Sweating Out Ciprofloxacin Selects Multiresistant Staphylococcus Epidermidis
Abstract & Commentary
Synopsis: The excretion of antimicrobial agents in sweat might explain the presence on the skin of resistant Staphylococcus epidermidis that are responsible for most of the infections related to foreign bodies such as intravascular catheters.
Source: Høiby N, et al. Excretion of ciprofloxacin in sweat and multiresistant Staphylococcus epidermidis. Lancet 1997;349:167-169.
Six of these enterprising authors took 750 mg drug twice daily for seven days and measured the concentration of ciprofloxacin in their sweat to see what impact, if any, there was on the development of resistance among the axillary and nasal Staphylococcus epidermidis. Sweat was induced by pilocarpine-iontophoreses for 30 minutes in the axilla and 30 mcL was collected using a 20 mm paper disc. Average concentrations of ciprofloxacin 2.5 h after the first, fifth, and 13th tablet taken at 07:00 h were 2.2, 2.5, and 5.5 mg/L respectively. All isolates of Staphylococcus epidermidis were susceptible to 0.125-0.375 mg/L ciprofloxacin before drug intake but four different resistant strains (determined by restriction fragment length polymorphism) were recovered in the axilla an average of 2.7 days and all within a week after the first intake of ciprofloxacin. The same four genotypes were recovered in the nose an average of 18 days (range, 8-34 days) after the first tablet had been taken. The strain designated 1 was recovered from all six volunteers and strain 2 from only one person; both strains were resistant to 32 mg/L or more ciprofloxacin and also to more than 8 mg/L methicillin, 8 mg/L or more trimethoprim, erythromycin, and gentamicin, and to more than 5 mg/L sulphonamide but were susceptible to 1 mg/L or less clindamycin, tetracycline, and co-amoxiclav (Augmentin), as well as 2 mg/L or less fusidic acid, 4 mg/L or less teicoplanin, and to 8 mg/L or less amikacin. Strains designated 3A and 3B were found in all six and three volunteers, respectively, and both were less resistant to ciprofloxacin (MIC 4-12 mg/L) and susceptible to all the aforementioned compounds except for methicillin. Resistant strains 1, and either 3A or 3B were found at least once in all the subjects and could still be detected almost six weeks after the end of treatment. The authors conclude that the excretion of antimicrobial agents in the sweat might explain the presence on the skin of resistant Staphylococcus epidermidis that are responsible for most of the infections related to foreign bodies such as intravascular catheters. They also raise the question of whether other antibiotics are also excreted in the sweat.
COMMENT BY J. PETER DONNELLY PhD
Although it might seem obvious that antibiotics should appear in the sweat, surprisingly, until now, no one seems to have taken any notice, hence the complete absence of data. Yet, as the authors allude to, multiresistant Staphylococcus epidermidis are commonplace in hospitals and are particularly troublesome in hemato-oncology wards where fluoroquinolones are regularly used for prophylaxis. Indeed, more than a decade ago, before the introduction of these compounds, Hamilton-Miller and Iliffe (J Med Microbiol 1985;19:217-226) had shown the frequency of these strains to be higher among those treated for malignant disease than among other patients and suggested that this might be due to the use of co-trimoxazole as prophylaxis. That should have given the impetus at least to one research group to attempt to understand the mechanism involved and, in essence, undertake a study such as the one done by this Danish group. However, it didn’t.
Since several liters of sweat can be produced in a single day, it should really come as no surprise that the resistant strains of Staphylococcus epidermidis should be detected so rapidly among the skin flora of the axilla that provides a fertile niche for many different sorts of bacteria besides staphylococci and is constantly bathed in sweat. The hands are also in constant contact with the axillae and nose and, as is well known, people do not always keep their hands to themselves. One consequence of this has been shown in a recent study of the family members of acne sufferers treated sequentially with antibiotics such as trimethoprim, a tetracycline, erythromycin, or clindamycin who were significantly more likely to harbor staphylococci with similar resistance patterns to those found by Høiby et al, albeit on their cheeks, than were those in a control population (Miller YW, et al. J Antimicrob Chemother 1996;38:829-837). Similar close contact might also explain the presence of strains 1 and either 3A or 3B in the nose or on the axillae of each of the subjects in the Danish study at some time during the study but not before intake of ciprofloxacin. As Hawkey pointed out in a commentary on the paper in the same issue of The Lancet, it seems unlikely that these strains could have evolved independently .
These data show that antibiotic pollution is not confined to the patient and that collateral damage can and does occur. They also provide a ready explanation for the occurrence of multiresistant staphylococci so frequently encountered in patients with foreign bodies. The ease and speed with which antibiotic-resistant staphylococci can be selected in patients and spread beyond them to close contacts should also serve as a further caution against the "frivolous and profligate use of a precious resource," namely antibiotics.
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