In United States, the rate of bacterial meningitis has declined dramatically with the introduction of vaccines for both Haemophilus influenzae type b (Hib) and Streptococcus pneumoniae. Over the last two decades, the epidemiology of bacterial meningitis has consequently changed with decreased cases among young individuals but a larger burden among the older adults (median age of patients has increased from 30.3 to 41.9 years).2,5 In third world countries that lack effective vaccination programs, the incidence and case fatality rate of bacterial meningitis remain elevated.5,6,7
Studies on meningitis during pregnancy have been limited to case reports, case series, and one nationwide confidential enquiry.1,8–24 The only available estimated incidence is 0.5 cases of pneumococcal meningitis per 100,000 successful pregnancies reported in a study from the Netherlands.7 Based on the review of these case reports and case series, the overall maternal mortality rate may be as high as 32% and the fetal loss rate 27%.
Pathogenesis, Risk Factors, and Microbiology
Central nervous system (CNS) infections are classified based on the site of infection: encephalitis—infection of cerebral cortex; meningitis—infection of meninges (pia mater, arachnoid, and dura mater); brain abscess—cerebral cortex; subdural abscess—between dura and arachnoid layers; and epidural abscess—immediately above the dura.25 The tight junctions in the CNS capillaries form a limited permeable barrier (blood-brain barrier) that protects the CNS from invading pathogens and toxic substances. However, it also prevents entry of immunoglobulins, complement, and antibiotics, thereby limiting the host’s initial immune defense mechanism allowing the rapid progression of CNS infections. Table 3-1 shows the pathophysiological time line of bacterial meningitis.26
TABLE 3-1Pathophysiological Time Line of Bacterial Meningitis41 |Favorite Table|Download (.pdf) TABLE 3-1 Pathophysiological Time Line of Bacterial Meningitis41
|Early Events ||Intermediate Events ||Late Events |
Proinflammatory cytokines shower and initial bacterial invasion within subarachnoid space
Subpial encephalopathy induced by cytokines and other mediators
Breakdown of “blood-brain barrier” with migration of leukocytes and cerebral edema
|Impaired cerebral blood flow from rising intracranial pressure and vasculitis ||Focalizations |
|Fever, headache ||Confusion, meningeal signs, low CSF glucose ||Impaired consciousness, elevated CSF pressure and protein, focal symptoms ||Obtunded, seizures, and focal neurological signs ||Paralysis, cognitive impairment, coma, and risk for death |
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