The New Tuberculosis

Snider, Dixie E.; Roper, William L.

doi:10.1056/nejm199203053261011

Cited by 366 publications

(160 citation statements)

References 10 publications

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“…31 A presença de linhagens MDR reflete deficiências no controle da TB, o que dificulta o tratamento e a prevenção da doença, causando sua difusão. É necessário conhecer a suscetibilidade aos diferentes fármacos de uma linhagem individual a fim de se iniciar um tratamento com a combinação de fármacos mais adequada.…”

Section: Introductionunclassified

Tuberculose resistente: revisão molecular

et al. 2002

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ResumoO progresso na compreensão dos mecanismos de resistência aos fármacos usados no tratamento da tuberculose tem permitido o desenvolvimento de novos métodos para a detecção da tuberculose resistente. A resistente aos fármacos representa uma ameaça para os programas de controle da tuberculose. Para tanto, é necessário conhecer o padrão de sensibilidade das linhagens para fornecer o tratamento adequado. Os estudos moleculares dos mecanismos de ação dos fármacos antituberculose têm elucidado as bases genéticas da resistência aos fármacos em Mycobacterium tuberculosis. Os mecanismos de resistência aos fármacos na tuberculose são causados por mutações cromossomais em diferentes genes da bactéria. Durante a exposição aos fármacos, há uma pressão seletiva favorecendo o desenvolvimento de linhagens resistentes. A tuberculose multirresistente é um problema nacional e internacional que traz sérias dificuldades para o controle global da doença. Realizou-se uma revisão sobre os mecanismos moleculares associados à resistência aos fármacos com ênfase nas novas perspectivas para detectar os isolados resistentes. AbstractProgress to understanding the basis of resistance to antituberculous drugs has allowed molecular tests for detection of drug-resistant tuberculosis to be developed. Drug-resistant tuberculosis poses a threat to tuberculosis control programs. It is necessary thus to know drug susceptibilities of individual patient's strain to provide the appropriate drug combinations. Molecular studies on the mechanism of action of antituberculous drugs have elucidated the genetic basis of drug resistance in M. tuberculosis. The mechanisms of drug resistance in tuberculosis are a result of chromosomal mutations in different genes of the bacteria. Upon drug exposure there is a selective pressure for such resistant mutants. Multidrug-resistant tuberculosis is a health problem of increasing significance for the whole global community. This paper reviews the molecular mechanisms associated with drugresistance as well the new perspectives for detecting resistant isolates. Current Comments Atualização

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Section: Introductionunclassified

Tuberculose resistente: revisão molecular

et al. 2002

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“…A more alarming aspect of tuberculosis is the emergence of multidrug-resistant strains of M. tuberculosis (MDRTB) that is a widespread phenomenon (Snider & Roper 1992, Frieden et al 1993, Iseman 1993, Kato-Maeda et al 1999. The common finding has been a high rate of primary resistance to isoniazid (INH) and to the combination of isoniazid and rifampin (RIF) (Garcia-Garcia 2000) and a high rate of resistant (17.2%) to all the four commonly used antimycobacterial agents for treatment and prophylaxis of TB, including RIF (Granich et al 2000, Singh & Kaur 2004.…”

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confidence: 99%

Detection of rifampin resistance patterns in Mycobacterium tuberculosis strains isolated in Iran by polymerase chain reaction-single-strand conformation polymorphism and direct sequencing methods

Isfahani¹,

Tavakoli²,

Salehi³

et al. 2006

Mem. Inst. Oswaldo Cruz

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“…Isonicotinic acid hydrazide (isoniazid [INH]) has been a potent and clinically important antituberculosis drug since its introduction in 1952 (2), but the emergence of INH-resistant mutants has limited its efficacy (10). While neither the mode of action nor the cellular target of INH has been elucidated, it has been suggested that peroxides and peroxidases are needed to activate INH (14,17) and that the in vivo target may be mycolic acid synthesis (5,15).…”

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Effects of peroxides on susceptibilities of Escherichia coli and Mycobacterium smegmatis to isoniazid

Rosner

Storz

1994

Antimicrob Agents Chemother

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Escherichia coli strains were previously found to be susceptible to the antituberculosis drug isonicotinic acid hydrazide (isoniazid [INH]) when they carried certain mutations that also sensitize them to peroxides: a deletion in oxyR, a redox-sensitive regulator of hydrogen peroxide-inducible genes, or mutations in both katG and ahpCF, OxyR-regulated genes encoding hydroperoxidase I, and an alkyl hydroperoxide reductase.

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The New Tuberculosis

Cited by 366 publications

References 10 publications

Tuberculose resistente: revisão molecular

Tuberculose resistente: revisão molecular

Detection of rifampin resistance patterns in Mycobacterium tuberculosis strains isolated in Iran by polymerase chain reaction-single-strand conformation polymorphism and direct sequencing methods

Effects of peroxides on susceptibilities of Escherichia coli and Mycobacterium smegmatis to isoniazid

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