A Brief Overview of Infectious Bursal Disease in Poultry
Neeteesh Kumar1, D.Niyogi2 , D.P. Srivastava3 , K.K.Tripathi4 ,Vibha Yadav5 ,Arunima singh6 ,Akshit Tyagi6
1PhD Scholar, Department of Veterinary Pathology
- Professor & Head, Department of Veterinary Pathology
- SMS ,KVK PG College Ghazipur
- Assistant Professor, Department of Veterinary Pathology
- Assistant Professor, Department of Veterinary Microbiology
- PG Scholar, Department of Veterinary Pathology
College of Veterinary Science & Animal Husbandry, A.N.D.U.A.T., Kumarganj, Ayodhya, U.P. – 224229
Corresponding author email: dr.dpsrivastava56@gmail.com
Introduction
Infectious bursal disease, caused by the infectious bursal disease virus (IBDV), affects young domestic hens all over the world. Symptoms include listlessness, watery diarrhea, ruffled feathers, and dehydration. The morbidity rate is high, and the fatality rate is typically low, although some virulent strains cause mortality rates of 60% or greater. Diagnostic methods include macroscopic and microscopic lesions in the cloacal bursa, as well as molecular detection of the viral genome. Vectored and attenuated live virus vaccines can be used to stimulate active immunity in chicks when maternal antibodies decline. Infectious bursal disease (IBDV) is a viral infection that affects young domestic chickens all over the world. Listlessness, watery diarrhoea, ruffled feathers, and dehydration are among the clinical indicators. The morbidity rate and mortality rate are both high.
History
Infectious bursal illness afflicts young domestic hens globally. Classical strains reigned until the introduction of mutant IBDV strains in 1986. The vvIBDV strains were discovered in Europe in 1989 and spread to the Middle East, Asia, and Africa. They were discovered in South and Central America in 1999 and in the United States in 2009. Infectious bursal disease is very infectious. IBDV is shed in feces and spread from house to house by fomites. Variant IBDV strains usually induce subclinical infection in chickens, but some layer chicken breeds may have low mortality rates (< 10%). Classical IBDV strains can generate clinical indications of disease and moderate mortality rates (< 40%), but vvIBDV strains can result in high mortality rates (> 60%). The flock morbidity rate is normally 100%, while the mortality rate can range from 5% to more than 60%, depending on the virus strain and chicken breed. Layer breeds tend to have greater mortality rates than broiler chickens. Chickens are most vulnerable to clinical illness between 3-6 weeks, when immature B lymphocytes dominate the bursa and maternal immunity has decreased. However, serious illnesses have been seen in Leghorn chicks as young as 18 weeks. In clinical infections, illness onset occurs after a 3- to 4-day incubation period.
Etiology
The infectious bursal disease virus (IBDV), a double-stranded RNA virus (Avibirnavirus gumboroense) from the Birnaviridae family, causes infectious bursal disease. IBDV virions, like other birnaviruses, are not enclosed and have an icosahedral, single-shelled shape.
Two IBDV serotypes have been reported. Serotype 1 viruses infect hens, and there can be antigenic diversity across strains. Antigenic drift is mostly responsible for this antigenic diversity, but antigenic variations can also emerge via genome homologous recombination. Serotype 1 field strains exhibit wide ranges of virulence.
Virus strains can be classified according to their phenotype as subclinical, classically virulent, or extremely virulent (vv). They can also be classified based on the antigenicity of the hypervariable region of viral protein 2 (VP2) as classical.
Immunosuppression is directly related to the loss of B cells; however, immunosuppression and related secondary infections are common in birds that recover from the illness. The severity of immunosuppression is determined by the virulence of the infecting virus and the age of the host.
Clinical Finding
Depending on the IBDV strain and maternal immunity, infectious bursal illness in young chicks might be symptomatic or subclinical. Infection results are determined by the chicken’s age and breed, as well as the virus’s virulence. Infections that occur before the age of three weeks are typically asymptomatic.
Fig 1: Shows Hemorrhagic bursitis in IBD infected birds
All pathogenic IBDVs generate lesions in the cloacal bursa (Fabricius bursa) in both clinical and subclinical illness states.
Initially subclinical illnesses are the most important manifestation of the disease in terms of economic damage. They produce severe, long-lasting immunosuppression by destroying immature cells in the cloacal bursa, thymus, and spleen.
The humoral (B cell) immune response is the most significantly impacted, while the cell-mediated (T cell) immunological response is damaged less severely.
After a 3-4 day incubation period, clinical symptoms may include: Severe prostration and incoord ination.
Symptoms may include watery diarrhea, soiled vent feathers, vent picking, and cloacal irritation.
