Clonal Spread of Carbapenem Non-susceptible Acinetobacter baumannii in an Intensive Care Unit in a Teaching Hospital in China.
10.3343/alm.2012.32.6.413
- Author:
Qiao ZHONG
1
;
Weidong XU
;
Yuanjian WU
;
Hongxing XU
Author Information
1. Department of Laboratory Medicine, Suzhou Municipal Hospital Affiliated Nanjing Medical University, Suzhou, China. zhongqiao83@yahoo.com.cn
- Publication Type:Original Article
- Keywords:
MLST;
Molecular epidemiology;
Acinetobacter baumannii
- From:Annals of Laboratory Medicine
2012;32(6):413-419
- CountryRepublic of Korea
- Language:English
-
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-beta-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.
