A prudent approach to screening for and treating tuberculosis

DR. REZNIK is assistant professor of pediatrics and DR. OZUAH is professor and interim university chairman, both at Albert Einstein College of Medicine, Children's Hospital at Montefiore, Bronx, N.Y.

The authors have nothing to disclose in regard to affiliations with, or financial interests in, any organization that may have an interest in any part of this article.

Many more children have latent TB infection (LTBI) than have active TB. We must identify and treat both groups-latent and active-if we are ever to eliminate TB disease in children.

The stages of TB

A person who has been exposed to someone who has TB falls into one of three classifications⁵ :

1. Exposure. The patient has had contact with someone who has pulmonary TB, but he shows no clinical manifestations and has a negative tuberculin skin test.

2. Latent infection.M tuberculosis has replicated within the lungs. The tuberculin skin test is positive, the chest radiograph is normal or shows only small calcifications or granuloma, and no signs or symptoms of disease are present.

3. TB disease. The patient has clinical manifestations of TB and radiographic evidence of disease.

Transmission of infection

Mycobacteria are nonmotile, nonspore-forming, pleomorphic, weakly gram-positive rods. The diagnostic hallmark of mycobacteria is the capacity to form stable mycolate complexes with certain aryl methane dyes, called acid-fastness.⁵

M tuberculosis is spread person to person via the respiratory route. Children usually aquire TB infection from adults. Young children are less contagious than adults-they have a lower burden of mycobacteria, and cavitary lesions are rare among young children. Also, young children do not cough as effectively as adults.

Droplets containing M tuberculosis complex become airborne when a person with pulmonary or laryngeal TB coughs, sneezes, speaks, laughs, or sings. Infected droplets dry, then become droplet nuclei and remain suspended in air for hours. After inhalation, the droplet nucleus is carried down the bronchial tree and implants in a respiratory bronchiole or alveolus.

The organisms grow slowly in alveolar macrophages for two to 12 weeks, until they reach sufficient number (usually 10³ to 10⁴ ) to elicit a reaction to the tuberculin skin test (TST). Before the development of cellular immunity, tubercle bacilli spread via lymphatics to the hilar lymph nodes and via the bloodstream to distant sites, such as kidneys, bones, brain, and upper lung fields.¹

In people with intact cell-mediated immunity, collections of activated T cells and macrophages form granulomas that limit multiplication and spread of the organism, resulting in LTBI.