Brevundimonas diminuta infections and its resistance to fluoroquinolones

Abstract

Objectives: To report infections caused by Brevundimonas diminuta and antibiotic studies of this Gram-negative bacterium. Patients and methods: Seven patients with infection and eight bacterial strains were studied. Tests included antibiotic susceptibility and analysis of the DNA gyrase and topoisomerase genes and the effect of efflux pump inhibitor Phe-Arg-β-naphthylamide (PANA). Results: The patients all had underlying disease of cancer. The infections involved bloodstream (one case), intravascular catheter (four cases), urinary tract (one case) and pleural space (one case of empyema). Fever up to 39.2°C characterized these infections, which resolved upon treatment by combination antibiotics. Microbiologically, all organisms were resistant to multiple fluoroquinolones and cefepime, but were susceptible to amikacin, imipenem and ticarcillin/clavulanate. These quinolone-resistant B. diminuta strains were probably selected out by the prophylactic use of a quinolone in six of these patients. Additionally, the B. diminuta type strain ATCC 11568^T that was isolated before the quinolone era from water was also resistant to ciprofloxacin and intermediate to levofloxacin, suggesting intrinsic quinolone resistance. The DNA gyrase and topoisomerase of six analysed strains all contained GyrA Ala-83 and Met-87, GyrB Leu-466 or Thr-466, and ParC Gln-57, Val-66 and Ala-80 that were probably the cause of fluoroquinolone resistance. PANA had nearly negligible effect. Conclusions: B. diminuta is intrinsically resistant to fluoroquinolones and can be selected out to cause infections.