Stürenburg Enno, Kühn Alexandra, Mack Dietrich, Laufs Rainer
Institut für Infektionsmedizin, Zentrum für Klinisch-Theoretische Medizin I, Universitätsklinikum Hamburg-Eppendorf, Martinistrasse 52, D-20246 Hamburg, Germany.
J Antimicrob Chemother. 2004 Aug;54(2):406-9. doi: 10.1093/jac/dkh334. Epub 2004 Jun 16.
In recent years, cefotaximases of the CTX-M type have become a predominant cause of resistance to extended-spectrum cephalosporins in Gram-negative bacteria. Although most enzymes provide higher levels of resistance to cefotaxime than to ceftazidime, mutants with enhanced catalytic efficiency against ceftazidime have recently been described. This report identifies another ceftazidime-resistant mutant of the CTX-M class of enzymes.
Two ceftazidime-resistant strains, Escherichia coli IFI-1 and Klebsiella pneumoniae IFI-2, were isolated from a 46-year-old man during treatment of postoperative peritonitis with ceftazidime. Susceptibility testing, mating-out assays, isoelectric focusing as well as PCR and sequencing techniques were carried out to investigate the underlying mechanism of resistance.
E. coli IFI-1 and K. pneumoniae IFI-2 exhibited a clavulanic acid-inhibited substrate profile that included extended-spectrum cephalosporins. Notably, both strains had up to a 32-fold higher level of resistance to ceftazidime than to cefotaxime. Further characterization revealed that a novel bla(CTX-M) gene encoding a beta-lactamase with a pI of 8.9 was implicated in this resistance: CTX-M-23. Along with the substitutions D114N and S140A, CTX-M-23 differed from CTX-M-1, the most closely related enzyme, by a P167T replacement in the active-site omega loop, which has not previously been observed in other CTX-M enzymes. By analogy with what was observed with certain TEM/PSE/BPS-type beta-lactamases, the amino acid substitution in the omega loop may explain ceftazidime resistance, which has only rarely been reported for other CTX-M enzymes.
The emergence of a new ceftazidime-resistant CTX-M-type mutant provides evidence that these enzymes are able to broaden their substrate spectrum towards ceftazidime, probably due to substitutions in the active-site omega loop.
近年来,CTX-M型头孢他啶酶已成为革兰氏阴性菌对广谱头孢菌素耐药的主要原因。尽管大多数酶对头孢噻肟的耐药性高于头孢他啶,但最近已报道了对头孢他啶催化效率增强的突变体。本报告鉴定了CTX-M类酶的另一种头孢他啶耐药突变体。
从一名46岁男性术后腹膜炎患者接受头孢他啶治疗期间分离出两株头孢他啶耐药菌株,即大肠埃希菌IFI-1和肺炎克雷伯菌IFI-2。进行药敏试验、接合试验、等电聚焦以及聚合酶链反应(PCR)和测序技术,以研究耐药的潜在机制。
大肠埃希菌IFI-1和肺炎克雷伯菌IFI-2表现出对克拉维酸敏感的底物谱,包括广谱头孢菌素。值得注意的是,两株菌对头孢他啶的耐药水平比对头孢噻肟高32倍。进一步鉴定表明,一种编码pI为8.9的β-内酰胺酶的新型bla(CTX-M)基因与这种耐药性有关:CTX-M-23。除了D114N和S140A替换外,CTX-M-23与最密切相关的酶CTX-M-1的不同之处在于活性位点ω环中的P167T替换,这在其他CTX-M酶中尚未观察到。与某些TEM/PSE/BPS型β-内酰胺酶的情况类似,ω环中的氨基酸替换可能解释了头孢他啶耐药性,而其他CTX-M酶很少有这种耐药性报道。
一种新的头孢他啶耐药CTX-M型突变体的出现证明,这些酶能够扩大其对头孢他啶的底物谱,这可能是由于活性位点ω环中的替换所致。