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TUBERCULOUS MENINGITIS Tuberculous Meningitis

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TUBERCULOUS MENINGITIS Tuberculous Meningitis TUBERCULOUS MENINGITIS TUBERCULOUS MENINGITIS The rising incidence of HIV has seen a concomitant rise in the incidence of tuberculous meningitis. P BILL Pierre Bill’s interests are neuromuscular MB ChB, FCP (SA), FRCP(Lond) disorders, tropical neurology and under- graduate and postgraduate teaching. Emeritus Professor and Consultant He is currently President of the College Department of Neurology of Neurologists within the Colleges of Inkosi Albert Luthuli Central Hospital and Medicine of South Africa. University of KwaZulu-Natal Durban Recently there has been a resurgence of tuberculosis (TB) an aerobic Gram-positive rod that stains poorly owing in developed and developing countries. This is due to the to its thick cell wall that contains lipids, peptoglycans, increasing prevalence of HIV, overcrowding in the urban and arabinomannans. The Ziehl-Neelsen stain uses the population and in abnormal communities (prisons, refugee properties of the cell wall to form a complex that prevents colonies, and concentration camps), poor nutritional status, decolourisation by acid or alcohol. appearance of drug-resistant strains of TB, ineffective TB control programmes, and increase in migration to the The development of TBM is a two-step process. M. developed world from countries where TB is prevalent. tuberculosis bacilli enter the body by droplet inhalation, the Compared with pulmonary TB, which has been the subject initial point of infection being the alveolar macrophage. of many clinical trials, the pathogenesis, diagnosis and During the localised infection within the lung (primary treatment of tuberculous meningitis (TBM) have received complex) there is a short but significant bacteraemia that little attention. How the disease kills or disables those can seed bacilli to other organs in the body. In about 10% it infects is poorly understood; the best diagnostic tests of cases the primary complex does not heal but progresses are controversial, and the optimum treatment with and tuberculous pneumonia develops, with heavier and antituberculosis drugs is not known. The only certainties more prolonged bacteraemia. Dissemination to the CNS lie in the fatal consequences of missed diagnoses and is more likely, particularly if miliary TB develops. In those management. It has been estimated that about 10% of who develop TBM, bacilli seed to the meninges or brain patients with extrapulmonary TB have CNS involvement. parenchyma, forming small subpial or subependymal foci, Involvement of the CNS in TB is five times more frequent in called Rich foci, after the original studies of Rich and HIV-positive than in HIV-negative patients. McCordick. These foci may remain dormant for many years. The second step in the development of TBM is rupture of EPIDEMIOLOGY the Rich focus into the subarachnoid space. This heralds the onset of TBM. Before HIV, the most important determinant for the development of TBM was age. In populations with a high The release of M. tuberculosis bacilli into the subarachnoid TB prevalence, the peak age for TBM is 0 - 4 years. In space results in a local T lymphocyte-dependent response, populations with a lower TB prevalence, most TBM cases characterised macroscopically as caseating granulomatous occur in adults, risk factors being alcoholism, diabetes inflammation. The numbers and types of white cells in the mellitus, malignancy, and recent corticosteroid use. Co- CSF help differentiate TBM from other forms of meningitis, infection with HIV now dwarfs these risk factors, and but little is known of their role in disease pathogenesis. increases the lifetime risk of developing clinical TB. HIV also increases the risk of developing extrapulmonary TB and in In 75% of children the onset of TBM is less than 12 months particular TBM – a risk which increases as the CD4 cell after the primary infection. count diminishes. Three general processes produce the subsequent AETIOLOGY, PATHOGENESIS AND PATHOLOGY neurological pathology: adhesion formation, an obliterative vasculitis, and an encephalitis or a myelitis. Adhesions TBM was first described as a pathological entity in 1836, result from the thick, gelatinous basal meningeal exudate and Robert Koch demonstrated that TB was caused by that develops after the inoculation of bacilli into the Mycobacterium tuberculosis in 1882. M. tuberculosis is subarachnoid space. The exudate is particularly marked September 2006 Vol.24 No.9 CME 505 pg505-511.indd 505 9/12/06 8:44:58 AM TUBERCULOUS MENINGITIS Compared with pulmonary 1-β and tumour necrosis factor, fontanelles develop in infants. Nausea, which promote granuloma formation. vomiting and altered sensorium may TB, which has been the Tubercles consist of mononuclear