The capsular polysaccharide complex from Bacteroides fragilis promotes the formation of intra-abdominal abscesses--a pathologic host response to infecting microorganisms. This complex consists of two distinct polysaccharides, each with repeating units that have positively charged amino groups and negatively charged carboxyl or phosphate groups. Analysis of these polysaccharides as well as other charged carbohydrates before and after chemical modification revealed that these oppositely charged groups are required for the induction of intra-abdominal abscesses in a rat model.
Clindamycin-associated enterocolitis in hamsters was studied to detect and characterize a transmissible agent. It was found that the disease could be transferred by cecal contents and filtrates of cecal contents (pore size of filter, 0.02 micron) obtained from animals after administration of clindamycin. Subsequent work showed that enterocolitis could be produced with broth cultures of a species of Clostridium recovered from cecal contents of animals with clindamycin-induced disease. The cell-free supernatant of this strain also caused enterocolitis. Cecal contents from animals with clindamycin-induced disease incubated with gas gangrene antitoxin failed to cause intestinal lesions. These experiments indicate that clindamycin-associated colitis in hamsters is due to a clindamycin-resistant, toxin-producing strain of Clostridium.
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