Neisseria are Gram-negative diplococci. N. meningitidis and N.onorrhoeae are the only two bacteria in this group that are commonly pathogenic to humans. Meningococcal infection Meningococci (N. meningitidis) are ubiquitous. However, group A is commonly found in Africa and group B on the European and American continents. The incidence of groups C, Y and W135 infections is steadily rising worldwide. Group A is responsible for epidemics of meningitisand group Band C for sporadic infections. Its virulence is attributed to the polysaccharide capsule (which resists phagocytosis) and the lipopolysaccharide-endotoxin complex (which is responsible for its clinical toxicity). Transmission is by droplet infection or direct contact. Humans are the only known reservoirs. Following transmission, N. meningitidis colonize the nasopharynx preferentially because of the humidity, increased carbon dioxide tension and specific receptor substances synthesized by the nasopharynx to which they adhere. Invasiveness of the organism appears to be almost solely dependent on the amount of specific antimeningococcal bactericidal antibody in the host. A history of a recent viral respiratory infection is common.
Four major clinical syndromes due to meningococci are recognized:
MENINGOCOCCAEMIA may occur alone or in association with eningitis. It is characterized by the presence of headache, fever, malaise and myalgia. The patient looks toxic, and has tachycardia and tachypnoea. Skin manifestations occur early and consist of a purpuric rash and/or petechiae that also affect the conjunctivae.
FULMINANT MENINGOCOCCAEMIA (Waterhouse- Friderichsen syndrome) occurs in about 10% of patients. It is characterized by an extremely rapid downhill clinical course, with extensive haemorrhage into the skin, hypotension, shock, confusion, coma and death within a few hours of the onset of symptoms. Disseminated intravascular coagulation (DIC), due to activation of the complement system, may further complicate the clinical picture. Haemorrhage into the adrenal glands mayor may not be present. Without prompt treatment, the mortality rate approaches 100%.
MENINGOCOCCAL MENINGITIS presents with fever, nausea, vomiting, headache, photophobia, altered consciousness and neck rigidity. The clinical presentation is indistinguishable from other acute bacterial meningitides.
CHRONIC MENINGOCOCCAEMIA is rare. It is characterized by intermittent fever, a maculopapular rash, arthralgia and splenomegaly. Blood cultures are positive during bacteraemic episodes. N. meningitidis may also rarely result in polyarthritis, pericarditis and nephritis.
This is established by demonstrating meningococci In body fluids such as blood, CSF, petechial or joint aspirates. The CSF is turbid with an increase in neutrophils and protein. Counterimmunoelectrophoresis and latex agglutination to the polysaccharide antigen of group A, C, D and Y have recently been found useful.
Benzylpenicillin is the treatment of choice, the dose being 1.2-2.4 g i.v. 4-hourly for adults started immediately on suspicion of diagnosis. Cefotaxime is equally effective.Chloramphenicol (75-100 mg kg- 1) is the drug of choice in individuals allergic to penicillin. Resistance to penicillin has been reported. Treatment for shock and ole should be instituted. Steroids should be used in children with meningococcal meningitis.On discharge from hospital, rifampicin should be given-see below.
PREVENTION AND CONTROL
Penicillin does not affect the carrier state. Family contacts of patients are protected effectively by rifampicin 600 mg two times daily for 2 days. Immunoprophylaxis with a quadrivalent vaccine against group A, C, Y and WI35 organisms is effective and is recommended when travelling to high-risk places-Africa, Asia, South America, Middle and Far East.