Antimicrobial resistance in Bacteroides

Abstract

Antimicrobial resistance in Bacteroides species has a direct impact on the selection of chemotherapy for anaerobic infections. Multiple studies have documented differences in susceptibility patterns related to individual hospitals, geographic areas, and antibiotic-prescribing practices. Resistance to beta-lactam antibiotics, tetracycline, clindamycin, and metronidazole has been documented in Bacteroides species. The prime mechanism for beta-lactam resistance is the production of beta-lactamases, including penicillinases, cephalosporinases, and the metallo-beta-lactamases that can hydrolyze imipenem. Resistance to tetracycline is mediated by ribosomal protection by the tetQ class. Resistance to clindamycin is mediated by ribosomal modification. Metronidazole resistance may be caused by a combination of decreased antibiotic uptake, decreased nitroreductase activity, and decreased pyruvate:ferredoxin oxidoreductase activity accompanied by increased lactate dehydrogenase activity. Most disturbing is the appearance of resistance to multiple agents in the same organism. Understanding the mechanisms of resistance and the mechanisms of action of these drugs not only will lead to the design of new antimicrobial agents but will permit informed selection of therapy for bacteroides infections.