Reimche Jennifer L, Kirse Daniel J, Whigham Amy S, Swords W Edward
Department of Microbiology and Immunology, Wake Forest School of Medicine, Winston-Salem, NC 27106, USA.
Department of Otolaryngology, Wake Forest School of Medicine, Winston-Salem, NC 27106, USA.
Pathog Dis. 2017 Feb;75(1). doi: 10.1093/femspd/ftw112. Epub 2016 Dec 11.
The inflammatory middle ear disease known as otitis media can become chronic or recurrent in some cases due to failure of the antibiotic treatment to clear the bacterial etiological agent. Biofilms are known culprits of antibiotic-resistant infections; however, the mechanisms of resistance for non-typeable Haemophilus influenzae biofilms have not been completely elucidated. In this study, we utilized in vitro static biofilm assays to characterize clinical strain biofilms and addressed the hypothesis that biofilms with greater biomass and/or thickness would be more resistant to antimicrobial-mediated eradication than thinner and/or lower biomass biofilms. Consistent with previous studies, antibiotic concentrations required to eliminate biofilm bacteria tended to be drastically higher than concentrations required to kill planktonic bacteria. The size characterizations of the biofilms formed by the clinical isolates were compared to their minimum biofilm eradication concentrations for four antibiotics. This revealed no correlation between biofilm thickness or biomass and the ability to resist eradication by antibiotics. Therefore, we concluded that biofilm size does not play a role in antibiotic resistance, suggesting that reduction of antibiotic penetration may not be a significant mechanism for antibiotic resistance for this bacterial opportunist.
被称为中耳炎的炎性中耳疾病，在某些情况下可能会由于抗生素治疗未能清除细菌病原体而变为慢性或复发性疾病。生物膜是导致抗生素耐药性感染的已知罪魁祸首；然而，不可分型流感嗜血杆菌生物膜的耐药机制尚未完全阐明。在本研究中，我们利用体外静态生物膜试验来表征临床菌株生物膜，并探讨了这样一个假设，即与较薄和/或生物量较低的生物膜相比，生物量和/或厚度更大的生物膜对抗菌介导的根除更具抗性。与先前的研究一致，消除生物膜细菌所需的抗生素浓度往往远高于杀死浮游细菌所需的浓度。将临床分离株形成的生物膜的大小特征与其对四种抗生素的最小生物膜根除浓度进行了比较。这表明生物膜厚度或生物量与抵抗抗生素根除的能力之间没有相关性。因此，我们得出结论，生物膜大小在抗生素耐药性中不起作用，这表明抗生素渗透减少可能不是这种机会致病菌产生抗生素耐药性的重要机制。
