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. 2022 Aug 26;10:136. doi: 10.1186/s40168-022-01327-7

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© The Author(s) 2022

Open AccessThis 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 — Genetic context of AMR gene families unique to NS infants. From the de novo assembly, open reading frames were annotated using Prokka, and resistance genes were predicted using RGI main. The Prokka annotations are the colored arrows, and the RGI main predictions are labeled on each ORF. The genes are shown grouped into their respective AMR gene families: (A) AAC(3) gene family, (B) CTX-M beta-lactamase family, (C) OXA beta-lactamase family, (D) streptogramin vat acetyltransferase family (NS = not supplemented preterm)