An outbreak of bla OXA-51-like- and bla OXA-66-positive Acinetobacter baumannii ST208 in the emergency intensive care unit

Abstract

A series of clinical isolates of drug-resistant (DR) Acinetobacter baumannii with diverse drug susceptibility was detected from eight patients in the emergency intensive care unit of Tokai University Hospital. The initial isolate was obtained in March 2010 (A. baumannii Tokai strain 1); subsequently, seven isolates were obtained from patients (A. baumannii Tokai strains 2–8) and one isolate was obtained from an air-fluidized bed used by five of the patients during the 3 months from August to November 2011. The isolates were classified into three types of antimicrobial drug resistance patterns (RRR, SRR and SSR) according to their susceptibility (S) or resistance (R) to imipenem, amikacin and ciprofloxacin, respectively. Genotyping of these isolates by multilocus sequence typing revealed one sequence type, ST208, whilst that by a DiversiLab analysis revealed two subtypes. All the isolates were positive for blaOXA-51-like and blaOXA-66, as assessed by PCR and DNA sequencing. A. baumannii Tokai strains 1–8 and 10 (RRR, SRR and SSR) had quinolone resistance-associated mutations in gyrA/parC, as revealed by DNA sequencing. The ISAba1 upstream of blaOXA-51-like and aminoglycoside resistance-associated gene, armA, were detected in A. baumannii Tokai strains 1–7 and 10 (RRR and SRR) as assessed by PCR. Among the genes encoding resistance–nodulation–division family pumps (adeB, adeG and adeJ) and outer-membrane porins (oprD and carO), overexpression of adeB and adeJ and suppression of oprD and carO were seen in isolates of A. baumannii Tokai strain 2 (RRR), as assessed by real-time PCR. Thus, the molecular characterization of a series of isolates of DR A. baumannii revealed the outbreak of ST208 and diverse antimicrobial drug susceptibilities, which almost correlated with differential gene alterations responsible for each type of drug resistance.

Mechanisms Efflux Pumps of <i>Acinetobacter baumannii</i> (MDR): Increasing Resistance to Antibiotics

“…With various reported a MIC dimness of adeIJK mainly the resistance of A. baumannii to β-lactamines, lincosamides, fluoroquinolones, chloramphenicol, trimethoprime, and fusidic acid has been noticed [57]. The selection of the majority gene adeJ, will lead to an amplification in the sensitivity of chloramphenicol, macrolides, lincosamides, tetracyclines and quinolones and β-lactams [58] [59]. The regulation of adeIJK is less complex than that of adeABC, but at about 750 -850 kbp of adeIJK operon there is a regulator adeN belonging to the class of tetR [35].…”

A Epidemiological Investigation of a Nosocomial Outbreak of Multidrug-Resistant <i>Acinetobacter baumannii</i> in a Critical Care Center in Japan, 2011&ndash;2012

“…isolates identified as MDRAB was isolated from as few as 4.4z of the hospitals JANIS assessed. Although nosocomial MDRAB outbreaks have been reported in Japan (7,8), the prevalence of MDRAB infection or colonization in Japan is much lower than in other countries (9). Therefore, it is important to contain nosocomial outbreaks of MDRAB and maintain low prevalence rates of MDRAB infection and colonization in Japan.…”

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“…The resistance genes were examined via a multiplex PCR for bla OXA-23-like , bla OXA-24-like , bla OXA-51-like , bla OXA-58-like , and ISAba1 genes, as described previously [2,[10][11][12]. The amplification of the bla OXA-51-like genes was performed as described previously [6,11].…”

“…The RNA templates were extracted using the RNeasey ® Mini Kit (QIAGEN GmbH). The expression of three different resistance-nodulation-division (RND) family pump-encoding genes (adeB, adeG, adeJ) and two outer membrane porin-encoding genes (oprD and carO) were analyzed by quantitative RT-PCR using the StepOnePlus TM Real-Time PCR System (Applied Biosystems) [2,[16][17][18]. The three previously characterized genes adeB, adeG and adeJ encoded the RND pumps in the adeABC, adeFG and adeIJK operons, respectively.…”

“…Acinetobacter baumannii is a strictly aerobic, non-fermenting, non-fastidious, non-motile, catalase-positive, oxidase-negative, gram-negative bacteria that is known to be a major pathogen of nosocomial infection in immunocompromised patients [1]. Outbreaks of antimicrobial-resistant A. baumannii have become a major clinical problem [1][2][3]. All strains of A. baumannii possessed a chromosomally encoded bla OXA-51-like , some of which provided resistance to carbapenems when the molecular milieu around the gene promoted its expression, such as ISAba1 [4].…”