Campylobacter are a frequent cause of diarrhoea in man. The in-vitro susceptibility of all species to the fluoroquinolones and the good response observed in early clinical trials has led to the proposal that these agents may be useful in the treatment of campylobacter enteritis and other more complicated campylobacter infections. However, fluoroquinolone-resistant campylobacters have been reported in up to 50% of isolates from man. The numbers of resistant isolates varies both between and within countries, factors associated with this include foreign travel, local usage of fluoroquinolones, especially in animal husbandry, and whether the microbiology laboratory tests for susceptibility to fluorinated agents, or just nalidixic acid. Fluoroquinolone-resistant campylobacter have emerged during therapy with fluoroquinolones and been responsible for treatment failure. The mechanism of resistance in most isolates is due to mutation in the gyrA (at threonine 86) gene which encodes the A subunit of DNA gyrase. The suggestion of cross resistance to non-quinolone antibiotics, such as tetracycline and/or erythromycin, is probably explained by coincidental occurrence in isolates already resistant to such drugs. The proposal that the veterinary use of fluoroquinolones has led to the selection of fluoroquinolone-resistant campylobacters in poultry which then enter the food-chain to infect man has been viewed as controversial. In the UK fluoroquinolone were only licensed for this use in 1993; it will be interesting to see whether resistant isolates increase the number, thereby lending support for this hypothesis.