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<article xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" article-type="letter"><?properties open_access?><front><journal-meta><journal-id journal-id-type="nlm-ta">Emerg Infect Dis</journal-id><journal-id journal-id-type="iso-abbrev">Emerging Infect. Dis</journal-id><journal-id journal-id-type="publisher-id">EID</journal-id><journal-title-group><journal-title>Emerging Infectious Diseases</journal-title></journal-title-group><issn pub-type="ppub">1080-6040</issn><issn pub-type="epub">1080-6059</issn><publisher><publisher-name>Centers for Disease Control and Prevention</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">30334732</article-id><article-id pub-id-type="pmc">6199982</article-id><article-id pub-id-type="publisher-id">18-0465</article-id><article-id pub-id-type="doi">10.3201/eid2411.180465</article-id><article-categories><subj-group subj-group-type="heading"><subject>Letters to the Editor</subject></subj-group><subj-group subj-group-type="article-type"><subject>Letter</subject></subj-group><subj-group subj-group-type="TOC-title"><subject>Acquired Resistance to Antituberculosis Drugs</subject></subj-group></article-categories><title-group><article-title>Acquired Resistance to Antituberculosis Drugs</article-title><alt-title alt-title-type="running-head">Acquired Resistance to Antituberculosis Drugs </alt-title></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Aung</surname><given-names>Htin Lin</given-names></name></contrib><contrib contrib-type="author"><name><surname>Nyunt</surname><given-names>Wint Wint</given-names></name></contrib><contrib contrib-type="author"><name><surname>Fong</surname><given-names>Yang</given-names></name></contrib><contrib contrib-type="author"><name><surname>Russell</surname><given-names>Bruce</given-names></name></contrib><contrib contrib-type="author"><name><surname>Cook</surname><given-names>Gregory M.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Aung</surname><given-names>Si Thu</given-names></name></contrib><aff id="aff1">University of Otago, Dunedin, New Zealand (H.L. Aung, B. Russell, G.M. Cook); </aff><aff id="aff2">Ministry of Health and Sports, Yangon, Myanmar (W.W. Nyunt); </aff><aff id="aff3">Massey University, Palmerston North, New Zealand (Y. Fong); </aff><aff id="aff4">Ministry of Health and Sports, Naypyitaw, Myanmar (S.T. Aung) </aff></contrib-group><author-notes><corresp id="cor1">Address for correspondence: Htin Lin Aung, Sir Charles Hercus Health Research Fellow, Department of Microbiology and Immunology, School of Biomedical Sciences, University of Otago, PO Box 56, Dunedin, New Zealand; email: <email xlink:href="htin.aung@otago.ac.nz">htin.aung@otago.ac.nz</email></corresp></author-notes><pub-date pub-type="ppub"><month>11</month><year>2018</year></pub-date><volume>24</volume><issue>11</issue><fpage>2134</fpage><lpage>2134</lpage><related-article id="d35e101" related-article-type="commentary-article" ext-link-type="pubmed" xlink:href="29460735" vol="24" page="524">1. <string-name><surname>Loutet</surname><given-names>MG</given-names>
</string-name>, <string-name><surname>Davidson</surname><given-names>JA</given-names>
</string-name>, <string-name><surname>Brown</surname><given-names>T</given-names>
</string-name>, <string-name><surname>Dedicoat</surname><given-names>M</given-names>
</string-name>, <string-name><surname>Thomas</surname><given-names>HL</given-names>
</string-name>, <string-name><surname>Lalor</surname><given-names>MK</given-names>
</string-name>. <article-title>Acquired resistance to antituberculosis drugs in England, Wales, and Northern Ireland, 2000&#x02013;2015.</article-title>
<source>Emerg Infect Dis</source>. <year>2018</year>;<volume>24</volume>:<fpage>524</fpage>&#x02013;<lpage>33</lpage>. <pub-id pub-id-type="doi">10.3201/eid2403.171362</pub-id>
</related-article><kwd-group kwd-group-type="author"><title>Keywords: </title><kwd>Food safety</kwd><kwd>drug-resistant</kwd><kwd>Myanmar</kwd><kwd>tuberculosis</kwd><kwd>tuberculosis and other mycobacteria</kwd><kwd>whole-genome sequencing</kwd><kwd>antimicrobial resistance</kwd></kwd-group></article-meta></front><body><p><bold>To the Editor:</bold> We read with great interest the article by Loutet et al. on acquired resistance to antituberculosis drugs in low-burden settings, such as England, Wales, and Northern Ireland (<xref rid="R1" ref-type="bibr"><italic>1</italic></xref>), and support their assertion that detecting acquired resistance should be a priority in high-burden settings. This objective is particularly urgent in Myanmar, where tuberculosis (TB) is highly endemic (<xref rid="R2" ref-type="bibr"><italic>2</italic></xref>) and drug-resistant TB is present through both acquired drug resistance and direct transmission. Unfortunately, the overwhelming number of TB cases precluded routine phenotypic drug susceptibility testing (DST) of first- or second-line drugs, so we began using whole-genome sequencing (WGS), which enabled us to more rapidly diagnose drug-resistant TB (<xref rid="R3" ref-type="bibr"><italic>3</italic></xref>). Here, we briefly describe 2 cases of acquired antituberculosis drug resistance detected by WGS. </p><p>Patient A, diagnosed with rifampin-susceptible TB by Xpert (Cepheid Inc., Sunnyvale, CA, USA), received a treatment regimen containing first-line drugs but failed to achieve smear conversion at the 3-month follow-up. WGS indicated that the isolate was resistant to isoniazid, streptomycin, and rifampin. WGS and phenotypic DST of the isolate at baseline revealed it was resistant to isoniazid and streptomycin. Isolates from before and after treatment differed by 2 single-nucleotide polymorphisms, suggesting that rifampin resistance was acquired during therapy (<xref rid="R4" ref-type="bibr"><italic>4</italic></xref>). Patient B was diagnosed with rifampin-resistant TB and reported that he had started multidrug resistant (MDR) TB treatment 6 months earlier but failed to continue the treatment. WGS and phenotypic DST showed the case had been MDR TB (resistant to isoniazid, rifampin, and streptomycin, but sensitive to amikacin) at baseline but had become pre&#x02013;extensively drug resistant (amikacin resistance was acquired during treatment). </p><p>Loutet et al. showed that WGS provides an effective way to evaluate TB drug resistance in low-endemicity settings (<xref rid="R5" ref-type="bibr"><italic>5</italic></xref>). We believe WGS is even more vital to help direct MDR TB treatment in high-burden settings, to halt the continued spread of TB. </p></body><back><fn-group><fn fn-type="citation"><p><italic>Suggested citation for this article</italic>: Aung HL, Nyunt WW, Fong Y, Russell B, Cook GM, Aung ST. Acquired resistance to antituberculosis drugs. Emerg Infect Dis. 2018 Nov [<italic>date cited</italic>]. <ext-link ext-link-type="uri" xlink:href="https://doi.org/10.3201/eid2411.180465">https://doi.org/10.3201/eid2411.180465</ext-link></p></fn></fn-group><ack><p>Ethics approval for this study was given by the Ethics Review Committee of Department of Medical Research, Yangon, Myanmar.</p><p>This work was supported by the New Zealand Health Research Council (grant number 15/648 and 18/024).</p></ack><ref-list><title>References</title><ref id="R1"><label>1. </label><mixed-citation publication-type="journal"><string-name><surname>Loutet</surname>
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