严重耐药铜绿假单胞菌:耐药机制及治疗策略综述

Q4 Biochemistry, Genetics and Molecular Biology Acta Microbiologica Bulgarica Pub Date : 2023-09-01 DOI:10.59393/amb23390302
S. Sowmyanarayan, R.V. Kavitha
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引用次数: 0

摘要

铜绿假单胞菌是一种严重耐药的病原体,是全世界免疫缺陷患者发病的原因。这种细菌对几种抗生素具有独特的抵抗力。许多耐药机制,如可靠的外排泵、细胞膜通透性降低、酶机制使抗菌药物失活以及抗生素靶点的修饰,使细菌能够在不利条件下存活。该细菌耐药的原因和程度已被清楚地阐明。这种病原体在关键基因中表达几种突变的能力使其具有致命性。常见细菌物种固有的和获得的抗菌素耐药性的持久威胁被广泛研究,为公众设计更新和有效的治疗方法。一些研究已经在处理铜绿假单胞菌感染的方法上进行了工作。对受严重影响的患者给予最高水平的最新抗生素和联合治疗。噬菌体治疗的现代治疗策略已经在临床前进行了测试。彻底治愈铜绿假单胞菌感染的问题陈述尚未得到建设性的解决。
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Critically Resistant Pseudomonas aeruginosa: a Short Review on the Mechanisms of Resistance and Therapeutic Strategies
Pseudomonas aeruginosa is a critically resistant pathogen that is responsible for the morbidity of immunodeficient patients throughout the world. The bacterium possesses unique resistance to several antibiotics. Numerous resistance mechanisms like reliable efflux pumps, reduced permeability of the cell membrane, inactivation of antimicrobial drugs by enzymatic mechanisms and modification of antibiotic target sites enable the survival of the bacteria in adverse conditions. The causes and extent of antibiotic resistance in this bacterial species have been elucidated clearly. The ability of the pathogen to express several mutations in crucial genes makes it lethal. The everlasting threat of intrinsic as well as acquired antimicrobial resistance in common bacterial species is studied extensively to devise newer and effective therapeutics for the general public. Several studies have worked on the methods to deal with P. aeruginosa infections. The highest level of the newest antibiotics along with combinatorial therapy is administered to severely affected patients. Modern therapeutic strategies of bacteriophage therapy have been tested preclinically. The problem statement of curing P. aeruginosa infections thoroughly is yet to be resolved constructively.
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来源期刊
Acta Microbiologica Bulgarica
Acta Microbiologica Bulgarica Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
0.40
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0
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