as in the
case of shock), or it may be delayed for hours to days (as in
the case with exposure to nephrotoxic drugs).
The duration is highly variable, but it usually persists
about 1 or 2 weeks.
The oliguric phase is characterized by predictable fluid
and electrolyte imbalances including alterations in hydration, hyponatremia, hyperkaliemia, metabolic acidosis and
hyperphosphatemia.
Clinical signs typically develop during the oliguric phase
of ATN, including gastrointestinal, hematological and neurological manifestations. Gastrointestinal disorders are common and include anorexia, vomiting, mucosal ulceration and
hemorrage.
This hemorrage results primarily from defective platelet
function, but may also be associated with thrombocytopenia,
decreases in various coagulation factors and defects in capillary function.
Progressive anemia and neurological disorders characterized by lethargy, depression, stupor and coma may occur
during the oliguric phase.
Transition from the oliguric to the diuretic phase heralds
the onset of re-establishment of tubular continuity, dissolution and/or mobilisation of intratubular casts, and return to
near normal patterns of renal perfusion.

Diagnosis of acute renal failure


ARF may be recognized by an abrupt onset of azotemia
or oliguria, rapidly progressive azotemia, or sudden onset of
clinical signs of uremia in a previously healthy patient.
A preliminary diagnosis of ARF is based on evidence
from medical history, previous data concerning renal function and lack of phisical evidence of CFR (e.g. weight loss,
poor haircoat condition, rubber jaw, growt retardation in
puppies).
Usually, physical examination of patients with ARF typically reveals good nutritional status.
Diagnostic plans should be directed toward:

MAIN PROGRAMME

Med Vet
Private Practitioner, Moncalieri - Italy

112

1) identifying life-threatening complications,


2) localizing the cause of ARF (e.g. pre-renal, post-renal or
primarly renal failure),
3) determining urine volume,
4) differentiating ARF from CRF,
5) determinig the etiology of ARF,
6) monitoring patient response to therapy.
It is particularly important to obtain an urine sample for
analysis and culture before initiating fluid therapy because
fluid therapy may cause concentrated urine to become dilute, making diagnosis of prerenal azotemia difficult. In addition, fluid therapy may alter the urine sediment causing erroneous interpretation.

4th European FECAVA SCIVAC Congress

to less than 7.10, acidosis may:


1) reduce cardiac contractility and the inotropic response to
catecholamines,
2) predispose to ventricular arrhytmias,
3) promote neurologic signs ranging from lethargy to coma.

Volume depletion
At the time of diagnosis, most patients with ARF have
some degree of volume depletion. Although volume depletion can usually be detected by physical examination, physical changes can be subtle, particularly when fluid loss has
occurred quickly and recently.

Medical emergencies in ARF


Infection
Several life threatening complications may occur in patients with ARF, they are hyperkaliemia, metabolic acidosis,
severe anemia, volume depletion, sepis.

Hyperkalemia
Hyperkalemia is a common complication of oliguric
acute primary renal failure and urinary tract obstruction. It is
less commonly associated with non-oliguric acute primary
renal failure and is rarely associated with prerenal azotemia
unless prerenal azotemia results from Addisons disease. Detection of bradycardia or other cardiac dysrhytmias should
alert one to the possibility of hyperkalemia.
Hyperkalemia is confirmed by determination of serum
potassium concentrations; however, electrocardiography
provides a rapid means of detecting hyperkalemia. Typical
electrocardiographic changes observed with mild to moderate hyperkalemia include tall, peaked T waves, slowing of
the heart rate, flattening of P waves and prolongation of the
P-R intervals and QRS complex.
Patients with azotemia, hyperkalemia, hyponatremia
may have hypoadrenocorticism (Addisons disease), in this
case the major disadvantage of administering hormone replacement therapy for ARF is that the catabolic effect of corticosteroid administration may increase the magnitude of
azotemia.

Metabolic acidosis
Metabolic acidosis is a relatively common finding in
ARF. The magnitude of renal dysfunction appears to be a
poor predictor of metabolic acidosis.
Acidosis may be more common in patients with oliguric
ARF than nonoliguric ARF, but not all patients with oliguric
ARF have significant metabolic acidosis.
Therefore diagnosis of metabolic acidosis should be
based on evaluation of blood bicarbonate (or total CO2) concentration and, if available, blood pH. Urine pH is not reliable guide to systemic acid-base status.
Clinical effects of acidosis are usually minimal unless
blood pH is less than 7.20U. However, when blood pH drops

Infection may be a cause or complication of ARF. Dilute


urine, oliguria, anuria and urinary obstruction predispose to
urinary tract infection. Furthermore uremia is characterized
by reduced immunocompetence. Because of these factors,
infection is an important cause of morbidity and mortality in
uremic patients.
Often infections are related to invasive diagnostic and
therapeutic procedures such as vascular and expecially urinary catheterisation. Careful attention to detail and intelligent decisions regarding application of use of catheters and
invasive diagnostic and therapeutic procedures will dramatically reduce the incidence of infection-related mortality.
Examination of urinalysis, urine culture, and a complete
blood cell count are indicated to rule out infection as a cause
or complication of ARF. When fever, physical examination,
or laboratory findings indicate the probability of infection,
its location and cause should be vigorously sought so that
the most appropriate and least nephrotoxic antimicrobial
therapy may be initiated.

Underlying disease processes


Patients may die of the diseases process which initiated
ARF (e.g. acute pancreatitis, sepsis, shock, hypercalcemia,
ethylene glycol intoxication) rather than from ARF or its
complications. Therefore, diagnosis and initiation of specific therapy for diseases which may have precipitated ARF
should be a high priority.
The history, physical examination and urinalysis are usually sufficient to rule-out prerenal and postrenal causes of
azotemia.

Renal biopsy
Renal biopsy may help to differentiate acute from chronic renal failure. In addition, it may provide an etiologic diagnosis and allow assessment of the potential reversibility of
renal injury. However, since renal biopsy is an invasive procedure which entails several risks, it should not be performed unless necessary. Not every patient with ARF re-

4th European FECAVA SCIVAC Congress

Prognosis of acute renal failure


The prognosis for dogs and cats with acute primary renal
failure has been generally considered poor. It is best determined by response to therapy. However, the outcome may
not become apparent for days to weeks following diagnosis.
While it is often difficult to offer an accurate prognosis
early in the course of acute primary renal failure, severe,
progressive hyperkaliemia, metabolic acidosis and uremic
symptoms are negative prognostic indicators. In absence of
these factors, patient treatment and monitoring should be
continued, even if azotemia continues to increase.

Treatment of acute renal failure


Although therapy designed to eliminate the cause(s) of
ARF will not directly result in repair of renal lesions, it will
minimize the severity and extent of renal damage. Symptomatic and supportive therapy designed to minimize deficits
and excesses in fluid, electrolyte, acid-base and nutritional
balance, will often allow life to be sustained intil the body
can restore adequate renal structure and function.
Because many of the complications of ARF are medical
emergencies, it is often necessary to initiate therapy before
diagnostic evaluation can be completed. Furthermore, treatment of ARF should be modified according to patient response to therapy, that is assessed by comparing pre-treatment and serial post-treatment data.
Patient with severe metabolic disturbances may require
frequent laboratory and clinical evaluation, whereas patients
with less severe disturbances generally require less frequent
monitoring.

Fluid therapy
Most patients with ARF are volume depleted before induction of therapy. However, the decision to administer fluid therapy should be based on clinical assessment of hydration, in order to correct volume depletion, regardless of urine volume.
Because hypovolemia and hypotension cause oliguria
and may contribute to the genesis of ATN or predispose to
further renal damage, volume depletion should be rapidly
corrected. Patients should be rehydrated with replacement
fluid via an aseptically placed intravenous catheter.
In most cases, cristalloids, like lactated Ringers solution
are satisfactory. However, if a large amount of fluid has been
lost, in order to help the increase of the blood oncotic pressure, it is advisable to administer plasma-expanders solution
(colloids), up to 20 ml/kg of body weight.
Urine volume and other contemporary losses (e.g. vom-

iting and diarrea) greatly influence fluid requirements during


the maintenance and recovery phases of ARF. Measurement
of urine volume may provide a particularly useful guide to
fluid therapy during the diuretic phase of ATN. Patients are
predisposed to dehydration during this phase because involuntary urine losses are often great. In order to prevent dehydration, the volume of parenteral fluids administered and
oral fluids, should consider also the amount of urine volume,
contemporary fluid losses and insensible fluid losses (about
20 to 25 ml/kg/day).

Therapy of potassium and acid-base


imbalance
Hyperkaliemia is commonly associated with oliguric
ARF and may cause skeletal muscle weakness, reduce cardiac contractility and cause a variety of cardiac conduction
disturbances.
If serum potassium concentration exceed 8.0 mEq/l, or if
serious cardiotoxiticy occurs, therapy with sodium bicarbonate, glucose, with insulin, or calcium gluconate should
be considered. Of these drugs, sodium bicarbonate (0.5 to
1.0 mEq/kg body weight over 15 minutes) is commonly
used first because many hyperkalemic patients also require
this drug for treatment of concurrent metabolic acidosis. Administration of glucose (20% at the dose of 0.5 to 1.0 gm/kg
body weight) and insulin (1 unit each 3 grams of glucose administered) or calcium gluconate (10% solution, not exceed
0.5 to 1.0 gm/kg body weight) are indicated primarily for
rapid correction of severe hyperkalemic cardiotoxicity.

Oliguria versus non oliguria


Therapy specifically designed to convert oliguria to nonoliguria should be considered only for oliguric patients unresponsive to fluid volume replacement. In this case use of
diuretics alone or associated with vasoldilators should be
considered.
Furosemide has been the most commonly used diuretic
in canine and feline patients. Initially it should be administerd intravenously at the dose of 1-2 mg/kg body weight. If
no substantial diuresis develops within one hour after administration, the dose may be doubled (4 mg/kg). If this dose
also fails to induce diuresis, the dose may be further increased to 6 mg/kg body weight.
If diuresis still does not occur, the combination of
furosemide and dopamine may be considered.
Mannitol is an osmotic diuretic commonly used to treat
oliguric ARF. Mannitol has at least three theoretical advantages over furosemide:
1) it may enhance renal function by minimizing renal tubular cell swelling via its osmotic properties,
2) mannitol exerts its diuretic effects along the entire
nephron and therefore may directly affect the proximal
tubule,
3) mannitol may expand the extracellular fluid volume.
The major disadvantage of mannitol is the potential for
vascular overload if oliguria persists. Therefore it should be

MAIN PROGRAMME

quires renal biopsy.


Today, with the use of automated biopsy instruments
guided by ultrasound inspection of the kidney and a correct
anesthesia protocol and technique, kidney biopsy may be
performed within a very acceptable margin of safety for the
patient.

113

114

avoided in overhydrated oliguric patients. Mannitol (20% 25% solution) is administered intravenously over 5 to 10 minutes at a dose of 0.25 to 0.5 g/kg body weight. If substantial
diuresis ensues, administration of mannitol can be repeated
every 4 to 6 hours, or administered as maintenance infusion (8
to 10% solution) during the initial 12 to 24 hours of treatment.
Because reduced renal flow may contribute to the pathogenesis of ARF, vasodilators are the logical therapy for patients with ARF. Dopamine, a precursor of norepinephrine,
has been suggested for patients that are unresponsive to osmotic and/or loop diuretics. Infusion of low doses of
dopamine reduces renal vascular resistance and increases renal flow, particularly to the inner renal cortex. Dopamine
should be administered by intravenous infusion at the rate of
1 to 3 g/kg body weight/min, using an intravenous fluid administration pump or under close supervision to assure accurate fluid delivery rate.

Dietary management
Clinical manifestations of uremia are improved by combination of a correct dietary protein amount and pharmacologic control of uremic gastritis and vomiting. It limits the
catabolic effects of starvation and may be performed also using enteral or parenteral feeding.

4th European FECAVA SCIVAC Congress

Control of uremic vomiting


Uremic gastritis is a major cause of vomiting in patients
with renal failure.
Cimetidine and ranitidine have been recommended for
control of uremic hemorragic gastritis because they block
gastrin-stimulated gastric hyperacidity. For dogs in uremic
crises, cimetidine is given intravenously at an initial dose of
10 mg/kg body weight every 12 hours (5 mg/kg for cats) and
ranitidine is administered at 2 mg/kg.
Once uremic gastritis has been controlled and oral
medication may be tolerated, cimetidine can be administered orally at a dose of 5 mg/kg every 12 hours for 2 to 3
weeks.
The dosage is reduced to 5 mg/kg given once daily for 2
to 3 weeks before being withdrawn. Dosage recommendations for cats are approximately one-half of the canine dose.
Because uremic vomiting may also result from stimulation
of the chemoreceptor trigger, intravenously administered
centrally-acting antiemetics may be useful in controlling
vomiting. However, hypotension and sedation are potential
pitfalls associated with antiemetic therapy. Chloropromazine
(0.5 mg/kg), prochlorperazine (0.13 mg/kg q 6 hrs),
trimethobenzamide (3 mg/kg q 8 hrs) are centrally-acting
antiemetics which may help to control nausea and vomiting
in uremic patients.

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115

Surgical treatment of most common diseases


of tortoises
Leonardo Brunetti

Carapace and plastron fractures


Living in home gardens tortoises are subject to injuries
caused by mowers, cars, electric gates, children and pets. As
for turtles they can easily fall down from their enclosures or
from the balconies.
These fractures have to be stabilized as soon as possible,
so its necessary to advise the owner, even over the phone,
how an emergency bandage can be done, that is by binding
up the shell with some sticky tape and keeping the animal
away from further traumas.
As soon as it reaches the veterinary practice, an inspection of the fracture and a clinical examination must be done,
to establish the reptiles general health.
If we are in front of prostrate and dehydrated subjects,
first we must give some fluids by intraperitoneal or intrabone injection.
When it is necessary we must treat the shock and the internal haemorrhage. As a cover, an antibiotic therapy is always advisable.
The success of the operation largely depends on the timeliness with which the patient is taken to the veterinary practice. Contaminated but recent fractures (1-4 hours) have a
better prognosis than the ones with a small bacterial infection but having taken place a longer time before (>4 hours).
The most frequent situation for tortoises living in gardens is when the fracture has happened 1 or 2 days before.
In this case its better to wait some days before proceeding
with orthopaedic treatment, in order to stabilise the patient
and control the infection.
Before the re-establishment, the patient must be washed
with an antiseptic solution (i.e. a soap solution of iodine
povidone). Any foreign material (soil, grass, stones) must be
removed. We can use an elevator and the anatomic forceps
to lift carefully the carapace and the plastron, where its possible, spraying the under part with a warm sterile physiologic solution.
After having removed the largest foreign materials, the
patient must be washed again with an antiseptic solution.
Every part of the patient, including the ones not interested in the fracture must be submitted to a surgical scrub, because it will be necessary to handle the whole body of the
patient, especially the smallest subjects, in the re-establishment treatment.
It may be useful to do an X-ray on the entire animal, to
highlight possible fractures on the spine and /or on bones of

the limbs.
The X-ray examination may also reveal the presence of
foreign materials.

Linear composed fractures


These are usually the easiest to treat. After having made
a careful curettage in the above described way, we stabilise
the fracture trying to keep up some pressure between the
ends of the fracture. If the displacement is small or absent, it
may be sufficient to put a cerchage wire all around the patient (Fig. 1).
However, if between fracture ends there is a certain
looseness, its possible to put a cerchage wire on detached
points along the fracture line (Fig. 2).
A different approach is necessary when the composed
linear fracture is placed on zones where the animals movement operates a particular traction on the edges of the frac-

Figure 1

Figure 2

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Med Vet
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4th European FECAVA SCIVAC Congress

ture, as for example it happens when there is a fracture between the humeral and the pectoral scutes of the plastron. In
this case its necessary to join the two techniques: 1) the detached suture stitches by cerchage wire and 2) the application of the cerchage all around the carapace. Once the fracture is stabilized, we can apply some acrylic resin for dental
use(with catalyst), or some two components vitrified stucco,
normally used for small repairs on boats and cars. This proceeding is necessary to reinforce the structure and to obtain
the impermeability of the interested zone.

Decomposed multiple fractures


We often must treat subjects with multiple fractures both
on the carapace and the plastron. In this case we must behave as if being in front of a puzzle, trying to preserve and
put together again the different pieces, in the best way, along
the fracture lines. The depressed fragments must be kindly
lifted by elevators, and the ones not connected with the vascular system removed. When the mosaic is composed, we
can go on putting the single pattern wire suture along the
fracture line trying to stabilize the structure. The cerchage
wire must be passed through two holes, previously made by
a drill, along the edges of the shell bits to be rebuilt with the
help of a wire passer or with a suitable diameter needle put
in one of the two holes to work as a guide.
In this case too, at the end of the rebuilding surgery we
must put on some resin or some other suitable material to
give a mechanical help to the shell and to keep up impermeability and asepsis in the coelomatic cavity.

loss of matter from the shell, we can hope in a complete recovery of the animal.
We use the following technique to repair the matter loss:
a surgical sponge is put inside the sinus caused by the trauma, then a piece of X-ray film is put on the sponge. This film
has already been exposed, passed in autoclave and cut according to the necessity. Some small cuts will be made along
the edges of the film to allow it to fit the shape of the tortoise
shell (Fig. 5).
The piece of film has to be longer than the shell zone to
be recovered and it will be glued along its edges by a histocompatible cianoacrylic glue or by two components epossidic resin glue. The edges of the film are then covered by
some acrylic resin (with catalyst) for dental use or vetrified
stucco (with hardener) or with a glue containing two components to keep impermeability and asepsis inside the treated area.
As an alternative we have used successfully acetate
sheets, in place of X-ray film. The desired rebuilding materials are those which offer a low heating, a strong mechanic
resistance and a low price.

BRACHIAL PLEXUS

Fractures with loss of matter


Shell lesions with loss of matter caused by mowers are
among the most frequent ones among home tortoises.
A complete neurological examination should be performed, in addition to the examination first described, because in chelonians, vertebrae are fused with dermal bones,
(Fig. 3) and a dorsal fracture of the carapace can interest the
spinal cord and the brachial and lumbosacral plexuses (Fig.
4). If the spinal cord is safe, even in front of an important

Figure 4

CORNEAL
SCUTE DERMAL
BONE
NEURAL
ARCH

LATERAL
PROCESS
CENTRUM
SPINAL
CORD

Figure 3

Figure 5

LUMBO SACRAL PLEXUS

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117

Turtles will have to remain in dry zone for weeks or


months, until they are healthy again; they are put in a clean
water pool only to eat.
Tortoises can go back to their gardens a few days after
the operation.
A chelonian having such an important trauma must not go
into hibernation during the first winter following the lesion.
Figure 6

Its necessary to cut the plastron to reach the coelomic


cavity in chelonians.
The usual approach is through abdominal and femoral
scuti but may also be cranial or caudal or lateral, depending
on the organs we have to reach and / or possible present
fractures.
A rectangular wedge must be done on the plastron by a
cutting blade. To enable the wedge to turn over, the bone and
horny layers of three sides must be completely cut, while the
ones of the fourth side must be cut only in some parts, preserving the vascolarization.
During the cutting it is vital to cool the plastron by a cold
sterile physiological solution dripping on the part.
When the bone is drifted and the periostium is taken
away the underlying abdominal musculature is showed
clearly. Now it is the moment to make an incision on the
coelomic membrane, where two venous sinuses run down on
each side of the middle line.- Be careful to save the venous
sinuses (only for drastic measures one of them may be cut).
Celiotomy may be used for a lot of procedures: dystocia,
cystotomy for cystic calculi, gastro-intestinal foreign bodies
removal, lesions of the coelomic cavity organs following
shell fracture traumas. In this particular case we always try
to reach the coelomic cavity trough the fracture lines in order to avoid further damage on the patients stiff structure.
When the surgery is finished and the wedge is placed
back in the original position some acrylic resin for dental use
has to be put on the surface of the plastron.

Surgical treatment of penis prolapse


Penis prolapse is rather frequent both for turtles and tortoises. Normally the organ prolapsed for physiologic or
pathologic causes may have an oedema with a probable consequent paraphimosis.
If we are lucky and the animal is taken in time to the veterinary practice, so that the paraphimosis interested tissues
are in good condition, it is possible to place back the penis.
At first it is necessary to wash carefully the wounded
area with a chlorhexidine soap solution, then the organ has
to be sprayed with a sterile physiologic solution. Now we
proceed with a compressive manual pressure to reduce the
oedema and contemporaneously we have to push the penis
inside the cloaca. This operation is often difficult, but it is
necessary to repeat it many times until we are successful.
When the organ is replaced we have to put one or two sutures on the cloaca opening to tishten it, in order to avoid another prolapse (Fig. 6). The residue opening cloaca has to be

sufficient to permit the passage of fecal and urinary product.


The suture will be left in situ for 2-3 weeks. During this period the original causes of prolapse must be found and resolved.
When the patient is taken too late to the veterinary practice and there are some ulcerated and necrotic areas on the
surface of the prolapsed penis, it is necessary to cut the organ off. This amputation doesnt cause any urinary problems
because a reptiles penis has only a copulative function and
it doesnt contain the urethra.
The surgical technique is rather easy: the organ which
has a seminal groove, being kept in physiological position,
is held by an assistant and a continuous pattern mattress suture is applied on its base, then the suture has to be tightened. At this point it is possible to cut off the necrotic part
but there are some devices to consider:
1) the suture must be done with very close sutures to control
the haemorrhage caused by the resection of penis sinus
bodies.
2) an end of suture material must be left to hold it by a mosquito, so as not to lose the organ in the cloaca when we
are replacing it back and to control possible haemorrhages of the penis remaining part.

Surgical treatment of cloacitis


Female tortoises living in small gardens together with a
lot of males often present some cloacitis for the too frequent
coupling.
Cloacal lesions are often complicated by miasis.
The surgical treatment of cloacitis consists in removing
necrotic tissues and every larvae by an accurate curettage.
Then we have to reconstruct the cloacal orifice.
The suture material used is nylon monofilament. Sometimes an anal scutes plastronectomia is necessary, to have
easy access to the cloacal zone.
Sutures will be left in situ between 20 days and two
month, depending on the recovery time.
It is opportune to keep only one male with 4-5 females in
the same garden to prevent this usual pathology.

Surgical treatment of abscesses


Abscesses are rather usual in chelonians where they appear as firm lumps under the skin or under muscles in various zones, especially in the auricular regions (turtles) and in
axillary, inguinal and pericloacal zone (tortoises).
Surgical treatment is necessary because, unlike mam-

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Celiotomy

118

mals, neutrophili granulocytis are not able to colliquate the


pus, permitting a spontaneous draining outside.
The abscess will be completely removed, being careful
to cut off the capsula. We make an incision on the skin above
the lump, and we isolate the lump after drying up the surrounding tissues. The remaining cavity will be sutured with
nylon monofilament and the sutures will be removed 2 or 3
weeks after.

4th European FECAVA SCIVAC Congress

If some delicate structure is present near the lump, we


can use an alternative technique. After cutting the skin above
the lump we take away the infected solid matter with a
Wolkmanns spoon or other adequate instrument. Then we
wash the cavity with a solution composed of hydrogen peroxide, iodopovidone (or chlorhexidine) and physiological
solution, 1-2 times a day for some days. In this case, it can
be unnecessary to suture the remaining cavity.

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119

Ultrasonography in the diagnosis of the urinary tract


diseases in dogs and cats
Claudio Bussadori

The ultrasound examination is a rapid and secure technique, which allows a valuation of the position, dimension
and the parenchyma morphology of the organ in exam.
This methodic by now is large diffused and constitutes
the preferential techniques of imagine of the urinary apparatus, as it reveals, respect to the radiology, a major sensibility and specificity in the diagnostics of the urinary and
nephrological pathologies.
The ultrasound examination can be also used to guide the
withdrawal of bioptic samples through percutaneous way,
which permits histological examinations in a bloodless manner.
The observed pathology alterations can be classified in
many standards: in this specific case we applied the classification on the ground of the structural modifications which
are pointed out in ecografy, considering the different pathologies who can determine them. Since there are not described
some pathology aspects of ultrasound examinations, these
are been located in the classification on the ground of the
macroscopic or microscopic modifications and the analogy
with other pathologies which echografic aspects are known.

tern. The echogenicity is correlated to the cellular type,


which are involved, to the vascular system, to the grade of
haemorrage and to the presence of necrotic phenomenons.
The solid uniform hyperechoic masses can have an aspect
similar to the cysts, without demonstrating lateral acoustic
shades and posterior reinforcement, but with an evident survey of the internal echoes increasing the gain. The lesion of
the lynphosarcoma, the tumor most common of the cat is
characteristic of a weak vascular system, are ipoecogen. The
hypoechoic lesion has a connective tissue or mineral deposit: among these are part of it, the calcification, the infarct,
the fibrous zone and the gathering of gas.
The type of complex mass lesion shows a mosaic of different echogenic areas: in differential diagnosis we can distinguish tumors, granulomas, organized haematoms recent
infarcts. The most tumor types, described with vary echopattern in small animals are haemangiosarcoma, renal blastoma, adenocarcinoma, condrosarcoma, cancer or papilloma
of transit cells.

Diffused lesions
KINDNEY
Parenchyma modification of the kidneys.
Focal cyst lesion
The cystic renal lesion includes a group of hereditary and
acquired diseases, often verified on occasion. The renal cyst
are most roundish with thin and regular walls and the contains without echo frames; they are characterized by the
presence of artificials which are the reinforcement of the
posterior walls and the refraction.
The distinction treated from the human medicine between polycystic autosomic recessive or infantile renal disease and policystic autosomic dominant renal disease or of
the adult can be adapted in veterinary medicine to the feline
species in which this pathology is frequent.
Other tumors localized with characteristics alike the
cysts are the haematomas and the abscesses.

The solid focal lesion


This kind of lesion can have an hyperechoic, hypoechoic
or isoechoic aspect with a regular or subtle sonographic pat-

The renal cortex can present itself hypoechoic, like the


lynphosarcomatic infiltration or iperechogenic, like the Ethylene Glycol Toxicity, in the interstitial and glomerular
nephritis, in the acute tubular necrosis, in the nephrocalcinosis, and in the renal sclerosis.
It has also been signalized in the lynphosarcoma of cats
and the infective peritonitis.
Sonographic findings includes focal hyperechoic of the
corticomedullary junction but it is considerated a characteristic lesion of the Ethylene Glycol toxicity (medullar rim
sign). We can also observe it in the vasculitis due to the
FIP, in acute tubular necrosis and in interstitial chronic
nephritis.

Volume decreasing Sclerosis


- With loosing of the distinction between the cortical and the
medullar.
We observe it in the renal displasia, which is the result of
a disorganization of the organogenesis probably for a hereditary autosomic recessive character.

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Med Vet, Dipl ECVIM


Private Practitioner, Milan - Italy

120

In the policystic kidney with microcysts the presence of


lots of little interfaces can determine a diffused hyperechogenicity without any distinction between cortical and
medullar.
- With decrease of the cortical-medullar correlation.
We find it in pathologies with a progressive course, like
the tubule-interstitial nephropathology of the Norvegian
Elkhound and the Fanconi del Basenji Syndrome.

