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HISTORY
The first outbreak of the disease was recorded in 1926, in Java, Indonesia and in 1927 by
Doyle in Newcastle -upon- Tyne , England .
In India , the disease was first recorded at Ranikhet (U.P.) in Kumoan hills (Nainital
District, Uttaranchal) by Edward in 1927. Hence the name Ranikhet disease.
The name, Newcastle disease was coined by Doyle as a temporary measure to avoid a
descriptive name that might be confused with other diseases. Later, it became clear that
other less severe diseases were caused by viruses indistinguishable from NDV.
In the United States , a relatively mild respiratory disease, often with nervous signs, was
first described in the 1930 and subsequently termed pneumoencephalitis.
It was caused by a virus indistinguishable from NDV in serological tests. Subsequently,
numerous NDV isolations that produced extremely mild or no disease in chickens was
made around the world. In India , it is the most important disease of poultry.
ETIOLOGY
Causative agent: Paramyxovirus type1 (PMV-1 belongs to the genus Avulavirus, family
Paramyxoviridae).
Based on the disease produced in chickens, NDVs have been classified into five
pathotypes
o Viscerotropic velogenic: The NDVs cause a highly virulent form of the disease.
Haemorrhagic lesions are characteristically present in the intestinal tract.
o Neurotropic velogenic: These NDVs cause high mortality following respioratory
and nervous signs.
o Mesogenic: These NDVs cause low mortality following respiratory and some
times nervous signs.
o Lentogenic: These respiratory NDVs cause mild or inapparent respiratory
infection.
o Asymptamatic: The enteric NDVs cause inapparent enteric infection.
SUSCEPTIBLE SPECIES
ND occurs in domestic fowl, turkeys, pheasants, pigeons, quail and guinea fowl.
Ducks and geese are susceptible but severe disease is rare.
Many species of wild birds are also susceptible.
Chickens are the most and waterfowl the least susceptible of domestic poultry.
Psittacines (parrots) are highly susceptible and can excrete virus for long periods.
Epidemiology
Virulent NDV strains are endemic in poultry in most of Asia , Africa , and some countries
of North, Central, and South America.
Other countries, including the USA and Canada , are free of those strains and maintain
that status with import restrictions and eradication by destroying diseased poultry.
Cormorants, pigeons, and imported psittacine species have also been sources of virulent
NDV infections of poultry.
Low virulence NDV is prevalent in poultry and wild birds, especially waterfowl.
Infection of domestic poultry with low virulence NDV contributes to lower productivity.
Transmission
Infected birds shed virus in exhaled air, respiratory discharges, and feces.
Virus is shed during incubation, during the clinical stage, and for a varying but limited
period during convalescence.
Virus may also be present in eggs laid during clinical disease and in all parts of the
carcass during acute virulent infections.
Chickens are readily infected by aerosols and by ingesting contaminated water or food.
Infected chickens are the primary source of virus, but other domestic and wild birds may
be sources of NDV.
Transfer of virus, especially in infective feces in which virus may be present in high titre,
by the movement of people and contaminated equipment is the main method of spread
between poultry flocks.
The virus has been found to survive for several days on the mucous membrane of the
human respiratory tract and has been isolated from sputum.
Human infections, with flu-like symptoms and conjunctivitis, have been reported.
PATHOGENESIS
CLINICAL FINDINGS
Sudden death
Depression
Prostration
Diarrhoea
Facial edema
Cyanosis of comb (See the picture)
Mortality - 100%
LESIONS
Young chickens and those dying peracutely may have no lesions especially in birds that
only show nervous signs.
Remarkable lesions are usually observed only with VVND and they include
Haemorrhage in intestine
Petechial haemorrhage in proventiculus
Enlarged and necrotic caecal tonsils
Necrosis and haemorrhage in lymphoid aggregates in intestine
Splenic necrosis on capsular surface
Nervous system lesions are not seen regardless of pathotypes
In contrast, the lesions in birds infected with lower virulence NDV strains may be limited
to respiratory tract
Congestion and mucoid exudates seen in the respiratory tract, especially in trachea (see
the picture below) with opacity and thickening of the air sacs (airsacculitis).
Secondary bacterial infections will increase the severity of the respiratory lesions.
Ovarian follicle - Flaccid, haemorrhagic stigmata
Oviduct - haemorrhage and discolouration.
MICROSCOPIC LESIONS
DIAGNOSIS
PREVENTION
Live lentogenic vaccines, chiefly B1 and LaSota strains, are widely used and typically
administered to poultry by mass application in drinking water or by spray.
Alternatively, individual administration is via the nares or conjunctival sac.
Healthy chicks are vaccinated as early as day 1-4 of life. However, delaying vaccination
until the second or third week avoids maternal antibody interference with an active
immune response.
Mycoplasma, some other bacteria, and other viruses affecting the respiratory tract, if
present, may act synergistically with some vaccines to aggravate the vaccine reaction
after spray administration.
Oil-adjuvanted inactivated vaccines are also used following live vaccine in breeders and
layers and may be used alone in situations where use of live virus may be
contraindicated.
In countries where virulent NDV is endemic, a combination of live virus and inactivated
vaccine can be used; or alternatively, if permitted by law, a live mesogenic strain vaccine
may be used in older birds.
The frequency of revaccination to protect chickens throughout life largely depends on the
risk of exposure and virulence of the field virus challenge.
ZOONOTIC RISK
Newcastle disease viruses, whether virulent field viruses or live vaccine, can produce a
transitory conjunctivitis in humans, but the condition has been limited primarily to
laboratory workers and vaccination teams exposed to large quantities of virus.
Before poultry vaccination was widely practiced, conjunctivitis from NDV infection
occurred in crews eviscerating poultry in processing plants.
The disease has not been reported in people who rear poultry or consume poultry
products.
INTRODUCTION
Other names
o Gumboro disease
o Infectious Bursal Disease (1972)
o Infectious bursitis
o Avian nephrosis (1962)
Acute highly contagious infection of chickens
Birna virus ( ds RNA) - Birna = two
B- Lymphocytes are the primary target cells
Bursa, lymphoid organ, is severely affected
First report in Gumboro (Delware District of USA)
Economically significant, because
o Heavy mortality in 3 – 6 wks old chickens and older
o Severe prolonged immunosuppression of chickens infected at an early age
Immunosuppression leads to
o Vaccination failures
o Escherichia coli infection
o Gangrenous dermatitis
o Inclusion Body hepatitis – anaemia syndrome
Etiology
Serotype 1 IBDV
World wide distribution
Antigenic variation
Variation in virulence - from apathogenic to highly virulent strains
50 % mortality
Tropism for B-Lymphocytes of the bursa and their depletion
Serotype 2 IBDV
Wide spread
No pathogenic/ Immunosuppressive
Affects chickens, turkeys, ducks
Serotype 1 and 2 IBDV infects turkeys and ducks but no disease
Transmission
IBD: PATHOGENESIS
(click here for animation)
B - cells and their precursors are the main target cells
T- Lymphocytes are relatively unaffected
Renal pathology (swollen with urate deposits and cell debris) are due to severely swollen
bursa
Mechanism for muscular haemorrhage is not known (may be due to interference of virus
with the normal blood clotting mechanism)
Bursal infection in early life can result in impaired immune responses
Consequences
o Lowered resistance to diseases
o Suboptimal ( inadequate) responses to vaccination
Susceptible age - 3 -6 wks of age
Subclinical infection in younger than 3 wks —> immunosuppression
o Chemical bursectomy (using cyclophosphamide) in 3 day old chicks and
subsequent challenge at 4 wks —> Resistant to disease
o Similar results in surgically bursectamised 4 wks old chickens ( with mild
necrosis of lymphatic tissue and 1000 times less viral production) but 100%
mortality in control non-bursectamised birds
CLINICAL SIGNS
Severity depends upon age, breed, and MDA level of the chick as well as the virulence of
virus
Acute form
o Incubation period: 2- 3 days
o 3 -6 wks old chicks are affected
Signs
o Depression
o White watery diarrhoea
o Soiled vent
o Anorexia
o Ruffled feathers
o Reluctance to move
o Closed eyes and death
Morbidity - 10 – 100%
Mortality
o 0 - 20% (Normally)
o 90 – 100% (VVIBDV)
Milder form - Little or No signs Suboptimal (growth) / response to vaccination
Course of the disease
o Short, leading to death or recovery (in individual bird)
o Mortality reaches a peak 3-5 days after infection
GROSS PATHOLOGY
Dehydration of carcass
Muscular haemorrhage (thigh and pectoral) (see the picture - below), some times at the
junction of proventriculus and gizzard (see the picture - below).
Haemorrhages of pectoral leg muscles are typical of IBD
Intestine with excess mucus
Bursa
MICROSCOPICAL LESIONS
Bursa
Spleen - Moderate lymphoid cell necrosis
Thymus and caecal tonsil - Lymphoid cellular reaction (early stage), but less extensive
damage
Harderian gland - Depletion of plasma cells
Kidneys - Non - specific
Liver - Mild perivascular infiltration of monocytes.
DIAGNOSIS
Based on history, clinical signs and gross lesions ( for acute disease)
Differential diagnosis is required (for subclinical IBD)
Serological test
Immunoperoxidase staining
Immunofluorescence (in frozen bursal sections or smears)
Virus isolation (rarely) - Time consuming process
Inoculation of suspected bursa into 10 – 11 days old embryonated eggs
Some strains grow on Chick embryo fibroblast, vero cells or certain lymphoblastoid cell
cultures
Abs may develop after infection (detected by NT,ELISA, Precipitation test). It is useful
when MDA declines below detectable levels)
Nucleic acid probe, Ag-capture ELISA (using MCAbs.,), RT-PCR
DIFFERENTIAL DIAGNOSIS
Coccidiosis
Ranikhet disease
Haemorrhagic syndrome of muscles and other haemorrhages
Avitaminosis A
FLKS
Water deprivation with swollen kidneys
Excess renal urates.
INTRODUCTION
ETIOLOGY
HOST
SPREAD
Direct
Airborne transmission (common)
Faeces
Fomites
Eggs
IB - PATHOGENECITY
CLINICAL SIGNS
Respiratory form
Reproductive form
Macroscopical lesions
Respiratory tract
Serous, catarrhal, or Caseous exudates in the trachea and bronchi, generally without
haemorrhage
Caseous plugs may be found in the lower trachea and bronchi of chicks that die
Air sacs are thickened and opaque
Secondary bacterial infections in meat-type birds, especially with coli form bacteria,
produce caseous airsacculitis, perihepatitis, and pericarditis. Small areas of pneumonia
may be observed around the large bronchi.
Reproductive tract
Kidney
Swollen, pale kidneys, with tubules and ureters distended with urates
In layers, urolithiasis is associated with virus infection and certain dietary factors
Microscopical lesions
Marked hyperplasia of epithelium (circle) lining the Moderate infiltration of mononuclear cells (yellow
mucosa. arrows) and mild congestion (green arows)
DIAGNOSIS
ILT - PATHOGENECITY
CLINICAL SIGNS
MACROSCPICAL LESIONS
Peracute form
Acute form
Trachea showing aggregation of necrotic debris due to Trachea showing haemorrhagic content in the lumen and
sloughened mucosa. severe congestion of mucosa.
Mild form
Caseous exudate
Excess mucous
Conjunctivitis
MICROSCOPICAL LESIONS
Degenerative changes
Swollen cells
Loss of cilia
Desquamation
Inflammatory changes
DIAGNOSIS
Clinical signs
Demonstration of inclusion bodies
Serological tests includes FAT,IP,ELISA,PCR,AGID,VN,IFA
Learning objectives
To know the etiological factors and to understand the pathogenesis of two important
lymphoproliferative diseases - Marek's disease and lymphoid leucosis
To recognize the clinical signs manifested by the affected birds
To become familiar with the macroscopic and microscopic lesions of the disease
To know the mechanisms behind the immunosuppression produced by the viruses
To learn the diagnostic methods to confirm the disease
To know the different between Marek's disese and lymphoid leucosis
Virus on CAM
INTRODUCTION
PATHOGENESIS
Complete virions (Borrel granules) accumulate within the inclusion bodies (Bollinger
bodies)
Virus —> Epithelial cells —> Proliferation ( Cell to cell)
Entry of virus into blood —> Viraemia
No gross pathology of organs, but viral multiplication in liver, spleen —> Secondary
viraemia
CLINICAL SIGNS
Nodular proliferative skin lesions in non feathered parts – Head, Neck, Legs, Feet
Spread is gradual
Poor weight gain , poor egg production
Papule —> vesicles —> pustules —> crust/scab —> scar
Less mortality (may be high due to complications)
Gross lesions
Cutaneous form- Nodules (due to hyperplasia involving epidermis and underlying hair
follicles) and other features as in signs.
Diphtheretic form- Slightly elevated white opaque nodules develop on mucous
membranes —> Yellow, cheesy, necrotic pseudo-diphtheretic or diphtheretic membrane
—> on removal bleeding ulcers.
Dry pox: Nodules on the comb and mouth Wet pox: Trachea showing severe congestion (yellow) and
with edematous eyelid adhesion of caseous plaques (green)on the mucosal surface.
Microscopical lesions
DIAGNOSIS
Cutaneous form
o Based on clinical signs (Easy)
o Demonstration of intracytoplasmic eosinophilic inclusions - Borrel bodies
(virions) - By scrapping from the lesions and smears made on glass slides with
suitable stain
Diphtheretic form
o Based on clinical signs (Difficulty)
o Formation of ulcer, on removal of lesions, helps to differentiate it from ILT and
Hypovitaminosis - A
Inoculation test
DIFFERENTIAL DIAGNOSIS
Pantothenic acid
Biotin deficiency
Vitamin A deficiency
Infectious Laryngotracheitis
Other respiratory diseases in poultry
Injuries caused by external parasites and cannibalism.
INTRODUCTION
Avian influenza (AI) viruses infect domestic poultry and wild birds.
In domestic poultry, AI viruses are typically of low pathogenicity (LP), causing
subclinical infections, respiratory disease, or drops in egg production.
However, a few AI viruses cause severe systemic infections with high mortality.
This highly pathogenic (HP) form of the disease has historically been called fowl plague.
In most wild birds, AI viral infections are subclinical.
ETIOLOGY
LP viruses are distributed worldwide and are recovered frequently from clinically normal
shorebirds and migrating waterfowl. Occasionally, LP viruses are recovered from
imported pet birds and ratites.
The viruses may be present in backyard flocks and other birds sold through live-poultry
markets, but most commercially raised poultry in developed countries are free of AI
viruses.
The HP viruses arise from mutation of some H5 and H7 LP viruses and cause devastating
epizootics.
