DRUG RESISTANCE IN TUBERCULOSIS

https://doi.org/10.1016/S0891-5520(05)70397-4Get rights and content

America's first campaign to control tuberculosis began in 1889 when Hermann Biggs, together with Prudden and Loomis, wrote a report to the New York City Board of Health on the prevention of pulmonary tuberculosis.77 Because of Biggs' contributions to the field, his name is carved on the facade of the London School of Hygiene and Tropical Medicine together with twenty others who have made significant contributions to the improvement of public health. Biggs and others of our predecessors steadily made progress in the war against tuberculosis. Thus, tuberculosis cases declined as a result of sanitoriums, public health campaigns, chest X-rays, and most dramatically, through advances in tuberculosis drug therapy.

Despite progress in the promotion of public health and quality care, communities were surprised in the mid 1980s by the appearance of a new disease in the United States: drug-resistant tuberculosis. How could this have happened? By 1970, the seeds for disaster had been sown; categorical federal funding for tuberculosis control was phased out and replaced with general public-health block grants to the states. As a result, many states decided to spend less money in the fight against tuberculosis. It has been more than 12 years since the Centers for Disease Control and Prevention (CDC) first observed a deviation from the expected decline in the numbers of tuberculosis cases.10 The resurgence of tuberculosis in inner cities largely has been attributed to the acquired immunodeficiency virus epidemic, however, Brudney and Dobkin7 clearly showed that worsening economic and social conditions, including an increase in homelessness, contributed substantially to the increase in tuberculosis. In 1993, Mark Chassin (then New York State Commissioner of Health) extended this view and summarized it in this way: “Clearly, the challenge is not only in medicine and in public health, but also social, economic, and political.”12

Section snippets

Dimensions of the Problem

The emergence of Mycobacterium tuberculosis strains resistant to antituberculosis agents has recently received increased attention owing largely to the dramatic outbreaks of multidrug-resistant tuberculosis in HIV-infected patients in New York and Florida.11 These outbreaks have been characterized by delayed diagnoses, inadequate treatment regimens, high mortality, and significant rates of nosocomial transmission.24 Furthermore, increased surveillance has shown that drug-resistant tuberculosis

CONCLUSIONS FOR PATIENT TREATMENT

In summary, we would recommend that health care providers treating tuberculosis patients give consideration to the following seven items during diagnosis and treatment:

  • •

    Patients should be treated with a combination of drugs. Those at increased risk for drug-resistant disease should be started on a four-drug rather than a three-drug regimen.

  • •

    Directly observed therapy (DOT) reduces the risk of developing drug resistance.

  • •

    Antimicrobial therapy should be adapted to the results of the

References (83)

  • A. Telenti et al.

    Detection of rifampin-resistant mutations in Mycobacterium tuberculosis

    Lancet

    (1993)
  • S. Valway et al.

    False positive diagnosis of multidrug-resistant tuberculosis due to laboratory contamination [abstract]

    Tubercle Lung Dis

    (1994)
  • Y. Zhang et al.

    Molecular mechanisms of isoniazid: a drug at the front line of tuberculosis control

    Trends Microbiol

    (1993)
  • A. Banerjee et al.

    inhA, a gene encoding a target for isoniazid and ethionamide in Mycobacterium tuberculosis

    Science

    (1994)
  • J.S. Blanchard

    Molecular mechanisms of drug resistance in Mycobacterium tuberculosis

    Annu Rev Biochem

    (1996)
  • T. Bodmer et al.

    Mutation position and type of substitution in the β-subunit of the RNA polymerase influence in vitro activity of rifamycins in rifampin-resistant Mycobacterium tuberculosis

    J Antimicrobiol Chemother

    (1995)
  • M.A. Brow et al.

    Differentiation of bacterial 16S rRNA genes and intergenic regions and Mycobacterium tuberculosis katG genes by structure-specific endonuclease cleavage

    J Clin Microbiol

    (1996)
  • K. Brudney et al.

    Resurgent tuberculosis in New York City—Human immunodeficiency virus, homelessness, and the decline of tuberculosis control programs

    Am Rev Respir Dis

    (1991)
  • L.E. Bryan

    Bacterial Resistance and Susceptibility to Chemotherapeutic Agents

    (1982)
  • G. Canetti

    Present aspects of bacterial resistance in tuberculosis

    Am Rev Respir Dis

    (1965)
  • Centers for Disease Control

    Tuberculosis—United States, first 39 weeks

    MMWR Morb Mort Wkly Rep

    (1985)
  • Centers for Disease Control

    Nosocomial transmission of multidrug-resistant tuberculosis among HIV-infected persons—Florida and New York, 1988–1991

    MMWR Morb Mort Wkly Rep

    (1991)
  • M.R. Chassin

    Health challenges for the 1990s

    NY State J Med

    (1993)
  • C.P. Chaulk et al.

