Disseminated coccidioidomycosis in a mandrill baboon (Mandrillus sphinx): a case report.

A case of disseminated coccidioidomycosis caused by a dimorphic fungus Coccidioides immitis in a mandrill baboon (Mandrillus sphinx) was diagnosed following radiography, ultrasound-guided aspiration of thoracic lesions, and aspiration cytology of skeletal lesions of the left sixth rib. The diagnosis was confirmed by fungal culture and serum quantitative immunodiffusion for antibodies against C. immitis.

Hernia en masse.

Described is the case of a patient who developed symptoms compatible with small bowel obstruction approximately 16 hours after a difficult self-performed left inguinal hernia reduction. Exploratory laparotomy was performed, and release of an incarcerated loop of ileum was performed. A large inguinal hernia defect also was found, and this was repaired with a Cooper's ligament repair. The patient recovered uneventfully.

Actinomycin D before and during primary and secondary anti-Forssman immunoglobulin hemolysin responses in rabbits.

The effects of actinomycin D were studied on successive stages of the primary and secondary (anamnestic) anti-Forssman immunoglobulin hemolysin responses induced in rabbits by the antigen, sheep red blood cells. (Fully developed anamnestic reactivity was tested 1.5-2 months after the start of an untreated initial response.) The stages of both responses include induction by antigen, the latent period, the acute rise of hemolysin to peak titer, and the decline afterwards. This antibiotic modified both responses significantly in ways strikingly similar to those produced by large doses of x-rays. It was injected in a sublethal amount (0.08 mg/kg) at selected times before or after a test intravenous injection of 10(8.3) sheep erythrocytes/kg. Given within several days before the antigen, it delayed and depressed peak titer, whereas given during induction and the latent period, it delayed and enhanced peak titer. Given during the acute rise, its effect decreased, and given during the decline after peak titer, it only produced erratic slight rises in titer. It is suggested that delayed and depressed peak titers are associated with both known activities of sublethal doses of actinomycin D, i.e., cytotoxicity and inhibition of RNA synthesis, whereas enhanced peak titers are brought about by the presence of nucleic acid degradation products released by the cytotoxicity of actinomycin D at the critical time of active RNA synthesis in the latent period. Effects of actinomycin D differed quantitatively in the two responses. During the initial response, delayed depression was not apparent as soon and did not last as long, whereas delayed enhancement was more pronounced. In terms of the cells operating in the two responses, the data indicate that immunologically competent initial cells, as compared to memory cells, are more easily stimulated, are not injured as quickly, recover more rapidly, and overcompensate for the injury for a longer time. In addition, in untreated controls, recruitment of immunologically competent initial cells appears to be largely inhibited during induction of memory cells. Otherwise, decline of the secondary response would be less abrupt.