INFECTIOUS BURSAL DISEASE IN POULTRY, ITS DIAGNOSIS, TREATMENT AND CONTROL
Dr. Prabjot Singh (MVSc), Dr. Shilpa Sood (Associate Professor),Dr. Satuti Sharma (PhD Scholar), Dr Meenakshi (MVSc), Division of Veterinary Pathology, F.V.Sc & AH, SKUAST- Jammu, J&K, India (181102)
Infectious bursal disease, IBD (also known as Gumboro disease, infectious bursitis and infectious avian nephrosis) is a highly contagious disease of young chickens caused by infectious bursal disease virus (IBDV), characterized by immunosuppression and mortality generally at 3 to 6 weeks of age. IBDV is a non-enveloped, double-stranded RNA (dsRNA) virus belonging to the Birnaviridae family. The disease was first discovered in Gumboro, Delaware in 1962. It is economically important to the poultry industry worldwide due to increased susceptibility to other diseases and negative interference with effective vaccination. In recent years, very virulent strains of IBDV, causing severe mortality in chicken, have emerged in Europe, Latin America, South-East Asia, Africa and the Middle East. Infection is via the oro-fecal route, with affected bird excreting high levels of the virus for approximately 2 weeks after infection.
It causes heavy mortality in the chickens of 3 weeks of age. It causes immunosupression which leads to vaccination failure, E.coli infection, gangrenous dermatitis, & inclusion body hepatitis.
Incidence and distribution
The first report of a specific disease affecting the bursa of Fabricius in chickens was made by Cosgrove in 1962 The first cases were observed in the area of Gumboro, in Delaware (United States of America [USA]), which is the origin of the name, although the terms ‘IBD’ or ‘infectious bursitis’ are more accurate descriptions. Between 1960 and 1964, the disease affected most regions of the USA, and reached Europe in the years 1962 to 1971. From 1966 to 1974, the disease was identified in the Middle East, southern and western Africa, India, the Far East and Australia.. Infectious bursal disease is currently an international problem: 95% of the 65 countries that responded to a survey conducted by the Office International des Epizooties (OIE) in 1995 declared cases of infection, including New Zealand which had been free of disease until 1993. These findings led to the adoption of a specific resolution of the International Committee of the OIE during the 63rd General Session in May 1995.
Epidemiology Host range
Only chickens (Gallus gallus) develop IBD after infection by serotype 1 viruses. Turkeys (Meleagris gallopavo) may be asymptomatic carriers of serotype 2 and at times, of serotype 1 viruses whose pathogenicity for turkeys is ill-defined. The Pekin duck (Cairina moschata) can also be an asymptomatic carrier of serotype 1 viruses.
Anti-IBDV antibodies have been detected in guinea-fowl (Numida meleagris), common pheasants (Phasianus colchicus) and ostriches (Struthio camelus) which have also been demonstrated to carry serotype 2 viruses. Neutralising or precipitating antibodies have been detected, inter alia, in various species of wild duck, goose, tern, puffin, crow and penguin, which may mean that wild birds act as reservoirs or vectors.
The virus can be transmitted mainly from infected to susceptible birds through water, feeds, droppings and formites. Other means of transmission such as through the intermediary role of vermines like the lesser meal worm, mites and mosquitoes have also been reported . The disease is characterized by a short incubation period of 2-3 days.
Morbidity and mortality
Infectious bursal disease is extremely contagious. In infected flocks, morbidity is high, with up to 100% serological conversion, after infection, whilst mortality is variable. Until 1987, the field strains isolated was of low virulence and caused only 1% to 2% of specific mortality. However, since 1987 an increase in specific mortality has been described in different parts of the world. In the USA, new strains responsible for up to 5% of specific mortality were described. At the same time, in Europe and subsequently in Japan, high mortality rates of 50% to 60% in laying hens and 25% to 30% in broilers were observed. These hypervirulent field strains caused up to 100% mortality in specific-pathogen-free (SPF) chickens.
