Worms and TB Susceptibility

Effect of Worm Infection on TB Susceptibility

Background. Tuberculosis and intestinal helminth infections have similar epidemiology. Because helminths have been shown to bias the immune system away from the cell-mediated immunity required for intracellular infections, we hypothesized that treating the infection has the potential to augment anti-mycobacterial immunity.

Methods. A double-blind, randomized, placebo-controlled trial was performed in 144 healthy adults in the Amazon. Anti-mycobacterial immunity was quantified in vivo using tuberculin skin-testing and in vitro as interferon-γ secretion in response to specific tuberculosis antigens. These tests and stool parasitology were performed at recruitment and four weeks after deworming with three daily doses of 400 mg albendazole or placebo.

Results. Stool microscopy at recruitment diagnosed intestinal helminths in 48% of 126 participants. 40% were infected with Ascaris lumbricoides, 12% Trichuris trichuria, 6.3% hookworms, and 3.2% Strongyloides stercoralis. Deworming augmented the response to the tuberculin skin test following albendazole therapy (P=0.03) but not after placebo. Similarly, the in vitro quantification of anti-mycobacterial interferon-γ responses increased after albendazole therapy (P=0.02) but not placebo. Consequently, 38% (53/138) of baseline Quantiferon assays were positive at recruitment, and albendazole caused 17% (9/53) of the initially negative tests to become positive, compared with 0/49 after placebo (P=0.003).

Conclusion. Treating intestinal helminths augmented anti-mycobacterial immunity in vitro and in vivo. This suggests that antihelminthic treatment may modify the interpretation of these tuberculosis infection tests and antihelminthic therapy should be evaluated as a strategy for reducing tuberculosis susceptibility.



	Effect of Worm Infection on TB Susceptibility Background. Tuberculosis and intestinal helminth infections have similar epidemiology. Because helminths have been shown to bias the immune system away from the cell-mediated immunity required for intracellular infections, we hypothesized that treating the infection has the potential to augment anti-mycobacterial immunity. Methods. A double-blind, randomized, placebo-controlled trial was performed in 144 healthy adults in the Amazon. Anti-mycobacterial immunity was quantified in vivo using tuberculin skin-testing and in vitro as interferon-γ secretion in response to specific tuberculosis antigens. These tests and stool parasitology were performed at recruitment and four weeks after deworming with three daily doses of 400 mg albendazole or placebo. Results. Stool microscopy at recruitment diagnosed intestinal helminths in 48% of 126 participants. 40% were infected with Ascaris lumbricoides, 12% Trichuris trichuria, 6.3% hookworms, and 3.2% Strongyloides stercoralis. Deworming augmented the response to the tuberculin skin test following albendazole therapy (P=0.03) but not after placebo. Similarly, the in vitro quantification of anti-mycobacterial interferon-γ responses increased after albendazole therapy (P=0.02) but not placebo. Consequently, 38% (53/138) of baseline Quantiferon assays were positive at recruitment, and albendazole caused 17% (9/53) of the initially negative tests to become positive, compared with 0/49 after placebo (P=0.003). Conclusion. Treating intestinal helminths augmented anti-mycobacterial immunity in vitro and in vivo. This suggests that antihelminthic treatment may modify the interpretation of these tuberculosis infection tests and antihelminthic therapy should be evaluated as a strategy for reducing tuberculosis susceptibility.
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