INTRODUCTION
Theoretical concern about the development of antibiotic
resistance emerged almost immediately upon the discovery of penicillin. In fact, Alexander Fleming reportedly
said of his discovery, “The bacteria will not take this sitting down.†Just as Fleming and others predicted, bacterial resistance became a true clinical concern for dermatologists in the 1980s, when the first reports emerged of the resistance of Propionibacterium acnes to oral antibiotics.1 Subsequent studies
have documented acne treatment failure associated with resistance to topical antibiotics.2
Beyond dermatology practice, antibiotic resistance has now become
recognized as a worldwide health concern. The increasing prevalence of methicillin-resistant Staphylococcus aureus (MRSA) has emerged as perhaps the most notable sign of the consequences
of resistance and is probably the most widely recognized resistance concern in the general public. As public health officials, health care professionals, and even international governmental organizations continue to suggest strategies to combat resistance, as dermatology providers we may have to be more conscious of our use of antibiotics, especially for the treatment of acne. One of the well-established acne treatments, benzoyl peroxide (BP), has reemerged as an important tool in treating acne while minimizing resistance. New findings suggest that BP may not only help to reduce antibiotic resistance when used in combination with antibiotics,
but may also be sufficient to reduce P acnes when used alone as monotherapy without an antibiotic.
The Problem of Resistance
Initial reports of the resistance of P acnes to oral and topical antibiotics raised alarm in the dermatology community. Importantly P acnes resistance rates have been estimated to be as high as 60% in some patient populations.3 Across the health care field, concern about long-term antibiotic use and subsequent
resistance risk has grown alongside the number of reports of community-acquired MRSA skin and soft tissue infections.
4,5 One report suggested that in the 10-year period from 1988 to 1998, rates of MRSA at select dermatology outpatient clinics increased by nearly 10-fold, accounting for 11.9% of all S aureus strains in 1998—up from 1.5% in 1988.4 Concern about MRSA in both the medical and lay communities was amplified
by the recent emergence of the multidrug-resistant MRSA USA300 clone in San Francisco and Boston.5
Clinicians have largely associated the greatest risk for resistance
with the use of oral antibiotics; however, recent research confirms that resistance to topical antibiotics is prevalent among S aureus isolates.6 Globally, resistance to erythromycin is most common. In North America, 57.8% of resistant S aureus strains were resistant to erythromycin. MRSA is the second most common form of resistance globally as well as in North America, accounting for about one-third of global resistance and for 36.9% of resistance in North America. Clindamycin resistance
is the third most common, with rates of 21.5% globally and 22.5% in North America (Table 1).6
Understanding Resistance
Scientists have elucidated the processes by which bacterial resistance emerges. Bacteria are adept at developing and transferring
resistance, and they can do so rapidly. The phenomenon of “survival of the fittest†applies to antibiotic therapy and bacterial
resistance. Those bacteria that demonstrate resistance to an
