Infectious Bronchitis(IB)

• IB is an acute, highly contagious, viral disease of

chickens, upper respiratory tract disease
• Chracterised by respiratory signs: gasping,
sneezing, coughing and nasal discharge
• Severe renal disease associated with nephrotroic
strains
• Marked decrease in egg production
• Infections of IB along with Mycoplasma and E.coli
is common
 Occurence
• IB occurs naturally only in chickens
• All ages are susceptible
• Present in all countries
Historical information
• 1930 IB first observed in young chicks
• 1940’s IB serious disease of laying flocks causing marked
loss in egg production
• 1960’s nephrogenic strains observed
• 1936 IB virus first isolated, multiple serotypes in 1956
• 1950’s vacicnation commercially available
 Etiology
• IB is caused by Corona virus, only causes disease
in chickens
• Worldwide in distribution
• Virus fairly labile and can be destroyed by many
common disinfectants
• The virus can survive in 50% glycerin in most
mailed tissue specimens
• Fresh trachea and lungs from infected chickens
appropriate sample for virus isolation
• Antigenic variations among IB viral strains exist and
many serotypes identified and has capacity to
mutate
• Four common serotypes conecticut, Massachusetts,
Arkansas 99 and 072 used for vaccine production
• Cross protection among serotypes is highly variable
• Nephrotropic strain can induce significant mortality
 Epizootilogy
• Transmission of IB is by inhalation of virus containing
droplet expelled by infected, coughing chickens
• Aerosal transmission occurs
• Spread of infection in a flock is rapid
• Spread by fomites can occur
• Virus in contaminated premises can persist for 4
weeks under favourable condition
• Fewer birds may remain carriers and shedders of
virus for months after infection
The severity of disease and body system
involved are influenced by
• Strain of the virus
• Age , strain , immune status of chicken
• Cold stress
• Co infection with Mycoplasma gallisepticum,
E. coli can exacerbate disease
 Clinical signs
Respiratory syndrome is the most common in
birds of all ages
Baby chicks
• Coughing, sneezing, trachial rales
• Conjunctivitiis and dyspnoea
• Nasal and occular discharge
• Morbidity is virtually 100%
• Signs can develop 48 hrs post infection
• Weakness, depression and huddling near heat
source
• Feed consumption and weigt gain reduced
• Mortality in young chicks is negligible unless
complicated by another infectious agent
• Nephropathogenic strain can cause initial
respiratorysigns, depression, ruffled feathers,
increased water intake and high mortality(30%)
Laying chickens
• Coughing, sneezing, and rales
• Nasal or occular discharge
• Lacrimation and facial swelling
• Egg production drops rapidly upto 50%
• Effects can last for 6-8 weeks or longer
• Eggs are often soft shelled or misshapened with thin,soft,
wrinkled, rough, pale shells, smaller and
• Most outbreaks mortality is appox. 5% can be as high as
60%
• Cause damage to the functional oviduct
• Egg albumin may be watery
• Air sacculitis due to secondary bacterial
infection eg E. coli, Mycoplsma gallisepticum
• Swollen pale kidneys and urolithiasis in pullets
induced by nephrotropic strain
 Lesions
• Mild to moderate inflammation of upper
respiratory tract
• The trachea, sinuses and nasal passages may
contain erous, catarrhal or caseous exudates
• Severe air sacculitis: marked thickening and
opacity with much exudate in air sac,
• complicated by E. coli: caseous air sacculitis,
perihepatitis and pericarditis
• Older birds are more resistant
• Yolk material present in peritoneal cavity and
Ovarian fllicles appear flaccid
• Abnormalities of oviducts particularly middle third
• Oviduct may be hypoplastic or cystic and deposit
of eggs in the abdominal cavity
• Infection with nephropathogenic strains results in
swollen Kidneys, pale in colour and ureter and
tubules distended with urates in young birds
Infectious bronchitis(IB)
Histopathology
• Trachea shows hyperplasia of the epithelium
• Trachea and brnchi show loss of cilia and
sloughing of epithelium
• Sub epithelial mucosa shows congestion,
oedema, haemorrhages, heterophils and
lymphocytic infiltration
• Mucopurulent exudate in tracheal lumen
• Junction of Isthmus and magnum show atrophy of
epithelium , loss of cilia and focal accumulation of
