Tuberculous meningitis

Within a granuloma the Mycobacterium organism lives inside macrophages and dendritic cells and is maintained in a stable state by TNF-α.

Patients usually have headache, malaise, confusion and emesis.

It causes permanent neurological injury, and death, in a high proportion of affected persons through local inflammatory complications and stroke.

Is the severest form of infection, resulting in death or severe neurological defects in greater than half of those affected, despite treatment.

Can result in arachnoid fibrosis which may lead to hydrocephalus, obliterative endarteritis causing arterial occlusions and brain infarction.

Treated with corticosteroids results in reduced cerebrospinal fluid inflammation and earlier time to recovery.

Dexamethasone  was shown not to improve outcomes in most patients with TB meningitis and advanced HIV.

With suspected tuberculous meningitis spinal fluid should be evaluated for AFB (Acid fast bacilli) with smear and culture, which are the gold standard.

Associated with a paucity of bacteria with fewer than 1 bacillus per ml of CSF requiring a large volume of CSF to isolate the organism.

5ml is minimal volume of CSF acceptable for CSF studies, and 10 cc would be ideal.

CSF fluid must be centrifuged at 3000g for at least 15 minutes to sediment by centrifugal force the buoyant mycobacteria

Treatment with steroids improves survival in patients older than 14 years, but does not improve disability or death rate.

Treatment with steroids decreased death rate in children.

Prevalent in developing countries.

In industrialized nations sporadically seen in poor and immigrant populations.

Diagnosis in western nations may be delayed since the disease is of low prevalence, of variable presentation and the nonspecific findings on CSF analysis.

CSF analysis shows a moderate pleocytosis, with neutrophils and mononuclear cells or mononuclear cells with elevated protein levels, with glucose being moderately low or normal.

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