Abstract
Primary infection with the nematode Trichinella spiralis in rats elicits changes in intestinal motility (Castro et al., 1976). Experiments were designed to determine whether similar changes occur in immunized hosts given challenge infections. Intestinal motility was measured by following the transit of radioactive chromium through the small intestine of rats that were immunized by infection with 8 X 103 larvae. Six weeks after immunization animals were operated on to implant duodenostomy catheters. Eight days after the operations, the rats were divided into two groups. Animals in one group were challenged with 8 X 103 larvae, whereas those in the second group served as unchallenged, immunized controls. Three, 4 and 5 days postinfection 5Cr was injected directly into the duodenum of the catheterized animals. Propulsion of the isotope through the small bowel was allowed to progress for 15 min. At the end of this time animals were killed, their intestines were removed and divided into 10 equal segments, and the distribution of radioactivity in each segment was determined. The leading edge of radioactivity in both the control and the challenged rats traversed 70% of the gut length. The regression of percent radioactivity present in each segment of gut length yielded a slope of -16.39 for the control group and -17.08 for the challenged animals. The difference between these values was not significant. Both slopes, however, were greater than that obtained by plotting similar data collected from rats given a primary infection of 8 X 103 larvae. In the latter group of animals the front of the radioactivity traversed 100% of the gut length. Results support the conclusion that a secondary inoculum of T. spiralis larvae, in contrast to a primary inoculum of equal size, fails to elicit changes in intestinal motility. Abnormal motility patterns have been proposed as a causal factor underlying symptoms related to the gastrointestinal (GI) tract during some enteric parasite infections (Roche and Layrisse, 1966; Symons, 1966; Domingo and Warren, 1969). Definitive evidence of changes in motility caused by helminths recently evolved from studies of animals infected with T. spiralis (Schanbacher et al., 1975; Castro et al., 1976). Despite pathological consequences, altered motility resulting from infection may have a regulatory effect on the course of parasitism. McCoy (1940) suggested that enhanced intestinal transit was responsible for the rapid expulsion by previously infected rats of a secondary dose of T. spiralis larvae. Larsh and Hendricks (1949) postulated that an age-dependent difference in intestinal transit was responsible for variations in the intestinal distribution of T. spiralis between young and old mice. Our study was undertaken to determine, by direct measurement of intestinal propulsion, whether rats that were immunized to T. spiralis Received for publication 9 November 1976. * This study was supported by NIH Grant AI11361. G. A. Castro is the recipient of NIH Research Career Development Award AI-00087. responded to challenge infection by eliciting changes in normal intestinal motility. It was anticipated that information gained from this study would help elucidate the possible role of altered motility in resistance to the parasite. MATERIALS AND METHODS Initially, 12 Sprague Dawley rats (Sprague Dawley, Madison, Wisconsin) weighing 214 + 6 g (mean ? S.E.) were infected with 8 X 103 T. spiralis larvae by oral intubation of excysted parasites obtained from infected mouse skeletal muscle (Castro and Fairbairn, 1969). All animals were fed a stock diet (Lab Blox, Allied Mills, Inc., Chicago, Ill.) and given water ad lib. Six weeks after this immunizing infection, intraduodenal catheters were implanted in the 12 rats. The animals were anesthetized with 20 mg ketamine hydrochloride (Ketaject, Bristol Laboratories, Syracuse, N.Y.) administered intraperitoneally. After shaving the nape and abdomen, a midline abdominal incision was made through the peritoneum about 1.5 cm down from the xyphoid angle. Using a hemostat, a silastic catheter (0.50 mm inside diameter, 1.50 mm outside diameter) was passed along the right side, between the skin and musculature starting at the midline incision and exiting through a small cutaneous puncture made in the midscapular region. The other end of the catheter was passed through the musculature of the right abdominal wall into the abdominal cavity and then directly into the intestine through a small puncture approximately 3 cm distal to the
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