Infectious bursal disease (IBD) emerged in 1957 as a clinical entity responsible for acute morbidity and mortality in broilers on the Delmarva peninsula. The condition spread rapidly and was recognized throughout the U.S. broiler and commercial egg production areas by 1965. Early attempts to isolate the etiologic agent were impeded by a lack of specific-pathogen-free (SPF) eggs and by deficiencies in viral and serologic techniques. By 1967, the highly infectious nature of the agent was recognized. Reliable methods were developed to isolate the virus in embryonated eggs and to adapt it to tissue culture. The agent was characterized as a virus belonging to a new taxonomic group in 1976. The immunosuppressive property of IBD virus was first recognized in 1970 and was confirmed in structured trials in 1976. An early method of control involved planned infection of chickens. This technique lowered IBD mortality but often resulted in immunosuppression and further dissemination of field virus. A live attenuated vaccine was then developed, based on mild field isolates passaged in SPF eggs. This vaccine was federally licensed as the first of its kind for interstate use in 1968. It remains widely used today in breeders as a primer and in the control of very virulent IBD in many countries. The first two decades following emergence of IBD were characterized by close cooperation among scientists in academia, the biologics industry, and the USDA. By 1976, mortality caused by IBD was effectively controlled by vaccination. However, the more subtle effects of immunosuppression and the tremendous economic impact of the disease were just starting to be appreciated. Recognition of Delaware variants in the mid-1980s and emergence of very virulent forms of the condition in Europe and Asia beginning in 1989 attest to the continuing importance of IBD.

The polymerase chain reaction (PCR) technique was applied to the detection of infectious bursal disease virus (IBDV). Reverse transcription followed by the PCR was used to amplify a portion of IBDV genome. A set of primers that specify a 150-base-pair segment of IBDV genome was chosen from an Australian strain of IBDV. Standard challenge strain and variant strains A, D, E, G, and GLS-5 of IBDV serotype 1 and OH strain of serotype 2 from infected bursae were subjected to reverse transcription, followed by 30 cycles of PCR. A single band of the PCR product (DNA) of the expected size from each strain of IBDV was visible on polyacrylamide gels stained with ethidium bromide. Using the same primers, no PCR product was detected from genomic nucleic acids of turkey hemorrhagic enteritis virus, infectious bronchitis virus, reovirus, Salmonella enteritidis, Escherichia coli, and uninfected bursae. The PCR could be efficiently performed on serially diluted IBDV RNA and could detect 2 femtograms of IBDV RNA. The identity of the PCR products was confirmed by direct sequencing. The PCR is a specific and sensitive method for the detection of IBDV.

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In two experiments primary and secondary hemagglutination titers of chickens were determined in response to intravenous injections of 1 mL of a 5% suspension of sheep red blood cells (SRBC). All birds received the primary injection at 4 wk of age. In the first experiment, equal numbers of male and female birds were randomly selected to receive the secondary injection at 2, 4, 6, and 8 wk following the initial injection. Based on the level of IgG antibody to SRBC, all postprimary injections affected an anamnestic response. Furthermore, the anamnestic response obtained following the 6 and 8-wk postprimary injection was significantly higher than those obtained with injections 2 or 4 wk after the primary injection. In the second experiment, secondary injections were administered either 3 or 6 wk after the primary injections. The anamnestic response of birds receiving the 6-wk postprimary injection was higher than those injected 3-wk after the primary injections.

Viruses from three commercially available modified-live infectious bursal disease virus vaccines were propagated in tissue culture. Following this, a series of 32P-labeled probes was generated using the entire RNA genome as template for formation of randomly primed cDNAs. These probes were tested against dot blots of the three vaccine strains, as well as the USDA standard challenge strain and one field-origin strain. Dot blots were made of both crude tissue extract and LiCl-precipitated RNA genome. All three probes detected the standard challenge and field strains. Although differences in probe binding could be quantified among the strains, cross-hybridization indicated considerable homology within genomic regions preferentially transcribed under the experimental conditions.