PELVIS
The ultrasound examination is certainly indicated as the
gold standard examination when there is a suspect of pathology of the first part of the urinary duct.
It is possible to find physiologic symptoms of pyeloectasia (how it happens in the diuresi caused of drugs or pathologic symptoms (how it happens in the case of traumas, obstruction of the urine flow, infective pathologies).
An other frequent pathology in cats and dogs is the hydronephrosis, or rather the dilatation of the pelvis and the calyx secondary to the urinary accumulation caused of obstructions: it is important to distinguish the renal vein in the
presence of a possible extended urinary duct (control the expectoration of the vena cava).
To be able to distinguish the pyeloectasia caused of an
obstruction from a pyeloectasia which has not an origin obstructive, like the obstructive pyelonephritis, it has been estimated in the dog the use of the resistivity index (RI) or
Pourcelot index (you reach out to it dividing the difference
between the systolic top speed with less diastolic speed multiplied with the systolic top speed measured out at the level
the arcuate artery): recently the results are pointing out a low
sensibility and specificity with an high percent of falsehood
negatives, even if it is spotted that the falsehood negatives
could be lower in to 24 hours after the obstruction.
It is possible to express a diagnosis of pyelonephritis
when there are present contemporary two or more of the following signs: dilatation of the pelvis or the proximal part of
the urinary duct, presence of an hyperechoic bed in the
pelvis or in the proximal part of the urinary duct, hypo or
hyperechoic areas in cortex or medullar, loss of the differentiation corticomedullar.

URINARY BLADDER
The bladder for its anatomical position and for its anechoic contents is fit for an ultrasound examination. In the
condition of physiological or artificial fullness, constitutes
an excellent acoustic window and besides represents an important point of reference.

4th European FECAVA SCIVAC Congress

mally indicative of cystitis. We can see urinary polyps in the


bladder wall, typical of the polypoid cystitis or else a neoplasm eziology: these proliferations have to be differentiated
from blood clots adherent to the wall, trying to determinate,
with a patient rotation, with localized abdominal wall compression with the sonographic sound or with a bladder washing with sterile saline a neoplasm shifting that happens if it
is an haematomic agglomerate. In case of neoplasm it can be
associated a certain disorganization of the wall architecture.
Its important that the wall investigation is done accurately, to evidence localized thickness (usually cranioventral) that means cystitis and parietal diverticul presence:
these can be hereditary or acquired, have to be accurately analyzed to find the presence of neoplasm or calculus inside
the diverticolo. Since infect the diverticulum wall is deprived of the muscular component it results an almost always partial emptiness, favoring the persistence of oncogenic stimulus contact to the diverticolar urothelial mycoses
or easier the appearance of chronicle or recidivist infection
of the urinary ways.
The convex bladder wall determinates the appearance
of an artificial due to the sound refraction that simulates a
continuous interruption that disappears changing the sound
orientation.
The vegetating forms appear as solid and homogeneous
structures, with an echogenecity lower than the echogenecity of the bladder wall, with plant base such large to interrupt the continuity of the bladder inside jetting out into
the inside of the viscera.
For now infiltrating neoplasm determinate a thickness
and a rigidity of the bladder wall with an alteration of the
echografic structure: these can present a redoubt component
of the bladder lumen and are difficult to identify.
The possibility to evidence a neoplasm depends essentially of the dimension (the sonographic threshold to evidence a neoplasm are 5 millimeter) and of its seat (the neoplasm which are localized in the neck of the bladder are difficult to identify). Its easier to find the neoplasm localized
in the caudal part of the urinary bladder and trigone, rarely
in the cranial part of the urinary bladder.
If we examinate the cranial part of the trigone sometimes
its possible to recognize the intraparietal part of the urethras
which can be confused with neoplasm, because it appears
like a little convex form with regular walls: for that it is useful to observe if there are coupled structures and to point out
the turbulence created by the urinary peristaltic waves by
coming out the uretery outlets. The persistent uraco that goes
to the umbilicus can appear as a diverticulum or as an anechogic tubular structure cranial to the bladder; the uracal
cysts usually cranial of the bladder have thin walls and anechoic contents.

Contens
Bladder wall
The bladder wall appears as a reflecting line without any
discontinuity, whose thickness varies with the state of fullness: it is important to considerate pathologic only a substantial increasing of thickness in an expanded bladder nor-

Normally the urine is, as said, anechoic: presence of


blood or other fine urinary sediment can generate inside diffused, pointed formed echoes, which go slowly to sediment.
This phenomenal must not be confused with artificial due to
the wrong position in the bladder lumen of echoes borned

outside of the ultrasound bunch periferic portions structure:


this artificial shows as an echigenic band parallel to the dorsal bladder wall, similar to sediment deposit, which is not
possible to resupend shaking or balloting the bladder, which
doesnt move changing animal position and modifies itself
with the sound orientation.

121

The gas inside the bladder normally hyatrogen origin, is


hyperechoic, creates reverb and moves itself to an higher position: if the animal is in a dorsal recumbence it can be confused with the proximal sound reverb; in this case it can be
used a spacer or easier it has to be reexamined the animal in
standing position.

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123

Pathophysiology and treatment


of pericardial diseases
Claudio Bussadori
Med Vet, Dipl ECVIM
Private Practitioner, Milan - Italy

Anatomy and functions of the pericardium


The pericardium holds the heart and is composed by an
external part or lamina parietalis pericardii and an internal
part or lamina visceralis pericardii: the pericardial space
contains normally a small amount of serous liquid (0.5-15
ml in the dog). Although it is not an essential anatomic
structure, it is able to perform important functions: containment and protection of the heart, limitation of the acute dilatation, maintenance of the cardiac geometry and of the
ventricular compliance, modulation in the ventricular diastolic refilling phase, protection of the heart from infections
or adhesions, increasing of the diastolic relation between the
two ventricles.
The measurements of the intrapericardial pressure of a
normal heart is, unfortunately, not easy to obtain: this value is nevertheless very important in the study of pericardial
diseases. At this subject it is important to remember that
the transmural pressure of each ventricle is obtained by the
difference between the diastolic intracardiac pressure and
the intrapericardial and is independent from gravity. The
intrapericardial pressure is strictly connected to the right
atrial pressure and is comparable to the filling pressure of
the right ventricle when in a range between 0 and 20
mm/Hg. This value emerged from the utilization of intrapericardial balloon catheter (Santamore) which have
been demonstrating how, in a normal heart, the catheters
with open lumen were underestimating the values of the
pericardial pressure.
Moreover the pericardial pressure is not homogeneous in
each cardiac segment, but is higher at the level of the free
wall of the left ventricle (Hoit). It is not the pressure of a liquid which has to be equal in various regions, but it is a contact surface pressure, which means the pressure of a liquid
plus its deformation powers.

Etiology of pericardial diseases


The pericardial diseases in the dog are distinguished in
congenital (pericardial agenesia, periton-pericardio-diaphragmatic hernia) or acquired: this last ones can be classified depending on the type of effusion, which can be transudative (congestive heart failure, cysts, hypoalbuminemia
or other reasons of increased vasal permeability), exudative: infectious diseases, particularly bacterial and mycotic,
while the viral pericardial pathologies are more common in
bovine and feline species, the pericarditis in uremic syndromes are more frequent in the human species. Bleedings
occur in neoplasm: cardiac tumor, tumor of the heart base,
hemangiosarcoma, receptoma, pericardial celioma, lymphosarcoma, in idiopathic benign pericarditis, external trauma or heart rupture.
In the dog the major causes of pericardial effusion are the
neoplasm forms and the benign idiopathic pericarditis. The
definition benign is refereed to the human pathology while
in the dog this pathology frequently causes heart tamponade:
the etiology of this form is unknown in both species, even if
hyphotesis suggest an immunological genesis in both species.

Pathophysiology
The haemodynamic effects of the pericardial effusion are
related to the volume of the fluid, the compliance of the myocardium and the time that occurs. The physiological intrapericardial pressure in dogs varies around the values of atmosphere pressure (from -3.8 to 3.8 mm/Hg): this condition
enables the cardiac filling especially in the inspiratory
phase. After the gathering of fluid in the pericardial cavity
the intrapericardial pressure increases, joining first the atmosphere pressure and then further on to higher values,
while in the meantime there is an increasing of the right ventricle diastolic pressure.
The cardiac tamponade is a clinical syndrome, which
generates a cardiac emergency: it develops from an uncontrolled increasing of the intrapericardial pressure, this limits
the ventricular compliance which causes a significant obstacle to diastolic filling.
The pericardium is extremely resistant to acute stretching, while it is able to extend in a progressive way if the
stretching is continued. So this is the reason why even a
small increase of pericardial fluid developing suddenly can

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The author describes pathophysiology and the more


common causes of pericardial diseases furthermore are described guidelines for clinical and Echo-Doppler diagnosis
and staging of pericardial tamponade.
For treatment are described the most utilized medical
therapy and the technique of percutaneous pericardiotomy
using balloon catheter.

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lead to a severe cardiac tamponade, while an effusion of two


or more liters which accumulates slowly can associate only
with a small increase of intrapericardial pressure causing
better tolerated haemodynamic effects.
In slowly developing effusions we have at first only clinical signs of right cardiac failure and only in the following
phases of the process we have the clinical signs of emergency. The intrapericardial pressure increases then until it
causes a critical compression of the outside of the cardiac
walls, able to induce a diastolic collapse of the right atrium
and ventricle and the reduction of the ventricular volume followed by a systolic deficit of the left ventricle, inducing an
hypertension of the venous district and a hypotension of the
arterial district with severe compromise of cardiac output.

Clinical signs
The symptoms depend on the seriousness of the cardiac
tamponade. Slight tamponade in its initial phase can be
asymptomatic.
During an acute tamponade the clinical signs are particularly severe. We can have the lost of the cardiac impulse at
the palpation of the thorax, at the auscultation we have either
paraphoniac tones or tones that can not be detectable, noises
caused by preexistent murmurs, which sonorous is muffled
from the sonorous vibration caused by the passage through
the pericardial fluid.
A typical symptom is the paradox pulse, a huge decreasing (> 10 mm/Hg) of the arterial systolic pressure during inspiration. This phenomenon follows the reduction of the systemic venous drainage and the filling of the right ventricle
followed by reduction of the left filling and output. Central
venous pressure can, on the contrary, increase in the inspiratory phase determining a huge distention of the jugular veins.
To this clinical signs we can have the symptoms of a
backward heart failure like the enlargement of liver and
spleen and hepatojugular reflux. The decreased cardiac output causes also a secondary peripheral vasoconstriction,
with pallor mucosae, delay in the capillary filling, cold extremities (forward heart failure).

Electrocardiography
Electrocardiogram alteration are not pathognomic, but
are anyway significative if coupled with clinical signs and
enables the doubt of pericardial effusion. We can have voltage reduction of the ventricular complex (R<1 mV in D2)
associated to a normal a wave upper level of the ST segment
with under level of the P-R tract when even the atriums are
compromised. We can also observe phenomenon of electrical alternations, or cyclic variations of the QRS amplitude
due to the swinging of the heart inside the overdistended
pericardium (swinging heart).

Radiology
Moderate or massive pericardial effusions determinate

particular radiological alterations: the cardiac silhouette


shows an increasing of the transverse diameter without enlargement of the heart base. The profile of the cardiac shadow assumes a globular aspect without any sign of the auricles or of the atrioventricular junctions. The increased size
of the cardiac silhouette with its characteristically pumpkin shape is not proportional to the amount of liquid contented in the pericardium; in the same time the detection of
pleural effusions and hepatomegalia suggest a chronic
process. At the radiological examination of the thorax we
can also see the signs of the venous congestion and of the
low range, we can observe evident dilation of the caudal vena cava and the pulmonary veins while the pulmonary arteries are decreased and the lung appears hypovascular and radiolucent.
Before the advent of the echocardiography there was a
radiological method, called the diagnostic pneumopericardium, in this method there was the introduction, after pericardiocentesis, of atmospheric air or carbon dioxide in the
amount of half or less of the drained fluid, in that way it was
possible to obtain a good negative contrast for a radiological
study of the silhouette. This diagnostic proceeding can be
very helpful when there is a suspect of an effusion due to a
tumors etiology.
In those cases the association of a non selective angiography enables us to evidentiate the profile of the cardiac
chambers and of the big vessels, to better define the intrapericardial structure and their anatomical belonging.

Echocardiography
The echocardiogram is surely the technique that better
shows diagnostic utility, because it is highly specific and
sensible in the detection of pericardial effusion. In normal
conditions the pericardium is not visible as a distinct structure: if there is an effusion we have an anaechoic space between the echo reflected from the visceral pericardium and
the one reflected from the parietal pericardium, while they
normally reflect a single echo together.
Besides the detection of an effusion, echocardiography
consent to see the entity, the distribution and the grossly
physical characteristics of the fluid examined (for example
corpuscolated material). But an evaluation of the echodensity of the fluid within the pericardium depends too much on
the regulation of the echocardiographic instrument to be fully reliable, while the evidence of a lacertus fibrosus suggest
chronic inflammatory effusions or sometimes pericardial tumors like celiomas. A solid granular figure can lead to an intrapericardial hematoma, solid masses adherent to one of the
layer or infiltrating suggest tumors effusions. Echocardiography also grants an accurate evaluation of the level of the
haemodynamic commitment.
An important echocardiographic find is represented by
an excessive diastolic relation or a variation in concomitance
with the respiratory acts and the kinetics of the interventricular septum: the septum in the inspiratory phase, moves towards the left ventricle and in the espiratory phase, towards
the right ventricle. In other words, during the inspiration the
right ventricular cavity enlarges its volume, due to the in-

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Constrictive pericarditis
The diagnosis of chronic cardiac compression presents
great difficulties what allows to think that this pathology is
in effect more common of what it is believed, and that often
it is not identified, but it is important to identify this illness
because also if it has a particular severe prognosis in most of
the cases, it is surgically treatable. In this illness the clinical
signs of a commitment of the systemic and pulmonary venous drainage are evident as in the cardiac tamponade, but
only the echocardiography allows an non invasive diagnosis
of chronic cardiac compression, the bidimensional exam
shows a hyperlucent and a thickened pericardium, although
in truth, this report is extremely dependent from the operator, instead there is always an evidenced biatrial enlargements with normal seized ventricles. With the M-mode the
left ventricle shows a backward movement of the septum in
early diastole (early diastolic dip) and a fast early diastolic
excursion of the posterior wall; this aspect of the early diastolic phase shows that the left ventricle suddenly fills in protodiastole while subsequently the filling interrupts. We can
see a flattening of the posterior wall in mid and late diastole,
which represents the haemodynamic corresponding of the
square root sign.
The Doppler exam highlights a sharp deceleration of the
transmitral and transtricuspidal diastolic flows, this report is
common to restrictive cardiomyopathy, but in this last one
we do not have an inspiratory reduction of the flows which
is quiet evident in the constrictive pericarditis.

Treatment
The ultrasound tecnique enables a correct therapeutical
approach for the percutaneous pericardiocentesis, which
represents the procedure used for the stabilization of the patient in the acute phase and the resolution of the pericardial
tamponade. The method we use in those cases provides, if
the conditions of the patient allows it, the positioning of the
dog in a right lateral recumbency on a special table for
echocardiography, if the patient is not able to tolerate the recumbency this procedure can be performed with the animal
in a sitting or standing position. Under echographic guide a
needle of 18G is connected to a tube extension to a large syringe, the needle is introduced in the right forth intercostal
space under the costochondral junction, and through this
system it is possible to introduce physiological solution in
the pericardial sac in order to contrast the area containing the
tip of the needle. We chose the right approach because from
this side there is no risk of injury at the coronary vessels.
If this should be necessary, due to the relapse of the heart
tamponade, a second pericardiocentesis, can be considered.
In idiopathic pericarditis in order to obtain a radical resolution of the illness, and to avoid the evolution toward
chronic cardiac compression, we suggest a surgical subtotal
pericardiectomy, this can be executed in a traditional thoracotomy approach or through thoracoscopy.
In older dogs or animals in critical conditions, so that
they can not be subordinated to surgery we have used percutaneous pericardiectomy tecnique with a balloon catheter

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crease of the venous drainage in concomitance with the reduction of the left ventricular dimensions, the flattening, and
the dislocation of the septum towards the left ventricle. This
irregular movement is called the diastolic paradox septum.
Unfortunately it is not easy to measure this echocardiographic element and moreover it is not pathognomic for
pericardial effusion, but only for a diastolic compromising
of the left ventricle, which can occur also in other pathologies that causes an increasing of the right ventricular pressure like pulmonary hypertension, or pulmonary stenosis.
Better correlated to the relation between intrapericardial
pressure and right atrial pressure are the late diastolic collapse of the right atrium and the early diastolic collapse of
the right ventricle: with the increasing of the pericardial
pressure the right ventricle tends to remain longer in the diastolic phase. This echocardiographic signs are extremely
early and represent the beginning of the real cardiac tamponade, which start to express only when the intrapericardial
pressure, equalizing the diastolic pressure of the right atrium
causes its compression.
Another early echocardiographic sign of pericardial tamponade is the absence of the physiological reduction of the
diameter of the caudal vena cava during the inspiratory
phase, that should be around 50%: this phenomenon is
called vena cava plethora. This fact is strictly correlated
with the values of atrial pressure, index of vena cava collapsing lower than 35% is showing high values of right atrial pressure (Pepi).
The excursion of the caudal cava vein is appreciable and
measurable through a series of monodimensional scans, possibly obtained slowing the speed of sliding and detected at
the height of the diaphragmatic caval hiatus during the respiratory phases. The caval plethora is a very sensible echographic sign to point the venous drainage impediment, unfortunately not specific for cardiac tamponade, but only for
an important right diastolic dysfunction. Using the Doppler
method enables quantitative assessment of the inspiratory
reduction of the transmitral and transaortic speed of the fluid, associated to delayed opening of the mitral valve (in correspondence with the atrial systole) and a premature closing
of the aortic valve. (Appleton) (Schutzman).
Physiologically the aortic and transmitral flow have no
respiratory variation or if they have, only minimal (5%). In
the heart tamponade we can see respiratory reduction of the
mitral and aortic flow more than 25%, clear evidence of the
massive diastolic relation that occurs in the heart tamponade.
Analyzing the transmitral diastolic flow with the
Doppler, we can also highlight a reduction of the amplitude
and duration of the E wave, expressing a diastolic impediment in the first phase of the ventricular filling, or like in the
severe forms, were this only happens when we have the atrial contraction. In the massive forms the left ventricular filling is almost exclusively caused by the atrial contraction. In
physiological conditions the atrial contribution to the diastole is not higher than 25%, while in this cases it determinate
over the 50% of the diastolic volume: this phenomenon is
detected by the Doppler with a decreasing of the E/A ratio
and an increasing of the ratio between the A area and the integral of the whole transmitral flow. (Appellation).

125

126

(Cobb). This tecnique is executed under fluoroscopic control


with the dog in right lateral recumbence and after sedation.
With the help of the echographic guide the point were the
catheter will be introduced is chose, and in this point we
practice a local anesthesia, taking care to also include the
pleura parietalis. Then we introduce a needle of 16G through
the thorax wall to the pericardium, through this needle we
introduce in the pericardial sac a metal guide wire of 0.038
inches and 150 cm length, and through this guide we pass a
vascular dilator of 8 French until the pericardial sac, finally
removed the dilator, through the guide wire we introduce the
balloon catheter, the deflated balloon is placed through the
pericardial sac. For this use we need balloons that once inflated reach the diameter of 2-3 cm and the length of 4 cm.
The inflating of the balloon is executed with a 50% physiological solution and a contrast medium, the balloon is first
partially inflated, what enables us to highlight through fluoroscopy the depression on the balloon caused by the pericardial sac, if necessary we can move the balloon back and
forth. The balloon is then completely inflated until the waist
on it disappears, and kept like that for 2. This procedure has
given good results as a palliative therapy in tumors pericardial effusions, allowing the liquid formed in the pericardium
to pour in the thorax and to be reabsorbed.
In the benign idiopathic pericarditis with a possible immunological etiology there have been used many pharmacological therapies in order to reduce the immunitary response,
like corticoids, prednisolone 0.5-1 mg/kg. We experienced
(10 patients) the administration of azathioprine orally 1
mg/kg SID for a three months period after the first pericardiocentesis or in subjects which presented relapse after a
short time from the second pericardiocentesis.
During the treatment with Azathioprine we did not highlight secondary effects, besides a modest anemia and leu-

4th European FECAVA SCIVAC Congress

copenia. At this point of time in neither one of the subjects


treated there has been a relapse of important pericardial effusion.
The validity of this therapy surly needs further confirmations with treatments for a longer period of time and
groups of animals of greater numbers besides groups treated
with dummy.

Bibliography
Appleton C, Hatle L, Popp R: Cardiac tamponade and pericardial effusion:
respiratory variation in transvalvular flow velocities studied by
Doppler echocardiography. J.A.C.C. 1988;11:1020-1030.
Assanelli D, Lew W, Shabetai R, Le Winter M: Influence of the pericardium on right and left ventricular filling in the dog. J. Appl. Physiol.
1987; 63:1025-1032.
Cobb M.A. Boswood, G.M. Griffin and McEvoy F.J. Percutaneous balloon
pericardiotomy for the management of malignant pericardial effusion
in two dogs. Journal Small animal practice 1996; 37: 549-551.
Gibbs C, Gaskell CJ, Darke PGG, Wotton PR: Idiopathic pericardial hemorrage in dogs: A review of fourteen cases. J. Small Animal Pract.
23:483,1982.
Lopez-Sendom J, Garcia Fernandez M, Coma Canella I, Sotillo J, Silvestre
J: Mechanism of right atrial wall compression in pericardial effusion:
an experimental study in dogs; Journal Cardiovascular Ultrasonography 1988; 127-134.
Pepi M, Tamborini G., Barbier P., Doria E., Ecografia nello studio della fisiologia e della patologia del pericardio. Giornale Italiano di
Ecografia Cardiovascolare. Vol 4, N1 Marzo 1994.
Reed J.R. Pericardial diseases in Fox, Canine and Feline Cardiology
Churchill Livingstone 1988.
Santamore W, Constantinescu M, Little M: Direct assessment of right ventricular transmural pressure. Circulation 1987;75:744-747.
Schutzman J, Obarsky T, Pearce G, Klein A: Comparision of Doppler and
two-dimensional echocardiography for assessment of pericardial effusion. Am J Cardiology 1992; 70:1353-1357.
Sisson D, Thomas WP, Ruehl WW, Zinkl JG: Diagnostic value of pericardial fluid analysis in the dog. J Am Vet Med Assoc 184:51, 1984.

4th European FECAVA SCIVAC Congress

127

Disseminated intravascular coagulation:


State of the Art
Marco Caldin

Diagnosis of DIC, as well as many other aspects of this


fascinating intermediary mechanism of disease, is still a
rather complex phenomenon. We learned through the analysis of the DIC cases - as described in literature and through
ones we considered - that doesnt exist a single sign either of
laboratory or clinic, which can prove the existence of such a
clinical condition. Moreover often there are no correlation at
all between clinical-laboratory signs and autopsy findings.
That is why the diagnosis of DIC is a challenge for the internist who must evaluate critically clinical and laboratory
manifestations. For the clinical point of view in order to hypothesise the DIC, there must be a clinical entity able to
cause it. From the laboratory side the results must be evaluated in relationship with their sensibility and specificity towards the DIC.

then, exceeds the normal physiologic answers of compensation. Whereas in course of a low-grade DIC (compensatedchronic), the alterations are often only of the laboratory
kind, because the comsumption of the coagulant factors is
balanced by an increased production. Nevertheless the evolution from a phase to another, such as from normal to fulminant DIC, is very fast. This points out the dynamism of
the hemostatic balance.
Thrombotic manifestations, which are more difficulty visualized, bring to the production of microthrombes and
macrothrombes, that produce damages and sometimes a real
failure of the organs involved. Together with organ failure,
systemic signs of shock and metabolic acidosis appear deriving from a reduction in the tissue perfusion.

Laboratory features
Clinical features
Clinical signs deriving from DIC are generally those associated to the thrombohaemorrhagic disease. We must consider that it is quite easy for the physician to diagnose haemorrhagic events while it is more difficult to recognise the
thrombotic signs so our comprehension of the problem is only partial. We must add that the clinical picture shows also
the clinical signs deriving from the disease that has caused
the DIC. For that reason it is sometimes difficult to distinguish between cause and effect, that is to say between the
disease and its effects, i.e.,It is common the onset of liver
failure when there is a fulminant DIC, but it is also true that
liver failure is often the cause of the DIC.
The clinical signs combined with the haemorrhagic event
can be such as petechiae, ecchymosis, subcutaneous
haematomas, hemorrhagic diarrhoea and vomiting, hematuria, excessive post-traumatic (or post venipunctures)
bleeding.
According to our experience, hemorrhagic body effusions rarely are due to a DIC. When the clinician finds a hemorrhagic body effusion with laboratory signs of DIC
he/she must go on looking for the cause of it, since hemorrhagic manifestation depends from specific causes. In this
case the DIC emphasises the hemorrhagic events. Tipical example is the spleen hemangiosarcoma with abdominal effusion. Hemorrhagic manifestations are more frequent when
there is a fulminant DIC (decompensated-acute), when the
dynamic of the coagulation process first, and hemorrhagic

Data base (hemogram-biochemical profile-urynalisis) are


essential tools for a interpretation of the coagulative alterations. The data base often point out causes and the effects in
the DIC. As we said above, there is no single test able to diagnose the DIC. Nevertheless the laboratory tests are very important to evaluate the existence of the DIC. Unfortunately, as
far as we know, in veterinary licterature they are seldom considered in relation to their sensibility and specificity towards
the DIC. Besides the increasing number of the diagnostic
markers make us evaluate critically not only the new tests but
also the more traditional ones which have been revalueted in
the light of what we know. The data here reported refer to 71
DIC cases, analysed by one of the authors (M.C.).

Prothrombin time (PT)


Prothrombin time represents a global test which measures
the extrinsic pathway1 and the common pathway. It represents a direct measure of the factors I, II, V, VII, and X. When
one or more of these coagulation factors goes down to an
amount considerated critical (50-60 %), there in an increase
in PT. In the DIC the PT gets longer for different reasons:

Attualmente la divisione in due cascate coagulative ritenuta sorpassata


data la ormai comprovata relazione tra fattore VII e IX.

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Med Vet
Senior Lectures, Faculty of Veterinary Medicine, University of Padua - Italy

128

A. consumption of the factors involved in the extrinsic pathway and specially in the common pathway (fibrinogen).
B. Inactivation of the factors V and IX caused by the plasmin
C. Interference with fibrin monomer polymerization caused
by the FDP.
Sometimes in the DIC we assist also to a shortening of
the PT, because of the activated coagulation factors (thrombin and Xa).
In our research the PT has demonstrated a sensibility of
29% on 71 cases and it has also demonstrated a specificity
of 30%, showing the tendency to be alterated in the fulminant DIC together with the fibrinogen and platelets.

Activated partial thromboplastin time


(aPTT)
Activated partial thromboplastin time represents a global test which measures the intrinsic pathway 1 and the common pathway. It represents a direct measure of the factors
XII, XI, IX, VIII, prekallikrein, HWMK and more approximately of the factors I; II, V and X. In the DIC the lengthening and the shortening of the aPTT occurs for the same
reasons described for the PT. In our study the aPTT has
demonstrated a remarkable sensibility (73%), in spite of a
low specificity (30%), with the tendency to be alterated either in the fulminant DIC or in the low grade DIC. The great
sensibility of this test is probably due to the fact that the
aPTT evaluates in a more detailed way the intrinsic pathway,
which is mainly involved in the consumption of the coagulation factors.

Fibrinogen
During the DIC there is the consumption of fibrinogen
by the activation of the coagulation system which leads to its
trasformation to fibrin with diffuse thrombosis. Even if this
event occurs almost steadily, many times it does not determine a recognizable hypofibrinogenemia. This is due to a
considerable capacity of the hepatic synthesis in an acute or
chronic inflammatory process, when the liver increases the
synthesis of this coagulation factor concealing the consumption process. Furthermore collocation of fibrinogen to the
acute phase proteins may trasform this coagulant factor in a
protein sensible to other events different from the coagulation.When the fibrinogen level reduced at 75-100 mg/dl,
there is a lengthening of the PT and aPTT, and the PT seems
more sensible than aPTT to the hypofibrinogenemia. In our
series of 71 cases of DIC, fibrinogen appears of low sensibility (11%) but with a fairly good specificity (80%). Probably this depends by the low number of diseases that can reduce it (e.g. liver failure). Hypofibrinogenemia becomes evident during the fulminant DIC and it occurs a short time before the platelets consumption. If -in order to measure this
coagulation factor- we use a laboratory method based on
trasformation of fibrinogen to fibrin it can happen that artificious low values are recorded. This is due to the interference of the FDP in the conversion of fibrinogen into fibrin.

4th European FECAVA SCIVAC Congress

Thrombocytopenia/thrombocytopathia
In the DIC the low platelet count is due to the activation
of the coagulation process that causes the formation of microthrombes in the vascular bed. However as in the fibrinogen model,the presence of the inflammatory processes causing the DIC, or developping together with the DIC, can produce a reactive thrombocytosis that conceals the low level of
platelets.
High levels of platelet factor 4 and beta-thromboglobulina, document this fact, also if these markers are not pathognomonics. The alteration of the functional platelet is another aspect following the DIC.This is caused by the FDP coating of platelet membranes or the partial release of platelet
procoagulant material. Tests performed to document this fact
(bleeding time and platelets aggregation), have a unfavourable relationship between cost and benefit. In our series of 71 cases of DIC, a low platelets count shows a 13%
sensibility and a specificity of 90%, with the tendency to appear in fulminant DIC together with hypofibrinogenemia.

Schistocytes
Schistocytes, or red cell fragments, are end result of the
mechanical damage of the plasmatic membrane of eritrocytes against intravascularly fibrin strands. This event its
well documented by Bull and coworkers and it is more frequent in low-grade DIC. In fulminant DIC, often, the
process its so fast that there is not enough time to create a
extensive damage of the red cells.Other conditions that can
produce schistocytes are Heinz body anemia, iron deficiency, and laboratory artifacts.
In our series the sensibility of this test has been 20% and
the specificity 90%.

Fibrin(ogen) degradation products (FDP)


Plasmin degradation of the fibrin and the fibrinogen produces the FDP. The appearance of these products of degradation in blood shows the presence of plasmin. The FDPs
are constituted by the fragments X, Y, D and E. These fragments D and E are the most important from the diagnostic
point of view, and the commercial kit (thrombo-wellcotest)
which is generally used for FDP, measures these two fragments only.
The FDP are important not only for their diagnostic
meaning, but also for their anticoagulant activity that is responsible, together with the consumption of coagulant factors, of the haemorraghic syndrome that appears during the
DIC. They are considered ones of the most important inhibitors in blood. The derivation from fibrinogen, other than
fibrin, makes this diagnostic test less specific towards the
DIC. Nevertheless the DIC represents the clinical condition
that more frequently causes an increase of the FDP. There are
some other conditions that can produce a high level of FDP
through an increased production or a reduced elimination:
A. insufficiency of the mononuclear phagocytice system
which removes these products.

4th European FECAVA SCIVAC Congress

D-Dimers
The D-Dimers are the products of fibrins degradation.
They are the direct witness of the fibrinolytic activation, secondary to a coagulation process.
The D-Dimers are the most specific test to diagnose a
DIC, since they come only from the fibrin and not from the
fibrinogen as it happens to the fragments X, Y, D and E.
With regard to the DIC on 71 cases of DIC our research
has demonstrated a 82% sensibility and a 95% specificity.
We believe that, as in human medicine, also in dogs, the
D-Dimers appears to be the test most likely to be alterated in
confirmed DIC.

Antithrombin III (AT III)


The AT III, together with protein C, protein S, and components of the fibrinolytics system are physiologically the
most important naturally occuring anticoagulants proteins
The AT III regulates the blood haemostasis and defends the
organism against intravascular thrombosis2. It is an alpha-2globulin, produced by the liver (systemic action in blood)
and, to a lesser extent, it is produced by the vascular endotelium (local action). It inactivates thrombin and other
serine proteases in a progressive, irreversible manner. Antithrombin also inactivates other serine proteases, including
factors Xa, IXa, Xa, XIIa, and kallikrein, although with less
efficiency than for the inhibition of the thrombin.The rate of
AT III-mediated inactivation clotting factor is markedly enhanced by heparin (i.e., 2,000 folds compared to thrombin).
In DIC there is an increased consumption and consequently
a low level of AT III in blood. Diseases that can cause a low
level of AT III, besides the DIC are:
A. liver failure (reduced production).
B. Nephrotic syndrome (increased loss).
C. Protein loosing entheropathies (increased loss).
From a diagnostic point of view the AT III is less specific because there are quite many diseases which can influence
it. The low diagnostic aid from the AT III levels in diagnosing the DIC is related to the function of the molecule which
belongs to the acute phase proteins. Consequently, the AT III
levels undergo to fluctations in relationship to the entity of
the process. Since the AT III measures the patients anticoagulant capacity it must be considered as an indirect test for
the diagnosis of the DIC. In our DIC dogs, the sensibility
and specificity were respectively 48% and 60%. The AT III
levels might have great importance mostly in fulminant
DIC, where the consumption is greater than hepatic synthesis. The AT III is a good prognostic indicator. The prognosis
is guarded as much as the levels of AT III are reduced in
blood.

A list of suggested readings (MS Word97 or html format)


will be e-mailed by the authors if requested to
sanmarco@iperv.it

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B. Corticosteroids.
C. Liver failure.
D. Disfibrinogenemia (fibrinogens molecules not coagulated in test tube, cross-react with the policlonal antibodies
towards the fragments D and E).
E. Primary hyperfibrinolysis (clinical entity poorly described in veterinary medicine).
F. Artifacts deriving from the failing separation of the fibrinogen from fragments D and E cause a cross-reaction
with policlonal antibodies and the fibrinogen.
Besides positives in a clinical condition, different from
the DIC, you can find also some false negatives:
A. in the DIC with low activation of the fibrinolysis are produced only X fragments in the very early phase of plasmin degradation, which are not measured out by the traditional assays for FDP.
B. In the coagulation process which takes place in the testtube the D and E fragments can be trapped in the clot and
they can be present in a small quantity in the serum.
C. Excessive release of collagenase and elastase, originated
in leukocytes, which degrades the FDP producing false
negatives.
In spite of these difficulties, in the current veterinary literature the FDP are considered the mainstay of the diagnosis of the DIC.
In our study on 71 cases the FDP has demonstrated a
64% sensibility against a 55% specificity.

129

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131

Claw diseases in dogs and cats


Didier-Nol Carlotti

Summary
A figure of the anatomy of the canine claw is first presented. The clinical aspects of claw alterations and the diseases which cause such alterations in dogs and cats are reviewed, with emphasis on particular conditions: trauma,
bacterial infection, fungal infection, parasitic diseases, allergies, auto-immune diseases, Raynauds disease, keratinization disorders, genodermatoses, naevus and idiopathic
onychogryphosis, neoplasia. Claw diseases are often diagnostic and therapeutic challenges. A detailed case history, a
thorough physical examination and appropriate complementary examinations are required to establish a diagnosis of
claw diseases in dogs and cats. Therapy must be specific. In
all cases appropriate follow-up is most important.

Introduction
Nail disorders are relatively rare in companion animals,
particularly in comparison with nail disorders in man1,2,3,4,5,6.
In man, nail disorders are numerous and related to various
causes7. These include hereditary nail dystrophies, trauma,
bacterial infection, candidiasis, dermatophytosis, psoriasis,
eczema, lichen planus, nail disorders observed in systemic
diseases, Raynauds disease, arteritis, frost-bite.

Anatomy
Figure 1 shows the anatomy of the canine claw unit1,8,9.
The nail, or claw, is made of a thick stratum corneum. Claws
have prehensile, locomotor and offensive/defensive functions3,4. A fibro-myxoid body with an ovoid shape has been
discovered between the claw and the third phalanx in dogs
and cats9.

nail fold. Usually the area looks erythematous and oedematous. Oozing, crusting, and - less common - erosion and ulceration may be present (e.g. in auto-immune mediated dermatoses). In chronic cases, scaling, alopecia, lichenification
and hyperpigmentation may be observed.
Onychoschisis means fissuration (splitting) of the nail. It
can be caused by many inflammatory processes which alter
the nail structure and by trauma.
Onychorrhexis is the breaking of a nail which has become brittle for pathological reasons.
Onychogryphosis is a deformation of the claw. It appears
to be elongated and distorted. Usually this is caused by the
inflammation of the digit extremities, coupled with a perionyxis.
Onychomadesis is the sloughing off process for nails, it
is usually multiple.
Claw fracture is sometimes called onychoclasis.
Onyxis can affect only one nail (trauma, idiopathic onychogryphosis, neoplasia, and often dermatophytosis, although the latter can affect a few digits, not necessarily all
on the same foot). On the other hand multiple onyxis is observed in bacterial infections, leishmaniasis, allergic diseases, auto-immune disorders, Raynaud-like diseases, and
keratinization disorders.
Pruritus is rarely observed in cases of onyxis. It mainly
appears in cases of allergic dermatitis. Pain is more common,
particularly in cases of severe perionyxis, onychoschisis,
onychorrhexis and onychomadesis, particularly in bacterial
infections and immune-mediated disorders. It can be acute in
the case of nail fracture. It will only appear belatedly in cases of neoplasia. However, neither pruritus nor pain will be
noticeable in many cases, such as onychogryphosis (e.g. dermatphytosis, leishmaniasis, keratinization disorders, idiopathic onychogryphosis and the early stages of neoplasms).

Consideration of particular
diseases1,2,3,4,5,6,9,11
Clinical signs1,2,3,4
1 - Traumatic onyxis
Onyxis (or onychia) is by definition the disease of the abnormal looking nail. Often, but not always (e.g. trauma, neoplasia), an inflammatory process is responsible for the nail
alteration. Onyxis can be proximal (usually at the onset of
the disease), distal, or it may involve all the nail.
Perionyxis (or paronychia) is the inflammation of the

This is a very common disease in the dog. It usually affects only one nail, in particular the thumbnails (digit 1) on
the hind legs. The nail is more or less distally broken and pain
is usually observed. Diagnosis is clinically obvious. Therapy
consists in promptly removing the distal part of the nail with

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Med Vet, Dipl ECVD


Private Practitioner, Bordeaux - Merignac, France

132

forceps. A bandage is then applied for a few hours. If this is


done a few days after the fracture, systemic antibiotics should
be used for a week to prevent secondary bacterial infection.

4th European FECAVA SCIVAC Congress

serology and/or a parasitological examination (skin and/or


bone marrow cytology). Comprehensive therapy
(Lomidine, Glucantime, amphotericin B, allopurinol) and
a strict follow-up are mandatory.

2 - Bacterial onyxis
5 - Onyxis of canine ankylostomiasis
This disease exists in the dog but is much rarer in the cat.
In the latter, it is usually associated with an immunodeficient
state (FeLV and/or FIV infection, diabetes mellitus etc...). In
the dog it may be idiopathic or secondary to an underlying
disease (such as hypothyroidism, or even Cushings disease). Perionyxis, onychoschisis, onychorrhexis and onychomadesis are usually seen on several nails, with pain as
the primary complaint.
Diagnosis is made by cytology - which reveals a bacterial pus (degenerated neutrophils, phagocytosis), bacteriology and the response to therapy. Treatment must be based on
the removal of broken nails, topical antibacterial therapy and
long term systemic antibiotic therapy (based on bacterial
cultures and sensitivity testing, Staphylococcus sp. and
Gram negative rods often being cultured). Months of careful
therapy are needed, until the distal abnormal part of the nail
has disappeared. In all cases, and particularly in chronically
relapsing ones, an underlying disease should be suspected
and, if found, treated.
Bacterial pododermatitis, whatever the cause, often leads
to bacterial onyxis. Good examples are interdigital pyodermas due to demodicosis and allergic skin diseases. Perionyxis is a prominent feature in such cases. Therapy appropriate to the causal pododermatitis will cure the nail problem
if carried out for long enough.

3 - Dermatophytic onyxis
This is a rare cause of onyxis and perionyxis in the dog,
usually with one or a few digits being affected. In Aquitaine,
Microsporum gypseum and Microsporum canis have been
found to be the dermatophytes which most frequently cause
fungal onyxis. Alopecia of the corresponding digit is often
observed. Diagnosis is made by Woods light examination
which may reveal the fluorescence of the hair of the digit involved, direct examination and fungal culture of this hair,
and histopathology of the nail itself. Skin biopsy and the removal of the third phalanx are unnecessary. PAS staining of
the nail is mandatory and reveals the invasion of the nail keratine by the fungal hyphae.
Long-term antifungal therapy (griseofulvine, ketoconazole, itraconazole) is necessary until the abnormal part of the
nail disappears distally. This may take several months. Other
cutaneous lesions should be topically treated simultaneously.
Dermatophytic onyxis appears to be extremely rare in the cat.
The author has never made such a diagnosis in a feline.

4 - Onyxis of leishmaniasis
Onychogryphosis is a classic symptom of canine leishmaniasis. In the the enzootic area such a complaint justifies

Onychorrexis and onychomadesis can be seen in chronic


cases of pododermatitis caused by ankyostomiasis12. Diagnosis is made by cutaneous histopathology and coproscopy.

6 - Onyxis of allergic dermatites


An inflammatory skin disease of the digits (pododermatitis) is observed clinically in canine atopic dermatitis and
food allergy or intolerance. Onychogryphosis is frequent, often associated with perionyxis and redness of the hair on the
digits. The nails may appear reddish in dogs whose nails are
normally white.
A diagnosis is obviously reached by evaluating all the
symptoms observed in these diseases, by skin-testing, serology and elimination diets. Therapy includes allergen eviction, hyposentitization and symptomatic treatment (systemic
glucocorticoids, antihistamines, essential fatty acids, topical
antipruritic agents etc.).

7 - Onyxis of auto-immune dermatoses


These diseases usually affect several digits.
A - discoid lupus erythematosus/symmetrical lupoid onychodystrophy.
Discoid lupus erythematosus is a not so uncommon
cause of onyxis in the dog3,9,13. In fact, as the disease is symmetrical, as focal thickening and smudging of the basement
membrane zone are not seen and as direct immunofluorescence testing is negative, Danny Scott named this disease
Symmetrical Lupoid Onychodystrophy in 199511. Onychorrhexis and onychogryphosis are the main features of the
disease. Other lesions may be seen in other areas of the
body, but this is not always the case. Perionyxis is not always pronounced and skin biopsies of the nail bed area may
be unrewarding. Amputation of the third phalanx is often the
only way to reveal the typical hydropic and lichenoid interface dermatitis. Immuno-suppressive doses of glucorticoids
(prednisolone) may control the disease. Vitamin E and essential fatty acids (omega-3/omega-6 commercial compound) have been reported to be effective in some cases3,11.
B - pemphigus vulgaris.
Nails and nail beds may be affected in pemphigus vulgaris. Onychogryphosis and onychomadesis can be observed.
Severe perionyxis is also present, with erosions around the
nail bed which are a source of pain. Diagnosis is made by
histopathology either by skin biopsies around the claw or alternatively by amputation of the third phalanx. Biopsies of lesions in other body areas may be diagnostic. Only a guarded
prognosis should be made. Immunosuppressive therapy
should be carried out (glucocorticoids, azathioprine).

4th European FECAVA SCIVAC Congress

8 - Raynaud-like disease
In Man, Raynauds disease is due to a spasm of digital
arteries due to cold, which may be either secondary (e.g. to
SLE) or idiopathic. It is a cyanotic/hyperhaemic and painful
disease. Three female dogs (2 Boxers of 3 and 4 years of age
and a 5 year-old mongrel) were suspected by the author to
have a Raynaud-like disease. The patients were in severe
pain from several digts which from time to time looked
cyanotic. Onychogryphosis was prominent. Skin biopsies
were performed in 2 dogs around the claws and showed non
specific superficial dermatitis and a few Malassezia in the
stratum corneum in one dog. Direct immunofluorescence
testing was negative for IgG and C3. ANA test was negative
in the 3 dogs. Long term therapy with isoxsuprine, a vasodilatator, at the dose of 1mg/kg/day, was very helpful.

9 - Keratinization diseases
The author has seen severe mutiple onychogryphosis in
cases of canine ichthyosis. However, generalized skin lesions were prominent and histopathology of the lesions con-

firmed the diagnosis. Many cases responded partially to


retinoid therapy.
Some cases of zinc responsive dermatosis observed in
nordic dogs involve several digits. Two cases restricted to
the digits, with a prominent perionyxis and above all onychorrhexis were observed by the author in Malamutes (of 10
and 12 months of age respectively). Diagnosis was made by
histopathology, with biopsies taken around the nail bed.
There was a dramatic response to zinc sulfate supplementation (150 mg/kg BID) whereas zinc methionine had not been
very helpful.
Several cases of idiopathic nosodigital hyperkeratosis in
the older dog may be associated with mild multiple onychogryphosis.

10 - Genodermatoses
Ichtyosis is a hereditary keratinization disorder.
Onychogryphosis can be seen in canine dermatomyositis
(Collies, Shetlands, Beaucerons) and epidermolysis bullosa
(Beaucerons)14. Glucorticoids, vitamin E and pentoxifylline
are helpful. A similar hereditary condition could exist in the
cat, with onychomadesis15.

11 - Linear nevus and idiopathic


onychogryphosis
A case of congenital linear epidermal nevus ending in the
paw of a hindleg was diagnosed by the author in a 3 year old
Pyrenean shepherd, with a prominent onychogryphosis on 2
digits (and a secondary demodectic pododermatitis as well).
The nevus responded well to retinoid therapy (etretinate 1
mg/kg/day during 18 months followed by acitretin, at the
same dosage, during 8 months).
The author has seen multiple inverted papillomas in a 7
year old mixed French Spaniel associated with a severe onychogryphosis of only one digit. Papillomas can cause the development of cutaneous horns and potentially this claw alteration was linked to the skin disease.
Idiopathic onychogryphosis is observed in dogs. It usually affects one digit. Diagnosis is made by the elimination
of other possible causes. Regular removal of the nail affected is advisable.

12 - Neoplasms
Neoplasia of the nail fold is a common cause of onyxis
and onychomadesis in the old dog. Squamous cell carcinoma (which is often misleading since it looks like a non-healing wound), melanoma, and mast cell tumour are relitavely
frequent. However keratoacanthoma, inverted papilloma,
and eccrine adenocarcinoma may also be observed3. These
tumours affect only one digit usually, and necessitate agressive excision therapy. Melanoma and mast cell tumour may
metastase, although squamous cell carcinoma has a better
prognosis than usually believed if excision is carried out at
an early stage. Swelling is often prominent and pain is acute.

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C - pemphigus foliaceus and/or erythematosus.


Onychogryphosis and perionyxis can be observed in canine pemphigus foliaceus, particularly in severe forms of the
disease. When pemphigus foliaceus is exclusively confined
to the foot pads onychorrhexis is often observed. The author
has seen 2 cases of pemphigus erythematosus confined exclusively to the footpads, with onychorrhexis.
Diagnosis can be made by histopathology. In the extensive forms of the disease, biopsy of the skin lesions may be
diagnostic. In the localized forms, biopsy of the foot pads
and/or an amputation of the third phalanx may be diagnostic. Immunosuppressive therapy is necessary.
In the cat, pemphigus foliaceus is a possible cause of severe perionyxis. A thick pus is discovered in the nail bed.
Diagnosis is usually made by skin biopsy of the other skin
lesions. Glucocorticoid immunosuppressive therapy is
helpful.
D - bullous pemphigoid-like skin disease.
Severe multiple onychomadesis and/or severe onychogryphosis with ulcerative perionyxis may be seen in the
bullous pemphigoid group skin disease (a group of auto-immune disorders with subepidermal clefting as a common
feature). They may even be the prominent features of this
disease, making it a most painful one. Diagnosis is made by
biopsy of the skin lesions, particularly of the digits, if there
is ulceration around the nail bed. Alternatively, amputation
of the third phalanx of an affected digit may be the only way
to diagnose such a condition if only nail disease is present.
In one case, the author had the luck to establish a diagnosis
of bullous pemphigoid by removing nails from a dog with
onychomadesis; a small amount of skin tissue still attached
to the claw displayed the typical lesions of dermal-epidermal
clefting.
Therapy is not easy. Glucorticoid immunosuppression is
not always helpful.

133

134

4th European FECAVA SCIVAC Congress

Diagnosis is made by histopathlogy of the removed tumour


and radiographs of the digits often reveal bone lysis.
Multiple squamous cell carcinomas are seen in black
dogs, affecting several digits, with a slow growth rate. Excision therapy is mandatory.
Nail bed tumours are rarer in old cats. Those that do occur are squamous cell carcinoma, hemangiosarcomas, and
metatasis of primary lung carcinomas3.

inations are required to establish a diagnosis. The latter include cytology, bacteriology, mycology, histopathology (skin
biopsy around the nail bed or even third phalanx amputation,
sometimes very helpful) and immunological tests such as
skin-testing and elimination diets. Therapy must be specific.
In all cases appropriate follow-up is most important.

References
1.

Conclusion
Claw diseases in dogs and cats are often diagnostic and
therapeutic challenges. A detailed case history, a thorough
physical examination and appropriate complementary exam-

2.
3.
4.
5.
6.

DORSAL
EPIDERMIS
3rd PHALANX

DORSAL
MATRIX

7.
8.
9.
10.

11.

12.
13.
14.

VENTRAL
FOOTPAD
MATRIX
NAIL
VENTRAL
EPIDERMIS

15.

16.
Figure 1 - Anatomy of the canine claw

Scott DW, Miller WH, Griffin CE (1995), Muller and Kirks Small
Animal Dermatology, 5th edition, WB SAUNDERS Company,
Philadelphia.
Foil CS (1987), Disorders of the feet and claws, Proc. 11th KAL
KAN Symposium, 23-32.
Scott DW, Miller WH (1992), Disorders of the claw and clawbeds in
dogs, Compend Contin Educ Pract Vet, 14: 1448-1458.
Scott DW, Miller WH (1992), Disorders of the claw and the clawbeds
in cats, Compend Contin Educ Pract Vet, 14: 449-457.
White SD (1989), Pododermatis, Vet Dermatol, 1: 1-18.
Guagure E, Hubert B, Delabre C (1992), Feline pododermatitis, Vet
Dermatol, 3:1-12.
Du Vivier A (1980), Atlas of Clinical Dermatology, Gower Medical
Publishing Ltd, London.
Mueller RS, Sterner-Kock A, Stannard AA (1993), Microanatomy of
the canine claw, Vet Dermatol, 4: 5-11.
Carlotti DN (1995), Affections des griffes chez le chien et le chat,
Prat Md Chir Anim Comp, 30: 235-247.
Delabre C, Guagure E, Magnol JP (1993), Mise au point dune technique de coupe histologique de doigts de carnivores - applications
pratiques, Proc. 8es Journes du GEDAC, St-Malo.
Scott DW, Rousselle S, Miller WH (1995), Symmetrical Lupoid Onychodystrophy in Dogs: A retrospective Analysis of 18 Cases (19891993), J Amer Anim Hosp Ass, 31: 194 - 201.
Gross TL, Ihrke PJ, Walder EJ (1992), Veterinary Dermatopathology,
Mosby Year Book, St-Louis.
Remy I, Fontaine J (1992), Lupus rythmateux discode localisation unguale chez un chien, Proc Congrs CNVSPA, Paris, 314.
Fontaine J, Remy I, Clerxc C (1992), Epidermolyse bulleuse jonctionnelle familiale chez les chiots Bergers de Beauce, Proc Congrs
CNVSPA, Paris, 313.
Johnstone I, Mason K, Sutton R (1992), A hereditary junctional
mechanobullous disease in the cat, Proc 2nd Word Congress of Veterinary Dermatology, Montral, 1992, 111-112.
Goldschmidt MH, Shofer FS (1992), Skin tumors of the dog an the
cat, Pergamon Press, Oxford.

4th European FECAVA SCIVAC Congress

135

Its a coagulopathy. But couldnt it be ehrlichiosis?


C. Guillermo Couto

Summary
Spontaneous bleeding disorders are common in dogs.
Because canine ehrlichiosis can result in thrombocytopenia,
thrombopathia, and other coagulopathies, it frequently leads
to spontaneous bleeding.

Etiology and epidemiology


Canine ehrlichiosis (CE), also known as tracker dog disease, tropical canine pancytopenia, and canine hemorrhagic
fever, is caused by Ehrlichia canis, an obligated parasite of the
mononuclear cells, and it is distributed worldwide. It appear
that in German Shepherd dogs and Dobermann Pinschers, the
disease is more severe than in other breeds. This disease became prominent after a large number of military dogs developed CE during the Vietnam war. A neutrophilic strain of
ehrlichia has also been identified in dogs. Also, E. risticii (the
Potomac horse fever agent) may result in seropositivity without clinical signs in dogs. Recently, it was demonstrated that
E. risticii can result in seropositivity and transient fever, lymphadenopathy, and diarrhea in experimentally inoculated cats.
Another ehrlichia organism, E. platys, prevalent only in
the southeastern United States, can result in cyclic thrombocytopenia in dogs.
The vector and main reservoir of E. canis is the common
brown dog tick (Rhipicephalus sanguineous), which can
transmit the organisms for more than 5 months after engorgement with infected blood; the incubation period varies
from 7 to 21 days. The brown dog tick also can harbor
Babesia and Hepatozoon spp. This organism can also be
transmitted through blood transfusions.

Clinical features
Three common clinical phases are recognized for CE:
acute, subclinical, and chronic. The acute phase is common
in enzootic areas, and rare in other regions. It lasts approximately two to four weeks and consists of mild to severe clinical signs, secondary to lymphoid hyperplasia, pyrexia, and
cytopenias. Clinical signs and physical examination findings
include presence of ticks, pyrexia, depression, weight loss,
evidence of primary hemostatic bleeding, reactive lymphadenopathy and hyperplastic splenomegaly, dyspnea or

exercise intolerance due to pneumonitis, and occasionally,


central nervous system (CNS) signs. During this phase, the
titer may be negative, since it takes one to two weeks to develop sufficient antibody production (see below).
The subclinical phase occurs after the acute phase, may
last years, and is usually asymptomatic, although clinicopathologic abnormalities such as cytopenias and hyperglobulinemia may occur. An immunocompetent dog usually
eliminates the organism during this phase.
The chronic phase develops in dogs who cannot eliminate the organism, and is common in the non-enzootic areas.
Clinically, it is also characterized by lymphoreticular hyperplasia, cytopenias, and hyperglobulinemia. The clinical
signs begin one to four months post-inoculation, are variable
in severity, and include weight loss, pallor, evidence of primary hemostatic defects, generalized reactive lymphadenopathy, hyperplastic splenomegaly with extramedullary hematopoiesis, ocular changes (chorioretinitis,
anterior uveitis, hyphema, retinal hemorrhages), limb edema, and occasionally, CNS signs.

