An outbreak of respiratory illness due to Branhamella catarrhalis occurred in the intermediate care unit of a Veterans Administration hospital and involved patients and staff members. Four patients had pneumonia and four had bronchitis. Infected patients were placed in a cohort separated from noninfected patients and were treated. Pharyngeal culture was used to survey prevalence in staff and all other patients on the unit; three of 18 staff members and two of 19 asymptomatic patients were positive for B. catarrhalis. A case-control study showed that respiratory therapy, steroid use, and location within the unit were significant risk factors for B. catarrhalis infection or colonization. Strains from five patients and two staff members had identical bacterial restriction endonuclease digestion patterns with three different enzymes; these patterns were distinct from those of control strains. This study is the first to document an outbreak of B. catarrhalis infection confirmed with a typing system and thus establishes B. catarrhalis as a nosocomial pathogen.

The differences in sensitivity between NAT assays can be explained by the input of isolated viral nucleic acid in the amplification reactions. The FDA requirements for sensitivity of NAT blood screening assays can be met by the Gen-probe TMA, as well as by the AmpliScreen assays, particularly when combined with the NucliSens Extractor.

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Ciprofloxacin, one of the most active new quinolone antimicrobial agents, is bactericidal against a broad spectrum of gram-positive and gram-negative microorganisms, including Pseudomonas aeruginosa. Although P. aeruginosa is intrinsically less susceptible to most antibiotics than other clinically significant gram-negative organisms, 90% of P. aeruginosa strains are inhibited by ciprofloxacin at 0.5 ,ug/ml (7).There have been reports of decreased susceptibility to ciprofloxacin during therapy in clinical studies of P. aeruginosa infections (9, 10, 27, 35). These reports did not specify whether the decrease in susceptibility was due to the selection of naturally occurring resistant strains or the mutation of the original strain to a resistant variant.Kaatz and Seo (24), however, have described a P. aeruginosa strain whose identity was based on serotype, pyocin type, and plasmid profile. The MIC of ciprofloxacin for this strain increased from 0.57 to 5.42 ,ug/ml during parenteral therapy, with no significant change in susceptibility to other antibiotics. Resistance involved a decrease in the sensitivity of DNA synthesis to inhibition by ciprofloxacin, but the basis of this decreased sensitivity was not investigated further. Ogle et al. (31) analyzed 25 pairs of pre-and posttherapy isolates of P. aeruginosa from patients treated with imipenem, norfloxacin, or ciprofloxacin. Southern hybridization showed clonal identity between 23 of the 25 paired isolates, confirming the development of quinolone resistance rather than superinfection in these strains. The mechanism of this acquired resistance was not studied.Quinolones interfere with the activity of DNA gyrase (12,39), an essential bacterial topoisomerase that converts relaxed DNA to the supercoiled form. DNA gyrase has been isolated from a variety of bacteria (3,11,26,40) including P. aeruginosa (28). In vitro studies with P. aeruginosa PAO have shown that alterations in DNA gyrase (gyrA cfxA nalA mutations) or permeability (cfxB nfxB) can result in de-* Corresponding author. creased susceptibility to quinolones, including ciprofloxacin (32), norfloxacin (20), and nalidixic acid (22).To further understand the factors which mediate quinolone susceptibility in P. aeruginosa, we studied three clinical isolates of P. aeruginosa from a patient with a complicated infection. The MIC of ciprofloxacin increased from 0.5 ,ug/ml at the initiation of parenteral ciprofloxacin therapy to 16 ,ug/ml during therapy. All isolates were verified as the same strain by Southern hybridization with a strainspecific P. aeruginosa DNA probe (John Ogle, University of Colorado School of Medicine, Denver). To characterize the mechanisms involved in the acquisition of resistance to ciprofloxacin in vivo, we examined the outer membrane proteins (OMPs), lipopolysaccharide (LPS) content, antimicrobial susceptibilities, accumulation of ciprofloxacin, and DNA gyrase of these isolates. We provide evidence that the acquired resistance to quinolones in this clinical strain is primarily due to an altera...