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Clonal spread of carbapenem non-susceptible Acinetobacter baumannii in an intensive care unit in a teaching hospital in China.

ABSTRACT: BACKGROUND: This study was aimed to investigate the genetic diversity and antibiotic resistance profile of the nosocomial infection agent Acinetobacter baumannii from a medical intensive care unit (ICU) in a teaching hospital in Suzhou, China. METHODS: The genetic relationship among A. baumannii isolates in an ICU was investigated using multilocus sequence typing (MLST). The antibiotic resistance pattern was determined by performing an antibiotic susceptible test, which included an agar dilution method and an E-test method. Resistant determinants, e.g., carbapenemase genes, metallo-?-lactamases, and class 1 integron, were analyzed by specific PCR and DNA sequencing. RESULTS: In the present study, 33 non-duplicate isolates were identified as 5 existing sequence types (STs) (ST92, ST75, ST112, ST145, and ST345) and 1 new sequence type STn, which has a G-A mutation at nt268 on ropD40 of ST251. These results reveal limited diversity in carbapenem non-susceptible A. baumannii (CNSAb) isolates in our ICU, which are comprised of only 2 distinct STs, with ST92 and ST75 clustering into a clonal complex (CC) 92. Most CNSAb isolates (94.4%, 17/18) harbored the OXA-23 gene, while no carbapenem-susceptible A. baumannii (CSAb) isolates harbored it. In addition, 66.7% (22/33) isolates were positive for class 1 integrase, and gene cassette analysis showed there are 3 gene arrays among them, i.e., aacA4-catB8-aadA1 (77.3%, 17/22), aacA4 (22.7%, 5/22), and aacC1-orfX-orfX'-aadA1 (4.5%, 1/22). CONCLUSIONS: When all these data are combined, the antibiotic resistance and wide distribution of CNSAb isolates in our ICU are probably caused by expansion of the CC92 clone.

SUBMITTER: Zhong Q

PROVIDER: S-EPMC3486935 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature

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Clonal spread of carbapenem non-susceptible Acinetobacter baumannii in an intensive care unit in a teaching hospital in China.

Zhong Qiao Q Xu Weidong W Wu Yuanjian Y Xu Hongxing H

Annals of laboratory medicine 20121017 6

<h4>Background</h4>This study was aimed to investigate the genetic diversity and antibiotic resistance profile of the nosocomial infection agent Acinetobacter baumannii from a medical intensive care unit (ICU) in a teaching hospital in Suzhou, China.<h4>Methods</h4>The genetic relationship among A. baumannii isolates in an ICU was investigated using multilocus sequence typing (MLST). The antibiotic resistance pattern was determined by performing an antibiotic susceptible test, which included an ...[more]

PMID: 23130340

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Project description:Acinetobacter baumannii is an opportunistic pathogen primarily associated with multidrug-resistant nosocomial infections, for which polymyxins are the last-resort antibiotics. This study investigated carbapenem-resistant A. baumannii strains exhibiting an extensively drug-resistant (XDR) phenotype, including four isolates considered locally pan drug-resistant (LPDR), isolated from inpatients during an outbreak at a teaching hospital in Brazil. ApaI DNA macrorestriction followed by PFGE clustered the strains in three pulsotypes, named A to C, among carbapenem-resistant A. baumannii strains. Pulsotypes A and B clustered six polymyxin-resistant A. baumannii strains. MLST analysis of representative strains of pulsotypes A, B, and C showed that they belong, respectively, to sequence types ST1 (clonal complex, CC1), ST79 (CC79), and ST903. Genomic analysis of international clones ST1 and ST79 representative strains predicted a wide resistome for β-lactams, aminoglycosides, fluoroquinolones, and trimethoprim-sulfamethoxazole, with bla OXA-23 and bla OXA-72 genes encoding carbapenem resistance. Amino acid substitutions in PmrB (Thr232Ile or Pro170Leu) and PmrC (Arg125His) were responsible for polymyxin resistance. Although colistin MICs were all high (MIC ≥ 128 mg/L), polymyxin B MICs varied; strains with Pro170Leu substitution in PmrB had MICs > 128 mg/L, while those with Thr232Ile had lower MICs (16-64 mg/L), irrespective of the clone. Although the first identified polymyxin-resistant A. baumannii strain belonged to ST79, the ST1 strains were endemic and caused the outbreak most likely due to polymyxin B use. The genome comparison of two ST1 strains from the same patient, but one susceptible and the other resistant to polymyxin, revealed mutations in 28 ORFs in addition to pmrBC. The ORF codifying an acyl-CoA dehydrogenase has gained attention due to its fatty acid breakdown and membrane fluidity involvement. However, the role of these mutations in the polymyxin resistance mechanism remains unknown. To prevent the dissemination of XDR bacteria, the hospital infection control committee implemented the patient bathing practice with a 2% chlorhexidine solution, a higher concentration than all A. baumannii chlorhexidine MICs. In conclusion, we showed the emergence of polymyxin resistance due to mutations in the chromosome of the carbapenem-resistant A. baumannii ST1, a high-risk global clone spreading in this hospital.

