Subacute and subchronic toxicity of ethylene glycol administered in drinking water to Sprague-Dawley rats.

Subacute (10-day) and subchronic (90-day) toxicity studies of ethylene glycol (EG) were conducted in male and female Sprague-Dawley rats to provide the U.S. Environmental Protection Agency's (EPA) Office of Drinking Water with toxicity data for final preparation of a Health Advisory for the chemical. Ethylene glycol was administered in drinking water at concentrations of 0.5, 1.0, 2.0, and 4.0% for both sexes in the 10-day study. Based on a projected consumption rate of 100 ml/kg/day, the respective doses on a mg/kg/day basis would be 554, 1108, 2216, and 4432. These dose levels were also used in the 90-day study for females, but dose levels for the males in the 90-day study were 0.25, 0.5, 1.0, and 2.0% (227, 554, 1108, and 2216 mg/kg/day). At time of sacrifice necropsies were performed and tissues were prepared for histological evaluation. Blood samples were taken for hematology and clinical chemistry determinations. Body weights were measured weekly. Water and food consumption were determined three times weekly. No mortality occurred in the 10-day study. In the 90-day study 8/10 females and 2/10 males in the high dose group died prior to sacrifice. Body weights were suppressed in a dose response fashion for males and females. Hemoglobin, hematocrit, erythrocytes, and leukocytes were all significantly decreased in female rats receiving 4% EG for 10 days. The most significant histopathological findings, seen predominantly in males, were kidney lesions which included calcium oxalate crystals in tubules and pelvic epithelium; tubular dilation and degeneration; intratubular proteinaceous material; and inflammation in tubules and pelvic epithelium. At the same dose of ethylene glycol, males had more kidney lesions and much higher incidence and severity of lesions than the females.

Pneumatocele in a pig-tailed macaque (Macaca nemestrina).

Radiographic examination of a pig-tailed macaque (Macaca nemestrina) with pneumonia revealed a large pneumatocele. The pneumatocele, a thin-walled, partially fluid filled radiolucent area, occupied approximately one-third of the left thorax. Rapid resolution of the pneumatocele accompanied antimicrobial treatment of the pneumonia and coincided with clinical improvement. Severe pulmonary acariasis was found at postmortem 15 months later.

Acute gastric dilatation in nonhuman primates: review and case studies.

Acute gastric dilatation occurs sporadically in laboratory-housed nonhuman primates. Clinical histories often include chronic drug administration, food restriction, accidental overfeeding, and prior anesthesia. Monkeys may be found dead or may have clinical signs of colic, abdominal distention, and dyspnea. Death in untreated cases is due to impaired venous return and cardiopulmonary failure. Gastric distention with fermented gaseous ingesta and congestion of the abdominal viscera are the predominant lesions. The cause of acute gastric dilatation is unknown, but it probably is multifactorial. Two principal factors seem to be intragastric fermentation associated with Clostridium perfringens, and abnormal gastric function.

Acute gastric dilatation in nonhuman primates: review and case studies.

Acute gastric dilatation occurs sporadically in laboratory-housed nonhuman primates. Clinical histories often include chronic drug administration, food restriction, accidental overfeeding, and prior anesthesia. Monkeys may be found dead or may have clinical signs of colic, abdominal distention, and dyspnea. Death in untreated cases is due to impaired venous return and cardiopulmonary failure. Gastric distention with fermented gaseous ingesta and congestion of the abdominal viscera are the predominant lesions. The cause of acute gastric dilatation is unknown, but it probably is multifactorial. Two principal factors seem to be intragastric fermentation associated with Clostridium perfringens, and abnormal gastric function.

Infection of white carneaux pigeons (Columbia livia) with Mycobacterium avium.

Avian tuberculosis, caused by Mycobacterium avium, occurred in three White Carneaux pigeons. Clinical signs varied and included anorexia, lameness, torticollis, and the development of cutaneous nodules. Lesions at necropsy consisted of caseating hepatic, pulmonary, and cutaneous granulomas. In one animal, the marrow in several bones was replaced with caseous material. Histopathologically, the granulomas contained necrotic material and acid fast bacilli surrounded by epitheloid cells, giant cells, and lymphocytes. Treatment of affected animals was not attempted. False positive and false negative reactions occurred when intradermal tuberculin skin testing was done.