Meningococcal meningitis – causes, features, symptoms and treatment

Meningococcal meningitis occurs both in epidemics and sporadic forms. The causal organism is meningococcus (Nissseria meningitidis) a kidney shaped gram negative organism which can be classified into eight groups and out of which group A,B and C are the ones responsible for most of the infections. The organisms are commonly found in the nasopharynx of people who act as carriers and often the disease spreads by droplet infection. Carriers often outnumber overt cases, infect other people without themselves developing the disease. Principal causes of spread of the disease are over crowding and catarrhal disorder of the nose and throat. Children and young infants are more susceptible to suffer from it. It is uncommon after the age of 40.

Pathology

It is like in other cases of bacterial meningitis except for that in meningococcal meningitis brain is diffusely involved with resultant congestion, edema, perivascular hemorrhages and suppurative lesions. There may be focal areas of involvement. In fulminant form of meningitis, hemorrhages are found in the adrenals leading to adrenal failure and shock (Water House friederichsen syndrome).

Clinical features

Onset of meningococcal meningitis generally is acute with headache, fever, chills, neck rigidity and signs of meningeal irritation. Commonest age group is young children and adults. Incubation period is 3-5 days and there is history of preceding upper respiratory tract infection.

Onset may be gradual in some cases and fulminant in others. Pulse is slow. Headache and vomiting are rather of severe nature. Delirium may be severe and patient may pass into stupor and coma. Signs of meningeal irritation (photo-phobia: neck rigidity, kernig’s and brudzinski’s signs) are invariably present. Meningococcal meningitis is characterized by purpuric eruption and maculopapular rash in areas subjected to pressure. While purpuric eruption takes the form of petechiae appearing during the first 24 hours of illness, maculopapular rash appears before the fourth day first on the trunk and then on thighs and forearms.

As the disease progresses rise in intracranial pressure occurs. Pupils are dilated and react sluggishly. Diplopia, slight ptosis and divergent squint are common. Papilloedema may be present. Limbs are flaccid. Reflexes are diminished. There is loss of sphincter control. Development of stupor and coma are bad prognostic signs. Cases with fulminating type develop water house Frederich syndrome characterised by cyanosis collapse and shock.

Diagnosis

Meningococcal meningitis is to be differentiated from other forms of bacterial meningitis by its rash (purpuric and maculopapular). Other diseases to be differentiated include encephalitis, cerebral hemorrhage, meningitis and general infections (pneumonia, influenza, typhoid) simulating meningitis.

Investigations:

1. Blood count shows leucocytosis with rise in polymorphs.

2. Blood culture for meningococci may be positive in early stages.

3. CSF examination is the most important diagnostic aid. CSF pressure is raised. It is turbid and purulent in appearance. Protein content is raised. There is often a cob web formation. Sometimes CSF may coagulate due to high albuminous content. Glucose content is markedly reduced as well as chlorides (650-680 mg/100 ml). Cell count is increased, the cells being mainly polymorphonuclear. About 1000-2000 cells per cmm are present.

4. Gram’s stain of sedimented CSF does not readily identify meningococci. Meningococcal antigen may be demonstrated by immune electrophoresis (CIE) and ELISA test.

Complications and sequelae. A number of complications may occur in cases of meningococcal meningitis. These may be in the form of internal hydrocephalus, focal neurological damage (hemiplegia), paraplegia, aphasia, deafness and loss of vision. Uncommon complications include fibropurulent pericarditis, endocarditis, arthritis and nephritis. In the fulminant type, patient rapidly goes into stupor and coma. Death may occur in a short time. Cases of water house Frederich syndrome carry poor prognosis.

Cases where treatment has been delayed or inadequate these may be left with a chronic form of basal meningitis characterized by cranial nerve palsies, Hydrocephalus, neck retraction and paralysis.

Treatment of bacterial meningitis

1. Bacterial meningitis is an acute medical emergency and treatment must be instituted immediately. For adult patients with pneumococcal, meningococcal or Listeria meningitis drug of choice is Penicillin G 5- 10 million units intravenously every 6 hourly. Ampicillin in a dose of 300-400 mg/kg body weight daily intravenously is also an effective drug.

The third generation cephalosporins, cefotaxime (2 g I/V 4 hourly) or Ceftriaxone (2 g I/V once a day) are effectivie in pneumococcal, H. influenzae and meningococcal meningitis but not in listeria meningitis where trimethoprim, sulpha methoxazole (160 mg TMP+ 800 mg SMX) intravenously in drip twice a day is used.

2. Patients who are allergic to penicillin they can be treated with chloramphenicol (dosage 1 g I/v 6 hourly) or third generation cephalosporins.

3. Since these drugs (penicillin and ampicillin) enter the blood-brain barrier, intrathecal administration is not recommended.

4. Treatment must be continued for at least 7- 10 days. Progress of the case is observed by CSE Examination which becomes clear and its biochemistry returns to normal.

5. Look for any focus of infection in para nasal sinuses, mastoid or intracranial region. It should be adequately treated.

6. For raised intracranial tension intravenous Mannitol be given. It can be accompanied by high doses of steroids (Injection Dexamethasone 4 mg I/V 6 hourly). Supportive treatment consists of maintaining nutrition, fluid and electrolyte balance. Cases of Waterhouse friederichsen syndrome shall require intravenous fluids saline and high doses of steroids.

Prevention. A 23-valent pneumococcal vaccine is advocated in children with sickle cell disease, nephrotic syndrome asplenia for prevention against pneumococcus meningitis. This vaccine is effective in elder children and not of use in children below two years of age.

Similarly vaccine against serogroup A, C, Y and W-125 is effectively used for immunoprophylaxis against meningococcal meningitis. It is also not effective in children below two years of age. It takes one to two weeks for antibodies to develop after immunization. Since the period of risk is first two weeks after exposure, vaccination is not of much use in sporadic cases. However when there is an on going epidemic it may be used as part of an immun ization programme.

For contacts chemoprophylaxis with rifampicin (600mg daily for five day) is effective for eliminating colonization with the meningococcus and to prevent development of meningococcal infection.