Antibiotic Resistance of Propionibacterium acnes in Acne Vulgaris

Jil K. Swanson


Dermatology Nursing. 2003;15(4) 

In This Article

Abstract and Introduction


Acne vulgaris is a common skin disease affecting all ages. Antibiotics remain the most common prescribed agent for the treatment of acne. Improper use of antibiotics in the dermatological setting needs to be evaluated to prevent the increasing prevalence of antibiotic resistance.


Acne vulgaris is a common skin disease that involves individuals of all ages. It has been estimated to affect 79% to 95% of the adolescent population, 40% to 54% of individuals older than 25 years, and 12% of women and 3% of men in their mid ages (Cordain et al., 2002). Although not a fatal disease, it can produce both physical and emotional scarring, as well as psychological stress. Hence, treatment of the disease is important. Over the years, antibiotics have remained the most common prescribed agent for treating acne (Coates et al., 2002). In fact, each year 5 million prescriptions for oral antibiotics are dispensed for acne treatment (Stern, 2000). In an era of emerging antibiotic resistance, the use of antibiotics as a first choice of acne treatment should be re-evaluated to limit the development of antibiotic resistance. The purpose of this article is to address both topical and oral antibiotics used in treating acne vulgaris and their incidence of resistance to Propionibacteria acnes. Specifically, the most common topical antibiotics, including benzoyl peroxide, clindamycin, erythromycin, azelaic acid, and sodium sulfacetamide, will be discussed, as well as the most common oral antibiotics, including erythromycin, tetracycline, doxycycline, and minocycline.

The pathogenesis of acne vulgaris is a complex event, involving abnormal follicular hyperkeratination, the presence of P. acnes, increased sebum production, and inflammation at the site of pilosebaceous follicles (Thiboutot, 2002). P. acnes is an inhabitant of normal skin flora. It is implicated in the development of inflammatory acne by its ability to metabolize sebaceous triglycerides into fatty acids, which chemotactically attract neutrophils, as well as its capability to activate complement (Webster, 2002). The primary action of antibiotics is to decrease this organism on the skin and at the pilosebaceous follicles. For many years, antibiotics have been used frequently to treat acne vulgaris. Prior to the mid 1970s, resistance to P. acnes was not identified (Leyden, 1976). Since this time, however, antibiotic resistance has been increasing in prevalence within the dermatologic setting (Esperson, 1998). A 10-year study at the Leeds General Infirmary in the United Kingdom identified an increase in the prevalence of antibiotic-resistant strains from 34.5% in 1991 to 55.5% in 2001 (Coates et al., 2002). Furthermore, antibiotic resistance is not only a local concern in the United Kingdom, but a global problem, affecting populations in France, Germany, United States, Japan, and Australia (Ross et al., 2001).

Antibiotic resistance refers to when the minimum inhibitory concentration, the lowest concentration of an antibacterial agent that inhibits growth, is greater than the concentration obtained in vivo (Esperson, 1998). The development of antibiotic resistance is multifactorial. Although antibacterial agents are a primary factor in the development of resistance, there are many other factors involved, including the specific nature of the relationship of the bacteria to the antibiotic, how the antibacterial is used, host characteristics, and environmental factors (U.S. General Accounting Office, 1999). Even though the emergence of resistance coincided with the introduction of topical agents, a causal link between them and the development of resistance has not been proven, and may be a consequence of selective pressures from the extensive use of both topical and systemic agents (Coates et al., 2002). The first indication of antibiotic resistance to propionibacteria appeared in 1979 with the use of topical erythromycin and clindamycin (Crawford, Crawford, Stoughton, & Cornell, 1979).


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