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Review
. 2018 Jul;6(4):10.1128/microbiolspec.arba-0030-2018.
doi: 10.1128/microbiolspec.ARBA-0030-2018.

Antimicrobial Resistance in Mycoplasma spp

Affiliations
Review

Antimicrobial Resistance in Mycoplasma spp

Anne V Gautier-Bouchardon. Microbiol Spectr. 2018 Jul.

Abstract

Mycoplasmas are intrinsically resistant to antimicrobials targeting the cell wall (fosfomycin, glycopeptides, or β-lactam antibiotics) and to sulfonamides, first-generation quinolones, trimethoprim, polymixins, and rifampicin. The antibiotics most frequently used to control mycoplasmal infections in animals are macrolides and tetracyclines. Lincosamides, fluoroquinolones, pleuromutilins, phenicols, and aminoglycosides can also be active. Standardization of methods used for determination of susceptibility levels is difficult since no quality control strains are available and because of species-specific growth requirements. Reduced susceptibility levels or resistances to several families of antimicrobials have been reported in field isolates of pathogenic Mycoplasma species of major veterinary interest: M. gallisepticum and M. synoviae in poultry; M. hyopneumoniae, M. hyorhinis, and M. hyosynoviae in swine; M. bovis in cattle; and M. agalactiae in small ruminants. The highest resistances are observed for macrolides, followed by tetracyclines. Most strains remain susceptible to fluoroquinolones. Pleuromutilins are the most effective antibiotics in vitro. Resistance frequencies vary according to the Mycoplasma species but also according to the countries or groups of animals from which the samples were taken. Point mutations in the target genes of different antimicrobials have been identified in resistant field isolates, in vitro-selected mutants, or strains reisolated after an experimental infection followed by one or several treatments: DNA-gyrase and topoisomerase IV for fluoroquinolones; 23S rRNA for macrolides, lincosamides, pleuromutilins, and amphenicols; 16S rRNAs for tetracyclines and aminoglycosides. Further work should be carried out to determine and harmonize specific breakpoints for animal mycoplasmas so that in vitro information can be used to provide advice on selection of in vivo treatments.

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References

    1. Razin S. 1996. Mycoplasmas. In Baron S (ed), Medical Microbiology. University of Texas Medical Branch at Galveston, Galveston, TX.
    1. Taylor-Robinson D. 1996. Infections due to species of Mycoplasma and Ureaplasma: an update. Clin Infect Dis 23:671–682, quiz 683–684 10.1093/clinids/23.4.671. [PubMed] - DOI - PubMed
    1. Brown DR, Zacher LA, Wendland LD, Brown MB. 2005. Emerging mycoplasmoses in wildlife, p 383–414. In Blanchard A, Browning G (ed), Mycoplasmas: Molecular Biology, Pathogenicity and Strategies for Control. Horizon Bioscience, Norfolk, UK. [PubMed]
    1. Markham PF, Noormohammadi AH. 2005. Diagnosis of mycoplasmosis in animals, p 355–382. In Blanchard A, Browning G (ed), Mycoplasmas: Molecular Biology, Pathogenicity and Strategies for Control. Horizon Bioscience, Norfolk, UK.
    1. Waites K, Talkington D. 2005. New developments in human diseases due to mycoplasmas, p 289–354. In Blanchard A, Browning G (ed), Mycoplasmas: Molecular Biology, Pathogenicity and Strategies for Control. Horizon Bioscience, Norfolk, UK.

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