Intestinal Motility during the Enteric Phase of Trichinosis in Immunized Rats

Pathophysiology of Infectious Diarrhea

“…Alterations of the normal patterns of intestinal motor activity are now well described in a variety of experimental animal model s of bacterial (141)(142)(143)(144)(145)(146)(147)(148)(149)(150)(151)(152)(153)(154)(155)(156)(157)(158)(159), parasitic (160)(161)(162)(163)(164)(165)(166)(167)(168)(169)(170)(171), and viral (172) infectious enteritis, and have been associated with alterations in the rate of transit and diarrhea. While the subject of normal intestinal myoelectric or motor activity and its control mechanisms is beyond the scope of this article , several excellent reviews provide a more detailed discussion (173,174).…”

“…Alterations in intestinal motor activity have been described in association with a variety of parasitic infestations and appear to be part of an adaptive response contributing to expulsion of the organisms (161)(162)(163)(164)(165). Infection with coccidiosis (Eimeria magna) caused significant changes in the pattern of jejunoileal motility between 4 and 12 days postinfection in conscious rabbits (160).…”

“…Primary infection with the nematode parasite Trichinella spiralis is associated with an increased rate of transit in mice (161,162) and rats (163). The changes in intestinal myoelectric activity associated with both primary and secondary infection with this organism have been studied in the rat (163,164) and in the dog (165).…”

Structural relationships between immune cells and longitudinal muscle during a Trichinella spiralis infection in the rat intestine

“…In the case of Trichinella spiralis , the parasite resides briefly in the epithelial lining of the gut before the larvae gain access to the circulation and eventually encyst in skeletal muscle. Yet it is clear from in vivo studies that motility is altered during infection 9 , 10 and that changes in propulsive contractile activity are evident in extrinsically denervated segments of intestine during infection, 11 implying dysfunction in the motility apparatus within the gut wall – namely enteric nerves and muscle. Changes in longitudinal muscle include an increase in mass, reflecting both hypertrophy and hyperplasia 7 and in tension development.…”