Clinicopathologic features
The hematologic and serum biochemical findings consist
mainly of cytopenias and hyperproteinemia due to hyperglobulinemia. During the acute phase thrombocytopenia due
to peripheral destruction of platelets (ie; presumptively immune-mediated), regenerative anemia (due to immune hemolysis), leukocytosis with monocytosis, and a hypercellular bone marrow constitute common hematologic abnormalities; hyperproteinemia is present in a variable percentage of
cases, and it usually worsens with time.
Hyperglobulinemia and increased liver enzyme activities
(with or without hyperbilirubinemia) are the main serum
biochemical abnormalities during this phase.
During the chronic phase, clinicopathologic changes are
dominated by bi- or pancytopenia (with a hypocellular bone
marrow), lymphocytosis (up to approximately 15,000 lymphocytes/l), hyperglobulinemia and hypoalbuminemia due
to a polyclonal (or more rarely, monoclonal) gammopathy,
and proteinuria due to interstitial, lymphoplasmacytic
nephritis; in addition to hypocellularity, bone marrow aspirates usually reveal increased numbers of plasma cells. Occasionally, dogs with chronic ehrlichiosis and normal
platelet counts experience episodes of primary hemostatic

MAIN PROGRAMME

DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

136

bleeding; in those cases, a platelet dysfunction appears to be


the cause of the bleeding. Polyarthritis has also been recognized in dogs with chronic ehrlichiosis.

Diagnosis
A confirmative diagnosis of CE can be obtained by either: a) identifying the organism on cytologic specimens of
lymph node, spleen, or bone marrow; or b) obtaining a positive serology for E. canis. Ehrlichia organisms are rarely
identified in cytologic preparations, even retrospectively,
once a diagnosis has been confirmed by serology. Serology
for E. canis is usually performed by means of indirect immunofluorescent antibodies (IFA), a technique which is
highly sensitive and specific. Some degree of cross-reactivity with other ehrlichia organisms occurs, mainly E. equi, E.
risticii, and E. sennetsu, but no cross-reactivity exists with
Rickettsia rickettsi, the RMSF agent. Titers of 1:10 (the lowest dilution used by most laboratories) are considered diagnostic for infection, and may persist even after successful
treatment. Because detectable antibody titers do not occur
until after 7 to 21 days post-inoculation, paired serum titers
may be necessary in order to diagnose acute CE. Polymerase
chain reaction (PCR) is now widely used to diagnose CE.
Canine ehrlichiosis, as lymphoma and systemic lupus
erythematosus (SLE), can mimic a variety of disorders.
However, the main differential diagnoses in dogs with
chronic CE include multiple myeloma, lymphoma, chronic
lymphocytic leukemia, and SLE. Oftentimes, in a dog that
presents with a chronic history of weight loss, splenomegaly,
generalized lymphadenopathy, bi- or pancytopenia, bone
marrow plasmacytosis, and a monoclonal gammopathy, the
only one to differentiate between CE and multiple myeloma
is by obtaining a positive serology for E. canis. The same
holds true for dogs with chronic weight loss, mild lymphadenopathy and hepatosplenomegaly, lymphocytosis, and
a monoclonal gammopathy. Another disorder that is commonly mimicked by acute CE is immune-mediated thrombocytopenia (ie; isolated thrombocytopenia and increased
numbers of megakaryocytes in a bone marrow smear); in
these cases, immunosuppressive corticosteroid treatment
should be initiated in conjunction with tetracycline or doxycycline, until the results of the serology become available.

Treatment and prevention


Even though the clinical signs in dogs with CE can be
quite severe, response to treatment is usually remarkably
good. A notable exception is that of dogs with severe

4th European FECAVA SCIVAC Congress

chronic CE, in which response to treatment may be minimal. Recovery in dogs with acute forms and in dogs with
mild chronic forms occurs in 24 to 72 hours; complete recovery in dogs with chronic infection may take up to four
months. As discussed above, elevated titers (and a monoor polyclonal gammopathy) may persist for months or
years.
Tetracycline, and its derivative doxycycline, constitute
the mainstay of treatment (Table 1). They should be administered for 10 to 21 days and usually result in complete resolution of the clinical signs. However, serum titers may persist for several months (or even years).
Most textbooks recommend using tetracycline as the first
line of treatment; however, since a less expensive generic
doxycycline is available, we routinely use it to treat dogs
with CE at doses of 5 to 10 mg/kg, PO, SID to BID. Moreover, it appears to be more effective than tetracycline, and it
causes less yellowing of the teeth in pups than its parent
compound (tetracycline).
Doxycycline can also be used intravenously in dogs with
severe clinical signs or vomiting.
Chloramphenicol can also be used successfully to treat
CE. However, given its potential for marked hematologic
toxicity it is not the drug of choice for a cytopenic dog.
If treatment with tetracycline, doxycycline, or chloramphenicol fails to induce clinical or hematologic remission,
imidocarb dipropionate, and anticholinesterase agent not
available in the United States should be used.
It is administered as a single subcutaneous or intramuscular injection (5 mg/kg), which can potentially be repeated
in 2 to 3 weeks. It usually causes transient vomiting, diarrhea, shivering, and coughing, which resolve within minutes
to hours of the administration. As a general rule, intramuscular administration of drugs should be avoided in dogs with
thrombocytopenia or thrombocytopathia.
Supportive treatment in dogs with CE include administration of fluids and/or blood products, and possibly, corticosteroids to treat the underlying immune mediated disorder.
Immunosuppressive doses of corticosteroids, equivalent to
2-4 mg/kg of prednisone daily, do not appear to adversely affect the course of the disease when used concomitantly with
tetracycline or doxycyline. Anabolic steroids may be used in
attempts to stimulate hematopoiesis.
Prevention of CE centers around tick control, for which
a variety of products are available. Hunting dogs should be
tested and treated, since asymptomatic carriers can be a
source for continuous infection from ticks.
Prophylactic treatment with tetracycline (3 mg/kg, PO,
SID) or doxycycline (2-3 mg/kg, PO, SID) during tick season may prevent infection. All canine blood donors should
be tested for E. canis by serology.

4th European FECAVA SCIVAC Congress

137

Practical chemotherapy
C. Guillermo Couto
DVM, Dipl ACVIM
Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

Chemotherapy is commonly used in small animals with


malignant tumors. The basic principles, indications, contraindications, and practical applications of this treatment
modality will be discussed using case examples.

Cell and tumor kinetics


The mammalian cell cycle has 2 apparent phases: mitosis and resting phase. The resting phase is indeed composed of 4 phases:
synthesis phase (S): DNA synthesis occurs
gap 1 phase (G1): synthesis of RNA and enzymes needed
for DNA production occurs
gap 2 phase (G2): synthesis of the mitotic spindle apparatus occurs
gap 0 phase (G0): true resting phase.
The mitosis phase is termed M phase.
Several terms need to be defined prior to discussing
chemotherapy. Mitotic index (MI) refers to the percentage
of mitoses in a tumor mass. Growth fraction (GF) refers to
the proportion of proliferating cells within a tumor. Doubling time (DT) refers to the time required by a tumor mass
to double in size. In dogs they range from 2 days (for
metastatic osteosarcoma) to 24 days (for metastatic
melanoma), while in humans they range from 29 days (for
malignant lymphomas) to 83 days (for breast cancer). The
DTs depend upon the time spent in mitosis, cell cycle duration, GF and cell loss from death or metastases. Given our
knowledge on tumor kinetics, by the time a pulmonary
metastatic nodule is visualized on radiographs, it has
200,000,000 cells and weighs less than 150 mg (and it has
already divided 25 to 35 times).
As a general rule, most non-neoplastic tissues (with the
exception of bone marrow stem cells and intestinal crypt
epithelium) have low GF, low MI, and prolonged DT,
while most neoplastic tissues have high MI, high GF, and
short DT.
Surgical cyroreduction (debulking) of a tumor that
reached a plateau of growth will decrease the total number
of cells, thus increasing the MI and GF, and shortening the
DT. This will turn the neoplasm more susceptible to chemoor radiotherapy.

Indications and contraindications


of chemotherapy
Chemotherapy is primarily indicated for patients with
systemic (eg; lymphoma, leukemias) and metastatic neoplasms, although it can also be used for nonresectable,
chemoresponsive neoplasms which have been historically
refractory to radiotherapy or hyperthermia (primary
chemotherapy). It can also be used as an adjuvant treatment
following partial surgical debulking of a neoplasm (eg; partial excision of an undifferentiated sarcoma), and is indicated for control of micrometastatic disease following surgical
excision of a primary neoplasm (eg; cisplatin therapy after
limb amputation in dogs with osteosarcoma; VAC for dogs
with hemangiosarcoma). As a general rule, chemotherapy
should NEVER be used as a substitute for surgery, radiotherapy, or hyperthermia, or in patients with severe underlying multiple organ dysfunction (the latter will increase the
possibility of developing systemic toxicity).

Mechanism of action of anticancer drugs


The effects of anticancer drugs on a neoplastic cell population follow first order kinetic principles (ie: the number
of cells killed by a drug or drug combination is directly proportional to one variable, the dose used). Anticancer drugs
kill a constant proportion of cells, rather than a constant
number. Therefore, the efficacy of a drug or drug combination will depend upon the number of cells within a given tumor [eg; a drug combination that kills 99% of the cells in a
tumor containing 100,000,000 (109) cells will leave
1,000,000 (106) viable cells]. It should also be kept in mind
that different types of anticancer drugs kill tumor cells by
different mechanisms (see below).

Types of anticancer drugs


Anticancer agents are classified in the following categories:
alkylating agents
antimetabolites
antitumor antibiotics
plant alkaloids (or mitotic inhibitors)
hormones
miscellaneous

MAIN PROGRAMME

Summary

138

Alkylating agents cross-link DNA, thus preventing its


replication. Since they mimic the effects of radiotherapy
they are also referred to as radiomimetics. These drugs are
active during several phases of the cell cycle (ie; they are
cell cycle-nonspecific drugs). Alkylating agents commonly
used in pets with cancer include:
cyclophosphamide (Cytoxan)
chlorambucil (Leukeran)
melphalan (Alkeran)
cisplatin (Platinol) [DO NOT USE IN CATS!]
Antimetabolites exert their activity during the S phase of
the cell cycle (cell cycle phase-specific drugs). These drugs
are structural analogues of naturally occurring metabolites
(fake metabolites) that substitute for normal purines or
pyrimidines. The following antimetabolites are commonly
used in small animal cancer patients:
cytosine arabinoside (Cytosar-U)
methotrexate (Methotrexate)
5-fluoruracil (5-FU) [DO NOT USE IN CATS!]
6-thioguanine (6-TG)
6-mercaptopurine (PuriNethol)
azathioprine (Imuran)*
Antitumor antibiotics act by several mechanisms, the
most importants of which appear to be cross-linking of DNA
and inhibition of protein synthesis. They include:
doxorubicin (Adriamycin)
bleomycin (Blenoxane)
actinomycin D (Cosmegen)
mitoxantrone (Novantrone)
Plant alkaloids are derived from the periwinkle plant
(Vinca rosea) and the May apple plant (Podophyllum peltatum ). They disrupt the mitotic spindle and are therefore cell
cycle phase-specific (active during M phase). Commonly
used plant alkaloids include:

*Commonly used as an immunosuppressive drug.

4th European FECAVA SCIVAC Congress

vincristine (Oncovin)
vinblastine (Velban)
etoposide or VP-16 (VePesid)
Hormones are commonly used for the treatment of hemolymphatic malignancies or endocrine-related tumors.
Commonly used hormones include:
prednisone
testosterone
estrogens
progestagens
With the exception of corticosteroids, the use of hormones is not recommended since they are associated with
significant side effects in animals.
Finally, miscellaneous agents include drugs whose
mechanism of action is either unknown or different from the
ones listed above. Miscellaneous agents commonly used in
small animal cancer patients include:
DTIC (DTIC)
l-asparaginase (Elspar)

References
Bech-Nielsen S, Reif JS, Brodey RS: The use of tumor doubling time in
veterinary clinical oncology. J Amer Vet Radiol Soc 17:113-116,
1976.
Couto CG: Principles of chemotherapy. In Proceedings 10th Annual Kal
Kan Symposium for the Treatment of Small Animal Diseases. 1986,
pp 29-36.
Couto CG: Practical chemotherapy. In Nelson RW and Couto CG: Essentials of Small Animal Internal Medicine. St. Louis, Mosby-Yearbook,
1992, p 842-846.
Dorr RT and Fritz WL: Cancer Chemotherapy Handbook. New York, Elsevier, 1980.
Helfand SC: Principles and applications of chemotherapy. Vet Clin North
Amer 20:987-1013, 1990.

4th European FECAVA SCIVAC Congress

139

Complications of chemotherapy
C. Guillermo Couto

Summary
Chemotherapy is commonly used in small animal practice. Although this treatment modality is associated with a
high prevalence of adverse effects in people, toxicity in dogs
and cats is minimal and they usually preserve excellent quality of life. This lecture will discuss the common toxicities of
chemotherapy, emphasizing recognition and management.

Most anticancer agents are relatively nonselective in that


they not only kill rapidly dividing neoplastic tissues, but also some of the rapidly dividing tissues in the host as well
(eg; villal epithelium, bone marrow cells). In addition, they
are similar to other commonly used agents (eg; digitalis glycosides) in that they have low therapeutic indices (ie; narrow
therapeutic-to-toxic ratios).
Because anticancer agents follow first order kinetic principles (ie; the fraction of cells killed is directly proportional
to the dose used), increasing the dose of a particular drug
will increase the proportion of neoplastic cells killed, but it
will also enhace its toxicity. This is commonly seen when a
tumor relapses and higher doses of a previously used drug
are utilized.
Because toxicity is generally directed against rapidly dividing tissues, given the short turnover rate of bone marrow
and villal epithelial cells, myelosuppresion and gastrointestinal signs are the most common toxicities encountered
in practice. Other rare complications of chemotherapy include anaphylactoid (or anaphylactic) reactions, dermatologic toxicity, pancreatitis, cardiotoxicity, pulmonary toxicity, neurotoxicity, hepatopathies, and nephropathies. Table 1
lists anticancer drugs commonly used in small animals and
their toxicities.
In addition to the direct effects of the drugs on different
organ systems, rapid killing of certain neoplastic cells (ie;
lymphoma cells) can lead to rapid metabolic derangements
that result in acute clinical signs which mimic those of drug
toxicity (ie; depression, vomiting, diarrhea). This syndrome
is referred to as acute tumor lysis syndrome (ATLS).
Overall, the prevalence of toxicity of different
chemotherapy protocols is considerably lower in dogs and
cats (approximately 5% to 40%) than in humans (75% to
100%) treated with similar drugs or combinations. A recent
survey of owners whose pets had been treated with a variety
of chemotherapy protocols at The Ohio State University Vet-

erinary Teaching Hospital revealed that over 80% of those


questioned considered their pets quality of life to be equal
to or better than that prior to initiating chemotherapy.

Hematologic toxicity
The high mitotic rate and growth fraction (ie; 40 to 60%)
of the bone marrow cells predispose this organ to toxicity
from anticancer drugs. Hematologic toxicity represents the
most common toxicity of chemotherapy, and oftentimes results in temporary or permanent discontinuation of the offending agent/s due to severe (and often life-threatening) cytopenias. Agents commonly implicated in this type of toxicity are listed in Table 1.
When one considers the bone marrow transit times and
circulating half lives of blood cells, it is easy to anticipate
which cell line will be affected. For example, the bone marrow transit time and circulating half life of RBCs in the dog
are approximately 7 days and 120 days, those of the platelets
are 3 days and 4 to 6 days, and those of granulocytes are 6
days and 4 to 8 hours, respectively. Therefore, it is anticipated that neutropenia will occur first, followed by thrombocytopenia; anemia induced by chemotherapeutic agents is
extremely rare in dogs and cats, and, if it occurs, is of a late
onset (3 to 4 months after initiation of therapy). Other patient (eg; malnutrition, old age, concurrent organ dysfunction) and tumor factors (eg; bone marrow infiltration, widespread parenchymal organ metastases) can also effect the
degree of cytopenia.
Although thrombocytopenia is probably as common as
neutropenia, it is rarely severe enough to cause spontaneous
bleeding, and it will therefore not be discussed at length. In
general, in most dogs and cats with chemotherapy-induced
thrombocytopenia the platelet counts remain above 50,000
cells/l; spontaneous bleeding does not usually occur until
platelet counts fall below 30,000/l. Thrombocytosis is
common in cats and dogs receiving vincristine.
Neutropenia usually constitutes the dose-limiting cytopenia and occasionally leads to life-threatening sepsis. For
most drugs, the nadir usually occurs 5 to 7 days after treatment, and the neutrophil counts return to normal values
within 36 to 72 hours of the nadir. Patients with neutrophil
counts under 2,000 cells/l should be closely monitored for
the development of sepsis, although overwhelming sepsis
rarely occurs with neutrophil counts of 1,000/l.

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DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

140

4th European FECAVA SCIVAC Congress

Table 1. Toxicity of anticancer agents commonly used in dogs and cats


Drug
A.

B.

C.

D.

E.

Hematologic

GI

Anaphylaxis

Dermatologic
Pancreatitis

ALKYLATING AGENTS
Busulfan (Myleran)
Chlorambucil (Leukeran)
Cyclophosphamide (Cytoxan)
Melphalan (Alkeran)

++
+/++/+++
++

+/++
+/-

+/- A1
+/-A
+A
+/-A

?
?
?
?

ANTIMETABOLITES
Cytosine arabinoside (Cytosar-U)
5-Fluoruracil (5-FU)
6-Mercaptopurine (Purinethol)
Methotrexate (Methotrexate)
6-Thioguanine (Thioguanine)
Azathioprine (Imuran)

++/+++
++
+/++
+/+++
+/++
+/+++

+/+/++
+/++
+/+++
+
+/++

+A
+A +/-H2
+A
+/++A
+/++A
+A

+/?
+/++
?
?
+/++

ANTITUMOR ANTIBIOTICS
Doxorubicin (Adriamycin)
Bleomycin (Blenoxane)

++/+++
-

+/+++
-

+/++
-/+

++AH +++S3
+H

+/++
?

+
+/+/++

+++4

+A ++S
+A ++S
+A

?
?
?

PLANT ALKALOIDS (MITOTIC INHIBITORS)


Vincristine (Oncovin)
+/++
Vinblastine (Velban)
++/++
Etoposide (VePesid)
+/+++

+/+++

+/-

(see other)
-

++
?

MISCELLANEOUS
Dacarbazine (DTIC)
Cis-platinum (Platinol)

++/+++
+/-

++/+++
++/+++

+A
+A

+/++
?

L-asparaginase (Elspar)
Hydroxyurea (Hydrea)

F.

HORMONES
Prednisone
Estrogens

+/+/+++

+/+/-

+++
-

+/+++A

Other

Cystitis

Liver?

Cardiac
Lungs

+++
?

Cushings

Renal
Lung5

1A: alopecia; 2H: hyperpigmentation; 3S:perivascular sloughing; 4 when administered IV; 5 in cats.

The pathogenesis of sepsis in neutropenic patients is as


follows: chemotherapy-induced death and desquamation of
gastrointestinal crypt epithelial cells occurs simultaneously
with myelosuppression; enteric bacteria are absorbed
through the damaged mucosal barrier into systemic circulation; the numbers of neutrophils in circulation are not sufficient to phagocytose and kill the invading organisms; as a
consequence, microbial colonization of multiple organs occurs, and death ensues unless the patient is treated appropriately.
From the clinical standpoint, it is important to identify
the septic neutropenic patient, since the cardinal signs of inflammation (ie; redness, swelling, increased temperature,
pain, and abnormal function) may be absent due to insufficient numbers of neutrophils available to participate in the
inflammatory process. The same holds true for radiographic
changes compatible with inflammation; for example, dogs
with neutropenia and bacterial pneumonia diagnosed on the
basis of cytologic and microbiologic findings in transtracheal washes, oftentimes have normal thoracic radiographs.

As a general rule, when a severely neutropenic patient (neutrophil count <500/l) presents with marked pyrexia (T
>104), the pyrexia should be attributed to bacterial pyrogens
until proven otherwise, and the patient should be treated aggressively with empirical antimicrobial therapy (see below).
In addition, neutropenic patients with severe constitutional
signs (eg; depression, vomiting, diarrhea) and normal or low
body temperature should be regarded as septic and treated
aggressively. At the VTH-OSU, every neutropenic dogs and
cat with fever or nonspecific clinical signs is considered to
be septic until proven otherwise.
All patients undergoing chemotherapy should be current
on their immunizations. However, hematologic monitoring
the patient on chemotherapy constitutes the most effective
way to prevent severe, life-threatening sepsis secondary to
myelosuppression. Complete blood counts (CBCs) should
be obtained weekly or every other week when using myelosuppressive protocols, and the myelosuppressive agent/s
should be temporarily discontinued (or their doses decreased) if the neutrophil count is below 2,000 cells/l or if

the platelet count is below 50,000 cells/l. Discontinuing the


offending agent/s for 2 or 3 administrations is usually sufficient for the cell counts to return to the normal range. When
therapy is reinstituted, it is recommended that only 75% of
the initial dose be used, escalating doses over 2 to 3 weeks
until the initially recommended dose (or a dose which does
not result in marked cytopenias) is reached.
Clinically, neutropenic patients can be classified as
febrile or afebrile. Neutropenic febrile patients should be approached aggressively, since they are usually septic. Thus,
fever in a neutropenic patient constitutes a medical emergency. The following protocol is currently used in neutropenic febrile patients at the VTH-OSU (Table 2). The patient undergoes a thorough physical examination in search of
a septic focus, an indwelling intravenous catheter is placed
aseptically and intravenous fluids are administered as required. All anticancer agents with the exception of corticosteroids are discontinued at once (corticosteroids should be
discontinued gradually, since patients on chronic steroid
therapy can develop episodes of acute hypoadrenocorticism
when the drug is abruptly discontinued). Blood samples for
CBC; serum electrolyte, blood glucose, and blood urea nitrogen (BUN) concentrations are obtained immediately; a
urine sample for urinalysis and bacterial culture is also obtained. Two to three sets of aseptically collected blood samples can be obtained for aerobic and anaerobic bacterial cultures and antibiotic susceptibility tests at 30 minute intervals
(this is usually not necessary, since the bacterial isolates are
quite predictable - see below). After collecting the second
set of samples for blood cultures, therapy with an empirical
bacteriocidal antibiotic combination is instituted. We prefer
a combination of gentamicin (2.2 mg/kg, IV, TID) or
amikacin (6-10 mg/kg, IV, TID) and cephalothin (40 mg/kg,
IV, TID) since most bacterial isolates in these patients are
Enterobacteriaciae and staphylococci, organisms commonly
susceptible to these agents. Once the neutrophil count returns to normal and the patient is clinically normal (usually
within 72 to 96 hours), the antibiotic combination is discontinued and the patient is released with instructions to administer sulfadiazine-trimethoprim (ST) at a dose of 13-15
mg/kg, PO, BID for 5 to 7 days.
Neutropenic afebrile asymptomatic patients can be
treated as outpatients with discontinuation of the drug/s as

Table 2. Management of neutropenic febrile


dogs and cats
search for septic focus (PE, rads, US)
IV catheter
blood for CBC and biochemical profile
LRS solution (40-60 ml/kg for dogs and 20-30 ml/kg for cats)
discontinue chemo drugs (except for corticosteroids)
antibiotics
cephalotin 40 mg/kg, IV, tid
gentamicin 2.2 mg/kg, IV, tid or amikacin 6-10 mg/kg, IV, tid*
after patient stabilizes, decrease rate of IV fluids to 60-90
ml/kg/day
* if the patient is oliguric or anuric, do not administer aminoglycoside until
after the urinary bladder is palpable (ie; there is diuresis).

141

above plus ST (15 mg/kg, PO, BID); if the patients is


afebrile but has constitutional signs, he/she should be considered to be septic and treated as described above. If the
neutropenia is not severe (ie; 2,000 cell/l), no therapy is
needed, and the patient should only be monitored by the
owner. Owners should be instructed to monitor their pets
rectal temperature twice daily, and call the veterinarian if
pyrexia develops, in which case the patient is treated as neutropenic and febrile. Sulfa-trimethoprim combinations eliminate the aerobic intestinal flora, but preserve the anaerobic
bacteria, which are an important component of the local defense system, due to their ability to produce local antibiotic
factors. In addition, ST is active against a large number of
pathogens isolated from cancer patients, provide therapeutic
blood and tissue concentrations, and also provide high intragranulocytic concentrations.
Myelosuppression may be alleviated by using lithium
carbonate (10 mg/kg, PO, BID), granulocyte colony stimulating factor (G-CSF) at a dose of 5-10 g/kg SQ bid, or
products which stimulate release of endogenous G-CSF (eg;
bacterial products).

Gastrointestinal toxicity
Although less frequent than myelosuppression, gastrointestinal toxicity is a relatively common complication of cancer chemotherapy in pets. From the clinical standpoint two
major types of gastrointestinal complications can occur:
nausea/vomiting and gastroenterocolitis.
Although controlled studies are not available, nausea and
vomiting are not apparently as common in pets as in humans
(when using similar drugs and dosages). Drugs associated
with nausea and vomiting in dogs include DTIC, cisplatin,
doxorubicin, methotrexate, and actinomycin D; doxorubicin
and cyclophosphamide frequently result in nausea/vomiting
in cats (Table 1).
Acute nausea and vomiting caused by injectable drugs
can be alleviated by administering the offending agents by
slow intravenous infusions. If they persist despite slow administration, the use of antiemetics such as metoclopramide
(Reglan) at a dose of 0.1 to 0.3 mg/kg, IV, SQ, or PO TID,
or prochlorperazine (Compazine) at a dose of 0.5 mg/kg,
IM, BID to TID is indicated.
Gastroenterocolitis from anticancer agents is rare. Drugs
which occasionally cause mucositis include methotrexate,
5-fluoruracil, actinomycin D, and doxorubicin; it occurs
rarely with other alkylating agents such as cyclophosphamide. Of the drugs listed above, only doxorubicin (Adriamycin) and methotrexate (Methrotrexate) appear to be of
clinical importance. In my experience, Collies and Collie
crosses, Old English Sheepdogs, and West Highland White
terriers appear to be extremely susceptible to doxorubicininduced enterocolitis.
Doxorubicin-induced enterocolitis is characterized by
the development of hemorrhagic diarrhea (with or without
vomiting), primarily of large bowel type, 3 to 7 days after
administration of the drug. Supportive fluid therapy (if necessary) and treatment with therapeutic doses of bismuth subsalicylate-containing products (Pepto Bismol, 3 to 15 ml or

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4th European FECAVA SCIVAC Congress

142

1/2 to 2 tablest PO, TID to QID) are usually effective in controlling the clinical signs, which usually resolve in 3 to 5
days. Although anecdotal, if the patient is at risk for gastroenterocolitis (ie; one of the breeds mentioned above, prior history of this toxicity), administration of Pepto-Bismol
from days 1 to 7 of the treatment may alleviate or prevent
these signs. Gastroenteritis associated with oral methotrexate administration usually develops after the patient has been
receiving this drug for a minimum of two weeks.

