The increasing prevalence of antibiotic-resistant Streptococcus pneumoniae is of growing public health concern. The aim of this study was to assess resistance rates of S. pneumoniae to penicillin and other antimicrobial agents. Between November 1997 and February 1998 in a community health centre in Marcory, an Abidjan suburb, 138 S. pneumoniae strains were isolated from the nasopharynxes of 218 apparently healthy children aged 3-60 months. The sensitivity of the isolates was tested using the Kirby-Bauer method. In isolates with a possibly abnormal sensitivity to the Kirby-Bauer test, minimum inhibitory concentrations (MIC) were estimated using the E-test. Antimicrobials tested included penicillin G, amoxycillin, cefotaxime, cotrimoxazole, tetracycline, chloramphenicol, erythromycin, rifampicin and vancomycin. Twelve of 108 isolates (8.7%) had reduced sensitivity to penicillin G, and in three of them the MIC for penicillin reached at least 2 micrograms/ml. Resistance to amoxycillin and cefotaxime was lower than to penicillin (2.2%). With regard to cotrimoxazole, 37% were moderately resistant and 15.2% highly resistant. The lowest resistance rate observed was to rifampicin (2.2%) and the highest was to tetracycline (57.2%). Rates of resistance to erythromycin and chloramphenicol were 11.6% and 2.9%. All strains were sensitive to vancomycin. Multidrug resistance (MDR) was detected in 9.4% of S. pneumoniae isolates. In children, epidemiological surveillance of resistance can be monitored by bacteriological surveys, as shown in this study.
Thirty Mycobacterium tuberculosis strains (8: INHR/INHR, 12: INHR/RIFS, 10: INHS/RIFS) were examined against MICs of epiroprim (EPM) and isoniazid (INH) separately or in association. EPM alone proved to be insufficiently active against the various mycobacterial isolates (MIC ≧256 µg/ml). The observed average sensitivity to the association of EPM plus INH was, in contrast, considerably increased, as reflected by reduced MICs and lower percentages of resistant strains. MICs ranged between 16 and 32 µg/ml EPM and 2 and 4 µg/ml INH for INHR strains. All INHS isolates were inhibited by a concentration of 0.125 µg/ml EPM and 0.06 µg/ml INH. The fractional inhibitory concentration indices indicated an additive activity on INHR/RIFR strains and a synergistic activity on INHR/RIFS and INHS/RIFS strains. The synergistic activity of this drug association needs to be confirmed in an animal model.
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