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Fourteen laboratories participated in a collaborative study of a freeze-dried preparation of anti-infectious bursal disease virus serum to assess the suitability of the serum as a standard for use in the infectious bursal disease virus neutralization test. Ten laboratories carried out micro-virus neutralization tests and six carried out plaque reduction tests, two laboratories carrying out both tests. When titres were expressed as a proportion of that obtained for a reference preparation there was a marked reduction in variation between results from different laboratories. The use of a reference preparation was therefore of value when comparing results from different laboratories. It is proposed that the reference preparation used in this study be used as a standard to facilitate the comparison of results from different laboratories. The proposed standard contains by definition 10,000 UK units.

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Three inactivated porcine parvovirus vaccines were tested for efficacy in 66 susceptible gilts. The gilts were challenged with virulent virus on the 40th day of gestation. All the vaccines provided excellent protection against fetal mortality despite insignificant serological responses to one of them. Good protection was obtained with two of the vaccines even when the dose was substantially reduced. Unvaccinated controls had very few viable fetuses.

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Avian reovirus vaccines of the S1133 strain, used indirectly in the dams of challenged chicks, were found to confer protection against clinical signs and/or deaths resulting from the use of both homologous and heterologous challenge strains. There was some protection against every strain used, although this did vary in degree. It was difficult to relate this variation in protection to the differences in in vitro neutralization of the strains by S1133 antiserum, though there were some similarities.

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A live infectious bursal disease virus vaccine increased in virulence when passaged six times in susceptible birds, as judged by damage to the bursa of Fabricius. It is suggested that the increase in virulence of this vaccine was due to the selection of a virulent subpopulation which had been present in the vaccine since its original isolation from the field and which had not been eliminated during its attenuation by passage in cell culture. The vaccine was then plaque purified and a virus strain was selected which protected against challenge, did not damage the bursa and appeared not to passage in birds.

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Four different oil emulsion infectious bursal disease virus (IBDV) vaccines were inoculated into four-week-old specific pathogen-free chickens. At weekly intervals for five weeks, sera were obtained from the vaccinated birds and from uninoculated control birds and examined for antibodies against IBDV by enzyme-linked immunosorbent assay (ELISA), the quantitative agar gel precipitin (QAGP) test and the virus neutralisation (VN) test. There was a highly significant correlation between the mean responses to all tests; the highest correlation (0.818) was between VN and QAGP and the lowest (0.573) between QAGP and ELISA. Generally the ELISA detected positive sera earlier than the VN test which in turn was more sensitive than the QAGP test. The ELISA and QAGP test were less variable, more reproducible and easier to perform than the VN test.

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Two chicken flocks, vaccinated with different inactivated infectious bursal disease vaccines, and one unvaccinated flock provided chicks with high and low levels of and no maternally derived immunity. Following challenge at three ages with a subclinical strain of infectious bursal disease virus the chicks were assessed for bursal damage and suppression of the immune response to Newcastle disease virus. Both high and low levels of maternally derived antibody prevented immunosuppression but the lower level provided only partial protection against bursal damage.

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The depression of response of Brucella abortus strain 19 caused by an infectious bursal disease vaccine virus given to chicks at one day old was shown to persist for four weeks. Histological examination of the bursa of Fabricius showed a gradual repopulation by bursal lymphocytes, after initial damage, concomitant with the development of a humoral response.

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An experiment was performed to determine the results of the interaction of a mild infectious bursal disease vaccine and two different levels of maternal antibody in chicks, at various ages after hatching, as judged by protection against challenge with virulent infectious bursal disease virus. Maternal antibody of both high and low initial levels prevented effective vaccination at 1 and 14 days of age but by 28 days of age the vaccine was effective in birds of both initial antibody levels. Only the high initial level of antibody showed itself to be protective against all of the effects of challenge, while the low level, though it reduced or eliminated deaths, was unable to prevent bursal lesions and acted as a hindrance to vaccination. There was no evidence that vaccination significantly reduced the protective effects of maternal antibody.

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Two infectious bursal disease vaccines were administered to separate groups of maternally immune and susceptible chickens at various ages. Vaccine B caused no damage to the bursae of chickens examined histologically at nine and 20 days after vaccination. The bursae of chickens given vaccine A were shown to be severely damaged when similarly examined. Both vaccines protected all the susceptible groups against challenge, but only vaccine A protected the groups of maternally immune chickens. Susceptible chickens vaccinated at one day of age with vaccine A showed a lowered response to Hitchner B1 Newcastle disease vaccine given at 14 days of age, judged by the haemagglutination-inhibition response and Newcastle disease challenge. The performance of the Newcastle disease vaccine was not affected in chickens given vaccine B. Bedding used by birds given vaccine A was shown to be capable of transmitting vaccinal virus to susceptible chickens, causing severe bursal damage.

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Two freeze dried turkey herpes virus vaccines A and C, of similar virus content were administered in graded doses to groups of day old chicks which were genetically susceptible to Marek's disease. Immediately after vaccination the chicks were challenged by contact with 4-weeks-old birds that had been infected at one day of age with virulent Marek's disease virus strain HPRS 16. Assessment of protection against Marek's disease was based on the absence of gross lesions after a 15 week observation period and a significant difference in the protective capacity of the 2 products was found. From the relationship between protection and vaccine dose that was obtained with vaccine C it was calculated that 0.48 of a field dose protected 50% of the birds. Vaccine A provided no significant protection at any dose level. Isolation of vaccinal virus 3 weeks after administration of graded doses of vaccines A and B revealed that a significantly higher dose of vaccine A was required to produce viraemia in vaccinated birds. Determination of viraemia at intervals following inoculation of one field dose of the vaccines demonstrated that Vaccine A also induced a less rapid response than the other 2 vaccines. These effects were not related to the virus content of the vaccines.

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