2A-S3-3

 

Tuberculous meningitis

Calil Kairalla Farhat

Federal University of Sao Paulo - Brazil

 

Tuberculosis remains the most important infectious disease in the world, specially in developing countries, where it is also one of the biggest Public Health issues under discussion.

Since there’s been a lack of attention to this disease from the past decades, the number of cases has been increased around the world, which brought this problem to a new status of re-emerging disease by WHO. The increasing numbers of AIDS have contributed a lot to the current situation, and because of that even the classification as a persistent disease is appropriate.

The incidence rates of tuberculosis in American countries varies from 7-9 per 100.000 (Canada, Cuba, Trinidad-Tobago) to 100-350 per 100.000 (Honduras, Bolivia).

Tuberculous meningitis is the most severe presentation of tuberculosis and occurs in children between 3 months and 10 years of age, usually from 3 months to 3 years of age.

It starts from a primary complex, frequently pulmonary, and then there is hematogenous dissemination, producing small caseous foci situated in the brain or meninges.  The rupture of this foci causes discharge of tubercle bacilli directly in the subarachnoid space. A gelatinous exudate is developed in the pia-arachnoid, in the brain, infiltrates the walls of meningeal arteries and veins – with inflammation, caseatiion and obstruction – and extends to small vessels into the cortex, leading to infarcts.

The interference of the inflammatory process with the normal flow of the cerebrospinal fluid and with its absorption, and the predilection for the base of the brain explains the symptoms and the frequent involvement of the optic chiasm and the third, sixth, and seventh nerves.

The clinical course of the disease can be divided into three stages, each one with a duration of nearly two weeks.

1.         apathy, personality change, anorexia, irritability and some fever (temperatures not very elevated).

2.         signs and symptoms of central nervous system involvement, demonstrating meningeal damage: drowsiness, stiff neck, inequality of the pupils, vomiting, convulsions and signs of cranial nerves involvement (III, VI, VII).

3.         Signs of severe neurologic damage (decerebration, decortication), with irregular pulse and respirations, opisthotonus, coma.

Important aspects for the diagnosis are:

-            history of contact with a person with tuberculosis

-            tuberculin skin test – for children who didn’t receive BCG vaccination.

-            Chest roentgenogram

-            Cerebrospinal fluid analysis, with often the following findings:

increase in cellularity – 50 to 500 white blood cells per mm3, with polymorphonuclear leucocytes predominant

decreased glucose level .high concentrations of protein content (sometimes it can be observed the development of a pellicle on standing fluid)

spinal fluid culture – results after only 30 to 60 days, with less than 50% of positivity

Other valuable diagnostic methods:

gastric wash culture

enzyme-linked immunosorbent assay (ELISA) – for IgG and IgM antibodies to purified protein derivative (PPD) and bacille Calmette-Guérin (BCG) – sensibility of 90% and specificity of 89%.

computed tomography

magnetic resonance imaging

polymerase chain reaction (PCR)

As for evolution of the cases, the most important aspect is still “the earlier diagnosis the better prognosis” well know principle. Treatment must start promptly after diagnosis, and patients need to be followed closely, since the long term basis of therapy frequently leads to treatment disruption.

Very young age, the occurrence of convulsions, hydrocephalus and vasculitis are generally poor prognostic factors.

Long-term sequelae of this disease are more frequent and severe if diagnosis and treatment delay: blindness, deafness, intracranial calcification, diabetes insipidus, obesity, paraplegia, and mental retardation.