Homepage

History
Introduction
Molecular
 Characteristics

Pathogenesis
Clinical IBD
Subclinical IBD
Contol of IBD
Worldwide vv IBDV
Variant IBDV

Diagnostics and Prevention

Diagnostic Services
RT/PCR-RFLP
Sample Collection
 
Electrophoresis
RT/PCR
RT/PCR-RFLP

Light Cycler Modern PCR equipment

Penguin-IBDV Collaboration with the UK

Molecular Groups

Publications

 

Pathogenesis of IBDV

Clinical IBD:

In the clinical disease, morbidity can be seen in nearly 100% of the flock and mortality can range from 0% to over 50% with some very virulent IBDV (vvIBDV) strains. Immunosuppression is presumably transient in the clinical disease.

Subclinical IBD:

The subclinical disease occurs when IBDV breaks through maternal immunity. The degree of immunosuppression varies depending on the virulence of the virus strain and when the infection occurs. Immunosuppression is greater the closer the infection occurs to hatch and because the birds are a young age, the immunosuppression caused is permanent. The IBDV strains that cause subclinical disease in the face of robust maternal immunity are usually antigenic mutant forms of the virus. These viruses have been called variants because they vary antigenically from known vaccine strains.

Pathology:

Gross lesions can be seen for the most part on the bursa of Fabricius. The bursa may be swollen, or show signs of hemorrhage. In some cases, however, no lesions are observed and the bursa shrinks in size.

Control of IBD:

Infectious bursal disease virus is endemic throughout the world and is very stable in the environment. The virus is resistant to most disinfectants and thus control is only practical through the use of vaccination. Since it is important to protect chicks during the first weeks of life, breeder flocks are vaccinated so maternal immunity is passed to their progeny. The maternal immunity protects chickens from infection during the critical first two weeks of life when IBDV is capable of causing a permanent immunosuppression.

Maternal immunity does not protect against the clinical form of IBD. Vaccination against the clinical form of the disease is practiced but its success can vary because timing the administration of the vaccine with the waning maternal immunity is difficult. In addition, antigenic variability among wild-type IBDV strains makes it important to select the most antigenically appropriate vaccine.

Worldwide distribution of vvIBDV:

The vvIBDV strains can cause an acute clinical disease characterized by devastating mortality. The Office of International des Epizooties (OIE) estimates that IBD is present in more than 95% of the Member Countries. The acute clinical form of IBD caused by vvIBDV isolates has been observed in over 80% of these countries. It has been reported in Europe, Asia, Africa, South America and Central America. I am not aware of any vvIBDV reports in the United States, Australia or New Zealand.

Worldwide distribution of variant IBDV:

The actual distribution of variant IBDV strains around the world is difficult to ascertain because of the subclinical nature of the disease they cause. These strains may go unreported because an appropriate diagnostic test was not available or the subclinical disease went unnoticed because the acute clinical form of the disease was considered to be an economically more immediate problem. It is clear that antigenic variants of IBDV are widespread in the United States. These viruses have also been identified in Australia, Canada, Central America and South America.