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流感嗜血杆菌中β-内酰胺耐药机制

Mechanisms of beta-lactam resistance in Haemophilus influenzae.

作者信息

Gutmann L, Williamson R, Collatz E, Acar J F

机构信息

Laboratoire de Microbiologie Médicale, Hopital Saint-Joseph, Paris, France.

出版信息

Eur J Clin Microbiol Infect Dis. 1988 Oct;7(5):610-5. doi: 10.1007/BF01964237.

Abstract

Haemophilus influenzae has become increasingly resistant to beta-lactam antibiotics. Three major mechanisms, both enzymatic and non-enzymatic, are involved. Enzymatic resistance is mainly due to production of a TEM-1 plasmid-mediated beta-lactamase, and in some cases to a new enzyme ROB-1. Of the non-enzymatic mechanisms, decreased permeability due to alteration of outer membrane proteins seems to be rare in comparison to decreased affinity of penicillin-binding proteins for beta-lactam antibiotics. Enzymatic resistance is present in about 10-20% of clinical isolates, while non-enzymatic resistance is present only in 2-4%.

摘要

流感嗜血杆菌对β-内酰胺类抗生素的耐药性日益增强。这涉及三种主要机制,包括酶促机制和非酶促机制。酶促耐药主要是由于产生了TEM-1质粒介导的β-内酰胺酶,在某些情况下是由于一种新的酶ROB-1。在非酶促机制中,与青霉素结合蛋白对β-内酰胺类抗生素的亲和力降低相比,外膜蛋白改变导致通透性降低似乎较为少见。约10%-20%的临床分离株存在酶促耐药,而非酶促耐药仅存在于2%-4%的分离株中。

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