Depopulation and quarantine programs are used to quickly eliminate the HP viruses.
The incubation period is highly variable and ranges from a few days to 1 wk.
Transmission between individual birds is by ingestion or inhalation. Experimentally, cats
have been infected with 1 strain of H5N1 Asian HP AI following respiratory exposure,
ingestion of infected chickens, or contact with infected cats.
Potentially, domestic house cats could serve as a transmission vector between farms, but
the ability of other AI viruses, including other H5N1 strains, to infect cats is unknown.
Transmission between farms is the result of breaches in biosecurity practices, principally
by movement of infected birds or contaminated feces and respiratory secretions on
fomites such as equipment or clothing.
Airborne dissemination may be important over limited distances.
Even in the absence of secondary pathogens, HP viruses cause severe, systemic disease
with high mortality in chickens, turkeys, and other gallinaceous birds.
In peracute cases, clinical signs or gross lesions may be lacking before death.
However, in acute cases, lesions may include:
Cyanosis and edema of the head, comb, and wattle;
Edema and discoloration of the shanks and feet due to subcutaneous ecchymotic
hemorrhages;
Petechial haemorrhages on visceral organs and in muscles; and
Blood-tinged oral and nasal discharges.
A.I.- Severe edema and congestion of A.I.- Edema with paler necrotic areas in
kidney pancreas (red arrow)and congested
duodenum (Black arrow) .
Clinical signs, severity of disease, and mortality rates vary depending on AI virus strain
and host species.
DIAGNOSIS
ETIOLOGY
Vaccines can prevent clinical signs and death. Furthermore, viral replication and
shedding from the respiratory and GI tracts may be reduced in vaccinated birds.
Specific protection is achieved through autogenous virus vaccines or from vaccines
prepared from AI virus of the same haemagglutinin subtype.
Antibodies to the viral neuraminidase antigens may provide some protection. Currently,
only inactivated whole AI virus and recombinant fowlpox - AI-H5 vaccines are licensed
in the USA .
The use of AI vaccine requires approval of the state veterinarian.
In addition, use of H5 and H7 AI vaccines in the USA requires USDA approval.
Treating LP-affected flocks with broad-spectrum antibiotics to control secondary
pathogens and increasing house temperatures may reduce morbidity and mortality.
Treatment with antiviral compounds is not approved or recommended. Suspected
outbreaks should be reported to appropriate regulatory authorities.
ZOONATIC RISK
Avian influenza viruses exhibit host adaptation and rarely infect humans, usually as
isolated individual cases without human-to-human transmission.
In the 1997 Hong Kong outbreak, the risk factor for human infection was direct contact
with infected poultry, but not the handling, cooking, or consumption of poultry meat.
In 2004, HP AI of strain H5N1 infected poultry and wild birds in 9 Asian countries.
In Thailand and Vietnam , 37 human cases were confirmed, with a case fatality rate of
68%.
Learning objectives
To know the etiological factors and to understand the pathogenesis of two important
lymphoproliferative diseases - Marek's disase and lymphoid leucosis
To recognize the clinical signs manifested by the affected birds
To become familiar with the macroscopic and microscpical lesions of the disease
To know the mechanism behind the immunosuppression produced by the viruses
To learn the diagnostic methods to confirm the disease
To know the difference between Marek's disease and lymphoid leucosis
INTRODUCTION
Chickens are the most important natural host for Marek’s disease virus, a highly cell-
associated but readily transmitted alpha herpes virus with lymphotropic properties of
gamma herpes viruses.
Quail can be naturally infected and turkeys can be infected experimentally. However,
severe clinical outbreaks of Marek’s disease in commercial turkey flocks, with mortality
from tumors reaching 40-80% between 8-17 wk of age, were reported recently in France,
Israel, and Germany.
In some of these cases, the affected turkey flocks were raised in proximity to broilers.
Turkeys are also commonly infected with turkey herpes virus, an avirulent strain related
to Marek’s disease virus. Other birds and mammals appear to be refractory to the disease
or infection.
Marek’s disease is one of the most ubiquitous avian infections; it is identified in chicken
flocks worldwide.
Every flock, except for those maintained under strict pathogen-free conditions, may be
presumed to be infected.
Although clinical disease is not always apparent in infected flocks, a subclinical decrease
in growth rate and egg production may be economically important.
ETIOLOGY
Three serotypes of the cell-associated herpes virus are recognized. Serotypes 1 and 2
designate virulent and avirulent chicken isolates, respectively; serotype 3 designates the
related avirulent turkey herpes virus. Serotypes 2 and 3, as well as attenuated serotype 1
viruses, have been used as vaccines.
Serotypes are identified by reaction with type-specific monoclonal antibodies or by
biological characteristics such as host range, pathogenicity, growth rate, and plaque
morphology.
Currently, virulent serotype 1 strains are further divided into pathotypes, which are often
referred to as mild (m), virulent (v), very virulent (vv), and very virulent plus (vv+)
Marek’s disease virus strains.
PATHOGENESIS
Typically, affected birds show only depression before death, although emaciation may be
noted.
A transient paralysis syndrome (unilateral leg paresis) has been associated with Marek’s
disease, causing a characteristic posture of one leg held forward and the other held
backward as lesions progress. (see the pictures below)
Chickens become ataxic for periods of several days and then recover. This syndrome is
rare in immunized birds.
Enlarged nerves are one of the most consistent gross lesions in affected birds (see the
pictures below).
Various peripheral nerves, but particularly the vagus, brachial, and sciatic, become
enlarged and lose their striations.
Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the
liver (see the pictures below), spleen, gonads, heart, lung, kidney, muscle, and
proventriculus.
MD affected liver showing tumour nodules ( MD affected liver showing massive invasion of
arrows) of varying sizes on its surface. tumour into th hepatic parenchyma. (Red
arrow-Single nodule; Yellow arrow- Multiple
nodules)
Lymphoid infiltrates may expand the iris muscle and distort the shape of the pupil (See
the pictures below).
Enlarged feather follicles (commonly termed skin leukosis) (see the pictures below) may
be noted in broilers after defeathering during processing and are a cause for
condemnation.
The bursa is only rarely tumorous and more frequently is atrophic. Histologically, the
lesions consist of a mixed population of small, medium, and large lymphoid cells plus
plasma cells and large anaplastic lymphoblasts.
These cell populations undoubtedly include both tumor cells and reactive inflammatory
cells. When the bursa is involved, the tumor cells typically appear in interfollicular areas.
DIAGNOSIS
Usually, diagnosis is based on enlarged nerves and lymphoid tumors in various viscera.
The rareness of bursal tumors helps distinguish this disease from lymphoid leukosis also,
Marek’s disease can develop in chickens as young as 3 wk of age, whereas lymphoid
leukosis typically is seen in chickens >14 wk of age. Reticuloendotheliosis, although rare,
can easily be confused with Marek’s disease because both diseases feature enlarged
nerves and T-cell lymphomas in visceral organs.
A diagnosis based on typical gross lesions may be confirmed histologically, or better, by
demonstration of predominant T-cell populations and Marek’s viral DNA in lymphomas
by histochemistry and PCR, respectively.
Furthermore, Marek’s disease lymphomas will usually lack evidence of clonally
integrated avian retroviruses or alteration of the cellular oncogene c-myc.
CONTROL
Vaccination is the central strategy for the prevention and control of Marek’s disease.
The efficacy of vaccines can be improved, however, by strict sanitation to reduce or delay
exposure and by breeding for genetic resistance.
Probably the most widely used vaccine consists of turkey herpes virus.
Bivalent vaccines consisting of turkey herpes virus and either the SB-1 or 301B/1 strains
of serotype 2 Marek’s disease virus has been used to provide additional protection
against challenge with virulent serotype 1 isolates.
Several attenuated serotype 1 Marek’s disease vaccines are also available; of these, the
CV1988/Rispens strains appears particularly effective.
A synergistic effect on protection, noted mainly between serotype 2 and 3 strains, has
prompted the empirical use of other virus mixtures.
Because vaccines are administered at hatching and require 1-2 wk to produce an effective
immunity, exposure of chickens to virus should be minimized during the first few days
after hatching.
Vaccines are also effective when administered to embryos at the 18th day of incubation.
In ovo vaccination is now performed by automated technology and is widely used for
vaccination of commercial broiler chickens, mainly because of reduced labor costs and
greater precision of vaccine administration.
Proper handling of vaccine during thawing and reconstitution is crucial to ensure that
adequate doses are administered.
Cell-associated vaccines are generally more effective than cell-free vaccines because they
are neutralized less by maternal antibodies.
Under typical conditions, vaccine efficacy is usually >90%. Since the advent of
vaccination, losses from Marek’s disease have been reduced dramatically in broiler and
layer flocks.
However, disease may become a serious problem in individual flocks or in selected
geographic areas (eg, the Delmarva broiler industry).
Of the many causes proposed for these excessive losses, early exposure to very virulent
virus strains appears to be among the most important.
Using fowl pox virus and herpes virus of turkeys as vectors, experimental recombinant
vaccines have been shown to be effective against challenge with virulent Marek’s disease
virus.
INTRODUCTION
Under natural conditions, lymphoid leukosis has been the most common form of the
leukosis / sarcoma group of diseases seen in chicken flocks, although recently myeloid
leukosis has become prevalent.
Members of the leukosis / sarcoma group of avian retroviruses, including avian leukosis
viruses that were formerly placed in a subgenus termed avian type C oncorna viruses
have recently been termed alpha retroviruses.
Members of this group of viruses have similar physical and molecular characteristics and
share a common group-specific antigen.
Avian leukosis occurs naturally only in chickens. Experimentally, some of the viruses of
the leukosis/sarcoma group can infect and produce tumors in other species of birds or
even mammals.
The infection is known to exist in virtually all chicken flocks except for some SPF flocks
from which it has been eradicated.
The frequency of infection has been reduced substantially in the primary breeding stocks
of several commercial poultry breeding companies.
In recent years this control program has expanded, and infection has become infrequent
or absent in certain commercial flocks.
The frequency of avian leukosis tumors even in heavily infected flocks is typically low
(<4%), and disease is often inapparent.
Up to 1.5% excess mortality per wk has been reported in commercial broiler- breeder
flocks naturally infected with subgroup J avian leukosis virus.
ETIOLOGY
Chickens are the natural hosts for all viruses of the leukosis/sarcoma group; these
viruses have not been isolated from other avian species except pheasants, partridges, and
quail.
Avian leukosis virus is shed by the hen into the albumen or yolk, or both; infection
probably occurs after the onset of incubation.
Congenitally infected chickens fail to produce neutralizing antibodies and usually remain
viraemic for life.
Horizontal infection after hatching is also important, especially when chicks are exposed
immediately after hatching to high doses of virus, eg, in feces of congenitally infected
chicks or in contaminated vaccines.
Horizontally infected chickens have a transient viraemia followed by antibody
production.
The earlier the infection, the more likely it is to lead to tolerance, persistent viraemia,
and tumors.
Other factors known to increase the susceptibility of chickens to horizontal infection
include the absence of maternal antibodies and the presence of endogenous retroviruses,
especially those associated with the late feathering (K) gene.
Tumors are more frequent in congenital than in horizontal infections, but many more
chickens are exposed horizontally than congenitally.
Rates of embryo transmission typically are 1-10%; virtually all chicks in an infected flock
are exposed by contact.
Congenital and, in some cases, early horizontal infection can induce permanent carrier
states characterized by shedding of virus or antigen into the environment and into eggs.
Late infection (ie, inoculation at 12-20 wk of age) is unlikely to lead to virus shedding.
The virus is not highly contagious compared with other viral agents and is readily
inactivated by disinfectants.
Transmission can be reduced or eliminated by strict sanitation.
After the infection is eradicated, standard disease control and sanitation practices can
keep chicken flocks free of the disease.
The role of males in transmission of avian leukosis virus is uncertain.
Infected cocks apparently do not influence the rate of congenital infection of progeny.
Cocks may act only as virus carriers and sources of contact or venereal infection to other
birds.
PATHOGENESIS
Chickens with lymphoid leukosis show nonspecific clinical signs including inappetence,
weakness, diarrhea, dehydration, and emaciation.
Infected chickens become depressed before death. Palpation often reveals an enlarged
bursa and sometimes an enlarged liver.
Infected birds may not necessarily develop tumors, but they may lay fewer eggs.
Diffuse or nodular lymphoid tumors are common in the liver (see the picture
below) spleen, and bursa, and are found occasionally in the kidneys, gonads, and
mesentery.
Involvement of the bursa has been considered virtually pathognomonic, although bursal
lymphomas are now known to also be induced by reticuloendotheliosis virus.
Sometimes the bursal tumors are small and observed only after careful examination of
the mucosal surface of the organ.
Usually, no enlargement of peripheral nerves is apparent, although such lesions have
been noted after experimental inoculation of subgroup J virus.
Microscopically, the tumor cells are uniform, large lymphocytes. Mitotic figures are
frequent.
Outbreaks of neoplasms other than lymphoid leukosis such as myelocytomas,
haemangiomas, and renal tumors have also been noted in meat-type chickens infected
with subgroup J avian leukosis virus.
Myelocytomatosis and skeletal myelocytomas may cause protuberances on the head,
thorax, and shanks.
Myelocytomas may develop in the orbit of the eye, causing hemorrhage and blindness.
Haemangiomas may be seen in the skin, appearing as “blood blisters,” which may
rupture causing hemorrhage.
Renal tumors may cause paralysis due to pressure on the sciatic nerve. Microscopically,
especially in cases of myelocytomas induced by subgroup J avian leukosis virus, the liver
shows a massive intravascular and extravascular accumulation of myelocytes
characterized by the presence of cytoplasmic eosinophilic granules.
Most strains of leukosis/sarcoma viruses also induce non lymphoid tumors (including
sarcomas), erythroblastosis, myeloblastosis, myelocytomas, haemangiomas,
nephroblastomas, osteopetrosis, and related neoplasms.
The nature of the tumors and their frequency depend on virus and chicken strain, age,
dose, and route of infection.
Occasional outbreaks of predominantly one type of tumor are seen in the field. The Rous
sarcoma virus, a member of this group, has been widely studied in the laboratory.
Each strain usually causes a predominantly neoplastic disease and can be distinguished
on the basis of pathogenicity.
Some viruses (eg, Rous sarcoma and erythroblastosis viruses) contain a viral oncogene
that leads to neoplasm induction within a short incubation period, but such viruses are
rare in the field.
Viruses with a viral oncogene are often defective for replication and require the presence
of a non defective helper virus to replicate.
DIAGNOSIS
Because avian leukosis virus is widespread among chickens, virus isolation and the
demonstration of antigen or antibody have limited or no value in diagnosing field cases
of lymphomas.
