Biofilms in Dermatology

Aron G. Nusbaum, BS; Robert S. Kirsner, MD, PhD; Carlos A. Charles, MD


Skin Therapy Letter. 2012;17(7) 

In This Article


Acne affects approximately 45 million individuals in the United States with most patients aged 12–24 years old, where the prevalence has been shown to be as high a s 85%.[30] Evidence for the presence of biofilms in acne is predominantly derived from the ability of Propionibacterium acnes (P. acnes) to form biofilms both in vitro and on implanted medical devices. In addition, sequencing of the P. acnes genome reveals the presence of genes involved in the production of EPS and QS molecules.[31] P. acnes strains isolated from acne patients form biofilms in vitro that are characterized by increased lipase activity as compared to planktonic organisms.[32] This may explain a pathogenic role for P. acnes biofilms in acne, as lipase is not only a well known virulence factor, but it also produces irritant fatty acids that promote inflammation[33] and enhance P. acnes adhesion to the sebaceous follicle.[34] Keratin plugging has long been considered a key component of acne pathogenesis, and the adhesive properties of the EPS produced by P. acnes biofilms in sebum may be responsible for the tenacious binding of keratinocytes to the infundibular epithelium.[35] The observed clinical trend towards decreased efficacy of topical antibiotics may be explained by their usage over time or by the presence of biofilms, as biofilm-associated P. acnes exhibits increased resistance to commonly used anti-acne agents.[36] In addition, the extended length of treatment necessary for acne to respond to oral antibiotics further suggests that biofilms are a key pathogenic factor in this condition.[37] An in vitro study[32] evaluating multiple anti-acne agents alone or in combination found that only 0.1% triclosan, 5% benzoyl peroxide + 0.5% erythromycin, and 5% benzoyl peroxide + 1% clindamycin were effective in both reducing biofilm mass and killing >99% of biofilm-associated P. acnes. Interestingly, 5% benzoyl peroxide alone was ineffective unless combined with erythromycin or clindamycin, possibly as a result of antibiotics inhibiting protein synthesis and, therefore, making P. acnes cells vulnerable to benzoyl peroxide generated radicals. It should be noted that although 30mM azelaic acid was bactericidal, it did not reduce biofilm mass. Minocycline was the only agent in its class that removed biofilm and displayed the greatest bactericidal effect of all the tetracyclines tested. It has been postulated that the success of isotretinoin therapy may be related to reduction of sebaceous gland size with a subsequent decrease in sebum production, thus depleting the nutrient source for P. acnes biofilm.[35] The effectiveness of photodynamic therapy may also be due to an indirect effect on biofilms mediated by decreased sebaceous gland activity.[38] Future acne therapies may incorporate specific biofilm production antagonists or agents that alter the physical and biochemical properties of the pilosebaceous unit in order to create an unfavorable environment for P. acnes biofilm.[39]


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