Tuberculosis Screening

Tuberculosis, caused by Mycobacterium tuberculosis, is an infection that occurs on a spectrum between latent and clinical disease. Clinical disease, termed active tuberculosis, is most frequently characterized by pulmonary disease, but extrapulmonary manifestations can also be observed. After initial infection, patients can progress to active tuberculosis or eliminate the organism via the innate immune response or T-cell immunity. Most are noted with latent tuberculosis infection (LTBI) characterized by M tuberculosis in a dormant state with no evidence of any symptoms. These patients have the highest reactivation risk within the first two to five years of initial infection, during which LTBI can progress to active tuberculosis. Lifetime reactivation risk is estimated at 5% to 10% and increases with immunosuppression. Therefore, those with LTBI are at risk for developing active tuberculosis and infecting others while risking personal morbidity and mortality. The global mortality of tuberculosis infection was estimated at 1.4 billion by the World Health Organization and 1.3 billion by the Global Burden of Disease study in 2013. As patients with LTBI do not exhibit any symptoms, LTBI incidence has to be estimated. In 2014, the global incidence of latent tuberculosis infection (LTBI) calculated via mathematical modeling was 23%. An estimated 10.4 million new infections were noted in 2015. Screening for M tuberculosis infection is essential for public health, as it allows patients with LTBI to receive preventative treatment. The goal of testing for LTBI is the identification of those at high risk of developing tuberculosis. The decision to test should presuppose a decision to treat if the result is positive. Providers should be committed to following up on test results, offering tuberculosis-preventative treatment, and monitoring for adherence and tolerance of provided therapy. The tuberculin skin test (TST) and the interferon-gamma release assay (IGRA) are the current screening methods for measuring adaptive host immune response. During initial infection, M tuberculosis is encountered by alveolar macrophages, and antigen is presented to T-cells. Upon second exposure, TH1 cells release IGN-γ, which stimulates macrophages to release inflammatory cytokines. The TST measures the indirect evidence of this inflammatory reaction triggered by a reaction to purified protein derivative (PPD), a solution of antigens derived from M tuberculosis. In contrast, IGRAs measure the amount of IFN-γ released.