Gross characteristics of diagnostic significance include the tumorous involvement of the
liver, spleen, or bursa in the absence of peripheral nerve lesions. Tumors occur in birds
>14 wk old.
In lymphoid leukosis, the lymphoid cells are histologically uniform in character, large,
and contain IgM and B-cell markers on their surface.
Tumors can be differentiated from those of Marek’s disease by gross and microscopic
pathology (although this can be difficult in practice) and by molecular techniques that
demonstrate the characteristic clonal integration of proviral DNA into the tumor cell
genome with the associated disruption of the c-myc oncogene.
Lymphoid leukosis cannot easily be differentiated from B-cell lymphomas caused by
reticuloendotheliosis virus except by virologic assays; however, such tumors probably are
extremely rare.
ELISA kits for detection of antibodies to avian leukosis virus subgroups A, B, and J are
available commercially.
CONTROL
Learning objectives
INTRODUCTION
SPREAD
Ingestion is the usual route of entry. Virus is shed in the faeces for a period of several
days and it is quite resistant to environmental conditions.
It appears that some birds are enteric carriers and excrete virus in their droppings.
Infected litter is a source of the virus which is easily transmitted horizontally by fomites
and mechanical carriers. Vertical transmission is a very important means of virus
dissemination.
Transmission of the virus occurs through the egg, from infected to susceptible stock.
Egg transmission occurs during the period from the infection of susceptible laying hens
to the development of immunity, a period of 3-4 weeks.
PATHOGENESIS
In young chicks exposed to field strains, primary infection of the alimentary tract,
especially duodenum, is rapidly followed by a viraemia, and subsequent infection of the
pancreas and other visceral organs (liver, heart, kidney, spleen) and skeletal muscle, and
finally central nervous system.
Viral antigen is abundant in the CNS, where Purkinje cells and molecular layer of the
cerebellum are the favoured sites of virus replication.
Persistence of the viral infection is common in the CNS, alimentary tract and pancreas.
CNS and the pancreas are the only sites uniformly infected by egg-adapted strains.
Age at exposure is especially important in the pathogenesis. Birds infected at one day of
age generally die, where as those infected at 8 days develop paresis (partial paralysis) but
usually recover.
Infection at 28 days causes no clinical signs. Bursectomy but not thymectomy abolished
the age resistance. This indicated that humoral immunity was the basis of age resistance.
It is found that young age correlates with prolonged viraemia, persistence of virus in the
brain, and development of clinical disease
AE usually makes it appearance when chicks are 1-2 week of age. Affected chicks first
show a slightly dull expression of the eyes.
This is followed by a progressive ataxia from incoordination of the muscles, which may
be detected readily by exercising the chicks.
As the ataxia becomes more pronounced, chicks show an inclination to sit on their hocks
and finally, they come to rest, or fall on their sides (see the picture below).
AE: The lens of this bird's eye contains a large, roughly circular, well-demarcated pale
blue area of opacity. (Source: Cornell University)
LESIONS
The only gross lesions in chicks are whitish areas in the muscles of ventriculus, which are
due to masses of infiltrating lymphocytes.
In adult birds, no changes have been described except the lens opacities.
Microscopically, the main changes are in the CNS and some viscera. The peripheral
nervous system is not involved.
In the CNS, the lesions are those of a disseminated non-purulent encephalomyelitis, and
a ganglionitis of the dorsal root ganglia.
The most finding is a striking perivascular infiltration in all portions of the brain and
spinal cord, except cerebellum. Microgliosis occurs as diffuse and nodular aggregates.
The glial lesion is seen chiefly in the cerebellar molecular layer.
In the mid-brain, two nuclei- nucleus rotundus and nucleus ovoidalis – are always
affected with a loose microgliosis which is considered Pathognomonic. Another lesion of
Pathognomonic importance is central chromatolysis (axonal reaction) of the neurons in
the nuclei of thebrain stem, particularly those of the medulla oblongata.
The dying neuron is surrounded by satellite oligodendroglia.Later, microglia phagocytize
the remains. The central chromatolysis is never seen without an accompanying cellular
reaction.
Visceral lesions appear to be hyperplasia of thelymphocytic aggregates. In the
proventriculus, there only a few small lymphocytes in the muscular wall.
In AE, theses become dense lymphocytic foci (aggregates). This lesion is Pathognomonic.
Similar lesions occur in the ventriculus muscle, but unfortunately they also occur in
mArek’s disease.
In the pancreas, circumscribed lymphocytic follicles are normal, but in AE thenumber
increases several times.
In the myocardium, particularly in the atrium, there are aggregates of lymphocytes.
These are considered to be the result of AE.
DIAGNOSIS
The clinical signs, absence of gross lesions, and microscopic findings in the brain, spinal
cord and visceral organs together with the absence of other virus infections and
nutritional deficiencies affecting the nervous system, are strongly suggestive of avian
encephalomyelitis and are frequently used for presumptive diagnosis.
A definitive diagnosis requires demonstration of the virus by isolation and identification
or by other means.
Examination of smears from the brain, or cryostat sections stained by direct
immunofluorescence may also be used to demonstrate virus; positive results are
confirmatory and often unreliable.
A number of serological tests are available for determining the infection. These include
virus neutralization (VN) test, an indirect immunofluorescence test, immunodiffusion
and an ELISA test. Because of its specificity and sensitivity, rapidity of performance and
amenability to large-scale screening, the ELISA has replaced other tests for antibody,
including the assessment of efficacy of vaccination.
DIFFERENTIAL DIAGNOSIS
INTRODUCTION
This disease is usually seen in meat-producing chickens aged 3-7 weeks. However it has
also been recorded in birds as young as 7 days old, and as old as 20 weeks.
It is a rare disease in turkeys. It is characterised by a sudden increase in mortality. This is
normally between 2 and 10% of the flock but upto 30% has been described.
Significant mortality persists for only a few days.
ETIOLOGY
The etiology of the disease has not been properly established. There is no separate
inclusion body hepatitis virus.
Virtually every serotype of fowl Aviadenovirus group I have been isolated from the
naturally occurring cases of IBH.
Furthermore, all the adenovirus serotypes produce hepatitis when young SPF chicks are
inoculated parenterally.
Most experimental adenovirus infections produce basophilic inclusion bodies in the
hepatocytes whereas most natural cases produce eosinophilic intranuclear inclusion
bodies. If adenoviruses are involved in producing IBH, they appear to acta with some
other factor.
It has been suggested that immunosuppression produced by infectious bursal disease
(IBD) helps adenovirus to produce IBH. However many flocks undergoing combined
infections with these viruses remain healthy. Furthermore, outbreaks of IBH occurred in
both Northern Ireland and Newzealand before IBD virus was into those countries. Some
outbreaks of disease described as IBH closely resemble haemorrhagic syndrome/
infectious anaemia caused by Chicken anaemia virus.
Outbreaks of IBH which occurred in Australia in the early 1990s differ significantly from
the above. They occurred in much younger chicks (i.e. under 3 weeks of the age), have
caused higher mortality and predominantly basophilic inclusion bodies were present in
hepatocytes.
Adenoviruses have been isolated from field cases and have reproduced the disease
experimentally in chickens. In India, the disease has appeared as seasonal, especially
after monsoon, in the cold season. The mycotoxin stress seems to be another
predisposing factor besides IBD.
CLINICAL SIGNS
The disease is characterised by sudden onset of mortality, reaching highest after 3-4
days, and dropping on the 5th day, but some times continuing for 2-3 weeks.
Morbidity is low. Sick birds adopt a crouching position with ruffled feathers and die
within 48 hours, or recover.
Mortality may reach 10%, and sometimes as high as 30%. Overall feed conversion and
weight gain are usually decreased.
Anaemia, jaundice of the skin and subcutaneous fat, haemorrhages in various organs,
especially the muscles, and bone marrow degeneration are usually present, but vary in
severity.
In some outbreaks the bone marrow lesions are most prominent, and it has been
suggested that the disease should be called, “Hepato-myeloporetic disease”.
LESIONS
The liver in diseased birds is pale, friable and swollen, and frequently has haemorrhages.
Petechial or ecchymotic haemorrhagesmay be present in the liver and skeletal muscles.
Microscopically, there is a diffuse and generalized hepatitis, with intranuclear inclusion
bodies in the hepatocytes, which are often eosinophilic.
In the Australian outbreaks, basophilic inclusions predominated. Virus particles were
detected only in cells with basophilic inclusions.
Eosinophilic inclusions were composed of fibrillar granular material. IN the New zealand
outbreaks, inclusions were eosinophilic.
DIAGNOSIS
This depends on isolation and identification of the virus, and on serological tests.
Specimens of choice are faeces, pharynx, kidney, and affected organs, e.g. livers.
Virus isolation is best achieved by inoculating both a 10% suspension of the affected
organ and a a faeces suspension into cell cultures. Chicken embryo liver or lung cells, or
chick kidney cells, are all sensitive but chick embryo fibroblatss are relatively insensitive.
Antibody to the conventional adenovirus group antigen can be detected using the double
immunodiffusion (DID) test. The indirect immunofluorescent test is much more
sensitive and rapid, and is inexpensive. ELISA has been used to detect group antibodies,
and it is expensive and sensitive.
Demonstration of eosinophilic intranuclear inclusion body in Haematoxylin and eosin
staining in the hepatocytes of chickens in naturally occurring inclusion body hepatitis is
diagnostic.
INTRODUCTION
A viral disease, which was reported from Pakistan, affecting particularly broilers
and the losses varies from 10-20%.
An incomplete virus which requires another adenovirus for its multiplication and growth
is the cause of this disease and certain viral diseases such as adenovirus, IBH,
aflatoxicosis are said to be responsible for the outbreak of this disease.
On postmortem examination
Learning objectives
To know the etiological factors and to understand the pathogenesis of chicken infectious
agent, egg drop syndrome and avian nephrosis.
To recognize the clinical signs manifested by the affected birds.
To become familiar with the macroscopic and microscopical lesions of the disease.
To learn the diagnostic methods to confirm the disease.
To understand the mechanism of anemic condition caused by chicken infectious anemia
virus.
To know the effect of adeno virus on egg production and the different between EDS 76
and infectious bronchitis.
INTRODUCTION
SPREAD
PATHOGENESIS
Experimental studies have shown that anaemia and pathological changes associated with
CAV are produced only following parentral inoculation of high doses of CAV into
neonatal , fully susceptible (i.e. having no maternal antibody) chicks.
Chicks infected by contact with parenterally inoculated chicks are also resistant to
experimental disease but become infected and shed the virus.
Maternal antibody is protective. Chicks with maternal antibody usually show no disease
or anaemia following parentral inoculation, but may become infected and shed the virus.
Experimental dual infection of CIAV and immunosuppressive viruses such as
reticuloendotheliosis virus, virulent Marek’s disease virus and infectious bursal
disease(IBD) virus enhances the apparent pathogenicity of CAV, resulting in greater
mortality and more persistent anaemia and histological lesions.
In such dual infections the protective effect of maternal antibody to CAV may be
overcome.
In chicks dually infected with CAV and IBD virus, the age résistance was overcome and
contact-infected chicks also developed anaemia. CIAV has been shown to be
immunosuppressive.
Functional changes were detected in splenic lymphocytes and splenic and bone marrow
macrophages from both clinically affected and sub clinically infected chicks.
Following intramuscular inoculation of susceptible day- old chicks, CAV was consistently
recovered from all organs for upto 21 days after inoculation.
The principal sites of CAV replication are precursor T cells in the thymic cortex and in
haemocytoblasts in the bone marrow.
Destruction of these cells accounts for the immunosuppression and anaemia. However,
the virus also replicates in all lymphoid aggregates through out the body.
SIGNS
Disease occurs in theprogeny of breeder flocks which are infected for the first time with
the the virus fater they come into lay.
CIAV is vertically transmitted to the progeny. No clinical signs are seen in the parents.
However, around two weeks of age, the young chicks show variable mortality. This can
be as great as 60% but usually averages around 10%. The most characteristic changes in
infected are anaemia, aplasia of the bone marrow and atrophy of thymus, spleen and
bursa of Fabricius.
Anaemia is characterised by watery blood, increased clotting time and paler plasma.
Low haematocrit values ranging from 6-27% is due to pancytopaenia with markedly
decreased numbers of erythrocytes, white blood cells, and thrombocytes.
Affected birds are depressed and more or less pale. Haemorrhages may occur under the
skin and through out the skeletal muscles.
Enlarged livers and gangrenous dermatitis may also be present. Other names for this
condition are anaemia dermatitis syndrome, infectious anaemia syndrome,
haemorrhagic syndrome, and blue-wing disease.
Surviving chicks completely recover from anaemia by 20-28 days after infection.
However, retarded recovery and increased mortality may be associated with secondary
bacterial and viral infections. Secondary infections cause more severe clinical signs.
Subclinical infection of the progeny of immune breeder flocks is common. This occurs
soon after maternally acquired antibodies have disappeared at about 3 weeks of age.
MACROSCOPIC LESIONS
Though thymic atrophy is the most consistent lesion, bone marrow atrophy is the most
characteristic lesion. Femoral bone marrow is fatty, and yellowish and pink.
Thymic atrophy may result in a complete regression of the organ.
As infected chicks develop age resistance, thymic atrophy is a much more consistent
lesion than grossly visible bone marrow lesions. Bursal atrophy is less noticeable.
Haemorrhages in the proventricular mucosa, and subcutaneous and muscular
haemorrhages are some times associated with severe anaemia.
DIAGNOSIS
Outbreaks of clinical disease are normally diagnosed on the basis of the characteristic
signs and pathology. There is also usually a history of a common breeder flock, which is
often close to peak egg production.
Laboratory diagnosis is base on immunofluorescent or immunocyto chemicaldetection of
CIAV antigens in thymus or bone marrow. Viral DNA can also be detected in thymus or
bone marrow by insitu hybridization, dot blot hybridization or polymerase chain reaction
(PCR).
Virus isolation is not recommended because it is slow and expensive. Serum antibody to
CIAV can be detected by a variety of serological tests including serum neutrolisation,
indirect immunofluorescence and enzyme-linked immunosorbent assay (ELISA).
DIFFERENTIAL DIAGNOSIS
Runting and Stunting Syndrome, field rickets and Salmonella enteritidis septicaemia
were the conditions most likely to produce low weights and mortality in this age group.
All of these were excluded on the absence of typical pathology.
Sulphonamide toxicity and severe aflatoxicosis can induce haemorrhagic lesions and
aplastic anaemia, though these would not be expected to occur in the progeny of only 1
parent flock.
ETIOLOGY
The cause of EDS is an adenovirus that differs from aviadenoviruses and siadenoviruses
in that it agglutinates avian but not mammalian red blood cells to high titres.
