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拟杆菌属中的抗菌药物耐药性

Antimicrobial resistance in Bacteroides.

作者信息

Rasmussen B A, Bush K, Tally F P

机构信息

Infectious Disease Section, Lederle Laboratories, American Cyanamid Company, Pearl River, New York 10965.

出版信息

Clin Infect Dis. 1993 Jun;16 Suppl 4:S390-400. doi: 10.1093/clinids/16.supplement_4.s390.

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.

摘要

拟杆菌属中的抗菌药物耐药性对厌氧感染化疗方案的选择有直接影响。多项研究记录了与各个医院、地理区域及抗生素处方习惯相关的药敏模式差异。已证实拟杆菌属对β-内酰胺类抗生素、四环素、克林霉素和甲硝唑具有耐药性。β-内酰胺耐药的主要机制是β-内酰胺酶的产生,包括青霉素酶、头孢菌素酶以及可水解亚胺培南的金属β-内酰胺酶。对四环素的耐药性由tetQ类的核糖体保护介导。对克林霉素的耐药性由核糖体修饰介导。甲硝唑耐药可能是由于抗生素摄取减少、硝基还原酶活性降低、丙酮酸:铁氧化还原蛋白氧化还原酶活性降低以及乳酸脱氢酶活性增加共同作用所致。最令人不安的是同一生物体中对多种药物出现耐药性。了解耐药机制以及这些药物的作用机制不仅将有助于设计新的抗菌药物,还能为拟杆菌感染的治疗提供明智的治疗选择。

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