(Avian anemia virus infection, Blue wing disease, Anemia dermatitis syndrome, Hemorrhagic aplastic anemia syndrome) Etiology, Epidemiology, and Pathogenesis: The chicken anemia virus (CAV) virus is a 25 nm, nonenveloped, icosahedral virus with a single-stranded, circular DNA genome. The proposed classification of CAV is a new family of viruses, designated Circoviridae. Antibody to CAV occurs worldwide, and the disease has been described in most countries with a developed chicken industry. CAV is not known to infect birds other than chickens. CAV is transmitted horizontally by direct contact or contaminated fomites (fecal-oral route) and vertically through the embryonated egg. Most breeder flocks become infected and develop CAV antibody before they begin to lay fertile eggs. If egg-producing seronegative breeder flocks are infected, CAV will be vertically transmitted: as long as the hen is viremic (1-3 wk), hatched chicks will be CAV-infected. The proportion of vertically infected chicks is <5%, and they rapidly infect susceptible hatchmates via horizontal spread. If hens are seropositive, maternally derived antibody generally protects progeny from disease but not from infection. Chicks <1 wk old without maternal antibody to CAV can become infected and develop disease. Age resistance to disease (not infection) begins at ~1 wk and is complete 2 wk after hatching. However, the protective effects of maternal antibody and age resistance can be overcome by co-infection of CAV with immunosuppressive agents such as infectious bursal disease virus ( Infectious Bursal Disease: Introduction), herpesvirus (Marek’s disease, Marek’s Disease), and reticuloendotheliosis virus ( Reticuloendotheliosis). Many flocks of SPF chickens have antibody to CAV. Spread of infection by CAV-contaminated embryo- or cell-culture-derived vaccines and biologicals has not been documented. When day-old susceptible chicks are inoculated IM with CAV, viremia occurs within 24 hr. Virus can be recovered from most organs and rectal contents up to 35 days after inoculation. The principal sites of CAV replication are precursor T cells in the cortex of the thymus and hemocytoblasts in the bone marrow. Anemia results from destruction of the latter. CAV infection has adverse effects on proliferation responses of spleen lymphocytes and on production of T-cell growth factor and interferon by splenocytes. Some functional properties of macrophages are also adversely affected. Neutralizing antibody is detectable 21 days after infection and clinical, hematologic, and pathologic parameters return to normal ~35 days after infection. Clinical Findings and Lesions: Signs of illness or adverse effects on egg production do not occur when seronegative adult chickens become CAV-infected. However, clinical disease occurs in their progeny 12-17 days after hatching and persists until vertical transmission of the virus has ceased. Chicks are anorectic, lethargic, depressed, and pale. PCV is low (in chicks, anemia is defined as a PCV of <27), and blood smears often reveal anemia, leukopenia, or pancytopenia depending on the stage of the disease. Blood may be watery and clot slowly. Mortality rates usually are ~10% but may be >50% Organs are pale, and the thymus and bursa of Fabricius are small. Bone marrow is pale or yellow. Hemorrhage may be present in or under the skin, skeletal 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 clinicopathologic findings. Confirmation requires detection of virus antigens or DNA in the thymus or bone marrow. Virus isolation also can be used but is slow and expensive. To isolate CAV, laboratories must maintain MDCC-MSB1 cultures (a lymphoblastoid cell line derived from Marek’s disease tumor) or have susceptible (antigen- and antibody-negative) day-old chicks or chick embryos. A commercial ELISA is now available to detect serum antibodies to CAV and can be used to identify breeder flocks that are seronegative at point of lay and to monitor the efficacy of vaccination. Treatment and Prevention: There is no specific treatment. Secondary bacterial infections may be treated with antibiotics. No vaccines currently are available for use in the USA, although a live vaccine administered in the drinking water is available in some European 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 not without risk and cannot be unreservedly recommended. Because of the synergism between CAV and other immunosuppressive viruses, control of the latter is also important. Subclinical, horizontally acquired infection with CAV in the broiler progeny of seropositive parent flocks is associated with significantly impaired economic performance. At present, there is no means available to prevent these losses. |
