Penyakit penting pada unggas

akibat infeksi virus

Sri Murtini

Beberapa penyakit viral penting dalam

industri peternakan diIndonesia :

Avian reovirus
Infectious Bronchitis
Infectious Laryngotracheitis
Eggs Drops Syndrom
Pox virus

Infeksi Avian Reovirus

Agent : Reoviridae ----------Orthoreovirus
Avian Reoviruses :
are ubiquitous viruses in nature, and are commonly
isloated from a variety of tissues in poultry affected my
multiple disease conditions such as viral
arthritis/tenosynovitis, sttunting syndrome, respiratory
disease, enteric disease, and malabsorption syndrome.
85-90% reovirus non pathogenic
Host :
broiler breeders (meat type chickens) : 7-16 weeks
of age
Chicks :
2 weeks of age

Malabsorption syndrome :
1. Runting/Stunting
2. Poor pigmentation
3. Abnormal feathering
4. Skeletal abnormalities
5. Increased mortality
6. Enlarged proventriculus

Clinical Signs/Gross Lesions

Viral arthritis/tenosynovitis
1. Lameness
2. Joint swelling
3. Thickened/ruptured tendons

Post-mortem Findings
Rupture of the gastrocnemius tendon----------green
discoloration of the skin at the join
Erosion articular cartilage

Ptechie in synovial membranes

clear fluid in capsula-------2nd infection
Rupture digital flexor tendons
Gastrointestinal Distention (fluid and gas), pancreas
atrophy, proventriculus dilatation

Histopathology:
Eosinophilic intracytoplasmic inclusion bodies in
liver
Thickening of the tendon, oedema, hypertrophy and
hyperplasia of the synoviocytes
Villous proliferation and invasion imflamatory cells
of the synovial membranes

 Pathogenicity
Reoviruses have been identified as the etiology of other disease
conditions such as:
1. Arthritis/tenosynovitis
2. Runting/stunting
3.Pericarditis/myocarditis/hydropericardium
4. Hepatitis
5. Bursal and thymus atrophy

Prevention Strategies
1. Good Husbandry Programs
2. Biosecurity Programs
3. Vaccination Programs
Vaccination (Broiler Breeders)
Purpose:
1. Prevent VA in the breeders
2. Prevent egg transmission to progeny
3. Produce maternal antibodies for the progeny
Vaccination Strategies (Broiler Breeders)

Program 1:

Program 2:

1st Live
1st/2nd Live
2nd/3rd Live
1st Live
2nd Live
2nd/3rd Live
1st Killed
2nd Killed

1-2 Wks
3-8 W
8-16 Wks
1 week
3-4 Wks
6-8 Wks
10-14 Wks
14-20 Wks

SQ/Water
SQ/Water/Wingweb
SQ/Water/Wingweb
SQ/Water
SQ/Water
SQ/Wingweb/Water
SQ/IM
SQ/IM

Prevention
Select birds that are leukosis virus negative using serologic
methods to prevent spread of the disease.
Treatment
None.
Special note
It is immunosuppressive and a major cause of condemnation
in adult broiler breeders and layers. Tumors are a common
cause of condemnation in layer processing plants.

Poxviridae
Orthopoxvirus (image)

Largest and most complex of all viruses

Brick shaped
250 x 200 x 200 nm in size
Parapoxviridae are OVOID, 260 x 160 nm
Virions are complex
Core
Lateral bodies
Outer membrane
+ / - envelope
Core Dumbbell shaped, Contains viral DNA,
viral proteins
Lateral bodies unknown nature
+/ - Envelope
Genome is linear and double stranded
Largest genome of any animal virus
Encodes all transcription and replication
enzymes needed for viral genome

Poxviridae Subfamilies and Genera

Orthopoxvirus vaccinia
Parapoxvirus pseudocowpox virus
Avipoxvirus fowlpox virus
Capripoxvirus sheeppox virus
Leporipoxvirus Leooripoxvirus
Suiposvirus Swinepox virus
Molluscipoxvirus Myxoma virus
Yabapoxvirus Yaba monkey tumor virus

