Antibiotic Resistant Bacteria Colonizing Healthy Skin

The following release is a summary of a presentation at the 100th General Meeting of the American Society for Microbiology. Additional information on this and other presentations can be found in the General Meeting Press Kit online at http://www.asmusa.org/pcsrc/gm2000/presskit.htm.

Embargo Date/Time: Wednesday, May 24, 2:30 p.m.

Primary Author:
Anne Eady, Univ. of Leeds
44-113-223-5581
miceae@leeds.ac.uk

Each and every one of us is a walking culture collection of bacteria. Complex communities of resident bacterial species live on all exposed body surfaces including the skin, eye, upper respiratory tract, oral cavity and intestine. Although some of these bacteria are sensitive to antibiotics, many of them are resistant to the antibiotics we rely on daily to treat infection. Every time we are given a course of antibiotics our resident bacterial population is exposed to selective pressure. In order to survive, the bacteria develop resistance. Those that do not become resistant are replaced by those that are resistant. Although the changes are only transient, a proportion of the bacteria remain resistant for long periods of time after antibiotic therapy has ended. In this way the effects of repeated courses of antibiotics are cumulative.

Resident skin bacteria perform an important function. They use the secretions of our sweat and sebaceous glands (sebum is the grease that makes our skin look shiny) as nutrients and by their presence prevent colonisation by more harmful bacteria. When we are hospitalised and taking antibiotics, our resident flora is upset and this enables harmful bacteria (such as Staphylococcus aureus and Acinetobacter baumannii) to colonise our skin. These harmful bacteria can be passed between patients by hospital staff and sometimes they may cause infection. Because the organisms are usually multiply resistant, infections caused by them are often difficult to treat. In some patients, especially those on immunosuppressive therapy, resident skin bacteria can also cause infections. These organisms are generally not as resistant as those from the hospital environment. These problems are well understood by doctors who know how to manage them.

Not all antibiotics select for resistance in the skin flora. Those that do are delivered to the skin surface in bioactive amounts and what little evidence there is suggests that sweat may be the main route. Studies with the fluoroquinolone ciprofloxacin found the drug in sweat within hours of the first oral dose and resistant coagulase-negative staphylococci were detected in the axilla less than 3 days after starting therapy. In contrast aminoglycosides like gentamicin do not reach the surface of intact skin in inhibitory amounts and this may explain why staphylococcal resistance did not emerge until the introduction of extensive topical use. Of course, all systemically administered antibiotics reach the surface when the skin is broken or barrier function is abnormal (as in premature neonates).

In the community, antibiotic therapy for the common skin disease acne vulgaris a significant driver of resistance in the resident flora (not only of skin) and is frequently overlooked. Doctors are reluctant to treat patients with acute respiratory infections with even short courses of antibiotics because of concerns about resistance. These same doctors happily write prescriptions for several weeks oral or topical antibiotic treatment for acne despite the fact that duration of therapy is a primary driver of resistance. Acne patients are reservoirs of singly and multiply resistant coagulase-negative staphylococci which can be disseminated by desquamation or contact. Studies have shown that the skin flora of untreated close contacts of antibiotic treated acne patients is more similar in terms of resistance to that of the patients than of age and sex matched healthy control subjects. This observation suggests that selective pressure extends beyond the patients themselves, perhaps via the translocation of active drug from the patients' skin.

Acne is not an infection in the traditional sense and it can be managed by treatment regimens not involving antibiotics. However, a resident skin bacterium called Propionibacterium acnes is implicated in the formation of inflamed acne spots. The organism is a slow growing anaerobic bacterium with GC rich DNA and, unlike staphylococci, has no mobile genetic material. The only means it has to acquire resistance is by mutation or via the transfer of resistance genes from an unrelated species. Until this year resistance was invariably associated with chromosomal mutations in the genes that encode the target sites to which the antibiotics bind. This was true for erythromycin, clindamycin and tetracyclines. The level of resistance conferred was high enough to be clinically relevant in the case of oral administration but topical application could theoretically deliver enough drug to the skin to inhibit the resistant strains. A mobile resistance gene of corynebacterial origin carried