Mechanisms of resistance to trimethoprim, the sulfonamides, and trimethoprim-sulfamethoxazole.
Mechanisms of resistance to trimethoprim, the sulfonamides, and trimethoprim-sulfamethoxazole.
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对甲氧苄啶、磺胺类药物和甲氧苄啶-磺胺甲恶唑的耐药机制。
DOI：
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发表时间：
1982
期刊：
影响因子：
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通讯作者：
R. Then
中科院分区：
文献类型：
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作者：
R. Then
已知多种不同的机制导致对甲氧苄啶、磺胺类药物或甲氧苄啶-磺胺组合的天然或获得性耐药性。一些具有明显临床重要性的机制已经得到深入研究。其中包括独特的旁路机制，例如耐药性、质粒编码的二氢叶酸还原酶或二氢叶酸合成酶的合成；迄今为止，在其他药物耐药性的研究中还没有遇到过这种机制。本文重点关注过去很少讨论的几种耐药机制，包括甲氧苄啶或磺胺类药物的代谢改变和对氨基苯甲酸的过量产生，以及同时存在的不止一种机制。这些机制在临床分离株耐药性中的作用需要进一步研究。
A variety of different mechanisms are known to be responsible for either natural or acquired resistance to trimethoprim, the sulfonamides, or trimethoprim-sulfonamide combinations. Some mechanisms of obvious clinical importance have been studied intensively. Among these are unique bypass mechanisms such as the synthesis of drug-resistant, plasmid-coded dihydrofolate reductase or dihydropteroate synthetase; such mechanisms so far have not been encountered in studies of resistance to other drugs. This article focuses on several mechanisms of resistance that have rarely been discussed in the past, including metabolic alteration of trimethoprim or the sulfonamides and hyperproduction of p-aminobenzoic acid, and on the simultaneous presence of more than one mechanism. The role of these mechanisms in the resistance of clinical isolates requires further investigation.