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Updated: May 26, 2026
Rapid and Specific Detection of Acinetobacter baumannii Infections Using a Recombinase Polymerase Amplification/Cas12a-based System
Published on: April 25, 2025
Outbreak of imipenem-resistant Acinetobacter calcoaceticus-Acinetobacter baumannii complex harboring different
Yi-Tzu Lee1, Chang-Phone Fung, Fu-Der Wang
1Department of Medicine, Chutung Veterans Hospital, Chutung, Hsinchu County, Taiwan.
Background And Purpose:
To investigate the clinical and molecular epidemiology of the imipenem-resistant Acinetobacter calcoaceticus-Acinetobacter baumannii (IRAcb) complex during an outbreak in an intensive care unit (ICU).
Methods:
Forty-six clinical and 11 environmental isolates of the IRAcb complex were collected from the ICU of Taipei Veterans General Hospital, Taiwan between December 2003 and March 2004. These isolates were genotyped using pulsed-field gel electrophoresis (PFGE). Carbapenemase genes and their associated genetic structures were analyzed using PCR. Clinical data obtained from the patients were also reviewed and analyzed.
Results:
The isolates were identified at the genomic species level as A. baumannii (42 clinical and five environmental isolates) and Acinetobacter genomic species 13TU (four clinical and six environmental isolates). Both species were comprised of two pulsotypes, but those of A. baumannii were closely related (83% similar). IS1008-ΔISAba3-bla(OXA-58-like) and ISAba1-bla(OXA-51-like) were identified in 22 and 21 clinical isolates of A. baumannii, respectively (one isolate contained both). The ISAba3-bracketed bla(OXA-58-like) gene was detected in all isolates of Acinetobacter genomic species 13TU. Patient transfers between different sections of the ICU were important factors that contributed to the spread of the two pulsotypes of A. baumannii. However, among the A. baumannii isolates identified, only those carrying IS1008-ΔISAba3-bla(OXA-58-like) could be found in the environment, indicating an additional route of transmission. The prior use of carbapenem or cefepime was associated with the subsequent infection with A. baumannii carrying the ISAba1-bla(OXA-51-like) gene, while prior piperacillin/tazobactam use was associated with the subsequent infection with A. baumannii carrying the IS1008-ΔISAba3-bla(OXA-58-like) gene.
Conclusion:
A. baumannii isolates carrying different carbapenemase genes and their associated genetic structures might be transmitted or selected in different ways.
Insights
This study investigated imipenem-resistant Acinetobacter calcoaceticus-Acinetobacter baumannii (IRAcb) complex outbreaks in an ICU. Different carbapenemase genes in A. baumannii were linked to distinct transmission routes and antibiotic exposures.
Area of Science:
- Medical Microbiology
- Epidemiology
- Molecular Biology
Background:
- An outbreak of imipenem-resistant Acinetobacter calcoaceticus-Acinetobacter baumannii (IRAcb) complex occurred in an intensive care unit (ICU).
- Understanding the clinical and molecular epidemiology of this outbreak is crucial for infection control.
Purpose of the Study:
- To investigate the clinical and molecular epidemiology of the IRAcb complex during an ICU outbreak.
- To identify the genetic characteristics and transmission dynamics of the outbreak isolates.
Main Methods:
- Collected 46 clinical and 11 environmental isolates of the IRAcb complex.
- Utilized pulsed-field gel electrophoresis (PFGE) for genotyping.
- Analyzed carbapenemase genes and genetic structures using PCR and reviewed patient clinical data.
Main Results:
- Identified isolates as A. baumannii and Acinetobacter genomic species 13TU.
- Two pulsotypes of A. baumannii were closely related; one type was found in the environment, suggesting an additional transmission route.
- Specific carbapenemase genes (bla(OXA-58-like), bla(OXA-51-like)) were associated with different antibiotic exposures and transmission patterns.
Conclusions:
- A. baumannii isolates with different carbapenemase genes and genetic structures exhibit distinct transmission and selection mechanisms.
- Patient transfers and environmental contamination play roles in spreading resistant strains within the ICU.
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