4.6 Article

Distribution of Carbapenemase Genes among Carbapenem-Non-Susceptible Acinetobacter baumanii Blood Isolates in Indonesia: A Multicenter Study

Journal

ANTIBIOTICS-BASEL
Volume 11, Issue 3, Pages -

Publisher

MDPI
DOI: 10.3390/antibiotics11030366

Keywords

infectious disease; Acinetobacter baumannii; CNSAB; carbapenemase gene; resistant factor; Indonesia

Funding

  1. Indonesian Ministry of Higher Education [B/112/E3/RA.00/2021]
  2. Japan Initiative for Global Research Network on Infectious Diseases (J-GRID)
  3. Faculty of Medicine, Universitas Riau

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Carbapenem non-susceptible Acinetobacter baumannii (CNSAB) is a significant pathogen causing nosocomial bacteremia among critically ill patients worldwide. This study analyzed the genetic profiles of CNSAB isolates from bacteremia patients in Indonesia and found that they were mostly resistant to multiple antibiotic classes, but susceptible to tigecycline and trimethoprim-sulfamethoxazole. The bla(OXA-23-like) gene was identified as the predominant gene. A national surveillance system is needed to monitor the genetic profiles of CNSAB in Indonesia.
Carbapenem non-susceptible Acinetobacter baumannii (CNSAB) is an important pathogen that causes nosocomial bacteremia among critically ill patients worldwide. The magnitude of antibiotic resistance of A. baumanii in Indonesia is expected to be significant; however, the data available are limited. The aim of this study was to analyze the genetic profiles of CNSAB isolates from patients with bacteremia in Indonesia. CNSAB isolates from blood cultures of bacteremia patients in 12 hospitals in Indonesia were included. The blood cultures were conducted using the BacT/Alert or BACTEC automated system. The CNSAB were identified with either Vitek 2 system or Phoenix platform followed by a confirmation test using a multiplex polymerase chain reaction (PCR) assay, targeting the specific gyrB gene. The carbapenemase genes were detected by multiplex PCR. In total, 110 CNSAB isolates were collected and were mostly resistant to nearly all antibiotic classes. The majority of CNSAB isolates were susceptible to tigecycline and trimethoprim-sulfamethoxazole (TMP-SMX), 45.5% and 38.2%, respectively. The bla(OXA-51-like) gene was identified in all CNSAB isolates. Out of the total, 83.6% of CNSAB isolates had bla(OXA-23-like) gene, 37.3% bla(OXA-24-like) gene, 4.5% bla(NDM-1) gene, 0.9% bla(IMP-1) gene, and 0.9% bla(VIM) gene. No bla(OXA-48-like) gene was identified. The bla(OXA-23-like) gene was the predominant gene in all except two hospitals. The presence of the bla(OXA-24-like) gene was associated with resistance to tigecycline, amikacin, TMP-SMX and cefoperazone-sulbactam, while bla(OXA-23-like) gene was associated with resistance to TMP-SMX and cefoperazone-sulbactam. In conclusion, the bla(OXA-23-like) gene was the predominant gene among CNSAB isolates throughout Indonesia. A continuous national surveillance system needs to be established to further monitor the genetic profiles of CNSAB in Indonesia.

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