Nutrition and Health in a Developing World by Saskia de Pee Douglas Taren & Martin W. Bloem
Author:Saskia de Pee, Douglas Taren & Martin W. Bloem
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham
HIV coinfection is the single most potent risk factor for progression from infection to active disease, whether infection is from a new primary infection (e.g., recent exposure to bacteria) and/or reactivation of a latent infection (see Epidemiology section above). Since multiple exposures are possible, mixed (or multiple)-strain infections have been described, although the challenges to fully understanding the epidemiology (laboratory detection of mixed strains is difficult leading to gaps in knowledge), clinical (e.g., ability to comprehensively assess individual drug susceptibility/resistance with multiple strain infections), and population (e.g., transmission dynamics of competing strains, vaccine, and preventative therapy effects on circulating strains)-level implications are numerous [135]. Unlike many opportunistic infections that occur only with significant immunosuppression, TB can manifest with any degree of immunosuppression. If TB disease manifests in HIV-positive individuals who are not significantly immunosuppressed, then the disease course is similar to TB in HIV-negative individuals and is dominated by PTB in adults. If TB manifests once advanced HIV-associated immunosuppression has occurred, systemic disease involving multiple organs that lack well-defined granulomas with diffuse lesions is increasingly likely. Notably, all forms of EPTB have been described in HIV-associated TB, and this further complicates the clinical diagnosis of active TB in a resource-restricted setting. The specific nature of the immunological changes caused by HIV infection that drastically increase the likelihood of TB disease is complex and not fully understood [4, 136]. In general, untreated HIV infection leads to an absolute and functional decline in the cell-mediated immune response that is essential for maintaining lifelong immunological control of Mycobacterium spp. The destruction of T cells, specifically CD4+ cells in the granuloma by HIV, causes a change in the granuloma structure leading to the escape of viable bacilli.
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