Delayed cutaneous hypersensitivity response in tetanus toxoid sensitized rhesus monkeys: predictor of anergy and value in tuberculin skin testing.

The primary problem in using the tuberculin skin test in nonhuman primates is the clinical uncertainty concerning the animal's ability to elicit a delayed cutaneous hypersensitivity response. A negative tuberculin skin test can only be meaningful if the animal can produce a delayed cutaneous hypersensitivity reaction. Veterinarians deliberately sensitize animals to antigens in the form of prophylactic vaccination. Therefore, if nonhuman primates were deliberately sensitized to an antigen capable of producing a hypersensitivity response, that antigen should serve as a positive control for delayed cutaneous hypersensitivity reactions. Tetanus toxoid was chosen because repeated immunizations with this antigen is recommended routine medical practice for nonhuman primates housed outdoors. Twenty juvenile, male rhesus (Macaca mulatta) monkeys were selected for this study. The monkeys were assigned randomly to one of two groups of ten animals. The test group was vaccinated with tetanus toxoid intramuscularly at 1 month intervals for a total of three vaccinations. The control group was treated the same except saline was administered rather than tetanus toxoid. Following sensitization, the two groups of animals were challenged with tetanus toxoid intradermally. Eight of the ten monkeys in the test group responded to the tetanus toxoid while none of the control groups responded to the tetanus toxoid. Elicitation of a delayed cutaneous response in animals sensitized to tetanus antigen before challenge may serve as a positive control for delayed cutaneous hypersensitivity. This simple test may serve as a useful adjunct in making objective clinical decisions concerning anergy-suspect animals.

Antigenic variation of wild and vaccine rabies strains of Egypt.

Nineteen street rabies virus strains, isolated in Egypt from humans (two), dogs (nine), cats (two), farm animals (two), gerbils (three), and a jackal were antigenically analyzed. The Pasteur strain used for the preparation of human rabies vaccine, the Flury high and low egg passage stains (HEP, LEP) used for animal vaccines, and the challenge virus standard (CVS) strain were also assayed. All were examined by the indirect fluorescent antibody test, using a panel of 20 monoclonal antibodies against the nucleocapsid of rabies and rabies-related viruses. The rabies isolates demonstrated patterns of reactivity with the antinucleocapsid panel different from those of the Pasteur, HEP, and CVS strains. Representative human, dog, and rodent isolates were analyzed by neutralization tests in mice, with a second panel of 19 monoclonal antibodies against rabies and Mokola envelope glycoproteins. With this panel, the isolates demonstrated patterns of reactivity different from the vaccine strains. These data indicate antigenic variation between wild virus and vaccine strains.

Seasonal and sexual influences on rabbit atropinesterase.

Atropinesterase was found in 61.17% of 6686 New Zealand White rabbits of both sexes studied over 2.5 years. Significantly more males possessed the enzyme, there was a significant difference in atropinesterase frequencies in males versus females in the winter and summer seasons, and a significant decrease in the frequency of atropinesterase-positive females during the winter.

In vivo detection of rabbit atropinesterase.

The comparability of an in vivo rapid screening test for the presence of atropinesterase with an in vitro standard colorimetric test was assessed using 410 male and female New Zealand white rabbits. The results from both tests were in agreement in 405 of the 410 (98.8%) rabbits compared. One false negative and four false positive results occurred with the rapid screening test.

A genetic study of canine hip dysplasia.

Using scores taken from pelvic radiographs of 1,186 German Shepherd Dogs, heritability estimates of canine hip dysplasia (CHD) were obtained. As measured by either of 2 scores defined, CHD was found to be 22.0% heritable. In this colony, CHD was a moderately heritable condition. To make progress in selecting against CHD, use of the progeny test to identify superior replacement breeders was stressed.