Subfamily Entomopoxvirinae contains

viruses of insects

Viral replication cytoplasm

Avian Pox
Cause
Age group affected
Transmission

Clinical Signs + Lesions

Avipoxvirus
WW all ages
Break in skin allows virus in,
infected scabs can contaminate the
environment
Cutaneous form
Papule Vesicle Pustule Scab

Diptheritic form
Space occupying plaque in upper GI
and Resp
May cause suffocation

Morbidity + Mortality

Cutaneous form- 1-2% mort

Diptheritic form- up to 40% mort

Poxviridae
Avipoxvirus Fowlpox virus
Causes disease in chickens, turkeys,
guinea fowl, peacocks, pheasants and
other avian species.
Exact relationship between the
poxviruses of the different avian species
is not certain, but it has been shown
experimentally that the virus causing
one type of pox can give rise to disease
in other species and that infection with
one may stimulate protection against
another
E.g. milk maids

Poxviridae
Avipoxirus Fowlpox virus

Distribution worldwide
Hosts chickens, turkeys, pigeons, pheasants
etc.
Etiologic agent Avipoxvirus extremely
resistant to dessication and can survive in
exfoliated scabs for prolonged periods
Inclusions bodies Bollinger Bodies large
intracytoplasmic inclusions Borrel bodies
elementary bodies occur inside the Bollinger
bodies.
Borrel bodies are minute spherical bodies
obtained by tryptic digestion of Bollinger
bodies
Transmission occurs through small
abrasions in the mouth or through injuries to
the comb, wattle as a result of fighting,
pecking or other injuries
Mechanical transmission by mosquitoes,
ticks, biting flies and lice

Avian Pox Continued

Diagnosis

Control + Prevention

Treatment
Vaccine

Intracytoplasmic eosinophilic
inclusion bodies, viral
isolation, ELISA, viral material
will produce lesions in fertile
chicken eggs
Recovery gives long immunity,
live vax, eliminate cannibalism
with beak trimming
No treatment
Live vax

Poxviridae Epidemiology,
Pathogenesis and Immunity

Epidemiology
Poxviruses are resistant to ambient temperatures and can survive for many
months or years in dried scabs
Poxviruses are transmitted between animals by skin abrasions, aerosol to the
URT, mechanical transmission by arthropods

Pathogenesis and Immunity

Highly epitheliotropic causing cutaneous and systemic disease in birds and
wild and domestic mammals
Many are host specific, but orthopoxviruses infect a wide range of hosts
After cutaneous introduction or inhalation the virus gains access to the
systemic circulation through the lymphatics.
Multiplication of the virus at the skin wound may lead to direct access to the
blood and primary viremia.
Secondary viremia disseminates the virus back to the skin and other target
organs

Poxviridae
Pathogenesis, Immunity

Poxviruses induce lesions by a variety of mechanisms:

Degenerative changes in the epithelium
Lesions start as erytheamatous macules, become papular and then vesicular
Vesicles develop into umbilicated pustules POCK LESION
Pustules rupture and for a crust/scab
Lesions heal and leave a scar
Rupture of the pustule can lead to secondary bacterial infection

Proliferative lesions
Poxviruses replicating in epidermis may result in virus induced (encoded epidermal
growth factor) cellular hyperplasia
Poxviruses encode proteins which may counteract host defenses

Immunity varies from short lived like in parapoxvirus infections to prolonged in others

Poxviridae
Diagnosis
Virus isolation
Scrapings from skin lesions, vesicular lesions and crusts
Chorioallantoic membrane
Pock lesions not parapoxviruses DO NOT replicate in embryonated eggs
Cell culture
Poxviruse grow in a variety of cell cultures
Virus identification
Negative stain electron microscopy FAT etc.
Histopathology

Infectious Laryngotracheitis
Penyebab : Herpesvirus
Sensitivity: mild (halogen-detergents + iodophors, heating,
freezing (-18, -25 C !)

