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Tuberculosis, caused by Mycobacterium tuberculosis, is the most common mycobacterial disease in the world and remains a leading public health problem. Numerous other mycobacterial species are present in the environment and are most often termed atypical or nontuberculous mycobacteria. Like the attenuated vaccine Bacille Calmette-Guérin (BCG) they are generally poorly virulent, even so they can be at the origin of severe infections if the host immune response is impaired. It has been clearly demonstrated that the intrinsic virulence of a mycobacterial species is not the only factor determining disease severity, which is illustrated by the observation that the majority of individuals infected with M. tuberculosis do not develop clinical disease. Numerous arguments suggest that disease severity depends largely on susceptibility/resistance determined by the host genetic make up. In the following review we will discuss the studies on the genes implicated in complex predisposition to tuberculosis and Mendelian predisposition to disease caused by less virulent mycobacteria, proposing a continuous spectrum between those two types of predisposition.
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BACKGROUND: Although various hematologic abnormalities are seen in tuberculosis, immune thrombocytopenic purpura is a rare event. CASE PRESENTATION: We report a case of a 29 year-old male who was presented with immune thrombocytopenia-induced hemoptysis, macroscopic hematuria and generalized petechiae. The patient was found to have clinical, microbiological and radiological evidence of active pulmonary tuberculosis. The immune thrombocytopenic purpura was successfully treated with anti-tuberculous drugs combined with corticosteroids and high dose immune globulin therapy. CONCLUSION: Immune thrombocytopenic purpura can be one of the hematological manifestations of tuberculosis which has a global prevalence with increasing incidence secondary to HIV infection.
Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis. Protection against and pathogenesis of tuberculosis greatly depend on specific T lymphocytes, and it is generally assumed that CD4+ T cells--through lymphokine-mediated macrophage activation--are the major mediators of the host response to tuberculosis. In the present report, results from experimental tuberculosis studies in mice are summarized which indicate that both CD4+ and CD8+ T lymphocytes are generated during tuberculosis. Furthermore, evidence is presented that both T cell populations are involved in protection against and pathogenesis of tuberculosis and that the final outcome of the host response depends on an intricate balance between these two types of T cells.
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Fifty years after the introduction of the first effective antimicrobial agents against Mycobacterium tuberculosis, this pathogen continues to be a tremendous public health problem. The rise in the number of resistant strains and the difficulties involved in the therapy of tuberculosis in immunocompromised AIDS patients have renewed the interest in the development of effective vaccines. To evaluate whether a potential vaccine against tuberculosis could prevent infection by eliciting a protective antibody response, we reviewed the history of antibody-mediated immunity against tuberculosis. Review of the literature of the past 100 years demonstrates that there is sufficient evidence to conclude that antibody-mediated immunity can modify the course of infection in certain situations. Based on our findings and on what is known in other systems, we propose that the role of antibody-mediated immunity to M. tuberculosis be reexamined, using advanced technology.