Hypersensitivity reactions
Acute type I hypersensitivity reactions occasionally occur in dogs receiving parenteral l-asparaginase (Elspar) or
doxorubicin (Adriamycin), and are common in dogs treated with etoposide (VePesid). The reaction to doxorubicin
does not appear to be a true hypersensitivity reaction, since
this agent can induce direct mast cell degranulation independently of IgE mediation. Etoposide can be safely administered orally to dogs. Hypersensitivity reactions to anticancer agents are extremely rare in cats and will not be
discussed.
Clinical signs in dogs with hypersensitivity reactions are
primarily cutaneous and gastrointestinal. Typical signs begin
during or shortly after administration of the agent, and include head shaking (due to ear pruritus), generalized urticaria and erythema, restlesness, occasional vomiting, and
(rarely) collapse due to hypotension.
Most systemic anaphylactic reactions can be prevented
by pretreating the patient with H-1 antihistamines (ie;
diphenhydramine, 1-2 mg/kg, IM, 20-30 minutes prior to administration of the drug) and by administering certain drugs
(such as l-asparaginase) by the subcutaneous, intramuscular,
or intraperitoneal route, rather than intravenously. If the
agent cannot be given by any other routes (ie; Adriamycin),
it should be diluted and administered by slow intravenous
infusions. At the VTH-OSU we routinely pretreat dogs (but
not cats) with diphenydramine prior to administering doxorubicin or l-asparaginase.
Treatment of acute hypersensitivity reactions includes immediate discontinuation of the agent, administration of H-1
antihistamines (ie; diphenhydramine, 0.2-0.5 mg/kg, slow
IV), intravenous dexamethasone sodium phosphate (1-2
mg/kg), and fluids, if deemed necessary. If the systemic reaction is severe, the administration of epinephrine (0.1-0.3 ml of
a 1:1,000 solution, IM or IV) is indicated. Once the reaction
subsides, the administration of certain drugs such as Adriamycin may be continued. Intravenous H1 antihistamines
should be used with caution in cats, since they can cause
acute CNS depression leading to apnea.

Dermatologic toxicity
Dermatologic toxicity is rare in small animals. Three
types of dermatologic toxicities can occur: local tissue
necrosis due to extravasation, delayed hair growth or alopecia, and hyperpigmentation.
Local tissue necrosis due to extravasation of vincristine,

4th European FECAVA SCIVAC Congress

vinblastine, actinomycin D, or doxorubicin is occasionally


seen in dogs receiving these drugs; however, it is rare in cats.
Although the pathogenesis of this toxicity is poorly understood, these drugs are extremely caustic when given perivascularly, causing marked tissue necrosis 1 to 15 days after the
injection (earlier with the vinca alkaloids, and later with
doxorubicin and actinomycin D). As a consequence of this,
every effort should be made to ensure that these drugs are
administered intravascularly.
In order to prevent or minimize extravascular injection
of caustic drugs, they should be administered through a
small gauge (22 G to 23 G) indwelling intravenous catheter
(I prefer over-the-needle catheters such as the Terumo Surflo) or 23 G to 25 G butterfly catheters. I use the former for
doxorubicin and the latter for vinca alkaloid administration;
in cats, it is safe to administer doxorubicin through a butterfly catheter. Caustic drugs should be properly diluted prior
to administration (ie; vincristine to a final concentration of
0.1 mg/ml and doxorubicin to a concentration of 0.5 mg/ml),
and patency of the catheter should be assured by intermittently aspirating until blood appears in it. If the catheter is
not patent, it should be placed in another vein.
Despite careful intravascular injection, some dogs develop mild to moderate local tissue reactions (eg; erythema,
moist desquamation, and alopecia). This is common in
Golden Retrievers receiving vincristine, vinblastine, actinomycin D, or doxorubicin, and is believed to be due to selfinflicted damage after developing mild phlebitis or thrombophlebitis. These patients are managed as discussed below.
Recommendations for management of extravascular injections are listed in Table 3.
If despite these precautions a local tissue reaction occurs,
it will develop in approximately 1 to 7 days after perivascular injection of vinca alkaloids, and 7 to 15 days after actinomycin D or doxorubicin extravasation. Tissue necrosis is
far more severe with doxorubicin, since it is extremely caustic and it persists in the tissues for several weeks to months.
Clinical signs include pain, pruritus, erythema, moist dermatitis, and necrosis of the affected area; severe tissue
sloughing usually occurs. If mild local tissue reactions develop, they can be treated as described in Table 4.
In dogs and cats undergoing chemotherapy delayed hair
growth is more common than alopecia. This is in contrast
with human patients, in which severe scalp alopecia is a predictable complication of therapy. Excessive shedding is also
a common occurrence.
Alopecia appears to occur predominantly in wooly
(coarse) haired dogs such as poodles and Kerry blue terriers.
In short haired dogs and cats, it affects primarily the tactile
hairs. Although the exact reason why wooly haired dogs develop chemotherapy-induced alopecia is unknown, a prolonged anagen phase and synchronous hair growth, comparable to that existing in human scalp hair may make these
dogs prone to this toxic effect. Drugs commonly associated
with delayed hair growth or alopecia include cyclophosphamide, doxorubicin, 5-fluoruracil, 6-thioguanine, and hydroxyurea. Alopecia and delayed hair growth usually resolve
shortly after discontinuation of the offending agent.
Hyperpigmentation induced by anticancer agents is
rare in dogs and extremely rare in cats. Cutaneous hyperpig-

Table 3. Recomendations for the management


of perivascular injections of caustic anticancer drugs
in cats and dogs
1. Do not remove the IV catheter.
2. Administer 10 to 50 ml of sterile saline solution through the
catheter (in an attempt to dilute the agent).
3. With a 25 G needle administer 10 to 20 ml of sterile saline solution subcutaneously (SQ) in the affected area.
4. Inject 1 to 4 mg of dexamethasone sodium phosphate SQ in the
affected area (in an attempt to stabilize lisosomal and plasma
membranes).
5. Apply cold compresses or ice packs to the area for 48-72 hours
(to cause vasoconstriction and prevent local dissemination of the
drug, and to decrease local tissue metabolism).

Table 4. Recommended treatment for dogs that received


a perivascular injection of a caustic anticancer agent
1. Apply an antibiotic ointment (with or without corticosteroids) to
the affected area.
2. Bandage the area (and replace bandages daily).
3. Prevent the patient from causing self mutilation by using an elizabethan collar or a muzzle.
4. If there is no bacterial contamination (ruled out on the basis of
negative bacterial cultures or cytology), DepoMedrol can be injected subcutaneously (10 to 20 mg) in the affected area to alleviate pruritus and inflammation.
5. If severe necrosis or gangrene due to anaerobic contamination
occurs the area should be surgically debrided.
6. In severe doxorubicin-induced soft tissue necrosis, amputation
of the affected limb may be required.

mentation affecting the face, ventral abdomen and flanks is


quite common in dogs receiving doxorubicin-, actinomycin
D, and bleomycin-containing protocols.

Cardiotoxicity
Cardiotoxicity is a relatively rare complication of doxorubicin therapy in the dog, and appears to be extremely rare
in the cat. Two types of doxorubicin-induced cardiac toxicity are observed in dogs: an acute reaction during or shortly
after administration, and a chronic cumulative toxicity.
Acute doxorubicin toxicity is characterized by the development of cardiac arrhythmias (mainly, sinus tachycardia) during or shortly after administration. This phenomenon is
thought to be related to doxorubicin-induced histamine-mediated catecholamine release, since the sinus tachycardia
and hypotension can be prevented by pretreatment with H1
and H2 antihistamines. Several weeks or months after repeated doxorubicin injections, persistent arrhythmias, including ventricular premature contractions, atrial premature
contractions, paroxysmal ventricular tachycardia, second
degree AV blocks, and intraventricular conduction defects
develop. These rhythm disturbances are usually associated

143

with the development of a dilated cardiomyopathy, similar


to that seen spontaneously in large breed dogs and Cocker
Spaniels.
The hallmark of chronic doxorubicin toxicity in the dog is
the development of dilated cardiomyopathy after surpassing a
total cumulative dose of approximately 240 mg/m2. The cumulative cardiotoxic dose in the cat is unknown, but it appears
to be approximately 150 to 170 mg/m2. Clinical signs of toxicity in dogs are those of congestive heart failure (usually leftsided). Therapy consists of discontinuation of the drug and
use of cardiac drugs such as digitalis glycosides or non-glycoside inotropic agents. Once cardiomyopathy develops, the
prognosis is poor, since myocardial lesions are irreversible.
For a detailed discussion of treatment of dilated cardiomyopathy please refer to a standard internal medicine textbook.
Monitoring dogs receiving doxorubicin is critical to prevent the development of fatal cardiomyopathy. In this respect, dogs and cats with underlying rhythm disturbances or
impaired myocardial contractility, as determined by decreased fractional shortening on M-mode echocardiograms
should not receive doxorubicin. It is also recommended that
patients receiving doxorubicin undergo M-mode echocardiographic evaluation every three doxorubicin cycles (9
weeks) to assess myocardial contractility, and that administration of the drug be discontinued if decreased fractional
shortening occurs. The use of endomyocardial biopsies to
monitor cardiac toxicity from doxorubicin is impractical in
dogs and cats.
Several protocols have been devised in an attempt to
minimize doxorubicin-induced cardiomyopathy. Unfortunately, only three protocols have shown promise. Of these,
weekly low dose doxorubicin showed a significantly lower
frequency of histologic changes when compared to the conventional 3-weekly schedule in humans. I have been able to
administer total cumulative doses of 500 mg/m2 to two dogs,
when using 10 mg/m2 weekly. However, recent evidence
suggests that this schedule is not as effective in dogs with
lymphoma. A new compound termed ICRF-187 (or ADR
259) offers a promising means of reducing the chronic cardiotoxicity induced by doxorubicin; using this compound,
doses in excess of 500 mg/m2 have been administered to
dogs without significant cardiotoxicity. Unfortunately, this
compound is not commercially available. At the VTH-OSU
we administer doxorubicin as a slow bolus (20-30 minutes)
of a 0.5 mg/ml solution intravenously. This results in a relatively low peak plasma concentration of the drug, and decreases the risk of developing cardiotoxicity. Using this protocol we evaluate approximately one dog every 18 months
with clinical evidence of doxorubicin-induced cardiomyopathy; for reference, we administer approximately 4 gm of
doxorubicin per year, and a 70 lb dog receives an average
dose of 30 mg.

Urotoxocity
The urinary tract is rarely involved in adverse reactions
to anticancer agents in small animal patients. Only two specific complications are of clinical importance in pets with
cancer: nephrotoxicity and sterile hemorrhagic cystitis.

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144

Transitional cell carcinomas (TCCs) of the urinary bladder


associated with cyclophosphamide (CTX ) therapy can also
occur in dogs.
Nephrotoxicity is rarely observed in dogs and cats undergoing chemotherapy. Although several potentially
nephrotoxic drugs are commonly used in these species, only
doxorubicin (primarily in the cat), cisplatin (in the dog), and
intermediate- to high-dose methotrexate (in the dog) are of
concern to the clinician. Doxorubicin may be a potent
nephrotoxin in cats, and the limiting cumulative toxicity in
this species may be renal, rather than cardiac. Doxorubicin
may cause nephrotoxicosis in dogs with preexisting renal
disease, and in those concomitantly receiving other nephrotoxins, such as aminoglycoside antibiotics.
Sterile hemorragic cystitis is a relative commmon complication of chronic CTX therapy in dogs, but it is extremely rare in cats. Although rare, hemorrhagic cystitis may also
occur acutely or peracutely after the first dose of CTX.
Three dogs treated in our clinic with 100 mg/m2 of CTX IV,
and 4 dogs receiving 300 mg/m2 of CTX PO developed
acute clinical signs and urinalysis changes compatible with
sterile hemorrhagic cystitis after the first dose. Sterile cystitis apparently results from the irritating effects of one of
CTX metabolites (acrolein). Approximately 5% to 25% of
dogs, and 1% to 3% of cats treated with oral CTX develop
sterile hemorrhagic cystitis, which usually occurs after 18
weeks. Furosemide administered concomitantly with CTX,
appears to decrease the prevalence of cystitis.
Forced diuresis appears to prevent or minimize the frequency of this complication. I usually recommend administering the CTX in the morning, allowing the pet to urinate
frequently (if he/she is an indoor dog), salting the food, and
administering prednisone on the same day that the patients
receive the CTX (if the protocol calls for prednisone administration).
Clinical signs of serile hemorrhagic cystitis are similar to
those of other lower urinary tract disorders, and include pollakiuria, hematuria, and dysuria. Urinalyses are character-

4th European FECAVA SCIVAC Congress

ized by the presence of blood, with mildly to moderately increased numbers of white blood cells, and absence of bacteria. Treatment of this complication is aimed at discontinuing
the offending drug, forcing diuresis, diminishing inflammation of the bladder wall, and preventing secondary bacterial
infections. Discontinuation of CTX results in resolution of
the cystitis in most dogs within one to four months. In addition to discontinuing the drug, I administer furosemide
(Lasix), at a dose of 2 mg/kg, PO, BID for its diuretic effects; prednisone, at a dose of 0.5-1 mg/kg, PO, SID for its
antiinflammatory (and diuretic) effect; and a sulfadiazinetrimethoprim combination (Tribrissen), at a dose of 13-15
mg/kg, PO, BID to prevent secondary bacterial contamination. If despite this approach the clinical signs worsen, instillation of 1% formalin solution in water into the bladder
can be attempted. In two dogs thus treated, gross hematuria
resolved within 24 hours and did not reoccur. Intravesical infusion of a 25% to 50% DMSO solution may also alleviate
signs associated with cystitis in dogs.

References
Couto CG: Management of Complications of Cancer Chemotherapy. Vet
Clin North Amer 20:1037-1053, 1990.
Couto CG: Complications of cancer chemotherapy. In Nelson RW and
Couto CG: Essentials of Small Animal Internal Medicine. St. Louis,
Mosby, 1992, p 847.
Crow SE, Theilen GH, Madewell BR et al: Cyclophosphamide-induced
cystitis in the dog and cat. J Am Vet Med Assoc 171:259,1977.
Harvey HJ, MacEwen EG, Hayes AA: Neurotoxicosis associated with use
of 5-fluoruracil in five dogs and one cat. J Am Vet Med Assoc
171:277, 1977.
Knapp DW, Richardson RC, DeNicola DB, Long GG, Blevins WE: Cisplatin toxicity in cats. J Vet Internal Med 1:29, 1988.
Laing EJ, Miller CW, Cochrane SM: Treatment of cyclophosphamide-induced hemorrhagic cystitis in five dogs. J Am Vet Med Assoc
193:233, 1988.
Weller RE: Intravesical instillation of dilute formalin for treatment of cyclophosphamide-induced cystitis in two dogs. J Am Vet Med Assoc
172:1206, 1978.

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145

Fever of unknown origin in dogs


C. Guillermo Couto

Summary
Persistent fever in a patient in which a diagnosis cannot
be obtained is relatively common in practice. Fever of unknown origin can be due to infectious, immune-mediated,
neoplastic, or miscellaneous causes. The diagnostic and therapeutic approach to a patient with FUO will be discussed.

The term fever of undetermined (or unknown) origin


(FUO) is used quite liberally in veterinary medicine to describe a febrile syndrome for which a diagnosis is not evident. In human medicine, the term FUO refers to a febrile
syndrome of more than 3 weeks duration, which remains
undiagnosed after one week of thorough in-hospital evaluation. If the term FUO is used as recommended in the human
literature, very few dogs and cats will actually fit in that category. Therefore, this chapter will discuss the approach to a
dog with fever, which does not respond to antibacterial antibiotic treatment, and for which a diagnosis is not obvious
after obtaining a minimum data base (i.e.; CBC, serum biochemical profile, urinalysis).
In general, the clinician tends to assume that a dog with
fever has an infection, until proven otherwise. This appear to
be true in practice, since a large proportion of dogs with
fever respond to nonspecific antibacterial treatment. In most
of those patients, because the fever responds so promptly to
treatment, no clinicopathologic evaluation is performed.

Disorders associated with FUO


In humans, certain infectious, neoplastic, and immunemediated disorders are commonly associated with FUO. Approximately one third of the patients have infectious diseases; one third have cancer (mainly hematologic malignancies such as lymphoma and leukemia); and the remaining
one third have immune-mediated, granulomatous, or miscellaneous disorders. Ten to 15% of the patients with FUO remain undiagnosed despite intensive efforts to obtain a definitive answer.
However, to my knowledge, prospective or retrospective
studies of dogs with FUO are lacking in the veterinary literature. Based on the patients evaluated in our clinic and in reports from the literature, the most common cause of FUO
appear to be infectious diseases, followed by immune-medi-

ated, miscellaneous, and neoplastic disorders (Table 1). It


should be remembered that despite aggressive evaluation,
the cause of the fever cannot be determined in approximately 10% to 15% of the patients.
Table 1. Causes of fever of undetermined origin in dogs
Infectious
Bacterial
subacute bacterial endocarditis
brucellosis
tuberculosis
Lyme disease
suppurative infection
abscesses (liver, pancreas, stump pyometra)
prostatitis
diskospondylitis
pyelonephritis
peritonitis, pyothorax
septic arthritis
Rickettsial
ehrlichiosis, Rocky Mountain spotted fever, Salmon poisoning
Mycotic
histoplasmosis
blastomycosis
coccidioidomycosis
Protozoal
hemobartonellosis
babesiosis
hepatozoonosis
Chagas disease
leishmaniasis
Immune-Mediated
polyarthritis
vasculitis
meningitis
systemic lupus erythematosus
immune-hemolytic anemia (IHA)
steroid-responsive fever
Neoplastic
acute leukemia
chronic leukemia
lymphoma
malignant histiocytosis
multiple myeloma
necrotic solid tumors
Miscellaneous
metabolic bone disorders
drug-induced (tetracycline, enrofloxacin, penicillins, sulfa)
tissue necrosis
hyperthyroidism
idiopathic

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DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

146

Approach to the patient with FUO


A patient with FUO should be approached in a systematic fashion. In general, a three stage approach is used in our
clinic (Table 2). The first stage consists of a thorough history and physical examination, and a minimum data base. The
second stage consists of additional noninvasive and invasive
laboratory tests. The third stage consists of a therapeutic trial, and is instituted when no diagnosis is obtained after completing the second stage.
History and physical examination. Once a febrile patient fails to respond to antibacterial treatment, a course of
action must be formulated. A thorough history should be
obtained, and a complete physical examination should be
performed. The history rarely provides clues regarding the
cause of the fever; however, a history of ticks may suggest
the possibility of a rickettsial or hemoparasitic disorder, administration of tetracycline (mainly to cats) may suggest
the possibility of a drug-induced fever), and traveling to areas where systemic mycoses are endemic should prompt
further investigation by means of cytology, serology, or
fungal cultures.
During a physical examination, it is important to evaluate
the lymphoreticular organs, since a number of infectious and
neoplastic diseases affecting these organs (eg; ehrlichiosis,
RMSF, leukemia, systemic mycoses) may result in fever. An
enlarged lymph node or spleen should be evaluated cytologically by means of a fine needle aspiration (FNA); a sample
can also be obtained for bacterial and fungal culture and susceptibility through FNA, if the specimen is cytologically compatible with infection/inflammation. Any palpable mass/es or
swelling/s should also be evaluated by means of FNA.
The oropharynx should be inspected and palpated thor-

Table 2. Diagnostic evaluation of the dog with FUO


First Stage
CBC
Serum biochemical profile and thyroxine
Urinalysis
Urine bacterial culture and susceptibility
FNA of enlarged organs, masses or swellings
Second Stage
Thoracic and abdominal radiography
Abdominal ultrasonography
Echocardiogram
Serial blood cultures
Immune tests (ANA, RF)
Serum protein electrophoresis
Serology (see Table 1)
Arthrocentesis (cytology and culture)
Biopsy of any lesion or enlarged organ
Bone marrow aspiration (for cytology and bacterial/fungal culture)
Cerebrospinal fluid analysis
Leukocyte scanning
Exploratory celiotomy
Third Stage
Therapeutic trial (antipyretics, antibiotics, corticosteroids)

4th European FECAVA SCIVAC Congress

oughly, searching for signs of pharyngitis, stomatitis, or


tooth root abscesses. The bones should also be thoroughly
palpated, particularly in a young dog, since metabolic bone
disorders such as hypertrophic osteodystrophy, can result in
fever associated with bone pain. Palpation and passive motion of all joints is also indicated, in search of mono-, oligo,
or polyarthritis. A neurologic examination should be conducted to detect signs compatible with meningitis or other
CNS lesions.
The thorax should be ausculted carefully in search of a
murmur, which could indicate the presence of bacterial endocarditis. A thorough ocular exam may reveal changes suggestive of a specific etiology (eg; chorioretinitis in dogs with
ehrlichiosis).
Laboratory evaluation. A minimum data base consisting of a CBC, serum biochemical profile, urinalysis, and
urine bacterial culture and susceptibility should always be
obtained in dogs and cats with persistent fever. The CBC
may provide important clues regarding the cause of the fever
(Table 3). A serum biochemical profile is rarely diagnostic in
patients with FUO, although it provides indirect information
on parenchymal organ function. However, hyperglobulinemia and hypoalbuminemia may suggest an infectious, immune-mediated, or neoplastic disorder. Pyuria in a urinalysis is suggestive of a urinary tract infection (UTI); however,
lower UTIs rarely result in fever.
Finally, when a definitive diagnosis has not been obtained, a therapeutic trial of specific antibacterial/antifungal
agents or immunosuppressive doses of corticosteroids can
be initiated (see below).
If a dog presents with chronic fever and severe neutropenia, it must be determined if the neutropenia is the
cause or the consequence of the pyrexia (i.e.; which one
came first). Several clues from the physical examination and
CBC are helpful in establishing this. If the patient is severely ill, and the neutrophils in the blood smear are toxic (or
there is a pronounced left shift), the neutropenia is probably
the consequence of the fever (i.e.; there is neutrophil consumption due to bacterial infection, that initiated the fever).
If a dog is healthy (other than the fact that he/she has a
fever), and if the neutrophils do not exhibit toxic changes,
the most likely explanation is that the fever is secondary to
the neutropenia. The latter patients are likely to have steroidresponsive neutropenia.

Treatment
If a definitive diagnosis is obtained, a specific treatment
should be initiated. The problem arises when a definitive diagnosis cannot be arrived at. In these patients, changes in the
CBC usually represent the only laboratory abnormality
(Table 3). That is, results of bacterial and fungal cultures,
serology, imaging, and FNAs are negative (or the studies are
normal). If the patient has already been treated with a broad
spectrum bactericidal antibiotic, a therapeutic trial of immunosuppressive doses of corticosteroids is warranted.
However, prior to instituting this treatment, the owners
should be informed of the potential consequences of this approach (mainly, if the dog has an undiagnosed infectious dis-

Table 3. Hematologic changes in dogs with FUO


Hematologic change

Compatible with

Regenerative anemia

immune-mediated, hemoparasites,
drugs
infection, immune-mediated, tissue
necrosis, malignancy, endocarditis
infection, immune-mediated, tissue
necrosis, malignancy, endocarditis
leukemia, immune-mediated,
pyogenic infection, bone marrow
infiltrative disease, drugs
infection, immune-mediated, tissue
necrosis, lymphoma, endocarditis,
histiocytosis
ehrlichiosis, Chagas disease,
leishmaniasis, chronic lymphocytic leukemia
hypereosinophilic syndrome,
eosinophilic inflammation, lymphoma
rickettsiae, leukemia, lymphoma,
drugs, immune-mediated
infectious (chronic),
immune-mediated

Nonregenerative anemia
Neutrophilia with left shift
Neutropenia

Monocytosis

Lymphocytosis

Eosinophilia

Thrombocytopenia
Thrombocytosis

147

ease, death could occur from systemic dissemination of the


organism after initiating immunosuppressive treatment). In
patients with immune-mediated (or steroid-responsive)
FUO, the pyrexia and clinical signs usually resolve within
24 to 48 hours of initiating treatment; in that case, the patient
is treated with maintenance immunosuppressive therapy.
If no response to corticosteroids is observed, two courses of action remain. First, to release the patient on antipyretic drugs, such as aspirin (10-25 mg/kg, PO, BID in dogs and
10 mg/kg, PO, every third day in cats), with instructions to
return to the clinic for a complete reevaluation in one to two
weeks. Antipyretics should be used with caution, since as
discussed above, fever is a protective mechanism (i.e.; lowering the body temperature may be detrimental in a patient
with an infectious disease. Moreover, drugs such as dipyrone and banamine, can result in significant hypothermia,
which may have adverse effects for the patient. It should also be remembered that most nonsteroidal antiinflammatory
drugs, in addition to their ulcerogenic effects, can cause
blood cytopenias and result in tubular nephropathy when the
patient becomes dehydrated or receives other nephrotoxic
drugs. Second, antibiotic trials can be continued, using a
combination of bactericidal drugs (eg; a cephalosporin and
an aminoglycoside) for a minimum of 5 to 7 days.

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149

Recurrent infections in dogs


C. Guillermo Couto

Summary
Recurrent or persistent infections are usually the result of
congenital or acquired abnormalities of the immune system.
Some breeds appear to be at high risk for congenital immunologic defects. This lecture will discuss the diagnostic and therapeutic approach to dogs and cats with recurrent infections.

