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Respiratory exposure to Mycobacterium tuberculosis (Mtb) can result in a spectrum of immunological and clinical outcomes. At one extreme is “Mtb resistance,” a proposed state in which the innate immune system kills and clears organisms at the lung’s mucosal surface, staving off infection and eventual disease [1]. At the other extreme is “full-blown” tuberculosis (TB), symptomatic pneumonia that features systemic inflammation, expectoration of sputum that contains live Mtb, and classic signs of lung damage on chest X ray. In between these two extremes is a gradient of states that ranges from latent Mtb infection to subclinical disease. TB control strategies largely focus on identification and treatment of people with full-blown TB disease and provide scant guidance on how to identify and manage the spectrum of more “subtle” disease. Subclinical TB disease is inherently difficult to identify and research, resulting in …