• Mycobacterium tuberculosis review article
  • Hanieh Jafarvand Atashgah,1 Saman Hakimian,2,*
    1. M.sc student of Pathogenic Microbes Islamic Azad University Central Tehran Branch
    2. M.sc student of Pathogenic Microbes Islamic Azad University Central Tehran Branch


  • Introduction: Tuberculosis is an infection disease caused by Mycobacterium Tuberculosis which is first appeared roughly 2000 years ago and it's transmitted from person to person via droplets. MTB mixed infection is described as a disease state in which patient harbors more than one MTB strain at the same time either as a result of a single transmission involving multiple distinct strains or as result of multiple transmission events. These strains are largely categorized in to eight distinct genetic lineage. The different lineages are not only associated with particular geographical area , but they also have distinct pathogenic characteristics that influence disease transmission , treatment outcomes and antimicrobial drug.
  • Methods: Virulence factors of MTB can generally be divided in to two groups : Proteins and cell wall components. Rather than rashly inducing acute inflammation, MTB takes compromised countermeasures to enter into a quiescent latency status to elude host immune clearance. During the latency period, MTB employs a range of effector proteins to reinforce its living niches and counterbalance host immune defense.
  • Results: MTB possesses an arsenal of protein and lipid effector that influence macrophage functions and inflammatory responses. Tuberculosis modulates intracellular trafficking, undermines macrophages effector functions, control cell death way, impair antigen presentation and survives in diverse intracellular environment. MTB reduces the mitochondrial dependency to glucose and increases the mitochondrial dependency to fatty acid. Iron is essential for MTB but is severely limited in the human host. Secretion of protein tyrosine phosphatase ,ptpA, is essential for MTB inhibition of host macrophage acidification and maturation and it is a substrate of the protein tyrosine kinase ,ptkA, encoded in the same operon. There is evidence that MTB pathogens interact with Golgi-derived vesicles that contain enzymes implicated in innate immunity. MTB is able to subvert or neutralize host defenses early in the phagosome maturation pathway using wide variety of molecules and strategies. The most notable of MTB secreted protein is the protein tyrosine phosphatase (PtpA) which is essential for the growth of MTB within human macrophages. It inhibits macrophage V-ATPase staling phagosome acidification. Deletion of PtpA gene showed no effect on MTB growth nor its ability to initiate infections in human cells. Neutrophils are the most widely present cell population in patient with active TB. The immune response of T lymphocytes begins at the moment that MTB spreads inside the lymph nodes. . T lymphocyte are critical for prevention of primary disease from initial MTB and loss of CD4 T-cell through infections greatly exacerbate Tuberculosis susceptibility and reactivation of latent infection memory response is more effective if it's positioned at site of pathogen infection. The role of humoral adaptive immunity in TB is extremely uncertain. Complementmediated opsonization does not alter MTB survival. . There is an interaction between other disease and TB such as Covid19 or Diabetes . Covid19 decreases the number of TH1 and other immune cells which leads to TB infections. Diabetes is a major risk factor for the development of active and latent TB increased susceptibility to TB in patients with diabetes has been endorsed to several factors including direct effect related to hyperglycemia, Insulin resistance, indirect effect related to macrophage and lymphocyte function
  • Conclusion: TB drugs are administered in different combinations of four first line drugs (Rifampin , Isoniazid , Pyrazinamide and Ethanbutol) which form the core of treatment regimens in the initial treatment phase of 6-9 months. Several reasons account for the failure of TB therapy such as (i) Late diagnosis, (ii) Lack of time and administration of effective drugs, (iii) Lower availability of less toxic, inexpensive and effective drugs, (iv) Long treatment duration, (v) Nonadherence to drug regimen and (vi) Evolution of drug resistant TB strains.
  • Keywords: Mycobacterium tuberculosis, Infection, Drug resistance