lymphocytes and plasma cells
• Kidneys interstitial nephritis, show focal infiltration
of lymphocytes and plasma cells, tubules with
dilatation and hyaline casts
• The virus causes grannular degeneration, vacuolation
and desquamatin of the tubular epithelium
• Focal areas of necrosis may be seen
 Diagnosis
• VN
• ELISA
• Hi
• Isolation and identifiaction of virus: 9-12 days old SPF
chicken embryos-embryo, in seven days will show
dwarfing/stunting,curling
• Trachea, lungs, air sacs and kidneys are good source of
virus
• RT PCR
• FAT
• 12 days embryo inoculated with supernatant
containing IB virus develop lesions
• IB virus causes dwarfing and stunting of
embryos also amnion and allntois are
thickened and closely invest the embryos
• Egg fluid from inoculated embryos do not
haemagglutinate erythrocytes if IB virus is
present
 Infectious Laryngotracheitis
ILT
• ILT is an economically important acute viral
respiratory disease of chickens, pheasants and
peafowl
• It is highly contagious
• Chracterised by severe dyspnoea, coughing,
gasping, rales and expectoration of bloody exudate
Occurrence
• Most outbreaks in chickens occur in broilers more
than 4 weeks of age or in mature chickens
 Etiology
• ILT is caused by Gallid Herpes virus I(ILTV), 80-110nm in
size
• The virus is readily destroyed by many disinfectants.
• There is only one immunogenic strains although strains
varies in pathogenicity
• Herpes virus infection leads to the formation of type A
intranuclear inclusions
• Inclusions observed intracheal epithelial cells
occasionally in conjunctival epithelium and chorio
allantoic membrane of embryonated chicken eggs
 Epizootiology
• Some recovered chickens and vaccinated
chickens become carriers and shed virus for long
period of time
• Can shed virus following stress induced
reactivation
• Mechanical transmission of virus via fomites
• Lateral transmission
• Severe in adult birds but mild in chicks below 3
weeks of age
 Clinical signs
• Affected birds are anorectic and in active
• The birds below 3 weeks of age show conjunctivitis and
watery fluid between eyelids
• Marked dyspnoea, often with loud gasping sounds and
coughing
• Severely affected chickens often raise and extend their
head and neck during inspiration and make loud
wheezing sounds
• Expectoration of bloody mucoid exudate as a
cosequence of coughing and head shaking
• Extention of the during inspiration seen 5-12 days
after exposure
• Beaks, faces or feathers of occasional birds may be
bloody
• High morbidity and considerable mortality
• It is due to occlusion of the trachea by
haemorrhage or exudate
• Morbidity as high as 50-70%
• Mortality in 10-20% range
• Lowered egg production
• The disease also persists for 2-6 week in the flock
• Signs of low pathogenicity include conjunctivitis,
with watery eyes, lachrymation, nasal discharge,
swollen infraorbital sinuses and lowered egg
production
• Recovered birds remain carriers for life and
become a source of infection for susceptible birds
 Lesions
• Severe laryngotracheitis with bloody or
caseous exudate in the trachea
• Lesions vary from mucoid inflammation to
severe degeneration of the mucosa with
haemorrhage
• Inflammation may extend into bronchi and air
sacs
• In PM birds may have an occluding
pseudomembrane or caseous plugs in the
tachea
• Death occur due to suffocation
• Infected birds have a bloody beak or blod on
the face, head or feathers
• In less pathogenic outbreaks mild
conjunctivitis and sinusitis
• Microscopic examination of trachea of birds
killed during first few days of the disease may
reveal intra nuclear inclusion bodies in epithelial
cells
• Loss of goblet cells
• Cells lose cilia, becomes oedematous
• Similar inclusions can be demonstrated in the
chorioallantoic membrane of infected chicken
embryos and in infected tissue culture cells
 Diagnosis
• The clinical signs and chracteristic lesions
• Demostration of IN inclusions in the trachea and
conjunctiva mucosal epithelium during early stage of
the disease
• Immunofluorescence/ FAT: demontration of viral
antigen
• Chick Embryo inoculation- 10 days: growth of virus on
the chrioallantoic membrane(CAM)-typical plaques are
produced and inclusions can be demonstrated
• PCR
 Infectious Bursal disease
IBD
• Also known as Gumboro disease, Infectious bursitis
