Biomedical subjects

R L Cisneros

Publications and source records attributed to R L Cisneros.

23 records · Page 2Linked to original sources

PubMed1980

Clostridium difficile in gnotobiotic mice.

Germfree mice associated with Clostridium difficile developed intestinal disease characterized by polymorphonuclear cell infiltration of the lamina propria, diarrhea, and cecal cytotoxin concentrations positive at a 10(-6) dilution. The numbers of viable bacteria never exceeded 10(10) colony-forming units per g (dry weight). Despite the high toxin levels and chronic inflammation over a 30-day period, the mortality rate was low (less than 2%). Daily treatment of these animals with two oral doses of 2 mg of vancomycin resulted in stool levels of greater than 200 micrograms/ml, well in excess of the minimum inhibitory concentration for C. difficile. This therapy decreased viable cell density by 2 to 3 logs and increased the spore counts from 10(5.8) to 10(7.8) colony-forming units per g (dry weight) by day 7, and animals were free of detectable toxin. However, once therapy was stopped, viable bacteria and spore counts and cytotoxin concentrations returned to previous levels. Treatment of mice with concentrations of clindamycin shown to be inhibitory in vitro had no effect on C. difficile toxin titers or bacterial counts, although the appearance of a clindamycin-resistant population was noted. These data indicate that vancomycin, given orally, decreases the concentration of toxin, but C. difficile survive as spores. By contrast, large populations of vegetative cells and high cytotoxin levels persist when clindamycin is used, even at an inhibitory concentration.

Animals↗

PubMed1977

The capsular polysaccharide of Bacteroides fragilis as a virulence factor: comparison of the pathogenic potential of encapsulated and unencapsulated strains.

The pathogenic potentials of encapsulated and unencapsulated strains of Bacteroides fragilis were compared by use of a rat model of intraabdominal sepsis. Implantation of encapsulated B. fragilis alone resulted in abscesses in most recipients, whereas unencapsulated strains seldom produced this effect unless they were combined with another organism. Implants of heat-killed, encapsulated B. fragilis also resulted in abscess formation. Subsequent experiments suggested that the abscess-potentiating ability of encapsulated B. fragilis is related to the capsular polysaccharide. Implantation of 200 microgram of the purified capsular material alone or in conjuction with unencapsulated strains caused abscess formation in a majority of animals. Comparable results were not obtained with capsular polysaccharide from Escherichia coli O7:K1(L)"NM or with heat-killed Streptococcus pneumoniae type III. The capsular polysaccharide of B. fragilis appears to potentiate abscess formation and may represent a virulence factor for this species.

Abscess↗

PubMed1977

Clindamycin-associated colitis due to a toxin-producing species of Clostridium in hamsters.

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.

Animals↗

PubMed1977

Clindamycin-associated colitis in hamsters: protection with vancomycin.

Clindamycin and lincomycin produced a lethal enterocolitis in 65 of 67 Syrian hamsters. The administration of oral or parenteral vancomycin to recipients of clindamycin or lincomycin was uniformly protective in 49 patients. These results suggest that certain bacteria play a role in the pathogenesis of enterocolitis in this model.

Animals↗

PubMedDate not supplied

Animal model system for studying virulence of and host response to Bacteroides fragilis.

Experimental animal model systems have been used by many investigators to explore the pathogenicity of obligate anaerobes. During the last 15 years, research in our laboratory has utilized an experimental model for intraabdominal sepsis to define the contribution of obligate anaerobes to the infectious process. These studies have shown that obligate anaerobes are important components of the polymicrobic flora present during such infection. Moreover, certain anaerobes, such as Bacteroides fragilis, possess specific virulence factors, such as the capsular polysaccharide, that appear to be important to the infectious process. More recent research has used modifications of the original model system to evaluate the host immune response to B. fragilis. These studies indicate that immunization with the capsular polysaccharide provides a T cell-dependent immunity to abscess development when animals are challenged with B. fragilis. It has also been shown that the killing of B. fragilis is T cell dependent. The observations made with regard to B. fragilis in this animal model system are discussed.

Animals↗