Fatal encephalitis caused by Ochroconis gallopavum in a domestic cat (Felis domesticus).

Ochroconis gallopavum was identified as the causal agent of fatal encephalitis in a young, short-hair, domestic cat. The cat initially developed an ulcerated mass on the left side of the tongue and signs of pain in the abdomen. The tongue lesion was surgically removed and exploratory abdominal surgery revealed abnormalities suggestive of pancreatitis and peritonitis. During the month after surgery, the cat's health declined, manifested by sluggishness, loss of appetite and abnormal behaviour. Following a final rapid deterioration, the cat became non-responsive and was euthanized. Histologic examination of the brain, lung and mediastinal lymph node lesions revealed large numbers of pigmented, septate, branched, hyphal elements with swollen intercalary and terminal vesicles, and short chains of moniliform hyphal cells. Cultures of the mediastinal lymph nodes yielded a dematiaceous, thermotolerant fungus that was identified as O. gallopavum. This report describes the first well-documented infection in a cat caused by O. gallopavum.

A 90-day vapor inhalation toxicity study of decalin.

A subchronic 90-day inhalation study was conducted to determine the toxic effects of decalin, a commonly used industrial solvent. Experimental groups consisting of male and female beagle dogs, male and female Fischer-344 rats, and female C57BL/6 mice were continuously exposed to decalin concentrations of 5 or 50 ppm. An unexposed control group was also maintained. All dogs and a portion of each rodent group were sacrificed and examined at exposure termination, while the remaining rodents were held for observation up to 21 months postexposure. No distinct exposure-related lesions were noted in dogs. Dog body weights, organ weights, and blood clinical pathology were also normal. At exposure termination hepatocellular cytoplasmic vacuolization was noted in female mice exposed to both concentrations. This liver tissue change was reversible and was not a significant finding in female mice examined during the 21-month postexposure observation period. In male rats, decalin exposure produced nephropathy characterized by hyaline droplets, necrosis, and intratubular casts. Accentuated tubular degeneration and medullary mineralization were noted in exposed rats held for long-term postexposure observation. There was no associated abnormal increase in mortality nor alterations in serum, blood urea nitrogen, or creatinine levels. Female rats were free of decalin-induced renal damage. There was a slightly greater incidence of commonly occurring pituitary tumors in both mice and rats; however, the tumor incidence was not dose related. The results of this study suggest that the toxic effects of decalin are similar to those previously described for other hydrocarbon solvents and fuels.

Six month inhalation toxicity of fluomine dust.

Fluomine is a cobalt chelate of interest in life support systems of high altitude aircraft. Rats, mice, guinea pigs and dogs were exposed to fluomine particles for a six month period on an industrial-type schedule. Chronic exposure of the dust caused a statistically significant decrease in the mean body weights of the test rats when compared to their respective control group. The dust had irritative effects on the respiratory systems of rats and dogs at the highest exposure level. A concentration of 0.1 mg/m3 is a suggested threshold limit at or below which no serious effects should occur.

The mammalian toxicity of fluomine dust.

Fluomine is a cobalt chelate compound which complexes molecular oxygen and releases it on heating. This property has led to its use a a regenerable oxygen source in high-altitude aircraft. Investigations into the acute effects of exposure to fluomine by various routes were undertaken as first steps in the toxicological characterization of the material. Single-dose rat and mouse oral administration led to LD50 values of 123 mg/kg for male CF1 mice and 187 mg/kg for male Sprague-Dawley rats. The LC50 values for single four-hour inhalation periods varied from 112 mg/m3 for male rats to 416 mg/m3 for male mice. Fluomine proved to be highly irritating when instilled in the eyes of rabbits and to the lungs of rats on inhalation. Exposure of rabbit skin to the compound demonstrated moderate irritancy particularly in areas of abrasion. Positive reactions to intradermal challenge were demonstrated after both intradermal and inhalation sensitization of guinea pigs.

An epizootic of necrotic dermatitis in laboratory mice caused by Lancefield group G streptococci.

During a 7-mo period, mice from a group of 383 being used in a toxicology experiment developed severe progressive necrotic dermatitis, and some animals developed paralysis. The overall mortality rate for the group was 134/383 (35%). Seventeen mice were necropsied for bacteriologic and histopathologic examination. A streptococcus identified as Lancefield group G was isolated from the skin lesions of 15 of the mice, from 8 of 9 throats cultured, from 4 of 8 spleens, and occasionally from other sites. It was thought that the infections were initiated and perpetuated by bites from mice carrying the streptococcus in their mouth and throats. Microscopic examination of affected skin revealed necrotic dermatitis characterized by epithelial ulceration with suppuration. The skin lesions were reproduced in 6 of 15 mice inoculated with the isolated streptococcus.

Hepatic lesions in mice after continuous inhalation exposure to 1,1,1-trichloroethane.

Male CF-1 mice (24 to 34 gm.) were exposed to either 250 p.p.m. or 1000 p.p.m. of 1,1,1-trichloroethane in air continuously for 14 weeks. Control mice were exposed to room air. Serial sacrifice of exposed and control mice from 1 to 14 weeks demonstrated significant changes in the centrilobular hepatocytes of animals in the 1000 p.p.m. group. Moderate liver triglyceride accumulation was evident in the 1000 p.p.m. group and peaked at 40 mg. per gm. of tissue (wet weight) after 7 weeks of exposure. Partial recovery was indicated by a decrease in the hepatic triglyceride level of 16 mg. per gm. by 14 weeks of exposure to 1000 p.p.m. Electron microscopic evaluation revealed that cytoplasmic altertions were most severe in centrilobular hepatocytes in the 1000 p.p.m. group and were mild to minimal in the 250 p.p.m. group. These alterations consisted of vesiculation of the rough endoplasmic reticulum, with loss of attached polyribosomes, increased smooth endoplasmic reticulum, microbodies, and triglyceride droplets. Some cells had ballooned cisternae of the rough endoplasmic reticulum. Necrosis of individual hepatocytes occurred in 40 per cent of the mice exposed to 1000 p.p.m. for 12 weeks. This necrosis was associated with an acute inflammatory infiltrate and hypertrophy of Kupffer cells. Comparison of these findings to the results obtained by other investigators studying dichloromethane indicates that the pathologic alterations observed with 1,1,1-trichloroethane were similar to those observed with dichloromethane, except for different time courses of the effects and different degrees of recovery. The toxic effects of 1,1,1-trichloroethane were of a type similar to those produced by carbon tetrachloride, but they appeared to be much less severe.