Infectious bursal disease (IBD), also known as Gumboro, is a highly contagious viral infection of chickens that is seen worldwide. The severity of the disease will depend on the age and breed of chicken and the virulence of the virus. White Leghorns are more susceptible than broilers and brown-egg layers. Signs of the disease can include a rapid drop in feed and water consumption, mucoid (slimy) diarrhoea with soiling of the vent feathers, ruffled feathers, listless chicks with unsteady gait or sitting in hunched position, picking at own vent and sleeping with beak touching the floor.
Infections before 3 wk of age are usually subclinical (no detectable symptoms). Chickens are most susceptible to clinical disease at 3-6 wk, but severe infections have occurred in Leghorn chickens up to 18 wk old.
Early subclinical infections are the most important form of the disease because of economic losses. The disease can cause severe, long-lasting suppression of the immune system. Chickens that are immunosuppressed by early IBD infections do not respond well to vaccination and are more susceptible to other diseases, including those that don’t normally affect healthy chickens.
In clinical infections, onset of the disease is sudden after an incubation of 3-4 days. Mortality is usually low but can reach 20%. Recovery occurs in <1 wk, and broiler weight gain is delayed by 3-5 days. The presence of maternal antibody (antibody passed to the chick from the mother) will modify the way the disease progresses. Virulence of field strains of the virus varies considerably. Very virulent (vv) strains of the virus that cause high mortality and morbidity were detected first in Europe. These spread throughout the Old World in the last decade and in 1999 were in South America. The vv strains have not yet been detected in Australia.
Infectious bursal disease is caused by a birnavirus (IBDV) that is most readily isolated from the bursa of Fabricius, an organ of the immune system, but may be isolated from other organs. It is shed in the faeces and spreads between birds or by contact with a contaminated environment and is possibly also carried in the air on dust particles. The virus can be transferred from house to house on fomites (any inanimate object or substance that is capable of carrying infectious organisms from one individual to another) and rodents. The virus is very stable and difficult to eradicate from premises. There is no vertical transmission (from parents directly to offspring). Mealworms and litter mites may harbour the virus for 8 weeks, and affected birds shed large amounts of virus for about 2 weeks after infection.
There is no treatment for IBD but support therapies, such as vitamin and electrolyte supplements and antibiotics to treat any secondary bacterial infections, may reduce the impact of the disease.
Depopulation and rigorous disinfection of contaminated farms have achieved some limited success in preventing disease spread. Prevention is through good biosecurity and vaccination, including passive protection via breeders and vaccination of progeny depending on virulence and age of challenge. In most countries, breeders are immunised with a live vaccine at 6-8 weeks of age and then re-vaccinated with an oil-based inactivated vaccine at 18 weeks. Birds that have recovered from a natural infection have a strong immunity. Immunity in chicks after receiving a live vaccine can be poor if maternal antibody was still high at the time of vaccination.
There is a high degree of variation between naturally occurring IBD viruses and so a number of vaccines are available. Vaccines need to be selected based on the types of viruses present in the area. The disease is believed not be present in New Zealand. The Australian field strains of IBD are relatively mild and live vaccination of broilers is not regarded as necessary; the main method of control relying on vaccination of parent chickens and transmission of maternal antibody to the chicks.
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