Chicken Anemia Virus Infection (Chicken infectious anemia, Blue

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Chicken Anemia Virus Infection
(Chicken infectious anemia, Blue wing disease, Anemia dermatitis
syndrome, Hemorrhagic aplastic anemia syndrome)
Etiology, Epidemiology, and Pathogenesis :
Chicken anemia virus (CAV), a 52nm, nonenveloped, icosahedral
virus with a single-stranded, circular DNA genome, is the only
member of the genus Gyrovirus of the Circoviridae family. The
genome codes for 3viral proteins (VP). VP 1is the capsid protein,
but VP 5may be needed as a scaffold protein to allow proper folding
of VP1. VP3, or apoptin, is a nonstructural protein that induces
apoptosis in infected cells. CAV infects only chickens, although
antibodies have been detected in Japanese quail. The virus is
present worldwide based on serology and virus isolation. The
disease, chicken infectious anemia, has been described in most
countries where chickens are raised commercially .
Horizontal transmission of CAV is by the fecal-oral route and
perhaps by the respiratory route. Vertical transmission occurs
when seronegative hens become infected and continues until
neutralizing antibodies develop. Chicks hatched from these eggs
are viremic, and CAV can rapidly spread horizontally from these
chicks to susceptible, maternal antibody-negative hatchmates.
Roosters shedding CAV in the semen are another source of vertical
transmission. Vaccination of seronegative flocks prior to the onset
of egg production is recommended to prevent vertical
transmission .
Maternal antibody-negative chicks are susceptible to infection and
disease until 5-1wk of age. In contrast, maternal antibody-positive
chicks are protected from disease and probably from infection. Age
resistance to clinical disease, but not infection, begins at
approximately 1wk of age. The age resistance can be overcome by
coinfection of CAV with immunosuppressive agents such as
infectious bursal disease virus ( Infectious Bursal Disease:
Introduction), Marek’s disease herpesvirus ( Marek’s Disease), and
reticuloendotheliosis virus ( Reticuloendotheliosis ( .
Many SPF flocks developed antibodies to CAV during or after the
onset of sexual development. Spread of infection by CAVcontaminated embryo- or cell-culture-derived vaccines is possible .
When day-old susceptible chicks are inoculated IM with CAV,
viremia occurs within 52hr. Virus can be recovered from most
organs and rectal contents up to 32days after inoculation. The
principal sites of CAV replication are hemocytoblasts in the bone
marrow, precursor T cells in the cortex of the thymus, and CD 8
cells in the spleen. Replication in the first leads to anemia, while
replication in the latter two causes immunosuppression.
Neutralizing antibodies are detectable 51days after infection and
clinical, hematologic, and pathologic parameters return to normal
~ 32days after infection. CAV infection has adverse effects on
proliferative responses of spleen lymphocytes and on the
production of interleukin- 5and interferons by splenocytes.
Infection can cause a marked decrease in generation of antigenspecific cytotoxic T cells directed against other pathogens. In
addition to T-cell defects, macrophage functions such as Fcreceptor expression, phagocytosis, and antimicrobial activity may
be impaired. Subclinical, horizontally acquired infection with CAV in
broiler progeny of seropositive parent flocks may be associated
with impaired economic performance .
Clinical Findings :
Signs of illness or adverse effects on egg production do not occur
when seronegative adult chickens become infected. However,
vertical transmission or infection of maternal antibody-negative
chicks before 1wk of age can cause clinical disease 11-15days
after hatching or infection. Chicks are anorectic, lethargic,
depressed, and pale. PCV is low (in chicks, anemia is defined as a
PCV of ≤51), and blood smears often reveal anemia, leukopenia, or
pancytopenia depending on the state of the disease. Blood may be
watery and clot slowly. Mortality rates are variable but may be high
with secondary complicating infections .
Lesions: Organs are pale; the thymus is generally atrophied, and
the bursa of Fabricius may be small. Bone marrow is pale or yellow.
Hemorrhage may be present in or under the skin, muscle, and other
organs. Histologically, lymphoid cell populations are depleted in
primary and secondary lymphoid organs. Granulocytic and
erythrocytic compartments in the bone marrow are atrophic or
hypoplastic .
Diagnosis :
A tentative diagnosis is based on history, signs, and gross and
histopathologic lesions. Confirmation requires detection of virus or
viral DNA in the thymus or bone marrow. PCR and quantitative PCR
techniques are commonly used to demonstrate the presence of
CAV. Viral isolation can be used but is slow and expensive. To
isolate CAV, chloroform-treated extracts of tissues are inoculated in
MDCC-MSB 1or MDCC- 121cultures (a lymphoblastoid cell line
derived from Marek’s disease tumor) or into susceptible,
immunocompromised (antigen- and antibody-negative), day-old
chicks. Commercial ELISA kits are available to detect serum
antibodies to CAV and can be used to identify breeder flocks that
are seronegative prior to egg production and to monitor the efficacy
of vaccination .
Treatment and Prevention :
There is no specific treatment. Secondary bacterial infections may
be treated with antibiotics. Live vaccines are available for
vaccination of antibody-negative breeder flocks prior to the start of
egg production. Administration is by injection or by addition to the
drinking water depending on the type of vaccine available in
individual countries. In some areas, transfer of litter to
noncontaminated premises and the addition of crude homogenates
of tissues from affected chickens to the drinking water have been
used to ensure infection and seroconversion of parent flocks
before they begin to lay, thereby diminishing the risk of egg
transmission. However, these procedures are risky and not
recommended. Because of the synergism between CAV and other
immunosuppressive viruses, control of the latter is also important .
At present, there is no vaccine available to prevent subclinical
losses in broilers .
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