Although EDS virus apparently shares the Aviadenovirus group antigen, this can be
detected only by indirect means. It is now classified as a species, duck adenovirus A, in
the genus Atadenovirus.
In fact, EDS virus is a naturally occurring adenovirus of ducks, geese and other water
fowl that has infected domestic fowl.
It grows best in duck and geese cell cultures but also grows well in chick embryo liver
and chick kidney cells. All virus isolates belong to one serotype (DAdV-1).
SPREAD
PATHOGENESIS
Following experimental infection of laying infection, the virus grows to a limited extent
in the nasal mucosa. This is followed by a transient viraemia, with virus growth in
lymphoid tissue through out the body, especially spleen and thymus.
The infundibulum of the oviduct is consistently affected. At 8 days after infection there is
massive viral replication in the pouch shell gland region of the oviduct, and to a much
lesser extent , in other parts of the oviduct. This coincides with the occurrence of egg
shell changes. Both the eggs with normal and affected shells contain virus, both
externally and internally, for the next 2 -3 weeks.
Chicks hatched from these infected eggs often do not develop antibody but they may be
latently infected. At around peak egg production, the virus is reactivated and horizontal
spread occurs.
In a minority of cases there is horizontal spread of the virus between birds during the
growing period, but, as the amount of virus excreted is small, this spread is limited.
CLINICAL SIGNS
The first sign is usually loss of shell pigmentation. This is quickly followed by production
of thin-shelled, soft-shelled and shell-less eggs.
Egg shells may have focal thickening due to mineral deposits. However, ridging and
misshapen eggs are not a feature. There is a drop in egg production.
The birds are normally healthy but some times appear slightly depressed. Diarrhoea may
be noticed due to an excess of oviduct secretion in droppings.
Classical EDS is manifested by a sudden apparent fall in egg production around peak
production or by a failure to achieve or hold expected production.
MACROSCOPIC PATHOLOGY
Inactive ovaries and atrophied oviducts are often the only recognized lesons, and these
are not consistently present.
MICROSCOPIC PATHOLOGY
The main pathological changes occur in the pouch shell gland of oviduct. Virus replicates
in epithelial cell nuclei, and produces intranuclear inclusion bodies.
Many affected cells are sloughed into the lumen. There is a severe inflammatory
response involving macrophages, plasma cells and lymphocytes, together with variable
numbers of heterophils in the lamina propria and epithelium.
DIAGNOSIS
The combination of a sudden fall in egg production, associated with thin-shelled and
shell-less eggs in a apparently healthy birds, is almost diagnostic.
Virus isolation can be difficult because it is very difficult to identify the correct bird to
sample. The easiest method is to feed the affected eggs to susceptible hens.
Once they produce abnormal eggs, the pouch shell gland is harvested, and samples
inoculated into either duck kidney, or fibroblast cell cultures, or embryonated eggs. Virus
growth is detected by testing for haemagglutinins.
Detection of antibodies to EDS virus by the haemagglutination inhibition (HI) test using
fowl erythrocytes is sensitive and easy and is the diagnostic method of choice in
unvaccinated flocks.. ELISA is now also used.
DIFFERENTIAL DIAGNOSIS
EDS can be distinguished from Newcastle disease and influenza virus infections by the
absence of illness, and from infectious bronchitis by the eggshell changes that occur at or
just before the drop in egg production and by the absence of ridges and malformed eggs
sometimes seen in infectious bronchitis.
INTRODUCTION
SPREAD
ANV is distributed worldwide in the domestic fowl. Transmission readily occurs by direct
or indirect contact.
The most common method is probably through ingestion of faecally contaminated
material.
Egg transmission (vertical transmission) has been suggested on the basis of field
observations.
PATHOGENESIS
Only young chickens are known to develop clinical disease and distinct kidney lesions
when exposed to ANV. Following infection, the virus is first detected in faeces within 2
days, with maximum virus shedding at 4-5 days.
The virus is widely distributed, with maximum titres in the kidney and jejunum and low
titres in the bursa of Fabricius, spleen and liver.
The virus is consistently isolated from kidney, jejunum, and rectum, but not from brain
and trachea.
CLINICAL SIGNS
The clinical sign in one-day old chicks is only transient diarrhoea, but not all chicks show
the signs. Weight gain is depressed.
In the broiler chickens, symptoms vary from none ( subclinical) to outbreaks of the so-
called “runting syndrome” and baby chick nephropathy”.
LESIONS
Gross lesions in dead chicks are mild to severe discolouration and swelling in the
kidneys, and visceral urate deposits.
Chalk- like urate crystals are seen on the surface of the peritoneum and liver. The heart is
white due to heavy urate deposits on the surface of epicardium.
Microscopically, the primary changes consist of necrosis and degeneration of epithelial
cells of the proximal convoluted tubules with infiltration of granulocytosis and
interstitial nephritis of varying severity.
The degenerating epithelial cells show acidiphilic granules of various sizes in the
cytoplasm. Also, there is interstitial lymphocytic infiltration and moderate fibrosis.
In the later stages, lymphoid follicles develop. Virus particles and viral antigens can be
demonstrated in the degenerating epithelium by electron microscopy, and also by
immunofluorescence.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
Learning objectives
To know the etiological factors and to understand the pathogenesis of chicken infectious
agent, egg drop syndrome and avian nephrosis
To recognize the clinical sign manifested by the affected birds
To become familiar with the macroscopic and microscopical lesions of the disease
To learn the diagnostic mehtods to confirm the disease
To have a better understanding about the etiology, pathogenesis, clinical signs, lesions
and diagnosis of infectious stunting syndrome and reo viral infections
INTRODUCTION
Reoviruses are ubiquitous in chickens and turkeys; some strains become viraemic and
localize in the large joints, resulting in arthritis, tendinitis, and synovitis.
Most birds are thought to be susceptible to respiratory-intestinal strains of reo viruses.
Chickens and, to a lesser degree, turkeys are susceptible to viral arthritis, which is seen
worldwide.
Reoviruses also have been associated with pericarditis and myocarditis,
hydropericardium, pasting, malabsorption, and femoral head necrosis, although further
study is needed to define their role.
The disease is egg-transmitted and is of short duration except when lateral transmission
in a flock is prolonged.
Respiratory and digestive infections may occur but are of short duration; however, the
virus survives in tendon sheaths for extended periods.
The virus is spread via aerosols, fomites, and mechanical means, and is resistant to heat
and chemical inactivation.
Several antigenic subtypes of avian reoviruses have been identified; however, there
appears to be significant cross-protection among most of the isolates or subtypes.
Pathogenicity of the isolates varies widely. Serious outbreaks of viral arthritis are
followed by a decreased incidence in later hatch groups of birds from the same parent
flock.
This may be related to decreased egg transmission and development of parental
immunity.
Day-old chicks are more susceptible than older birds when exposed by natural means.
The earlier in life the chick is infected, the longer the virus persists in the tissues.
CLINICAL FINDINGS
The arthritic form (tenosynovitis) usually is seen in broilers 4-8 wk old as unilateral or
bilateral swellings of the tendons of the shank and above the hock; it can also be found in
much older chickens.
The birds walk with a stilted gait (click here for animation). In severely affected flocks,
rupture of the gastrocnemius tendon is frequent, and many cull birds are seen around
the feeders and waterers.
Mortality is 2-10% and morbidity 5-50%. Severely affected birds rarely recover; less
severely affected birds recover in 4-6 wk.
The infection is inapparent in many birds. Feed efficiency and rate of gain are decreased.
LESIONS
An acute, fulminating infection is occasionally seen in young chicks and embryos with
cardiomegaly, hepatomegaly, and splenomegaly with necrotic foci.
Edema of the tendons of the leg is marked, petechial hemorrhages develop in the
synovial membranes above the hock, and fusion and calcification of the tendon bundles
are common.
Blood clots and hemorrhages are seen with rupture of the gastrocnemius tendon.
Pitted erosions of the cartilage of the distal tibiotarsus are seen with flattening of the
condyles.
Histologically, the synovial cells are hypertrophied, hyperplastic, and infiltrated by
lymphocytes and macrophages.
The synovia contain heterophils and macrophages. Infiltration of heterophils or
lymphocytes, or both, between myocardial fibers is a constant finding.
However, the infiltrating heterophils are difficult to distinguish from the clusters of
young, proliferating heterophils (ectopic myelopoiesis) that are present in the heart
muscle of all young, rapidly growing broiler chickens.
DIAGNOSIS
There is no treatment. Maternal antibody prevents early infection in chicks and should
reduce or prevent egg transmission.
Because egg transmission is the principal means of spread, it is desirable to have the
breeder flock immune.
Such a program should be directed to the serotypes present in the flock.
Adult birds are less susceptible to clinical disease if exposed by natural routes
INTRODUCTION
Infectious stunting Syndrome (ISS) is a transmissible disease that is seen worldwide and
results in a variable percentage of runted and stunted birds.
It is also sometimes known as, ‘pale bird syndrome’, malabsorption syndrome’, ‘
infectious runting’ and ‘runting and stunting syndrome’.
The financial losses are caused by an increased number of culled birds, poor feed
conversion, reduced weight for age, and greater than expected variations in weight at
slaughter.
The disease has now been reported from most broiler growing countries of the world,
including India.
CAUSE
PATHOGENESIS
CLINICAL SIGNS
The percentage of affected chickens in a flock with ISS can vary from a few percent to
more than 90%. At 4-8 days, the stunted chickens are characterised by the retarded
feathering on their heads and necks, and pendulous abdomens. At about two weeks,
affected chickens are often called as, “yellow heads” because of the prominence of the
retained down feathers on the head and neck.
Broken and displaced primary wing feathers have given the disease names like”
helicopter feathering” or “ helicopter disease”. AT 2-4 weeks clinical signs include
lameness due to secondary osteodystrophy, poor weight gain, opisthotonous due to
secondary encephalomalacia and pale shanks.
One of the important features if the disease is the presence of severely stunted (runted)
MACROSCOPIC LESSIONS
Affected birds can be relatively small for their age and pale. The subcutaneous fat is pale
compared to normal, hence the name” pale bird syndrome”. They are not anaemic.
Intestines are distended and pale with poorly digested contents. This phenomenon has
been referred to as “malabsorption syndrome”. In chickens that have not recently
eaten,the intestine s contain clear watery or mucoid fluid and hence it is described
as”mucoid” or catarrhal enteritis. The thymus is reduced to a chain of small dark lobes,
and the bursa of Fabricius is usually swollen. Depending on the form of ISS, the pancreas
can be hard, atrophic and very pale.
In all forms of ISS, osteodystrophy is commonly seen in the affected birds of a few weeks
of age. Because of the osteodystrophy, the disarticulation of the hips during the necropsy
can easily result in a separation of femur head from the femur. This can also happen
during catching, transport and handling of the birds for slaughter.
chickens, which remain small despite their huge appetites.
MICROSCOPIC LESIONS
Intestinal lesions include villus atrophy, and necrosis and degeneration of enterocytes on
the sides of villi and crypts, associated with significant infiltration of lymphocytes and
macrophages into the villus and lamina propria.
Lesions are most pronounced in the mid-jejunum. Enterocytes and degenerate
macrophages reveal small cytoplasmic inclusions.
DIAGNOSIS
The etiological agent has not been characterised, and serological tests are not available.
Therefore, diagnosis depends upon characteristic features of the disease, namely severely
stunted ( runted) but active chickens with retained down feathers on the head and neck
at 2-3 weeks of age; and poor growth in a variable percentage of the remaining flock at 2-
4 weeks.
Learning objectives
INTRODUCTION
Escherichia coli is a normal inhabitant of the digestive tract of mammals and birds, and
most strains are non-pathogenic. Certain serotypes can cause disease in poultry.
Colisepticaemia, egg peritonitis, yolk sac infection, and coligranuloma ( Hjarre’s disease)
are the well recgnised results of E.coli infection infection. These conditions are
collectively grouped under the heading “ Colibacillosis”.
INTRODUCTION
Colisepticaemia
Signs are nonspecific and vary with age, organs involved, and concurrent disease.
Young birds dying of acute septicemia have few lesions except for enlarged, hyperemic
liver and spleen with increased fluid in body cavities.
Birds that survive septicemia develop subacute fibrinopurulent airsacculitis, pericarditis,
perihepatitis, and lymphocytic depletion of the bursa and thymus.
Colisepticaemia: Perihepatitis and pericarditis:Liver
showing a thin layer of fibrin adhering on its surface (Red
arrow) while the heart showing adhesion of thick yellowish
fibrin layer( Green arrow).
DIAGNOSIS
Unlike pathogenic E coli associated with illnesses in other animal species, avian isolates
are generally nonhemolytic on sheep (5%) blood agar.
Isolation of a pure culture of E coli from heart blood, liver, or typical visceral lesions in a
fresh carcass indicates primary or secondary colibacillosis.
Consideration should be given to predisposing infections and environmental factors.
Pathogenicity of isolates is established when parenteral inoculation of young chicks or
poults results in fatal septicemia or typical lesions within 3 days.
Pathogenicity can also be detected by inoculation of the allantoic sac of 12-day-old chick
embryos.
Resulting gross lesions include cranial and skin hemorrhages in addition to
encephalomalacia in embryos inoculated with virulent isolates.
Also known as “mushy chick disease” and “omphalitis’. This condition is one of the
common causes of mortality in chicks during the first week after hatching.E.coli can be
involved either as the primary and sole causative agent or as a secondary opportunist.
Yolk sac infection can be associated with a thickened navel , where the route of infection
is via the unhealed navel, orbacteria can multiply in the hatching egg following faecal
contamination of the shell.
Yolk sac infection can cause 100% mortality in a batch of chicks in the first week of life,
but deaths are usually between 5% and 10%. Other bacteria, such as Bacillus cereus,
staphylococci, Pseudomonas aeruginosa,Proteus Spp. And clostridia, can also cause yolk
sac infection, either on their own, or, more commonly together with E.coli.
E.coli multiplies rapidly in the intestines of newly hatched chicks and infection spreads
rapidly from chick to chick in the hatchery and brooders.
A hatching environment that is not sufficiently humid is often associated with a high
incidence of yolk sac infection.
Affected chicks appear depressed and have distended abdomen and a tendancy to
huddle.
Sometimes the navel is visibly thickened, prominent and necrotic. Affected carcasses
may show a distinctive, purifying smell.
Post-mortem examination reveals a septicaemic carcass with the subcutaneous and yolk
sac blood vessels engorged and dilated.
The lungs are usually congested and the liver and kidneys dark and swollen.
The striking finding is an inflamed unabsorbed yolk sac with the yolk abnormal in colour
and consistency.
