Inflammation of the meninges is called meningitis and may be caused by bacteria, viruses, fungi and other organisms in immune-compromised patients.
Infection may reach meninges as a result of direct spread as in case of fracture of skull or penetrating wounds or spread from within cases of intracranial abscess. Infection through the blood stream may result from focal infection, somewhere in the body such as empyema, pneumonia or osteomyelitis. Disseminated miliary tuberculosis is an important cause of tubercular meningitis. Similarly focus of infection in the cranium like mastoiditis, nasal air sinuses shall spread the infection to meninges.
Meningitis may be classified according to the organisms responsible for it.
1. Acute pyogenic meningitis due to Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, Staph. epidermidis, Listeria monocytogenes and organisms like E. coli, Proteus, Pseudomonas. Uncommon organisms include Salmonella, Shigella.
2. Meningococcal meningitis
3. Tuberculous meningitis
4. Acute lymphocytic choriomeningitis
Acute pyogenic meningitis
Commonest organism for acute pyogenic meningitis is streptococcus pneumoniae responsible in 30 to 50 per cent of cases in adults followed by haemophilus influenzae type B which mainly effects children. Other organisms include staphylococcus aureus which generally occurs post-operative in neuro-surgical patients Staph. Epidermidis producing meningitis associated with shunting procedures and group B streptocQcci and gram negative bacilli which are associated either with brain abscess, head injury or neuro-surgical procedures. Listeria monocytogenes is also a major pathogen responsible for causing meningitis in infants, elderly debilitated patients or those who are immuno suppressed.
Irrespective of the organisms causing meningitis pathology in all cases is the same. Infection once it breaches the protective wall of the meninges, rapidly spreads over the surface of the brain, spinal cord and expendymal lining of the ventricles. The brain and spinal cord are swollen and congested. The cortical veins become congested and convolutions on the surface of brain become flattened because of internal hydrocephalus which is due to inflammatory adhesion obstructing outflow of CSF from fourth ventricle.
Whole of CSF becomes turbid and purulent. Depending on the type of organism, inflammatory exudate may be located at various sites. In pneumococcal infection it is located more often on cerebral convexity while in H. influenzae, it is mainly basal. When the process is fulminant it may spread and involve the cranial nerves as well as ependymal surface of the ventricles.
All cases of acute pyogenic meningitis have the same clinical picture. Most of the time onset is acute characterized by fever coming with rigors, and headache which is very severe almost bursting in character. Increasing severity of headache maybe main symptom confined to frontal region and radiating down to the back. Vomiting is often present. Convulsions are seen more often in children especially with H. influenzae meningitis.
Because of meningeal irritation patient may be curled up in bed. There is neck rigidity, head retraction and Kemig’s sign is positive. Delirium is common and as the disease progresses patient passes into drowsiness and coma. There is severe degree of photo-phobia. Pupils are unequal and reaction is sluggish. Later on these become dilated and fixed. Ptosis may be seen because of raised intracranial tension and there is paralysis of occular muscles. Papilloedema is usually present.
Onset of meningitis may be insidious in children and elderly people. Rapid progress of the disease takes place in adults, it following a fulminant course. Limbs become flaccid. Reflexes are diminished. Incontinence of urine may take place and within 24- 48 hours, course becomes downhill.
Diagnosis of pyogenic meningitis shall depend on history (head injury, infection on skull air sinuses, respiratory infection like pneumonia, lung abscess, neuro-surgical operations etc) and clinical picture (fever, headache, neck rigidity, toxemia). Any patient coming with fever neck rigidity and confusion the diagnosis of meningitis should be considered.
1. Blood count. There is leucocytosis with rise in polymorph count.
2. CSF examination. It is the most important test. CSF pressure is raised. It is turbid and purulent pus like. Formation of a coagulum is often seen. Protein content is markedly increased while chloride content is reduced to 650 mg and glucose content is markedly diminished. Cells on microscopic examination are polymorphs and are present in thousands per cmm.
Lange’s colloidal gold curve is meningitic type. Grams stain of sedimented CSF is done to identify the causative agent. Pneumococci and H. influenzae are identified more readily. In cases where bacteria are not seen by Gram’s stain, staining with acridine orange and examination under a fluorescence microscope may be helpful in demonstrating bacteria not stained by Gram’s stain. CSF cultures are positive in 70 to 80 per cent of cases.
The measurement of bacterial antigens in the CSF by Latex Agglutination, radioimmunoassay and ELISA may be done to determine the presence of specific capsular polysacchride especially in cases of H. influenzae B and S. pneumoniae. Blood cultures are equally important since they shall provide clue to the causative agent.
3. All patients must have X-rays of chest, skull and sinuses to exclude the presence of infection (pneumonia, lung abscess, sinusitis, skull fracture etc).
A small percentage of cases of bacterial meningitis may be left with cranial nerve palsies and some with sensory hearing loss. Deafness is equally common. If focal neurological damage takes place there may be local signs of cerebral damage. Some children may be left with mental retardation. Epilepsy may develop. Persistent changes in level of consciousness should raise suspicion of internal hydrocephalus. Some children may be left with learning defects. Cases of pneumococcal meningiis in adults may pass into coma.
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