4.6 Article

Differences in the genome, methylome, and transcriptome do not differentiate isolates of Streptococcus equi subsp. equi from horses with acute clinical signs from isolates of inapparent carriers

Journal

PLOS ONE
Volume 16, Issue 6, Pages -

Publisher

PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0252804

Keywords

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Funding

  1. Link Equine Research Endowment, College of Veterinary Medicine & Biomedical Sciences, Texas AM University
  2. Department of Large Animal Clinical Sciences, College of Veterinary Medicine & Biomedical Science, Texas AM University
  3. Patsy Link Chair in Equine Research
  4. Swedish Research Council for Environment, Agricultural Sciences and Spatial Planning (FORMAS) [221-2013-606]

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Research using next-generation sequencing technologies found no significant or consistent differences in the genome, methylome, and transcriptome of isolates of the bacterium Streptococcus equi subsp. equi (SEE) from horses with acute clinical strangles and inapparent carrier horses. This suggests that adaptations of SEE to the host are unlikely to explain the carrier state of the pathogen. Instead, efforts to understand the carrier state of SEE should focus on host factors.
Streptococcus equi subsp. equi (SEE) is a host-restricted bacterium that causes the common infectious upper respiratory disease known as strangles in horses. Perpetuation of SEE infection appears attributable to inapparent carrier horses because it neither persists long-term in the environment nor infects other host mammals or vectors, and infection results in short-lived immunity. Whether pathogen factors enable SEE to remain in horses without causing clinical signs remains poorly understood. Thus, our objective was to use next-generation sequencing technologies to characterize the genome, methylome, and transcriptome of isolates of SEE from horses with acute clinical strangles and inapparent carrier horses-including isolates recovered from individual horses sampled repeatedly-to assess pathogen-associated changes that might reflect specific adaptions of SEE to the host that contribute to inapparent carriage. The accessory genome elements and methylome of SEE isolates from Sweden and Pennsylvania revealed no significant or consistent differences between acute clinical and inapparent carrier isolates of SEE. RNA sequencing of SEE isolates from Pennsylvania demonstrated no genes that were differentially expressed between acute clinical and inapparent carrier isolates of SEE. The absence of specific, consistent changes in the accessory genomes, methylomes, and transcriptomes of acute clinical and inapparent carrier isolates of SEE indicates that adaptations of SEE to the host are unlikely to explain the carrier state of SEE. Efforts to understand the carrier state of SEE should instead focus on host factors.

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