develop. A continuous low-grade fever subject of many clinical cells surrounding a necrotic (caseous) is present in about 80% of patients. trials, the pathogenesis, centre. The complex cellular immune diagnosis and treatment response in TB determines whether Cranial nerve abnormalities occur of tuberculous meningitis the host develops active disease. in one-quarter of patients, most (TBM) have received little Progression and expansion of the commonly a 6th nerve palsy. Choroidal caseous lesion may result in different tubercles are present in less than attention. types of CNS involvement. Tubercles 10% of patients, but are diagnostic that rupture into the subarachnoid of TB. Visual loss may develop owing BCG vaccination pro- space cause meningitis. Those deeper to optochiasmatic arachnoiditis, 3rd vides the best prophylaxis in the parenchyma of the brain or ventricular compression of optic chiasm spinal cord cause tuberculoma or from hydrocephalus, optic nerve against severe forms of TB, abscess. granuloma, and ethambutol toxicity. mainly meningitic and mil- Funduscopic examination may reveal iary. Most CNS TB is caused by papilloedema. Hemiplegia may occur M. tuberculosis. Non-tuberculous at the onset of the disease or at a later mycobacteria (NTM) are ubiquitous stage. Quadriplegia secondary to around the sylvian fissures, basal in the environment. They usually bilateral infarction or severe cerebral cisterns, brainstem and cerebellum, cause infection in persons with oedema is less common. Occasionally and contains lymphocytes, plasma immunosuppression, especially patients abnormal movements may be present, cells, macrophages and fibrin. with AIDS and very low CD4 counts including chorea hemiballismus, Blockage of the basal subarachnoid (< 10 cells/µl). Atypical bacteria athetosis, generalised tremors, cisterns, 4th ventricular outlet or infrequently produce meningitis or myoclonic jerks and ataxia. Seizures, aqueduct can result in obstruction of meningoencephalitis. Mycobacterium either focal or generalised, may occur the CSF and hydrocephalus. Adhesions avium is the most common aetiological during the illness. As the disease around the interpeduncular fossa and agent of this group. Mycobacterium progresses, increasing evidence of related structures can compromise fortuitum meningitis is a complication cerebral dysfunction sets in, with cranial nerves, particularly 2, 4 and of CNS surgery and trauma and apathy and irritability progressing to 6, and the internal carotid artery. is usually associated with abscess increasing lethargy, confusion, stupor An obliterative vasculitis may result and foreign bodies. Less frequently and coma. Spinal meningitis may in infarction and stroke syndromes. NTM infections are manifested result in root pain, spastic or flaccid These commonly occur in the territory as intracranial mass lesions, or paralysis and loss of sphincter control. of the internal carotid artery (ICA), rhombencephalitis. Diagnosis is made proximal middle cerebral artery (MCA) by culture of tissue, sputum, blood Although HIV-infected patients with TB and perforating vessels to the basal or CSF. Because NTM are ubiquitous are at increased risk of developing ganglia. Infarcts occur in about 30% bacteria, their isolation from a sample TBM, the clinical features and of cases, causing a range of disorders may represent contamination. However, outcome do not seem to be altered. ranging from hemiparesis to movement isolation from a sterile fluid such as These patients commonly have disorders. Haemorrhagic transformation CSF usually represents infection of the extrameningeal TB on admission. of infarcted tissue is not unusual. nervous system. In elderly patients with TBM, the The basal inflammatory process may presentation may be atypical. Signs extend into the parenchyma, resulting CLINICAL FEATURES of meningism may be absent, seizures in encephalitis. Brain tissue underlying occur more commonly, and CSF the exudate shows oedema, which can TBM is usually preceded by a findings may be atypical, and the CSF be marked throughout the hemispheres, prodromal period of 2 - 4 weeks of may even be acellular. perivascular infiltration, and a nonspecific symptoms such as fever, microglial reaction (known as border malaise, myalgia, and headache. A rare complication of TBM is zone reaction). Fifty per cent of patients have chest tuberculous encephalopathy, radiographic abnormalities, a history usually occurring in a young child The pathogenesis of TBM at a cellular of contact with a TB patient, and a with progressive primary TB. level is poorly understood. During the positive tuberculin skin test. In children The presentation is of reducing first 2 - 4 weeks of infection there is prodromal symptoms include irritability, consciousness level with few focal no immune response to the organism. poor
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