EGG PERITONITIS
A whole or partly formed egg may be impacted in the oviduct (see the pictures below).
A profuse pure growth of E.coli can be isolated from the oviduct and caseous inspissated
material.
Impaction of oviduct
The condition usually occurs as the cause of sporadic death in adult hens.
The clinical signs are non-specific and affected birds are usually found dead or die after
depression and loss of condition.
Post-mortem examination typically shows hard, yellow, nodular granulomas in the
mesentery and wall of the intestine ( see the picture), and particularly the caecum.
o Some times the liver is similarly affected and is hard, blotchy, discoloured and
swollen.
INTRODUCTION
Infectious coryza is an acute, highly contagious disease of the upper respiratory tract of
chickens.
A chronic respiratory disease can develop when complicated by other pathogens.
The disease occurs worldwide and causes economic losses due to an increased culling
rate in meat chickens and significant reduction of egg production in laying and breeding
fowl.
CAUSE
SPREAD
The main source of infection is clinically affected and carrier birds. As only a few viable
organisms are necessary for the infection, it can be transmitted by drinking water
contaminated by nasal discharge as well as by airborne means over a short distance.
Lateral transmission occurs readily by direct contact.
PATHOGENESIS
Adherence of the organism to the ciliated mucosa of the upper respiratory tract seems to
be the first step of the infection.
The capsule and the haemagglutination antigen play an important role in the
colonization.
Toxic substances released from the organism during the proliferation are associated with
production of lesions in the mucosa and appearance of the clinical signs.
The capsule may act as a natural defence substance against the bactericidal power of
complement through the alternate pathway.
As paragallinarum is a noninvasive bacterial agent with a strong tropism for ciliated cells
and migrates into the lower respiratory tract ( lungs, air sac) only after synergistic
interaction with other infectious agents and/or if encouraged by immunosuppression.
Factors that predispose to more severe and prolonged disease ( chronic respiratory
disease) include intercurrent infections with microorganisms such as infectious
bronchitis virus, laryngotracheitis virus, Mycoplasma gallisepticum, Escherichia
coli or Pasteurella spp. and unfavourable environmental conditions.
CLINICAL SIGNS
In severe cases, marked conjunctivitis with closed eyes, swollen wattles (wattle disease)
and difficulty in breathing can be seen.
Infectious coryza: Chicken showing bilateral
facial edema with marked swelling of
infraorbital sinus (blue arrow) and swollen
wattle in a natural case. Profuse nasal discharge
is also evident (green arrow).
Feed and water consumption is usually decreased resulting in a drop in egg production
or an increase in the rate of culls.
A reduction of egg production of more than 20% indicates multifactorial disease.
If complicated with other infectious agents a more severe and prolonged disease may
develop with the clinical picture of a chronic respiratory disease.
LESIONS
The upper trachea may be involved but the lungs and airs sacs are only affected in
chronic complicated cases.
Subcutaneous edema of the face and wattles is prominent.
Microscopically, marked loss of cilia and microvilli, cell edema, degeneration and
desquamation of mucosal and glandular epithelium, infiltration of leukocytes and
deposition of mucopurulent substances can be seen and followed by infiltration of mast
DIAGNOSIS
The history of a rapidly spreading disease, its clinical signs and lesions may allow a
tentative diagnosis.
The diagnosis has to be confirmed by cultural identification of the causal agent. Swabs
from an infraorbital sinus ( the nasal exudates is usually contaminated) of 2 or 3
diseased chickens should be cultured on blood agar plates cross-streaked with a feeder
organism such as Staphylococcus epidermidis.Swabs form the trachea and airsacs may
be taken, although H.paragallinarum is less frequently isolated from thes areas.
The organism should be identified by morphology, biochemistry and
immunofluorescence.
A number of serological tests are used for the examination of sera for specific antibodies
against H.paragallinarum. These include agglutination, haemagglutination inhibition,
and fluorescent antibody test.
cells into the lamina propria of the mucous membrane.
To know the etiological factors and to understand the pathogenesis of fowl cholera,
tuberculosis and sprochaetosis
To recognize the clinical signs manifested by the affected birds
To become familiar with the macroscopic and micriscopical lesions of the disease
To learn the diagnostic methods to confirm the disease
To know the basic mechanism of granuloma formation in tuberculosis
BOTULISM (LIMBERNECK)
SPREAD
PATHOGENESIS
Type C botulism can be caused by ingestion of preformed toxin. Because, the organism is
widely distributed in the gut, as indicated, dead birds provide conditions for C .
botulinumgrowth and toxin production.
Birds scavanging (i.e., searching for decaying flesh as food) such carcasses can readily
obtain enough toxin to become affected.
Botulism caused by A, B, and E rarely, and generally has been associated with
consumption of spoiled human food products fed to backyard chicken flocks.
The pathogenesis of botulism was once thought exclusively to be ingestion of preformed
toxin. There is growing evidence that C. botulinum type C produces toxin in the gut to
cause disease.
The term “toxico-infection” has been used to describe this form of the disease in broiler
chickens. Experimental evidence suggests caecum as the site of toxin production.
SIGNS
Clinical signs appear within a few hours of ingestion of the toxin. In chickens,
flaccid paralysis (i.e., lacking firmness of muscles) of legs, wings, neck and eyelids
are main features of the disease.
Initially, affected birds are found sitting and reluctant to move. If forced to walk,
they appear lame. Wings droop when paralysed.
Affected birds have ruffled feathers. Limberneck, the original and common name
for botulism, precisely describes paralysis of the neck. Because of eyelid paralysis,
birds appear comatose (in coma, unconscious), and may look dead.
Death results from cardiac and respiratory failure.
LESIONS
There are no gross or microscopic lesions. Sometimes, maggots or feathers may be found
in the crop.
DIAGNOSIS
The presumptive diagnosis of botulism is based on clinical signs and lack of gross or
microscopic lesions.
Definitive diagnosis requires detection of in serum, crop, or gastrointestinal washings
from sick birds.
The presence of toxin is confirmed by the injection of serum, or extracts of crop, or
intestinal contents, into mice.
Since toxin can be produced in decaying body tissues, material for examination should
be from living birds, or fresh Carcasses.
INTRODUCTION
CAUSE
The disease is caused by Clostridium perfringens type A or C in the large intestine and
caeca, and subsequent migration to small intestine where it produces toxins.
Alpha toxin produced by C.perfringens types A and C, and beta toxin produced by type C,
are believed responsible for intestinal and mucosal necrosis, the characteristic lesion of
the disease.
Both have been detected in faeces of chickens with NE. Predisposing factors include
outbreaks of coccidiosis, especially mild or subclinical, changes in diet, and inadequate
cleaning of houses, utensils and equipment.
SPREAD
Clostridium perfringens can be found i n faeces, soil, dust, contaminated feed and litter,
or intestinal contents.
Contaminated feed or litter are the main source of infection.
Fish meal is considered a particularly likely source of Clostridium
perfringens contamination.
PATHOGENESIS
CLINICAL SIGNS
The characteristic gross lesion of necrotic enteritis is a pseudo membrane attached to the
intestinal mucosa, primarily the small intestine.
The mucosa of the caecal pouches are not changed but the caecal tonsils and adjoining
narrow segments of the caeca may occasionally be affected.
The pseudo membrane which varies in entent, may be partly or entirely detached from
the viable mucosa, leaving behind a depression or a more extended smooth surface.
Necrotic enteritis: Jejunum showing marked Necrotic enteritis: Jejunum showing formation
thickening of mucosa due to edematous changes of greenish diptheretic membrane (green
(black arrow) and congestion (red arrow) with arrow) and tissue debris (red arrow) due to
diffuse brownish eruptions resembling the "dirty sloughed mucosa.
turkish towel" appearance.
The membrane may be white, yellow, green, brown or red. A yellow or green
discolourations is the most commonly found.
The affected gut segment may be dilated and soft with fluid contents, or the wall appear
turgid and rigid with dry and sparse luminal contents.
A detached pseudo membrane is occasionally found in the gut lumen. The contents of the
caecal pouches are often dark and dry.
Birds dying with NE often show a dark liver with dilated gall bladder, pale kidneys with
prominent lobular outlines, and dark and dry pectoral musculature indicating
dehydration.
The body condition depends on the course of disease. Birds dying with acute NE are in
good bodily condition.
Three main types of liver lesion may be found. The most common and most
characteristic is cholangiohepatitis.
Livers with the second type of lesion show light, randomly localized nodules ( focal
necroses and granulomas) of the liver parenchyma, and the third and most rare
type is massive liver necrosis causing a smaller or larger part of a liver lobe to be
homogenously discoloured.
MICROSCOPIC LESIONS
The characteristic feature is an aggregation of large, Gram-positive, rod-shaped bacteria
surrounded by necrotic tissue delineated from viable tissue by a zone of granulocytic
infiltration containing pyknotic cell nuclei.
The lesions are usually located within the lamina propria of the gut mucosa.
The least extensive lesions are limited to focal necroses comprising some epithelial and
stromal cells on the villus tips.
The deepest lesions may even affect the muscular wall of the gut.
Diagnosis
Differential Diagnosis
The similar lesions producing disease like coccidiosis and ulcerative enteritis should be
considered.
CAUSE
Gangrenous skin necrosis may be associated with various aerobic and anaerobic
bacteria; however, Clostridium septicum , Clostridium perfringens type A,
and Staphylococcusaureus , either singly or in combination are most often involved.
Combined infections are often more severe.
Young chicks immunosuppressed by infectious bursal disease or chick anemia virus are
predisposed. The disease may occur secondary to avian adenovirus or reticuloendothelial
virus infections as well.
Skin lesions due to trauma, wet litter, picking, or treading wounds may provide entry
sites for causative bacteria.
Systemic effects arise from invading bacteria and their elaborated exotoxins.
CLINICAL SIGNS
The first sign is usually a sudden dramatic increase in mortality in the affected flock.
Overall mortality is 10-60%. Affected chickens are extremely depressed, lethargic, and
prostrate, and die within 8-24 hr.
Red to black patches of moist, gangrenous skin are seen over the breast, abdomen, wing
tips, or thighs.
Feather loss or sloughing of the epidermis is common. When clostridial infection occurs,
palpation of the affected areas often reveals crepitation due to gas bubbles in the subcutis
and musculature.
LESIONS
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
INTRODUCTION
CAUSE
CLINICAL SIGNS
In acute disease there may be increased mortality without any obvious signs.
In other case signs may include depression, huddling, with ruffled feathers, anorexia and
watery droppings. Mortality in chickens vary from 2% to as high as 12%.
LESIONS
Gross lesions
Birds dying with acute disease show good condition and may have feed in the crop. More
protracted disease may lead to emaciation.
The most important lesions are found in the intestine, liver and spleen.
First, there are small, circular to lenticular mucosal ulcers affecting the small intestine,
caeca and upper large intestine.
The ulcers may penetrate as deep as the serosa, which may become perforated and result
in peritonitis. The ulcers may coalesce to form large areas with a pseudomembrane.
Small ulcers have a haemorrhagic border, which may be seen on the serosal and mucosal
surfaces.
A haemorrhagic border is less frequently found in larger lesions. Lesions with raised
edges may also be found.
In the liver, usually there are yellowish to grey necrotic lesions of varying size. The spleen
is enlarged and haemorrhagic.
Quail with acute disease may show haemorrhagic enteritis of the duodenum, with small
red spots visible on the serosal surface.
Microscopical lesions
Intestinal ulcers consist of small haemorrhagic and necrotic areas, often with clumps of
Gram-positive bacteria.
The ulcers involve villi and excreted into the the submucosa.
The ulcers sometimes reach as deep as the muscular coat and serosa.
Affected tissue is surrounded by granulocytes and mononuclear inflammatory cells.
Liver lesions consist of multifocal foci of coagulative necrosis that are often poorly
demarcated and with minimal inflammatory reaction.
Gram-positive bacteria are occasionally found within the necrotic foci.
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
INTRODCUTION
INTRODUCTION
Infectious, egg transmitted disease of poultry, especially chicks and turkey poults,
characterised by white diarrhoea, high mortality in young birds.
Cause: Salmonella pullorum.
Young chicks and turkey poults (Less than 4 weeks) commonly affected- very high
mortality (up to 100%) ; adults - asymptomatic carriers.
Not significant in other birds.
CLINICAL SIGNS
PATHOLOGY
Chicks
Growers
Arthritis - Hock joint - Enlarged due to the presence of excess orange coloured gelatinous
material around the joints.
Adults
DIAGNOSIS
Treatment of infected flocks to alleviate the perpetuation of the carrier state is not
recommended.
Control is based on routine serologic testing of breeding stock to assure freedom from
infection.
CLINICAL SIGN
Acute
Chronic
Sub acute
PATHOLOGY
Acute
Carcass appear septicaemic and jaundiced.
Subcutaneous blood vessels: hyperaemic and engorged.
Skeletal muscles: Congested and dark in colour.
Consistent finding: Dark reddish or almost blackish swollen friable liver with a
characteristic copper bronze sheen (glistening brightness on the surface).
Spleen: Enlarged
Small intestine: catarrhal enteritis with viscous, slimy, bile- tinged materials.
Characteristic feature: Dark brownish bone marrow.
Chronic
DIAGNOSIS
ETIOLOGY
Motile Salmonella serotypes, other than those in the S.arizonae sub genus are often
referred to as, “Paratyphoid (PT) salmonellae”.
These organisms can infect a wide variety of hosts , including humans.
In some cases they result in asymptomatic intestinal carriers and in some cases they
produce clinical diseases .
The most commonly isolated serotypes from chickens (i.e. PT salmonellae)
are: S.typhimurium , S. entritidis, S. hadar, S. montevideo, S.kentucky
and , S. heidelberg.
SPREAD
Paratyphoid salmonellae can be introduced into poultry from the following sources,
o Contaminated feed - Animal proteins containing feed : Fish meal, meat and bone
meal and poultry offal and feather meal.
o Vegetable proteins - They become contaminated with organisms either before or
after processing.
o Biological vectors - They can disseminate and amplify the organisms in poultry
flock.
o Insects - Cockroaches and meal worms (larvae of various beetles)
o Rats and mice - Important vectors of S.enteritidis in laying flocks.
VERTICAL TRANSMISSION
HORIZONTAL TRANSMISSION
Humans may also be salmonella excretors
Control of the disease is possible by means of high standard farm management, farm
hygiene and biosecurity
CLINICAL SIGNS
Disease is uncommon
Young chicks, poults or ducklings are commonly affected
Rarely in birds over 4 weeks of age
Mortality is usually less than 20% but exceptional case it reaches 100%.