and infectious avian nephrosis
• Infectious bursal disease is an acute, highly contagious,
viral disease of young chickens and turkeys
• Characterised by diarrhoea, vent picking, trembling,
incoordiation,
• Inflammation followed by atrophy of the Bursa of
fabricius
• Variable degree of immuno-suppression
 Occurence
• Occurs primarily in chickens
• Clinical signs and mortality are generally more
severe in birds 3-6 weeks old
• IBD may occur in chickens as long as they have a
functional Bursa of Fabricius(1-16 weeks of age)
• The younger the birds at the time infection the
more severe the immunosuppression increasing
susceptibility to pathogens
• Once the premises has been contaminated with
IBD virus the disease tends to reoccur, usually as
a subclinical infection
• In turkeys subclinical infection with IBD virus
occurs without immunosuppression
• Ducks can also be subclinically infected with no
resultant immunosuppressin
• Occurs in major poultry producing countries of
the world
 Historical information
• In 1962 IBD was reported in farms near
Gumboro, Delaware
• In Nepal, 1992/93 severe outbreaks in growing
birds
• Initially the disease was confused with a
variant form of IB accompanied by nephrosis
• Reported in many countries throught the
world
 Etiology
• IBD is caused by a Birna virus(Infectious Bursal Disease
Virus:IBDV) belonging to Birnaviridae
• The virus genome has two double stranded RNA
segments
• Two serotypes exist with only serotype 1 being
pathogenic and there are six strains causing
immunosuppression because of loss of B lymphocytes
• Serotype 2 strains of the virus infects chickens and
turkeys but have not caused clinical disease or
immunosuppression in these hosts
• IBDVs have been identified in other avian
species including Penguins
• The virus is very resistant to most disinfectants
and environmental factors
• It persists for months in contaminated houses
and for weeks in water, feed and droppings
• It can be transmitted by fomites
• It has some susceptibility to formalin and iodide
disinfectants
• The virus is lymphocidal and severely damages
Bursa of Fabricius
• The thymus, spleen and caecal tonsils are also
damaged but less severely
• it severely damages humoral response of
susceptible chicks when they are infected at less
than 3 wks of age
• Those chicks then do not respond properly when
vaccinated with other diseases
• IBH and gangrenous dermatitis occur frequenly
in such flocks
• Some live vaccines may have a similar potential
for damage as field infections
• The Passive transfer of maternal antibodies to
baby chicks is very important for the prevention
of early infections with virus
• Breeder flocks must be vaccinated
• Progeny from vaccinated flocks will resist
infection for 2-4 wks
• Passive immunity will interfere with
vaccinations and is necessary to vaccinate
chickens after maternal immunity has fallen
 Epizootiology
• The virus spreads rapidly from infected chicks and from
contaminated premises or fomites to susceptible chicks
• The disease is highly contagious
• Mortality is found to be higher in layers than broilers
• Transmission of virus through the egg does not occur
and no evidence of carrier state
• The lesser meal worm(Alphitobius diaperinus) harbours
the virus for weeks after an outbreak and may tranmit it
to susceptible birds
• The worm live in poultry litter
 Clinical signs
• Infection can be clinical and subclinical
• Infections before 3 weeks of age are usually
subclinical
• Subclinical infection cause severe longlasting
immunosuppression due to destruction of
immature lymphocytes in bursa of fabricius,
thymus and spleen
• Clinical disease is observed only after 3 wks of
age
• Chickens are most susceptible at 3- 6 weeks
when immature B cells populate the bursa and
maternal immunity has waned
• There is sudden onset in first outbreak
• Onset of disease occurs after Incubation period
of 3-4 days
• Severe prostration, incordination, Tremor,
unsteadiness, depression, anorexia and ruffled
feathers like in coccidiosis
• Diarrhoea and dehydration
• Occasionally voiding of blood and straining during
defaecation
• Vent picking
• Morbidity very high upto 100% and mortality can range
from 5% to >60% depending on strain of the virus
• Virulence of the field virus varies and can be naturally
