Despite advances in antimicrobial and general supportive therapies, central nervous system (CNS) infections remain a significant cause of morbidity and mortality in children. As classical signs and symptoms often are not present, especially in the younger children, diagnosing CNS infections is a challenge to the emergency department. Also, even for children who have had promptdiagnosis and treatment, a high frequency of neurologic sequelae remains. This often leads to legal action. The emergency clinician is faced with the daunting task of separating out those few children with CNS infections from the vast majority of children who come to the ED with less serious infections.
To develop bacterial meningitis, the invading organism must gain access to thesubarachnoid space. This is usually via hematogenous spread from the upper respiratory tract where the initial colonization has occurred. Less frequently, there is direct spread from a contiguous focus (eg, sinusitis, mastoiditis, otitis media) or through an injury, such as a skull fracture.
The most common causative organisms in the first month of life areEscherichia coli and group Bstreptococci. Listeria monocytogenes infection also occurs in patients in this age range and accounts for 5-10% of cases.Neisseria meningitidis infections occurring in the first month of life have been reported. From 30-60 days, group B streptococcal infection occurs frequently, and the gram-negative enterics decline in frequency. Streptococcus pneumoniae, Haemophilus influenzae, and N meningitidis occur rarely inthis age group. In those older than 2 months, S pneumoniae and N meningitidiscurrently cause the majority of the cases of bacterial meningitis. H influenzaemay still occur, especially in children who have not received the Hib vaccine.
The most common causative organisms (eg, N meningitidis, S pneumoniae, H influenzae) contain a polysaccharide capsule that allows them to colonize the nasopharynxof healthy children without any systemic or local reaction. A concurrent viral infection may facilitate the penetration of the nasopharyngeal epithelium by the bacteria. Once in the bloodstream, the polysaccharide capsule allows the bacteria to resist opsonization by the classical complement pathway and, thus, inhibit phagocytosis.
Unusual bacteria occasionally cause meningitis. Pasteurellamultocida is known to cause skin infections from cat or dog bites. A recent case described a 7-week-old infant with P multocida meningitis after exposure to dog saliva with no wound, emphasizing the need to protect young children from this pathogen. This infection, while rare, is associated with significant morbidity and mortality.
Salmonella meningitis should be suspected in any child with thisorganism grown at any other site in an unwell child or one younger than 6 months. Mothers known to be infected with Salmonella during pregnancy may put their child at risk. As therapy is different for Salmonella meningitis, while rare, it must be considered in the above situations.
The bacteremic phase allows penetration of the cerebrospinal fluid (CSF) through the choroid plexus. The CSF is poorlyequipped to control infection because type-specific antibodies do not penetrate the blood brain barrier well and complement components are absent or in low concentrations.
The cell walls of both gram-positive and gram-negative bacteria contain potent triggers of the inflammatory response. In the gram-positive bacteria, teichoic acid is considered the major pathogenic component. In gram-negativebacteria, lipopolysaccharide or endotoxin is the major pathogenic component. These components are released in the CSF during bacterial growth and especially with the lysis of bacterial cells. Antibiotic therapy causes a significant release of the mediators of the inflammatory response.
The mediators of the inflammatory response include cytokines (tumor necrosis factor, interleukin 1, 6, 8, 10),...
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