Acute respiratory disease

Conjunctivitis
Laryngitis
Tracheitis
(Histopathology: intranuclear inclusion body in
epithelial cells by 3 day PI)

Avian infectious laryngotracheitis virus

Acute disease of chicken, pheasants (3-9 month)

Respiration problems, bloody mucous secretion

Conjunctivitis - panophtalmitis
Mild - peracute disease
Antigenic uniformity, strains differ in virulence
Impact of environment (iritation of resp.tract, low
temperature, concurrent infections)

Laryngs
(left - normal) (medium - hyperemic) (right - fibrin)

Avian infectious laryngotracheitis virus

Virus latency in infected and vaccinated animals
Rezidual pathogenicity of vaccine strains
Cell immunity non-transmissible to the newborns

Avian infectious laryngotracheitis virus

Samples:

4-6 living animals

trachea, larynx - chilled, not frozen

Diagnostics
I.N. inklusions - trachea
IF test trachea
Izolation on EE (CAM), IFA identification
Differentiation of vaccine and field strains by REA

Laryngotracheitis
Synonyms: infectious laryngotracheitis (ILT),avian
diphtheria
History:
First described 1925
Perhaps observed earlier
Isolated (1930)
Named by AVMA (1931)
Caused by filterable virus (Beaudette 1937)
First major effective avian virus vaccine

REPLIKASI VIRUS
PROSES REPLIKASI TERJADI DI NUCLEUS
Virus penetrasi ke sel inang pada bagian clathrin- and caveolaeindependent endocytosis.
Genom DNA utas tunggal terlepas pada proses Uncoating dan penitrasi ke
nuklues
Genom DNA utas tunggal virus dikonversi menjadi DNA utas ganda melalui
peranan faktor sel inang ,
DNA virus tersebut ditranskripsi menjadi mRNAs virus .
mRNAs virus ditranslasi menjadi protein virus
Replication ini diduga dimediasi oleh protein Rep protein, yang akan
memproduksi DNA utas tunggal berbentuk bulat
DNA utas tunggal yang disintesa :
a) diubah menjadi DNA utas ganda dan berperan sebagai ceakan untuk
proses trankripsi dan replikasi
b) akan dibungkus oleh kapsid protein dan meghasilkan virus baru , virus
tersebut dilepaskan dari sel melalui budding

Laryngotracheitis
Incidence and Distribution

Worldwide distribution
Intensive rearing
Control
Layers and breeders
Typically well vaccinated/controlled
Broilers
Short life cycle; often not vaccinated unless regional
problems
Niche/Fanciers
May be endemic in some flocks

Laryngotracheitis
Hosts
Primarily in chickens
Usually older birds
Respiratory tract: viremia unlikely
Pheasants & pheasant crosses (sporadic)
Peafowl (rare isolate)
Turkeys (experimental)
Other birds resistant (ducks, pigeons, doves,
sparrows, crows, starlings, guinea fowl) May still
carry virus mechanically

Laryngotracheitis
Economic Significance

Not determined
Estimated millions of $$$ in US
Mortality
Decreased production
Meat, eggs, breeder potential, increased down time
Uniformity, feed conversion
Processing issues
Vaccination (vaccines, labor)
Waste disposal & storage
Labor (service responsibilities, transport, cleaning and

Laryngotracheitis Etiology

Alphaherpesvirus
Morphology/composition
Similar to other Alphaherpes viruses
Double stranded DNA (155kb)
Enveloped
Glycoprotein spikes (humoral and cell mediated
immunity)
Shape: Icosahedral
Size: 195-250 nm
Similar to MDV

Laryngotracheitis Strain classification

Importance: differentiation of wild-type field strains vs.
modified live vaccine strain
Antigenically homogenous Differ in pathogenicity

Laryngotracheitis Physical/Chemical Susceptibility

Susceptible to heat
100F (48 hours)
155F (15min ?)
Susceptible to many chemicals
Chloroform, ether, iodophors, cresols, lye
Hydrogen peroxide mist/fumigant (5%)

Laryngotracheitis Pathogenesis
Portal of entry :

Upper respiratory/ocular
Ingestion nasal epithelium
Horizontal transmission
Aerosolization of virus
Birds, feed, water
Contaminated litter
Fomites (equipment, boots, clothes, tires)
Moves slowly through flock
No vertical or egg transmission known

Laryngotracheitis Pathogenesis
Virus present in trachea for 6-10 days PI
Inflammation and necrosis (tracheal cores)
Necrotic cells, blood, inflammatory debris
High virus shed during infection
Leads to :
Death (asphyxiation)
Latent carriers
Latent carriers :
Trigeminal ganglion + tracheal epithelium
Persistent infection & intermittent shedding

