Inhalation toxicity of cyclooctadiene in rats.

Groups of 20 male Crl:CDBR rats each were exposed, whole-body, for six hours/day, for a total of nine exposures over a two-week period to concentrations of 52, 150, or 500 ppm of 1,5-cyclooctadiene vapor. A control group of 20 male rats was exposed simultaneously to houseline air. Ten rats per group were used for standard toxicological evaluations and ten rats per group for neurotoxicity testing. In the standard toxicology group, at the end of the exposure period, blood and urine samples were collected for clinical analyses, and five rats per group were sacrificed for pathologic examination. After a two-week recovery period, the surviving rats in the standard groups were also given clinical and pathological examinations. The neurotoxicity group was given a functional observational battery (FOB) test and motor activity evaluations after the fourth and ninth exposures. In addition, six of ten neurotoxicity rats per exposure group were given neuropathology evaluations at the end of the exposure period. In rats exposed to 500 ppm of 1,5-cyclooctadiene there was an absence of alerting response toward the end of the daily six-hour exposures. These rats appeared to recover within 1/2 hour after exposure. This effect was not observed in the other test groups. The FOB evaluation showed an increase in the number of rats found sleeping in the 500 and 150 ppm groups compared to controls after the last exposure, but there were no treatment-related effects in the motor activity evaluation. Since there were no other neurobehavioral findings and no toxicity findings in the 150 ppm group, the sleeping behavior in the 150 ppm group was considered insufficient evidence of an adverse effect. Clinical laboratory evaluation of the 500 ppm group showed urinary pH decreases at the end of the exposure period but not after the two-week recovery period. There were no other toxicologically important changes in urine analysis, hematologic, or blood chemistry evaluations attributable to the test compound. Histologic effects were found in the nose and kidneys of rats in the 500 ppm group. There was a mild degeneration/necrosis of nasal olfactory epithelium observed immediately after the exposure period and a mild degeneration/regeneration in this area observed after the two-week recovery. In addition, there were increased kidney weights in the 500 ppm group immediately after exposure along with increased hyaline droplets in the kidneys. These effects were reversible after the two-week recovery period. There were no significant nasal or kidney effects observed in the 150 and 52 ppm test groups, and no other organ weight or histological effects attributable to the test compound observed in the standard toxicology groups at either evaluation time. The neuropathologic evaluation showed only one minor lesion in one 500 ppm-group rat and this was not considered to be attributable to exposure to 1,5-cyclooctadiene. Based on the decreased alerting response observed in rats during exposure at 500 ppm, and on the effects observed in the nose, kidney, and urine in rats at this concentration, the no-observed-adverse-effect (NOAEL) level in this study was considered to be 150 ppm.

Acute sarcocystosis-like disease in a dog.

Two of 8 littermate Rottweiler dogs developed persistent diarrhea at 6.5 weeks of age. Dog 1 was euthanatized at 14 weeks of age and had hepatitis characterized by necrosis and mixed leukocyte infiltrations in association with a previously unrecognized Sarcocystis-like protozoon. The organism was free in the hepatocyte cytoplasm without a parasitophorous vacuole, had divided by schizogony, and stained with anti-Sarcocystis serum, but did not stain with anti-Toxoplasma gondii or anti-Neospora caninum serum in an immunohistochemical test. Dog 2 was euthanatized at 10 weeks of age. This dog had large necrotic, hemorrhagic mesenteric lymph nodes. Numerous T gondii tachyzoites were observed in association with these lesions. The organism divided by endodyogeny and stained specifically with anti-T gondii serum.

Acute canine ehrlichiosis: platelet survival and factor 3 assay.

Ten dogs experimentally inoculated with Ehrlichia canis were thrombocytopenic 14 days after inoculation. Circulating platelet concentrations had declined rapidly by postinoculation day 10, but remained at or slightly below the 14-day concentration during the remainder of the 42-day experimental period. The percentage of circulating megathrombocytes also increased to 8.7 times preinoculation concentrations indicating the existence of accelerated thrombocytopoiesis. The release of platelet factor 3 (PF-3) from normal canine platelets was delayed after incubation of the platelets in globulin fractions from infected dogs. Inhibition of PF-3 release was attributed to the effect of an unidentified substance present only in the dialyzed globulin fraction of infected canine serums. The presence of antiplatelet antibody in these dogs was not evident. Survival of 51Cr-labeled platelets was decreased in infected dogs, but was most abbreviated in infected dogs that were thrombocytopenic when injected with labeled platelets. Thus, accelerated nonantibody-mediated destruction of platelets contributes markedly to the development of thrombocytopenia in dogs with acute ehrlichiosis.

A comparison of several intradermal tuberculins in Macaca mulatta during an epizootic of tuberculosis.

During an epizootic of tuberculosis in rhesus monkeys, several intradermal test reagents were compared for accuracy in detecting tuberculosis and for strength of reaction elicited. A purified protein derivative of Mycobacterium bovis, similar to one which will probably be approved for official veterinary testing and thus eliminate tuberculin-mammalian intradermic from commercial production, was among those evaluated. None of the reagents was found to be superior to tuberculin-mammalian intradermic. Significant difference were not found in reaction strength between abdominal and palpebral test sites, but both together were about 10 per cent more sensitive than either alone. Mycobacterium bovis and Mycobacterium tuberculosis were both cultured and identified from this epizootic.