The immunopathology of tuberculosis, the mode of action of the Bacillus Calmette-Guérin, of the tuberculin and of the immunotherapy

Abstract

The outer surface of the cell membrane of Mycobacterium tuberculosis is made of carbohydrates and lipids that do not readily induce the formation of antibodies by the invaded host. The absence of antibodies against the outer cell membrane of wild strains explains the long persistence of the pathogen in the invaded host. Its immunopathology sequence proceeds in four complex steps, some generating an immunodeficiency. TB presents a pronounced phenotypic variation, with the result that strains thriving in different parts of the world differ widely immunologically. The bacterium is ubiquitous, and the claim that the infection affects a quarter of the human population is an understatement. The Bacillus Calmette–Guerin (BCG) vaccination is a primo-infection that may generate an immunodepression and favor the infection of immunodepressed hosts. The BCG vaccine elicits a vigorous cellular immune response that prevents proliferation. This explains why BCG does not protect against infection but prevents dissemination from the primary foci to other parts of the body. The mycobacterium Mycobacterium vaccae fails to elicit a cellular immune response at a par with that generated by BCG. However, it is far superior to BCG at the humoral immunity level. The boosting of the synthesis of nitric oxide is possible by food supplements, as an adjuvant to immunotherapy.