Tally F P, Cuchural G J, Bieluch V M, Jacobus N V, Malamy M H
Scand J Infect Dis Suppl. 1984;43:34-43.
Knowledge of the mechanisms of antimicrobial resistance and resistance transfer in anaerobic bacteria has been gained over the past several years. There is widespread resistance to the beta-lactam antibiotics in the B. fragilis group of organisms and there is emerging penicillin resistance in other Bacteroides species. These resistances are usually mediated by chromosomal beta-lactamases. There have been two new beta-lactamases described in Bacteroides; a penicillinase which inactivates ureidopenicillins and another that inactivates cefoxitin. The transfer of the common beta-lactamase, penicillinase, and cefoxitin resistance has been documented in B. fragilis. The mechanism of tetracycline resistance in B. fragilis is the lack of accumulation of intracellular drug; the resistance is widespread in anaerobic bacteria and is seen in two-thirds of the B. fragilis strains. The transfer of tetracycline resistance is common, however, no transfer factor has yet been isolated. Clindamycin-erythromycin resistance in Bacteroides was first recognized in the mid-1970s and transferable resistance was described in 1979. The mechanism of resistance is probably similar to macrolide-lincosamide-streptinogramin-resistance seen in aerobic bacteria. Two clindamycin resistance transfer factors, pBFTM10 and pIP410 (pBF4) have been described. A common resistance determinant found both on plasmids and chromosomes is widely distributed in nature and it probably resides on a transposon. DNA homology studies indicate that there is more than one type of clindamycin resistance in Bacteroides; a newly recognized clindamycin resistance determinant is transferable. Local outbreaks of clindamycin resistance have been noted in the United States and in Europe. The susceptibility of Bacteroides in the United States in 1983 from a multi-center study reveals a 5% incidence of resistance in B. fragilis and 1% in Bacteroides species. The rate of clindamycin resistance has remained steady over the past three years in the Bacteroides fragilis group.
在过去几年里，人们对厌氧菌的抗菌耐药机制及耐药性转移已有了一定了解。脆弱拟杆菌属的微生物对β-内酰胺类抗生素普遍耐药，而其他拟杆菌属物种中也出现了对青霉素的耐药性。这些耐药性通常由染色体β-内酰胺酶介导。在拟杆菌属中已发现两种新的β-内酰胺酶：一种青霉素酶可使脲基青霉素失活，另一种可使头孢西丁失活。在脆弱拟杆菌中已证实常见的β-内酰胺酶、青霉素酶及头孢西丁耐药性的转移。脆弱拟杆菌对四环素耐药的机制是细胞内药物蓄积不足；这种耐药性在厌氧菌中普遍存在，三分之二的脆弱拟杆菌菌株都有此耐药性。四环素耐药性的转移很常见，然而，尚未分离出转移因子。拟杆菌属对克林霉素-红霉素的耐药性最早于20世纪70年代中期被发现，1979年报道了可转移耐药性。其耐药机制可能与需氧菌中所见的大环内酯-林可酰胺-链阳菌素耐药性类似。已描述了两种克林霉素耐药性转移因子，即pBFTM10和pIP410（pBF4）。一种在质粒和染色体上都存在的常见耐药决定簇在自然界广泛分布，它可能存在于转座子上。DNA同源性研究表明，拟杆菌属中存在不止一种类型的克林霉素耐药性；一种新发现的克林霉素耐药决定簇是可转移的。在美国和欧洲已注意到克林霉素耐药性的局部暴发。1983年美国一项多中心研究显示，脆弱拟杆菌的耐药发生率为5%，其他拟杆菌属物种为1%。在过去三年里，脆弱拟杆菌属中克林霉素耐药率一直保持稳定。
