IRT and CMT β-lactamases and inhibitor resistance
IRT and CMT β-lactamases and inhibitor resistance
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DOI：
10.1111/j.1469-0691.2007.01849.x
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发表时间：
2008-01-01
影响因子：
14.2
通讯作者：
de la Pedrosa, E. Gomez G.
中科院分区：
文献类型：
--
作者：
Canton, R.;Morosini, M. I.;de la Pedrosa, E. Gomez G.
大肠杆菌对青霉素-β-内酰胺酶抑制剂组合的获得性耐药是由于：（i）由于小的多拷贝质粒或强启动子中存在bla（TEM-1）基因而导致青霉素酶过度产生;（ii）组成型AmpC头孢菌素酶过度产生;（iii）OXA型和耐药TEM（IRT）β-内酰胺酶。IRT酶通过TEM-1或TEM-2 β-内酰胺酶的突变事件出现，这些突变事件影响对γ-内酰胺酶抑制剂的底物亲和力。它们主要在社区患者的泌尿系感染中分离。流行率是可变的，取决于地理区域，检测方法和潜在的选择压力。这些酶可能演变成复杂的突变体（CMT酶），这也赋予耐药的超广谱头孢菌素。迄今为止尚未检测到具有IRT表型的CTX-M酶。需要对IRT酶进行新的研究，包括群体结构、与毒力性状的关联以及质粒分散。
Acquired resistance to penicillin-beta-lactamase inhibitor combinations in Escherichia coli is due to: (i) penicillinase hyperproduction due to the presence of the bla(TEM-1) gene in small multicopy plasmids or strong promoters; (ii) overproduction of constitutive AmpC cephalosporinase; and (iii) OXA-type and inhibitor-resistant TEM (IRT) beta-lactamases. IRT enzymes emerge via mutational events from TEM-1 or TEM-2 beta-lactamases that affect substrate affinity for v-lactamase inhibitors. They are mainly isolated in urinary infections from community patients. Prevalence is variable, depending on geographical area, detection methods and potential selection pressure. These enzymes may evolve into complex mutants (CMT enzymes), which also confer resistance to extended-spectrum cephalosporins. CTX-M enzymes with the IRT phenotype have not been detected to date. New studies of IRT enzymes, including population structure, association with virulence traits and plasmid dispersion, are needed.