Emergence of resistance in gram-negative bacilli during beta-lactam therapy: a challenge for the future.

J C Pechère
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Abstract

The means by which gram-negative bacilli can resist newer beta-lactam antibiotics are reviewed. A first situation is generated by mutants which produce great amounts of a chromosomal cephalosporinase. These cells are present (frequency: 10(-4) to 10(-7] within bacterial populations such as Enterobacter cloacae, and multiply after selection during therapy by third-generation cephalosporins or monobactams. A second problem arose by 1985, with the sudden development of plasmid-mediated beta-lactamases markedly active against third-generation cephalosporins. Some recent molecules, such as penems, are not affected by the two mechanisms mentioned above but remain exposed to other resistance problems. Notably Pseudomonas aeruginosa strains can develop resistance during therapy by imipenem thanks to specific alterations of the bacterial outer membrane. As a consequence of these resistance difficulties, new interpretations for susceptibility testing and new therapeutic approaches should be considered.

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在β -内酰胺治疗期间革兰氏阴性杆菌出现耐药性:未来的挑战。
本文综述了革兰氏阴性杆菌耐新β -内酰胺类抗生素的方法。第一种情况是由产生大量染色体头孢菌素酶的突变体产生的。这些细胞存在于阴沟肠杆菌等细菌群中(频率:10(-4)至10(-7)),在使用第三代头孢菌素或单巴坦治疗期间进行选择后繁殖。第二个问题出现在1985年,质粒介导的β -内酰胺酶突然出现,对第三代头孢菌素具有显著活性。一些最近的分子,如阴茎,不受上述两种机制的影响,但仍然暴露于其他抗性问题。值得注意的是,铜绿假单胞菌菌株在亚胺培南治疗期间可由于细菌外膜的特定改变而产生耐药性。由于这些耐药困难,应考虑对药敏试验的新解释和新的治疗方法。
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