![]() ![]() ![]() The protein content of the CSF is elevated, with low or low-normal glucose levels. Stage 3 disease with neurologic deficits and altered mental status bears grave long-term morbidity and mortality.ĬSF pleocytosis, initially polymorphonuclear, becomes lymphocyte-predominant. Stage 2 disease (with neurologic deficits) carries an increased risk of long-term morbidity. Focal nerve deficits typically involve the third and sixth cranial nerves and the optic chiasm.Ĭlinically, stage 1 disease presents with insidious onset of meningitis without focal neurologic deficits. ![]() Basilar vascular enhancement, infarcts as a consequence of vasculitis, and hydrocephalus are the radiologic hallmarks of the disease ( Figure 10). The base of the brain is most commonly affected by thick exudates that tend to obstruct cerebrospinal fluid (CSF) flow. Tuberculous meningitis is the result of lymphohematogenous spread or miliary dissemination of the disease: it occurs in about 2% of infected children. In patients with miliary TB, numerous lesions can be found in the lungs, liver, spleen, skin, bone marrow, myocardium, and brain ( Figure 9). Miliary TB may also be the consequence of a tuberculous focus (typically a lymph node) draining into a blood vessel. It may also manifest clinically as overwhelming miliary TB-typically in infants within the first few weeks after infection. It may remain occult and manifest months later as extrapulmonary TB. Lymphohematogenous spread of TB in children occurs early in the incubation period. Cellular immunity develops within 2 to 12 weeks this leads to the typical hypersensitivity responses of reactive tuberculin skin testing ( Figure 1), phlyctenular conjunctivitis ( Figure 2), erythema nodosum ( Figure 3), and serous effusions in the peritoneum, pleura, or joints (Ponçet's disease). From here, bacteria spread locally to regional lymph nodes (primary complex) or by early hematogenous dissemination to other organs. Mycobacterial multiplication occurs in alveolar macrophages surrounded by local inflammation (primary focus). Most children become infected through aerosol droplets from adult source cases. Co-infection with HIV or other viruses (particularly measles), malnutrition, and other chronic illnesses dramatically increase the risk of progression from latent infection to active disease. In children, the risk of active disease after infection is 43% in the first year of life this risk decreases to 24% in children 1 to 5 years old, and to 15% in those between ages 11 and 15 years. ![]() There is a 5% to 10% lifetime risk that TB will develop in an infected adult. (In children, 95% of pulmonary TB cases are smear-negative for acid-fast bacilli.) Moreover, the risk of disease progression and dissemination is much higher in children than in adults. Clinical findings are usually nonspecific, and mycobacteria are difficult to obtain. The diagnosis of TB is particularly difficult to make in children. Poverty, neglect of TB control programs, changes in population demographics (migration, aging), and the impact of HIV infection are all responsible. The incidence of this disease is increasing in sub-Saharan Africa and the countries of the former Soviet Union. The vast majority of infections-95%-occur in developing countries, where the disease accounts for 25% of avoidable adult deaths. More than 8 million people are infected every year. Tuberculosis (TB) remains one the most important infectious diseases in the world. ![]()
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