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초록
Background
Acinetobacter spp. is an important nosocomial pathogen for which increasing resistance to multiple antimicrobial agents has been observed. Prevalence of multidrug-resistant (MDR) Acinetobacter spp. in the intensive care unit (ICU) at a teaching hospital in Korea started to increase in 2008. The aim of this study was to determine the source of pathogen spread and to characterize the emerging strains at an early stage of outbreak.
Methods
Samples from respiratory instruments and fomites in the ICUs, as well as from the healthcare workers, were cultured to identify the sources of MDR Acinetobacter spp. Antimicrobial susceptibility was determined by the CLSI disk diffusion method. Pulsed field gel electrophoresis (PFGE) was performed for clinical and environmental isolates in or-der to determine clonality. Carbapenemase genes were detected by multiplex PCR. Infection control measures including peer-monitoring of hand washing, environmental cleaning and standard precautions were enforced.
Results
Among the samples from the ICU tools (105) and healthcare worker's hands (44), 31 (30%) and 2 (5%) respective samples yielded MDR Acinetobacter spp. Among the environmental samples, 90% were from respiratory-related equipment. The majority of clinical and environmental MDR Acinetobacter spp. (44/55) belonged to the pulsotype A. baumannii and carried both blaOXA-51-like and blaOXA-23-like genes. Even though infection-control measures were enforced, prevalence of MDR Acinetobacter spp. continues to increase.
Conclusion
An outbreak of MDR Acinetobacter spp. in a Korean hospital was caused by A. baumannii carrying the blaOXA-23-gene and was correlated with contaminated respiratory-related instruments in the ICUs. More intensive measures for nosocomial infection control are needed for successful prevention of Acinetobacter spread in hospitals.
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Fig. 1.
Number of patients with Acinetobacter spp. isolates in a Korean hospital in 2008. There was noticeable increase in Acinetobacter spp. isolation in the hospital; the number of patients of Acinetobacter isolates significantly increased from 62 in January to 168 in August, 2008. The resistance rate to carbapenem was also increased to more than 50%. More than 60% of the total isolates were from respiratory specimens.
Fig. 2.
PFGE patterns of Acinetobacter spp. isolates from ICU environment (A) and patients (B). The majority of the isolates from ICU environment and patients belonged to pulsotype A, indicating they are identical clones.
Table 1.
MDR Acinetobacter spp. isolated from the ICUs environment and healthcare worker's hands
Table 2.
Number of MDR Acinetobacter spp. isolates from clinical and environment samples according to the PFGE band patterns and OXA carbapenemase genes
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