{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:56:54Z","timestamp":1787025414151,"version":"build-2736575974"},"reference-count":16,"publisher":"Scientific Scholar","content-domain":{"domain":["ijdvl.com"],"crossmark-restriction":true},"short-container-title":["Indian J Dermatol Venereol Leprol"],"abstract":"\n Background<\/jats:title>\n \n Leprosy, caused by\n Mycobacterium leprae<\/jats:italic>\n , remains a significant public health challenge, particularly in endemic regions. While multidrug therapy (MDT) has been effective, the emergence of antimicrobial resistance (AMR) to key drugs such as rifampicin, dapsone, and ofloxacin threatens leprosy control programs. Resistance mechanisms include mutations in genes such as\n rpoB<\/jats:italic>\n (rifampicin),\n folP1<\/jats:italic>\n (dapsone), and\n gyrA<\/jats:italic>\n (ofloxacin). Drug resistance contributes to treatment failures, prolonged transmission, and the emergence of severe complications, necessitating enhanced surveillance and diagnostic capabilities.\n <\/jats:p>\n <\/jats:sec>\n \n Aims<\/jats:title>\n \n This study aimed to determine the rates of primary and secondary AMR in\n M. leprae<\/jats:italic>\n among multi-bacillary leprosy patients attending a tertiary care institute in Uttarakhand. It also sought to identify patterns of genetic mutations associated with resistance.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n This prospective, cross-sectional study was conducted from July 2022 to June 2024. Patients with a bacteriological index (BI) \u22652, fulfilling specific clinical criteria [treatment-naive, chronic or recurrent erythema nodosum leprosum (ENL), relapse or persistent positive morphological index (MI)] were recruited. Slit skin smears (SSS) were processed using polymerase chain reaction (PCR) -based gene amplification to detect mutations in\n rpoB<\/jats:italic>\n ,\n folP1<\/jats:italic>\n and\n gyrA<\/jats:italic>\n . Amplified DNA samples were sequenced and analysed for resistance-associated mutations. Demographic and clinical data, including type of leprosy, BI, MI, and treatment history, were also collected.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Out of 47 samples tested, 43 were successfully amplified. Resistance was detected in eight cases (17%). Primary resistance was noted in 4\/20 treatment-naive patients (20%). Rifampicin resistance, attributed to the F439L mutation, was the most common (n = 4). Dapsone resistance due to\n P55L<\/jats:italic>\n and\n P55S<\/jats:italic>\n mutations was identified in two cases, while ofloxacin resistance associated with\n A91V<\/jats:italic>\n and\n G89C<\/jats:italic>\n mutations was seen in two cases.\n <\/jats:p>\n <\/jats:sec>\n \n Limitations<\/jats:title>\n The study\u2019s findings are limited by its sample size and the focus on a single tertiary care centre, potentially restricting the generalisability of results. Additionally, not all samples were successfully amplified for analysis.<\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n This study underscores the critical need for routine AMR testing in high-risk leprosy cases. Regional variations in resistance patterns necessitate localised surveillance to guide effective treatment strategies. Enhanced diagnostic capabilities, patient education, and policy-level interventions are essential to combat the rising threat of AMR in leprosy.<\/jats:p>\n <\/jats:sec>","DOI":"10.25259\/ijdvl_1842_2024","type":"journal-article","created":{"date-parts":[[2025,10,11]],"date-time":"2025-10-11T07:18:39Z","timestamp":1760167119000},"page":"37-42","update-policy":"https:\/\/doi.org\/10.25259\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Resistance to anti-leprosy drugs in multi-bacillary leprosy patients: The need for transformative action"],"prefix":"10.25259","volume":"92","author":[{"given":"Rashmi","family":"Jindal","sequence":"first","affiliation":[{"name":"Department of Dermatology, Venereology and Leprosy, Himalayan Institute of Medical Sciences, Dehradun, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Itu","family":"Singh","sequence":"additional","affiliation":[{"name":"Department of Immunology, Stanley Browne Laboratory, The Leprosy Mission Trust India, Community Hospital, Delhi, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dikshita","family":"Goyal","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Venereology and Leprosy, Himalayan Institute of Medical Sciences, Dehradun, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arnav","family":"Mittal","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Venereology and Leprosy, Himalayan Institute of Medical Sciences, Dehradun, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anuj","family":"Saini","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Venereology and Leprosy, Himalayan Institute of Medical Sciences, Dehradun, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ritu","family":"Dhoundiyal","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Venereology and Leprosy, 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