Bacille Calmette-Guérin (BCG) is a live strain of Mycobacterium bovis developed by Calmette and Guérin for use as an attenuated vaccine to prevent tuberculosis and other mycobacterial infections. The vaccine was first administered to humans in 1921 and remains the only vaccine against tuberculosis in general use. Several new vaccines against tuberculosis are also in development, and many are designed to boost the effects of BCG [1,2]. One investigational vaccine has been shown effective in a phase III trial .
BCG is the most widely administered vaccine in the world; it has been given to over 3 billion individuals, principally in the setting of routine newborn immunization (as dictated by guidelines of the World Health Organization) . There are multiple BCG vaccines in use around the world produced by different manufacturers and administered by different schedules. In the United States, BCG was sometimes administered to healthcare workers at risk for tuberculosis (TB) until the middle of the twentieth century but was never adopted for routine childhood immunization. BCG has been recommended in the United States only for immune-competent children and adults who have high risk of ongoing exposure that cannot be avoided .
Issues related to host immunity, vaccine efficacy, administration, safety, and policy will be reviewed here. Although the major role of BCG is TB prevention, BCG vaccine is also effective for protection against leprosy, Buruli ulcer, and disease due to nontuberculous mycobacteria. In addition, it is used as an immunostimulant in the treatment of superficial carcinoma of the bladder. These topics are discussed in detail separately. (See "Epidemiology, microbiology, clinical manifestations, and diagnosis of leprosy" and "Buruli ulcer (Mycobacterium ulcerans infection)" and "Complications of intravesical BCG immunotherapy".)
MYCOBACTERIA AND HOST IMMUNITY
Virtually any prior mycobacterial infection (whether naturally acquired or vaccine induced) appears to produce some level of protection against subsequent disease due to tuberculosis and, in some cases, to other mycobacteria . Natural infections that confer protection against tuberculosis (TB) include prior contained infection with M. tuberculosis itself or prior infection with nontuberculous mycobacteria (NTM) [6,7]. These observations suggest that protection is conferred by the immune response to common mycobacterial antigens.
Prior latent infection with M. tuberculosis that has been contained provides as much as 80 percent protection against disease after subsequent exposure . However, prior active disease is associated with an increased risk of a second episode of active tuberculosis due to a different strain in both HIV-positive and HIV-negative persons [9-15]. (See "Microbiology and pathogenesis of tuberculosis", section on 'Host factors'.)