 Laryngotracheitis Pathogenesis
Spread to trigeminal ganglion 4-7 days PI
Found to be latent for up to 15 months
Stress may cause virus to recrudesce
Movement, reproduction, etc.
Carriers in flock for 16 months
racheal swabs ~ 2%
Organ cultures ~ 50%

 Laryngotracheitis Clinical Signs

Acute respiratory disease
Conjunctivitis almond eye (often first signs)
Nasal discharge
Moist rales, coughing, gasping
Dyspnea
Expectoration of blood (only in severe infections)
Decreased production
Egg production 5-15%: no problems with shell quality
Unthrifty birds
Recovery in ~7-28 days (usually 10-14 days)
Duration ~2-6 weeks in flock

Laryngotracheitis Clinical Signs

Incubation 6-12 days post infection (PI)
2-4 days experimentally
Severe
90-100% morbidity
5-70% mortality (usually 10-20%)
Mild (silent LT)
As low as 5% morbidity and 0.1% mortality
Males slightly more susceptible

Adenoviruses aden = gland (Greek)

Adenoviruses

first isolated from adenoid tissue

Key Features:

1.

Icosahedral capsid (80 nm)

2.

Larger dsDNA genome (35 kbp): 30-40 genes

3.

Encodes own DNA polymerase and factors that regulate cellular processes

4.

Many animals are infected by multiple serotypes

5.

Mainly associated with mild respiratory disease

6.

Highly immunogenic. Fairly resistant

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Adenoviruses

Adenovirus Structure

fibre

penton
hexon

DNA
terminal protein

39

Adenoviruses

Importance of Adenoviral capsid

1.

Fibre and penton bind to proteins on the cell surface- determine tissue
infectivity.

2.

Adenoviruses can cause red blood cells to clump (haemagglutination).

Mediated by the fibre. Used for diagnosis- haemagglutination-inhibition
(HI) test.

3.

Hexon is the most abundant capsid protein and the major target for the
infected animals immune system. Immunity is long-lasting.

40

Egg Drop Syndrome 76

Cause

Age group affected

Transmission

Clinical Signs + Lesions

Diagnosis
Vaccine

Adenovirus Infection Type 3

Chicken layers + ducks
Pharynx and feces
Loss of color in pigmented
eggs, drop in egg production,
thin to shell less eggs, rough
shell, inactive and atrophied
oviducts, edema in uterus
Viral Isolation
Inactivated vax: 14-16wk
pullets

Avian Adenoviruses

Adenoviruses

1. Egg
drop
syndrome
(EDS76)- first reported in
1976. Infects pouch shell
gland with soft-shelled and
shell-less eggs produced,
with no clinical signs.
Effectively eradicated from
most countries.
2.

Turkey adenovirus 2- haemorrhagic enteritis of turkeys and marble

spleen disease of pheasants. Also causes immunosuppression. Controlled
by vaccination.

3.

Avian adenovirus 1- causes bronchitis in quails. Control by isolation and

decontamination.
42

INFECTIOUS BRONCHITIS

43

SIFAT VIRUS IB
VIRUS CORONA
LABIL, MUDAH MATI
MUDAH BERMUTASI
44

SIFAT VIRUS IB
AYAM YANG SEMBUH MASIH
MENGELUARKAN VIRUS
HINGGA BEBERAPA MINGGU
SERANGAN SAAT MUDA
MENYEBABKAN AYAM CACAT
PERMANEN PADA OVIDUCT
45

SIFAT PENYAKIT IB

AKUT
SANGAT CEPAT MENULAR
SELURUH DUNIA TERPAPAR
MENYERANG UMUMNYA AYAM MUDA
MENYERANG SALURAN REPRODUKSI
DAPAT MENYERANG GINJAL
MENURUNKAN PRODUKSI TELUR
MENURUNKAN KUALITAS TELUR
46

2. Infectious Bronchitis (IB)

Gejala klinis pernafasan

Ginjal pembendungan, kadang ada

endapan asam urat

Ayam masa produksi yang mati :

ditemukan telur dalam oviduct
dengan kerabang tipis atau dlm
keadaan pecah.

