Difference between revisions of "Chicken Anaemia Virus Disease"
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Revision as of 23:03, 28 June 2011
Also known as: Chicken anaemia— Blue wing disease (BWD) — Anemia dermatitis syndrome— chicken infectious anaemia avian anemia virus infection— Avian infectious anaemia— Chicken anemia virus infection— Hemorrhagic aplastic anemia syndrome— Infectious chicken anamia—CAV — Chicken infectious anemia virus (CIAV) — Chicken anaemia agent (CAA)— Avian infectious anaemia virus— Avian infectious anemia virus— Circovirus— Chicken infectious anaemia virus (CIAV) .
| Scientific Classification | |
|---|---|
| Kingdom | Virus |
| Family | Circoviridae |
| Genus | Circovirus |
| Species | Chicken anaemia virus |
Introduction
Chicken anaemia virus disease is commonly referred to as chicken anaemia, chicken infectious anaemia and blue wing disease. It is caused by the chicken anaemia virus (CAV), which is a non-enveloped icosahedral single stranded DNA (ssDNA) virus. CAV is 23-25 nm diameter and is part of the Circoviridae, composing of a small circular genome of negative sense. The virus iis difficult to eradicate as it is very hardy and resistant to high temperatures, acidic pH (pH3), chloroform and commercial disinfectants. CAV can be destroyed with hypochlorite and iodophor and formalin can reduce its infectivity. It is also morphologically and antigenically different to other circoviruses such as Porcine circovirus (PCV) and Psittacine beak and feather disease virus (PBFDV).
CAV produces three types of proteins of VP1 (52kDA), VP2 (24 kDA) and VP3 (14 kDA) kDa . Structural protein VP1 is the intracellular form of the capsid protein and VP2 is found in small amounts in the purified virus. Vaccines need to contain both of these to be antigenic. VP3 is involved in apoptosis which involves the programmed and controlled death of a cell. This process does not involve the lysis of the cell and therefore limits damage to surrounding cells and tissues. It also initiates pathogenicity and apoptosis of infected stem cells in the bone marrow (BM), resulting in damage to the BM. As a result the virus inhibits the production of red blood cells (RBC), white blood cells (WBC) and platelets. Lymphoid tissues are also affected. Due to its apoptotic properties VP3 has the potential to be an anti-cancer agent. It is not considered a zoonosis.
CAV is difficult to grow but can be grown in chickens, embryonated eggs and in cell culture. The most commonly used cell line is MDCC-MSB1 (a Marek’s disease transformed chicken lymphocyte cell line) [1], [2]. Virus production in this way may lead to the potential for Marek’s disease virus contamination of vaccines.
Signalment
The disease affects chickens but can also affect quail. Vertical transmission is of particular importance within intensive breeding populations. Disease is more severe in chicks. Fomites may assist the transmission of the virus. Immunity occurs once the bird has become infected.
Clinical Signs
Clinical signs are dependent on the age of the bird. Chicks develop clinical signs within two weeks of hatching if infected via vertical transmission. Chicks older than 14 days old do not show any clinical signs if infected via horizontal transmission.
Clinical signs consist of pale; comb, wattle, eyelids, legs and carcass, anorexia, weakness, stunting, unthriftiness, weight loss, cyanosis, petechiation and ecchymoses, lethargy and sudden death. Neurological signs include, dullness, depression and paresis.
Epidemiology
The disease can be spread both horizontally and vertically, resulting in clinical and subclinical infections, respectively. CAV isolates can be distinguished by using restriction endonuclease analysis of amplified DNA, but only a single serotype has so far been detected. Chicks hatching from layers of naive flocks over a period of 3 to 6 weeks, show clinical signs after 10-14 days of age. After this period the breeder layers develop sufficient CAV antibodies to stop the transmission of the virus to the egg. Mortality peaks during the third week of life around 5 to 10% but can be as high as 60%. Horizontal transmission can occur in older chickens that lack maternal derived antibodies from faecal-oral route, fomites and as the virus is excreted by a small number of vertically infected hatch mates.
Distribution
Worldwide distribution including commercial poultry and in specific pathogen free (SPF) flocks
Diagnosis
Diagnosis can be made on the above clinical signs and decreases in haematocrit from normal ranges (32-37.5%) to below 27% and increases in the amount of immature blood cells. Virus isolation can confirm diagnosis of disease but growth of CAV in cell cultures can be difficult. Levels of infection can be estimated by the detection of raising antibody titres and many diagnostic tests have been develop that include; immunoperoxidase staining, ELISA [3], PCR, dot blot hybridisation and indirect immunofluorescence [4]. Post mortem finding include severe atrophy of the lymphoid organs. The thymus, bursa of Fabricius, and to a lesser extent the spleen are all affected by a depletion of lymphocytes and sequential hyperplasia of reticular cells. Common finding include haemorrhages throughout the skeletal muscle and subcutaneous tissue and pale watery bone marrow. Severe aplasia of the bone marrow occurs and haematopoietic cells are replaced with adipose tissue, giving the bone marrow its watery texture and characteristic change in colour from red to yellow. Differential diagnosis:
Treatment
There is no specific treatment for infected birds with this virus and culling is likely to be the most appropriate option for commercial flocks.
Control
Vertical spread of the disease can be controlled by the vaccination of breeding hens with both live attenuated and wild vaccines that reduces the vertical transmission rate. Wild type vaccines are cheaper but can increase horizontal transmission rates and hidden reduction in production of older birds. At a farm level rigorous cleaning with hypochlorite, iodoform or formalin is recommended and biosecurity is important to try and erradicate on farm infections.
References
- ↑ Yuasa, N. (1983). Propagation and infectivity titration of the Gifu-1 strain of chicken anemia agent in a cell line (MDCC-MSB1) derived from Marek's disease lymphoma. National Institute of Animal Health Quarterly, Japan, 23(1):13-20; 18 ref.
- ↑ Goryo, M., Suwa, T., Matsumoto, S., Umemura, T., Itakura, C. (1987). Serial propagation and purification of chicken anaemia agent in MDCC-MSB1 cell line. Avian Pathology, 16(1):149-163; [7 fig.]; 18 ref.
- ↑ Todd, D., Mawhinney, K.A., Graham, D.A., Scott, A.N.J.,(1999) Development of a blocking enzyme-linked immunosorbent assay for the serological diagnosis of chicken anaemia virus. Journal of Virological Methods, 82(2):177-184; 17 ref.
- ↑ Sun, W., Wu, Z.Q., Hu, Q.H., Li, S.X., Li, G., (1999). Preliminary research on the diagnosis of chicken infectious anaemia by PCR, dot-blot-hybridization assay and indirect immunofluorescence assay'. Journal of Nanjing Agricultural University, 22(3):69-72.
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