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How molecular epidemiology has changed what we know about tuberculosisBy the mid-1980s, the US public health community considered tuberculosis to be under control, and a plan was established for its elimination by 2010.Between 1989 and 1992, however, the number of cases increased, and in response, scientists and public health officials reinvigorated research and control programs.These efforts have now turned the tide, and the number of cases of tuberculosis in the United States is again decreasing, being down 31% from the peak of the resurgence. 1During this time, researchers and disease controllers came together in a relatively new field, molecular epidemiology.This endeavor combines molecular methods for identifying individual strains of bacteria with conventional epidemiologic methods to investigate the determinants and distribution of disease.Together they can establish transmission links, identify risk factors for transmission, and provide insight into the pathogenesis of tuberculosis.Bacterial DNA fingerprinting is performed using restriction fragment-length polymorphism analysis that yields a unique pattern for unrelated clinical organisms and an identical pattern for strains isolated in outbreak settings.It can, however, be used only to track transmission between persons with active disease because the technique requires a viable culture of Mycobacterium tuberculosis. 2n this review, we present a summary of what has been learned about transmission dynamics and the pathogenesis of M tuberculosis since the first description of DNA fingerprinting in 1989 and the implication of these lessons for tuberculosis control. TUBERCULOSIS CAN PROGRESS RAPIDLY FROM INFECTION TO DISEASEThe natural history of tuberculosis starts with the exposure to M tuberculosis.
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Midori Kato‐Maeda (2000) studied this question.
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