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Abstract
A slide agglutination technique identifying 10 serogroups of Clostridium difficile (A,B,C,D,F,G,H,I,K and X) has been described previously. In this study, we have used the hamster to compare the ability of the 10 serogroup reference strains to colonise and produce disease. Groups of four hamsters were each given a single intraperitoneal injection of either clindamycin or cefoxitin, and an oral challenge dose of C. difficile. The time taken to establish faecal colonisation and the length of survival after colonisation were monitored. All hamsters treated with cefoxitin became colonised by day 3 and those challenged with the cytotoxigenic strains of serogroups A,C,H and K developed colitis and died. Among those challenged with the non-toxigenic strains of groups B,D,I and X and the toxigenic strains of groups F and G, faecal colonisation was established without signs of disease. This demonstrates that there are differences in virulence even among toxigenic strains of C. difficile. The same phenomenon was observed after treatment with clindamycin but the pattern of colonisation was quite different with some strains. In the hamsters challenged with toxigenic strains of groups C and K and non-toxigenic strains of groups D and I, which are highly resistant to clindamycin, the response was the same as with cefoxitin. The results were different with strains which were susceptible to clindamycin. Some animals became colonised much later than those treated with cefoxitin but the mortality was similar. The remaining animals became colonised by day 3, not by the challenge organism but by another strain which always belonged to serogroup D or C; the source of these organisms was thought to be either previously undetected faecal carriage or the environment. Four animals infected by a toxigenic serogroup-C strain died. Another five, colonised by a non-toxigenic serogroup-D strain survived even though they had been challenged with a strain of a virulent serogroup. This protective effect and the differences in the potential to colonise after clindamycin therapy may warrant further investigation in man.
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