    Eleven years of community-based directly observed therapy for tuberculosis

    JAMA

    (1995)
  • D.L. Cohn et al.

    Drug-resistant tuberculosis: review of the worldwide situation and the WHO/IUATLD Global Surveillance Project

    Clin Infect Dis

    (1997)
  • M.J. Colston et al.

    Homologous recombination, DNA repair, and mycobacterial recA genes

  • G.W. Comstock et al.

    Preventive therapy

  • J. Crofton et al.

    Streptomycin resistance in pulmonary tuberculosis

    Br Med J

    (1948)
  • E.R. Dabbs et al.

    Ribosylation by mycobacterial strains as a new mechanism of rifampin inactivation

    Antimicrob Agents Chemother

    (1995)
  • L. Deng et al.

    Recognition of multiple effects of ethambutol on metabolism of mycobacterial cell envelope

    Antimicrob Agents Chemother

    (1995)
  • V. Deretic et al.

    Mycobacterium tuberculosis is a natural mutant with an inactivated oxidative-stress regulatory gene: implications for sensitivity for isoniazid

    Mol Microbiol

    (1995)
  • A. Dessen et al.

    Crystal structure and function of the isoniazid target of Mycobacterium tuberculosis

    Science

    (1995)
  • S.W. Dooley et al.

    Multidrug-resistant tuberculosis [editorial]

    Ann Intern Med

    (1992)
  • M.R.W. Ehlers

    The wolf at the door: some thoughts on the biochemistry of the tubercle bacillus

    S Afr Med J

    (1993)
  • W. El-Sadr et al.

    Directly observed therapy for tuberculosis: The Harlem Hospital experience, 1993

    Am J Publ Hlth

    (1996)
  • J.O. Falkingham et al.

    Plasmids

  • M. Goble et al.

    Treatment of 171 patients with pulmonary tuberculosis resistant to isoniazid and rifampin

    N Engl J Med

    (1993)
  • E.P. Gormley et al.

    Transfer of plasmid RSF1010 by conjugation from Escherichia coli to Streptomyces lividans and Mycobacterium smegmatis

    J Bacteriol

    (1991)
  • G. Hatfull

    The molecular genetics of Mycobacterium tuberculosis

    Current Topics Microbiol Immunol

    (1996)
  • B. Heym et al.

    Missense mutations in the catalase-peroxidase gene, katG, are associated with isoniazid resistance in Mycobacterium tuberculosis

    Mol Microbiol

    (1995)
  • B. Heym et al.

    Mechanisms of drug resistance in Mycobacterium tuberculosis

    Current Topics Microbiol Immunol

    (1996)

    • Cited by (38)

    • Mycobacteria

      2017, Infectious Diseases, 2-Volume Set

    • Mycobacterial Infections of Bones and Joints

      2016, Kelley and Firestein's Textbook of Rheumatology: Volumes 1-2, Tenth Edition

    • Mutation pattern in rifampicin resistance determining region of rpoB gene in multidrug-resistant Mycobacterium tuberculosis isolates from Pakistan

      2014, International Journal of Mycobacteriology
      Citation Excerpt :

      Drug resistance mostly develops by mutational interplay rather than acquisition of resistant genes transfer from other bacteria. Drug resistance in MTB isolates has widely been investigated and is generally thought to be caused by spontaneous mutations [3,5,19]. Emergence of MDR-TB is a serious challenge for clinicians; it arises mostly due to rpoB gene mutations [20].

    • Molecular characteristics of MDR Mycobacterium tuberculosis strains isolated in Fujian, China

      2014, Tuberculosis

    • Mycobacterial Infections of Bones and Joints

      2012, Kelley's Textbook of Rheumatology: Volume 1-2, Ninth Edition

    • A mutation in Mycobacterium tuberculosis rpoB gene confers rifampin resistance in three HIV-TB cases

      2010, Tuberculosis
      Citation Excerpt :

      However, rates of both acquired and primary rifampin monoresistant MTB are increasing worldwide.5,6 Risk factors for rifampin monoresistant MTB include HIV co-infection, previously treated TB or inappropriately treated TB.5–7 Patients with monoresistance to rifampin tend to have poor treatment outcomes requiring longer hospital stays and treatment courses.7–9

    View all citing articles on Scopus

    Address reprint requests to Max Salfinger, MD, Wadsworth Center, New York State Department of Health, Albany, NY 12201–0509

    *

    This article is dedicated to Mary Pangborn, PhD, the Wadsworth Center scientist who in the mid–1940s recovered and refined cardiolipin, the chemically defined antigen used for the past 50 years in the serodiagnosis of syphilis.

    View full text
    Copyright © 1997 W. B. Saunders Company. Published by Elsevier Inc. All rights reserved.