Project description:Background:A. baumannii is a common nosocomial pathogen known for its high transmission potential. A high rate of carbapenem-susceptible Acinetobacter calcoaceticus-Acinetobacter baumannii (ACB)-complex in clinical specimens led to the implementation of a pathogen-based surveillance on a 32-bed surgical intensive care unit (SICU) in a German tertiary care centre. Methods:Between April 2017 and March 2018, ACB-complex isolates with an epidemiological link to the SICU were further assessed. Identification to the species level was carried out using a multiplex PCR targeting the gyrB gene, followed by RAPD, PFGE (ApaI) and whole genome sequencing (WGS, core genome MLST, SeqSphere+ software, Ridom). Additional infection prevention and control (IPC) measures were introduced as follows: epidemiological investigations, hand hygiene training, additional terminal cleaning and disinfection incl. UV-light, screening for carbapenem-susceptible A. baumannii and environmental sampling. Hospital-acquired infections were classified according to the CDC definitions. Results:Fourty four patients were colonized/infected with one or two (different) carbapenem-susceptible ACB-complex isolates. Fourty three out of 48 isolates were classified as hospital-acquired (detection on or after 3rd day of admission). Nearly all isolates were identified as A. baumannii, only four as A. pittii. Twelve patients developed A. baumannii infections. Genotyping revealed two pulsotype clusters, which were confirmed to be cgMLST clonal cluster type 1770 (n?=?8 patients) and type 1769 (n?=?12 patients) by WGS. All other isolates were distinct from each other. Nearly all transmission events of the two clonal clusters were confirmed by conventional epidemiology. Transmissions stopped after a period of several months. Environmental sampling revealed a relevant dissemination of A. baumannii, but only a few isolates corresponded to clinical strains. Introduction of the additional screening revealed a significantly earlier detection of carbapenem-susceptible A. baumannii during hospitalization. Conclusions:A molecular and infection surveillance of ACB-complex based on identification to the species level, classic epidemiology and genotyping revealed simultaneously occurring independent transmission events and clusters of hospital-acquired A. baumannii. This underlines the importance of such an extensive surveillance methodology in IPC programmes also for carbapenem-susceptible A. baumannii.

Project description:Acinetobacter baumannii is a common cause of healthcare-associated infections (HAI) worldwide, mostly occurring in intensive care units (ICUs). Extended-spectrum beta lactamases (ESBL)-positive A. baumannii strains have emerged as highly resistant to most currently used antimicrobial agents, including carbapenems. The most common mechanism for carbapenem resistance in this species is β-lactamase-mediated resistance. Carbapenem-hydrolyzing class D oxacillinases are widespread among multidrug-resistant (MDR) A. baumannii strains. The present study was conducted to determine the presence and distribution of blaOXA genes among multidrug-resistant A. baumannii isolated from ICU patients and genes encoding insertion sequence (IS-1) in these isolates. Additionally, the plasmid DNA profiles of these isolates were determined. A total of 120 clinical isolates of A. baumannii from various ICU clinical specimens of four main Jordanian hospitals were collected. Bacterial isolate identification was confirmed by biochemical testing and antibiotic sensitivity was then assessed. PCR amplification and automated sequencing were carried out to detect the presence of blaOXA-51, blaOXA-23, blaOXA-24, and blaOXA-58 genes, and ISAba1 insertion sequence. Out of the 120 A. baumannii isolates, 95% of the isolates were resistant to three or more classes of the antibiotics tested and were identified as MDR. The most frequent resistance of the isolates was against piperacillin (96.7%), cephalosporins (97.5%), and β-lactam/β-lactamase inhibitor combinations antibiotics (95.8%). There were 24 (20%) ESBL-producing isolates. A co-existence of blaOXA-51 gene and ISAba1 in all the 24 ESBL-producing isolates was determined. In addition, in the 24 ESBL-producing isolates, 21 (87.5%) carried blaOXA-51 and blaOXA-23 genes, 1 (4.2%) carried blaOXA-51 and blaOXA-24, but all were negative for the blaOXA-58 gene. Plasmid DNA profile A and profile B were the most common (29%) in ESBL-positive MDR A. baumannii isolates while plasmid DNA profile A was the most common in the ESBL-negative isolates. In conclusion, there was an increase in prevalence of MDR-A. baumannii in ICU wards in Jordanian hospitals, especially those having an ESBL phenotype. Thus, identification of ESBL genes is necessary for the surveillance of their transmission in hospitals.

Dataset Information

Clonal spread of carbapenem non-susceptible Acinetobacter baumannii in an intensive care unit in a teaching hospital in China.

Publications

Clonal spread of carbapenem non-susceptible Acinetobacter baumannii in an intensive care unit in a teaching hospital in China.

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