The fundamental pathobiology of tuberculosis (TB) is known to most clinicians. Mycobacterium tuberculosis is transmitted from person to person by inhalation of infectious aerosol droplets. Bacilli invade macrophages and dendritic cells in the lung, disseminate systemically, and trigger a T-helper type 1-skewed adaptive immune response that usually curbs bacillary growth prior to any manifestations of TB disease. The resulting latent TB infection (LTBI) is controlled for the lifetime of most individuals, but approximately 5 to 10% of infected persons will progress to active TB disease,1most often within 2 years of infection. In countries with high TB disease rates, a substantial proportion of new cases arise by exogenous re-infection, but in the United States most TB cases represent reactivation of LTBI,2providing a strong rationale for treating LTBI as an approach to reduce the incidence of TB disease. A strategic plan for the elimination of TB in the United States issued in 1989 by the Centers for Disease Control and Prevention and the Advisory Committee for the Elimination of Tuberculosis set an interim target TB case rate of 3.5 per 100,000 population by 2000 with the goal of eliminating TB (defined as < 1 case per million population) by 2010.3The first goal was not met; in 2006, the TB case rate was 4.6 per 100,000. Nonetheless, the TB rate in 2006 was the lowest since reporting began in 1953.4 The decline in annual TB rates has slowed since 2000, due in part to the disproportionate contribution of immigrants from high-prevalence countries.