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INTRODUCTION

  • 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.

PATHOPHYSIOLOGY

  • The development of bacterial meningitis involves four main processes: (1) mucosal colonization and bacterial invasion of the host and CNS, (2) bacterial replication in the subarachnoid space, (3) pathophysiologic alterations resulting in progressive inflammation, and (4) increased intracranial pressure (ICP) and cerebral edema leading to neuronal damage.

  • The critical first step in the acquisition of acute bacterial meningitis is nasopharyngeal colonization of the host by the bacterial pathogen. Most cases of acute bacterial meningitis probably occur following bacteremia, but the high incidence of pneumococcal meningitis in patients with sinusitis and otitis media suggests that direct spread to the CNS can also occur.

  • 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.

  • A common characteristic of most CNS bacterial pathogens (eg, H. influenzae, Escherichia coli, 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 lysis 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.

  • 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.

CLINICAL PRESENTATION

  • Signs and symptoms of acute bacterial meningitis include fever, nuchal rigidity, altered mental status, chills, vomiting, photophobia, and severe headache. Up to 95% of patients exhibit at least two of the following symptoms: fever, nuchal rigidity, headache, and altered mental status. 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, apnea purpuric rash, and convulsions.

  • 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.

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

  • CSF culture is the gold standard for diagnosis of bacterial meningitis ...

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