Antibiotic resistance of biofilms

Antibiotic resistance of biofilms
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DOI:
10.1080/08927019609386290
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发表时间:
1996-01-01
期刊:
影响因子:
2.7
通讯作者:
Gilbert, P
Gilbert, P
中科院分区:
生物学3区
文献类型:
--
作者:
Foley, I;Gilbert, P

文献摘要

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微生物生物膜对抗生素、杀生剂或消毒剂的处理非常顽固,这些药物可以充分控制浮游模式下生长的相同微生物。这种耐药性很大程度上归因于胞外聚合物基质中生物膜细胞的组织。虽然这种胞外聚合物不太可能阻碍抗菌剂的扩散和进入底层细胞,但它们将在化学上熄灭活性杀生剂,如氯和过氧物,并结合高电荷的抗生素,如妥布霉素和庆大霉素,从而为更深层的细胞提供一些保护。胞外酶结合在糖萼内,能够降解处理剂,将进一步减少敏感化合物的进入。然而,扩散限制不太可能是微生物生物膜耐药特性的唯一调节因素,此外,在整个生物膜群落中建立的氧气和营养的梯度将导致远离可获得的养分的点的生长速度大大降低。缓慢的生长速度,以及相关的严格反应的诱导,进一步加剧了这种抗性。最后,最近有证据表明,微生物附着在表面促进了浮游生物培养中通常不表达的基因的表达。这些基因的表达是否以改变细胞对抗菌剂的反应的方式改变了表型,仍有待证实。
Microbial biofilms are notably recalcitrant towards treatment with antibiotics, biocides or disinfectants that would adequately control the same organisms growing in planktonic mode. Much of this resistance has been attributed to an organisation of the biofilm cells within exopolymer matrices. Whilst such exopolymers are unlikely to hinder the diffusion and access of antimicrobial agents to the underlying cells, they will chemically quench reactive biocides such as chlorine and peroxygens, and bind highly charged antibiotics, such as tobramycin and gentamycin, thereby providing some protection to the more deep lying cells. Extracellular enzymes, bound within the glycocalyx and able to degrade the treatment agents, will further reduce the access of susceptible compounds. Diffusion limitation however, is unlikely to be the sole moderator of the resistance properties of microbial biofilms, in addition, gradients of oxygen and nutrients established across the biofilm community will cause growth rates to be much reduced at points remoted from the accessible nutrient. Slow growth rates, and the associated induction of stringent responses further contribute towards this resistance. Finally, there have been recent demonstrations that attachment of microorganism to surfaces promotes the expression of genes that are not normally expressed in planktonic culture. Whether or not the expression of such genes alters the phenotype in a manner which alters the response of the cells to antimicrobial agents remains to be demonstrated.