多药耐受
金黄色葡萄球菌
抗生素
微生物学
细菌
生物
渗透性休克
基因
突变
抗生素耐药性
遗传学
生物膜
作者
Ahmad Nasser,Shiva Jahanbakhshi,Mohammad Mehdi Soltan Dallal,Maryam Banar,Azin Sattari-Maraji,Taher Azimi
出处
期刊:Current Pharmaceutical Biotechnology
[Bentham Science]
日期:2023-04-14
卷期号:24 (15): 1898-1915
被引量:3
标识
DOI:10.2174/1389201024666230411110002
摘要
Relapse infection usually results from resistance to the antibiotic, acquired genes, or persister cells. Persister cells are formed through mutation, reduced activity or metabolically inactive pathways induced by antibiotics, harassing conditions, low ATP, and malnutrition. These factors provide the ground for bacteria to grow slowly. Such a slow growth rate makes traditional antibiotics ineffective against persister cells. Staphylococcus aureus (S. aureus), in addition to this form, can be observed in Small Colony Variants (SCVs), L-forms, and dormant, all of which are characterized by at least one feature, i.e., slow growth. Despite their slow growth, they are metabolically active in terms of stringent SOS and cell wall stress responses. The stress response involves resistance against harassing conditions, and it survives until it is reactivated later. The present study aims to discuss the mechanisms of all persister cell formations, circumstances involved, gene mutation, and adoptable strategies against it.
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