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In 2013, 400 cases of meningococcal meningitis were reported in the United States.1 These cases included 70 mortalities, as well as many patients who were disabled. Although the incidence of meningococcal meningitis is low, morbidity and mortality are high.
Each year clusters of meningitis cases break out in the U.S. in the fall and winter months, particularly among adolescents and young adults. Sixty percent of patients with meningitis are adolescents or young adults.2 Patients commonly present to a primary care provider early in the infection when it appears to be an upper respiratory infection or influenza.
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Early diagnosis is challenging; however, fulminant meningococcal infection can occur in less than 24 hours.3 The rapid surge of the infection often leaves the patient and primary care provider in an emergency situation.
What causes meningococcal meningitis?
Small outbreaks of bacterial meningitis are most often caused by one of two microorganisms — Neisseria meningitides or Streptococcus pneumonia.4,5 Both are highly resistant, encapsulated bacteria that enter the body via droplet infection in the upper respiratory tract. Another name for N. meningitides is meningococcus; hence, the name, meningococcal meningitis.
Meningococcus is the organism most often associated with outbreaks of epidemic proportion. Approximately 10% to 34% of the population are carriers of N. meningitides and have this microorganism in their nasopharynx.6,7 It is unclear why some individuals remain as carriers and others develop meningitis.
Meningococcus is an aerobic, Gram-negative diplococcus with a thick outer capsule. Disease is caused by one of six serotypes; A,B,C,X, Y or W-135; each has a slightly different outer capsule and occurs in different geographic locations.6 For example, in the U.S, most meningococcal organisms are serotypes B, C, or Y; in sub-Saharan Africa, the most common serotype is A.6
Meningitis involves inflammation of the pia and arachnoid membrane, the inner layers of the meninges. From the nasopharyngeal mucosa, the microorganism enters the bloodstream and then crosses the blood-brain barrier into the subarachnoid space and cerebrospinal fluid (CSF).
Once in the CSF, the bacteria elicit a profound inflammatory reaction, triggering macrophages and immunoglobulins to attack the microbes. However, the thick polysaccharide bacterial capsule resists phagocytosis and immunoglobulin assault. In addition, the bacteria secrete toxins that affect the brain parenchyma and stimulate apoptosis of neurons8.