47

Perubahan Patologi
Perubahan Bentuk Telur

Cangkang telur tipis

Bentuk telur yang abnormal

48

ANTIGEN
PERMUKAAN
MUDAH BERUBAH
49

Avian Infectious Bronchitis

Cause
Age group affected
Transmission

Clinical Signs
Most common URI
in the US

Coronavirus
Chickens only, all ages
Inhalation of virus
containing droplets,
carriers, survive up to 4 wks
in environment
Marked decrease in egg
prod, soft shelled eggs with
watery albimen, gasping
resp, sneezing, coughing

AIB continued
Lesions
Morbidity + Mortality
Diagnosis
Control + Prevention
Treatment
Vaccine

Cheesy exudate at tracheal

bifurcation, ocular and
nasal discharge in young
chicks
Morbidity: 100%;
Mortality: 50%
Viral isolation, ELISA
Vax
No effective tx, broad
spectrum ABs may prevent
complications
Modified live or killed Vax

VAKSIN IDEALNYA MAMPU

MENCIPTAKAN
IMUNITAS YANG MENSTERILKAN

BUKAN UNTUK IB ATAU

PENYAKIT LAIN YANG
HIDUPNYA DI MUKOSA
52

FACTORS INFLUENCING SUSCEPTIBILITY

Virus
Strain
Dosage
Route of exposure

Host
Age: Common in birds 12-24 weeks of age
Sex: Female are more susceptible
Immune status

Avian encephalomyelitis
Avian encephalomyelitis (AE) is a viral disease
of young chickens caused by a virus from the
Hepatovirus family and characterised by
central nervous system signs (Epidemic
Tremors). Primarily a viral infection of poultry,
chickens, turkey and pheasants.

Kingdom

Virus

Family

Picornaviridae

Genus

Hepatovirus

Species

Avian encephalomyelitis-like virus 1

Avian encephalomyelitis
First reported in 1932, the virus grows in the
yolk sac and brain of the chicken embryo in
eggs from nonimmune hens. Most prevalent
in chickens 1 to 6 weeks of age.

 Susceptible chickens more than 5 weeks old

will develop antibodies to AE, but do not show
clinical signs at the time of infection.

 AE occurs world wide and occurs in all seasons

of the year, but most cases are reported from
January to June.

 Egg-passage transmission from infected hen to

chick is the most common mode of spread,
but direct contact of susceptible hatchlings
with infected birds accounts for spread within
the flock. Indirect spread via fecal
contamination of feed and water also occurs.
The virus can survive at least 4 weeks in
droppings.

Clinical signs
Clinical signs appear at 7 to 10 days of age. Tremors
of the head and neck are presumptive of the disease
in the flock hence the name "Epidemic tremor".
Affected chicks first may show a dull expression of
the eyes, followed by progressive in coordination,
sitting on hocks, tremors of the head and neck, and
finally paralysis or prostration. Muscular tremors are
best seen by exercising the bird. Affected birds are
inactive; some may refuse to walk or walk on their
hocks.

 Chickens of all ages are susceptible, but clinical signs of

encephalitis only develop in those younger than four weeks.
The disease is similar in turkeys and chickens. Following
initial dull expression of the eyes, the following signs are
seen:
progressive ataxia with the chick losing control of legs,
sitting on its haunches and falling onto its side;
tremor of the head and neck.
Ataxia progresses to paralysis and death results from
inability to feed or drink, or through being trampled. Some
birds recover, and others may survive with persistent
clinical signs. In susceptible adult birds, infection is usually
sub-clinical, although there may be a transient drop in egg
production.

 Diagnosis is confirmed by fluorescent antibody

test, virus isolation and agar gel precipitin test.
AE must be differentiated from other
encephalitic diseases such as ND, EEE, MD etc.

 There is no treatment for acute outbreaks.

Control is through prevention. Affected
birds should be removed, killed and
incinerated. Recovered chicks are
unthrifty. Prove good nursing during
outbreaks will help with mortality.
Prevention is by selecting hatching eggs
from immune breeder flocks. Lifetime
immunity is acquired through vaccination
or recovery from a natural outbreaks.