attenuated, very virulent(vv), vvIBD can cause high
mortality
 Lesions
• Initially Bursa is enlarged to twice the normal
size, severely edematous and reddened
• It may contain haemorrhages
• It can become enlrged with yellowish coloured
transudare on the surface
• Th swelling recedes about the 5th day and
bursa atrophies rapidly from the 8th day
onward
• Increased mucus in intestine
• Haemorrhages are common in thigh and
pectoral muscles and at the junction of
proventriculus and gizzard(vvIBDV)
• Some IBDV virus can cause atrophy of Bursa
Infectious bursal disease( Gumboro disease)
• The kidneys may be swollen, ureters may contain urates
• Necrotic lesions / atrophy of other lymphoid organs eg
Thymus, spleen particularly with highly virulent IBD
virus
• Microscopically in the Bursa , lymphoid follicle
depletion and destruction followed by atrophy
• Similar changes occur in spleen thymus and caecal
tonsils
• Some strains of the virus cause few clinical signs and
minimal gross acute changes in the bursa
 Diagnosis
• Clinical signs and lesions
• AGPT
• ELISA
• VN
• Microscopic bursal lesions for lymphocyte
depletion in Bursal follicles
• Direct FAT
• RT-PCR
 Chicken infectious anaemia
CIA, Blue wing disease
• Anemia Dermatitis syndrome, Haemorrhagic
Aplastic Anemia syndrome
• Chicken infectious anaemia (CIA) is a disease
of chickens caused by an unclassified virus
• It is characterised by aplastic anaemia,
decreased weight gain, lymphoid depletion,
subcuaneous and intramuscular haemorrhage
and immunodepression
Occurence
• CIA is ubiquitus in all major chicken producing
countries of the world
Historical information
• CIA virus was first isolated in Japan in 1979
• Previously described as Blue wing disease,
aplastic anaemia and haemorrhagic anaemia
 Etiology
• CIA virus(CAV), 25 nm, has a circular, single
stranded, negative sense, DNA similar to porcine
circo virus.
• Previuosly described as circo virus
• Gyrovirus genus of Anelloviridae family
• CIA virus is difficult to isolate due to restricte cell
lines suitable for propagation
• Most chicken embryo cell lines and chicken embryos
are resistant to infection or produce low virus yields
 Epizootiology
• Ubiquitous in poultry producing areas of the world
• Chicken are the only known hosts
• All ages are susceptible to infection but clinical disease is
seen only during the 1st 2-3 weeks
• Age resistance is delayed by simultaneous infection with
IBD
• Vertical and horizontal transmission occurs by faecal-oral
route
• Contaminated litter is a common source of virus
introduction
 Clinical signs
• Anaemia characterised by hematocrit values
ranging from 6-27% (normal 35%)
• Nonspecific clinical signs include depression,
paleness, anorexia, lethargy and
• Reduced weight gain
• Watery and slowly clotting blood,
• High mortaliy in secondary infections
• Morbidity and mortality rates vary depending
upon immune status due to other infections
eg IBD, MD or reticuloenditheliosis
• Mortality is usually 5-10% buy can reach 60%
• Anemia, leukopenia pancytopenia in blood
smears
 Lesions
• Organs are pale, the thymus is generally
atrophied
• Gangrenous dermatitis and blue wing
diseasehymic atrophy
• Fatty yellowish bone marrow
• Bursal atrophy can also be seen
• Bone marrow is pale or yellow
• Swollen mottled liver
• Haemorrhages in the mucosa of the
proventriculus, subcutis and muscles
• Lesions of secondary bacterial infections
• Microscopcal lesions with depletion of lymphoid
cells in primary and secondary lymphoid organs
specially of thymic cortex
• Granulocytic and erythrocytic compartments in
bone marrow atrophic or hypoplastic
Chicken Infectious anaemia(CIA)
CIA contd
 Diagnosis
• Clinical signs and gross lesions
• Isolation and identification of the virus by
bioassay in susceptible 1 day old chicks
• ELISA
• VN
• Indirect immunofluorescence
• PCR
 Marek’s disease
• Marek’s disease is a highly contagious herpes
virus(MDV) induced neoplastic disease of chickens
• Polyneuritis, Fowl paralysis, Range paralysis,
Neurolymphomatosis
• One of the most Ubiquitous infections
• It is characterised by infiltration of various nerve
trunks and organs with pleomorphic lymphoid
cells(T cells lymphomas) and peripheral nerve
enlargement
Occurrence
• Important primarily in chickens rarely
