The majority of 'classic' skin and soft tissue infections are due to extracellular bacteria and are characterized by the presence of a polymorphonuclear inflammatory response. Impetigo, ecthyma, erysip-
elas, cellulitis, folliculitis and furunculosis are examples of such common infections. Recruitment, activation and functionality of polymorphonuclear cells in infected skin is dependent upon the correct production of chemokines and interleukins such as IL-8, the proper display of surface integrin molecules by polymorphonuclear cells, the upregulation of endothelial cell counter-integrin receptor molecules such as intercellular adhesion molecule 1 (ICAM-1), the presence in polymorphonuclear cells of normal phagocytic and enzymatic capabilities, and a preserved ability of polymorphonuclear cells to degranulate.
Impetigo results from a superficial infection of skin, usually by group A streptococci or Staphylococcus aureus. Infectious manifestations begin with formation of thin-roofed vesicles that rapidly pustulate and rupture. Dried, purulent discharge results in the formation of a characteristic, adherent, golden-brown crust. The vesico-pustule forms between the stratum corneum and the stratum granulosum, and the inflammatory response is predominately polymorphonuclear in nature. The most serious complication is that of streptococcus-specific antibody-as-sociated glomerulonephritis that can occur approximately 2 weeks after the cutaneous infection. Bullous impetigo also results from a superficial infection of skin but is caused by locally invasive phage-group 2 S. aureus that produces a toxin, exfoliatin. The action of this toxin results in the formation of bullae that contain S. aureus organisms and many polymorphonuclear cells. Bullous impetigo is not associated with the development of glomerulonephritis.
Erysipelas is a superficial cellulitis of skin and is most frequently caused by group A streptococci. Involved skin is usually red or brawny and is markedly indurated. The classic skin lesion rapidly expands peripherally. Edema is usually marked. Vesicles, bullae and petechiae may follow in involved skin. The patient may be febrile and systemically ill. Histopathologic examination of involved skin discloses marked vascular dilatation, extensive edema, and prominent infiltration by invading streptococci, especially of dermal lymphatic vessels. A polymorphonuclear cell infiltrate predominates.
Cellulitis is an acute, spreading infection of the deeper dermis and subcutaneous tissue and is most frequently caused by staphylococcal or streptococcal species. Infections with many other bacterial and fungal species have, however, been documented. The organisms proliferate in dermal and subcutaneous structures, and infection imparts an edematous, erythematous, inflamed appearance to involved skin. The advancing margin is less distinct than that seen with erysipelas. Leukocytosis, regional lymphadeno-pathy, local abscess formation and bacteremia can complicate the infectious process. The dermatolo-gical response is predominantly polymorphonuclear in nature.
Folliculitis is an infection of hair structures. Although most cases are due to gram-positive organism such as S. aureus, gram-negative bacteria such as Pseudomonas aeruginosa and fungal species can also be causative agents. Superficial folliculitis is characterized by pustule formation at the follicular opening. Deep folliculitis can manifest as a furuncle, or boil; or as a carbuncle, with extensive deep pustular involvement of the dermis and deeper structures. A polymorphonuclear cell infiltrate predominates in both superficial and deep folliculitis. Deep folliculitis can be complicated by fever, leukocytosis, bacteremia, local abscess formation, sinus tract formation and local tissue necrosis.
Individuals with defects in polymorphonuclear cell recruitment or functionality often have recurrent and chronic infections of the skin. For example, individuals with chronic granulomatous disease (CCD) are deficient in activity of the multicomponent cellular enzyme NADPH oxidase and are predisposed to skin infections with catalase-positive organisms such as S. aureus which are often chronic and recurrent. NADPH oxidase is crucial in generating the oxidative burst required to kill many catalase-positive bacteria, and a deficiency in the activity of NADPH oxidase often necessitates a compensatory host response that is granulomatous in nature.
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