Recurrent or persistent infections are usually the results


of congenital or acquired abnormalities of the immune system. Although canine clinical immunology is not a well developed speciality, great progress has been made over the
past decade in elucidating the underlying immunologic abnormalities in dogs with recurrent infections.
Congenital immunodeficiency syndromes in dogs can
affect the humoral, cellular, or phagocytic systems, either
singly or in combination. Humoral immunodeficiency syndromes include IgA deficiency in beagles, Shar-pei and, possibly, German shepherd dogs; IgM deficiency in Doberman
pinschers (not well documented); C3 deficiency in Brittany
spaniels; and transient hypogammaglobulinemia in
Samoyeds. These dogs usually suffer from recurrent upper
and lower respiratory tract infections, dermatitis, and enteritis; some beagles with selective IgA deficiency also experienced grand mal seizures.
Cellular immunodeficiency syndromes are apparently
less common; a T-cell abnormality has been documented in
Weimaraners with pituitary dwarfism and in Bull Terriers
with lethal acrodermatitis. The disease in Weimaraner pups
was characterized by retarded growth and recurrent respiratory and gastrointestinal infections. Necropsy findings in the
affected dogs included hypoplastic thymuses with absence
of thymic cortex. Several related Bull Terriers with growth
retardation, progressive acrodermatitis, chronic pyoderma
and paronichia, pneumonia, and diarrhea exhibited significantly decreased lymphocyte blastogenesis in response to
PHA stimulation. Other diseases with inconsistent cell-mediated immunologic abnormalities include Pneumocystis
carinii infection in Dachshunds, systemic aspergillosis, generalized demodicosis, and protothecosis.
Abnormalities in the phagocytic system have been well
documented in dogs. They may occur as a consequence of
decreased numbers of circulating phagocytes (ie; in grey
collies with cyclic hematopoiesis), or as a consequence of
abnormal phagocytic function (ie; defective neutrophil ad-

hesion in Irish setters with granulocytopathy syndrome; defective bactericidal capacity in Doberman pinschers with recurrent respiratory infections). Setters with deficiency of
surface adhesion proteins have recurrent episodes of omphalophlebitis, gingivitis, lymphadenitis, pyoderma, respiratory infections, pyometra, and fulminant sepsis. Affected
Dobermans exhibited recurrent episodes of rhinitis and
pneumonia that responded transiently to antibiotic therapy.
Immunodeficiency syndromes affecting more than 1 arm
of the immune system have been documented in a family of
Basset Hounds, and in several related Weimaraners. In the
former, severe growth retardation and early death were associated with low serum IgG and IgA concentrations, and
with abnormal lymphocyte blastogenesis in response to
PHA. In the latter, recurrent sytemic or multifocal infections
were associated with low serum IgG and IgM concentrations
and with impaired neutrophil chemiluminescence.
Acquired immunodeficiency syndromes include canine
distemper virus and parvovirus infections, and generalized
demodicosis. In addition, the use of systemic anticancer
agents may result in variable degrees of immunosuppression.
The type of infectious agent and the pattern of infection
are usually determined by the nature of the defect. For example, defects in the humoral immunity usually result in infections with pyogenic organisms affecting one or more
sites; defects in T-cell function result in viral, fungal, or protozoal infections that are usually widespread; abnormalities
in the phagocytic system may result in skin, respiratory,
meningeal, or systemic infections with pyogenic or enteric
organisms. Therefore, the type and pattern of infection will
dictate what test/s should be used in these patients.
Several diagnostic tests can be used in the evaluation of
dogs with suspected immunodeficiency. Some of these tests
(ie; neutrophil function tests; lymphocyte blastogenesis) require fresh blood samples (ie; need to be done within 4
hours) and specialized laboratory equipment; they are therefore of limited use to general practitioners and are limited to
teaching or research institutions. Other tests, however, can
be done of serum samples and can therefore be mailed to referral laboratories.
The following are some of the tests that can be used to
evaluate patients with recurrent infections:
humoral immunity: serum protein electrophoresis, immunoelectrophoresis, radial immunodiffusion for Ig levels, complement levels;
cellular immunity: lymphocyte blastogenesis in re-

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DVM, Dipl ACVIM


Department of Veterinary Clinical Sciences - College of Veterinary Medicine
The Ohio State University - Columbus, Ohio - USA

150

sponse to ConA, PWM, and PHA; enumeration of circulating T-cells; NK cell assays;
phagocytic system: nylon wool adhesion; migration under agarose; phagocytosis of bacteria, yeasts, or latex;
phagocytosis of opsonized particles; chemiluminescence;
nitroblue tetrazolium reduction test; bacterial killing assay.
Clinical management of these patients includes use of
the appropriate antimicrobial drugs on the basis of identification of the etiologic agent. If an infectious agent cannot be
isolated and the patient appears to have a bacterial infection,
bacteriocidal antibiotics that attain high intraleukocyte concentrations (ie; sulfa-trimethoprim) should be used.

4th European FECAVA SCIVAC Congress

References
Felsburg PJ: Immunodeficiency. In Kirk RW (ed): Current Veterinary Therapy IX. WB Saunders, Philadelphia. 1986, pp 439-444.
Degen MA, Breitschwerdt EB: Canine and feline immunodeficiencies Part I. Comp Cont Educ 8:313-323, 1986.
Degen MA, Breitschwerdt EB: Canine and feline. immunodeficiencies Part II. Comp Cont Educ 8:379-386, 1986.
Couto CG, Giger U: Congentital and acquired neutrophil function abnormalities in the dog. In Kirk RW (ed): Current veterinary Therapy X.
WB Saunders, Philadelphia. in press.
Guilford WG: Primary immunodeficiency diseases of dogs and cats. Comp
Cont Educ 9:641-650, 1987.

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151

Emergency care of pet birds


Lorenzo Crosta

Summary
Emergencies are still frequent with avian patients. Pet
bird owners must understand the importance of preventive
medicine, but they should also be educated by competent
professionals. Even more important is for veterinarians and
technicians to be trained to deal properly with avian emergencies. This paper takes into consideration the general aspects of these cases, like staff education, patient stabilization
and fluid therapy. Afterwards a short list of equipment and
tools for avian emergencies is given. Finally the most frequent emergencies in avian medicine are considered.

Introduction
Avian medicine is one of the latest veterinary specialization, and the progress and developments in this field have
been remarkable in the past few years. What still differentiates avian medicine from other veterinary specializations, is
preventive medicine with all those regular appointments,
like vaccinations, check-ups and others, which make the relationship between veterinarian and bird owner more constant, therefore increasing the chances for a sub-clinical or
still inapparent disease, to be diagnosed. To make matters
worse birds have a peculiar way of hiding symptoms of disease; this seems to be a necessity for birds to look healthy to
any possible predator. If this attitude is an advantage in the
wild, it makes it very difficult to understand how serious a
birds disease can be, so symptoms seem to appear and develop very suddenly and birds presented to a veterinarian are
often emergencies.
Obviously many emergencies, like traumas and toxicosis, do not have any relation with preventive medicine, but if
the owners of some of these patients could have been trained
on good bird management, their pets would not have needed
the veterinarians help.

Staff training
As weve just seen with avian emergencies time is often
so short that a proper training of all the clinics staff is really making the difference. The veterinarian should understand all the physiological and pathophysiological aspects of
the avian patient, furthermore she/he must have a good

knowledge of pharmacodynamics in birds, at least of the


drugs most frequently used in these emergencies. Technicians should know how to act rapidly and with certain ease
with these particular patients, without creating any risk for
the bird. Everybody should also know perfectly where all
the emergency equipment is located; all these points help
achieve the first aim of emergency medicine: patient stabilization. It is also very important for a technician to complete
a detailed form regarding the patients history.
Last but not least, considering the zoological variety of
the avian patients, the practitioner should be able to taxonomically locate the presented bird. This could be very important, as the same symptom can have a different diagnostic meaning in different bird species. So while the veterinarian waits for tests results and the chance to make a sure diagnosis, she/he can make a presumptive one, which must
take into consideration the patients species.

Patient stabilization
Stabilization of the avian patient follows the same procedures as those of emergency treatment in mammals, but
we must not forget that birds are easily stressed and this
could depend on the fact that they are always prey to a
predator bigger than themselves. This continous condition of
vulnerabilty induces a bird to appear healthy, especially
when faced with a potential predator like man. For these reasons during emergencies, before handling the bird it is very
important to observe it in its enclosure, as this will make it
feel less threatened. A first important step is to observe carefully the depth and rate of breathing: a rapid and superficial
breathing may show a critically ill and hypothermic bird, as
so happens during septicemia; while dyspnoea or laboured
breathing may indicate a disease which involves the respiratory system directly. In these cases it is always better to put
the patient in a heated cage supplied with oxygen, allowing
the bird to rest and calm down before handling. In the meantime, if it has not already been done, a complete clinical history of the bird can be compiled. If the bird can be weighed
or we already know its weight, we can be able to calculate
the exact dose of the drugs we intend to use; otherwise the
birds weight can be estimated according to the ideal weight
of that particular species. If the bird can be handled it is better not to stress it with forced restraint, but to anesthetize it
with isoflurane: this will allow us to proceed without risk, to

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dress wounds, temporarily fix fractures, collect blood, swabs


and other diagnostic specimens, and administer the preliminary drug therapy.

Fluid replacement therapy


Fluid therapy is a very important tool in the case of avian
emergencies, but we must pay attention to some facts that
differentiate birds from mammals: normally, a healthy birds
water intake varies from 5 to 30% of its body weight, according to the birds species, body weight and type of food.
Theoretically this determines a degree of variability in the
fluid requirements of sick birds, too. Anyway, as a general
rule, the mean fluid need of a bird can be estimated at 50
ml/kg b.w./day. It is important to assess the dehydration degree of the patient, expressed in percent, together with its
ideal body weight, which will allow a good estimation of the
fluid requirements per day. Lactated Ringers solution is
generally used, warmed to 100.4 to 102.2 F (38 - 39 C),
while the route of administration may change according to
many factors.
Oral route: this is the easiest way of fluid or drug administration to birds, but it is not suitable for emergencies.
Severely sick birds might regurgitate fluids and suffocate.
Subcutaneous route: birds do not have much subcutaneous tissue and their skin is not as elastic as that of mammals. However, the subcutaneous route is used to replace
fluids in moderately dehydrated birds. Small fluid amounts
can be injected in different sites on a birds back, or bigger
amounts can be injected in the axilla or flank region, where
we are less likely to inject fluids in an air sac. For these reasons subcutaneous administration is used primarily for
maintenance fluid therapy.
Intravenous route: this is the most direct route for administration of fluids in birds too, in a word it is definitively the emergency route of fluid administration. The most
used vessels for this purpose are the right jugular vein, the
ulnar vein and the medial metatarsal vein. Blood vessels of
birds are easily visible, but they are very fragile and lack
elastic fibers, therefore placing an intravenous catheter in
bird is simply done, but to leave it in place for long periods
may be difficult. Consequently intravenous catheters are
placed during isoflurane anesthesia or in very depressed patients. In this way sufficient fliud volumes can be administered quickly (10 ml/kg b.w. over the first five minutes, to be
repeated every 3 - 4 hours for the first 12 hours, then every
8 hours for the following 48 hours). In very calm birds it is
possible to leave an intravenous catheter in the ulnar vein;
while the medial metatarsal vein is preferred in Anseriformes (ducks and geese), in Columbiformes (pigeons and
doves), in various long-legged birds and in some birds of
prey. This last vein, if cannulated, can be managed as the
cephalic vein of dogs and cats.
Intraosseous route: in birds it is considered a very good
alternative to intravenous administration; furthermore to
leave an intraosseous catheter in place, in a bird, is more
easy than to leave an intravenous one. The way to place intraosseous catheters in avian patients is the same as used in
mammals; the bones of choice are the ulna and the tibiotar-

4th European FECAVA SCIVAC Congress

sus: in the first bone a distal access is used, in the latter a


proximal one. To avoid the bone cortex blocking the needle
channel, spinal needles are preferred. As happens in mammals, the major risk of this procedure are bone infections;
furthermore often an infusion pump is often needed to help
the fluid pass through the intraosseous catheter.

Equipment for avian emergencies


- Incubators
- Gram scale
- Fluid warming chamber
- Nebulizer
- Circulating warm-water blanket, Heat lamps
- Towels for restraint
- Isoflurane anhaestesia machine
- Face masks for anhaestesia induction
- Respiratory monitor
- Small endoscopes, flexible and rigid
- Small endotracheal tubes
- Sterilized air sac tubes
- Radiosurgical unit
- Leg band cutter
- Haemostatic sticks
- Intravenous catheters, 20 - 24 G
- Variety of spinal needles
- Infusion pump
- Microdrip IV administration sets
- Parrot mouth speculums
- Vetwrap like bandages, cut into small sizes
- Slides and cover slips
- Heparinized microhematocrit tubes
- Blood smears stains
- Microbiology swabs

Common avian emergiences


- shock (septic, toxic, traumatic)
- toxicosis
- seizures
- major wounds
- oiled birds
- frostbite
- head trauma
- open fractures
- haemorrhagiae
- hypoglicemia
- hypocalcemia
- tight leg band
- apnoea
- acute dyspnoea
- tracheal foreign bodies
- beak fractures
- tongue lesions
- crop wounds
- crop burns
- g.e. foreign bodies
- gastric impaction

- cloacal prolapse
- egg binding
- oviduct prolapse
- phallus prolapse

Literature
Crosta L, (1992), Uccelli e inquinamento da petrolio e derivati, metodi di
trattamento e rilascio. Ob. e Doc. Veterinari, 12: 27 - 32.
Crosta L, (1997), La visita clinica del paziente aviare: principali punti di
repere, contenimento manuale e farmacologico e dosaggio di alcuni
farmaci di comune impiego. Veterinaria, 11 (2): 115 - 129.

153
Degernes LA: Trauma Medicine. In: Ritchie BW, Harrison GJ and Harrison
LR, (1994), Avian Medicine: Principles and Application, Wingers
Publishing, Lake Worth, pp. 417 - 433.
Heidenreich M, (1997), Birds of Prey, Medicine and Management. Blackwell Science Ltd, Oxford, pp. 98 - 101.
Jenkins JR: Avian Critical Care and Emergency Medicine. In: Altman RB,
Clbb SL, Dorrestein GM and Quesenberry K, (1997), Avian Medicine
and Surgery, W.B. Saunders Company, Philadelphia, pp. 839 - 863.
Quesenberry K and Hillyer EV: Supportive Care and Emergency Therapy.
In: Ritchie BW, Harrison GJ and Harrison LR, (1994), Avian Medicine: Principles and Application, Wingers Publishing, Lake Worth,
pp. 382 - 416.
Redig PT: Management of medical emergencies in raptors. In: Redig PT,
(1993), Medical Management of Birds of Prey, 3rd ed, St. Paul, pp.
13 - 21.

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155

Emergency care and medical stabilisation


of reptiles
Stephen John Divers

Summary
The veterinary care of reptiles has progressed a great
deal over the past decade or so. Current practice has built
upon the foundations laid down by pioneers such that the
veterinary surgeon is now able to offer a comparable level
of care for reptiles as has been available for the more domestic animals for many years. However, with increasing
skill comes increasing expectations, and reptile clinicians
are now being increasingly asked to deal with critically sick
animals. This paper hopes to introduce the clinician to the
important aspects of providing emergency care for reptiles.
Emphasis is made of the importance of a through history and
clinical examination, diagnostic investigations and medical
stabilisation including parenteral fluid therapy. Some common emergency scenarios are also discussed.

Introduction
Reptile emergencies do occur; the tortoise attacked by a
dog, the iguana with hypocalcaemic tetany, the septicaemic
python. The basic approach to emergency reptile medicine
follows along similar lines to domestic animal medicine,
however reptile medicine also throws up a number of other
problems1. Reptiles are ectothermic and have a metabolic
rate comparable to 1/7 that of mammals. Their slower metabolism generally results in the slower clinical manifestations
of disease. Therefore, the clinician will often be presented
with a moribund reptile that was in apparently good health
the previous day. Some of these cases are true medical emergencies but many represent the terminal presentation of a
chronic illness.

History
In cases of true emergency, it may be essential to admit
and commence treatment (e.g. oxygen therapy) prior to taking a complete history, but in such cases a history should be
taken by a veterinary nurse or the veterinarian at the earliest
convenience. The importance of a detailed history must never be overlooked and may actually help in determining
whether the current situation is truly acute or merely the terminal stage of chronic disease2. Historical details of interest
include:

temperature and thermal environment (power cuts,


heater malfunction, electrocution, breeding programme).
Lighting (sunlight, artificial UVB lights, how old, lightreptile distance, electrocution).
Hide-outs, substrate (wet, mouldy), furniture (fallen
rocks or branches).
Recent changes in husbandry (last 6-12 months).
Other reptiles in direct contact with current patient (their
health, clinical signs).
Recent additions to collection (last 6-12 months, quarantine).
Appetite and food intake (reduced, increased, slow deterioration, complete anorexia, duration, food types, supplements).
Water intake and humidity (observed drinking, increase
or decrease, unknown).
Changes in behaviour (courtship, mating, egg
laying/birth, tremors, depression, lethargy).
Owners records (weights, snout-vent measurements,
Jackson ratio, ecdysis, routine treatments, other medications.)

Clinical examination
In cases of true emergency, it may be essential to admit
and commence treatment prior to performing a complete examination. Nevertheless a thorough clinical exam is always
indicated and should be performed as soon as possible2. The
examination should be systematic and cover all available
systems. Traumatised areas including severe burns, fractures
and wounds must be handled carefully to avoid further damage. During the examination;
Confirm species, sex and age.
Obtain an accurate weight and length, and an appreciation of overall body condition (pelvic limb and tail muscle
coverage, poverty lines).
Obtain an appreciation of respiratory and cardiovascular
function; head extended and open mouth breathing, glottal
discharge, increased respiratory efforts at rest and when unrestrained, buccal mucous membrane colour, demeanour
(active or lethargic), auscultation or Doppler for heart rate
and peripheral pulse rate.
Obtain an appreciation of metabolic disturbances and hydration; tremors, seizures, moribund, urate tophi in mucous
membranes of mouth, reduced skin elasticity, skin tenting,
swollen limbs/jaw, pyramiding or saddle-like shell.

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The Exotic Animal Centre - Essex - United Kingdom

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Obtain an appreciation of the integument; abscessation,


swellings and discharges, erythema and petechial haemorrhages, burns, lacerations and penetrating injuries.
Obtain an appreciation of the gastro-intestinal tract; buccal cavity, cloaca, coelomic palpation.
Obtain an appreciation of the urogenital system; if possible palpate kidneys, coelomic cavity for bladder stones and
eggs.
Obtain an assessment of the musculoskeletal system;
limbs, jaw, swellings, fractures, muscle loss, cachexia.

Trauma
In cases of severe and continued bleeding haemostasis
can be achieved by the application of local pressure bandages. Identified vessels may be permanently or temporarily ligated using nylon or vascular clips, or repaired under
isoflurane or local anaesthesia to maintain important vascular supplies. The application of calcium or adrenaline impregnated swabs and radiosurgery are also useful in the control of haemorrhage.
Prolapses of gastrointestinal tract through penetrating
coelomic wounds should be cleaned and replaced as long as
the intestinal segment is viable and has no lacerations that
will lead to the leakage of gut contents. The wound is then
packed with sterile swabs soaked in dilute povidone-iodine
solution or metronidazole solution (Torgyl, 5 mg/ml, Rhone
Merieux) and bandaged using plastic film. In cases of intestinal laceration, the site should be packed with moist sterile swabs, maintaining the intestine outside the coelomic
cavity and the whole area bandaged as before until surgery
can be undertaken.
Cloacal, penile, colonic and bladder prolapses should be
replaced if at all possible. If surgery is thought necessary
the area can be bandaged using moist swabs and plastic
film to prevent dehiscence until the operation can be safely
undertaken.
Traumatised soft tissues including limbs, tail, flanks and
shell should be treated in much the same way as for domestic animals. If medical stabilisation is required before
surgery then immobilising the area, covering with sterile
gauze and bandaging will prevent further damage and contamination. Burns are particularly prone to infection and the
liberal use of topical silver sulphadiazine cream (Flamazine,
1%, Smith and Nephew) cream is recommended.
Bite wounds tend to be superficial lacerations but deep
penetrating wounds should not be sutured, but treated as infected wounds.

Drowning
Tortoises kept in garden enclosures seem particularly
prone to drowning and may not be recovered from the pond
for several hours. These animals are often presented in a
moribund state. In very unresponsive cases (no deep pain response or corneal reflex) it is wise to obtain e.c.g. evidence
that the reptile is still alive before proceeding. Whatever the
species, position and tape an endotracheal tube in place, and

4th European FECAVA SCIVAC Congress

hold the animal head down. Pump the limbs of chelonia,


massage the thorax of lizards or lung field area of snakes to
aid evacuation of water. This should encourage voiding of
any fluid remaining within the lung fields. Inflate the lungs
with either air or pure oxygen and give intravenous
doxapram (Dopram-V, 20 mg/ml, Willows Francis) at 5-10
mg/kg i.v. to help stimulate respiration. Until spontaneous
breathing returns (which may take minutes or hours) the reptile should be maintained on a respiratory monitor and given intermittent positive pressure ventilation 2-4 times every
minute. Cases of drowning in freshwater seldom require fluid therapy unless severe cardiovascular or respiratory compromise continues. However, cases of drowning in marine
water will often lead to rapid water loss from the lungs and
dehydration. In these cases fluid therapy is recommended.
The prophylactic use of broad spectrum antibiotics is advisable as secondary pneumonia is not uncommon.

Hypothermia and hyperthermia


Severe hypothermia can result from heating failure or
more commonly delayed national and international transportation. Slow sustained warming is essential as too rapid a
rise in core temperature may cause further compromise.
Gradual increase in environmental temperature to the
species-specific POTZ (preferred optimum temperature
zone) over 4-24 hours depending on degree of hypothermia
is usually sufficient. In severe cases fluid therapy using
warm fluids may also be beneficial.
Hyperthermia is less common than burns, however, constant exposure to temperatures above the POTZ and approaching the species-specific critical high temperature (often 35-45C) will lead to heat stress. Open mouth breathing,
increased respiratory effort and collapse are common signs.
Immediate reduction of the environmental temperature to
the lower end of the species specific POTZ is required. In severe cases, fluid therapy using cooler but not refrigerated
fluids (20-30C) may be beneficial.

Intestinal obstruction and constipation


Gastro-intestinal obstructions may be due to gravel,
stones, bark, balls, rubber suction devices, elastic bands, abscesses, neoplasia, intussusception, ileus, renal enlargement,
cloacitis, faecoliths and parasites. Characteristic signs include regurgitation, tenesmus and diarrhoea, and less commonly blood in faeces or vomitus. Coelomic palpation may
reveal discernible masses within the gastro-intestinal (or reproductive) tract.
In such cases electrolyte and fluid imbalances should be
corrected. Faecal analysis may reveal parasites that should
be treated. In cases of constipation, it is important to consider predisposing factors including renal disease, but until the
reptile is stable and a thorough investigation can be undertaken, the use of oral laxatives or water enemas may be tried.
Once stable, radiography and endoscopy should be used
to diagnose the problem and appropriate measures can then
be taken where necessary.

Pneumonia
Reptiles lack a functional diaphragm and therefore have
great difficulty in coughing. In cases of pneumonia, infectious exudates tend to accumulate reducing the functional
area of lung. Once the functional pulmonary reserve has
been exceeded the reptile will present with increased respiratory effort at rest, and a possible glottal discharge. Providing a high oxygen environment will help alleviate the signs.
In severe cases with confirmed radiographic fluid lines, it is
often helpful to insert a small catheter down the trachea into
the lung fields and aspirate as much exudate as possible. The
exudate should then be submitted for laboratory analysis. In
moribund lizards sedation or isoflurane anaesthesia is seldom necessary for lung exudate aspiration.

Medical stabilisation
Assessment of dehydration,
metabolic disturbances and fluid therapy
Hydration status can be assessed in much the same way
as other animals, including reduction in skin elasticity, dull
and wrinkled skin. This must not be confused with normal
ecdysis (skin shedding). Pre-treatment blood samples are
very useful in evaluating hydration status and biochemical
derangements in reptiles. Although there is relatively little
published data on observed haematology and serum/plasma
biochemistry values, serial blood samples offer the best assessment of hydration status and response to therapy.
Preferred reptile venepuncture sites:
SnakesVentral tail vein, caudal to cloaca; The needle is angled
at 45-90 (craniodorsal) and placed in the ventral mid line
in-between paired caudal scales. A 5/8-1 21-25 g needle is
advanced, avoiding the hemipenes of males, while maintaining a slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Avoid the hemipenes of
males.
Cardiocentesis; The snake is restrained in dorsal recumbency and the heart located at a point 22-33% from the snout
to the vent. The heart is palpated and immobilised using the
thumb and forefinger and a 23-25 g 5/8-11/2 needle is advanced at 45 in a craniodorsal direction into the apex of the
beating ventricle. Blood often enters with each heart beat.
LizardsVentral tail vein; A 5/8-1 21-25 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect.
Ventral abdominal; A 5/8-1 23-25 g needle is advanced
in the ventral mid line in a craniodorsal direction. The vein
lies just below the abdominal musculature and it is difficult
to apply post-sampling pressure which makes haemorrhage
a concern.
Tortoises, turtles and terrapinsDorsal tail vein; A 5/8 21-25 g needle is angled at 45-90
and placed, as cranial as possible, in the dorsal mid line of

157

the tail. The needle is advanced while maintaining a slight


negative pressure. If the needle hits a vertebral body, withdraw slightly and redirect. The exact position, size and even
presence of this vessel may vary between species.
Right jugular; A 5/8 23-25 g needle is positioned lateral
at the level of the tympanic scale, and directed caudally midway down the neck. It is important to maintain post-sampling pressure to avoid haematoma formation.
Subcarapacial vein; The head is pushed inside the
coelomic cavity and a needle (bent to 60-75) is inserted in
the mid line just caudal to where the skin of the neck attaches to the cranial rim of the carapace. Advance the 5/8-1 2325 g needle in a dorsal direction and maintain slight negative
pressure. It is important to maintain post-sampling pressure
to avoid haematoma formation.
There are a variety of other venepuncture sites including
the brachial plexus and femoral plexus, however they usually provide smaller samples which are more often contaminated by lymphatic fluid.
CrocodiliansVentral tail vein; A 1-3 18-23 g needle is angled at 6090 and placed in the ventral mid line about 1/4 to 1/3 of the
way down the tail. The needle is advanced while maintaining slight negative pressure. If the needle hits a vertebral
body withdraw slightly and redirect. Larger crocodilians
(over 1.5 m in length) may require chemical restraint using
a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with neostigmine), and it may be necessary to use large spinal needles (3-8) to reach the vein.
Supravertebral vein; A 1-2 20-23 g needle is inserted at
90 in the mid line just caudal to the occiput. The needle is
advanced to just dorsal to the spinal cord, while maintaining
a slight negative pressure. Larger crocodilians (over 1.5 m)
may require chemical restaint using a neuromuscular blocking agent (e.g. 0.4-1.0 mg/kg gallamine, reversable with
neostigmine).
Intramuscular injections can be given into the epaxial
muscles of snakes and proximal forelimb muscles of chelonia, lizards and crocodilians.
The daily water requirements for reptiles have not been
conclusively determined. Published literature suggests that
reptiles may be rehydrated by providing fluids at a rate of
10-50 ml/kg/day, but 15-30 ml/kg/day appears more appropriate for the vast majority of species5,6,7. Rehydration can
take several days to a week or more and it is wise to rehydrate slowly.
Dehydration in reptiles may be characterised as isotonic,
hypotonic or hypertonic5. Hypotonic dehydration is most
commonly associated with prolonged anorexia and hypertonic dehydration associated with water deprivation or an inability to drink. Isotonic dehydration can occur following
haemorrhage, emesis, diarrhoea and tissue damage. Water
balance in reptiles differs from that of mammals as, per unit
body weight, reptiles have a higher percentage of total body
water (63.0-74.4%) and a higher percentage intracellular
water (45.8-58.0%).8 These values appear to be highest in
freshwater species, lower in terrestrial reptiles and lowest in
marine reptiles, with the concentration of isotonic saline in
non-marine reptiles being 0.8%9. This has led to the recommendation that standard 0.9% normal saline solutions be

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4th European FECAVA SCIVAC Congress

158

slightly diluted for use in reptiles to facilitate the intracellular diffusion of water. Four suggested fluid solutions for parenteral administration in reptiles are:
1) Two parts 2.5% dextrose in 0.45% sodium chloride and
one part Ringers or equivalent electrolyte solution5.
2) One part 5% dextrose in 0.9% sodium chloride, one part
lactated Ringers and one part sterile water.
3) Nine parts 0.9% sodium chloride and one part sterile
water.
4) 0.18% sodium chloride and 4% glucose.
All fluids given by any route must be warmed to the
species-specific PBT (often 30-35C) prior to administration.
Bathing, oral, subcutaneous and intracoelomic fluid administration must not be overlooked, however intravenous
or intraosseous routes offer the best fluid therapeutic approach in emergency situations. Intravenous catheterisation
is not easy in reptiles and cut-down procedures are often required under local or isoflurane anaesthesia. In large lizards,
cephalic and abdominal vein catheterisation has been employed, while the right jugular is most accessible in the chelonia. In snakes, the right jugular can be catheterised using a
cut-down technique. The incision site is located 12 abdominal scales cranial to the heart and two lateral scales to the
right. A 2-3 cm incision reveals the jugular just medial to the
ribs, which can then be catheterised with a 50-100 mm (24) 20-23 g catheter. In larger snakes it is possible to place
an intracardiac catheter. The heart is located and immobilised as described previously for blood sampling, and a 2575 mm (1-3) 22-23 g catheter is inserted just caudal to the
heart apex and advanced cranially into the ventricle. In all
cases of venous catheterisation, the catheter must be securely sutured to the skin and bandaged in place. Fluid infusion
is best controlled by a syringe driver. Most intravenous
catheters can be left in place for up to 72 hours, or up to 36
hours in the case of intracardiac catheters.
Intraosseous infusion is an easier technique that is available for use in lizards, small crocodilians and chelonia. In
lizards and small crocodilians a 19-38 mm (3/4-11/2) 20-25 g
spinal needle (or 16 mm 5/8 25 g hypodermic needle for
very small species) is inserted into the proximal tibia. The
limb is flexed and the tibial tuberosity located. The needle is
inserted distally while holding the body of the tibia. Correct
positioning can be verified by the aspiration of bone marrow,
low resistance to flushing with heparinised saline, or radiography. Greater care must be exercised when dealing with osteodystrophic lizards as limb fractures are a potential complication. In chelonians, the intraosseous needle can be inserted into the distal tibia or the medullary cavity of the vertical shell that connects the carapace and plastron. Intraosseous needles are taped in position using zinc oxide
tape, incorporating a loop of the extension line to reduce
catheter tension. Syringe drivers are used to control the infusion rate. The author has used this intraosseous technique
in reptiles as small as 75 grams and considers it the parenteral route of choice.
Infusion rates for intravenous and intraosseous administration are similar. As a general guide 0.8-1.4 ml/kg/hour is
suitable for rehydration purposes, but in cases of severe dehydration, shock or during surgery the author has used 5
ml/kg/hour for up to 3 hours without ill effect.

