We used two PCR reactions: in the first the complex-specific insertion sequence IS986/IS6110 was used to specifically detect DNA from Mycobacterium tuberculosis complex bacteria; in the second, conserved sequences of the mycobacterial groEL gene were used to detect DNA from mycobacteria other than M tuberculosis.
We conclude that DNA amplification in combination with lysozyme lysis can be used routinely in clinical laboratories as a rapid and sensitive test for the diagnosis of tuberculosis.
To further study this aspect, we stimulated T cells from normal human blood donors with synthetic peptides (each of approximately 15 amino acids in length) from the heat shock protein 65 of Mycobacterium tuberculosis-M. bovis.
Cytogenetic effects of 4 common anti-tubercular drugs, isoniazid (H), streptomycin (S), rifampicin (R) and pyrazinamide (Z), in 3 different combinations (2 SHRZ, 2 HRZ and 2 H2R2Z2) were evaluated in the lymphocytes of tuberculosis patients undergoing chemotherapy, in order to estimate their mutagenic potential in combination.
Cytogenetic effects of 4 common anti-tubercular drugs, isoniazid (H), streptomycin (S), rifampicin (R) and pyrazinamide (Z), in 3 different combinations (2 SHRZ, 2 HRZ and 2 H2R2Z2) were evaluated in the lymphocytes of tuberculosis patients undergoing chemotherapy, in order to estimate their mutagenic potential in combination.
Non specific indicators of tuberculosis are generally unhelpful although the bromide partition test and assay of the enzyme adenosine deaminase in cerebrospinal fluid appear to be of value in the diagnosis of tuberculous meningitis.
We demonstrate here that human T cells from healthy individuals and disease sites are able to recognize determinants within the 65 kD protein that are either specific for M. tuberculosis or are conserved between GroEL of mycobacterial, E. coli or human origin.
For the Gc system, the phenotypic frequencies did not differ significantly, but the PGM1 system showed a significant difference in the tuberculosis patients compared to controls.
Such genes include the murine MHC class I gene, Ld (toxoplasmosis), HLA-BW53, HLA DRB1* 1302-DQ B10s01 and TNF2 (malaria), murine Nramp (toxoplasmosis, leishmaniasis and tuberculosis), gene(s) modulating the T-helper type 1 and type 2 dichotomy (leishmaniasis, leprosy and HIV infection) and the natural killer cell complex (cytomegalovirus infection).
Compared with healthy tuberculin reactors, Mycobacterium tuberculosis-stimulated peripheral blood mononuclear cells from tuberculosis patients had diminished production and mRNA expression of the Th1 cytokines gamma interferon and interleukin 2 (IL-2), with no change in production and mRNA expression for the Th2 cytokines IL-4, IL-10, and IL-13.
When AMPLICOR MTB results were compared with resolved results, i.e., a specimen grew M. tuberculosis or was obtained from a patient with a clinical diagnosis of tuberculosis, the sensitivity, specificity, positive predictive value, and negative predictive value for the AMPLICOR MTB test were 66.7, 99.6, 91.7, and 97.7%, respectively.
When AMPLICOR MTB results were compared with resolved results, i.e., a specimen grew M. tuberculosis or was obtained from a patient with a clinical diagnosis of tuberculosis, the sensitivity, specificity, positive predictive value, and negative predictive value for the AMPLICOR MTB test were 66.7, 99.6, 91.7, and 97.7%, respectively.
We developed an algorithm that can be used to make an initial choice of a probe (either Mycobacterium tuberculosis complex [MTB] or M. avium complex [MAC]) for use in testing respiratory specimens.
We developed an algorithm that can be used to make an initial choice of a probe (either Mycobacterium tuberculosis complex [MTB] or M. avium complex [MAC]) for use in testing respiratory specimens.
The granulomatous immune response in tuberculosis is characterized by delayed hypersensitivity and is mediated by various cytokines released by the stimulated mononuclear phagocytes, including tumor necrosis factor-alpha (TNF alpha) and IL-1 beta.
M. tuberculosis cell wall component LAM acts similarly to LPS in activating mononuclear phagocyte cytokine TNF alpha and IL-1 beta release through CD14 and synthesis at the transcriptional level; both cytokines are key participants in the host immune response to tuberculosis.
We demonstrated that the Mycobacterium tuberculosis cell wall component lipoarabinomannan (LAM) is a very potent inducer of IL-1 beta gene expression in human monocytes and investigated the mechanism of this effect.
This finding, together with the emerging information on almost total sequence homology between the murine and human Nramp genes suggests that this gene may be responsible for the phenotype of resistance or susceptibility to tuberculosis.