Recovery takes <1 week, and broiler weight gain is delayed by 3-5 days. The existence of maternal antibodies affects the disease’s clinical progression.
Lesions
The lesions found after necropsy will vary depending on the strain of IBDV.
For strains that cause disease, the cloacal bursa becomes edematous and has a yellowish transudate on the surface. Hemorrhages on the serosal and mucosal surfaces are occasionally seen.
Strains of vvIBDV induce comparable cloacal bursa lesions, as well as congestion and bleeding in the pectoral and leg muscles. Some IBDV strains can produce cloacal bursa atrophy in the absence of visible symptoms.
Chickens that have survived from IBDV infections have tiny, atrophied cloacal bursas as a result of bursal follicle destruction and failure to regenerate.
Diagnosis
- Historical background.
- Finding macroscopic and microscopic lesions in the cloacal bursa.
- Detection of IBDV RNA
- Isolating IBDV viras RNA.
The presence of macroscopic lesions in the cloacal bursa is used to make an initial diagnosis of infectious bursal illness. The bursa is then examined under a microscope to look for lymphocyte depletion in the follicles.
Molecular methods of diagnosis are most commonly employed to detect IBDV in diagnostic samples. IBDV is most commonly isolated from the cloacal bursa; however, it can also be isolated from other organs. The RT-PCR test is utilized to detect the viral genome in cloacal bursa tissue.
Genomic alignment and phylogenetic studies of the VP2 coding region were utilized to further classify the viruses into genogroups. For molecular diagnostic tests, samples are often taken after maternal antibodies have decreased.
IBDV can be isolated from 8- to 11-day-old IBDV antibody-free chicken embryos that have been inoculated with diseased birds. The chorioallantoic membrane is more vulnerable to infection than the allantoic sac.
Some IBDV strains can also be isolated from cell cultures, including chicken embryo fibroblasts, cloacal bursa cells, and established avian and mammalian cell lines.
IBDV strains tailored for cell culture exhibit a cytopathic effect and can be used for viral titration and neutralization experiments.
IBDV antibodies can be detected in convalescent chicks by serologic testing. To quantify IBDV antibodies, commercially available ELISA kits are commonly utilized.
Treatment and Controle
Infectious bursal illness has no known cure. Therefore, control and prevention are crucial.
Rigorous cleaning of polluted farmland after depopulation has had poor success. IBDV is highly stable in the environment and difficult to eliminate from buildings.
Live, attenuated virus vaccines derived from chicken embryos or cell cultures with varying low pathogenicity can be administered via eye drop, drinking water, or SC routes at 1-21 days of age. Maternal antibodies can affect vaccine replication and consequently immunological response, but more virulent vaccine strains can override larger quantities of maternal antibody.
Vectored vaccines expressing the IBDV VP2 protein in the herpesvirus of turkeys (HVT) can be given in ovo or at hatch. These vaccinations are unaffected by maternal antibodies. Vaccinations containing live, attenuated viruses bound to antibodies (immune-complex vaccinations) are also available for in ovo or hatch injection.
High levels of maternal antibody during early brooding of chicks in broiler flocks (and in some commercial layer farms) can reduce early infection, subsequent immunosuppressive effects, or both.
Breeder flocks should be immunized one or more times during the growth season, once with a live, attenuated virus vaccine and again right before egg production with an oil-adjuvanted, inactivated vaccine.
Inactivated vaccines derived from chicken embryos, bursas, or cell cultures are available.
The latter vaccinations produce greater, more consistent, and longer-lasting antibody concentrations than live, attenuated virus vaccines.Breeder flocks’ immunological state should be checked on a regular basis using a quantitative serologic test such as viral neutralization or ELISA. If antibody levels fall, chickens should be revaccinated to provide appropriate immunity to their offspring.
Vaccination campaigns should try to use vaccines that closely match the field viruses’ antigenic profiles. Diagnostic testing for field strain genetic sequences can help determine the best immunization strategy.
Conclusion
IBD is one of the most prevalent immunosuppressive illnesses in the poultry sector. Despite the fact that the existing IBDV LAV against classical strains works effectively in many cases, the introduction of novel antigenic variation, pathogenic reassortants, and highly virulent strains, which are unaffected by classical vaccination strain-elicited immunity, is posing new issues [46, 47, 48]. The poultry sector urgently requires the development of IBDV-LAV against antigenic variants and highly virulent strains.
Key Points
Infectious bursal disease,caused by a virus, affects young chickens worldwide.
IBDVattacks immature B cells and suppresses immunity, resulting in subsequent infections in convalescent birds.
Aclinical examination of the cloacal bursa and molecular identification of the viral genome are used for diagnosis.
Vaccination of breeder flocks induces maternal immunity in young chicks for control.