observed in turkeys and jungle fowl
• Qual can be naturally infected
• The disease most cmmonly occurs in young
sexually mature chickens 2-7 months old but
can occur at virtually any age beyond 3 weeks
 Historical information
• 1907, Hungarian Veterinarian Joseph Marek
first description of MD
• 1924 USA first report
• 1967 herpesvirus was isolated and identified
 Etiology
• Marek’s disease virus is a member of te genusardi
virus within the subfamily Alphaherpesvirinae
• Herpes viruses associated with Marek’s disease
are classified into three serotypes
• Gallid alphaherpes virus 2(MDV Serotype 1)
isolates are ubiquitous in chickens and vary from
pathtypes designated as mild(m), virulent(v), very
virulent (vv) and very virulent plusvirulent
plus((vv)
• Gallid alphaherpes virus 3(Serotype 2) isolates
are common in chickens and are nononcogenic
• Meleagrid alphaherpes virus 1(turkey herpes
virus, MDVSerotype 3)represent avirulent virus
strain isolated from tukeys and chickens and
commonly used asvaccines against Marek’s
disease
• The three serotypes have considerale antigenic
cross reactivity
• The virus can be grown in cultured chicken embryo
kidney cells and in duck embryofibroblsts
• It produces distinct cytopathic effect with intranuclear
inclusions in those cells
• The virus is tightly bond to living cells and in this form
is very labile
• Cell free virus is released from the feather follicle
epithelium and is relatively resistant to environmental
factors
• Susceptible to common disinfectants
 Epizootiology
• Infected chickens shed virus conatining feather follicle
dander, which is a source of infection for other
chickens by respiratory route
• Carrier birds can shed virus throughout their lifetimes
• The disease is very contagious and infectious dander
can be disseminated over long distances
• Dander containing infectious enveloped virus
particles is the most important means of transmission
• The virus matures into a fully infective, enveloped
form in the epithelium of the feather follicle from
which it is release into environment
• It my survive for months in poultry house litter or
dust
• Dust or dander from infected chickens is effective
in transmission
• Mareks disease virus is not vertically transmitted
 Pathogenesis

• Pathogenesis of Marek’s disease can be described in

four phases of infections
• 1- Early productive and restrictive virus infection cusing
mainly degenerative(cytolytic) changes
• 2- Latent infection
• 3- Asecond phaseof cytolytic , productive – restrictive
infection causing permanent immuno suppression
• 4- A proliferative phase involving non-productively
infected lymphoid cells which may or may not progress
to lymphoma formation
 Clinical signs
• The incidence of Marek’s Disease is quite
variable in commercial flocks and depends on
• Strain and dose oof the virus
• Age exposure
• Maternalantibody
• Host gender and genetics
• Satrain and dose of the vaccine virus
• Sveral environmental factors including stress
• Birds with visceral tumours are depressed are
often cachectic prior to death
• Birds with lymphoid infiltration of peripheral
nerves may demostrate partial paralysis
• Blindness is associated with lymphoid
infiltration of the iris
• Clinical signs do not appear prior to 3 weeks of
age and peak between 2-7 months
 Lesions
• Gross enlargement and yellowing and loss of cross
striations of peripheral nerves(vagus, brachial and
sciatic nerves)
• Discoloration of the iris
• Enlargement of feather follicles withreddening(skin
leukosis)
• Visceral tumours involving liver, heart, spleen, gonad,
kidney, muscles,proventriculus and other organs and
tissues
• Bursa frequently atrophic
• Microscopically the lymphomas are
characterised by a mixture of pleomorphic
lymphocytes
• The tumor cells appear in interfollicular areas
• A few of these are true tumour cells that carry
T cell surface antigens and a tumour
associated antigen(MATSA)
Marek's disease
 Diagnosis
• History, age of birds affected and location of
neoplastic lesions in affected chickens
• Marek’s disease often occurs in 2-5 months
old( sexually immature) chickens but can occur
after onset of egg production
• Nerve involvement
• Absence of bursal lesions
• Pleomorphic lymphocytes cmprising lesions
• Exhibiting MATSA
Avian Leukosis Complex/ Sarcoma viruses

