Resistance to fluoroquinolone antibacterials has emerged in a limited form, largely amongst certain specific species and often restricted to single clones of these pathogens. Mediated by chromosomal mutation, the major mechanisms are alterations in gyrase subunits and reduced penetration associated with decreased outer membrane protein production. Resistance is most commonly seen to emerge amongst pathogens with higher than average initial MICs, particularly affected species being Pseudomonas aeruginosa and the staphylococci. Resistance is more likely to be encountered when such pathogens are exposed to concentrations at or below the MIC, which may result either from underdosage, the presence of the organism in a sequestered site, e.g. bone or prostate, or from confounding factors such as the presence of pus, indwelling prostheses or interactions which reduce absorption from the gastrointestinal tract. Repetitive use of these agents and continued use of fluoroquinolone precursors, such as nalidixic acid, may also contribute to resistance emergence. Most resistance is appearing amongst hospitalised patients and much of the apparent burden reflects horizontal cross-infection of many patients by a single resistant clone. There is very limited data linking increasing community use of fluoroquinolones with resistance emergence amongst pathogens such as Escherichia coli. In the main, the emergence of resistance can be anticipated and perhaps prevented or avoided for the sorts of risk groups and pathogens described. The use of adequate dosage by appropriate routes of administration in suitable patients and implementation of surveillance procedures for those at risk will minimise such problems. Policies for the effective use of these valuable agents should be part of everyday practice in hospitals.

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SUMMARYMoxifloxacin is a novel 8‐methoxyquinolone with enhanced potency against important Gram‐positive pathogens, notably Streptococcus pneumoniae. It retains class activity against Gram‐negative bacteria. Currently available for oral use, it has a prolonged half‐life, enabling once‐daily administration and reflecting balanced renal and hepatic elimination. Clinical trials have demonstrated an excellent safety record with minor class effects in the skin and gastrointestinal systems. Potential for phototoxicity is minimal and moxifloxacin is free of clinically significant neurological, hepatic or cardiac effects. Investigated primarily in respiratory infections, moxifloxacin has shown excellent performance in community‐acquired pneumonia (both pneumococcal and atypical), acute exacerbations of chronic bronchitis and acute maxillary sinusitis. It is available in many European countries and in the US where it is rapidly establishing clinical acceptance and formulary inclusion. (Int J Clin Pract 2000; 54(5): 329‐332)