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. 2021 Jun 14;11:12472. doi: 10.1038/s41598-021-91905-w

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© The Author(s) 2021

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/.

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An overview of the different resistance mechanisms at the gene and protein level in the studied E. coli and K. pneumoniae isolates. The presence of beta-lactamase genes and proteins in the 78 E. coli and 109 K. pneumoniae isolates are shown in (A, C). The presence of 16S ribosomal RNA methyltransferase (16S-RMTase) and aminoglycoside modifying enzyme (AME) genes and proteins are shown in (B, D) for E. coli and K. pneumoniae, respectively. For each isolate, present genes were depicted in purple, proteins in blue and susceptible, intermediate and resistant phenotypes in green, orange, and red, respectively. Genes that were partly present and genes that were less than 80% similar to their reference genes were depicted with a dotted pattern. Isolates were clustered based on presence of the depicted AMR genes.

An overview of the different resistance mechanisms at the gene and protein level in the studied E. coli and K. pneumoniae isolates. The presence of beta-lactamase genes and proteins in the 78 E. coli and 109 K. pneumoniae isolates are shown in (A, C). The presence of 16S ribosomal RNA methyltransferase (16S-RMTase) and aminoglycoside modifying enzyme (AME) genes and proteins are shown in (B, D) for E. coli and K. pneumoniae, respectively. For each isolate, present genes were depicted in purple, proteins in blue and susceptible, intermediate and resistant phenotypes in green, orange, and red, respectively. Genes that were partly present and genes that were less than 80% similar to their reference genes were depicted with a dotted pattern. Isolates were clustered based on presence of the depicted AMR genes.