MYCOBACTERIUM TUBERCULOSIS COMPLEX (MTC)


Table of contents :


  • Mycobacterium africanum
  • Mycobacterium bovis
  • Epidemiology
  • Transmission
  • Mycobacterium tuberculosis
  • Genomics
  • Proteomics
  • Transmission
  • Mycobacterium microti

  •  
  • Epidemiology
  • Transmission
  • Symptoms & signs
  • Laboratory examinations
  • Prevention
  • Web resources


  • Epidemiology : A person with recently diagnosed culture-confirmed, extensively drug-resistant pulmonary tuberculosis (XDR TB) traveled on the following 2 extended flights (more than 8 hours in duration) in May 2007: A 2nd round of TB evaluation and testing should be done because a negative
    TST or QFT-G result obtained less than 8 weeks after exposure may be
    considered unreliable for excluding latent tuberculosis infection (LTBI).
    Transmission : Pathogenesis : the development of a strong Th1-mediated adaptive immune response is considered of main importance for host defense against the intracellular pathogen Mycobacterium tuberculosis. The induction of a cellular immune response is not only dependent on the engagement of the TCR but also requires co-stimulation. In order to study the role of the co-stimulatory molecule of the tumor necrosis factor receptor family member CD27 during murine M. tuberculosis infection, we intranasally infected wild-type (WT) and CD27 knockout (KO) mice with 105 colony-forming units M. tuberculosis. Whereas there were no differences in bacterial growth, inflammation and IFN-g production by CD4+ and CD8+ lymphocytes in the lungs early after infection, the number of splenic CD8+ T cells producing the key Th1 cytokine IFN-g was lower in CD27 KO mice than in WT mice. After 6 weeks, CD27 KO mice had 3.6-fold higher mycobacterial counts in their lungs and displayed more pulmonary inflammation and increased numbers of infiltrated leukocytes. Despite these differences early in infection, an equal number of WT and CD27 KO mice died during a 43-week observation period and lung bacterial loads and inflammation were comparable in the surviving animals. CD27 does not contribute to the local IFN-g-mediated response and long-term protection against M. tuberculosisref. CD44highCD62Llow effector CD4 T lymphocytes generated during the course of mycobacterial infection can be segregated into 2 subsets on the basis of CD27 receptor expression. Only the CD27low subset exhibited a high capacity for IFN-g secretion, indicating that low CD27 expression is characteristic of fully differentiated effector CD4 T lymphocytes. CD27low IFN-g-producing CD4 T lymphocytes accumulate in the lungs but are rare in LNs. Several factors contribute to their preferential accumulation. First, CD27low CD4 T lymphocytes present in the LN are highly susceptible to apoptosis. Second, circulating CD27low CD4 T cells do not enter the LN but efficiently migrate to the lungs. Third, CD27high effector CD4 T cells that enter the lungs down-regulate CD27 expression in situ. In genetically heterogeneous mice that exhibit varying susceptibility to tuberculosis, the accumulation of mature CD27low CD4 T cells in the lungs correlates with the degree of protection against infection. Thus, we propose that terminal maturation of effector CD4 T lymphocytes in the periphery provides the host with efficient local defense and avoids potentially harmful actions of inflammatory cytokines in lymphoid organsref.
    => tuberculosis (TB) / "White Plague" : the bacillus may colonize (primary tuberculosis) every organ (rare in exocrine glands and URT) except muscle tissues due to lactic acid sensitivity : Resistance in HLA-DR4 haplotype, susceptibility in HLA-Bw15+. The supersusceptibility to tuberculosis 1 (sst1) genetic locus on mouse chromosome 1 contains the intracellular pathogen resistance 1 (Ipr1) gene, whose expression is upregulated in the sst1 resistant macrophages after activation and infection (but is not expressed in the sst1 susceptible macrophages) limiting the multiplication not only of M. tuberculosis but also of other intracellular bacteria as Listeria monocytogenes, switching a cell death pathway of the infected macrophages from necrosis to apoptosisref. RF in 10-25%.
    Susceptibility : genetic defects in the IFN-g response pathway cause unique susceptibility to intracellular pathogens, particularly mycobacteria, but are rare and do not explain mycobacterial disease in the majority of affected patients. Acquired defects such as anti-IFN-g autoantibodies may cause a similar immunological phenotype and thus explain the occurrence of disseminated intracellular infections in some patients without identifiable immune deficiencyref.
    Laboratory examinations  : Prevention : Web resources:

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