Clinical signs are not specific, but similar irrespective of the serotypes
Ruffled feathers and drooping wings , depression, closure of eyes and reluctance to move
Diarrhoea with pasting of feathers around the (pasty) vent is common
Visual impairment due to corneal opacity or caseous plaques in the eye ball
MACROSCOPIC LESIONS
Lesions vary from the complete absence to a septicaemic carcass- with the congestion of
lung, liver, spleen and swollen kidney
Chicks - Unabsorbed yolk sac is a common feature.
Birds survive the acute septicaemic phase.
o Discrete (separate) necrotic lesions in the lungs, liver and heart
o Peritonitis
o Haemorrhagic enteritis
The most characteristic lesion is typhilitis (inflammation of caeca) with the caeca
distended by hard white necrotic cores.
DIAGNOSIS
Salmonellae remain among the leading sources of food-borne illness throughout much of
the world
The paratyphoid infection in birds (salmonellosis) acquire great importance because of
the human illness caused from the consumption of contaminated poultry products.
Treatment
Control
Strict sanitation in the hatchery, fumigation of hatching eggs, pelleting of feed to destroy
salmonellae, cleaning and disinfection of poultry houses, rodent control, and use of
competitive exclusion products.
Several antibacterial agents help prevent mortality but cannot eliminate flock infection.
Maintenance of poultry in confinement and exclusion of all pets, wild birds, and rodents
help prevent introduction of infection.
PATHOGENESIS
Associated with the lipid A portion of Salmonella cell wall lipopolysaccharide (LPS)
Proteinaceous toxin
The overall virulence of salmonella depends mainly on the initial degree of mucosal
invasiveness
CHAPTER-10: FOWL CHOLERA, SPIROCHAETOSIS AND
TUBERCULOSIS
Learning objectives
To know the etiological factors and to understand the pathogenesis of fowl cholera,
tuberculosis and spirochaetosis
To recognize the clinical signs manifested by the affected birds
To become familiar with the macroscopic and microscopical lesions of the disease
To learn the diagnostic methods to confirm the disease
To know the basic mechanism of granuloma formation in tuberculosis
INTRODUCTION
SOURCE OF INFECTION
PATHOGENESIS
CLINICAL SIGNS
PATHOLOGY
Peracute
o Marked congestion of the carcass
Acute disease
o Multiple petechiae through out the viscera
o Multiple pin-point necrotic foci in the liver (click here for animation)
Sub acute
o Edema of lungs (especially in turkeys)
o Pneumonia
o Perihepatitis
Chronic
o Caseous arthritis of hock and foot joint swelling,
o Induration of one or both wattles (in chicken) (click here for animation)
o Caseous exudate in the middle ear ( torticollis)
DIAGNOSIS
Presumptive diagnosis can be made from clinical signs, lesions or isolation of the
organisms.
Confirmative diagnosis can also be made on the above three.
Demonstration of the organisms confirms the disease
o In peracute disease : Impression smears the liver or smears of heart will reveal
bipolar organisms in methylene blue stain.
o In pneumonic form : Smears from lungs will reveal the organisms.
Isolation and identification of the organisms
o Depends on cultural and biochemical procedures
o Laboratory animal inoculation
TREATMENT
Sulfonamides and antibiotics are commonly used; early treatment and adequate dosages
are important.
Sulfaquinoxaline sodium in feed or water usually controls mortality, as do
sulfamethazine and sulfadimethoxine.
Sulfas should be used with caution in breeders because of potential toxicity.
High levels of tetracycline antibiotics in the feed (0.04%), drinking water, or
administered parenterally may be useful.
Penicillin is often effective for sulfa-resistant infections.
PREVENTION
INTRODUCTION
Soft ticks of the genus Argas are the main reservoirs of the organisms.
The organisms must depend on the ticks for its continued existence.
Not all the species of Argas act as biological vector of spirochaete.
Argus persicus is the important vector.
B.anserina is capable of surviving in either the bird or environment for long periods.
PATHOGENESIS
Ticks become infective 6-7 days after biting a host and remain infective up to 488 days.
Birds gets organism from salivary gland through bite of the infected ticks
Outbreaks are common during warm, humid seasons
Recovered birds are not carriers
CLINICAL SIGNS
Birds are visibly sick with cyanosis or pallor, especially of comb and wattle
Dullness, anorectic, ruffled feathers, huddled-up appear
Greenish diarrhoea (containing excess bile and urates, probably resulting from anorexia
and increased water consumption)
Characteristic feature: An abrupt elevation in body temperature due to the presence of
spirochaetes in the circulation
Rapid loss of body weight
Later, Paresis (partial paralysis) or paralysis, anaemia and coma
Body temperature is subnormal just prior to death
Recovered birds: Emaciated and may have paralysis of one orboth wings or legs
LESIONS
Macroscopic lesions
Most characteristic: Marked enlargement and mottling of the spleen. Splenomegaly may
not be visible when the birds are infected with low virulent strains or in early stage
Liver: Enlargement with small haemorrhages and pale foci
Kidney: Swollen and pale with urates visible in ureters
Intestine: Contents are usually green and mucoid and there is variable degree of
haemorrhage, especially at the proventriculus and gizzard junction
Pericardium: Mild pericarditis (some times) by sparing other serous memb.
Microscopic lesions
Spleen
Liver
Organisms in tissue
DIAGNOSIS
INTRODUCTION
Avian tuberculosis occurs throughout the world in many avian and some mammalian
species and in domestic poultry it is generally seen in mature stock kept in conditions of
poor management.
It usually runs a protracted course, causing reduction in condition, reduced egg
production and eventually death.
Although loss in a flock is intermittent it is invariably in adult fowls and this, together
with the culling of unthrifty birds and the depression in egg production, can cause
serious economic loss.
The infection is of importance also because the disease occurs in wild birds, pigs, rabbits
and mink.
EPIDEMIOLOGY
Cause
HOSTS
It is probable that all species of bird can be infected but susceptibility among domestic
species seems to be in the following order: chickens, ducks, geese and, least susceptible,
turkeys, in which it is relatively uncommon.
Ike disease is observed most commonly in older poultry because of the greater
opportunity for infection with age and the generally long incubation period. However,
occasionally, heavy losses may occur in pullets on multiage sites where the infection is
endemic and the standards of hygiene poor.
Came birds, particularly pheasants, are also susceptible. Some birds kept in zoological
gardens seem to be prone to tuberculosis, perhaps because of the difficulty in adequately
cleaning and disinfecting pens.
Cage birds may also succumb to avian tuberculosis but tuberculosis in parrots and
canaries may also be caused by M. bovis or M. tuberculosis.
Surveys show that many species of wild bird become naturally infected and in some
instances a predisposing factor is their close association with infection in domestic stock.
Among mammals Al. avium can cause progressive disease in swine, rabbits and mink
and can cause sensitivity in cattle to the skin tuberculin rest.
SPREAD
In the transmission of infection the most important source of the organism is the
infected host, including domestic poultry, game birds and per or wild birds. Next in
importance, because of the prolonged survival of Al avium outside the body of the host,
are items contaminated with the droppings and excrement of such birds. These
commonly include litter, contaminated pens and pasture, equipment and implements
that come into contact with infected hosts, and the hands, feet and clothing of
attendants.
‘Swill’ containing offal or trimmings from ruberculous fowl or pigs can also be a source of
infection.
Eggs would seem to be only of minor importance in the spread of avian tuberculosis.
Tubercular lesions have occasionally been noted in the reproductive tract (ovary and
oviduct of the female and testes of the male) and tubercie bacilli have been reported,
rarely, in the eggs laid by tuberculous hens. However, there is no evidence to suggest that
chicks hatched from such eggs are likely to be infected or that disease is likely to be
introduced into a flock by this means.
INFUENCING FACTORS
The infections are worldwide but disease varies between and within countries. In
domestic poultry lack of hygiene in management and the age of the birds influence the
appearance of the disease since the organism is highly resistant in the environment and
within the host is generally associated with a long incubation period.
SIGNS
Signs may be prolonged over a period of weeks or months before death. There is
generally progressive but slow loss of condition and accompanying loss of energy and
increasing lethargy.
Although the appetite usually remains good, there is eventually gross emaciation with
marked atrophy of the sternal muscles, with the ‘keel’ becoming prominent or even
‘knife-edged’.
The face and comb become pale and sometimes jaundiced and the comb is shrunken and
often there is persistent diarrhoea with soiling of the tail feathers.
Occasionally a bird will show a hopping, jerky type of locomotion, which is usually
unilateral and is thought to be associated with tubercular lesions of the bone marrow of
the leg bones or joints. Some may adopt a sitting position.
Occasionally, birds may die suddenly in good bodily condition and yet show advanced
lesions of tuberculosis.
In such eases rupture of the affected liver or spleen with consequent internal
haemorrhage is often the precipitating cause of death.
LESIONS
Gross lesions, in the chicken, are most commonly seen in the intestines, liver, spleen and
bone marrow but may be found in any organ or tissue.
Irrespective of the organ involved, the lesions are typical tubercular granulomata. They
are irregular, grey-white nodules, varying in size from pinpoint to large masses of
coalescing tubercular material.
‘When cut through, the nodules are firm and caseous and the centres may be a pale
yellow colour, particularly those from the bone marrow. Those in the liver and intestine
may show bile staining. llae liver and spleen are often grossly enlarged and occasionally
rupture, resulting in blood in the body cavity and sudden death.
The smaller tubercles in these organs can be readily enucleated from the surrounding
tissue, particularly when they protrude from the surface. Such protrusion of tubercles
from the surface of the spleen gives rhe organ an irregular, ‘knobbly’ appearance.
The wall of the intestine is invariably studded with similar lesions, varying in size from a
millimetre to several centimetres in diameter. They usually involve the whole thickness
of the intestinal wall and eventually ulcerate into the lumen of the intestine, with
consequent discharge of bacilli and probably constituting the major source of infection
within the droppings.
The bone marrow of the long bones of the legs frequently contains tubercular nodules,
which can best be seen macroscopically if the bones are split longitudinally, particularly
in the region of the femoro-ribiotarsal and tibiotarsal—tarsometatarsal joints. They are
pale yellow in colour and vary in size and number. This is one of the distinctive features
of tuberculosis in the chicken.
The lungs are less frequently affected in the domestic chicken but more commonly in
waterfowl. Tubercle bacilli have been isolated from some eases of arthritis affecting the
phalangeal joints (‘bumble foot’) in the fowl.
DIAGNOSIS
The clinical signs and gross lesions are strongly indicative of avian tuberculosis and the
demonstration of acid/alcohol-fast tubercle bacilli in lesions or sections is supportive of
this. There is seldom any difficulty in demonstrating the organisms, which are often
present in very large numbers, particularly in young lesions and those from the bone
marrow.
Cultural examination, or even chick inoculation of suspect material, may be necessary
when organisms are few or for isolation and identification of the causal agent. The agent
can also be identified by DNA techniques.
Immunological tests are also of value in the recognition of infected birds during life.
They include the tuberculin test, an agglutination test and ELISA.
The tuberculin test in the fowl consists of injection of 0.05-0.1 mL of avian tuberculin
into one wattle using a needle about 1 cm long and of 25 gauge.
The other wattle remains uninjected as the control. When testing a flock it is usual to
inject the tuberculin into the wattle on the same side for each bird.
The needle is introduced at the lower edge of the wattle and is directed upwards into the
centre.
The test is read 48 h after the injection of tuberculin, although some positive reactions
may be observed sooner than this.
The test is read by palpating the two wattles simultaneously between the first finger and
thumb of each hand.
A positive reaction is recognized by a hot, soft, edematous swelling of the injected wattle,
which maybe twice the size of the uninjected one or even larger.
Most uninfected birds will show no reaction in the injected wattle and occasional small,
firm, pea-like swellings can usually be ignored.
The accuracy of the test, relative to gross lesions seen at necropsy, in detecting infected
birds is about 80%. However, birds in an advanced stage of infection may give no
reaction. It is possible, however, that such birds would be thin or emaciated on handling
during the testing of a flock and thus arouse suspicion of tuberculosis.
Various modifications of the site of inoculation of tuberculin have been suggested for
turkeys, ducks and other birds but this test has not yet proved to be reliable for these
species. For these the whole-blood, stained antigen agglutination rest may be preferable.
In this test a drop of antigen (a suspension of avian tubercle bacilli) is mixed with a drop
of blood from the bird under test. A positive reaction is indicated by agglutination within
1 mm. The distinct advantage of this test is that birds have only to be handled once;
however, its lack of specificity must be considered.
DIFFERENTIAL DIAGNOSIS
Learning objectives
INTRODUCTION
Several Mycoplasma spp have been isolated from avian hosts; M. gallisepticum , M.
iowae , M. meleagridis , and M. synoviae are the most important.
Mycoplasmas are fastidious bacteria, 0.3-0.8 µm in diameter; they lack a cell wall and
require a rich growth medium containing serum.
They do not survive for more than a few days outside the host and are vulnerable to
common disinfectants. Each has distinctive epidemiologic and pathologic characteristics.
M. gallisepticum infection is commonly designated as chronic respiratory disease in
chickens and as infectious sinusitis in turkeys.
Infection may also be seen in pheasants, chukar partridges, and peafowl. Infection in
pigeons, quail, ducks, geese, and psittacine birds should be considered.
Passerine-type birds are quite resistant, although M. gallisepticum is the major cause of
natural outbreaks of conjunctivitis in wild house finches (Carpodacus mexicanus) in the
eastern USA.
The disease is worldwide. Its effects are most severe in large commercial operations
during winter.
M. gallisepticum is the most pathogenic avian mycoplasma; however, strains may differ
markedly in virulence. Primary isolation is made in enriched broth medium containing
10-15% serum, then plated on agar.
Typical colonies are identified by immunofluorescence.
In the USA, most breeder flocks are free of M. gallisepticum , and outbreaks are due to
lateral transmission from infected chickens; however, in some parts of the world, egg
transmission is a major source of infection.
The incidence of egg transmission is highly variable, ranging up to 30-40% during the
first 2 mo after infection of susceptible birds in production.
The transmission rate then lessens and is inconsistent (0-5%) until the end of
production.
Birds infected before the onset of production transmit through the egg at a much lower
rate, if at all.
The infection may be dormant in the infected chick for days to months, but when the
flock is stressed, aerosol transmission occurs rapidly and infection spreads through the
flock.
Live virus vaccination, natural virus infection, cold weather, or crowding may initiate the
spread.
In addition, the infection may be carried by personnel (especially from an infected to a
clean flock), fomites, or introduction of infected birds.
In many flocks, the source of infection cannot be determined.
The epithelium of the upper air passages is most susceptible to infection; however, in
severe, acute disease the infection is also found in the lower respiratory tract.
