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. 2024 Dec 2;13:88. doi: 10.1186/s40249-024-01262-9

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Anti-PGL-I IgM in PB and MB leprosy patients. Sera from PB (n = 76) and MB (n = 133) leprosy patients were examined by PGL-I QURapid. Leprosy patients were stratified for bacterial index (BI 0: n = 76; BI 1–3: n = 21; BI 4–6: n = 112). Ratio (R-)values (Y-axis) were calculated by dividing the peak area of the test line (T) by the peak area of the flow control line (FC). A Kruskal–Wallis test with Dunn’s correction for multiple testing was performed to determine the statistical significance between three groups (P-values: **P ≤ 0.01, ***P ≤ 0.001, ****P ≤ 0.0001)