Pohlod D J, Saravolatz L D, Somerville M M
Department of Medicine, Henry Ford Hospital, Detroit, Michigan 48202.
J Antimicrob Chemother. 1988 Oct;22 Suppl D:35-41. doi: 10.1093/jac/22.supplement_d.35.
Susceptibilities of methicillin-resistant Staphylococcus aureus (MRSA, n = 32), methicillin-sensitive S. aureus (MSSA, n = 32), and S. epidermidis (SE, n = 24) were determined to fleroxacin, amifloxacin, ciprofloxacin, difloxacin, enoxacin, norfloxacin, and ofloxacin. All organisms were isolated from the blood of patients with infective endocarditis. MRSA and MSSA MIC90s were less than 1.0 mg/l of fleroxacin, ciprofloxacin, difloxacin, and ofloxacin while amifloxacin and norfloxacin produced MIC90s of less than 2.0 mg/l and enoxacin MIC90s of less than 4.0 mg/l. For S. epidermidis MIC90s were less than 1.0 mg/l of all quinolones except amifloxacin whose MIC90 was less than 2.0 mg/l. Two strains from each staphylococcal group were used in time-kill trials performed with all seven quinolones. Within 8 h, all quinolones colony counts were decreased by one log. At 24 h, most quinolones decreased MRSA, MSSA, and SE colony counts by two to four logs; however, exceptions were found with (1) difloxacin, enoxacin, and norfloxacin against MRSA, (2) ciprofloxacin and enoxacin against MSSA, and (3) ciprofloxacin against SE in which all colony counts increased one to three logs in 24 h. When quinolone time-kill trials did not show a decrease in colony counts at 24 h, the MIC's for the 24 h growth showed a four- to 250-fold increase when compared with pre-trial MICs. No selection or emergence of resistant organisms was found with fleroxacin, amifloxacin or ofloxacin.