Guidelines for the Diagnosis and Treatment of Meningococcal Meningitis
Meningococcal disease may present as meningitis, septicaemia or a combination of the two. Generally, meningitis has a gradual onset, with fever, headache and neck stiffness as the most frequent clinical symptoms. In contrast, fulminant septicaemia may develop within hours, and is characterised by hypotension, disseminated intravasal coagulation (DIC), petecchial bleedings and shock. Mortality with septicaemia often reaches 30%. It is of vital importance to diagnose and treat meningococcal disease rapidly. Conventionally, diagnosis is based on culture of the bacterium Neisseria meningitidis from blood or cerebrospinal fluid (CSF) or on microscopy of Gram-negative diplococci in the CSF. Direct bacterial antigen (capsular polysaccharide) detection methods have readily become available. These tests are rapid and do not require the presence of viable bacteria, but their sensitivity and specificity is low. During the last few years, a number of polymerase chain reaction (PCR) tests for the detection of bacterial nucleic acids have been developed. PCR tests are rapid, specific, extremely sensitive, does not require viable bacteria and may allow direct typing of the bacterium. The drug of choice for treating meningococcal disease is benzylpenicillin. In some rare cases, the sensitivity of N. meningitidis to penicillin is decreased, and ceftriaxone or cefotaxime may be used instead. The severe clinical signs in septicaemia are mainly caused by bacterial endotoxins which are part of the bacterial cell wall and are also released from viable bacteria. Antibiotics do not prevent the effects of endotoxins and supportive therapy to control increased intracranial pressure, hypovolaemia, DIC and shock, are also needed. Following the first case of meningococcal disease in a population, the infection may spread causing one or more secondary cases. The ideal prevention of meningococcal disease is by vaccination. However, no vaccine against group B meningococcal disease exists, and group A and C vaccines have not been implemented in most vaccination programmes. Prevention of the primary case is therefore not achievable, but secondary infection can be prevented by eradication of the disease-causing strain in healthy contacts with chemoprophylaxis.
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