Send to

Choose Destination
See comment in PubMed Commons below
Kekkaku. 1995 Nov;70(11):645-50.

[The mode of infection of tuberculosis--analysis using molecular epidemiologic methods].

[Article in Japanese]

Author information

Research Institute of Tuberculosis, Japan Anti-Tuberculosis Association Matsuyama 3-1-24, Tokyo, Japan.


In the 1950's, evidence showed that INH-resistant Mycobacterium tuberculosis organisms were attenuated in both virulence and pathogenicity in animals, and it was postulated that these bacilli might also be attenuated in their virulence to humans. Subsequent studies, however, indicated that all INH-resistant strains should not be considered as being attenuated in their virulence to humans. The general conclusion was that patients excreting INH-resistant organisms are somewhat less infectious to their contacts than patients excreting INH-susceptible organisms. Insertion sequences are suitable tools for the diagnosis and epidemiology of tuberculosis because of the highly variable copy number and variability of insertion sites in the chromosome. This variability allows the subtyping of M. tuberculosis strains by restriction fragment length polymorphism (RFLP) analysis. Patients with the same RFLP pattern constitute an epidemiologically linked cluster. Clustering indicates recent infection and rapid progression to clinical illness. Nearly one thirds of new cases of tuberculosis in San Francisco are the result of recent infection. In Thailand, tuberculosis has now emerged as the most common opportunistic disease associated with HIV infection. Cluster analysis showed the risk of progression to active tuberculosis among individuals infected with HIV. Ther have been numerous outbreaks of multidrug-resistant tuberculosis in the United States. Most of such outbreaks have primarily involved persons infected with HIV, who are thought to have been exposed to the strains in medical or correctional facilities.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center