Difference between revisions of "Chicken Anaemia Virus Disease"

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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) '''''.
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{{OpenPagesTop}}
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{{Podcasts
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|link = https://bloomsbury.mediacore.tv/podcasts/wikivet-english/chicken-anaemia-virus-disease}}
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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''
Line 13: Line 16:
 
|sub-order          =
 
|sub-order          =
 
|super-family      =
 
|super-family      =
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|family            = Circoviridae
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|family            = [[Circoviridae]]
 
|sub-family        =
 
|sub-family        =
 
|genus              = Circovirus
 
|genus              = Circovirus
 
|species            = Chicken anaemia virus
 
|species            = Chicken anaemia virus
 
}}
 
}}
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==Introduction==
 
==Introduction==
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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.
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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)]].   
  
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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.
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CAV produces '''three types of proteins''': '''VP1''' (52kDA), '''VP2''' (24 kDA) and '''VP3''' (14 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). Virus production in this way may lead to the potential for Marek’s disease virus contamination of vaccines.
  
 
==Signalment==
 
==Signalment==
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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 .
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The disease affects '''chickens''' but can also affect quail. Poultry that have previously been exposed to CAV and have CAV antibodies develop immunity.  '''Disease is more severe in chicks.'''
 +
 
 
==Clinical Signs==
 
==Clinical Signs==
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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.
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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.
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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==
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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.
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The disease is mainly spread by '''vertical transmission''', which is of particular importance to intensive breeding populations. The '''age''' of the bird has a marked effect on the '''development of clinical signs'''.'''Chicks hatching''' from infected layers of naive flocks (vertical transmission) '''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%. '''Older chicks''' (>14 days old) that become infected via faecal-oral route (horizontal transmission) '''do not exhibit clinical signs''' but the '''growth and health of the birds may be affected'''. Fomites may assist the transmission of the virus.
  
 
==Distribution==
 
==Distribution==
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'''Worldwide'''  distribution including commercial poultry and in specific pathogen free (SPF) flocks
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'''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. ''' 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 <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>.
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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]].  
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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.
+
 
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'''Differential diagnosis''':
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''' 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]], PCR and indirect [[immunofluorescence]].
 +
 
 +
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==
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There is no specific treatment for infected birds with this virus and culling is likely to be the most appropriate option for commercial flocks.
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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==
 
==Control==
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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.
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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.  
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==References==
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<references/>
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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
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|flashcards = [[Blue Eye Disease Flashcard]]
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|flashcards = [[Chicken Anaemia Virus Disease Flashcards]]
 
}}
 
}}
  
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==References==
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Schat, K.A. and van Santen, V.L. (2008) '''Chicken Infectious Anaemia'''. In: '''Diseases of Poultry, 12th Edition''' (eds. Saif, Y.M., Fadly A.M., Glissen J.R., McDougald L.R., Nolan L.K., Swayne D.E.) ''Wiley-Blackwell'', pp 211-235
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 +
Todd, D. and McNulty, M.S. (2007) '''Circoviridae'''. In: '''Poultry Diseases, 6th Edition''' (eds. Pattison, M., McMullin, P., Bradbury, J., Alexander, D.) ''Saunders, Elsevier'', pp 398-405
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{{CABI source
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|datasheet = [http://www.cabi.org/ahpc/?compid=3&dsid=89195&loadmodule=datasheet&page=2144&site=160 chicken anaemia virus] and [http://www.cabi.org/ahpc/?compid=3&dsid=89194&loadmodule=datasheet&page=2144&site=160 chicken anaemia]
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|date =18 June 2011
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}}
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<br><br>
  
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[[Category:To Do – CABI review]]
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{{Dave Cavanagh
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|date = 23 August 2011
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}}
  
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{{OpenPages}}
  
 
[[Category:Circoviridae]]
 
[[Category:Circoviridae]]
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[[Category:Avian Viruses]]
 
[[Category:Lymphoreticular and Haematopoietic Diseases - Birds]]
 
[[Category:Lymphoreticular and Haematopoietic Diseases - Birds]]
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[[Category:To Do - Jaimie Meagor]]
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[[Category:CABI Expert Review Completed]][[Category:CABI AHPC Pages]]

Latest revision as of 13:21, 17 August 2012


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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: VP1 (52kDA), VP2 (24 kDA) and VP3 (14 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). 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. Poultry that have previously been exposed to CAV and have CAV antibodies develop immunity. Disease is more severe in chicks.

Clinical Signs

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 is mainly spread by vertical transmission, which is of particular importance to intensive breeding populations. The age of the bird has a marked effect on the development of clinical signs.Chicks hatching from infected layers of naive flocks (vertical transmission) 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%. Older chicks (>14 days old) that become infected via faecal-oral route (horizontal transmission) do not exhibit clinical signs but the growth and health of the birds may be affected. Fomites may assist the transmission of the virus.

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, PCR and indirect immunofluorescence.

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
FlashcardsFlashcards logo.png
Flashcards
Test your knowledge using flashcard type questions 		Chicken Anaemia Virus Disease Flashcards


References

Schat, K.A. and van Santen, V.L. (2008) Chicken Infectious Anaemia. In: Diseases of Poultry, 12th Edition (eds. Saif, Y.M., Fadly A.M., Glissen J.R., McDougald L.R., Nolan L.K., Swayne D.E.) Wiley-Blackwell, pp 211-235

Todd, D. and McNulty, M.S. (2007) Circoviridae. In: Poultry Diseases, 6th Edition (eds. Pattison, M., McMullin, P., Bradbury, J., Alexander, D.) Saunders, Elsevier, pp 398-405


CABIlogo

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 18 June 2011.

This article has been expert reviewed by Prof Dave Cavanagh BSc, PhD, DSc

Date reviewed: 23 August 2011



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