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The results of an overview of early (90-240 min) and late (24 hours or more) patency and of stroke rates for each of the three commercially available thrombolytic agents, streptokinase, alteplase, and anistreplase are presented. Studies included in this analysis are all those published between 1985 and March 1992 and focus on the licensed dosage regimens of each agent. The rates of early and late patency for streptokinase were 64.7% and 80.8%; for alteplase, 66.6% and 73.7%; and for anistreplase, 72.1% and 84.5%. The rates of total and hemorrhagic stroke for streptokinase were 0.69% and 0.17%; for alteplase, 1.27% and 0.50%; and for anistreplase 0.91% and 0.38%. These results provided evidence that the rates of early and late patency appeared to be greatest for anistreplase and that the rates of stroke are within "acceptable" ranges for all three thrombolytic agents with streptokinase affording the lowest rate.

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The development of a double-well ELISA test for the detection of turkey rhinotracheitis (TRT) virus antibody in turkey and chicken sera, utilising a streptavidin-biotin detection protocol is described. This test was compared with a conventional ELISA, which detects antibody using a peroxidase-labelled anti-turkey IgG. The double-well streptavidin-biotin ELISA was more sensitive than the conventional ELISA, and, due to the consistently low background values obtained, was further modified to a single-well ELISA test. Antibody titres obtained using the single-well streptavidin-biotin ELISA were similar to those obtained using the conventional ELISA. A microtitre serum neutralisation test for TRT virus read using an indirect immunoperoxidase (IIP) detection protocol after 48 h was also developed and compared to the standard neutralisation test employing a 7 day incubation and read by CPE. The specificity of the single-well streptavidin-biotin ELISA was confirmed using the rapid (IIP) serum neutralisation test.

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Sera from a flock of naturally infected commercial turkeys were tested for antibodies against turkey rhinotracheitis virus using an indirect immunofluorescence test with infected turkey embryo tracheal organ cultures, a serum neutralisation test using chick embryo fibro-blasts or liver cells and an ELISA. Antibodies were detected by all tests within 5 days of the appearance of clinical respiratory disease. Serum neutralising antibodies detected in chick embryo fibroblasts rapidly achieved their peak titres and were decreasing by day 13. ELISA antibodies peaked on day 13. On days 13 and 34 significant correlations were obtained for immunofluorescence and ELISA and for ELISA and microneutralisation in fibroblasts. For both the latter tests there was a good correlation between the results obtained for individual birds within the flock on days 13 and 34. ELISA and serum neutralisation in chick embryo fibroblast monolayers would appear to be sensitive and reliable tests for detecting circulating antibodies against turkey rhinotracheitis virus in commercial flocks.

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Twenty-four laying turkey hens shown to be free of antibodies to turkey rhinotracheitis virus were inoculated intranasally with an isolate of the virus. A mild respiratory disease developed between 5 and 9 days post infection (pi). Two birds were selected at random at intervals between days 1 and 20 pi, killed and tissues examined for the presence of virus. At autopsy between days 2 and 12 abnormalities were found in the oviducts including the deposition of inspissated albumen. Yolk material was occasionally found in the abdominal cavity and there was one instance of egg peritonitis. Eggs with abnormal shells were found in the uterus on days 3 and 9. By direct immunofluorescence (IF) staining, virus was detected in the trachea between days 1 and 7 pi and in the turbinates between days 2 and 5 pi. Virus could also be isolated from these sites using turkey embryo tracheal organ cultures but this method was slightly less sensitive than IF for these tissues. No virus was demonstrated in the lungs or air sacs. Viral antigens were detected by IF in the epithelium of the uterus on day 7 pi and in this and all other regions of the oviduct on day 9 pi. Virus was isolated only from middle magnum and vagina on day 9 pi. On other occasions up to 20 days pi the above tissues and spleen, ovary, liver, kidney and hypothalamus were all negative for virus. Antibodies detected by ELISA and serum neutralisation both reached, high titre by 12 days pi and were maintained at a high level (Iog2 12-15) throughout the period of observation (89 days).

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An inactivated Salmonella hadar vaccine was administered to parent turkey stock and the progeny were subjected to challenge with S hadar. There was some evidence that eggs from vaccinated birds were more resistant to growth of the organism. When compared with similarly infected poults from unvaccinated parents, a markedly different serological picture and pattern of salmonella excretion was seen. It appeared that the passive immunity induced by the vaccine encouraged the faster establishment of other gut Enterobacteriacae, even in the presence of large numbers of S hadar.

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