No abstract

A lethal enterocolitis was induced in hamsters by oral or parenteral administration of clindamycin in amounts comparable to those used in treatment of humans. The intestinal lesions were characterized histologically as an acute inflammatory reaction with pseudomembrane formation and resembled the lesions seen in humans with antibiotic-induced colitis. Results of quantitative stool cultures showed the numbers of Peptostreptococcus and Corynebacterium decreased in animals with colitis after challenge with 100 mg of clindamycin/kg, while numbers of Escherichia coli, Streptococcus faecalis, and clindamycin-resistant Clostridium sordellii and Clostridium difficile increased. Bacteria were not seen within the intestinal lesions. Viruses were not isolated from hamsters with colitis. Although the pathogenesis of this syndrome is not completely established, the evidence is consistent with the hypothesis that the disease is caused by clostridial toxins and that the production of these toxins by organisms within the intestines is enhanced by the effects of clindamycin upon the bowel flora.

Forty-four neoplasms were found at necropsy in 115 gerbils from a colony of wild-caught, and first- or second-generation laboratory-raised gerbils. Ten species of gerbils varying from 24 to 61 months of age were affected. The neoplasms occurred in 18 primary locations and included nine neoplasms previously unreported in gerbils. Unusual neoplasms included several squamous cell carcinomas of middle ear, squamous cell carcinoma of ventral marking gland, and Hodgkin's-like lymphoma. Neoplasms were a significant cause of morbidity and mortality in these aging animals.

The significance of fever in response to a bacterial infection has been investigated using the lizard Dipsosaurus dorsalis as an animal model. These lizards develop a fever of about 2°C after injection with the bacterium Aeromonas hydrophila . To determine whether this elevation in body temperature increases the resistance of the host to this infection, as measured by survival, lizards were infected with the live bacteria and placed in a neutral (38°C), low (34° or 36°C), or high (40° or 42°C) ambient temperature. An elevation in temperature following experimental bacterial infection results in a significant increase in host survival.

Antigens were extracted from a virulent isolate of Pasteurella multocida (serotype 3,12,15:D) with potassium thiocyanate, and a vaccine was prepared. Pasteurella-free rabbits were vaccinated intranasally and intraconjuctivally twice with a 2-week interval and challenged intranasally with the homologous P. multocida serotype 2 weeks after the second vaccination. The vaccinated rabbits produced serum immunoglobulin G and nasal mucosal immunoglobulin A against P. multocida. The vaccine protected the challenged rabbits against clinical disease and death; however, otitis media was not prevented, and microscopic inflammatory lesions were occasionally noted in the lungs and nasal turbinates. In contrast, nonvaccinated, challenged rabbits became febrile, dyspnic, depressed, and anorectic, and five of six died within 4 days of challenge with severe lesions including pneumonia, pleuritis, otitis media, and bacteremia. The vaccine prevented death and colonization of challenge organisms in the blood and lung, but did not prevent colonization of the middle ear. The vaccine alone did not cause clinical disease or gross lesions, but did produce microscopic pulmonary inflammatory lesions.