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Molecular epidemiological survey of bacteremia by multidrug resistant Pseudomonas aeruginosa: the relevance of intrinsic resistance mechanisms.

Authors :
Dantas, Raquel Cristina Cavalcanti
Silva, Rebecca Tavares e
Ferreira, Melina Lorraine
Gonçalves, Iara Rossi
Araújo, Bruna Fuga
Campos, Paola Amaral de
Royer, Sabrina
Batistão, Deivid William da Fonseca
Gontijo-Filho, Paulo Pinto
Ribas, Rosineide Marques
Source :
PLoS ONE; 5/8/2017, Vol. 12 Issue 5, p1-14, 14p
Publication Year :
2017

Abstract

The bacterial factors associated with bacteremia by multidrug-resistant and extensively drug-resistant P. aeruginosa, including overexpression of efflux pumps, AmpC overproduction, and loss/alteration of the OprD porin in isolates that are non-Metallo-β-Lactamase producing were analyzed in a retrospective study. Molecular analyses included strain typing by Pulsed Field Gel Electrophoresis and identification of key genes via qualitative and quantitative PCR-based assays. Previous use of carbapenems and tracheostomy was independently associated with the development of bacteremia by extensively drug-resistant and multidrug-resistant strains of P. aeruginosa. A high consumption of antimicrobials was observed, and 75.0% of the isolates contained amplicons with the bla<subscript>SPM-1</subscript> and bla<subscript>VIM</subscript> genes. Of the 47 non-Metallo-β-Lactamase isolates, none had another type of carbapenemase. However, the isolates exhibited high rates of hyperproduction of AmpC, loss of the OprD porin (71.4%) and the presence of MexABOprM (57.1%) and MexXY (64.3%). This study suggests that in non-Metallo-β-Lactamase isolates, the association of intrinsic resistance mechanisms could contributes to the expression of multidrug-resistant/extensively drug-resistant phenotypes. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
19326203
Volume :
12
Issue :
5
Database :
Complementary Index
Journal :
PLoS ONE
Publication Type :
Academic Journal
Accession number :
122916447
Full Text :
https://doi.org/10.1371/journal.pone.0176774