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Biomedical subjects

C A Wanke

Publications and source records attributed to C A Wanke.

41 records · Page 3Linked to original sources

Small-bowel colonization alone is a cause of diarrhea.

Bacterial overgrowth in the small bowel is known to occur in patients with persistent diarrhea, but it has been unclear if colonization alone causes fluid secretion. We studied isogenic, nontoxigenic Escherichia coli strains with colonizing factor antigen II (CFA/II) (1392+) and without CFA/II (1392-) in 18-h rabbit ileal loops. Neither strain produced fluid, but quantitative cultures of rabbit ileal loops with the CFA/II-positive strain had a mean of 10(3) more CFU of bacteria per cm2 than did cultures of rabbit ileal loops with the CFA/II-negative strain or a negative control (P less than 0.05). Of 11 rabbits given strain 1392+ via the small bowel in the reversible ileal tie model, 7 became colonized (mean, 10(10.4) +/- 1.6 CFU/cm2) over 72 h, and all 7 developed diarrhea and had gross gut fluid accumulation, versus none of 10 rabbits given strain 1392- (mean, 10(3.6) +/- 1.9 CFU/cm2) (P less than 0.05). Both strains grew equivalently in vitro. The mechanism by which this E. coli strain which colonizes small-bowel mucosa but produces no recognized toxins causes fluid accumulation and diarrhea in a rabbit model at 72 h remains to be elucidated.

Animals↗

Viral hepatitis and gastroenteritis transmitted by shellfish and water.

The epidemiology and clinical presentation of water-borne viral diseases, including shellfish-associated viral illnesses, are discussed in this article. Hepatitis A virus, Non A-Non B hepatitis and the agents of viral gastroenteritis, Norwalk agent, Snow Mountain agent, rotavirus, the small round viruses, caliciviruses, and astroviruses are included. The technical problems associated with evaluating the viral contamination of water or shellfish are noted.

Disease Outbreaks↗

A medium chain triglyceride-based diet in patients with HIV and chronic diarrhea reduces diarrhea and malabsorption: a prospective, controlled trial.

Our objective was to determine whether a medium-chained triglyceride (MCT)-based diet, compared to a long-chain triglyceride (LCT)-based diet, conveys a beneficial effect on diarrhea and fat malabsorption in human immunodeficiency virus (HIV)-infected individuals with chronic diarrhea and weight loss. A secondary objective was to evaluate the pathogens associated with the diarrhea and to evaluate whether the etiologic agent was a determinant of response to the nutritional intervention. Prospective, randomized double-blind comparative trial was conducted in 24 adult patients with HIV, diarrhea of greater than 4-wk duration, fat malabsorption, and loss of 10-20% of ideal body weight, these patients were recruited from our outpatient infectious disease clinic. Evaluations of diarrheal pathogens were made by complete stool examination, upper and lower endoscopy with quantitative culture, and biopsy. Body composition determinations, and measurements of fat, carbohydrate, and vitamin absorption pre- and postintervention. Patients were randomly assigned to one of two complete nutritional products with either medium- or long-chain triglyceride fat exclusively for 12 d followed by treatment of infectious pathogens. Ten patients were found to have Microsporidium and 9 patients had no identifiable pathogen. All patients responded to intervention with both nutritional products overall with 45% fewer stools, decreased stool fat and weight, and a significant increase in urine nitrogen. The group that received the MCT product demonstrated significantly decreased stool number (mean 4 to 2.5), stool fat (mean 14 to 5.4 g), and stool weight (mean 428 to 262 g) compared with baseline (P < 0.01 for all). Patients with both species of microsporidia and with pathogen negative diarrhea had good response. We found that HIV patients with diarrhea, regardless of etiology, and documented fat malabsorption may benefit symptomatically from a diet composed of an MCT-based liquid supplement.

Adult↗

Recombinant human tumor necrosis factor and recombinant murine interleukin-1 alter the binding of Escherichia coli to intestine, mucin glycoprotein, and the HT29-C1 intestinal cell line.

Little is known about the effects of cytokines at the intestinal mucosal surface on the adherence of bacteria. We examined the effects of recombinant tumor necrosis factor (TNF) and interleukin-1 (IL-1) on the adherence of various strains of Escherichia coli to intestinal mucosa in vivo and in in vitro models. We studied the effects of TNF or IL-1 injected intraperitoneally on the ability of a rabbit enteric pathogen (RDEC-1) and a nonpathogenic E. coli (1392-) to colonize rabbit small bowel and found that there was a trend toward increased colonization by the RDEC-1 organisms in the TNF-treated rabbits, and a significant increase in colonization by the RDEC-1 organisms in the IL-1-treated animals (P < 0.01). Both TNF and IL-1 altered the density and the level of glycosylation of the small bowel mucus glcoprotein purified from the treated and untreated rabbits, and TNF treatment significantly increased the number of bacteria bound by this purified mucin (P < 0.01 for all strains). HT29-C1 intestinal cells in tissue culture were also grown in media with TNF or IL-1 and used in bacterial binding assays. The cells provided with media with 50 pg/mL of either cytokine bound significantly more of the three bacterial strains than cells in untreated media (P < 0.01 for all strains). The cytokines TNF and IL-1 have the potential to alter bacterial adherence to intestinal mucosa in vivo and in vitro; additional studies to clarify the role that these alterations in adherence may play in the clinical syndromes characterized by increased levels of intestinal cytokines are warranted.

Animals↗