Difference between revisions of "Avian Leukosis Virus"

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== Diagnosis  ==
 
== Diagnosis  ==
  
History, signalment and clinical signs are indicative of the disease, but differentials such as [[Mareks Diesease|Marek's disease]] and coligranuloma need to be excluded.  
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History, signalment and clinical signs are indicative of the disease, but differentials such as [[Mareks Disease|Marek's disease]] and coligranuloma need to be excluded.  
  
 
Necropsy can be carried out and lesions seen will include focal grey to white tumours, initially in the bursa, then liver, spleen, kidney etc. The liver may be very large. Microscopic examination will reveal lymphoplastic cells.
 
Necropsy can be carried out and lesions seen will include focal grey to white tumours, initially in the bursa, then liver, spleen, kidney etc. The liver may be very large. Microscopic examination will reveal lymphoplastic cells.

Revision as of 10:34, 28 March 2011


Introduction

This virus is of the family Retroviridae, which is a family of viruses that eventually all cause tumours. There are three subgroups of this virus to note. Groups A and B are found in 10% of layers and cause occasional B cell leukosis, J has been found in up to 40% of broilers causing up to 10% of deaths by myeloid tumors. All three subgroups are transferred vertically and horizontally. Vertical transmission is most important by infection of the egg white in infected breeders (who are long-term carriers), lateral transmission is poor but infection may occur by the faecal-oral route, especially in young birds. The causative viruses are rapidly inactivated at ambient temperature and on exposure to most disinfectants.

The disease is complex and has various manifestations such as lymphoid leukosis, myeloblastosis (see Sero-type J), erythroblastosis, osteopetrosis, myxosarcomas, fibrosarcomas and other tumours. It affects chickens worldwide with susceptibility varying considerably among different strains and types of stock, with layers being more susceptible to lymphoid leukosis.

Morbidity is low but mortality is high in many cases of the disease.

Clinical Signs

Signs include depression, emaciation, weight loss and enlargement of the abdomen, liver or bursa. However, many birds are asymptomatic.

Diagnosis

History, signalment and clinical signs are indicative of the disease, but differentials such as Marek's disease and coligranuloma need to be excluded.

Necropsy can be carried out and lesions seen will include focal grey to white tumours, initially in the bursa, then liver, spleen, kidney etc. The liver may be very large. Microscopic examination will reveal lymphoplastic cells.

Control

Selective breeding has now controlled the virus type J and may lead to eradication of this group. This has been done by identifying hens whose eggs testing positive for antigen in albumin and removing them from the flock.

Control measures include general good hygiene, management systems such as an 'all in/ all out'  production system and removal of the litter after every batch. It is also important to control arthropods especially mites.


References

Bridger, J and Russell, P (2007) Virology Study Guide, Royal Veterinary College

Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial

Jordan, F, Pattison, M, Alexander, D, Faragher, T, (1999) Poultry Diesease (Fifth edition), W.B. Saunders

Randell, C.J, (1985) Disease of the Domestic Fowl and Turkey, Wolfe Medical Publication Ltd

Saif, Y.M, (2008) Disease of Poultry (Twelfth edition), Blackwell Publishing