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Acinetobacter baumannii-induced infective endocarditis: new insights into pathophysiology and antibiotic resistance mechanisms

期刊

FUTURE MICROBIOLOGY
卷 17, 期 16, 页码 1335-1344

出版社

FUTURE MEDICINE LTD
DOI: 10.2217/fmb-2021-0279

关键词

Acinetobacter species; antibiotic resistance; epidemiology; infective endocarditis; pathophysiology; therapeutic targets

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This review discusses the possible disease and antibiotic resistance mechanisms involved in infective endocarditis caused by Acinetobacter species, especially A. baumannii, and suggests potential treatment options.
Plain language summary Infective endocarditis (IE), known as inflammation of the thin membrane that lines the inside of the heart, results from infections from microbes (e.g., Staphylococcus, Streptococcus and Acinetobacter species and, less commonly, fungi). IE caused by a special microbe called the Acinetobacter species is an uncommon condition with substantial death rates globally. Although it is not common, IE caused by Acinetobacter species, especially A. baumannii, might be difficult to treat due to increased antibiotic resistance. Therefore, it is important to understand the possible disease and antibiotic resistance mechanisms of A. baumannii during IE. This review explains the possible underlying disease mechanisms involved in IE caused by A. baumannii and highlights the potential antibiotic resistance mechanisms, suggesting possible treatment options for IE caused by A. baumannii. Infective endocarditis (IE), characterized by inflammation of the endocardial surface of the heart and its valves, results from infections caused by Staphylococcus, Streptococcus and Acinetobacter species and less commonly fungi. Acinetobacter-induced IE is a relatively rare condition with significant morbidity and mortality worldwide. Notably, its mortality rate is greater than that of endocarditis induced by Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens and Kingella kingae. Although it is rare, Acinetobacter-induced IE caused by A. baumannii might bring unique therapeutic challenges such as increased antibiotic resistance. Therefore, it is vital to understand perfectly the possible pathophysiologic and antibiotic resistance mechanisms adopted by A. baumannii during IE. This review discusses the probable underlying pathomechanisms involved in A. baumannii-induced IE and highlights the potential antibiotic resistance mechanisms, suggesting therapeutic targets for A. baumannii-induced IE.

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