Difference between revisions of "Chicken Anaemia Virus Disease"
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| − | Also known as: ''''' Chicken | + | Also known as: '''''Chicken Anaemia — Blue Wing Disease — BWD — Anemia Dermatitis Syndrome — Chicken/Avian Infectious Anaemia — Hemorrhagic Aplastic Anemia Syndrome — Infectious Chicken Anaemia — CAV — Chicken Infectious Anaemia Virus — CIAV — Chicken Anaemia Agent — CAA''''' |
{{Taxobox | {{Taxobox | ||
|name =''Scientific Classification'' | |name =''Scientific Classification'' | ||
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|sub-order = | |sub-order = | ||
|super-family = | |super-family = | ||
| − | |family = Circoviridae | + | |family = [[Circoviridae]] |
|sub-family = | |sub-family = | ||
|genus = Circovirus | |genus = Circovirus | ||
|species = Chicken anaemia virus | |species = Chicken anaemia virus | ||
}} | }} | ||
| − | |||
==Introduction== | ==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 | + | 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 [[:Category:Circoviridae|Circoviridae]], composing of a small circular genome of negative sense. The virus is '''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 Circoviruses|''Porcine circovirus'' (PCV)]] and [[Psittacine Beak and Feather Disease| ''Psittacine beak and feather disease virus'' (PBFDV)]]. |
| − | CAV produces '''three types of proteins''' of '''VP1''' (52kDA), '''VP2''' (24 kDA) and '''VP3''' (14 kDA) kDa . | + | 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) <ref name=" Yuasa, 1983">Yuasa, N. (1983) | + | 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) <ref name=" Yuasa, 1983">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. </ref> <ref name=" Goryo et al., 1987"> 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. </ref>. Virus production in this way may lead to the potential for Marek’s disease virus contamination of vaccines. |
==Signalment== | ==Signalment== | ||
| − | The disease affects '''chickens''' but can also affect quail. | + | The disease affects '''chickens''' but can also affect quail. Disease is more '''severe in chicks'''. <u>Immunity occurs once the bird has become infected.</u> |
==Clinical Signs== | ==Clinical Signs== | ||
| − | Clinical signs are '''dependent''' on the '''age''' of the bird. | + | 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 | + | 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== | ==Epidemiology== | ||
| − | Fomites may assist the transmission of the virus and the disease can be '''spread both horizontally and vertically''', resulting in '''clinical and subclinical infections, respectively''' and the latter being of particular '''importance''' to '''intensive breeding populations'''. '''Chicks hatching''' from infected layers of naive flocks '''show clinical signs after 10-14 days of age'''over a '''period of 3 to 6 weeks. After which the breeder layers develop sufficient CAV antibodies to stop the transmission of the virus to the egg. | + | Fomites may assist the transmission of the virus and the disease can be '''spread both horizontally and vertically''', resulting in '''clinical and subclinical infections, respectively''' and the latter being of particular '''importance''' to '''intensive breeding populations'''. '''Chicks hatching''' from infected layers of naive flocks '''show clinical signs after 10-14 days of age''' over a '''period of 3 to 6 weeks. After which 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'''. | + | <u>'''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'''.</u> |
CAV isolates can be distinguished by using restriction endonuclease analysis of amplified DNA, but only a single serotype has so far been detected. | CAV isolates can be distinguished by using restriction endonuclease analysis of amplified DNA, but only a single serotype has so far been detected. | ||
==Distribution== | ==Distribution== | ||
| − | '''Worldwide''' distribution including commercial poultry and in specific pathogen free (SPF) flocks | + | '''Worldwide''' distribution including commercial poultry and in specific pathogen free (SPF) flocks. |
==Diagnosis== | ==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. | + | 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 [[Haematopoiesis - Overview|immature blood cells]]. |
| − | Post mortem finding include severe atrophy of the lymphoid organs. | + | |
| + | ''' 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 developed that include immunoperoxidase staining, [[ELISA testing|ELISA]]<ref name=" Todd et al., 1999">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. </ref>, PCR, dot blot hybridisation and indirect [[immunofluorescence]]<ref name=" Sun et al., 1999">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. </ref>. | ||
| + | |||
| + | 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. | ||
==Treatment== | ==Treatment== | ||
| Line 52: | Line 54: | ||
==Control== | ==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. | + | 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 to eradicate on farm infections. | ||
{{Learning | {{Learning | ||
|flashcards = [[Chicken Anaemia Virus Disease Flashcards]] | |flashcards = [[Chicken Anaemia Virus Disease Flashcards]] | ||
}} | }} | ||
| + | |||
| + | ==References== | ||
| + | |||
| + | <references/> | ||
[[Category:Circoviridae]] | [[Category:Circoviridae]] | ||
| + | [[Category:Avian Viruses]] | ||
[[Category:Lymphoreticular and Haematopoietic Diseases - Birds]] | [[Category:Lymphoreticular and Haematopoietic Diseases - Birds]] | ||
| − | [[Category:To Do - | + | [[Category:To Do - Jaimie Meagor]] |
Revision as of 22:11, 9 July 2011
Also known as: Chicken Anaemia — Blue Wing Disease — BWD — Anemia Dermatitis Syndrome — Chicken/Avian Infectious Anaemia — Hemorrhagic Aplastic Anemia Syndrome — Infectious Chicken Anaemia — CAV — Chicken Infectious Anaemia Virus — CIAV — Chicken Anaemia Agent — CAA
| 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 is 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. Disease is more severe in chicks. 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
Fomites may assist the transmission of the virus and the disease can be spread both horizontally and vertically, resulting in clinical and subclinical infections, respectively and the latter being of particular importance to intensive breeding populations. Chicks hatching from infected layers of naive flocks show clinical signs after 10-14 days of age over a period of 3 to 6 weeks. After which 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.
CAV isolates can be distinguished by using restriction endonuclease analysis of amplified DNA, but only a single serotype has so far been detected.
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 developed 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.
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 to eradicate on farm infections.
| Chicken Anaemia Virus Disease Learning Resources | |
|---|---|
 Test your knowledge using flashcard type questions |
Chicken Anaemia Virus Disease Flashcards |
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.