Abstract
Relatively few investigations have dealt with the pathogenesis of the intestinal phase of trichinosis. This is especially true in human infection which is usually diagnosed only after the disease has progressed into the extraintestinal stage. In guinea pigs administered graded doses of Trichinella spiralis larvae the gut phase is accompanied by diarrhea and weight loss, the intensity of which is directly dependent on the size of the worm burden (1).
Interestingly, the small intestine of animals with these symptoms is characterized by histopathology similar to that reported for humans with malabsorption syndromes, and the capacity of the gut to transport glucose actively is greatly reduced (2). Since the transport of glucose is mediated through the brush border of the gut epithelium, it is probable that other physiologic functions associated with this region, including the activity of digestive enzymes such as disaccharidases (3) are adversely affected and may contribute to the clinical picture.
Presently, the physiologic basis of diarrhea in trichinosis is not well understood, although diarrhea as a clinical entity may be caused by various intestinal malfunctions, including deranged absorption and impaired digestive processes (4). Despite the general assumption that the failure of parasitized animals to gah weight at normal rates is related to anorexia, weight loss cannot be attributed entirely to this factor (1). To establish the possibility that helminth-induced diarrhea and weight loss are related, in part, to impaired digestive function, the activity of maltase, sucrase, trehalase, and palatinase in the small intestine of control guinea pigs was compared to that of animals infected with Trichinella.
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