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I am reading Murray Microbiology book.

Some facts

  • M. tuberculosis is an intracellular pathogen.
  • At the time of exposure, M. tuberculosis enters the respiratory airways and infectious particles penetrate to the alveoli where they are phagocytised by alveolar macrophages.
  • In contrast with most phagocytised bacteria, M. tuberculosis prevents fusion of the phagosome with lysosomes (by blocking the specific bridging molecule, early endosomal autoantigen 1 [EEA1]). NB probably here something relevant
  • At the same time, the phagosome is able to fuse with other intracellular vesicles, permitting access to nutrients and facilitating intravacuole replication.
  • Phagocytised bacteria are also able to evade macrophage killing mediated by reactive nitrogen intermediates formed between nitric oxide and superoxide anions by catalytically catabolising the oxidants that are formed.
  • Dissemination to any body site occurs most commonly in immunocompromised patients, like HIV patient.
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3 Answers 3

If you read this article, you will find that CD4+ and CD8+ T-cells are probably the major mediators of the immune response against M. tuberculosis. Since HIV severely depletes the number of CD4+ T-cells (and to a lesser extent other kinds of lymphocytes), it stands to reason that the frequency of infection and virulence will be substantially increased in such patients.

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Thank you very much for your answer! I extended it by reading Murray and adding the result below. –  Masi Feb 4 at 8:22

I think one reason for greater virulence is the fact that M.tuberculosis prevents fusion of the phagosome with lysosomes.

I think this picture is little relevant here

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I am thinking what is happening in these two parts here:

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This answer does not provide enough support why there is greater virulance in HIV patients than in normal people. And particularly why the preventation of the fusion of the phagosome with lysosomes leads to it.

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Extension to Kanchi's answer by using Murray Microbiology textbook

Dissemination to any body site occurs most commonly in immunocompromised patients, like HIV patient. CD4+ and CD8+ T-cells are the major mediators of the immune response against M.tuberculosis. Since HIV severely depletes the number of CD4+ T-cells (and to a lesser extent other kinds of lymphocytes), it stands to reason that the frequency of infection and virulence will be substantially increased in such patients. In patients with HIV infection and with a low CD4 T-cell count, the disease usually appears before the onset of other opportunistic infections, is twice as likely to spread to extrapulmonary sites, and can progress rapidly to death.

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