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  • Central Nervous System (CNS) infections include a wide variety of clinical conditions and etiologies: meningitis, meningoencephalitis, encephalitis, brain and meningeal abscesses, and shunt infections. The focus of this chapter is meningitis.


  • Central nervous system infections are the result of hematogenous spread from a primary infection site, seeding from a parameningeal focus, reactivation from a latent site, trauma, or congenital defects in the CNS.

  • Passive and active exposure to cigarette smoke and the presence of a cochlear implant that includes a positioner, both increase the risk of bacterial meningitis.

  • CNS infections may be caused by a variety of bacteria, fungi, viruses, and parasites. The most common causes of bacterial meningitis are Streptococcus pneumoniae, group B Streptococcus, Neisseria meningitidis, Haemophilus influenzae, and Listeria monocytogenes.

  • The critical first step in the acquisition of acute bacterial meningitis is nasopharyngeal colonization of the host by the bacterial pathogen. The bacteria first attach themselves to nasopharyngeal epithelial cells and are then phagocytized into the host's bloodstream.

  • A common characteristic of most CNS bacterial pathogens (eg, H. influenzae, Escherichia coli, and N. meningitidis) is the presence of an extensive polysaccharide capsule that is resistant to neutrophil phagocytosis and complement opsonization.

  • The neurologic sequelae of meningitis occur due to the activation of host inflammatory pathways. Bacterial cell death causes the release of cell wall components such as lipopolysaccharide, lipid A (endotoxin), lipoteichoic acid, teichoic acid, and peptidoglycan, depending on whether the pathogen is gram-positive or gram-negative. These cell wall components cause capillary endothelial cells and CNS macrophages to release cytokines (interleukin-1, tumor necrosis factor, and other inflammatory mediators). Proteolytic products and toxic oxygen radicals cause an alteration of the blood–brain barrier, whereas platelet-activating factor activates coagulation, and arachidonic acid metabolites stimulate vasodilation. These events lead to cerebral edema, elevated intracranial pressure, cerebrospinal fluid (CSF) pleocytosis, decreased cerebral blood flow, cerebral ischemia, and death.


  • Meningitis causes CSF fluid changes, and these changes can be used as diagnostic markers of infection (Table 36–1).

  • Clinical presentation varies with age; generally, the younger the patient, the more atypical and the less pronounced is the clinical picture.

  • Patients may receive antibiotics before a diagnosis of meningitis is made, delaying presentation to the hospital. Prior antibiotic therapy may cause the Gram stain and CSF culture to be negative, but the antibiotic therapy rarely affects CSF protein or glucose.

  • Classic signs and symptoms include fever, nuchal rigidity, altered mental status, chills, vomiting, photophobia, and severe headache. Kernig and Brudzinski signs may be present but are poorly sensitive and frequently absent in children.

  • Clinical signs and symptoms in young children may include bulging fontanelle, apneas, purpuric rash, and convulsions, in addition to those just mentioned.

  • Purpuric and petechial skin lesions typically indicate meningococcal involvement, although the lesions may be present with H. influenzae meningitis. Rashes rarely occur with pneumococcal meningitis.


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