AETIOLOGY & CHARACTERISTIC OF VIRUS
Infectious bursal disease (IBD) is a highly contagious viral disease of young/ immature chickens caused by infectious bursal disease virus (birnavirus) which is most readily isolated from the bursa of Fabricius (BOF) also called cloacal bursa. Bursa of fabricius is round out-pouching of the cloaca and one of the four primary lymphoid tissues (organs) where maturation of lymphocytes occurs though may be isolated from other organs.
The disease was first discovered in Gumboro, Delarware. It causes necrosis and atrophy of BOF. It is characterized by immunosuppression, high morbidity, pecking of vent, whitish diarrhoea, depression, dehydration, prostration and necrosis of the lymphoid follicles of the BOF and kidney in birds of between 3 to 6 weeks and maximum of 12 weeks of age.
While chicken of between 3 to 12weeks of age with highly active cloacal bursa are more susceptible to disease, birds over 12 weeks are resistant to challenge and will show no clinical signs unless infected by highly virulent strains
The virus can survive in a wide range of environmental conditions; remains viable from pH 2-12 but is inactivated only in 70⁰C for 30 minutes (can survive heat of 60⁰C for 90 minutes, temp of 25⁰C for 2 days and 20⁰C for 3 years). It is also resistant to some disinfectants but 2 % solutions of chloramines, halamide, and formaldehyde are effective against the virus
IBDV can survive in infected poultry houses for 122 days after removal of infected birds or beddings and in contaminated water or feed for 52 days. It is resistant to heat, ultraviolet radiation
IBDV can infect a wide range of domestic birds but only chickens show clinical signs of disease.TRANSMISSION
The main route of transmission is faecal-oral and the virus is shed for up to 2 weeks post-infection in large amounts, transferred from farm house to farm house by fomites. It is very stable and difficult to eradicate from premises.
Chickens infected with the IBD virus shed the virus in their faeces. Feed, water, and poultry house litter become contaminated. Other chickens in the house become infected by ingesting the virus. IBDV can also be spread by the nematode parasite, Alphitobius diaperinus (lesser mealworm)Fig 1 Alphitobius diaperinus (lesser mealworm)
Because of the resistant nature of the IBD virus, once a poultry house becomes contaminated, the disease tends to recur in subsequent flocks plus the ease of transmission (mechanically) among farms by people, equipment and vehicles. Wild birds are thought to be mechanical vector
IBD is not zoonotic (cannot spread between animals and humans.)MORTALITY AND MORBIDITY
IBD is extremely contagious. In infected flocks, morbidity is high up to 100% whilst mortality may be up to 30% but range of 57% has been reported in Nigeria
The birds are anorexic with the proventriculus (crop) being empty, depressed. There is ataxia (neurological signs consisting of lack of voluntary coordination of muscle movements), vent pecking which is whitish and pasted with watery diarrhoea, ruffled feathers, trembling and prostration, initial high temperature which becomes subnormal shortly after death. Mortality usually begins within 7days. Chicks in infected pen are not able to run when excited. The virulence varies massively and so can disease severity. Initial outbreaks are usually the most severe and recurrent cases are milder with lower mortality and frequently go undetected
POST MORTEM (PM) LESIONS
On post-mortem examination, the cloacal bursa is initially swollen, oedematous and occasionally hemorrhagic then later turns from white to cream and a gelatinous yellow transudate covers the serosal surface of the BOF early in infection. Carcasses are dehydrated, often with darkened (congestion and haemorrhage) pectora, thigh and leg muscles. This is due to the IBD virus interference with the normal blood clotting mechanism. Many petechiae may be visible in the thigh and pectoral muscle masses. Mucus may also be present within the intestines. In advanced disease, renal changes (swollen kidney) may be evident due to prolonged dehydration. Grey foci may also be visible on an enlarged spleen.
Chickens that have recovered from IBDV, (7-8 days post infection) have small, atrophied, cloacal bursas due to the destruction and lack of regeneration of the bursal follicles
The dead carcasses (dead body of the animal) are dehydrated, often with haemorrhages in the pectoral, thigh and abdominal muscles.
The lesions in the bursa of Fabricius are progressive. In the beginning, the bursa is enlarged, oedematous and covered with a gelatinous transudate.
There is depletion of the BOF which will be replaced with hetrophils, cellular debris and hyperplastic endothelial cells, haemorrhagic areas in the BOF. Histopathological lesions are mostly observed in lymphoid tissues like BOF, spleen, thymus and cecal tonsils.
• In the BOF, there is erosion and corrugation of epithelium, degeneration of the follicle, necrosis and oedema
• Necrosis of lymphocytes of the thymus
• Kidneys have interstitial haemorrhage, perivascular accumulation of lymphoid cells, oedema, tubular and glomerular necrosis
Involves consideration of
i. the flock’s history
ii. the clinical signs of sudden onset and short crises period with rapid recovery of the entire flock (5-7 days) as well as spiked mortality curve and
iii. the PM lesions of the cloacal bursa and haemorrhages of the breast and thigh muscles
iv. Diagnosis is confirmed by post-mortem or laboratory testing on islolation of the virus from bursa or kidney
Chickens less than 3 weeks of age present no clinical signs of disease, while chickens greater than 3 weeks of age present clinical signs as described. The severity of the clinical signs will depend upon the factors described. Confirmation of a diagnosis of clinical IBD can be made at necropsy by examining the BF during the early stages of disease for characteristic gross lesions.
During later stages of disease it is difficult to confirm a diagnosis of IBD by examining only shrunken, atrophied BF, as other diseases (for example, Marek’s disease, mycotoxicosis) produce similar changes. In birds less than 3 weeks of age or in young chickens with maternal antibodies, IBD virus infections are usually subclinical. Thus, typical clinical signs are not present, and diagnosis should be supported by histopathologic study of suspect BF, serologic studies, or by virus isolation.
Acute disease is usually recognised in a flock by rapid onset, high morbidity diarrhoea with a spike in mortality and rapid recovery. Diagnosis is confirmed by post-mortem or laboratory testing.
IBDV antigen can be detected in cloacal bursa or splenic samples by Agar Gel Precipitation or Immunofluorescence. Reverse Transcription – Polymerase Chain Reaction (RT-PCR) is commonly used to detect IBDV. Antibody- Enzyme Linked Immuno-Sorbent Assay (ELISA) can be used for serological diagnosis within a flock.
No treatment is available rather symptoms are treated (supportive therapy) as it manifests with antibiotics and multivitamins. Maintain a good temperature in poultry house especially in young birds. Recovery is usually rapid in an infected flock.
• Effective biosecurity program and Hygienic measures with appropriate disinfectants are imperative. Rigorous disinfection of contaminated farms after depopulation has achieved limited success though
• Effective breeder Vaccination Program is also usually required. The highly infectious nature of IBD coupled with the extreme resistance of IBD virus has made vaccination a necessity in major poultry producing areas.
Both live and inactivated forms are available. Timing is difficult due to interference of maternally-derived antibody, but oil adjuvanted vaccines can extend maternal immunity to 5 weeks. Vaccination can cause immunosuppression and a degree of bursal damage.
Vaccines are given intraocular (I/O) or in drinking water (per os) to chicken after 1 week of age and then booster dose also given after 2 weeks to support the maternal antibody.
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