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The risk of global epidemic replacement with drug-resistant Mycobacterium tuberculosis strains

McBryde, Emma S., Meehan, Michael T., Doan, Tan N., Ragonnet, Romain, Marais, Ben J., Guernier, Vanina and Trauer, James M. 2017, The risk of global epidemic replacement with drug-resistant Mycobacterium tuberculosis strains, International journal of infectious diseases, vol. 56, pp. 14-20, doi: 10.1016/j.ijid.2017.01.031.

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Title The risk of global epidemic replacement with drug-resistant Mycobacterium tuberculosis strains
Formatted title The risk of global epidemic replacement with drug-resistant Mycobacterium tuberculosis strains
Author(s) McBryde, Emma S.
Meehan, Michael T.
Doan, Tan N.
Ragonnet, Romain
Marais, Ben J.
Guernier, VaninaORCID iD for Guernier, Vanina orcid.org/0000-0002-0960-3874
Trauer, James M.
Journal name International journal of infectious diseases
Volume number 56
Start page 14
End page 20
Total pages 7
Publisher Elsevier
Place of publication Amsterdam, The Netherlands
Publication date 2017-03
ISSN 1201-9712
1878-3511
Keyword(s) Antibiotic resistance
Communicable disease control
Mathematical modelling
Tuberculosis
Antitubercular Agents
Epidemics
Global Health
Humans
Incidence
Models, Biological
Mycobacterium tuberculosis
Risk Assessment
Tuberculosis, Multidrug-Resistant
Tuberculosis, Pulmonary
Science & Technology
Life Sciences & Biomedicine
Infectious Diseases
MULTIDRUG-RESISTANT
ANTIBIOTIC-RESISTANCE
PHARMACOKINETIC VARIABILITY
POPULATION PHARMACOKINETICS
MDR-TB
RIFAMPIN
TRANSMISSION
MUTATIONS
COST
MECHANISM
Summary Objectives
Multidrug-resistant tuberculosis (MDR-TB) is a threat to tuberculosis (TB) control. To guide TB control, it is essential to understand the extent to which and the circumstances in which MDR-TB will replace drug-susceptible TB (DS-TB) as the dominant phenotype. The issue was examined by assessing evidence from genomics, pharmacokinetics, and epidemiology studies. This evidence was then synthesized into a mathematical model.

Methods

This model considers two TB strains, one with and one without an MDR phenotype. It was considered that intrinsic transmissibility may be different between the two strains, as may the control response including the detection, treatment failure, and default rates. The outcomes were explored in terms of the incidence of MDR-TB and time until MDR-TB surpasses DS-TB as the dominant strain.

Results and conclusions
The ability of MDR-TB to dominate DS-TB was highly sensitive to the relative transmissibility of the resistant strain; however, MDR-TB could dominate even when its transmissibility was modestly reduced (to between 50% and 100% as transmissible as the DS-TB strain). This model suggests that it may take decades or more for strain replacement to occur. It was also found that while the amplification of resistance is the early cause of MDR-TB, this will rapidly give way to person-to-person transmission.
Language eng
DOI 10.1016/j.ijid.2017.01.031
Field of Research 0605 Microbiology
1108 Medical Microbiology
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2017, The Authors
Free to Read? Yes
Use Rights Creative Commons Attribution Non-Commercial No-Derivatives licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30108626

Document type: Journal Article
Collections: School of Medicine
Open Access Collection
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.