Cantón R, Morosini M I, de la Maza O Martín S, de la Pedrosa E Gomez G
Servicio de Microbiología, Hospital Universitario Ramón y Cajal, Madrid, Spain.
Clin Microbiol Infect. 2008 Jan;14 Suppl 1:53-62. doi: 10.1111/j.1469-0691.2007.01849.x.
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 beta-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.
大肠埃希菌对青霉素 - β - 内酰胺酶抑制剂联合制剂获得性耐药的原因如下：（i）由于小多拷贝质粒中存在bla(TEM - 1)基因或强启动子导致青霉素酶过度产生；（ii）组成型AmpC头孢菌素酶过度产生；以及（iii）OXA型和抑制剂耐药TEM（IRT）β - 内酰胺酶。IRT酶通过影响对β - 内酰胺酶抑制剂底物亲和力的突变事件从TEM - 1或TEM - 2β - 内酰胺酶产生。它们主要在社区患者的泌尿系统感染中分离得到。其流行率因地理区域、检测方法和潜在选择压力而异。这些酶可能演变成复杂突变体（CMT酶），其也赋予对超广谱头孢菌素的耐药性。迄今尚未检测到具有IRT表型的CTX - M酶。需要对IRT酶进行新的研究，包括群体结构、与毒力特征的关联以及质粒传播情况。