There is a marked interaction between respiratory viruses, Escherichia coli ,
and M. gallisepticum in the pathogenesis of chronic respiratory disease.
Once infected, birds remain carriers for life.
CLINICAL FINDINGS
11.1.Chronic Respiratory
Disease(CRD): Gasping: Chick showing typical sign
of "Oral breathing" due to occlusion of respiratory tract
with exudate.
DIAGNOSIS
INTRODUCTION
M synoviae was first recognized as an acute to chronic infection of chickens and turkeys
that produced an exudative tendinitis and bursitis; it now occurs most frequently as a
subclinical infection of the upper respiratory tract.
M synoviae infection is also a complication of airsacculitis in association with Newcastle
disease or infectious bronchitis.
It is seen primarily in chickens and turkeys, but ducks, geese, guinea fowl, parrots,
pheasants, and quail may also be susceptible.
Serum (preferably swine serum) and nicotinamide adenine dinucleotide are required for
growth on artificial media.
ETIOLOGY
M. synoviae is egg-transmitted, but the rate is low (probably <5%), and some hatches of
progeny may be free of infection.
Egg transmission is greatest during the first 1-2 mo after infection of susceptible
breeders.
Lateral transmission is similar to that of M. gallisepticum , but the rate of spread is
generally more rapid.
M. synoviae isolates vary widely in pathogenicity. Isolates from cases of airsacculitis are
more apt to produce air sac lesions than isolates from synovial fluid or membranes.
Some strains produce the typical clinical disease of synovitis.
The paucity of natural outbreaks of clinical synovitis in chickens in recent years may be
related to the adaptation of M synoviae to the respiratory tract; however, clinical
synovitis in turkeys is relatively common.
CLINICAL FINDINGS
Although slight rales may be present in birds with respiratory infection, usually no signs
are noticed.
Younger birds, especially those under stress or suffering concurrent infections, are more
likely to be affected.
Outbreaks of infectious synovitis occur most commonly in chickens at 4-6 wk and in
turkeys at 10-12 wk. Lame birds tend to sit.
The more severely affected birds are depressed and are found around the feeders and
waterers. Swellings of the hocks and footpads are seen.
Morbidity is 2-15%, and mortality 1-10%. The effect on egg production is minimal, but
instances of egg production losses have occurred.
LESIONS
In the respiratory syndrome, airsacculitis occurs when the bird is stressed from
Newcastle disease, infectious bronchitis, or improper ventilation.
In many cases, air sac lesions resolve after 1-2 wk. Early in synovitis, the liver is enlarged
and sometimes green.
The spleen is enlarged, and the kidneys are enlarged and pale.
A yellow to gray, viscid exudate is present in almost all synovial structures; it is most
commonly seen in the keel bursa, hock, and wing joints.
In chronic cases, this exudate may become inspissated and orange.
DIAGNOSIS
A presumptive diagnosis can be based on the lesions and clinical signs, but laboratory
confirmation is necessary.
Skeletal abnormalities must be eliminated as the cause of lameness.
The disease must be differentiated from viral tenosynovitis and from staphylococcal and
other bacterial infections.
The serum plate agglutination or ELISA test is used to detect infected flocks, but cross-
reactions with M gallisepticum and other nonspecific reactions may occur.
Reactors are confirmed as positive by haemagglutination-inhibition or by isolation and
identification of the organism.
PCR may be used to rapidly detect the organism in infected tissues.
In turkeys, the agglutination test for M synoviae may not be reliable.
Serologic testing and isolation similar to those for M gallisepticum have resulted in
eradication of the infection in most primary breeder flocks of chickens and turkeys.
Administration of a tetracycline antibiotic in the feed may be beneficial in treatment or
prevention of synovitis.
When airsacculitis is a problem, preventive antibiotic therapy during the time of
respiratory reaction to Newcastle disease and infectious bronchitis vaccine may be
helpful.
Medication of breeder flocks is of little value in preventing egg transmission.
INTRODUCTION
M. iowae was originally thought to be of low pathogenicity in producing air sac lesions in
chickens and turkeys, but it is a potentially important cause of reduced hatchability in
turkeys.
Antigenicity and pathogenicity vary considerably among M iowae strains.
M. iowae is resistant to 1% bile salts, and an enriched medium similar to those used for
other avian mycoplasmas is suitable.
Infection was common in turkey flocks in Europe and North America, but the infection
rate has now been reduced by intensive eradication efforts in breeding stocks.
It is a relatively uncommon infection of chickens. M. iowae is egg transmitted, but little
is known of other aspects of its epidemiology.
Many strains of M. iowae are lethal to turkey embryos.
After experimental inoculation of young poults, stunting, poor feathering, and various
skeletal deformities such as tenosynovitis and chondrodystrophy develop, but the
mechanism is unknown.
These effects have not been recognized in the field, probably because most infected birds
die before hatching. Older birds appear to be quite resistant.
Affected turkey breeder flocks show no clinical signs other than reduced hatchability
(usually 2-5%).
In many flocks, the hatchability returns to normal after 1-2 mo.
Most embryos die during the mid to late stages of incubation.
Dead turkey embryos are edematous, congested, and stunted; they may have clubbed
down.
Poults challenged in ovo or at 1 day of age may develop various skeletal deformities such
as rotated tibia, deviated toes, chondrodystrophy, or erosion of the articular cartilage of
the hock joint.
Feathers may also be poorly developed. Chicks challenged at 1 day of age may develop
tenosynovitis and ruptured tendons.
Turkeys apparently have a poor antibody response, and no reliable serologic test is
available.
Diagnosis relies on isolation and identification of the causative agent.
The best method of control is to maintain flocks free of M. iowae ; however, because
serology is unreliable, this may be difficult.
Dipping hatching eggs in solutions of enrofloxacin has significantly reduced losses in
hatchability.
INTRODUCTION
INCIDENCES
Considerable variation in virulence among strains and also among species of host
Turkeys are most susceptible and then ducks and pigeons
Chickens are rarely affected
The serotypes which infect birds are different from those of mammals. However, avian
strains of Chlamydia psittaci can infect humans
Currently, six serotypes of Chlamydia psittaci are known to infect birds
The disease in humans contracted from turkeys is usually more severe than that from
psittacine birds
Avian chlamydiosis in birds is usually systemic and some times fatal.
SPREAD
PATHOGENESIS
CLINICAL SIGNS
Human
o Sudden onset of febrile illness with upper respiratory involvement,
o Pneumonia and debility
o Although it is not usually fatal, significant death occurs
Birds - Clinical signs vary with age, species of birds and strain of the organism
Turkey, Duck, Pigeons
o Depression with ruffled feathers
o Anorexia, conjunctivitis, Purulent nasal discharge
o Tracheitis with rales (some times)
o Grey-green diarrhoea with blood
Death may be sporadic or more in a flock.
Mortality is likely to be higher in parrots than in parakeets.
Recovered birds may excrete the organisms for longer period.
Chickens are rarely affected (although susceptible).
PATHOLOGY
Vary and are dependent on the severity and acute nature of the disease
Mortality vary from 0 to 30%
Gross lesions
o Serofibrinous exudate on serosal surfaces
o Pericardium - Inflammatory changes
o Lungs - Congestion
o Air sacs - Thickening due to clouding of walls
o Liver and spleen- Enlargement & Softer and small necrotic foci and petechiae
MICROSCOPIC LESIONS
Spleen
Liver
Kidneys
Lungs
Intestine
Erosion of mucosa
Infiltration of lamina propria and sub mucosa with lymphocytes an plasma cells
LCL (Levinthal, Coles, and Lillie) bodies
DIAGNOSIS
ZOONOTIC IMPORTANCE
ETIOLOGY
The two major species of fungus Aspergillus which cause aspergillosis in poultry are,
o Aspergillus fumigatus
o Aspergillus flavus
Other species include A.terreus, A.glaucus, A.niger, A.nidulans, A.amstelodami and
A.nigerscens
These organisms are common soil saprophytes, occurring in decaying vegetative matter
and feed grains.
They grow on organic matter in warm humid environments
Fungal hyphae are 4 -12 m m in diameter and bear conidiopores producing conidia
(spores) 2 - 6 m m in diameter that are easily spread in air.
ASPERGILLOSIS: TRANSMISSION
ASPERGILLOSIS: LESIONS
Macroscopical lesions
Older lesions
o Contain pleomorphic hyphae up to 12 m m in dia.
o Air-filled cavities may appear green to black due to development of pigmented
conidiophores
o Fungi tend to proliferate within the granuloma and rarely invade adjacent tissue
in immunocompetent birds.
Trachea: Yellow caseous plaques adherent to the mucosal surface that some times
occluding the lumina.
Syrinx: Caseous, gelatinous, or less commonly mucopurulent exudate.
Brain: white to yellow circumscribed areas either in cerebellum or cerebrum.
Ocular form: Extensive keratoconjunctivitis
Aspergillosis: Brooder pneumonia: Pancreas showing severe
congestion (red arrow) with multifocal paler necrotic areas (blue
arrow) and more vascularisation of duodenal serosa in Aspergillus
sp., infection of chicken.
Microscopical lesions
Air sacs
DIAGNOSIS
DIFFERENTIAL DIAGNOSIS
The clinical signs of avian aspergillosis are dependent upon the organ systems involved
Pulmonary aspergillosis is differentiated from other respiratory diseases by
granulamatous lesions at necropsy
o Exudative fibrinous or purulent air sacculitis and pneumonia are also frequently
seen in the following cases
Mycoplasmosis
Colibacillosis
Fowl cholera
Chlamydiosis
o If granulamatous lesions predominate , the following ones should also be
considered
Mycobacteriosis
Other mycoses
INTRODUCTION
FAVUS - PATHOGENESIS
FAVUS - DIAGNOSIS
INTRODUCTION
AFLATOXICOSIS
ETIOLOGY
Aflatoxin is found in corn (maize), peanuts, cottonseed, millet, sorghum and other feed
grains. A. flavus produces the majority of the toxin and gives it its name, but aflatoxin is
also produced Aspergillus parasiticus.
Both fungi are ubiquitous in the environment, contain toxigenic and nontoxigenic
strains, and produce aflatoxin in warm (30—35°C), high-humidity (0.90—0.99 activity)
conditions.
Handling or storage of grains in these conditions any where may also stimulate
production. Stressing host plants by insect damage, drought, poor nutrition or delayed
harvest increases afiatoxin production.
Naturally occurring aflatoxin contains aflaroxins B1, B2, C1 and C2, but aflatoxin B1 is
usually in the highest concentration and is the most toxic.
Aflatoxin is stable once formed in grain, and is not degraded during normal milling and
storage. Other toxins produced with aflatoxins under field conditions may play a
synergistic role in toxicity.
HOST
Young poultry are most sensitive to afiatoxin than adults. There are also large species
differences, with ducks being 10 times more sensitive than chickens, and turkeys
intermediate between the two.
PATHOGENESIS
CLINICAL SIGNS
Aflatoxicosis does not usually induce mortality directly, although high levels (>10 ppm)
may be lethal.
The most economically significant effects of aflatoxicosis on growing birds are decreased
growth and poor feed conversion (>1 ppm). There is also a marked decrease in resistance
to infections such as salmonellosis, coccidiosis, infectious bursal disease and candidiasis,
with resultant increased condemnations at processing (>0.5 ppm). Poultry manifesting
aflatoxicosis may also have failure of normal pigmentation and increased
bruising (>0.5 ppm).
Intoxicated adult hens have decreased egg production and the hatchability of those eggs
that are produced is reduced (>2 ppm).
In adult breeder males testicular weights and sperm counts are reduced.
Insemination of hens with semen from affected males has shown decreased fertility in
some studies and no significant reduction in others.
LESIONS
Lesions will depend on the age of the host and the dose of toxin and can include enlarged
Iivers which become friable and yellow with increasing dose, kidney and spleen
enlargement, diminution of the bursa of Fabricius, thymus and testes. Petechial
haemorrhages or bruises after trauma are also increased because of decreased clotting
factor synthesis and increased capillary fragility.
ETIOLOGY
Ochratoxicosis occurs less frequently in poultry than aflatoxicosis but is more lethal
because of its acute toxicity. Its name derives from Aspergillus ochraceus, the first
fungus shown to produce it.
Most naturally occurring cases have been associated with ochratoxin produced by P
enicillium veridicatum but five other species of Aspergillus and six other species
of Penicilliumproduce it as well.
Ochtatoxin is a dihydroisocoumarin derivative linked to L-3-phenylalanine.
Ochratoxin A and the dechlorinated B form occur naturally but ochratoxin A is the most
toxic and is produced in greater quantities.
HOST
Young poultry are most sensitive to ochtatoxin ingestion and ducks are seven times more
sensitive to the acute effects than chickens.
Quail and turkeys are also more sensitive to ochratoxicosis than chickens.
SPREAD
PATHOGENESIS
Acutely intoxicated birds are depressed, dehydrated and often polyuric (>4 ppm) and die
in acute renal failure.
Survivors will be stunted, poorly feathered, and have increased clotting times, anaemia
and immunosuppression (>0.6 ppm). There may be loss of pigmentation and reduced
weight gain (>2 ppm).
Laying hens may have delayed sexual maturity or develop wet droppings, causing
increased numbers of stained eggs. There is also a decrease in egg production and
hatchability (>2 ppm), and poor performance in progeny derived from intoxicated hens.
LESIONS
Affected kidneys are white to tan, swollen, hard and may have white pinpoint urate
crystals. If damage is extensive enough to cause renal failure there is dehydration,
hyperuricaemia and visceral urate deposition.
Pasty white urates are deposited on pericardial, perihepatic, peritoneal and articular
surfaces. These deposits may be mistaken for inflammatory exudate but their true nature
can be determined by microscopic examination of impressions or smears, or histological
sections.
More commonly, birds survive in compensated renal failure and kidneys appear
enlarged, fibrotic and pale.
In addition to the renal lesions there is mild to moderate fatty change and glycogen
deposi tion in hepatocytes, resulting in yellow enlarged livers. There is also some mild
decrease in bursal and thymic size consistent with immunosuppression.
INTRODUCTION
ETIOLOGY
Trichothecene mycotoxins occur frequently in wheat, corn (maize) and other grains used
for poultry feed production and are produced by many species of Fusarium,
Stachybotrysand at least three other genera. They also produce many nontrichothecene
mycotoxins, some of which may exacerbate the clinical effects of the trichothecenes
present.
Fusarium and Stachybotrys grow at many temperatures but toxin production is highest
in cold ( <20°C), moist conditions.
