Infectious Bursal Disease is a widely prevalent contagious viral disease occuring in brooding and growing stage of chickens causing significant morbidity and low mortality rate. There is initial enlargement of bursa of Fabricius followed by atrophy (regression).
Distribution
Infectious Bursal Disease is prevalent in almost all the states of the country. In West Bengal and Orissa the outbreak has occured with significant toll to the broiler birds. Tamil Nadu and Andhra Pradesh have suffered a lot for this devastating disease. It usually occurs in birds having the age group of 3-6 weeks. In India, the disease was first reported by Mohanty (1971). Jayaramaih and Malik (1974) made isolation and characterization of the virus. The disease in now occuring in very virulent form causing high mortality. Some farms in Maharashtra suffered initially with very virulent Infectious Bursal Disease problem. Subsequently, the virulent form could be noticed in other states of the country. Ajinkya (1980) reported heavy mortality due to RD in association with Infectious Bursal Disease in broiler chicks in Maharashtra. Precipitation of latent infections like aplastic anaemia, gangrenous dermatitis and inclusion body hepatitis have been recorded. The sero-prevalence of the disease has been reported in different states of India where the disease existed as subclinical or inapparent form.
The very virulent form of the disease with 40 to 70% mortality along with very virulent Newcastle disease has been found to occur from West Bengal to Orissa; Vishakhapatanam, Hydrabad-Chittor-Nellore of Andhra Pradesh and Namakkal of Tamil Nadu. It has also been spread to Maharashtra, Karnataka including Gujarat and Madhya Pradesh.
Aetiology
The disease is caused by double stranded RNA virus. About three serotypes have been identified. The virus can be propagated in chorio-allantoic membrane. The virus can be isolated in cloacal bursal cell culture. Cell culture adapted strains cause cytopathic effects. There is significant variation between strains of the virus.
The virus is resistant to ether, chloroform and common antibiotics, but can be inactivated by 1% solution of formalin or cresol within one hour.
Susceptible Hosts
Young chicks of 2-9 weeks of age are most susceptible. Both broilers and layers may suffer. Outbreak has been recorded in artificially reared pheasants. Guinea fowls, quails and pigeons are resistant to natural infection.
Mode of Transmission
The virus is very stable and difficult to remove from the poultry houses. It is discharged through the faeces and is spread from poultry shed by fomites. The virus is very much contagious in nature and transmitted through direct contact. The infection may spread from contaminated environment. The infected poultry shed may remain infective for 122 days even after removal of the infected birds. The virus may remain alive for around 6 months in dry litter and for more than a year in unused dry poultry sheds. The disease occurs more in commercial farms and remains prevalent throughout the year.
Pathogenesis
The virus exerts lymphocidal action and thus distorts and destroys the immune system. The recovered birds remain immuno-suppressed and they have very poor response to vaccine.
The virus causes severe long lasting immuno depression. This depression is due to destruction of immature lymphocytes in the cloacal bursa, thymus and spleen. The humoral (B-cell) response is grossly affected although cell mediated (T-cell) response is also appreciably reduced.
Immuno suppressed birds show very poor response against vaccine like Ranikhet disease, Infectious bronchitis, Inclusion body hepatitis and Marek’s disease.
Affected and recovered birds are more prone to get infected with other infectious agents. Concommitment infections with Ranikhet disease, infectious laryngotracheitis, infectious bronchitis, Marek’s disease, E. coli, Salmonellosis, coccidiosis, anaemia, gangrenous dermatitis, IBH have been recorded.
Very virulent infectious bursal disease has been found to be associated with Ranikhet disease and inclusion body hepatitis. Aflatoxin in feed has been found to be responsible for suppressing immunity right from first week of age in chicks resulting in poor uptake of Infectious Bursal Disease vaccinations. Faulty brooding temperature especially in severe winter lead severe stress on flocks immune response resulting in increased Infectious Bursal Disease problem.
Clinical Findings
The presence of maternal antibody and age interfere with manifestation of clinical signs.
The infections may be divided into two types.
(i) Sub-clinical infections: Here the clinical manifestations are less obvious. But, the birds remain dull and depressed. Birds less than 3 weeks of age remain in such form. The morbidity rate is more but mortality is less. But, there is possibility of mortality even upto 100% when the predisposing factors, infections with other pathogens. This form is very much important to the flock raisers from economic stand point.
(ii) Clinical infections: Birds show severe depression, incoordination, watery diarrhoea, soiled vent feathers, vent picking and cloacitis. Mortality ranges from 20% to 30%. There is retardation of body weight and there is recovery within a week. Concurrent infections alter the clinical manifestations. Maternal antibody may also deviate the cause of the disease.
Recently, VVIBD has been recorded. Affected birds showed the signs of dullness and ruffled feathers with prostration and emitting creamy coloured faeces. The mortality pattern during the course of 5-7 days average 50-150-500-200-50-25-5 (from first to seventh day) in an Hock of 1000 to 2000 birds. This type of mortality is ascribed as Classical SPIKE MORTALITY OF VVIBD.
Treatment
There is no effective treatment. Symptomatic treatment against liver and kidney disorders may be attempted. Signs of dehydration should be checked by hydration therapy with oral fluid and electrolytes. Attempt should be made to stimulate immunity. For this drugs like E care SE Zeetress, Stress rouk and vitamins like A, E, C may be tried.
Control
- Strict hygienic and sanitation measures are to be adopted i.e. biosecurity and farm disinfection.
- Visitors should be discouraged to enter the farm.
- Thorough disinfection of personnel should be made. They should use separate farm overall clothing.
- Layers and broilers are to be reared in separate cage. They should no be kept in close viscinity.
- Depopulation of affected birds should be made.
- All the poultry equipments should be sterilized.
- All the dead birds should be disposed by burning.
- Droppings should be removed and treated with formalin before discarding.
- The house should be disinfected or fumigated before introduction of new batch of chicks. Complete disinfection should be made including roof, walls, flooring. For this, Idophore compound e.g. Safegaurd, Polysan, Formaldehyde, Gluteral dehyde e.g. Attak, Kohrsolin, VIrkons may be used. This disinfection should be made between chick replacement and during attack.
- Lime/washing soda in foot baths and infected premi9ses is to be arranges.
- Transportation van, Empty feeders, gunny bags, egg trays are to be disinfected.
- Proper disposal of litter between chick replacement period and during outbreak is to be done to control spreading of infection.
Vaccine
Broiler flocks should possess high level of parenteral antibody to sustain the initial phase of life. Breeder flocks should be vaccinated during growth period by live vaccine and be revaccinated before egg laying with inactivated vaccine.
Commercial vaccines are available in the form of (a) Lukert type strain vaccine (b) Intermediate type strain vaccine (c) Inactivated vaccine.
