Individuals with skin of color may develop a wide range of cutaneous infections involving either gram-positive or gram-negative organisms.
In most cases, these infections do not differ significantly from those that occur in the general population.
Staphylococcus aureus and Streptococcus pyogenes are the two major gram-positive organisms that are most often implicated in common skin and soft tissue infections.
Gram-negative infections of the skin occur more commonly in children, patients with diabetes, and immunocompromised patients.
Although empirical antibiotic treatment is an important first step in treating bacterial infections, once the diagnosis is established, treatment should then be dictated by the antibiotic sensitivities of the cultured organism.
BACTERIAL BIOFILMS AND THE SKIN
The human body plays host to a diverse world of bacteria, both as single-celled planktonic organisms and in sessile groups. Microbial flora of the skin largely exists within biofilms, sessile bacterial communities encased in an extracellular matrix, with the ability to communicate and regulate its own growth and metabolism.1 Biofilms exist in both healthy and pathologic skin and may be protective or destructive, influencing host inflammatory cells and host metabolism and conferring antibiotic resistance. Therapeutic approaches to dermatologic disease have shifted recently, as biofilms may require more than traditional culture-based treatment.2
Biofilm studies are revealing new information about the skin’s bacterial environment. These studies help explain why noninfectious diseases like acne vulgaris, miliaria, and atopic dermatitis respond to antibiotics and why certain lesions have anatomic predilections.2 More alarming however, are in vitro studies of biofilms that are 50 to 500 times more resistant to antibiotics than their planktonic counterparts.3,4 This is due to several mechanisms: a physical barrier that prevents antibiotic diffusion,5 slowed growth and metabolism of centrally located organisms that escape peripheral antibiotic activity, regulatory genes that change bacterial phenotype in response to environmental stress, spore-like forms that shut down antibiotic targets,6 and frequent gene transfer through genomic islands of horizontally acquired DNA segments.7 The complex interaction between biofilms and antibiotic therapy demands attention from the dermatologist, as inappropriate usage with sub-minimum inhibitory concentrations may enhance biofilm formation and confer further resistance.8,9
The widespread use of antibiotics for bacterial skin infections contributes to the emergence of resistant organisms and poses a serious threat to public health. Dermatologists wrote approximately 9.5 million prescriptions for oral antibiotics in 2009 alone,10 and antibiotic resistance is growing among normal skin flora. The first penicillin-resistant Staphylococcus aureus was discovered in 1941, shortly after the drug’s introduction. Up to 78% of all staphylococcal skin infections are now due to methicillin-resistant S. aureus (MRSA).11 MRSA continues to display resistance to a range of drugs, including mupirocin, erythromycin, clindamycin, tetracycline, sulfonamides, chloramphenicol, cephalosporins, and quinolones.12
Propionibacterium acnes, the bacteria involved in acne formation, is just ...