Spontaneous exocrine pancreas hypoplasia in specific pathogen-free C3HeB/FeJ and 101/H mouse pups causes steatorrhea and runting.

Under specific pathogen-free conditions, 1.3% to 1.8% of litters born in our inbred 101/H and C3HeB/FeJ mouse colonies had pups with steatorrhea and runting. Clinically affected male and female pups were first identified when they were from 14 to 25 d old. Unaffected littermates were healthy and were weaned successfully. Postmortem findings in 8 clinically affected mice included a small, poorly differentiated exocrine pancreas comprising cytokeratin-negative duct-like structures but lacking recognizable acinar cells with their normal carboxypeptidase B-positive zymogen granules. Endocrine pancreas islets were unremarkable and contained insulin-positive beta cells and glucagon-positive alpha cells. There was mild inflammation of the hindgut but no evidence of intestinal pathogens or marked inflammation or necrosis of pancreas, either alone or as part of a multisystemic inflammatory condition. Sera from pups in 4 affected litters did not contain antibodies to reovirus 3, mouse coronavirus, rotavirus, or mouse adenovirus 2. Furthermore, 4 sets of parental mice and sentinel mice from the facility were negative for 13 viruses, bacteria, and parasites. C3HeB/FeJ and 101/H inbred strains may be genetically predisposed because the steatorrhea and runting was absent in 13 other mouse strains and subspecies bred in the specific pathogen-free facility. This condition resembles exocrine pancreas hypoplasia, but the inheritance is complex. A wider implication is that runting coupled with steatorrhea are phenotypic criteria to suspect pancreatic disease that could be used in the context of a mouse N-ethyl-N-nitrosourea-mutagenesis program to identify potential mutants with defects in pancreas development.

[Pathophysiological significance of steatorrhea as well as of hydroxystearic acids in the feces of calves with diarrhea]. / Pathophysiologische Bedeutung von Steatorrhoe sowie von Hydroxystearinsäuren im Kot von Durchfallkälbern.

UNLABELLED: The objective of this study was to determine the digestibility of milk lipids in calves with diarrhoea, the pathophysiological effects of fat intake on the course of the disease and the conversion of malabsorbed longchain fatty acids to secretory effective hydroxy fatty acids by the intestinal flora. ANIMALS: 32 male calves of the breed "Deutsches Fleckvieh" with spontaneous occurring diarrhoea, age 3-14 days. Reference group: 6 clinically healthy calves of the same age group. Feed: whole milk, daily ration corresponding to 10% of the BM, divided into 3 meals; supplementary oral rehydration solution as required. METHODS: Quantitative collection of the faeces excreted over a period of at least 72 hours, determination of fatty acids and glycerides, identification and quantification of hydroxystearic acids in the faeces by gas chromatography; calculation of the apparent digestibility of the milk lipids. RESULTS: The apparent digestibility of the milk lipids was in part considerably reduced in direct relation (r = 0.8) to the severity of the diarrhoea. In the case of daily fecal outputs of over 50 g/kg BM (watery diarrhoea), the apparent fat digestibility was reduced below 50%. Even so, the apparent digestibility correlated positively with the milk intake (r = 0.5). The fat excretion in the patients showed an average of 1.4 g/kg BM/24 h and was thus nearly nine times higher in comparison to the reference group (0.16 g/kg BM/24 h). In the case of severe diarrhoea, fat excretion rates of over 2 (up to max. 5.8) g/kg BM in 24 hours were recorded. However, in the main (approx. 70%) it was not glycerides but nonesterified fatty acids. A part of the longchain fatty acids were converted to hydroxy fatty acids by the intestinal flora. It was possible to quantify alpha-, 10(9)- and 12-hydroxystearic acids individually in the faeces of both healthy calves and those with diarrhoea. However, the total concentration of hydroxystearic acids in the faces of 26 out of 32 patients was considerably under the secretory effective concentration of 2 mmol/kg (mean = 1.5 mmol/kg), the other six lay between 2.9 and 11.6 mmol/kg. Only a weakly positive correlation (r = 0.23 or 0.24) existed between the amount of milk intake and the fecal concentration resp. excretion of hydroxystearic acids. CONCLUSIONS: There was no evidence that the consumption of milk lipids influenced the diarrhoea negatively. In individual cases, it could not be completely excluded that fluid and electrolyte absorption was affected by hydroxystearic acids produced in the intestine, but the quantitative effects of this process are of minor significance in comparison to other diarrhoea inducing factors.