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Human populations are rarely exposed to one pathogen alone. Particularly in high incidence regions such as sub-Saharan Africa, concurrent infections with more than one pathogen represent a widely underappreciated public health problem. Two of the world’s most notorious killers, malaria and tuberculosis, are co-endemic in impoverished populations in the tropics. However, interactions between both infections in a co-infected individual have not been studied in detail. Both pathogens have a major impact on the lung as the prime target organ for aerogenic  Mycobacterium tuberculosis  and the site for one of the main complications in severe malaria, malaria-associated acute respiratory distress syndrome (MA-ARDS). In order to study the ramifications caused by both infections within the same host we established an experimental mouse model of co-infection between  Mycobacterium tuberculosis  and  Plasmodium berghei  NK65, a recently described model for MA-ARDS. Our study provides evidence that malaria-induced immune responses impair host resistance to  Mycobacterium tuberculosis . Using the natural routes of infection, we observed that co-infection exacerbated chronic tuberculosis while rendering mice less refractory to  Plasmodium.  Co-infected animals presented with enhanced inflammatory immune responses as reflected by exacerbated leukocyte infiltrates, tissue pathology and hypercytokinemia accompanied by altered T-cell responses. Our results - demonstrating striking changes in the immune regulation by co-infection with  Plasmodium  and  Mycobacterium  - are highly relevant for the medical management of both infections in humans.

Natural Transmission of Plasmodium berghei Exacerbates Chronic Tuberculosis in an Experimental Co-Infection Model