In most cases, meningitis occurs as a complication of a primary bacteremia. The inflammatory response to the products of bacterial multiplication may result in alteration of the permeability of the blood-brain barrier with extension of infection and inflammation to the brain itself. The resulting brain edema, increased intracranial pressure, decreased cerebral blood flow, and vascular thrombosis produce neuronal injury. Less commonly, meningitis occurs via the hematogenous route from a distant primary focal infection, direct extension from adjacent infection, or following head injury with cribriform plate fracture. The incidence of meningitis is highest between the ages of birth and 2 years, with age-related peak risks during the neonatal period and between 3 and 8 months. Host defense factors resulting in impaired splenic function or immunodeficiency are associated with increased risk for sepsis and meningitis.

The pathogenic organisms responsible for bacterial meningitis parallel those responsible for sepsis. In the neonatal period, group B Streptococcus and E. coli predominate. In older infants and children, S. pneumoniae and N. meningitidis are the likely pathogens. Although penicillin-resistant strains of S. pneumoniae are increasing in frequency, there is no evidence that these organisms are more virulent.38 Infants and children who have not received the HIB vaccine continue to be at risk for HIB meningitis.

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