Author:
Mojica María F.,De La Cadena Elsa,Ríos Rafael,García-Betancur Juan Carlos,Díaz Lorena,Reyes Jinnethe,Hernández-Gómez Cristhian,Radice Marcela,Gales Ana C.,Castañeda Méndez Paulo,Munita José M.,Pallares Christian José,Martínez José R. W.,Villegas María Virginia
Abstract
ObjectivesIdentify molecular mechanisms responsible for the in vitro non-susceptibility to ceftolozane/tazobactam (TOL) in a group of 158 clinical isolates of Pseudomonas aeruginosa from five Latin American countries collected before the introduction of TOL into the clinical practice.MethodsClinical isolates of P. aeruginosa (n = 504) were collected between January 2016 and October 2017 from 20 hospitals located in Argentina, Brazil, Chile, Colombia, and Mexico. Minimum inhibitory concentrations (MICs) to TOL were determined by standard broth microdilution and interpreted according to CLSI breakpoints. Initially, production of carbapenemases in TOL non-susceptible isolates was assessed by Rapidec® followed by qPCR to detect blaKPC, blaNDM-1, blaVIM, and blaIMP. Illumina® WGS was performed for isolates in which non-susceptibility to TOL was not mediated by carbapenemases.ResultsA total of 158 (31.3%) isolates were non-susceptible to TOL. In 74 (46.8%) of these isolates, non-susceptibility to TOL was explained by the production of at least one carbapenemase. WGS revealed that some isolates carried ESBLs, mutated blaPDC and ampD, associated with decreased susceptibility to TOL.ConclusionSubstitutions found in PDC and carbapenemase production were the most common presumed mechanisms of resistance to TOL detected in this study. This study shows that epidemiological surveillance is warranted to monitor the emergence of novel mechanisms of resistance to TOL that might compromise its clinical utility.
Subject
Microbiology (medical),Microbiology
Cited by
5 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献