Role-Of-Infectious-Bursal-Disease-IBD-Gumboro-In-Poultry-Industry-Its-Diagnosis-And-Control-Measures.

The infectious bursal disease is caused by a birnavirus (infectious bursal disease virus; IBDV) that is isolated from the bursa of Fabricius.

Author: Dr. Maria Jamil1, Dr. Kashif Saleemi1, Dr. Ali Raza2, Dr. Muhammad Tahir Aleem3

Infectious bursal disease, also known as Gumboro disease, infectious bursitis and infectious avian nephrosis, is a highly contagious disease of young chickens and turkeys caused by infectious bursal disease virus, characterized by immunosuppression and  generally at 3 to 6 weeks of age. Infection before 3 weeks of age is usually subclinical. But severe infection has occurred in Leghorn chickens up to 18 weeks of age. The cloacal bursa becomes enlarged with yellowish coloured transudate, haemorrhages on the serosal and mucosal surface and atrophy of bursa, with reduction of B lymphocyte which leads to immunosuppression in birds.  In IBD mortality can reach up to 100% and morbidity ranges from 5-60%. Death is usually higher in layer breeds as compared to broiler chickens. Recovery occurs within less than 1 week.

The infectious bursal disease is caused by a birnavirus (infectious bursal disease virus; IBDV) that is isolated from the bursa of Fabricius. It is shed in the faeces and transferred from house to house by fomites. It is very steady and hard to eliminate from the premises. There is only horizontal transmission no transmission from hen to chick and mealworms and litter mites can harbor the virus for upto 8 weeks. Infected birds may shed large quantity of virus for up to 2 weeks after exposure. Two serotypes of IBDV have been recognized. The serotype 1 viruses cause disease in chickens and, within them, antigenic distinction may occur among strains. Antigenic variation may also exist through genome homologous recombination. Serotype 2 strains of the virus infect chickens and turkeys but have not caused clinical disease or immunosuppression in these hosts.

Flock morbidity is typically 100%, and mortality can range from 5% to greater than 60% depending on the strain of virus and breed of chicken. Mortality is typically higher in layer breeds compared with broiler chickens. Recovery occurs in less than one week, and broiler weight gain reduced by 3–5 days. The existence of maternal antibody will change the clinical course of the disease.

Sequential changes in bursa (course of disease 7-8 day):

       

Normal bursa

3 day post infection

4 day post infection

5 day post infection

6 day post infection

7 day post infection

8 day post infection

After 3 days bursa become enlarged due to oedema, then upto 5th days after exposure goes on increasing that is  about double of day 3rd. There will be cheesy material in bursal folds and hemorrhagic. After that size start to reduce and at day 8 the size of the bursa is of 1/3rd of that of the original size.

Symptoms of Gumboro:

IBD is seen in young domestic chickens worldwide and is caused by IBDV. The clinical disease often occurs quite suddenly with a rapid increase in mortality rate. The clinical sign includes trembling, ruffled feathers, poor appetite, dehydration, huddling, vent pecking, and depression. The majority of the lesions are found in the bursa of Fabricius when birds are necropsied.

Diagnosis:

  • Macroscopic and microscopic lesions in the cloacal bursa and molecular identification of the viral genome are used to diagnose the disease.
  • Diagnosis can be accomplished by molecular detection of the viral VP2 gene using RT-PCR
  • Sequence analysis of the VP2 gene is used to identify the IBDV genotype
  • Virus isolation in chicken embryos or chicken embryo fibroblast cell cultures is possible but often not necessary
  • In 8-11-day-old antibody-free chicken embryos IBD virus can be isolated with inoculation from birds in the initial stages of the disease. The chorioallantoic membrane is more sensitive to inoculation than is the allantoic sac.
  • In cell cultures some strains of IBD virus can also be isolated that include mammalian cell line, chicken embryo fibroblasts, cells from the cloacal bursa, and established avian.

Treatment and control measures against IBD

For IBD no proper treatment only use the supportive therapies such as vitamin and electrolyte supplements and antibiotics to treat the infection. Any secondary bacterial infections may decreased the control of the disease. Clearance and complete disinfection of pollutened farms have attained some limited success in avoiding the disease spread.

Vaccination to induce maternal immunity in young chicks is initially used to control the disease. Vectored and live attenuated vaccine can be used to induced active immunity in chicks as a maternal antibody. In most countries, at 6-8 week of age breeders are protected with a live vaccine at 6-8 then at 18 week of age re-vaccinated with an oil-based inactivated vaccine. Birds that are recovered from a natural infection having strong immunity. If at the time of vaccination maternal antibody was still high, immunity in chicks that obtain the live vaccine would be poor.

  1. Department of Pathology, Faculty of veterinary science, University of Agriculture, Faisalabad
  2. Department of Microbiology, Faculty of veterinary science, University of Agriculture, Faisalabad
  3. MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, 210095 Nanjing, P.R.China

Author: Dr. Maria Jamil1, Dr. Kashif Saleemi1, Dr. Ali Raza2, Dr. Muhammad Tahir Aleem3