Abstract
BackgroundOn a global scale, nearly two billion persons are infected with Mycobacterium tuberculosis. From this vast reservoir of latent tuberculosis (TB) infection, a substantial number will develop active TB during their lifetime, with some being able to transmit TB or Multi-drug- resistant (MDR) TB to others. There is clinical evidence pointing to a higher prevalence of infectious diseases including TB among individuals with Diabetes Mellitus (DM). Furthermore, ageing and diabetes mellitus may further aggravate protein-energy malnutrition (PEM), which in turn impairs T-lymphocyte mediated immunologic defenses, thereby increasing the risk of developing active TB and compromising TB treatment. This article aims to a) highlight synergistic mechanisms associated with immunosenescence, DM and PEM in relation to the development of active TB and b) identify nutritional, clinical and epidemiological research gaps.MethodsTo explore the synergistic relationship between ageing, DM, tuberculosis and PEM, a comprehensive review was undertaken. The MEDLINE and the Google Scholar databases were searched for articles published from 1990 to March 2015, using different MESH keywords in various combinations.ResultsAgeing and DM act synergistically to reduce levels of interferon gamma (IFN- γ), thereby increasing susceptibility to TB, for which cell mediated immunity (CMI) plays an instrumental role. These processes can set in motion a vicious nutritional cycle which can predispose to PEM, further impairing the CMI and consequently limiting host defenses. This ultimately transforms the latent TB infection into active disease. A clinical diagnostic algorithm and clinical guidelines need to be established for this population.ConclusionGiven the increase in ageing population with DM and PEM, especially in resource-poor settings, these synergistic tripartite interactions must be examined if a burgeoning TB epidemic is to be averted. Implementation of a comprehensive, all-encompassing approach to curb transmission is clearly indicated. To this end, clinical, nutritional and epidemiological research gaps must be addressed without a delay.
Highlights
On a global scale, nearly two billion persons are infected with Mycobacterium tuberculosis
TB infection occurs when a susceptible person inhales droplets containing Mycobacterium tuberculosis bacteria, which travel through the respiratory tract to the alveoli
In aged individuals the up-regulation of the major histocompatibility complex (MHC) class I and II expression as well as the antigen presentation capacity are reduced in dendritic cells, [32] which as a corollary diminishes interleukin 2 production and reduces T-cell proliferation
Summary
Nearly two billion persons are infected with Mycobacterium tuberculosis. From this vast reservoir of latent tuberculosis (TB) infection, a substantial number will develop active TB during their lifetime, with some being able to transmit TB or Multi-drug- resistant (MDR) TB to others. Ageing and diabetes mellitus may further aggravate protein-energy malnutrition (PEM), which in turn impairs Tlymphocyte mediated immunologic defenses, thereby increasing the risk of developing active TB and compromising TB treatment. TB infection occurs when a susceptible person inhales droplets containing Mycobacterium tuberculosis bacteria, which travel through the respiratory tract to the alveoli. An additional challenge to TB control efforts is the global increase in multi-drug resistant TB (MDR-TB), defined as TB caused by strains resistant to at least isoniazid and rifampin. In 2013, the World Health Organization (WHO) reported that 3.6 % of the new cases and 20.2 % of the previously treated cases had MDR-TB [3]
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