Mechanisms of resistance and resistance transfer in anaerobic bacteria: factors influencing antimicrobial therapy.
The resistance of anaerobic bacteria to a number of antimicrobial agents has an impact on the selection of appropriate therapy for infections caused by these pathogens. Resistance to penicillin in Bacteroides fragilis has long been recognized. Most resistance is due to chromosomal beta-lactamases that are cephalosporinases. Two new enzymes that inactivate the ureidopenicillins and cefoxitin have been described in B. fragilis. The most common mechanisms of cefoxitin resistance is by the blocking of penetration of the drug into the periplasmic space. The transfer of beta-lactamase and penicillinase and of cefoxitin resistance has been demonstrated. Penicillin resistance in other Bacteroides is mediated by a penicillinase. Chloramphenicol resistance is mediated by a chloramphenicol acetyltransferase and by nitroreduction in anaerobic bacteria. Anaerobic bacteria are resistant to aminoglycosides because these organisms lack the oxidative transport system for intracellular drug accumulation. Metronidazole resistance, which is rarely encountered, is mediated by a decrease in nitroreduction of the compound to the active agent. Clindamycin-erythromycin resistance in B. fragilis is probably similar to macrolide-lincosamide-streptogramin resistance in aerobic bacteria. Two transfer factors, pBFTM10 and pBF4, which confer resistance to clindamycin have been described; the resistance determinant on them is widely distributed in nature. Tetracyline resistance in B. fragilis is mediated by a block in uptake of the drug. Transfer of tetracycline resistance is common; however, no transfer factor has been isolated. Transfer has been proposed to occur via a conjugal transposon. The special characteristics of the infected site influence the outcome of antimicrobial therapy, particularly in abscesses.(ABSTRACT TRUNCATED AT 250 WORDS)
D000038:Abscess / Q000188:drug therapy; D000900:Anti-Bacterial Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001421:Bacteria, Anaerobic / Q000187:drug effects* / Q000502:physiology; D001424:Bacterial Infections / Q000188:drug therapy; D001442:Bacteroides Infections / Q000188:drug therapy; D001441:Bacteroides fragilis / Q000187:drug effects / Q000502:physiology; D002701:Chloramphenicol / Q000494:pharmacology; D002981:Clindamycin / Q000494:pharmacology; D004251:DNA Transposable Elements; D004352:Drug Resistance, Microbial; D004917:Erythromycin / Q000494:pharmacology; D006801:Humans; D007769:Lactams; D008795:Metronidazole / Q000494:pharmacology; D011815:R Factors; D013752:Tetracycline / Q000494:pharmacology
D000900:Anti-Bacterial Agents; D004251:DNA Transposable Elements; D007769:Lactams; D008795:Metronidazole; D002981:Clindamycin; D004917:Erythromycin; D002701:Chloramphenicol; D013752:Tetracycline