70 - Superficial Bacterial Skin Infections and Cellulitis

Providing a permeability barrier, which prevents both the loss of water and electrolytes and the invasion of pathogens, the skin has a primary protective function. Intact skin is resistant to colonization and invasion of bacteria via a number of mechanisms. The outermost layer of the epidermis, the stratum corneum, constitutes the principal barrier against infection. The stratum corneum consists of corneocytes (anucleated keratinocytes or skin cells), and an outer lipid matrix. Corneocytes fit together in an overlapping fashion, making penetration by organisms difficult; they are shed from the skin after approximately 14 days, thus pathogenic organisms have limited time to invade further into the epidermis. The lipid matrix surrounding corneocytes is acidic, providing antimicrobial activity against pathogenic organisms, including Staphylococcus aureus and Streptococcus species. Keratinocytes also participate in innate immunity via secretion of antimicrobial peptides (AMPS) such as human β-defensins, canthelicidin, psoriasin, and dermicidin. AMPs are small peptides with broad-spectrum antimicrobial activity against bacteria, viruses and yeast. Production of AMPs by keratinocytes is stimulated by inflammatory cytokines produced in the skin as a result of injury or inflammation and by invasive organisms via pathogen-associated molecular patterns (PAMPs). Resident bacteria on the skin provide additional protection against infection by preventing colonization with pathogenic organisms via competitive binding to cell surface receptors, and by the production of toxic substances called bacteriocins that inhibit the growth of similar bacteria. Skin microflora generally can be categorized into two groups: resident flora and transient flora. Resident florae establish secure attachments to the skin, are present in stable numbers, and are able to tolerate an acidic environment. Transient florae are introduced from the environment and only attach if the skin is disrupted. Group A streptococcus (GAS, Streptococcus pyogenes) and S. aureus are the most common transient bacteria on the skin that cause infection. Many different bacteria are considered to be normal, resident flora, and each organism has a predilection for specific anatomic locations and for hosts of a particular age. The skin becomes colonized with microorganisms during the birth process and through contact with the environment. Infants born vaginally acquire Staphylococcus epidermidis during passage through the vaginal canal; and within hours, coryneform bacteria also are found on neonatal skin. The dry surface of the stratum corneum is colonized by micrococci and coagulase-negative staphylococci (CoNS), while coryneform organisms and gram-negative bacilli prefer moist, intertriginous areas. Propionibacterium spp. grow in hair follicles and sebaceous glands, and are mainly found after puberty, when sebaceous activity increases. Hair follicles are colonized by micrococci and CoNS superficially; Corynebacterium and Propionibacterium spp. are found deep in follicular canals. Transient colonization of the skin by pathogens is facilitated by factors that harm the resident flora, including elevated temperature, humidity, and antibiotic therapy. When a pathogen achieves successful colonization of the skin, the other cutaneous defense mechanisms must also be overcome before infection commences. Therefore, the main determinant of cutaneous infection is the balance between the virulence of the organism and the defense mechanisms of the host. Compromised cutaneous barrier function occurs in patients with chronic dermatitis and premature infants, making their skin more susceptible to pathogenic colonization and cutaneous infection. Primary bacterial infection of the skin can involve the epidermis, dermis, or subcutaneous tissue, whereas soft-tissue infections extend deeper, to the fascia or muscle. Superficial skin infections are mainly limited to the epidermis and dermis; although secondary inflammation can involve the subcutis. Several types of lesions can form in the skin as the result of a primary infectious process (Table 70-1); however, a pathogen usually produces a characteristic primary lesion with a characteristic pattern of spread. When cutaneous bacterial infection occurs, recognition of the type and depth of lesion produced are helpful in determining the likely causative agent. Primary, superficial bacterial infections of the skin and cellulitis are the focus of this chapter (Table 70-2). Other infectious agents (viruses, fungi) that sometimes resemble these bacterial infections are discussed briefly.