Trichothecenes are therefore associated with cool climates, particularly when grain
harvests have been delayed into the winter months or infected grain has been stored in
cold conditions. This is distinct from aflatoxin or ochratoxin production and thus
simultaneous contamination with these toxins is rare. There are approximately 80
chemically related sesquiterpinoid trichothecene mycotoxins described, but most is
known about the effects of the 1 2, 1 3-epoxytrichothecenes T-2, hydroxy T-2 (HT-2),
diacetoxyscirpenol (DAS, anguidine) and deoxynivalenol (DON, vomitoxin). It is not
known if these four compounds cause most field cases of trichothecene mycotoxicosis.
Zearalenone (F2) also falls in this category but its effects in commercial poultry are
minimal.
HOST
PATHOGENESIS
SIGNS
There is reduced feed intake, weight gains and feed efficiency, also, anaemia and poor
feathering with broken feather shafts.
Affected adult birds will develop oral ulcers, decreased egg production, decreased shell
quality and hatchability (>20 ppm 1-2).
LESIONS
Ulcers are found at the commissures of the mouth, on the hard palate adjacent to the
beak and the palatine cleft, and on the dorsal surface of the tongue (>2ppmT-2).
Ulcers are not usually produced further down the oesophagus unless the birds eat large
amounts of feed rapidly. There may be reduction in size of the bursa of Fabricius and
thymus glands of young birds and birds may show anaemia and pale bone marrow.
It should be noted that oral ulcers are not specific, since dietary copper sulphate (>200
ppm) and other caustic or traumatic dietary ingredients induce identical lesions.
INTRODUCTION
Several other mycoroxicoses have been rarely described in poultry but the overall
economic significance of these toxicoses is low.
o Citrinin
o Oosporein
o Fusarium fungi
o Moniliformin
o Fusarochromanone (TDP-1)
o Ergotism
o Diagnosis of mycotoxicoses
CITRININ
OOSPOREIN
FUSARIUM FUNGI
Fusarium fungi produce a wide variety of other mycotoxins. Some strains of Fusarium
moniiforme produce fumonisins, a group of water-soluble mycotoxins associated with
equine encephalomalacia and swine pulmonary edema. Poultry are apparently more
resistant.
Ingestion of 325 ppm by turkey poults and 250 ppm by broiler chicks is required to
decrease feed intake and bodyweights.
MONILIFORMIN
ERGOTISM
DIAGNOSIS OF MYCOTOXICOSES
The clinical signs, gross and histopathological lesions may be helpful but not specific.
The results of feeding trials with the suspect feed to reproduce the field toxicosis are also
of value but it may be difficult to obtain replicate feed samples. Samples of suspect feed
and mouldy clumps for feeding trials and chemical analysis should be collected directly
from the trough in the poultry house.
Samples can be rapidly screened for aflatoxin, ochraroxin, T-2, DON and fumonisin with
commercially available solid or liquid phase competitive enxyme-linked immunosorbent
assay (ELISA) tests.
These inexpensive rapid tests can be done in minutes with material on the farm or in the
feed mill and yield generally excellent results. Positive tests should be confirmed by most
rigorous analytical chemical methods, including thin layer chromatography, high-
performance of liquid chromatography, grass chromatography, mass spectrophotometry,
or monoclonal antibody technology. Such confirmation requires the capability of the
diagnostic laboratory for both analysis and interpretation.
Learning objectives
CLASSIFICATION OF PARASITES
CLASSIFICATION OF PARASITES
INTRODUCTION
TREATODES
Trematodes (flukes) are flat, leaflike, parasitic, organisms belonging to the phylum
Platyhelminthes, class Trematoda
They differ from cestodes (class: Cestoda) in having a digestive system, and they do not
form proglottids
The life cycle of all trematodes parasitizing birds requires a molluscan as an intermediate
host; some species also use a second intermediate host
Since adult trematodes and larval metacercariae invade almost every cavity and tissue of
birds, they may show up unexpectedly at necropsy
Flukes are less host-specific than tape worms. Therefore, wild birds often introduce
infection in areas where domestic poultry is reared
Since many snails live in ponds and streams, ducks and geese are the most frequently
parasitized
Out of all the trematodes, the oviduct fluke (Prosthogonimus sp.), which is a frequent
parasite of many species of wild birds, some times cause problems with ducks and
chickens.
Prosthogonimus macrorchis , oviduct fluke has caused economic losses to poultry
producers by
o Drastically reducing egg production after a recent infection
o Occasionally being enveloped within a hen’s egg and later discovered by a
complaining customer
Other organs invaded by the flukes include,
o Metacercarial cysts in the skin of chickens and turkeys ( Collyriclum faba )
o Small adult flukes in the conjunctival sac of the eye ( Philopthalmus gralli)
o Adults in the liver, pancreas, and bile duct of duct of ducks and turkeys (
Amphimerus elongatus )
o Adults in the collecting tubules of the excretory system of chickens, turkeys, and
pigeons ( Tanaisa bragai )
o Adults and eggs in the circulatory system of ducks by three species of blood fluke;
and
o Fourteen flukes that invade various areas of the digestive tract
A high percentage of chickens and turkeys may be infected with tapeworms if they are
reared on range or in back yard flocks
These parasites are found more frequently in warmer seasons., when intermediate hosts
are abundant
Many species of tape worms are now considered rare in intensive poultry farming
because the birds do not come in contact with intermediate hosts
Tape worms or cestodes are flattened, ribbon shaped, usually segmented worms.
The term, proglottid is used to describe these individual segments
One to several gravid proglottids are shed daily from the posterior end of the worm.
Each proglottid contains one or more sets of reproductive organs, which may be become
overcrowded with eggs as the maturing proglottid becomes a gravid proglottid
Tape worms are characterised by complete absence of digestive tract and obtain their
nutritional nourishment by absorption from the intestinal contents of the host
Duodenum , jejunum or ileum are the usual site for attachment.But one
species, Hymenolepis megalops is found in the cloaca or bursa of Fabricius of ducks
CESTODES - PATHOGENESIS
DIAGNOSIS
DEVELOPMENT OF NEMATODES
Eggs of some nematodes require only a few days to complete embryonation; others
require several weeks.
In case of nematodes with direct life cycle, the final host becomes infected by eating
embryonated eggs containing second stage larvae or free larvae.
In case of those with indirect life cycle, the intermediate host ingests the embryonated
eggs or free larvae, and retains the larvae within the body tissues.
The final host becomes infected either by eating the infected intermediate hosts or by
injection of the larvae by a blood-feeding arthropod.
Eggs of some nematodes require only a few days to complete embryonation ; others
require several weeks.
In case of nematodes with direct life cycle, the final host becomes infected by eating
embryonated eggs containing second stage larvae., or free larvae.
In case of those with indirect life cycle, the intermediate host ingests the embryonated
eggs or free larvae, and retains the larvae within the body tissues.
The final host becomes infected either by eating the infected intermediate hosts or by
injection of the larvae by a blood-feeding arthropod.
INTRODUCTION
A.galli eggs are ingested by grass hoppers or earth worms, hatch , and are infective to
chickens. However, no development of the larvae occurs.
Under optimum conditions of temperature and moisture, eggs in the droppings become
infective in 10 – 12 days; under less favourable conditions, a long timer time is necessary.
Eggs are quite resistant to low (non-freezing) temperatures.
ASCARIDIA GALLI - PATHOGENECITY
Synergism with other diseases like coccidiosis, infectious bronchitis produce harmful
effects
A.galli have also been shown to transmit avian reoviruses
Some times, A.galli is found in the hen’s eggs as they migrate, from the cloaca, up the
oviduct with subsequent inclusion in the egg
Infected eggs can be detected by candling
INTRODUCTION
It infects chicken, turkey, duck, goose, guinea fowl, pigeon, and quail.
They are seen in the small intestine and the caecum.
They are the smallest of the nematodes.
Highly pathogenic when they are present in large numbers.
Different species parasitize different parts of the alimentary tract.
Life cycle may be direct or indirect.
The most common and pathogenic is Capillaria obsignata, a hair-like worm , which has a
direct life cycle.
Gross lesions - In some cases, catarrhal exudate in the upper intestine and thickening of
the wall
INTRODUCTON
Heterakis gallinarum (caecal worm) infects chicken, turkey, duck, goose pheasant and
quail
The larval and adult H.gallinarum inhabit the caeca
Adult worms are small and white
The male is 7-13 mm long while the female is 10-15 mm long in length
The eggs are thick-shelled, ellipsoidal, unsegmented when deposited, and
undistinguishable from those of A.galli.
PATHOGENECITY
INTRODUCTION
TRANSMISSION
The most important natural route of transmission is within the egg of Heterakis
gallinarum.
Ingestion by caecal worms in the caecal lumen.
They enter into the nematode eggs which are ultimately shed in the host species and are
available to infect further hosts.
The role of heterakis as vectors is very important, because they are also parasites of birds
and protect the histomonads within their egg during transmission from bird to bird.
The earthworm may also act as a transport host in which heterakis larvae may hatch but
remain viable and infected with histomonads in the earthworm tissues.
Besides the earthworms, insects such as flies, grass-hoppers, and crickets may serve as
mechanical vectors.
CLINICAL SIGNS
In turkeys
o Anorexia, drowsiness, dropping of the wings, closed eyes, and sulphur-yellow
droppings.
o Blackhead is an accurate term , since the head may or may not be cyanotic, nor it
is unique to histomoniasis.
o Mortality may be high, reaching a peak about a week after the onset of signs.
In chicken
o Infection may be mild and go unnoticed or may be severe and cause high
mortality.
o Sulphur coloured droppings seen in turkeys are seldom found in chickens, but
blood caecal discharges have been observed.
o Sometimes, gross pathology in chickens may resemble caecal coccidiosis.
MACROSCOPIC LESION
MICROSCOPICAL LESION
Caecum
Earlier changes
Hyperaemia and heterophilic infiltration in caecal wall
Later changes
Liver
Earlier changes
Later changes
DIAGNOSIS
Diagnosis can be made from the characteristic gross lesions which remain clearly visible
long after death.
If confirmation is required, stained sections from the periphery of liver lesions will reveal
rounded up organisms.
Identification of living organisms in the wet preparations from caecal lesions is a little
difficult. It requires fresh material and a heated microscope stage.
INTRODUCTION
ETIOLOGY
Two species have been described in birds, Cryptosporidium baileyi and C. meleagridis.
Cryptosporidium baileyi causes both respiratory and intestinal disease, whereas C.
meleagridis is associated with enteric disease only.
Cryptosporidia infect chickens, turkeys, ducks, geese, and several others.
Isolates do not have rigid host specificity.
LIFE CYCLE
Excystation (Infective Sporozoite Release)
Thick-walled oocysts are ingested by the host and reach the intestine where sporozoites
excyst and penetrate the microvillus borders of ileal enterocytes.
This stage of development occurs in a parasitophorous vacuole, characterized as an
intracellular but extracytoplasmic space.
Other Eimeriorina do not exhibit such behavior and confine themselves to intracellular,
intra-cytoplasmic domains
Fertilization
Intestinal infection
Respiratory infection
HISTOPATHOLOGY
Respiratory cryptosporidiosis
A large number of parasites through out the epithelium lining the trachea and bronchi.
Epithelial hyperplasia.
Thickening of the mucosa by mononuclear cell infiltrations with some heterophils.
Loss of cilia, and discharge of mucocellular exudate into the airways.
DIAGNOSIS
TRANSMISSION
Since C.baileyi can infect a variety of birds, it is possible that wild birds may serve
as carriers
Learning objectives
To understand the role of nutrients (vitamins / minerals) in the various body functions
of the birds.
To become familiar with peculiar clinical signs due to deficiency of such vitamins /
minerals.
To learn the pathological features during the deficiency conditions.
INTRODUCTION
There are a great variety of clinical conditions that are induced by nutritional deficiencies
and imbalances. These may arise from,
o Gross deficiency in the ration supplied to poultry
o Antagonism between nutrients
o Destruction or inactivation during feed manufacture
o Impaired absorption or metabolic disorder that renders supply inadequate
A specific mineral or trace element deficiency generally produces characteristic signs,
reflecting specific metabolic functions; For eg,
o Fat soluble vitamins A and E are involved with membrane integrity
o Water soluble vitamins and trace elements with enzyme systems
o Very profound effects may be brought about by a deficiency of minute amounts of
these nutrients at the site required
GENERAL INFORMATION
VITAMIN- A
The term vitamin A covers a number of physiological forms (retinol, retinoic acid,
retinaldehyde and retinyl ester)
Retinol is the most common form in nature
It is a fat-soluble vitamin found primarily in animal products such as liver and fish oils
Beta carotene is the precursor of vitamin A
Maize containing more amount of beta carotene. Wheat based diets are assumed to have
no background vitamin A activity
VITAMIN- A
Key function
Deficiency symptoms
VITAMIN- D
KEY FUNCTIONS
Vitamin D, as the renal metabolite 1,25-dihydroxycholecalciferol (following initial
hydroxylation in the liver to the 25-hydroxy product), has the main function of
o Inducing the synthesis of calcium-binding proteins
o Controlling intestinal absorption
o Blood translation of calcium
DEFICIENCY SYMPTOMS
GENERAL INFORMATION
The term vitamin E covers a range of tocopherols and tocotrienols that all have vitamin E
activity
o The key form for poultry is the a -tocopherol
o Sources: Cereal germs, most oilseeds and leafy plants
o Vitamin E may be described as a naturally occurring antioxidant
KEY FUNCTIONS
DEFICIENCY SYMPTOMS
EXUDATIVE DIATHESIS
Capillary wall lesions lead to increased vascular permeability, with resulting blood and
plasma leakage; this accumulates subcutaneously, particularly over the breast and under
the wings, also intramuscularly and in the pericardial sac.
The condition is prevented by and responsive to vitamin E and selenium.
The usual treatment is vitamin E via drinking water.
Nutritional muscular dystrophy frequently occurs with exudative diathesis and tends to
occur when vitamin E deficiency is accomplished by deficiency of sulphur-containing
amino acids (methionine and cysteine) in chicks, turkey poults and duckling.
Microthrombosis of arterioles and smaller capabilities cause occlusion, which gives rise
to degeneration and necrosis of muscle fibres, seen as pale streaks mainly in breast and
thigh muscles (hence the reference to white muscle diseases).
Prevention and treatment are by vitamin E supply, as previously described.
GENERAL INFORMATION
KEY FUNCTION
DEFICIENCY SYMPTOMS
Microbial synthesis occurs is the caecum and large intestine and as result deficiency
is very rare, especially in adult birds, although the supply of vitamin derived from
microbial synthesis is thought only to be of benefit if faeces are consumed.
Chicks can exhibit delayed blood clotting as a result of deficiency
Oral administration of antibacterial drugs such as sulfaquinoxaline and some other
sulpha drugs are stated to be antagonistic to vitamin K activity