• Avian leukosis(ALV) sarcoma group are caused by

Alpharetrovirus genus of the family Retroviridae
• Retroviridae contains a diverse group of RNA
viruses(tumor viruses)
• These viruses contain reverse transcriptase, RNA
dependant DNA polymerase
• Infection leads to uncotrolled cellular
proliferation
• Neoplastic diseases of mature chickens
• It comprises lymphoid leucosis,
erythroblastosis and myeloblastosis,
myelocytomatosis
• A variety of tumors such as fibrosarcoma,
hemangiomas and nephroblstomas and bone
disorder osteopetrosis
Lymphoid leukosis is a neoplastic disease of poultry
characterised by
Enlargement of liver by infiltrating lymphoblasts
• A gradual onset in a flock,
• Persistent low mortality,
• Neoplasia of the bursa of Fabricius
• With metastasis to many other internal organs: liver,
spleen and kidney
• A new strain of ALV “J” causes myeloid
leucosis(myelocytomatosis
 Occurence
• Lymphoid leukosis associated mortality is most
common in chickens of >16weeks of age
• Incidence highest at about sexual maturity
• The disease is world wide in distribution
• With ALV J meat type of chickens appear to be
more susceptible than layers
Historical information
• 1868 first report of LL by Roloff
 Etiology
• Caused by a family of retroviruses known as avian
lekosis viruses
• Classified into 10 groups
• A,B,C,D,E,F,G,H, I and J
• Sub group A are more common and most frequently
associated with LL
• Sub group B occasionally isolated and C and D are rare
• Subgroup E viruses are common rarely associated with
neoplasms(non-oncogenic)
• Subgroup F,G,H, and I viruses primarily cause
leukosis in species other than chickens
• ALV J viruses have extensive antigenic
variations within the strain
• The viruses can be cultured in chicken embryo
fibroblasts but produce no cytopathology and
are detected by antigen tests
 Epizootiology
• Chickens are the natural hosts for all virusesof the
leukosis/sarcoma groups
• These viruses have not been isolated from other
avian species exceptpheasants, patridges and quail
• Vertical transmission through eggs is most
important
• Chickens also can be infected by contact exposure
particularly with ALV-J which is more efficient in
horizontal transmission
 Pathogenesis
• Lymphoid leukosis is a clonal malignancyof the
bursal dependent lymphoid system
• Transformationinvarirably occurs in the intact bursa,
often as early as 4-8 weeks after infection
• Tumors are often not detectable until 14 weeks of
age,
• Death rarely occurs before 14 wks of age and is
frequent around time of sexual maturity
• The tomors are composed entirely of B lymphocytes
 Clinical signs
• Chickens with LL have few typical clinical signs
• These may include anorexia, weakness, pale comb,
shrivelled, diarrhoea, dehydration and emaciation
• Lossof egg production
• Many birds with tumors are unthrifthy or emaciated and
have pale head parts
• Enlargement of the abdomen may result from massive
enlargement of the liver
• Flocks with high infection rates experience depressed
egg production
 Lesions
• There are no external lesions
• Lymphomas seen in many organs in chickens
of > 16 weeks of age,
• Diffuse or nodular tumors are common in liver,
kidney, ovary, mesentery and Bursa of
Fabricius-pathognomonic
• Microscopically the tumor cells are
uniform,large lymphoblsts
• Mitotic figures are frequent
• Hemangiomas may also be seen
• Microscopically the neoplastic cells in tumours
are uniformly lymphoblastic and cells are
pyroninophilic
• The tumors originates from B cells
Avian lymphoid leukosis
 Diagnosis
• History, clnical signs, gross and histopatholgy
• Consideration of age of affected chicken
• The course of disease and pattern of mortality in
the flck, location of gross lesions
• Involvement of Bursa of Fabricius always present
• In contrast to MD bursal tumors are
intrafollicular causing nodular enlargment
• Immunohistochemistry, PCR, virus isolation
 DD of Avian tumors
Gross lesions
organ MD LL
Liver +++ +++
Spleen +++ +++
Nerves +++ -
Skin +++ +
Gonads +++ +++
Heart +++ +
Bursa + +++
Itestine + ++
Lungs +++ ++
Kidneys +++ +++
 DD of Avian tumors
Gross lesions
characteristic MD LL
Histology
Pleomorphic + -
Uniform blast cells - +
Antigens
MATSA + -
Ig M + +++
B cell + +++
T cell +++ +
Age of occurrence
Peak time 2-7 4-10
Limits >1 >3