Antibiotic resistance in Burkholderia species.
The genus Burkholderia comprises metabolically diverse and adaptable Gram-negative bacteria, which thrive in often adversarial environments. A few members of the genus are prominent opportunistic pathogens. These include Burkholderia mallei and Burkholderia pseudomallei of the B. pseudomallei complex, which cause glanders and melioidosis, respectively. Burkholderia cenocepacia, Burkholderia multivorans, and Burkholderia vietnamiensis belong to the Burkholderia cepacia complex and affect mostly cystic fibrosis patients. Infections caused by these bacteria are difficult to treat because of significant antibiotic resistance. The first line of defense against antimicrobials in Burkholderia species is the outer membrane penetration barrier. Most Burkholderia contain a modified lipopolysaccharide that causes intrinsic polymyxin resistance. Contributing to reduced drug penetration are restrictive porin proteins. Efflux pumps of the resistance nodulation cell division family are major players in Burkholderia multidrug resistance. Third and fourth generation β-lactam antibiotics are seminal for treatment of Burkholderia infections, but therapeutic efficacy is compromised by expression of several β-lactamases and ceftazidime target mutations. Altered DNA gyrase and dihydrofolate reductase targets cause fluoroquinolone and trimethoprim resistance, respectively. Although antibiotic resistance hampers therapy of Burkholderia infections, the characterization of resistance mechanisms lags behind other non-enteric Gram-negative pathogens, especially ESKAPE bacteria such as Acinetobacter baumannii, Klebsiella pneumoniae and Pseudomonas aeruginosa.
Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute and Institute for Therapeutic Innovation, University of Florida, Gainesville, FL, USA; Department of Microbiology Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO, USA.
Katherine A
KA
Rhodes
Department of Molecular Genetics and Microbiology, College of Medicine, Emerging Pathogens Institute and Institute for Therapeutic Innovation, University of Florida, Gainesville, FL, USA. Electronic address: hschweizer@ufl.edu.
Herbert P
HP
Schweizer
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D019117:Burkholderia / Q000187:drug effects* / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity; D019121:Burkholderia Infections / Q000188:drug therapy / Q000382:microbiology / Q000473:pathology; D042726:Burkholderia mallei / Q000187:drug effects* / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity; D016957:Burkholderia pseudomallei / Q000187:drug effects* / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity; D027081:DNA Gyrase / Q000235:genetics / Q000378:metabolism; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics*; D015964:Gene Expression Regulation, Bacterial; D019450:Genes, MDR; D005896:Glanders / Q000188:drug therapy / Q000382:microbiology / Q000473:pathology; D006736:Horses; D006801:Humans; D008554:Melioidosis / Q000188:drug therapy / Q000382:microbiology / Q000473:pathology; D018272:Porins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism; D013762:Tetrahydrofolate Dehydrogenase / Q000235:genetics / Q000378:metabolism
D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D018272:Porins; D013762:Tetrahydrofolate Dehydrogenase; D027081:DNA Gyrase
Antibiotics resistance; Burkholderia; Burkholderia cepacia complex; Glanders; Melioidosis