4th European FECAVA SCIVAC Congress

Haemorrhage
In cases of severe haemorrhage a PCV evaluation is warranted. If the PCV is below 0.05L/L then a single whole
blood transfusion may be indicated. Blood should only be
collected from healthy reptiles preferably of the same
species and from the same collection to avoid cross-colony
infection. However, the author has taken blood from Hermanns tortoises (Testudo hermanni) for transfusion into a
leopard tortoise (Geochelone pardalis), and has taken blood
from a green iguana (Iguana iguana) for transfusion into a
common tegu (Tupinambis teguixin) without obvious ill-effects. Cross matching does not appear necessary, at least for
a one-off transfusion. The donor reptile can provide 7 ml/kg
blood which can be collected into a heparinised syringe for
immediate administration to the recipient. Alternatively,
blood may be collected into citrate-phosphate-dextrose and
administered later. Catheterisation of the right jugular of
donor and recipient tortoises facilitates blood collection and
transfusion. In lizards, collection and transfusion via the
ventral tail vein appears to work well. In snakes a jugular
catheter or cardiac catheter should be utilised. Blood has also been administered via an intraosseous catheter in iguanas.
Reptiles are able to cope with much greater blood loss than
mammals, and so blood transfusion is only required in dire
circumstances when the animal is very depressed following
acute and severe haemorrhage. Usually, the administration
of intravenous or intraosseous fluids is acceptable. Colloids
are less frequently used in reptiles because much of the water loss is from the intracellular space rather than plasma, but
in cases of acute haemorrhage their use is commendable.

Laboratory investigation
Basic biochemistries can be run on many in-house practice laboratories (e.g. Vettest 8001) with a reasonable degree
of accuracy. Uric acid must always be undertaken as a level
of over 1000 umol/l in an anorexic reptile tends to indicate
severe azotaemia (pre-renal, renal or post-renal). Above
1487 umol/l uric acid may start to precipitate out and cause
gout. However, post-prandial elevations of uric acid can occur normally in many species, particularly snakes, and so
short-term elevations of uric acid may not carry such a poor
prognosis. Consistently high or rising uric acid levels above
1500 umol/l, despite intensive fluid therapy, tend to carry
the worst prognosis. Urea and creatinine are poor indicators
of dehydration and renal disease and are not considered
clinically useful. PCV and total protein are useful for assessing dehydration and are relatively inexpensive permitting serial assessments at a viable cost. The inclusion of glucose in parenteral fluids may be important in supporting
cachexic reptiles and should certainly be used in cases of severe hypoglycaemia. Another metabolic disorder, severe
hypocalcaemic tetany, will benefit from the inclusion of calcium in the infusion fluid. However, it is important to consider concurrent control of any pre-existing hyperphosphataemia (diuresis, phosphate binders) to avoid soft tissue
mineralisation.

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159

Observed serum biochemistry ranges used to assess dehydration and biochemical imbalances in selected reptiles
(Adapted from references 3 and 4, and the authors unpublished observations)

PCV (%)
TP (g/l)
Urea (mmol/l)
Creatinine (mmol/l)
Uric acid (umol/l)
Glucose (mmol/l)
Calcium (mmol/l)
Phosphorus (mmol/l)
Sodium (mmol/l)
Chloride (mmol/l)
Potassium (mmol/l)

Gila
monster

Tortoise
(Testudo sp)

Box
tortoise

Boa
constrictor

Rat snake

Caiman

25-38
50-78
0-0.7
42-80
70-140
9.4-16.0
2.2-3.5
1.5-3.0
140-183
102-125
1.3-5.2

25-30
60-85
na
na
100-1000
2.5-6.0
2.2-3.5
1.4-2.9
150-190
114-130
4.1

19-40
50-75
0.25-6.70
20-150
75-200
2.6-5.2
2.7-3.6
0.8-1.5
120-158
98-128
4.0-7.0

20-38
40-50
na
na
100-200
2.0
2.5-3.5
0.9-1.7
130-149
104-108
4.6-4.7

20-32
46-80
0-1.67
0-26.5
75-250
0.6-4.0
2.5-5.5
0.8-1.6
130-152
104-124
3.0-5.7

20-30
40-70
na
na
75-250
na
2.5-6.3
2.1-3.1
130-160
125-147
4.1-5.2

26
50-65
na
na
175
4.1-6.3
2.3-3.8
1.3-2.9
139-150
109-132
3.8-7.9

Electrolyte imbalances will usually resolve as renal perfusion and function is restored, however if carefully monitored the correction of acid-base and electrolyte imbalances
may be attempted in a similar manner to mammals.
A complete blood count takes time and may well be beyond the capabilities of a practice laboratory, especially outside normal office hours. Nevertheless, a haematocrit tube
can provide a PCV, semi-quantitative estimate of total white
blood cell count and an idea of plasma colour and character.
In a full haematocrit tube, the first 1% of the buffy coat represents approximately 10109/L and every additional 1%
adds a further 5109/L. This is obviously not very inaccurate
but will provide an idea of whether a reptile has a WBC of
5109/L or 50109/L. In addition, a fresh blood smear
stained with DiffQuik will also permit the rapid assessment
of a white blood cell differential, with particular reference to
heterophils, azurophils and lymphocytes along with any
leukocyte toxic changes.
Any discharges, fluids or superficial tissues can be sampled for impression smear cytology using DiffQuik stains. It
is important to submit blood, tissues and aspirates for culture
and sensitivity before commencing broad spectrum antimicrobial therapy. Enrofloxacin and ceftazidime are safe,
broad antibiotics that are commonly employed. In cases of
suspected septicaemia, i.v. or i.o. ceftazidime and amikacin
may be employed but beware of the nephrotoxic effects of
aminoglycosides.

Hospitalisation
Once the acute emergency is over and the animal is on
continuous fluid therapy it is vital that the reptile is maintained in a suitable thermal environment, at the species-specific POTZ (often 25-35C). All metabolic and physiological processes are dependent upon environmental temperature and all your hard work will be undone if the animal is
left overnight in a cold kennel with a hot water bottle! Oxygen therapy can continue in the hospital vivarium and monitoring using peripheral pulse oximetry is useful.

Nutritional support is usually secondary to rehydration,


but in cases of severe starvation complete parenteral nutrition
can be attempted. The oral route is preferred although the intravenous administration of lipid emulsions may be feasible.
The author prefers Critical Care Formula (Vetark) as an initial oral electrolyte and maltodextrin, protein and amino acid
mixture. This can later be replaced by Hills a/d for carnivores
and insectivores or commercial human baby foods (vegetable
and fruit varieties lacking dairy products) for herbivores.
More recently, the use of Pretty Pets complete herbivorous
reptile diets (tortoise and iguana) have been utilised with apparent success by simply adding warm water and mixing into a thick slurry. It must be stressed that such exclusive diets
should only be used on a short term basis and that once the
reptile has started to improve, efforts must be made to provide a more varied, natural diet. Most reptiles will be very
weak and therefore food material should be placed directly
into the stomach using feeding needles or stomach tubes. The
head should be kept elevated for a prolonged period using
foam or sand bags to avoid regurgitation.
Once stabilised further investigation (radiography, ultrasonography, endoscopy etc.) and surgery can proceed.

Key words
Reptile, emergency, trauma, shock, haemorrhage,
drowning, gastro-intestinal obstruction, hypothermia, hyperthermia, pneumonia, fluid therapy.

References
1.
2.
3.

4.

Boyer, T.H. (1994). Emergency care of reptiles. Semin Avian Exotic


Pet Med 3:210-216.
Divers, S.J. (1996). Basic reptile husbandry, history taking and clinical examination. In Practice 18:51-65.
Stein, G. (1996). Hematologic and blood chemistry values in reptiles.
In: Reptile Medicine and Surgery, p473-483 (Ed. D. R. Mader). WB
Saunders, Philadelphia.
Divers, S.J., Redmayne, G. and Aves, E.K. (1996). Haematological

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Green
iguana

160

5.

6.

4th European FECAVA SCIVAC Congress


and biochemical values of 10 green iguana (Iguana iguana). Veterinary Record 138:203-205.
Jarchow, J.L. (1988). Hospital care of the reptile patient. In: Exotic
Animals. (Eds. E.R. Jacobson and G.V. Kollias). Churchill Livingstone, New York.
Klingenberg, R.J. (1996). Therapeutics. In: Reptile Medicine and
Surgery, p 299-321 (Ed. D. R. Mader). WB Saunders, Philadelphia.

7.

8.
9.

Pokras, M.A., Sedgwick, C.J. and Kaufman, G.E. (1992). Therapeutics. In: Manual of Reptiles. (Eds. P.H. Beynon, M.P.C. Lawton and
J.E. Cooper). BSAVA, Cheltenham.
Thorson, T.B. (1968). Body fluid partitioning in the Reptilia. Copeia
3:592.
Marcus, L.C. (1981). Veterinary Biology and Medicine of Captive
Amphibians and Reptiles. Lea and Febiger, Philadelphia.

4th European FECAVA SCIVAC Congress

161

Hemogram interpretation revisited


Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Time spent critically reviewing all aspects of the complete hemogram is diagnostically rewarding. This, coupled
with newer automated technology better enables clinicians
to detect sample errors and potential errors as well as
graphically depicting cells. Automated technology also improves the identification of appropriate and abnormal cells,
and may reduce labor time as well as providing more objective quantitative information about blood samples.

Introduction
The following is considered a COMPLETE hemogram:
Examining red blood cells
1. Red blood count
2. Hemoglobin concentration
3. Packed cell volume or hematocrit
4. Mean cell volume
5. Mean cell hemoglobin
6. Mean cell hemoglobin concentration
7. Reticulocytes
8. Reticulocyte production index
9. Metarubricytes
10. Red cell morphology and cytograms
11. Histogram of red cell volume distribution
12. Total protein
Determining inflammation
12. Fibrinogen
13. Sedimentation rate
Examining platelets
14. Platelet count
15. Mean platelet volume
16. Platelet morphology
Examining leucocytes
17. White blood cell count corrected for metarubricytes
18. Differential white blood cell count in absolute values
Immature forms
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Degenerated cells
Unidentifiable cells

19. White blood cell morphology


20. Leucocyte cytogram

The relationship between hemoglobin,


hematocrit, and the red cell indices plus
the histogram of red cell volume
distribution
The hemoglobin concentration is probably the most accurate (and the red cell count the least accurate) of the three
analytes needed to calculate the red cell indices. The packed
cell volume is the number derived from packing red cells by
centrifugation in a glass tube. It is similar to but not necessarily the same as the hematocrit which is a calculated number. If the red cell indices are within the reference interval
(this is the new jargon for normal range), then the relationship between hemoglobin and hematocrit is steady. That is to
say, the hemoglobin multiplied by 3 should approximate the
hematocrit or the hematocrit divided by 3 should approximate the hemoglobin. Any significant departure from this ratio suggests laboratory error. If the red cell indices are not
within the reference interval the ratio is not valid.
It is important to recall the red cell indices are MEAN
values. Therefore it takes a lot of abnormally sized cells to
move the MCV out of range. It takes a significant decrease
in hemoglobin production to drop the MCHC. Abnormal indices provide free useful information. However normal indices require further examination of the hemogram. Responsive anemias, responsive to hemolysis or blood loss, usually
become macrocytic and hypochromic. Macrocytic normochromic anemias suggest aberrant red cell maturation and
are often the first signs of impending marrow dysplasia or
neoplasia. Most clinical anemic presentations are normocytic and normochromic requiring additional examination of
the hemogram and, perhaps, additional testing. Microcytic
hypochromic anemias suggest blood loss. In younger animals this often is associated with parasitism. In older animals ulceration and/or neoplasia is suggested. Histograms of
red cell volume distribution is a relatively new measurement
allowing visualization of erythrocyte volume variability.
Disturbances of red cell production that result in altered
red cell size are more readily detected. These histogram abnormalities alert the technologists or clinicians to the presence of unusual red cell volumes when the mean values of
the red blood cell indices are within the reference interval.

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Summary

162

Reticulocytes and nucleated red cells


Reticulocytes are an index of marrow erythroid production and effective delivery to the vascular space. Reticulocytes are observed in blood smears stained with vital
stains. Polychromasia, virtually the same as reticulocytes,
is observed in Romanowsky (Wrights) stained smears.
Reticulocytes, to be interpreted properly, in dogs and cats,
must be adjusted for packed cell volume and erythropoietin
production. The reticulocyte production index is one attempt at understanding how responsive is bone marrow
erythropoiesis.
Metarubricytes are the only nucleated red cells that
should ever be observed in peripheral blood smears. Red cell
precursors younger than these often suggest marrow dysplasia or neoplasia. Since nucleated red cells inflate the white
cell count, whenever nucleated red cells are present the
white cell count should be corrected. Nucleated red cells are
never an indication of red cell response unless accompanied
by reticulocytes in numbers exceeding nucleated red cells
(sans unitage).
Clinicians should be capable of developing a diagnostic
differential scheme for the presence of nucleated red cells
and/or reticulocytes in nonanemic patients as well as anemic
patients.

Red cell morphology


It is almost too mundane to think of red cell morphology
in only terms such as polychromasia, poikilocytosis, anisocytosis and occasional spherocytosis. There are many red
cell shapes and sizes that are diagnostically useful. A few include codocytes and stomatocytes which also may be observed in immune-mediated hemolysis, burr cells in advanced glomerulonephritis, acanthocytes in some forms of
cholestatic disease, schistocytes associated with disseminated intravascular coagulation, Heinz bodies when hemoglobin is oxidized, and blister cells observed in hypersplenic
diseases. There are many more helpful red cell changes...

Red cell cytograms


The typical erythrocyte cytogram plots each red cell by
the size of the cell and the hemoglobin content. The cytogram is compared to appropriate cytograms for the species
in question. This technology allows for the earlier detection
of iron deficiency anemia and documentation of active erythropoiesis. These are just several examples.

Total protein, fibrinogen, erythrocyte


sedimentation rate, icterus index
The only way red cell mass can be viewed critically is
with total protein quantitation. Dehydrated patients may
mask mild anemias. Blood loss is often clinically obvious
and is supported by lowered proteins. Younger animals have
lower proteins (less immunoglobulins) than do older ani-

4th European FECAVA SCIVAC Congress

mals. Fibrinogen and erythrocyte sedimentation rate are


helpful additions to our diagnostic armamentaria as regards
inflammation. They often increase, preceding changes in the
leucogram and return towards normal before the leucogram
does. Decreases in fibrinogen are associated with disseminated intravascular coagulation. Marked increases in fibrinogen quantitation and erythrocyte sedimentation rate are
associated with renal or neoplastic diseases.
Icterus index is a way of making an objective assessment
of patient jaundice. Plasma color is compared to potassium
dichromate standards and given a number value. Comparative aspects become evident on patient reexamination or
when speaking to a colleague about the patient. Regularly
inspecting plasma color and clarity often reveals free hemoglobin or lipemia.

Platelet count, platelet morphology,


and mean platelet volume
Platelet numbers should be critically assessed. It is simply not enough to receive a report that platelet numbers are
increased, adequate, or decreased. In patients that have
primary hemostatic defects, diagnostic and therapeutic decisions must be based on absolute numbers. In addition, large
platelets suggest young platelets. Platelet granularity is observably affected by some diseases and some drugs. Oval to
cigar-shaped platelets often suggest occult bleeding. Mean
platelet volume (MPV) is a new measurement designed to
enable us to view platelet size distribution. The detection of
microthrombocytosis in immune mediated thrombocytopenia is but one example of the advantage of determining
MPV. Another example is the detection of macrothrombocytes and active response to thrombocytopenia.

White cell count, distribution,


and morphology
White cells counts must be corrected for increased numbers of nucleated red cells. Additionally, the white cell count
is use to calculate absolute numbers of individual cell types.
Percentage distribution is not informative and often leads to
misdiagnoses. Included among the categories of cells in the
white cell differential should be cells called unclassifiable
and degenerated. These additional categories are an alert
to the presence of neoplastic cells and/or toxic cells.
The difference between a stress leucogram - mature neutrophilia, monocytosis, lymphopenia, and eosinopenia - and
an inflammatory leucogram - left shift - must be grasped.
Regenerative and degenerative left shifts are useful diagnostic academic terms which affect therapies.
The neutrophil to lymphocyte ratio is 3:1 in dogs and 2:1
in cats. These differences allow quantification of response
comparatively between the two species. Dogs often mount
an elegant response to a lesion or process. Cats, given the
same degree of insult, mount a lesser response. Ratio inversions are significant.
Nonspecific evidence of systemic toxicity is revealed
when neutrophil morphology changes. Vacuolation, toxic

4th European FECAVA SCIVAC Congress

granulation, and hypersegmentation, when observed, require


additional patient examination in order to determine the
cause of these morphological changes.

163

detect toxicity, detect modest eosinophilias, and detect blast


cells in early leukemic patients.

Recommended reading
There are several leucocyte cytograms now available.
These are the peroxidase cytogram and the basophil cytogram. The peroxidase cytogram plots each leucocyte by
cell size and peroxidase activity and the computer draws
lines around cell clusters that are distinctly different from
each other and allows an automated leucocyte differential
count. The basophil cytogram strips away leucocyte cytoplasm and plots naked leucocyte nuclear size and density. Interpretation of the basophil cytogram is based on the shape
of the cell cluster. The shape can determine individual leucocyte types and numbers, detect left shifts automatically,

Tvedten H. Advanced hematology analyzers interpretation of results. Vet


Clin Path 1993; 22:72-80.
Weiser MG. Sizing of animal erythrocytes using sulfate-based diluent. Vet
Clin Path 1985; 14:7-9.
Weiser MG. Modification and evaluation of a multichannel blood cell
counting system for blood analysis in veterinary hematology. J Amer
Vet Med Assoc 1987; 190:411-415.
Northern J, Tvedten HW. Reports of retrospective studies. Diagnosis of microthrombocytosis and canine immune-mediated thrombocytopenia
in dogs with thrombocytopenia: 68 cases (1987-1989). J Amer Vet
Med Assoc 1992. 200: 368-372.
Kocher WD. Autoimmune hemolytic anemia in: Atlas of automated cytochemical cytology. Edited by Simson, Ross, Kocher. Tarrytown NY,
Technicon Instruments 1988. 26-27.

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Leucocyte cytograms

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165

Special hematology diagnostics


Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Leucocyte cytograms

Hemogram
Red cell cytograms
Mean platelet volume and cytogram
Leucocyte cytograms
In-house blood typing
Feline transfusion medicine
Detection of antibodies on red cells
Use of erythropoietin
Use of granulocyte-colony stimulating factor
Hemostasis
Primary hemostasis - the buccal mucosal bleeding time
Secondary hemostasis - PIVKA
Tertiary hemostasis - D-Dimer

There are several leucocyte cytograms now available.


These are the peroxidase cytogram and the basophil cytogram. The peroxidase cytogram plots each leucocyte by
cell size and peroxidase activity and the computer draws
lines around cell clusters that are distinctly different from
each other and allows an automated leucocyte differential
count. The basophil cytogram strips away leucocyte cytoplasm and plots naked leucocyte nuclear size and density. Interpretation of the basophil cytogram is based on the shape
of the cell cluster. The shape can determine individual leucocyte types and numbers, detect left shifts automatically,
detect toxicity, detect modest eosinophilias, and detect blast
cells in early leukemic patients.

HEMOGRAM

In house blood typing

Red cell cytograms

A simple in-house card test for feline red cell antigens


A, B, and AB and canine DEA 1.1. The dog has eight different blood types identified as dog erythrocyte antigens (DEA)
1.1, 1.2, 3, 4, 5, 6, 7, and 8. The use of DEA 1.1 and 1.2 positive blood products that are crossmatch incompatible may
cause hemolysis. Controversy exists as to whether DEA 7 is
an important determinant in canine transfusion reactions.
Ideally canine blood negative for DEA 1.1, 1.2 and 7 should
be used as it conforms with the concept of universal donor
blood. In random source, first time canine transfusion of
noncrossmatched or typed blood the transfusion reaction
rate is approximately fifteen percent. Again, transfusion reaction indicates that the materials transfused are not effective and are causing a physiologic burden on an already burdened patient - reasons to blood type and crossmatch. Recently there has been suggestions that the only significant
canine antigen is DEA 1.1. Donors blood products negative
for DEA 1.1 that are crossmatch compatible have a much reduced chance of transfusion reaction.

The typical erythrocyte cytogram plots each red cell by


the size of the cell and the hemoglobin content. The cytogram is compared to appropriate cytograms for the species
in question. This technology allows for the earlier detection
of iron deficiency anemia and documentation of active erythropoiesis. These are just several examples.

Mean platelet volume


Platelet numbers should be critically assessed. It is simply not enough to receive a report that platelet numbers are
increased, adequate, or decreased. In patients that have
primary hemostatic defects, diagnostic and therapeutic decisions must be based on absolute numbers. In addition, large
platelets suggest young platelets. Platelet granularity is observably affected by some diseases and some drugs. Oval to
cigar-shaped platelets often suggest occult bleeding. Mean
platelet volume (MPV) is a new measurement designed to
enable us to view platelet size distribution. The detection of
microthrombocytosis in immune mediated thrombocytopenia is but one example of the advantage of determining
MPV. Another example is the detection of macrothrombocytes and active response to thrombocytopenia.

Feline blood groups


and transfusion medicine
Three feline blood groups have been described: A, B,
and AB. The feline blood group system is different than that
in dogs because the occurrence of natural isoantibodies is

MAIN PROGRAMME

Special hematology diagnostics

166

common. Approximately 70% of all type B cats have anti-A


antibody in a high enough titer to cause decreased RBC survival and acute hemolysis. As little as 5 ml of incompatible
blood is enough to cause a fatal reaction. In 35% of all type
A cats anti-B is present but usually in low titer; reaction in
these animals is less frequent. Although the incidence of
type B cats in the United States is low, many purebred cats
(excepting the Siamese) such as the Cornish and Devon Rex,
British shorthair, Abyssinian, and Himalayan cats have a
high frequency of B blood types. Crossmatching is strongly
recommended for all cats about to receive blood or blood
products. The presence of natural isoantibody always result
in decreased RBC survival posttransfusion. Mean RBC survival is approximately 30 days in cats of the same blood type
and less than 10 to 14 days in cats with differing blood types.
Donor cats should be screened for red cell parasites,
heartworms and feline leukemia virus (FeLV), feline infectious peritonitis (FIP), and feline immunodeficiency virus
(FIV). At 2 week intervals 10 ml/kg can be collected. The
use of citrate-phosphate-dextrose-adenine (CPD-A1) is the
recommended anticoagulant. Heparin is contraindicated as
it activates platelets and antithrombin III and can result in
many unwarranted and disparate reactions including hemorrhage.
When delivering feline whole blood taken in a citrate anticoagulant care must be taken not to cause hypocalcemia,
which may be severe and even lethal. Citrate is a strong calcium chelator. Caution must also be used not to induce volume overload. Generally if less than 20% of blood volume
is delivered to a normovolemic but anemic feline patient
during an 8 hour period, volume overload does not occur. As
mentioned, cats have a normal blood volume of approximately 70 ml/kg.

Detection of antibodies on red blood cells


The ability to detect antibody in IHA will depend on the
characteristics of the antibody. Agglutination occurs readily
with IgM antibodies and poorly, if at all, with IgG antibodies. This is due to the fact that the larger IgM molecule can
span the distance imposed by mutually repulsive forces that
keep rbcs separated. When this happens IgM forms a lattice
and agglutination occurs. Additionally a sufficient amount
of antibody must be present for this phenomenon to occur.
The direct antiglobulin test (DAT; Coombs reaction) involves the species specific production of an antiantibody
thus allowing agglutination to occur in vitro. The majority of
autoimmune antibodies in human animals and nonhuman
small animals are IgG1 and the remainder are predominantly IgG3. The use of antiIgG and anticomplement 3 antisera
can aid in the determination the pattern of antibody or complement fixation in IHA. The antiglobulin test results are
then of four types:
a) antibody alone is fixed, generally antiIgG but no antiC3. In human animals this reaction is generally associated with specific blood groups and with specific
drug-induced IHA.
b) both IgG and C3 are found to be present on the rbc.
This indicates that IgG antibody is capable of fixing

4th European FECAVA SCIVAC Congress

complement. This pattern in human animals is seen in


SLE and in idiopathic IHA. This never occurs when
drugs are involved.
c) complement only is fixed; antiIgG does not cause agglutination. This kind of DAT reaction has several
causes. The antibody may not be IgG. The antibody
may have low affinity due to temperature. Papainization of the rbcs may result in a positive immmunoglobulin test because papain will increase the
ability of the antibody to interact with the rbc surface
antigen.
d) the test is negative. This results when the test is not
performed in both cold and warm environs, when the
affinity of the DAT antibodies is too low, when there
are too few antibodies or complement molecules on
the rbc surface, or when the DAT antibodies are too
avid resulting in the prozone phenomenon that is, too
many antiantibodies cover the antigens and lattice
structures are prevented.
WHAT YOU SHOULD DO! - As the handling clinician
you must ask your laboratory a series of questions. First is
the DAT being uses species specific? Do they run positive
and negative controls on each patient? Was the test run in
both cold and warm environs? What dilutions were used to
overcome potential prozone phenomena (generally dilutions
out to 1:16 will do this)?
OTHER MEANS OF DIAGNOSIS - There does not
seem to be a major age or sex predisposition to IHA in nonhuman animals. There does seem to be a breed predilection
with Cocker Spaniels, Old English Sheepdogs, Poodles,
German Shepherds and Doberman Pinschers predominating.
The presence of spherocytes helps but there is a caveat here.
Unless a trained technologist or cytologist is reviewing the
smears, spherocytes often are incorrectly identified. Conversely without training spherocytes are often missed. With
feline and equine rbcs spherocytosis is often missed because
of the small cell size. Spherocytosis is suggested when the
MCV is below normal or at the low end of the reference interval despite the large numbers of reticulocytes which often
accompany IHA and when the MCHC is above the reference
interval. This results when smaller cells (spherocytes) are
present (MCV) and have only lost membrane without loss of
intracellular content (MCHC). Slappendel from the State
University of Utrecht suggests that performing a standard
osmotic fragility test at half strength will reveal increased
osmotic fragility in IHA patients. Attempting to cause or disperse agglutination has been singularly unrewarding in this
authors hands.
Increased reticulocyte production indices without clinical evidence of bleeding and without hypoproteinemia suggests hemolysis. The caveat here is that nonimmune hemolysis can occur and spherocytosis can occur without IHA (hypophosphatemia often causes spherocytosis).

Use of erythropoietin (Epo)


Erythropoietin is synthesized primarily in the peritubular
cells located in the inner cortex and outer medulla of the kidney although small amounts are synthesized in the liver. Re-

4th European FECAVA SCIVAC Congress

combinant EPO has been produced and is commercially


available. Like the natural hormone, the recombinant product acts preferentially on the late differentiation of CFU-E.
In the clinical trials in dogs it has had remarkable effects.
Not only is the anemia of end-stage renal disease effectively treated but activity seems to ameliorate many of the other
effects of renal disease such as hypertension, hyperkalemia,
and thrombotic tendencies. EPO appears to be a true hormone, acting at a distance from its site of production.

167

and hemogram above. Specific examination of the primary


hemostatic reaction is accomplished with the buccal mucosal bleeding time (BMBT). The BMBT is accomplished
with a bleeding time device and has been described. The
BMBT is sensitive to platelet dysfunctional states primarily
and to vascular dysfunction secondarily. The BMBT is not
performed when thrombocytopenia is pronounced.

Use of granulocyte-colony stimulating


factor (G-CSF)
G-CSF is most well known in veterinary medicine. G-CSF
has a molecular mass of 18 to 22 kilodaltons and is released
from fibroblasts and activated monocytes. The effect of GCSF is more restricted than that of GM-CSF and IL-3. G-CSF
enhances the differentiation and neutrophil function. G-CSF
increases neutrophil killing of tumor targets by a mechanism
of antibody-dependent cellular cytotoxicity (ADCC), and also
enhances phagocytosis. In clinical trials, G-CSF has been
shown to shorten the period of dangerous neutropenia following chemotherapy for neoplasia and the number of days antibiotics must be used to treat some septic processes. G-CSF
produces remarkable increases in neutrophil numbers without
affecting the numbers of monocytes and lymphocytes.

HEMOSTASIS
Examination of primary hemostasis-buccal
mucosal bleeding time
Primary hemostasis consists of vascular constriction,
platelet adhesion and platelet aggregation. It must be distinguished from secondary hemostasis - coagulation (fibrin formation) and tertiary hemostasis (fibrinolysis). Primary hemostasis has been partially examined in the microhematocrit

The PIVKA test (proteins induced by or involved in vitamin K antagonism or absence) is a specific test of vitamin
K deficiency. In fact, the PIVKA test often prolongs as much
as 24 hours before clinical signs may be observed. The PIVKA plasma is deficient in three of the four vitamin K coagulation proteins, factors II, VII, and X. The test is simple and
reproducible. It can be accomplished in-hospital and requires only the deficient plasma and a hot water bath.

Examination of tertiary hemostasis D-Dimers


The reference interval assessed for D-dimer in normal
dogs was 0.01-0.25 mcg/ml (mean = 0.13 mcg/ml). In the 71
cases of DIC the D-dimer concentration ranged from 0.05 to
3.93 mcg/ml (mean = 0.73 mcg/ml). With a cut-off of 0.25
mcg/ml, the calculated. sensitivity for D-dimers in the DIC
group was 82 percent. D-dimer can be detected and utilized
diagnositically in clinical canine medicine. D-dimer concentrations appear to be useful in the assessment of uncompensated canine DIC. Further research is needed to determine
the usefulness of this analyte in cases where DIC is suspected but not supported by current laboratory testing protocols.

References available on request

MAIN PROGRAMME

Examination of secondary hemostasis PIVKA

4th European FECAVA SCIVAC Congress

169

Clinical approach to anemia


Bernard F. Feldman

Case examination
A nine month old West Highland White Terrier was presented for elective castration but, during physical examination, the mucous membranes were noted to be pale. Despite
this the patient was bright, alert, responsive and afebrile. A
biochemical profile was essentially unremarkable but the hemogram had some unusual findings:
WBC/L 14,400 (12,400 neuts; 500 monos; 1000 lymphs;
500 eos)
RBC/L 2,400,000 (MCV 79; MCHC 34; MCH 27)
PCV%
19
Hbg/dL 6.5
T.P.g/dL 6.1
NRBCs 5/100 wbcs
Retics% 10
Icterus Index - normal
ESR (corrected) - negative 12
Polychromasia ++++, Anisocytosis +++++, Poik +,
Target ++, Lepto ++, Spherocytes -, Stomatocytes -,
Bowls -, Knizocytes -, Schisto -.
Abnormal test(s)? _________________________________
Diagnosis? _______________________________________
Why? ___________________________________________

Anemia
I. Hypoproliferative (nonresponsive anemia)
II Hyperproliferative (responsive anemia)
III. Variable response anemia
Anemia is NOT a disease, simply a sign of disease.
The evaluation of the patient with anemia requires the usual
careful history and physical examination, followed by laboratory screening that provides a complete hemogram:
Examination of red blood cells
1. Red blood count
2. Hemoglobin (Hc) concentration
3. Packed cell volume or hematocrit
4. Mean cell volume
5. Mean cell hemoglobin
6. Mean cell Hb concentration
7. Reticulocytes
8. Reticulocyte production index
9. Metarubricytes and other NRBCs

10. Red cell morphology and cytograms


11. Histogram of RBC vol. distribution
12. Total protein
Determining inflammation
13. Fibrinogen
14. Sedimentation rate
Examination of platelets
15. Platelet count
16. Mean platelet volume
17. Platelet morphology
Examination of leucocytes
18. White blood cell count corrected for metarubricytes
19. Differential white blood cell count in absolute values
Immature forms, neutrophils, lymphocytes,
monocytes, eosinophils, basophils, degenerated cells,
unidentifiable cells
20. White blood cell morphology
21. Leucocyte cytogram
Red Cell Indices - While the red cell indices reflect abnormalities in red blood cell production, changes in the indices are slow to occur (remember, they are mean values!)
and often lag behind the pathologic process. Despite the fact
that most clinical anemias are normocytic and normochromic, macrocytic normochromic anemias usually reflect maturation abnormalities (vitamin B12, folate, myeloproliferative disease), microcytic hypochromic anemias
specifically suggest iron deficiency in small animals, and
macrocytic hypochromic anemias are associated with intense red cell regeneration.
Reticulocyte Count - The percentage reticulocyte count
requires, at least, conversion to absolute values. The reticulocyte count in the dog requires several conversions to account for the normal bone marrow response to erythropoietin, and the length of time of bone marrow reticulocyte
maturation which is correlated with the degree of anemia.
These two conversions are often called the reticulocyte production index (RPI).
Hypoproliferative (nonresponsive) anemia - Anemia
as a disease sign is placed into one of several categories.
Anemia of inflammatory disease is modest, often undetectable, and clinically insignificant. Anemia associated
with acute hemorrhage presents little diagnostic challenge
and in the early stages is characterized as nonresponsive.
Anemia associated with chronic hemorrhage is associated,
in general, with parasitism in young animals and ulceration
of bleeding neoplasms in older animals and in the early

MAIN PROGRAMME

DVM, PhD, Dipl ACVIM


Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

170

stages is characterized as nonresponsive. Microcytosis and


hypochromasia, however, are slow to occur. Anemia associated with decreased erythropoietin production suggests the
clinician examine renal function, thyroid function or adrenal function. Production deficits, manifested by anemia and
or bicytopenia or pancytopenia suggests anemia associated
with bone marrow disease.
Hyperproliferative (responsive) anemia - Hemolysis
or Hemorrhage
Hemolytic Anemia is caused by fragmentation, phagocytosis, or intravascular lysis. The most common canine hemolytic anemia is immune-mediated hemolytic anemia
(IHA), which may be defined as a premature breakdown of
red cells and in the case of immune-mediation, premature
breakdown of red cells associated with antibodies. Among
the implicated antibodies are immunoglobulin G (IgG) and
IgM. When associated with the red cell at 37 degrees they
are considered warm reacting. When temperatures are below
35 degrees and antibody is associated with red cell membranes, the reaction is considered cold reacting. Both of the
aforementioned immunoglobulins, and especially IgM, can
fix complement. Complement- and/or phagocyte-mediated
red cell membrane damage result in swelling (spherocytosis)
or lysis (hemoglobinemia). When hemolysis is active the
erythroid marrow becomes responsive in three to five days.
Anemia of hemorrhage also becomes responsive in three to
five days.
Variable response anemia, anemia which is unpredictable in terms of its reticulocyte response is a maturation
abnormality due, most often, to vitamin B12 or folate deficiency. Intrinsic marrow disease, also potentially a maturation abnormality may also present similarly in the early
stages.

Causes of anemia - a summary


1. Iron deficiency - always nonresponsive
2. Inflammation - always nonresponsive
3. Marrow damage - always nonresponsive
4. Decreased erythropoietin - always nonresponsive
5. Hemorrhage - nonresponsive early; responsive later
6. Hemolysis - nonresponsive early; responsive later
7. Maturation abnormality - usually nonresponsive but
unpredictable

4th European FECAVA SCIVAC Congress

Initial approach to the anemic patient


The reticulocyte count is the only index of effective erythropoiesis. Proper usage requires: 1) conversion to an absolute quantity; 2) adjustment for the reduced hematocrit;
and 3) correction for the effect of erythropoietin on marrow
reticulocyte release. THESE ADJUSTMENTS RESULT IN
CALCULATION OF THE ADJUSTED RETICULOCYTE NUMBERS OR THE RETICULOCYTE PRODUCTION INDEX (RPI).
First: figure out the absolute quantity of reticulocytes. If
the canine mean red cell count is seven million, one percent
reticulocytes is seventy thousand reticulocytes - the reference interval would be thirty-five thousand to one hundred
five thousand reticulocytes per microliter.
Second: correct for the reduced hematocrit. Multiply the
absolute reticulocyte count by the patients hematocrit and
divide the result by the mean species hematocrit.
Third: correct for the effect of erythropoietin on reticylocyte release.

Erythropoietin
Erythropoietin (Epo) is inversely correlated with the red
cell count (or hematocrit). The lower the hematocrit the
higher the concentration of erythropoietin (except in renal
failure). The effects of erythropoietin include:
1. commits uncommitted stem cells to the erythroid line;
2. decreases the marrow maturation time for red cell development;
3. increases individual cell hemoglobin synthesis;
4. causes premature release of reticulocytes from bone
marrow.

Adjusting the reticulocyte numbers


the reticulocyte production index (RPI)
The average time for reticulocytes to mature in the dog
or cat is four and one-half days, three days occur in the marrow and one day in peripheral blood if the hematocrit is appropriate:
In the dog:

The laboratory evaluation of anemia is initiated by examination of the red cell indices - MCV, MCHC, and MCH.
If these indices are abnormal, this is essentially free information and gives specific direction. Examples are macrocytic hypochromic anemia which invariably suggests red cell
response and microcytic hypochromic anemia which suggests (at least) iron deficiency. However if the indices are
normal, normocytic and normochromic, examination of the
degree of red cell response - specifically the appropriateness
of the reticulocyte response - must be considered.

In the cat:

Development
in Marrow

in Peripheral
Blood

45
35
25
15

Laboratory evaluation of anemia

Hematocrit

3.5 days
3.0 days
2.5 days
1.5 days

0.5 days
1.5 days
2.0 days
2.5 days

32
24
16
10

3.5 days
3.0 days
2.5 days
1.5 days

1.0 days
1.5 days
2.0 days
2.5 days

To correct for the effect of erythropoietin on reticulocyte


release, after converting reticulocytes to absolute values and
adjusting for the reduced hematocrit, divide the final figure

4th European FECAVA SCIVAC Congress

of 3.5 million/ul, the absolute value is approximately


170,000/ul.
170,000 22% (patients Hct)/ 45% (mean canine Hct)
= 85,000/2.0 = 42,500.
This corrected absolute reticulocyte number is within the
reference interval observed for dogs with appropriate hematocrits. Thus, this patient must be considered nonresponsive

Initial characterization of anemia is it responsive? nonresponsive?


A RPI less than 2.0 = nonresponsive anemia.
A RPI greater than 2.0 = responsive anemia i.e., hemorrhage or hemolysis.

References available on request

MAIN PROGRAMME

by the number of days the average reticulocyte will live as a


reticulocyte based on the patients hematocrit (see charts
above).
For example, to determine red cell production over
basal rate:
If a canine patients hematocrit is 22 percent (mean normal is 45 percent) and the patients reticulocyte percentage
is 5 percent, is this patient responding appropriately to the
reduced hematocrit?
5% 22% (patients Hct)/ 45% (mean canine Hct) =
2.5/2.0 = 1.27 basal rate.
If 1.0 is basal rate, 1.27 over basal rate is nonresponsive!
Only patients with a corrected reticulocyte count over 2.0
are considered responsive, i.e. are responding from either
hemorrhage or hemolysis.
For example, to determine corrected absolute reticulocyte counts:
If the reticulocyte count is 5 percent of a red cell count

171

4th European FECAVA SCIVAC Congress

173

Interpretation of the blood smear.


Morphologic alterations of red and white cells
Bernard F. Feldman
DVM, PhD, Dipl ACVIM
Department of Biomedical Sciences and Pathobiology - Virginia-Maryland
Regional College of Veterinary Medicine - Blacksburg, Virginia - USA

Case 1 (C6) - Two year old, spayed female cat presented with anorexia, depression, and increased temperature.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x103/ul

8
5
3.45
43.5
33.3
15.5
0
0
Heinz bodies
Doehle bodies
640

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

6.7
230
2.0
500
0
306
294
0
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)

Case 2 (C8) - One year old intact male cat presented because of weight loss, anorexia and, hemorrhagic diarrhea.
On entry the PCV was 21%. These are data accumulated the next day.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x103/ul

7
2.3
3.12
44.5
30.3
15.5
0
0
Heinz bodies
Doehle bodies
0

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

3.2
320
2.0
3100
0
2330
670
100
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)

Case 3 (282) - Two year old Corgi-Cocker Spaniel spayed female was presented because of episodes of bleeding
for the past two weeks. There was gingival bleeding and some petecchiae on mucous membranes and on the abdomen.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x 103/ul 38
Plat morph

23
8.0
3.2
117
25.7
36
4
4+ aniso, polychr
toxic granulation
(200-400)
megathrombocytes

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected)/ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Metamyelocytes
Myelocytes

6.7
250
2.0
43500
9000
21400
4100
2200
800
0
3500
2500

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)
(0)

MAIN PROGRAMME

During this session we will examine a series of cases and discuss the morphologic alterations seen in blood and bone marrow preparations associated with those cases.

174

4th European FECAVA SCIVAC Congress

Case 4 (D13) - Six year old spayed femal Basenji dog presented because of chronic diarrhea.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x 103/ul
Plat morph

32
10.5
5.4
64
32
21
1.0
4
slight anisocytosis
immature
988
variably sized

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Metamyelocytes
Myelocytes

6.1
450
3.0
28100
4100
19000
1100
1000
900
0
1500
500

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)
(0)

Case 5 (289) - Neutered male Collie, 4.5 years of age presented because of nervousness, whining, crying, and pacing
(will not sleep).
PCV %
37
Hb g/dl
10.7
RBC x 106/ul
6.3
MCV fl
58.7
MCHC g/dl
28.9
MCH pg
16. 9
Retics %
4.8
Nrbcs/100wbc
28
RBC morph-slight aniso; polychr
WBC morph
normal
Plat x 103/ul
218
Plat morph
normal

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable
Damaged

6.2
200
3.5
9900
0
7500
1200
800
400
0
0
0

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)
(0)

Case 6 (298) - Six year old neutered male toy Poodle presented because of persistent diarrhea.
PCV %
47
Hb g/dl
17
RBC x 106/ul
5.12
MCV fl
91.7
MCHC g/dl
36.1
MCH pg
33.2
Retics %
0
Nrbcs/100wbc
0?
RBC morph-retained nuclei?
WBC morph
hypersegmented
Plat x 103/ul
332

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable

7.1
300
2.0
15100
151
8909
4454
755
831
0
0

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

Case 7 (297) - Two year old neutered male mixed breed cat presented with an acute history of anorexia and depression.
Temperature was subnormal, pulse 200/minute and respirations 32/minute. Mucous membranes were pale.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x103/ul

11
2.6
1.8
95.6
28.2
31
12
15
Heinz bodies
Doehle bodies
313

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

6.3
400
8.0
9400
0
8300
700
400
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)

4th European FECAVA SCIVAC Congress

175

Case 8 (C15) - Six and one-half year old neutered male cat presented with a two week history of anorexia, two day history
of vomiting and diarrhea. Temperature was elevated, there was marked splenic enlargement on palpation and on radiography.
The patient was dehydrated approximately 5%.
(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells
Unclassifiable cells

7.8
450
10.0
33700
?
4000
700
?
0
0
0
29000

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)
(0)

Case 9 (C11) - Male intact mixed breed cat presented because of anorexia and depression.
Mucous membranes were pale and icteric. On palpation the cat had hepatomegaly and splenomegaly. Temperature was subnormal.
PCV %
10
Hb g/dl
3.2
RBC x 106/ul
2.1
MCV fl
65
MCHC g/dl
31
MCH pg
29
Retics %
few
Nrbcs/100wbc
12
RBC morph some bowl forms
WBC morph
Doehle bodies
Plat x103/ul low
Platelet morphology not done

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)
Unclassifiable cells

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells

8.2
500
17.0
7900
?
1700
2500
?
0
0
0
3700

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)
(0)

Case 10 (C14) - Mixed breed neutered male cat presented because of lethargy and poor appetite.
Mucous membranes were pale. Temperature was subnormal.
PCV %
11
Hb g/dl
3.5
RBC x 106/ul
1.7
MCV fl
54
MCHC g/dl
34
MCH pg
26
Retics %
few
Nrbcs/100wbc
0
RBC morph aniso; megalo
WBC morph bizarre nuclei
Plat x103/ul low
Platelet morphology not done

(30-45)
(12-18)
(5-10)
(39-55)
(31-35)
(12.5-27.5)
(0.2-1.6)
(0)

(300-800)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Disintegrated cells
Unclassifiable cells

86.8
250
4.0
12000
200
9800
1500
300
200
0
0
0

(6.0-8.0)
(50-300)
(2-7)
(5500-19500)
(0-120)
(2500-12500)
(1500-7000)
(0-850)
(0-1500)
(0)
(0)
(0)

Case 11 (7 - 139339) - Two year old, mixed breed, spayed female dog presented because of persistent fever
and pale mucous membranes. On palpation and radiography abdominal fluid was found.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph normal
WBC morph
Plat x 103/ul

15
4.5
2.19
68.5
30
20.5
2.0
9

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

toxicity
44

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable

8.6
400
2.0
3700
1739
370
370
74
0
0
1147

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

MAIN PROGRAMME

PCV %
12
Hb g/dl
4.0
RBC x 106/ul
2.1
MCV fl
64
MCHC g/dl
32
MCH pg
29
Retics %
0
Nrbcs/100wbc
14
RBC morph
normal
WBC morph
Doehle bodies
Plat x103/ul clumped
(300-800)
Platelet morphology not done

176

4th European FECAVA SCIVAC Congress

Case 12 (139930) An Irish Setter spayed female, seven years of age was presented because of a swollen right salivary gland
(or perhaps, submandibular lymph node).
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph normal
WBC morph
Plat x 103/ul

24
8.2
3.26
73.6
34.2
25.3
0.8
2.3

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

toxicity
213

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Meta- and myelocyte

7.0
700
2.0
20500
3588
8610
1435
3793
102
0
2358: 615

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

Case 13 (140469) This patient, a Doberman Pinscher intact female, six years of age was referred because
of inappropriate reticulocyte numbers and leucocytosis.
PCV %
Hb g/dl
RBC x 106/ul
MCV fl
MCHC g/dl
MCH pg
Retics %
Nrbcs/100wbc
RBC morph
WBC morph
Plat x 103/ul

35
4.6
2.03
74.9
32
23.9
4.8
3.5
normal
many immature
138

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)

(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
Unclassifiable

7.1
500
29900
2541
14203
3140
9419
149
0
0

(6.0-8.0)
(200-400)
3 (2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(100-1250)
(0)
(0)

Case 14 (140682) Pomeranian, 12 year old intact female was presented for pyometritis. She was anorectic, depressed and weak.
Temperature was normal. Pulse was 180 per minute. The following data were obtained as a part of the presurgical screen.
PCV %
23
Hb g/dl
7.1
RBC x 106/ul
3.61
MCV fl
63.7
MCHC g/dl
30.9
MCH pg
19.7
Retics %
3.8
Nrbcs/100wbc
2
RBC morph poly; microcytes
WBC morph
many immature
Plat x 103/ul
456

(37-55)
(12-18)
(6-8)
(60-77)
(31-35)
(19-24)
(0-1.5)
(0)
Progranulocytes
(200-400)

Plasma Protein g/dl


Fibrinogen mg/dl
Icterus Index units
WBC (corrected) /ul
Band
Neutrophils
Lymphocytes
Monocytes
Blasts
Myelocytes; metas

7.3
500
2
123900
25400
73720
2478
6195
rare
rare
620; 15487

(6.0-8.0)
(200-400)
(2-7)
(6000-17500)
(0-400)
(3000-11500)
(1000-4800)
(150-1350)
(0)
(0)
(0)

4th European FECAVA SCIVAC Congress

177

Mycobacterial skin diseases


Luis Ferrer

Introduction
In general, mycobacteria are uncommon causes of skin
diseases. Three groups of mycobacterial skin diseases have
been recognized: cutaneous atypical mycobacteriosis, cutaneous tuberculosis and feline leprosy. In this lecture we will
focus predominantly in atypical cutaneous mycobacteriosis,
which is most prevalent in Europe.

Atypical mycobacteriosis
Etiology: most cases are due to rapidly growing mycobacteria included in Runyon group IV. These mycobacteria are nonchromogenic, rapidly growing, gram positive,
acid fast, aerobic, non-spore forming bacilli. Mycobacterium
fortuitum, M. phlei, M smegmatis and M. chelonei are the
most common species. They are ubiquitous in nature, specially in water, wet soil and intestines of ruminants, pigs and
other animals. They are non-pathogenic for animals under
normal circunstances. Infection is usually consequence of
trauma or fight wounds.1
Dogs and cats are quite resistent to infection by slow
growing atypical mycobacteria (Mycobacterium avium-intracellulare, M. genavense). They are classified as Runyon
group III and are acid fast, slender rods; non-chromogens.
Most reported cases have described disseminated disease
without cutaneous involvement, but cutaneous lesions have
been described in a few cases.2
Clinical signs: most patients present with a history of
trauma and non-healing lesions that have not responded to
antimicrobial therapy.
In atypical mycobacteriosis associated with rapidly
growing mycobacteria lesions consist in fistulous tracts and
purpuric macules and nodules that ulcerate. Ventral abdomen, inguinal region and legs are the most commonly affected body parts. Usually dogs and cats are systemically
unaffected and disseminated disease is rare.
In atypical mycobacteriosis due to slow growing mycobacteria (M. genavense, M avium-intracellulare) disseminated disease is rather uncommon. Cutaneous disease, when
exist, may present as nodules or diffuse subcutaneous
swellings. Anorexia, weight loss, lymphadenopathy,
splenomegaly and anemia have been reported in dogs and
cats with the disseminated form of the disease.3,4,5
Diagnosis: a complete physical examination and bichem-

ical evaluation (complete blood count, chemistry panel and


urinalysis) in patients suspected of mycobacterial infections
is recommended. If disseminated disease is suspected apropriate imaging techniques (RX, ultrasound) are recommended. In cat, FeLV and FIV infection should be investigated.
In most cases the definitive diagnosis is based on biopsy
plus culture or PCR. Histopathologic findings consist of
vatying degrees of granuloma formation, pyogranulomatous
dermatitis, cellulitis and panniculitis. Acid-fast bacteria are
observed in approximately 50% of cases. M. avium-intracellulare and M. genavense usually are present in larger numbers and are more commonly identified on cytology and
histopathology compared to the rapidly growing group IV
mycobacteria.
Polymerase Chain Reaction (PCR) is a very sensitive
and specific diagnostic tool. Most human hospitals run rapid
kits to detect mycobacteria in samples. There are also commercial kits to detect M. avium-intracellulare. The identification of other species can only be made in well equiped, experienced laboratories. The identification of the mycobacteria can also be made from paraffin embedded tissue samples
(after DNA extraction) allowing retrospective studies.
Treatment: prolonged courses of antibiotics and surgical
removal of infected tissue are the most effective treatments.
Antibiotic selection should be based, if possible, on culture
and senstivity results. Good choices while culture and sensitivity results are pending or lack include enrofloxacine and
clarithromycin.
Based on published reports fluoroquinolones, aminoglycosides, tetracyclines and clofazimine appear to be most effective.
Prognosis: guarded in all patients. Antibiotic resistance
in mycobacteria is becoming an increasing problem.

Cutaneous tuberculosis
Tuberculosis in dogs and cats has a worldwide distribution. The incidence of the disease, however, has decreased
with the decline of the disease in human beings and cattle.
Etiology: M. bovis or M. tuberculosis. In the case of M.
bovis dogs and cat contract the disease consuming infected
meat or milk. In the case of M. tuberculosis the disease is
contracted via airborne transmission from an infected human. Probably, the incidence is higher in cats than in dogs.
Clinical signs: respiratory and digestive systems are pri-

MAIN PROGRAMME

DVM, Dipl ECVD


Universitat Autonoma de Barcelona - Spain

178

marily affected. Cutaneous involvement is unusual but occasionly happens. Patients show draining tracts, noedules,
plaques, abscesses or ulcers. Patients usually are systemically ill with fever, weight loss and anorexia.
Diagnosis: history, clinical exam, biopsy, culture and
PCR. Biopsy specimens show nodular to diffuse pyogranulomatous dermati