ABSTRACT
This chapter reviews the epidemiology of neonatal necrotizing enterocolitis (NEC) with particular reference to the role of specific clostridial organisms in the pathogenesis of the syndrome. The identification of a primary pathogen or toxin may be delayed or masked by the events which ensue after the initial gastrointestinal (GI) injury. When the disease does present, it may demonstrate within a wide spectrum of signs, symptoms, severity, and mortality. The incidence of NEC was not altered nor the severity affected by human milk feedings. Past hypotheses related to the etiology of NEC all evoked GI ischemia as an important component for the pathogenesis of NEC. Certainly, clostridial organisms may become pathogens in infancy as evident by neonatal tetany and infantile botulism. The new organism may need to have the ability to bind to enterocytes in order to initiate the sequence of proliferation and toxin production.
