Preputial dermatitis in male guinea pigs (Cavia porcellus).
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Biomedical subjects
Publications and source records attributed to C M Lang.
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A case of gastric ruputre secondary to a trihobezoar occurred in a rabbit. A review of the literature showed that, although trichobezoars are common in rabbits, antemortem gastric rupture has not been reported previously.
A female squirrel monkey (Saimiri sciureus) had granulomatous lesions in the liver and colon. There were many fungal organisms in sections of liver and many of these organisms had multiple buds on their surface. Although we did not prepare fungal cultures, the appearance of the organisms was sufficient to identify them as Paracoccidiodes brasiliensis, the cause of paracoccidioidomycosis (South American blastomycosis).
Spontaneous diabetes mellitus, observed in a colony of guinea pigs, parallels in many ways the syndrome known as juvenile diabetes mellitus in man: elevated blood glucose levels; reproductive dysfunction in the female; degranulation and severe cytoplasmic vacuolation of beta cells, severe fatty degeneration of acinar cells, and hyperplasia of the islets of the pancreas; and a high frequency of abnormal pancreatic secretions. Islet-cell necrosis and insulinitis usually seen in viral infections was not observed. Microangiopathy, another characteristic of juvenile diabetes mellitus in man was demonstrated as a significant increase in the thickness of the basal membranes in peripheral capillaries. A glomerular lesion encountered in some of the diabetic guinea pigs was shown to be similar to the glomerular sclerosis seen in human diabetics. Although a definitive etiologic agent was not identified, the disease was clearly contagious in origin.
During an 18-month period, gastric dilatation was recognized in six guinea pigs from a colony with a monthly average of 253 animals. All of the affected guinea pigs were breeders and ranged in age from 8 to 26 months. Clinical signs were tachycardia, dyspnea, cyanosis, and marked abdominal distention. Macroscopic lesions included gastric volvulus, gastric dilatation, and splenic congestion.
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Spontaneous diabetes mellitus has been documented in a colony of guinea pigs. The contagious nature of the disease has been verified, but the nature of the infectious agent is not known. Animals from the original colony or animals exposed to the colony with normal glucose tolerance tests (GTT) became diabetic, as evidenced by elevated one- and four-hour GTT values, and in most cases have significant glycosuria. The severity of pathologic changes in the pancreatic islets parallel, in general, the severity of the clinical symptoms (glycosuria and abnormal GTT). Those animals with severe glycosuria and elevated FBS as well as one- and four-hour GTT values had the most pronounced degranulation and most prominent cytoplasmic inclusions in islet B cells. The severity of scarring in the islets can be correlated with the duration of the overt diabetic state. The other clinical parameters of note were elevated serum triglycerides, normal serum but elevated aortic cholesterol, and absence of ketonemia or ketonuria. The reproductive capacity of diabetic females was compromised. While the clinical manifestations are mild or variable, the presence of significant islet pathology is reminiscent of human juvenile diabetes mellitus. These findings lend support to the concept that infectious and/or immune mechanisms could be operative in the etiology and pathogenesis of human diabetes mellitus.
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Only some of the diverse factors that can affect drug disposition and response in laboratory animals have been identified at the present time. These numerous factors contribute to large day-to-day variations that have become a major problem impeding investigation of drug disposition and response in laboratory animals. Although these variations render many experiments difficult to interpret and produce large discrepancies in the literature, few published investigations using laboratory animals provide sufficient details to permit replication of the studies under similar conditions with respect to these variables. Thus, the importance of these variables in affecting results is apparently insufficiently recognized at present. Two commonly overlooked variables affecting the activity of hepatic microsomal enzymes (HME) in rodents and hence the rate at which rodents eliminate from their bodies many foreign compounds are the bedding under the wire mesh cage and the relative cleanliness of the environment. Numerous chemicals present in relatively low concentrations in the environment of the animal room can significantly alter HME activity. Representative of these chemicals are aromatic hydrocarbons in cedarwood bedding, eucalyptol from aerosol sprays, and chlorinated hydrocarbon insecticides, each of which induces HME activity, whereas ammonia generated from feces and urine accumulated in unchanged pans under cages may inhibit HME activity. Chloroform, identified as an environmental contaminant of the water and air of certain cities, exhibits sex and strain differences with respect to toxicity (LD50) in mice. After intraperitoneal injection, twice as much chloroform accumulated in the kidneys of males from the sensitive strain (DBA/2J) as from the resistant (C57BL/6J) strain. First generation offspring were midway between parental strains both with respect to LD50 and renal accumulation of chloroform.
In this study, 37 guinea pigs were classified, on the basis of histologic examination of the pancreas, into three categories: nondiabetic, latent diabetic, and overt diabetic. In order to compare the exocrine pancreatic function in these three groups of animals, pancreatic secretion was collected from each animal following an intravenous infusion of secretin and pancreozymin. Pancreatic enzyme activity, bicarbonate concentration, and the total volume of pancreatic secretion were all significantly decreased in guinea pigs with overt diabetes, but not in those with latent diabetes mellitus. Pancreatic histologic changes characteristic of both latent and overt diabetes were beta-cell hyperplasia and generalized fatty degeneration of the acini. Only the animals with overt diabetes showed total degranulation and severe vacuolation of theta-cells. The same type of exocrine pancreatic dysfunction observed in guinea pigs with spontaneous overt diabetes mellitus is found in human diabetics, and is particularly common in the juvenile type. The guinea pig, therefore, appears to be a suitable animal model for the study of human juvenile diabetes mellitus.
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Reduction of aniline hydroxylase activity, ethylmorphine N-dementhylase activity, and cytochrome P-450 content occurred in hepatic microsomes of rats kept under dirty conditions, defined as accumulation for 1 week of urine and feces in pans under the wire mesh cages. In comparison with rats that had urine and feces removed twice daily from such pans, rats kept over Kimpak bedding or over Litter Green, changed twice daily, also showed reduced drug-metabolizing activity in hepatic microsomes, but to a lesser degree than the dirty rats. Placement of a filter top on cages for 1 week also decreased drug-metabolizing activity. These experiments suggest that the relative cleanliness of an animal's environment can influence hepatic microsomal drug metabolism.
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