Division of Infectious Diseases, Department of Internal Medicine, Faculty of Medicine, Prince of Songkla University, Hat Yai, Thailand.
Department of Biomedical Sciences and Biomedical Engineering, Faculty of Medicine, Prince of Songkla University, Hat Yai, Thailand.
Clin Respir J. 2024 Jan;18(1):e13732. doi: 10.1111/crj.13732.
Biofilm formation is an important virulence factor of Acinetobacter baumannii. Here, we examined the biofilm formation of archived A. baumannii causing ventilator-associated pneumonia (VAP).
Eighteen and twenty isolates of A. baumannii causing bacteremic pneumonia and non-bacteremic pneumonia were included, respectively. Antimicrobial susceptibility testing was performed by broth microdilution method, while biofilm formation was evaluated by microtiter dish biofilm formation assay.
All 38 isolates were still susceptible to colistin and tigecycline, whereas almost all isolates were non-susceptible (intermediate to resistant) to several antimicrobial agents, especially ceftriaxone and cefotaxime. Approximately, 44% of bacteremic isolates and 50% of non-bacteremic isolates were classified as carbapenem-resistant A. baumannii (CRAB). Biofilm formation was detected in 42% of the studied isolates. Bacteremia among the patients infected with biofilm-producing isolates was significantly higher than in those infected with non-biofilm-producing isolates. The antimicrobial susceptibilities of A. baumannii with biofilm formation were lower than those without biofilm formation, but the differences did not have statistical significance. The patients infected with non-biofilm-producing isolates had good clinical and non-clinical outcomes than those infected with biofilm-producing isolates. The survival rate of patients diagnosed with VAP due to biofilm-producing A. baumannii was lower than in those patients diagnosed with VAP due to non-biofilm-producing isolates.
Biofilm formation of A. baumannii causing VAP was associated with antimicrobial resistance and bacteremia as well as unfavorable clinical outcomes.
生物膜形成是鲍曼不动杆菌的重要毒力因子。在这里，我们研究了引起呼吸机相关性肺炎（VAP）的存档鲍曼不动杆菌的生物膜形成。
分别纳入了 18 株和 20 株引起菌血症性肺炎和非菌血症性肺炎的鲍曼不动杆菌。采用肉汤微量稀释法进行抗菌药物敏感性试验，微量滴定板生物膜形成试验评估生物膜形成。
所有 38 株分离株仍对黏菌素和替加环素敏感，而几乎所有分离株对几种抗菌药物（尤其是头孢曲松和头孢噻肟）均表现为非敏感性（中介至耐药）。约 44%的菌血症分离株和 50%的非菌血症分离株被归类为耐碳青霉烯鲍曼不动杆菌（CRAB）。在研究的分离株中，有 42%的分离株可检测到生物膜形成。感染产生物膜分离株的患者发生菌血症的比例明显高于感染非产生物膜分离株的患者。具有生物膜形成的鲍曼不动杆菌的抗菌药物敏感性低于不具有生物膜形成的鲍曼不动杆菌，但差异无统计学意义。感染非产生物膜分离株的患者的临床和非临床结局要好于感染产生物膜分离株的患者。诊断为产生物膜鲍曼不动杆菌引起的 VAP 的患者的生存率低于诊断为非产生物膜鲍曼不动杆菌引起的 VAP 的患者。
引起 VAP 的鲍曼不动杆菌的生物膜形成与抗菌药物耐药性、菌血症以及不良临床结局有关。
