22 OP
METRONIDAZOLE (MTR) SUSCEPTIBILITY IN CLOSTRIDUM DIFFICILE

(CD) ISOLATES FROM CD-ASSOCIATED DIARRHEA (CDAD) TREATMENT FAILURES A~ND SUCCESSES.

Johnson S*, Sanchez JL, and Gerding DN.
VACHS, Lakeside and Northwestern U. Medical School, Chicago, IL, USA.

Despite high clinical efficacy, a small number of patients with CDAD do not respond to treatment with MTR. In light of recent documentation of MTR resistance in equine CD isolates we looked for evidence of MTR resistance in human CD isolates from CDAD cases obtained over a 10-year period from one institution. Between 1982 and 1991 14/632 (2%) patients with CDAD did not respond to MTR after 7 days of therapy. E-Test and agar dilution susceptibilities were performed on all available CD isolates (10) from the MTR-failure cases and 20 contemporary control CDAD patients who responded to MTR.

Restriction endonuclease analysis (REA) typing was also performed on all CD isolates. By E-Test, the mean ±SD MIC of MTR-failure associated CD isolates, 0.23±0.21 ug/mL (range = 0.064 to 0.75), was similar the mean ±SD MIC of MTR-success associated CD isolates 0.29±0.19 ug/mL (range = 0.094 to 0.75), P= 0.4. Agar dilution testing gave similar results and showed correlation with the E-Test results (0.58). The MIC of the CD isolate recovered from one patient after 10 days of MTR therapy was similar to the MIC of the originally recovered CD

isolate; 0.38 and 0.50 ug/mL, respectively. Recovered CD isolates belonged to 13 different REA groups and were randomly distributed between MTR-failure and MTR-success cases. Specific REA Types B1, K1, and Y1P were recovered from both

MTR-failure and MTR-success cases. No particular CD strain was associated with MTR treatment failure. No CD clinical isolates were found to be resistant to MTR. Clinical CDAD treatment failures with MTR could not be attributed to decreased susceptibility of the causitive CD isolate to MTR.