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Use of ciprofloxacin for treating leptospirosis – need for clinical trials

Specialist Registrar, Department of Medical Microbiology, Aberdeen Royal Infirmary & Honorary Lecturer, University of Aberdeen, Grampian University Hospitals NHS Trust, Foresterhill, Aberdeen AB25 2ZN, UK

Correspondence: Abhijit M. Bal (a.bal{at}abdn.ac.uk)

I read with interest the article in the Journal of Medical Microbiology by Sugunan et al. (2004). The authors describe a case of leptospirosis acquired after laboratory exposure. The patient was initially treated with doxycycline and later with ciprofloxacin.

Ciprofloxacin is a fluoroquinolone antibiotic. Its value in treating leptospirosis has not been firmly established. Shalit et al. (1989) demonstrated the usefulness of ciprofloxacin in an animal model of leptospirosis. However, only one leptospiral strain was used in their experiments conducted on a small number of animals. Takashima et al. (1993) determined the antimicrobial effects of quinolones on leptospires. Their data reveals that for all the five serogroups used in the study including serogroup Australis, there was at least a 32-fold difference between the minimal inhibitory concentration and the minimal bactericidal concentration of ciprofloxacin although the clinical significance of this finding is difficult to interpret. Using quantitative PCR for evaluating treatment of experimental leptospirosis, Truccolo et al. (2002) concluded that ofloxacin, a related fluoroquinolone, was unable to clear leptospiraemia.

Clinical trials for the use of ciprofloxacin in leptospirosis have not been carried out. In the report described, doxycycline was discontinued after 2 days due to its adverse effects and lack of clinical response (Sugunan et al., 2004). Penicillin would have been a natural choice at this stage. Most clinicians would treat leptospirosis with a 7 day course of appropriate antibiotics (Watt et al., 1988). The decision to discontinue pathogen-directed therapy of proven efficacy could not have been based on initial negative leptospiral serology. In my own experience, the microagglutination test has poor sensitivity for acute phase samples (Bharadwaj et al., 2002) and the dipstick IgM assay has a sensitivity of only 63 % early in disease (Gussenhoven et al., 1997). Delayed seroconversions are common in leptospirosis (Tappero et al., 2000).

Quinolones have been used in uveitis following leptospirosis (Mancel et al., 1999) but comparative trials have not been conducted and uveitis is a late localized immunological phenomenon rather than a direct effect of the organism. It is possible that limited observations suggest that quinolones could be useful in systemic leptospirosis. Clinical response in such cases could reflect the natural history of the illness but could also be due to a hitherto unproven effect of quinolones on leptospires. However, until such a time that their efficacy is proven, use of quinolones should probably be reserved for exceptional situations. Use of appropriate antibiotics reduces mortality due to leptospirosis from 4 % to 1 % (Guidugli et al., 2000).

Because of the apparent therapeutic response in the case described by Sugunan et al. (2004), their report could form a basis for future trials involving the use of ciprofloxacin in leptospirosis. Importantly, quinolones are available for oral administration, have excellent bioavailability and are generally well tolerated (Hooper, 2000), while the ß-lactam antibiotics may require parenteral administration, may lead to anaphylaxis and may give rise to Jarisch-Herxheimer reaction (Emmanouilides et al., 1994).

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