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  • Superficial nonfollicular infection, due to Staphylococcus aureus or group A Streptococcus, occurs more commonly in children (Fig. 18-1)

  • Lesions can begin as erythematous papules that evolve into a vesicle or pustule. The pustules may rupture leaving contagious honey-colored crusts

  • Treatment: topical mupirocin

  • Bullous impetigo is a toxin-mediated erythroderma (Fig. 18-2) is caused only by Staphylococcus aureus → exotoxin cleaves desmoglein 1 → separation of the epidermis at the granular layer

  • Clinical (seen most frequently in newborns)

  • Sharply demarcated flaccid bullae without surrounding erythema

  • Treatment: dicloxacillin or first-generation cephalosporin, topical mupirocin


Impetigo. (Used with permission from Dr. Steven Mays.)


Bullous impetigo. (Used with permission from Dr. Steven Mays.)


  • Differs from impetigo in that the dermis is ulcerated

  • Usually caused by group A beta-hemolytic streptococci (GABHS)

  • Clinical

    • Thick crusted ulcer that heals slowly and may produce a scar

    • Most commonly affects the lower extremities of children, persons with diabetes, and neglected elderly patient. Often occurs with lymphadenitis

  • Histology: ulceration to dermis with bacteria, crusting and an acute inflammatory infiltrate

  • Treatment: usually dicloxacillin or first-generation cephalosporin, parental antibiotics may be needed for widespread infection

Bacterial Folliculitis

  • Most cases caused by S. aureus (Fig. 18-3)

  • Superficial infection: (facial involvement is called Bockhart folliculitis): red papules/pustules, follicularly centered

  • Deep infection: (facial involvement = sycosis barbae); erythematous, fluctuant nodules

  • Lupoid sycosis: chronic form of sycosis barbae associated with scarring

  • Treatment: topical antibiotics, systemic antibiotics may be indicated


Folliculitis. (Used with permission from Dr. Steven Mays.)


  • S. aureus most commonly found (Fig. 18-4)

  • Clinical

    • Deep-seated nodules around hair follicle (inflammation involves the subcutis)

    • Multiple furuncles make a carbuncle, evolve from preceding folliculitis

  • Treatment: topical mupirocin and dicloxacillin; if large, then also need drainage


Furuncule. (Used with permission from Dr. Steven Mays.)


  • Cutaneous abscesses represent a collection of purulent debris in the skin (Fig. 18-5)

  • Usually Staphylococcus aureus (including possibly methicillin-resistant strains)

    • Methicillin-resistant S. aureus: altered cell wall transpeptidase (penicillin-binding protein 2a) carried on staph chromosome cassette mecA

      • – transfer by bacterial plasmids

    • Hospital-acquired methicillin-resistant Staphylococcus aureus (MRSA) usually carries mecA types I, II, and III

      • – resistance to clindamycin and macrolides (inducible clindamycin resistance detectable by the “D-zone” test). Community-acquired MRSA commonly carries SCCmec IV

      • – more antibiotic susceptibilities

      • – MRSA usually carries an ...

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