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莫拉克斯氏菌引起肺炎球菌肺炎中青霉素中和作用的实验证据。

Experimental evidence for Moraxella-induced penicillin neutralization in pneumococcal pneumonia.

作者信息

Hol C, Van Dijke E E, Verduin C M, Verhoef J, van Dijk H

机构信息

Eijkman-Winkler Institute for Medical and Clinical Microbiology, Utrecht University, Netherlands.

出版信息

J Infect Dis. 1994 Dec;170(6):1613-6. doi: 10.1093/infdis/170.6.1613.

Abstract

Resistance of microorganisms to antimicrobial agents is an increasing problem in the treatment of infectious diseases. In mixed infections, an interesting development can arise when one organism protects another from being killed by an antibiotic. Unfortunately, in the case of respiratory tract infections, experimental evidence of this development is poor. In this study, mice intranasally infected with a lethal number of pneumococci and treated with a curative dose of penicillin or amoxicillin died from pneumococcal pneumonia when they were coinoculated with beta-lactamase-producing Moraxella catarrhalis. beta-lactamase-negative M. catarrhalis did not show a similar indirect pathogenic effect. Treatment with a combination of amoxicillin and the beta-lactamase inhibitor clavulanic acid was not affected by beta-lactamase-producing M. catarrhalis. These findings help explain antibiotic failure in respiratory tract infections, even though the causative microorganism is sensitive to the antibiotic in vitro.

摘要

微生物对抗菌剂的耐药性在传染病治疗中是一个日益严重的问题。在混合感染中,当一种微生物保护另一种微生物不被抗生素杀死时,可能会出现有趣的情况。不幸的是,在呼吸道感染的情况下,这种情况的实验证据并不充分。在本研究中,经鼻腔感染致死剂量肺炎球菌并用治愈剂量青霉素或阿莫西林治疗的小鼠,当它们与产β-内酰胺酶的卡他莫拉菌共同接种时,死于肺炎球菌肺炎。β-内酰胺酶阴性的卡他莫拉菌未表现出类似的间接致病作用。阿莫西林与β-内酰胺酶抑制剂克拉维酸联合治疗不受产β-内酰胺酶的卡他莫拉菌影响。这些发现有助于解释呼吸道感染中抗生素治疗失败的原因,即使致病微生物在体外对该抗生素敏感。

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