ArticleVeterinary research2015
Correlation of hypothetical virulence traits of two Streptococcus uberis strains with the clinical manifestation of bovine mastitis.
Article in Veterinary research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Whole-Genome Sequencing Analysis Revealed High Genomic Variability, Recombination Events and Mobile Genetic Elements inAntibiotics (Basel, Switzerland) · 2025Article
- Potential factors involved in the early pathogenesis of Streptococcus uberis mastitis: a review.Folia microbiologica · 2021Review
- Transcription Profiling of Monocyte-Derived Macrophages InfectedFrontiers in genetics · 2019Article
- MicroRNA expression profiles of bovine monocyte-derived macrophages infected in vitro with two strains of Streptococcus agalactiae.BMC genomics · 2018Article
- Effect of the Essential Oil ofFrontiers in veterinary science · 2018Article
- Molecular and virulence characterization of highly prevalent Streptococcus agalactiae circulated in bovine dairy herds.Veterinary research · 2017Article
- Cellular and soluble components decrease the viable pathogen counts in milk from dairy cows with subclinical mastitis.The Journal of veterinary medical science · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Streptococcus uberis is a common cause of clinical and subclinical mastitis in dairy cattle. Several virulence mechanisms have been proposed to contribute to the species' ability to cause disease. Here, virulence characteristics were compared between S. uberis strains FSL Z1-048, which consistently caused clinical mastitis in a challenge model, and FSL Z1-124, which consistently failed to cause disease in the same model, to ascertain whether in vitro virulence characteristics were related to clinical outcome. Macrophages derived from bovine blood monocytes failed to kill FSL Z1-048 whilst reducing survival of FSL Z1-124 by 42.5%. Conversely, blood derived polymorphonuclear cells caused more reduction (67.1 vs. 44.2%, respectively) in the survival of FSL Z1-048 than in survival of FSL Z1-124. After 3 h of coincubation with bovine mammary epithelial cell line BME-UV1, 1000-fold higher adherence was observed for FSL Z1-048 compared to FSL Z1-124, despite presence of a frame shift mutation in the sua gene of FSL Z1-048 that resulted in predicted truncation of the S. uberis Adhesion Molecule (SUAM) protein. In contrast, FSL Z1-124 showed higher ability than FSL Z1-048 to invade BME-UV1 cells. Finally, observed biofilm formation by FSL Z1-124 was significantly greater than for FSL Z1-048. In summary, for several hypothetical virulence characteristics, virulence phenotype in vitro did not match disease phenotype in vivo. Evasion of macrophage killing and adhesion to mammary epithelial cells were the only in vitro traits associated with virulence in vivo, making them attractive targets for further research into pathogenesis and control of S. uberis mastitis.
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