Infectious Bursal Disease (IBD)

Infectious Bursal Disease (IBD) is also known as Gumboro disease, Avian bursitis and Infectious nephritis.

Infectious Bursal Disease (IBD) is an acute highly contagious viral disease of young chicken that affect lymphoid tissue primarily bursa of fabricius characterized by high mortality in chicks and prolonged immuno-supression.

Etiology

• Infectious Bursal Disease (IBD) is caused by an infectious bursal disease virus genus Avibirnavirus a member of the family Birnaviridae.  It is a non enveloped double stranded segmented RNA virus. It is very stable in an environment and difficult to eradicate from premises. The severity of infection is depends on age, breed of chicken and virulence of virus.
• The virus contains two segments A and B. The segment A encodes viral structural proteins VP2, VP3, VP4 and VP5. The VP2 elicits neutralizing antibody response. The segment B encodes VP1-involved in replication and transcription of virus and thus playing some role in the virulence of the virus. The strains of IBDV are Variant, classical and very virulent strain.

Epidemiology

• Infectious Bursal Disease (IBD) was first recognized as a specific disease entity by cosgrove in 1962 and was referred to as avian nephrosis because of extreme kidney damage succumb to infection.
• The first outbreak occurred in the area of Gumboro, Delaware, so it is called as Gumboro disease.
• In India this disease was first reported by Mohanty etal (1971) in Uttar Pradesh.
• Chicken are the only natural hosts for the virus in which natural infection occurs.
• All breeds are susceptible but, white leghorns breeds are more susceptible than other breeds.
• Variant IBDV induce little mortality with marked bursal lesions.
• Classical IBDV- induce-10-15 % mortality.
• Very virulent infectious bursal disease virus (vvIBDV) induce approximately 50-100% mortality.

Source of infection

• The virus shed in faeces of infected bird.

Transmission

• Ingestion of contaminated feed and water  with faeces of infected birds.
• Fomite transfer from infected shed to non infected shed.

Clinical manifestation

• Infectious Bursal Disease (IBD) occur as subclinical and clinical infection.
• Subclinical infection occur in less than 3 weeks of age.
• Clinical infection occur at 3-6 weeks of age, but severe infection occurred in white leghorn chicken upto 18 weeks old.
• Early subclinical infection is most important than clinical infection.
• Subclinical infection causes severe long lasting immunosuppression due to destruction of  immature lymphocytes in bursa of fabricius, thymus, spleen and atrophy of bursa.
• The humoral (B cell) immune response is severely affected and cell mediated (T cell) immune response  also affected to lesser extent, then bird become immunocompromised  and highly susceptible to other infection.

Clinical infection

• Incubation period is 2-3 days after exposure to virus.
• Chickens exhibit severe prostration, incordination, whitish or  watery diarrhoea, soiled vent feathers, vent picking and inflammation of the cloaca, anorexia, depression, ruffled feathers, trembling and death.
• Affected birds became dehydrated and subnormal temperature in terminal stages.
• Recovery occur within one week.
• Morbidity 100%, mortality 20-30%.

Necropsy Finding

• Bursa is highly enlarged twice or 2-4 times of its normal size after 3 days of infection. The affected bursa is swollen, edematous yellowish in colour and occasionally have haemorrhage.
• Haemorrhage at the junction of proventriculus and gizzard.
• Congestion and haemorrhage of the pectoral, thigh and leg muscle.
• Recovered bird has small atrophied cloacal bursa due to destruction and lack of bursal follicle after 12^th day of infection.

Diagnosis

• Based on clinical signs and lesions.
• Isolation by virus in embryonated chicken egg by  inoculation into chorioallantoic route.
• Isolation of virus in cell culture (cells from cloacal bursa) or chicken embryo fibroblast.
• The ELISA is most commonly used for evaluation of antibodies in serum. ELISA does not differentiate between antibodies to serotype1 and serotype 2.
• Virus neutralization test is used to identify antibodies to different serotype of IBDV.
• Quantitative agar gel precipitation test used for detection of antibodies in serum.

Differential diagnosis

• Coccidiosis
• Nephropathogenic strain of IBV
• Water deprivation syndrome

Treatment

• No therapeutic or supportive treatment has been found to change the course of the disease.

Prevention and Control

• Rigorous disinfection of contaminated farms after depopulation.
• Live vaccine of chicken embryo or cell culture origin (low pathogenic  virus) can be given through eye drops or drinking water route at  1-21 days of age.
• Breeder flocks should be vaccinated one or more times during growing period, first with live vaccine and again before egg production with oil adjuvanted inactivated vaccine. Which induce more uniform and persistent level of antibody than live vaccine.
• The immune status of breeder flocks should be monitored by periodical testing of flock with VNT and ELISA.
• Revaccination is followed to maintain adequate immunity to progeny, when antibody level is fall  down.
• IBD subunit vaccine has been attempted mainly from baculovirus. A baculovirus expressed recombinant VP2 protein has been used commercially in broiler breeds, and immunity transferred to their progeny.