Pseudomonas aeruginosa: resistance to the max.
Pseudomonas aeruginosa: resistance to the max.
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DOI：
10.3389/fmicb.2011.00065
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发表时间：
2011
影响因子：
5.2
通讯作者：
Poole K
中科院分区：
文献类型：
--
作者：
Poole K
铜绿假单胞菌本质上对多种抗菌素具有耐药性，并可在抗假单胞菌化疗期间产生耐药性，这两者都会损害由该生物引起的感染的治疗。对多种抗菌素的耐药（多药耐药）在铜绿假单胞菌中越来越普遍，有一些报告称，可以用一种药物粘菌素治疗泛耐药分离株。这种生物的获得性耐药性是多因素的，可归因于染色体突变和通过水平基因转移获得抗性基因。影响耐药性的突变变化包括多药外排系统的上调以促进抗菌药物的排出、ampC的抑制、ampC的改变以扩大酶的底物特异性（即扩展谱ampC）、外膜通透性的改变以限制抗菌药物的进入以及抗菌靶点的改变。P. aeruginosa耐药的获得性机制包括β-内酰胺酶，特别是可水解大部分β-内酰胺的广谱β-内酰胺酶和碳青霉烯酶、氨基糖苷修饰酶和提供高水平泛氨基糖苷抗性的16S rRNA甲基化酶。这种生物在体内以耐抗生素生物膜的形式生长的倾向，以及高频率产生耐抗生素突变体的超突变菌株的发生，也影响了抗假单胞菌化疗。由于治疗选择有限和耐药性增加，无法治疗的铜绿假单胞菌感染是否很快就会出现在我们身上？
Pseudomonas aeruginosa is intrinsically resistant to a variety of antimicrobials and can develop resistance during anti-pseudomonal chemotherapy both of which compromise treatment of infections caused by this organism. Resistance to multiple classes of antimicrobials (multidrug resistance) in particular is increasingly common in P. aeruginosa, with a number of reports of pan-resistant isolates treatable with a single agent, colistin. Acquired resistance in this organism is multifactorial and attributable to chromosomal mutations and the acquisition of resistance genes via horizontal gene transfer. Mutational changes impacting resistance include upregulation of multidrug efflux systems to promote antimicrobial expulsion, derepression of ampC, AmpC alterations that expand the enzyme's substrate specificity (i.e., extended-spectrum AmpC), alterations to outer membrane permeability to limit antimicrobial entry and alterations to antimicrobial targets. Acquired mechanisms contributing to resistance in P. aeruginosa include β-lactamases, notably the extended-spectrum β-lactamases and the carbapenemases that hydrolyze most β-lactams, aminoglycoside-modifying enzymes, and 16S rRNA methylases that provide high-level pan-aminoglycoside resistance. The organism's propensity to grow in vivo as antimicrobial-tolerant biofilms and the occurrence of hypermutator strains that yield antimicrobial resistant mutants at higher frequency also compromise anti-pseudomonal chemotherapy. With limited therapeutic options and increasing resistance will the untreatable P. aeruginosa infection soon be upon us?
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