The incubation period is very short: two to three days. In acute cases, the animals are exhausted, prostrated, dehydrated, suffer from watery diarrhoea, and feathers are ruffled. Mortality commences on the third day of infection, reaches a peak by day four, then drops rapidly, and the surviving chickens recover a state of apparent health after five to seven days. Disease severity depends on the age and breed sensitivity of the infected birds, the virulence of the strain, and the degree of passive immunity.
Macroscopic lesions observed principally in the bursa which presents all stages of inflammation following acute infection. Autopsies performed on birds that died during the acute phase (three to four days following infection) reveal hypertrophic, hyperaemic and oedematous bursas. The most severe cases are characterised by a major infection of the mucous membrane and a serous transudate, giving the bursal surface a yellowish colour. This appearance is often accompanied by petechiae and haemorrhages. By the fifth day, the bursa reverts to normal size and by the eighth day becomes atrophied to less than a third of the normal size. The affected animals are severely dehydrated, and many birds have hypertrophic and whitish kidneys containing deposits of urate crystals and cell debris. Haemorrhages in the pectoral muscles and thighs are frequently observed, probably due to a coagulation disorder . Certain variants from the USA are reported to cause rapid atrophy of the bursa without a previous inflammatory phase . Moreover, in the acute form of the disease caused by hypervirulent strains, macroscopic lesions may also be observed in other lymphoid organs (thymus, spleen, caecal tonsils, Harderian glands, Peyer’s patches and bone marrow.
In areas contaminated by IBDV, most broiler flocks have anti-IBDV antibodies when leaving the farm. Current serological tests cannot distinguish between the antibodies induced by pathogenic IBDV and those induced by attenuated vaccine viruses, so serological diagnosis is of little interest in endemic zones. Nonetheless, the quantification of IBDV-induced antibodies is important for the medical prophylaxis of the disease in young animals, in order to measure the titer of passive antibodies and determine the appropriate date for vaccination or in laying hens to verify success of vaccination . Serology is likewise essential to confirm the disease-free status of SPF flocks. Each serological analysis must include a sufficient number (at least twenty) of individual serum samples representative of the flock under study. A kinetic study requires at least two serological analyses separated by an interval of three weeks (paired sera).
The most widely used quantitative tests are the detection of precipitating antibodies by agar gel immunodiffusion (AGID) enzyme-linked immunosorbent assay (ELISA)).
Agar gel immunodiffusion is the simplest, but least sensitive technique. Results are obtained after an incubation period of 48 h. Variability in results may be due to the investigator, as well as the nature of the viral strain used as an antigen.
Serum neutralisation presents the disadvantages that specialized equipment and five days incubation are required. The technique is much more sensitive than AGID and correlates better with the level of protection of the subjects tested.
The ELISA is the most rapid and sensitive method, and presents the fewest variations due to the viral strain used as an antigen. Considerable inter- and intra-laboratory variability can occur with certain commercial kits. Although the correlation between results obtained using SN and ELISA is high, ELISA remains less sensitive, and does not detect low neutralizing titres which are sufficient to block vaccine administration (residual maternal antibodies). Enzyme-linked immunosorbent assays which use a recombinant VP2 protein as the sole antigen may be better correlated with protection.
- Commercial broilers- 13 day intermediate plus in drinking water.
- Commercial layers- 14 & 28 day standard intermediate plus in drinking water & on 21 day intermediate plus in drinking water.
- For breeder hen- Traditionally at prelay stage & midlay stage IBD inactivated vaccine is given to get high antibody titer.
Resistance Birds with maternal antibody are resistant due to high antibody titer. when antibody titer drops birds become susceptible. Very virulent strain can break the antibody barrier at young age. Older birds in which bursa is reduced in size & disappears are more resistant.
- Control thorough cleaning & disinfection of the houses between the flocks & the practice alI in , all out management. It delays infection & also provides time for vaccines to produce immunity.
- Hygienic & Sanitary precautions.
- Formaldehyde & Ionophores are found to be effective disinfectants.
- Removal of vectors like mealworms &
- Proper vaccination of birds & flock