Abstract

Fluoroquinolones are potentially useful for treatment of diarrhea caused by Escherichia coli and Salmonella enterica in calves and for treatment of pneumonia caused by Pasteurella multocida, P. haemolytica, Haemophilus somnus, Actinomyces pyogenes, and Mycoplasma bovis in calves and older animals. Fluoroquinolones can be used to treat human infections with β-lactamase producing P. multocida. Quinolones act by directly inhibiting bacterial DNA synthesis. Inhibition appears to occur by interaction of the drug with complexes composed of DNA and either of the two target enzymes, DNA gyrase and topoisomerase IV. Resistance to quinolones largely depends on chromosomal mutations. Emerging resistance to fluoroquinolones in Campylobacter isolated from humans has clearly been documented in numerous countries during the past decade. Early clinical trials of both community-acquired acute diarrhea and traveler's diarrhea caused by Campylobacter demonstrated that patients treated with a fluoroquinolone had good clinical response. Fluoroquinolones are effective for treatment and prevention of a wide range of bacterial infections in food and companion animals. Resistance is emerging, and limited alternatives make it important to preserve the effect of fluoroquinolones. Resistance in zoonotic bacteria, caused by use of quinolones in animals, is a concern for public health, because fluoroquinolones are important drugs in the treatment of human infections. Low-level resistance to fluoroquinolones in Salmonella and high-level resistance in Campylobacter causing human infections have emerged, in part, as a result of the use of fluoroquinolones in food animals. Fluoroquinolone resistance may decrease in bacteria from food animals following reductions in selective pressure.

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