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Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis.
Future Microbiol. 2012 Dec; 7(12):1389-99.FM

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.

Authors+Show Affiliations

Colorado State University, Department of Microbiology, Immunology & Pathology, IDRC at Foothills Campus, 0922 Campus Delivery, Fort Collins, CO 80523, USA. herbert.schweizer@colostate.edu

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Review

Language

eng

PubMed ID

23231488

Citation

Schweizer, Herbert P.. "Mechanisms of Antibiotic Resistance in Burkholderia Pseudomallei: Implications for Treatment of Melioidosis." Future Microbiology, vol. 7, no. 12, 2012, pp. 1389-99.
Schweizer HP. Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis. Future Microbiol. 2012;7(12):1389-99.
Schweizer, H. P. (2012). Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis. Future Microbiology, 7(12), 1389-99. https://doi.org/10.2217/fmb.12.116
Schweizer HP. Mechanisms of Antibiotic Resistance in Burkholderia Pseudomallei: Implications for Treatment of Melioidosis. Future Microbiol. 2012;7(12):1389-99. PubMed PMID: 23231488.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis. A1 - Schweizer,Herbert P, PY - 2012/12/13/entrez PY - 2012/12/13/pubmed PY - 2013/5/25/medline SP - 1389 EP - 99 JF - Future microbiology JO - Future Microbiol VL - 7 IS - 12 N2 - 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. SN - 1746-0921 UR - https://www.unboundmedicine.com/medline/citation/23231488/Mechanisms_of_antibiotic_resistance_in_Burkholderia_pseudomallei:_implications_for_treatment_of_melioidosis_ L2 - http://www.futuremedicine.com/doi/full/10.2217/fmb.12.116?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -