Publication: 23S rRNA and L22 ribosomal protein are involved in the acquisition of macrolide and lincosamide resistance in Mycoplasma capricolum subsp. capricolum
Authors
Prats-van der Ham, Miranda ; Tatay-Dualde, Juan ; Gómez-Martín, Angel ; Corrales, Juan Carlos ; Contreras de Vera, Antonio ; Sánchez López, Antonio ; de la Fe, Christian
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Publisher
Elsevier
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DOI
https://doi.org/10.1016/j.vetmic.2018.02.014
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info:eu-repo/semantics/article
Description
© 2018. Elsevier. This document is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
This document is the Accepted version of a Published Work that appeared in final form in Veterinary Microbiology. To access the final edited and published work see https://doi.org/10.1016/j.vetmic.2018.02.014
Abstract
Mycoplasma capricolum subsp. capricolum (Mcc) is one of the causative agents of contagious agalactia, and
antimicrobial treatment is the most commonly applied measure to treat outbreaks of this disease. Macrolides and
lincosamides bind specifically to nucleotides at domains II and V of the 23S rRNA gene. Furthermore, rplD and rplV
genes encode ribosomal proteins L4 and L22, which are also implicated in the macrolide binding site. The aim of this
work was to study the relationship between these genes and the acquisition of macrolide and lincosamide resistance
in Mcc. For this purpose, in vitro selected resistant mutants and field isolates were studied. This study demonstrates
the appearance of DNA point mutations at the 23S rRNA encoding genes (A2058G, A2059G and A2062C) and rplV
gene (Ala89Asp) in association to high minimum inhibitory concentration values. Hence, it proves the importance of
23S rRNA domain V and ribosomal protein L22 as molecular mechanisms responsible for the acquisition of macrolide
and lincosamide resistance in both field isolates and in vitro selected mutants. Furthermore, these mutations enable us
to provide an interpretative breakpoint of antimicrobial resistance for Mcc at MIC 0.8 µg/ml.
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