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InterLabService
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Company news

05.03.2019
Tuberculosis: multidrug resistance and contemporary risks

Tuberculosis (TB) caused by Mycobacterium tuberculosis (MTB) is the deadliest infectious disease more often appears in Central Asia, Eastern Europe and Russia and the associated global threat has worsened with the emergence of drug resistance, in particular multidrug resistant TB (MDR-TB).

TB1

Fig. 1. Countries in the three high-burden country lists for TB, TB/HIV and MDR-TB being used by WHO during the period 20162020, and their areas of overlap [1].

The tuberculosis situation is being closely monitored by World Health Organization (WHO), which developed a strategy of tuberculosis liquidation. In 2017 WHO reported that since 2000 less cases of getting tuberculosis appeared and during the period from 2006 till 2015 the amount of cases reduced 5,4% per year.

Nevertheless WHO is calling for attention to tuberculosis antibiotic resistance problem as 3.5% of newly diagnosed and 20.5% of previously treated patients had MDR-TB, defined as bacillary resistance to at least rifampicin and isoniazid. The highest levels of MDR-TB were found in Eastern Europe and Central Asia, with rates reaching 20% and 50%, respectively. An estimated 9% of MDR-TB patients had extensively drug-resistant TB [2]. TB control programs in many countries rely on rapid identification of cases for effective treatment of the disease. Importantly, the drug-resistant forms of TB require accurate diagnosis of the type of resistance to guide therapy and interrupt transmission of resistant organisms in communities [3].

Molecular tests for TB target spontaneous point mutations in specific genes or loci in the M. tuberculosis chromosome that are associated with drug resistance [4]. Rifampicin-resistance, which is the best understood of all anti-TB drugs, is associated with mutations in an 81 base pair region of the rpoB gene commonly referred to as the rifampicin resistance determining region (rpoB/RRDR). Mutations within the rpoB/RRDR confer resistance to rifampicin in majority of the rifampicin-resistant isolates [3], and three key mutations are reported to be predominant worldwide [3, 5, 6]. For isoniazid, mutations mainly in katG and inhA gene promoter, and infrequently ahpC, oxyR, kasA, furA and ndh genes, confer resistance to the drug [3, 7]. Approximately 64% of the phenotypic resistance to isoniazid globally is attributed to the katG/Ser315Thr mutation [7] with 67.2% in Georgia [8] and Mexico [9], 58% Pakistan [10], 71% Germany [11], 59% Italy [12], 56% Greece [13], and 43% Japan [14] incidence.

Our new AmpliSens MTC-MDR-FL kit is developed for detection of DNA mutations in Mycobacterium tuberculosis responsible for rifampicin resistance (572 codone of RRDR of rpoB gene) and isoniazid resistance (315 codone of katG gene and promotor region of inhA gene) by PCR method with hybridization-fluorescent detection of amplification products. Samples of DNA extracted from sputum, bronchoalveolar lavage, bronchial wash, pleural fluid, urine and Mycobacterium tuberculosis cultures might be used. We recommend using Amplisens MTC-MDR-FL kit when examining newly identified tuberculosis-positive patients for fast and correct treatment scheme using.

References:

  1. WHO Global tuberculosis report 2018
  2. Zhang, Y.; Yew, W-W. The International Journal of Tuberculosis and Lung Disease, Volume 19, Number 11, 1 November 2015, pp. 1276-1289(14)
  3. Campbell PJ, Morlock GP, Sikes RD, Dalton TL, Metchock B, Starks AM, et al. Molecular Detection of Mutations Associated with First- and Second-Line Drug Resistance Compared with Conventional Drug Susceptibility Testing of Mycobacterium tuberculosis. Antimicrobial Agents and Chemotherapy. 2011; 55(5):203241
  4. Pang Y, Lu J, Wang Y, Song Y, Wang S, Zhao Y. Study of the Rifampin Monoresistance Mechanism in Mycobacterium tuberculosis. Antimicrobial Agents and Chemotherapy. 2013; 57(2):893900
  5. Mariam DH, Mengistu Y, Hoffner SE, Andersson DI. Effect of rpoB Mutations Conferring Rifampin Resistance on Fitness of Mycobacterium tuberculosis. Antimicrobial Agents and Chemotherapy. 2004
  6. Sandgren A, Strong M, Muthukrishnan P, Weiner BK, Church GM, Murray MB. Tuberculosis Drug Resistance Mutation Database. PLoS Medicine. 2009
  7. Seifert M, Catanzaro D, Catanzaro A, Rodwell TC. Genetic Mutations Associated with Isoniazid Resistance in Mycobacterium tuberculosis: A Systematic Review. PloS one. 2015
  8. Shubladze N, Tadumadze N, Bablishvili N. Molecular patterns of multidrug resistance of Mycobacterium tuberculosis in Georgia. International journal of mycobacteriology. 2013
  9. Ramaswamy SV, Dou S-J, Rendon A, Yang Z, Cave MD, Graviss EA. Genotypic analysis of multidrugresistant Mycobacterium tuberculosis isolates from Monterrey, Mexico. Journal of medical microbiology. 2004
  10. Qazi O, Rahman H, Tahir Z, Qasim M, Khan S, Anjum AA, et al. Mutation pattern in rifampicin resistance determining region of rpoB gene in multidrug-resistant Mycobacterium tuberculosis isolates from Pakistan. International journal of mycobacteriology. 2014
  11. Tracevska T, Jansone I, Broka L, Marga O, Baumanis V. Mutations in the rpoB and katG genes leading to drug resistance in Mycobacterium tuberculosis in Latvia. Journal of clinical microbiology. 2002
  12. Jou R, Chen H-Y, Chiang C-Y, Yu M-C, Su I-J. Genetic diversity of multidrug-resistant Mycobacterium tuberculosis isolates and identification of 11 novel rpoB alleles in Taiwan. Journal of clinical microbiology. 2005
  13. Matsiota-Bernard P, Vrioni G, Marinis E. Characterization of rpoB mutations in rifampin-resistant clinical Mycobacterium tuberculosisIsolates from Greece. Journal of clinical microbiology. 1998
  14. Ohno H, Koga H, Kohno S, Tashiro T, Hara K. Relationship between rifampin MICs for and rpoB mutations of Mycobacterium tuberculosis strains isolated in Japan. Antimicrobial agents and chemotherapy. 1996

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