Diagnostic microbiology and infectious disease · 2025
Microbiological and clinical impact of aminoglycosides on KPC-producing Klebsiella pneumoniae bacteraemia with aminoglycoside-modifying enzymes.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Seong Jae Eun, Ahn Sang Min, Han Min, Lee Yong Seop, Lee Jung Ah, Kim Jae Hoon, Kim Jung Ho, Ahn Jin Young, Jeong Su Jin, Ku Nam Su, Yeom Joon Sup, Lee Hyukmin, Choi Jun Yong
Аннотация
BACKGROUND: Klebsiella pneumoniae (KPN) is a major pathogen associated with life-threatening infections. The global rise in carbapenem-resistant KPN, particularly Klebsiella pneumoniae carbapenemase (KPC)-producing strains, presents a treatment challenge. The efficacy of aminoglycosides against KPC-producing KPN strains carrying aminoglycoside-modifying enzyme (AME) genes remains unclear. This study evaluated the clinical and microbiological effects of aminoglycoside therapy on AME gene-bearing KPC-producing KPN bacteraemia.
METHODS: We conducted a retrospective cohort study on adults with amikacin-susceptible KPC-producing KPN bacteraemia at a South Korean tertiary hospital (2022-2024). Antimicrobial susceptibility was assessed using VITEK 2 and disc diffusion per Clinical and Laboratory Standards Institute guidelines. The blaKPC gene was detected via immunochromatography, whereas whole-genome sequencing identified blaKPC subtypes and AME genes. Clinical and microbiological outcomes were analysed based on aminoglycoside use.
RESULTS: Among 136 patients (mean age: 63.6 years), 98 received aminoglycoside therapy, and 38 did not. Intra-abdominal infections were the most common source. Microbiological clearance within one week was significantly lower in the aminoglycoside group (63.3 % vs. 84.2 %, (p = 0.005). Clinical improvement within three days was also lower (48 % vs. 73.7 %). Mortality rates (28-d: 26.5 % vs. 21.1 %, p = 0.660; in-hospital: 40.8 % vs. 34.2 %, p = 0.559) did not differ significantly. Multivariable analysis found no significant association between aminoglycoside use and 28-d mortality (odds ratio 0.99; 95 % confidence interval: 0.33-3.13, p = 0.988).
CONCLUSION: Aminoglycoside therapy did not improve clinical or microbiological outcomes in AME gene-bearing KPC-producing KPN bacteraemia, despite phenotypic susceptibility.
METHODS: We conducted a retrospective cohort study on adults with amikacin-susceptible KPC-producing KPN bacteraemia at a South Korean tertiary hospital (2022-2024). Antimicrobial susceptibility was assessed using VITEK 2 and disc diffusion per Clinical and Laboratory Standards Institute guidelines. The blaKPC gene was detected via immunochromatography, whereas whole-genome sequencing identified blaKPC subtypes and AME genes. Clinical and microbiological outcomes were analysed based on aminoglycoside use.
RESULTS: Among 136 patients (mean age: 63.6 years), 98 received aminoglycoside therapy, and 38 did not. Intra-abdominal infections were the most common source. Microbiological clearance within one week was significantly lower in the aminoglycoside group (63.3 % vs. 84.2 %, (p = 0.005). Clinical improvement within three days was also lower (48 % vs. 73.7 %). Mortality rates (28-d: 26.5 % vs. 21.1 %, p = 0.660; in-hospital: 40.8 % vs. 34.2 %, p = 0.559) did not differ significantly. Multivariable analysis found no significant association between aminoglycoside use and 28-d mortality (odds ratio 0.99; 95 % confidence interval: 0.33-3.13, p = 0.988).
CONCLUSION: Aminoglycoside therapy did not improve clinical or microbiological outcomes in AME gene-bearing KPC-producing KPN bacteraemia, despite phenotypic susceptibility.