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Normal human skin is colonized soon after birth by a large number of bacteria that live as commensals on the epidermis and in epidermal appendages (ie, the skin microbiome). For example, coagulase-negative Staphylococci (Staphylococcus epidermidis) are inoculated during vaginal passage and coryneform bacteria take up residence on neonatal skin shortly after birth. Within weeks after birth, neonatal skin is colonized with many different species of bacteria, fungi and viruses that comprise the human skin microbiome (see Chap. 16).

This chapter discusses superficial cutaneous infections and pyodermas. Pyodermas are infections of the skin that are pyogenic (ie, filled with pus). The majority of the cutaneous pyodermas are caused by Staphylococcus aureus or group A Streptococcus (GAS) (also known as Streptococcus pyogenes). These Gram-positive bacteria cause a broad clinical spectrum of infections ranging from superficial pyodermas to more invasive skin and soft-tissue infections (SSTIs; see Chaps. 151 to 153) depending on the organism, the anatomic location of infections, and on host factors. In addition, this chapter also discusses other common superficial bacterial skin infections, including pitted keratolysis, which is thought to be caused by Kytococcus sedentarius, Dermatophilus congolensis or other Corynebacterium spp., erythrasma, which is caused by Corynebacterium minutissimum, and trichobacteriosis, which is caused by Corynebacterium spp.



  • Staphylococcus aureus is the most common cause of superficial purulent skin infections (pyodermas).

  • Thirty percent of individuals are continuously colonized with S. aureus, and occasional carriage is found in up to 60% of healthy people. This represents a common source and risk factor for infection.

  • Contributing factors include immunosuppressive disorders, diabetes mellitus, atopic dermatitis, and preexisting tissue injury.

  • Local manifestations include impetigo, ecthyma, folliculitis, and furunculosis.

  • Systemic reactions include staphylococcal scalded-skin syndrome, staphylococcal scarlet fever, and staphylococcal toxic shock syndrome.

  • Pathology: dense neutrophilic infiltration.

  • Treatment: topical, oral, or parenteral antibiotics; change predisposing conditions, if possible. When planning therapy, consider antimicrobial resistance patterns.

Staphylococci are classified into 2 major groups: (a) coagulase-negative Staphylococci (S. epidermidis) and (b) coagulase-positive Staphylococci (S. aureus). Whereas S. epidermidis is primarily a harmless commensal bacterium found on the surface of human skin, S. aureus can be found as both a harmless commensal bacterium as well as an aggressive and deadly pathogen. In 1928, Alexander Fleming found that golden-colored S. aureus colonies were seen growing throughout a petri dish, except in one area contaminated by the mold Penicillium chrysogenum (also known as Penicillium notatum). This led to Fleming’s important discovery of penicillin and started the golden age of antibiotics. However, as antibiotic use became widespread so did the development of antibiotic resistance, which has complicated treatment of bacterial infections. These antibiotic-resistant bacteria include the widespread emergence of hospital-acquired and community-acquired methicillin-resistant S. aureus (MRSA) strains, as well as antibiotic resistance developing in commensal bacteria such as S. epidermidis. As a result, ...

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