Abstract

BackgroundAcinetobacter baumannii causes difficult-to-treat nosocomial infections, which often lead to morbidity due to the development of antimicrobial drug resistance and expression of virulence genes. Data regarding the association of resistance to colistin, a last treatment option, and the virulence gene expression of A. baumannii is scarce.MethodsWe evaluated the MLVA genotype, antimicrobial resistance, and biofilm formation of 100 A. baumannii isolates from burn patients, and further compared the in vitro and in vivo expression of four virulence genes among five colistin-resistant A. baumannii (Cst-R-AB) isolates. Five Cst-R-AB isolates were tested; one from the present study, and four isolated previously.ResultsOur results showed that reduced expression of recA, along with increased in vivo expression of lpsB, dnaK, and blsA; are associated with colistin resistance among Cst-R-AB isolates. Differences in virulence gene expressions among Cst-R-AB isolates, may in part explain common discrepant in vitro vs. in vivo susceptibility data during treatment of infections caused by Cst-R-AB.ConclusionsOur findings highlight the intricate relationship between colistin-resistance and virulence among A. baumannii isolates, and underscore the importance of examining the interactions between virulence and antimicrobial resistance toward efforts to control the spread of multidrug-resistant A. baumannii (MDR-AB) isolates, and also to reduce disease severity in burn patients with MDR-AB infection.

Highlights

  • Acinetobacter baumannii causes difficult-to-treat nosocomial infections, which often lead to morbidity due to the development of antimicrobial drug resistance and expression of virulence genes

  • Association of multi-drug resistant (MDR) profile with International clone (IC) types and biofilm formation index We further examined the association of the MDR profile of antimicrobial resistance of each isolate with the ability (See figure on page.) Fig. 1 Comparison of multi-loci variable-number tandem repeat analysis (MLVA) genotype diversity of 100 Acinetobacter baumannii isolates with their biofilm formation phenotype, as well as resistance to Clinical and Laboratory Standards Institute (CLSI) antimicrobial groups, and international clonal lineage to form biofilm as a virulence determinant, as well as the IC type of each isolate (Fig. 2a, b)

  • While the present study focused on the expression profile of four virulence genes among five Cst-R-Acinetobacter baumannii or A. baumannii (AB) isolates, the variation in the levels of virulence gene mitochondrial ribonucleic acid (mRNA) in vitro vs. in vivo conditions among Cst-RAB isolates could be due to a myriad of additional factors, such as differences between the cellular environment of the wound site as compared to the cell-free culture conditions

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Summary

Introduction

Acinetobacter baumannii causes difficult-to-treat nosocomial infections, which often lead to morbidity due to the development of antimicrobial drug resistance and expression of virulence genes. Data regarding the association of resistance to colistin, a last treatment option, and the virulence gene expression of A. baumannii is scarce. Acinetobacter baumannii is an opportunistic pathogen that can cause formidable infections among patients with burn wounds worldwide [1]. Bahador et al Ann Clin Microbiol Antimicrob (2018) 17:24 role in the high rate of treatment failure among wound infections caused by highly resistant A. baumannii isolates remains to be explored [14]. The expression of recA by A. baumannii isolates increases resistance to stress [19], while recA inactivation increases susceptibility to a variety of antimicrobial agents [15, 20]

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