Panel Discussion: Tuberculosis Research: Where (and How) Do We Go From Here?

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<h3>Nutritional Risk Factors for TB Progression: Results of a Longitudinal Cohort Study</h3><p>We followed a cohort of household contacts of microbiologically confirmed index TB patients over a one year period for TB infection and progression to disease. Among 6751 HIV-negative household contacts with viable baseline blood samples, 180 developed secondary TB during follow-up. We used risk set sampling to identify 709 matched controls from those who did not develop TB disease. After controlling for possible confounders, we found that vitamin A deficiency was associated with a 10-fold increase in risk of TB disease among household contacts (aOR 10.42; 95% CI 4.01–27.05; p &lt; 0.001). This association was dose-dependent with stepwise increases in TB disease risk with each decreasing quartile of vitamin A level. These data are consistent findings from recent studies among HIV infected individuals at risk for TB and with data that suggest that some measures of T-cell mediated immunity are improved by increasing Vitamin A to levels higher than those required to maintain normal vision.</p>

Megan Murray, Harvard University

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<h3>One of These Things is Not Like the Other One: Phenotypica Heterogeneity in Mycobacteria</h3><p>Diverse populations offer organisms an increased ability to survive when encountering stress. Unlike many rod-shaped organisms, mycobacteria are quite heterogeneous for size and shape. We find that this is reflected in metabolic heterogeneity, a characteristic important at the level of single cell survival in the face of treatment with the drug rifampin. This phenotypic heterogeneity is governed, in part, by the gene lamA. Mutants that lack lamA become less varied and are more rapidly killed by rifampin and antibiotics that target the cell wall. The encoded protein, LamA, has a role in establishing asymmetry at the time of cell division.</p>

Panel Discussion: Tuberculosis Research: Where (and How) Do We Go From Here?

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