No abstract

Genotypes of Mycobacterium tuberculosis causing disease were investigated in pulmonary tuberculosis patients admitted to two adjacent wards of a tuberculosis hospital in Delhi, India. Genetic markers, the insertion sequence IS6110, a direct repeat sequence, and a polymorphic GC-rich sequence supported the circumstantial epidemiologic link between eight strains of M. tuberculosis, suggesting their possible involvement in small-scale, interpersonal transmission of both drug-sensitive and drug-resistant tuberculosis. This is the first report of a suspected acquisition of M. tuberculosis among hospitalized patients in India. The use of multiple molecular typing markers and techniques unequivocally identified the exact clonality of strains isolated from the hospital. The result of this study emphasizes the need for more comprehensive investigation of high-risk situations for tuberculosis transmission and long-term follow-up analysis for identifying such instances of unsuspected transmission.

No abstract

Emerging evidence indicates that the causative agent of tuberculosis is more genetically and functionally diverse than appreciated previously. The impact of this variation on the clinical manifestation of the disease remains largely unknown. In addition, there exists significant variability in the immune status of the host governing susceptibility to tuberculosis. The effect of these variations on the host pathogen interaction was investigated by taking varying pathogen phenotypes (virulent H37Rv, a-virulent H37Ra and a multidrug resistant strain #591) and varying host (18 MDR-TB and 16 fresh TB patients and 10 healthy, BCG-vaccinated individuals). The key question was whether the intracellular survival of Mycobacterium tuberculosis (MTB) in human monocyte-derived macrophages (MDM), an attribute of pathogenic potential, can be modulated by the immune status of the hosts or phenotype of MTB. The findings of this study indicate that induction of TNF-α may not be a global indicator of virulence of a strain. TNF-α release may be differentially regulated in response to the same strain depending upon the immune status of the host. Moreover, the phenotype of the infecting MTB and the host's immune status played a comparable role in the intracellular survival of MTB. This picture supports the hypothesis that in addition to the phenotype variation of the mycobacteria, the immune status of an individual will greatly influence the outcome of the host-pathogen interaction. These results may have a bearing on the future endeavors in vaccine development and TB control strategy.