Publication:
23S rRNA and L22 ribosomal protein are involved in the acquisition of macrolide and lincosamide resistance in Mycoplasma capricolum subsp. capricolum

Simple item page
dc.contributor.authorPrats-van der Ham, Miranda
dc.contributor.authorTatay-Dualde, Juan
dc.contributor.authorGómez-Martín, Angel
dc.contributor.authorCorrales, Juan Carlos
dc.contributor.authorContreras de Vera, Antonio
dc.contributor.authorSánchez López, Antonio
dc.contributor.authorde la Fe, Christian
dc.contributor.departmentSanidad Animal
dc.date.accessioned2023-12-11T13:25:09Z
dc.date.available2023-12-11T13:25:09Z
dc.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.2018.02.014es
dc.description.abstractMycoplasma 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.es
dc.formatapplication/pdfes
dc.format.extent35es
dc.identifier.doihttps://doi.org/10.1016/j.vetmic.2018.02.014
dc.identifier.eisbnVeterinary Microbiology Volume 216, March 2018, Pages 207-211es
dc.identifier.issnPrint: 0378-1135
dc.identifier.issnElectronic: 1873-2542
dc.identifier.urihttp://hdl.handle.net/10201/136531
dc.languageenges
dc.publisherElsevieres
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectContagious agalactiaes
dc.subjectAntimicrobial resistancees
dc.subjectMacrolideses
dc.subjectrplV genees
dc.subject.odsObjetivo 3: Salud
dc.title23S rRNA and L22 ribosomal protein are involved in the acquisition of macrolide and lincosamide resistance in Mycoplasma capricolum subsp. capricolumes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
VETMIC_2017_1083_Revision 1_V0_R1.pdf
Size:
698.26 KB
Format:
Adobe Portable Document Format
Description:
Download
License bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
license.txt
Size:
2.26 KB
Format:
Item-specific license agreed upon to submission
Description:
Download
Collections
Informes o documentos de trabajo