2. Introduction
It is the disease of young chicken (less than 3weeks).
This disease was first seen in Japan during 1979 by Yuasa et al. (1979)
in commercially produced chickens. and is prevalent in all parts of the
word.
CAV has also been isolated from other species such as turkeys and
quails.
The disease is immunosupressive.
The other name of this disease are Chicken anaemia virus syndrome,
blue wing disease, anaemia dermatitis syndrome, hemorrhagic
syndrome.
It causes Anaemia, drop in lymphocytes,liver changes and
haemorrhages in all part of body .
The disease has recently been reported to be widely prevalent in India.
3. Etiology
Chicken anemia virus (CAV), a nonenveloped, icosahedral virus with a
single-stranded, circular DNA genome, is the only member of the Gyrovirus
genus of the Circoviridae family.
The genome codes for three viral proteins (VP).
VP1 is the capsid protein, but VP2 may be needed as a scaffold protein to
allow proper folding of VP1.
VP2 has also a dual-specificity protein phosphatase (DSP) activity, and
mutations affecting the DSP activity resulted in attenuation of virus
replication in vivo.
VP3, or apoptin, is a nonstructural protein that induces apoptosis in infected
cells.
Two other viruses with similar characteristics are the psittacine beak and
feather disease virus (PBFDV), and swine circovirus (SC).
The virus belong to single serotype.
This virus is remarkebely resistant which resist heating at 80ºC for 15 min.
and exposure to pH 3.Therefore difficult to erradicate.
Hypochloride type of chemicals is the most appropriate disinfectant to kill
the organism.
4. Transmission
Mechanical transmission : by the way of droppings, feeders, wateres
and growing place.
Horizontal Transmission : From chicken to chicken.
Chickens at any age are susceptible to infection by: Oral route and
Respiratory route.
Parent layer stock continues to excrete the Infectious Organism for
period of 6 weeks.
Acquired infection in older chicken lacking maternal antibody usually
originate from virus surviving in poultry houses between the flocks.
Verticle transmission :From hen through the hatching eggs to the chicks.
Emryo infection can be caused by semen of infected cocks.
It is the most importance means of spread and results in clinical
infection. Chick that hatch without maternal Antibodies are most
susceptible.
In Affected birds it simultaneously occur with Mareks and Bursal
disease, reticuloendothelial virus.
5. Pathogenesis
CAV is not highly contagious and it takes few weeks to spread
through an entire flock.
The disease occurs in those chicks which have no maternal
antibodies.
The main site of its growth are lymphoblast in the thymus and
haemocytoblast in bone marrow.
CAV can be found latent in SPF (Specific pathogen free) flocks
where the virus was detected in the ovaries, oviduct, testicles and
spleen of birds without obvious seroconversion until the birds came
into production.
6. Symptoms
Levels of thrombocytes and white blood cells are reduced and the
blood may be slow to clot.
The chicks are depressed ,dull, off fed, pale,slow weight gain and
very susceptible to secondary infection due to immunosupression.
Mortality: 10-60%.
The anaemia or paleness on comb, wattles ,eyelids and legs,
feather dropping, atrophy of thymus, spleen,bursa of fabricus.
Haemorrhages in muscle and skin region. Inflamation and necrosis
of skin.Gangrenous dermititis.
Enlargement of liver.
The drop in blood producing cells and T lymphocytes the anaemic
condition and immunosupression are observed.
Surviving chicks recover from anaemia by 20-28 days after
infection.This occurs after maternally acquired antibodies
disappeared at about 3 week of age.
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12. Post Mortem Findings
The marked reduction in size of thymus,bursa of fabricus and to lesser extent
the spleen.
The bone marrow changes from red colour to yellow or white colour.
Bone marrow in femur are fatty and yellowish.
Atropy of thymus result in complete disappearence of the organ.
The liver is often swollen.
Haemorrhages in the proventriculus ,under skin , in muscle associated with
severe anaemia.
Focal lesions (mostly in the wings) appear as ecchymotic skin haemorrhages.
This can be especially notorious at the end of the wings, hence the name
“Blue Wing Disease” used to describe this condition.
The tips of the wings may appear haemorrhagic and necrotic.
Decrease in the number haematopoietic cells is observed 4 –6 days post
infection. Followed by the appearance of large blastic cells.
The haematopoietic tissue is replaced by adipose tissue; this gives the bone
marrow a pale appearance.
13. Diagnosis
Important symptoms are useful to diagnosed the affected flocks.
ELISA
Commercial ELISA kits are available to detect serum antibodies
to CAV and can be used to identify breeder flocks that are
seronegative before egg production and to monitor the efficacy of
vaccination.
Serum neutralization test
Polymerase Chain Reaction.
To isolate CAV, chloroform-treated extracts of tissues are
inoculated in MDCC-MSB1(Morphogenesis-related protein)
or MDCC-147 cultures (both are lymphoblastoid cell lines
derived from Marek’s disease tumors) or into susceptible,
immunocompromised and maternal antibody–negative day-old
chicks.
14. Treatment
Treatment of secondary infection with appropriate
Antibodies.
The suplementation of Vitamin in drinking water.
Vaccine: NOBILIS CAV P4 (Live vaccine ) from 6
weeks of age onwards
15. Control
Preventive vaccination in breeder flock and in chicks.
Immunization of parent flocks several weeks before egg
production prevents outbreak in their progreny.
Vaccination should be performed about 13-15 week but never
later than 13-14 week before first collection of hatching eggs
to avaoid the risk of vaccine virus being spread through eggs.
Proper Management and hygiene.
Monitoring the flocks for the presence of virus antibody to
avoid vertically transmitted anaemia virus infection or to test
the efficacy of vaccination.
Vaccine: NOBILIS CAV P4 (Live vaccine ) from 6 weeks of
age onwards.
The breeding stock should be vaccinated at least 6 weeks
before .
