Staphylococcus aureus small colony variants, electron transport and persistent infections

Staphylococcus aureus small colony variants, electron transport and persistent infections
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DOI:
10.1016/s0924-8579(99)00170-3
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发表时间:
2000-01-01
影响因子:
10.8
通讯作者:
Proctor, RA
Proctor, RA
中科院分区:
医学2区
文献类型:
--
作者:
McNamara, PJ;Proctor, RA

文献摘要

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金黄色葡萄球菌可以突变形成一个称为小菌落变体(SCV)的细菌亚群。这些细菌具有由生长缓慢、缺乏色素、碳水化合物利用模式改变和毒素产生减少定义的特征表型。这种复杂的表型可以用电子传递的缺陷来解释。在临床分离株中,影响电子传递的最常见突变是编码甲基萘醌或血红素生物合成的操纵子。这些分离株是持续性抗生素耐药性感染的原因。这些感染的临床表现很容易用还原电子传递来解释。SCV在宿主细胞内存活,增加了复发感染的情况,并具有基于其改变的跨膜电位的新的抗性机制。此外,SCV提供了能量代谢和毒素产生之间的联系。这种联系可能是通过细菌对改变的NADH和ATP水平做出反应而起作用的。对这些信号通路的更全面了解可能会为开发改善葡萄球菌毒力和疾病的药物提供新的靶点。(C)2000年Elsevier Science B.V.和国际化疗学会。All rights reserved.
Staphylococcus aureus can mutate to form a sub-population of bacteria known as small colony variants (SCVs). These bacteria have a characteristic phenotype defined by slow growth, the lack of pigment, an altered pattern of carbohydrate utilization, and a reduction in toxin production. This complex phenotype can be explained by deficiencies in electron transport. In clinical isolates, the most common mutations that affect electron transport are in the operons encoding menaquinone or heme biosynthesis. These isolates are responsible for persistent antibiotic resistant infections. The clinical presentation of these infections is readily explained by a reduction electron transport. SCVs survive within host cells, increasing the instances of recurrent infections and have a novel mechanism of resistance based upon their altered trans-membrane potential. Additionally, SCVs provide a connection between energy metabolism and toxin production. This link may operate through the bacteria responding to altered levels of NADH and ATP. A more complete understanding of these signaling pathways may provide new targets for the development of drugs to ameliorate staphylococcal virulence and disease. (C) 2000 Elsevier Science B.V. and International Society of Chemotherapy. All rights reserved.