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==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 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 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 .  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.

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 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 .  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). '''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.

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.

==Clinical Signs==

==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 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.

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==

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.

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==

==Distribution==