[Current problems posed by staphylococcal infections in pediatric patients]

A PEDIATRIC PATHOGEN: Staphylococci remain one of the most important pathogenic agents leading to community-acquired infection in children. Over the last decades, there has been an evolution in the localizations of these infections: dramatic pleuropulmonary staphylococcal infection in newborns has almost entirely disappeared in developed countries. Conversely, skin infections and soft tissue infections as well as bone and joint localizations are frequent. The severity of these bone and joint infections has however declined allowing less aggressive therapeutic regimens. One of the current problems is the risk of emergence of meticillin-resistant strains causing community-acquired infections. Such infections have been very rare in France but careful monitoring is nevertheless necessary. NOSOCOMIAL INFECTION: Staphylococci are however the leading cause of nosocomial infections in children, particularly in intensive care units. All localizations are concerned, especially catheter-related septicemia and pneumonia. There has been an increasing trend for Staphylococcus aureus and coagulase-negative staphylococci infections. Most of the strains isolated are meticillin-resistant. TOXINS: Staphylococcus aureus secretes toxins leading to specific diseases: enterotoxins cause food-poisoning and exofoliatines cause generalized exfoliation and bullous impetigo. Staphylococcal scarlatina is related to the shock provoked by staphylococcal toxins: TSST-1 and entrotoxins. Staphylococcal toxic shock syndrome is a relatively new entity more frequently observed in adults but which was initially described in children. The disease may develop during any staphylococcal infection, particularly after superinfection of a skin burn or varicella. MECHANISM OF ACTION OF TOXINS: Staphylococcal toxins act like superantigens, capable of provoking polyclonal activation of a large number of T cells. This leads to the release of an important quantity of cytokines that intervene in the pathogenesis of toxic diseases. This polyclonal activation has been observed in other pediatric diseases of unknown origin but in which the involvement of staphylococcal toxins can be suspected. There is solid evidence in favor of staphylococcal toxins in Kawasaki syndrome. Likewise, these toxins could be implicated in sudden death syndrome in infants and in acute exacerbations of atopic exzema.