Impetigo in Children and Adolescents
Impetigo in Children and Adolescents
Because skin is a host mechanism of defense, unbroken skin is generally unaffected by coagulase-negative staphylococci (CoNS) and GABHS colonization. Teichoic acid mediates adhesion in the impetigo-causing microorganisms, but it requires fibronectin in order to colonize the skin. Fibronectin, a cell adhesion molecule that is not available on the surface of intact skin, allows for bacterial cells to attach to collagen and invade disrupted skin surfaces. (Table 1 lists various conditions that may predispose children to impetigo). Certain factors modify the skin's normal flora and enable transient colonization by GABHS and Saureus. These include humidity or high temperature, preexisting skin lesions, recent antibiotic treatment, and young age.
Colonization with GABHS occurs when infected individuals are in close contact with others. The normal flora of the skin becomes disrupted, allowing for the development of impetigo once the epidermis becomes affected with minor abrasions or insect bites. Often-times, patients who developed impetigo caused by streptococcus may have detectable GABHS in their nasal passages and throat up to 3 weeks after the development of lesions. These patients will not have symptoms of streptococcal pharyngitis since the strain of bacterium that causes impetigo (pattern D) is different from the strains causing pharyngitis (patterns A, B, and C).
Up to one-third of individuals are colonized with Saureus in the nostrils, and some of these patients experience recurrent impetigo around the lips and nose. Most healthy individuals only transiently host Saureus as part of their normal skin flora. In general, the bacteria are spread via direct skin contact and enter the surface of the skin through a broken site.
Pathophysiology
Because skin is a host mechanism of defense, unbroken skin is generally unaffected by coagulase-negative staphylococci (CoNS) and GABHS colonization. Teichoic acid mediates adhesion in the impetigo-causing microorganisms, but it requires fibronectin in order to colonize the skin. Fibronectin, a cell adhesion molecule that is not available on the surface of intact skin, allows for bacterial cells to attach to collagen and invade disrupted skin surfaces. (Table 1 lists various conditions that may predispose children to impetigo). Certain factors modify the skin's normal flora and enable transient colonization by GABHS and Saureus. These include humidity or high temperature, preexisting skin lesions, recent antibiotic treatment, and young age.
Colonization with GABHS occurs when infected individuals are in close contact with others. The normal flora of the skin becomes disrupted, allowing for the development of impetigo once the epidermis becomes affected with minor abrasions or insect bites. Often-times, patients who developed impetigo caused by streptococcus may have detectable GABHS in their nasal passages and throat up to 3 weeks after the development of lesions. These patients will not have symptoms of streptococcal pharyngitis since the strain of bacterium that causes impetigo (pattern D) is different from the strains causing pharyngitis (patterns A, B, and C).
Up to one-third of individuals are colonized with Saureus in the nostrils, and some of these patients experience recurrent impetigo around the lips and nose. Most healthy individuals only transiently host Saureus as part of their normal skin flora. In general, the bacteria are spread via direct skin contact and enter the surface of the skin through a broken site.
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