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- W2095871644 abstract "Burkholderia pseudomallei is the etiologic agent of melioidosis. This multifaceted disease is difficult to treat, resulting in high morbidity and mortality. Treatment of B. pseudomallei infections is lengthy and necessitates an intensive phase (parenteral ceftazidime, amoxicillin-clavulanic acid or meropenem) and an eradication phase (oral trimethoprim-sulfamethoxazole). The main resistance mechanisms affecting these antibiotics include enzymatic inactivation, target deletion and efflux from the cell, and are mediated by chromosomally encoded genes. Overproduction and mutations in the class A PenA β-lactamase cause ceftazidime and amoxicillin-clavulanic acid resistance. Deletion of the penicillin binding protein 3 results in ceftazidime resistance. BpeEF-OprC efflux pump expression causes trimethoprim and trimethoprim-sulfamethoxazole resistance. Although resistance is still relatively rare, therapeutic efficacies may be compromised by resistance emergence due to increased use of antibiotics in endemic regions. Novel agents and therapeutic strategies are being tested and, in some instances, show promise as anti-B. pseudomallei infectives." @default.
- W2095871644 created "2016-06-24" @default.
- W2095871644 creator A5018324088 @default.
- W2095871644 date "2012-12-01" @default.
- W2095871644 modified "2023-10-17" @default.
- W2095871644 title "Mechanisms of antibiotic resistance in <i>Burkholderia pseudomallei</i>: implications for treatment of melioidosis" @default.
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- W2095871644 doi "https://doi.org/10.2217/fmb.12.116" @default.
- W2095871644 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3568953" @default.
- W2095871644 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23231488" @default.
- W2095871644 hasPublicationYear "2012" @default.
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