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Home Journal Highlights Monitoring Antibiotic Resistance Evolution: an Interdisciplinary Approach
Monitoring Antibiotic Resistance Evolution: an Interdisciplinary Approach Print E-mail

 

Class A extended-spectrum beta-lactamases (ESBLs) have been reported with increasing frequency since they were first described in 1983. Now Teresa M. Coque of the microbiology department of University Hospital Ramón y Cajal Madrid, Spain, et al. show that the transnational emergence and spread of extended spectrum beta-lactamase TEM-24 was a multifaceted phenomenon involving old genes for ampicillin resistance, such as TEM-2, within old genetic platforms, and installed in the broad-host range IncA/C plasmid. That plasmid's broad range probably facilitated successive evolutionary events leading to capture of the TEM-24 gene in a multi-resistance region associated with defective Tn402 elements, says Coque. In any event, "the IncA/C plasmid was instrumental in spreading Enterobacter aerogenes, Klebsiella pneumoniae, and Proteus mirabilis, thus efficiently disseminating the dangerous TEM-24 beta-lactamase," she says. This work illustrates the complexity of the evolution of antibiotic resistance, she says. "Such complexity can only be addressed by a multilevel population biology/epidemiological analysis, simultaneously detecting genes, genetic platforms, integrons, transposons, plasmids, and clones, from multiple locations." Each of these genetic elements is both a "unit of selection" for evolutionary biologists, and a "unit of surveillance" for molecular epidemiologists. Preventing future antibiotic resistance will require an interdisciplinary approach, she says.

(A. Novais, F. Baquero, E. Machado, R. Cantón, L. Peixe, and T. M. Coque. 2010. International spread and persistence of TEM-24 is caused by the confluence of highly penetrating Enterobacteriaceae clones and an IncA/C2 plasmid containing Tn1696::TN1 and IS5075-Tn21. Antimicrob. Agents Chemother. 54:825-834.)