Glucose Malabsorption and Intestinal Histopathology in Trichinella spiralis-Infected Guinea Pigs

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Abstract
Intestinal malabsorption of glucose was induced in guinea pigs experimentally infected with Trichinella spiralis. In vitro and in vivo studies, carried out over a 28-day infection period, showed that the capacity of the small intestine to absorb glucose was significantly reduced in animals infected with 10,000 but not 5,000 larvae. Impaired absorption was first detected in the anterior 3/4 of the intestine on day 3 and for the 4th quarter on day 14 postinfection. The 1st and 2nd quarters were capable of normal glucose uptake on day 14, whereas uptake in the 3rd quarter remained impaired. On days 21 and 28 malabsorption was observed only in the 4th quarter. Impaired glucose uptake was associated with histopathology of the small in-testine similar to that reported for humans with malabsorption syndromes. A loss of normal villous pattern, aberrant epithelial cells, and inflammation of the lamina propria were observed during the course of infection. Chronologically, these alterations occurred in the anterior half of the intestine during early infection and later extended into the posterior intestine. Localization of adult T. spiralis in the small intestine was studied to determine if a relationship could be established between histopathology and the distribution of worms in the gut. There was a shift in the relative distribution of worms from the anterior to posterior end of the small intestine as infection time progressed. Only a small fraction of a dose of 10,000 larvae could be recovered from the small intestine following infection. Eight to 10% of the infective dose was recovered at various times during the 1st week, 1.8% on day 14, 0.2% on day 21, and only rarely were worms recovered on day 28. These findings have significance in revealing previously unknown components in the pathogenesis of trichinosis and in providing a rational basis for explaining, in part, weight loss and diarrhea in guinea pigs with this disease.