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MENINGOCOCCAL INFECTIONS

  • Etiology and Microbiology Neisseria meningitidis is a catalase- and oxidase-positive, gram-negative aerobic diplococcus with a polysaccharide capsule that colonizes humans only.

    • – Of the 13 identified serogroups, only 5—A, B, C, Y, and W135—account for the majority of cases of invasive disease.

    • – Serogroups A and W135 cause recurrent epidemics in sub-Saharan Africa. Serogroup B can cause hyperendemic disease, and serogroups C and Y cause sporadic disease and small outbreaks.

  • Epidemiology Up to 500,000 cases of meningococcal disease occur worldwide each year, with a mortality rate of ∼10%.

    • – Most commonly, meningococci asymptomatically colonize the nasopharynx; such asymptomatic nasopharyngeal carriage is detected in >25% of healthy adolescents and adults.

    • – Patterns of meningococcal disease include epidemics, outbreaks (e.g., in colleges, refugee camps), hyperendemic disease, and sporadic or endemic cases.

    • – Although most countries have predominantly sporadic cases (0.3–5 cases per 100,000 population), epidemics in sub-Saharan Africa can have rates as high as 1000 cases per 100,000 population.

    • – Rates of meningococcal disease are highest among infants, with a second peak in adolescents and young adults (15–25 years of age).

    • – Other risk factors for meningococcal disease include complement deficiency (C5–C9), close contact with carriers, exposure to tobacco smoke, and a recent URI caused by a virus or Mycoplasma species.

  • Pathogenesis Meningococci colonizing the upper respiratory tract invade the bloodstream through the mucosa only rarely, usually within a few days after an invasive strain is acquired.

    • – The capsule is an important virulence factor, providing resistance to phagocytosis and helping prevent desiccation during transmission between hosts.

    • – Severity of disease is related to the degree of endotoxemia and the magnitude of the inflammatory response.

    • – Endothelial injury leads to increased vascular permeability and hypovolemia, resulting in vasoconstriction and ultimately in decreased cardiac output.

    • – Intravascular thrombosis caused by activation of procoagulant pathways and down-regulation of anticoagulant pathways results in the characteristic purpura fulminans often seen in meningococcemia.

  • Clinical Manifestations The most common clinical syndromes are meningitis and meningococcal septicemia, with disease usually developing within 4 days of organism acquisition.

    • – A nonblanching rash (petechial or purpuric) develops in >80% of cases; early in the illness, the rash is often absent or may be indistinguishable from viral rashes.

    • – Meningococcal meningitis alone (without septicemia) accounts for 30–50% of cases.

      • This meningitis is indistinguishable from other forms of bacterial meningitis unless there is an associated petechial or purpuric rash.

      • Classic signs of meningitis (e.g., headache, neck stiffness, photophobia) are often absent or difficult to discern in infants and young children.

    • – Meningococcal septicemia alone accounts for ∼20% of cases and initially may present as an influenza-like illness (e.g., fever, headache, myalgias, vomiting, abdominal pain).

      • May progress to shock (e.g., tachycardia, poor peripheral perfusion, oliguria), decreased level of consciousness due to decreased cerebral perfusion, spontaneous hemorrhage (pulmonary, gastric, or cerebral), and ultimately multiorgan failure and death.

      • Poor prognostic factors include an absence of meningismus, hypotension, relatively low temperature (<38°C), leukopenia, and thrombocytopenia.

    • – Chronic meningococcemia presents as repeated ...

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