Infectious bursal disease (IBD) is widespread in many countries with intensive poultry industry. The causative agent is an RNA virus that belongs to Birnaviridae family. Two serotypes of IBDV exist. Serotype 1 strains originate from chickens, while serotypes 2 viruses are isolated from turkeys. Serotype 1 strains are further divided as classical, variant and very virulent. All the categories of young chickens are prone to the disease. Due to resultant immunosuppression the birds are exposed to secondary bacterial and viral infection that causes additional economic losses. The virus multiplies in the bursa of Fabricius inducing lymphocyte depletion (all strains) and inflammation (classical and very virulent strains). Approximately four days post infection, atrophy of bursa occurs followed by recovery process. Spleen, thymus and bone marrow are also damaged and the intensity of damage depends on the virus involved. Damages of these organs could be detected by pathohistological examination. The inflammatory response in bursa coincides with strong influx of CD3+ cells that take part in virus clearance and recovery. The disease can be controlled by the application of vaccination. Parent flocks are vaccinated with oil emulsion vaccines providing transfer of maternally derived antibodies to the progeny. In this way chickens are protected at an early age, while live vaccines provide protection during rearing. Live vaccines are classified as mild, intermediate and “hot”. Stronger vaccines can overcome high levels of maternal antibodies more efficiently and are recommended in questionable filed situation. Such vaccines may cause destruction of the bursa followed by a quick and full recovery. The knowledge about the antigenic structure of the virus leads to the production of genetically engineered vaccines that could be used in the future.
Arhives of Veterinary Medicine is an Open Access Journal.