Diabetes Mellitus as Hub for Tuberculosis Infection: A Snapshot

Abstract

Tuberculosis (TB) still remains the thorn in the flesh of efficient therapeutics affecting one-third of global population annually. There are several factors that enhance the susceptibility to TB infections including malnutrition, smoking, and immunocompromised conditions such as AIDS. In the recent years, growing body of evidence has gained considerable prominence which suggests that Diabetes Mellitus (DM) is individual risk factor leading to complicated TB infections. In this article the authors have attempted to summarize the link of type 2 DM with TB, the mechanistic action of how DM sensitizes for developing the active TB infection from the latent infection, and problems faced during treatment followed by possible preventive measures. We have tried to give account of the alterations that occurred in DM making a person more prone to develop TB.

Figure 1

Twin burden of TB infection and DM: TB infections are controllable in comparison to diabetics suffering from TB infection.

Figure 2

Predisposing factors endorsing TB in DM: DM leads to frequent development of latent to active TB having enhanced pathogenicity; compromised immunity causing loss in self-defense and the interaction of anti-TB drug with antidiabetic drugs causing decreased therapeutic index.

Figure 3

Implications of DM on TB: MTB resides as latent condition which could develop to active TB (shown by dotted arrow) but still is curable. Under diabetic condition immunocompromised state develops making condition prone to develop active TB (shown by bold arrows) which becomes incurable.

Figure 4

Mechanisms involved in enhancing TB infection during DM: during MTB infection the host innate immunity activates macrophages which causes phagocytosis and activates cytokines. Under nondiabetic condition cytokines become activated leading to ROS generation subsequently killing MTB. Under diabetic condition due to immunocompromised state the alteration in cytokine release leads to the survival of MTB due to suppressed ROS generation.