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Gut microbiota alterations linked to classical scrapie in sheep
Adelaida Hernaiz1, Laura Grasa2, Paula De Diego Abejón3
1Laboratorio de Genética Bioquímica (LAGENBIO), Facultad de Veterinaria, Universidad de Zaragoza, Zaragoza, Spain; Instituto Agroalimentario de Aragón-IA2 (Universidad de Zaragoza-CITA), Zaragoza, Spain.
Research in Veterinary Science
|September 27, 2025
Summary
Gut microbiota alterations are linked to prion diseases like scrapie in sheep. Specific bacterial phyla, Cyanobacteria and Lentisphaerae, increased in scrapie-infected sheep, suggesting a role in disease pathogenesis.
Area of Science:
- Microbiology
- Neuroscience
- Veterinary Medicine
Background:
- Growing evidence links gut microbiota to neurodegenerative diseases.
- The gut microbiota's role in prion diseases, such as scrapie, remains poorly understood.
- Prion diseases are caused by infectious misfolded prion proteins, affecting humans and animals.
Purpose of the Study:
- To investigate the gut microbiota composition in sheep with classical scrapie.
- To compare the gut microbiome of scrapie-infected sheep with healthy controls.
- To identify potential microbial biomarkers associated with scrapie pathogenesis.
Main Methods:
- 16S rRNA-based microbiome profiling of fecal samples.
- Analysis of gut microbiota composition in 10 scrapie-infected and 10 control sheep.
- Comparison of microbial richness, alpha diversity, and beta diversity between groups.
Main Results:
- Firmicutes and Bacteroidetes were the most abundant phyla in both groups.
- No significant differences in richness and alpha diversity were observed.
- Significant differences in beta diversity indicated altered gut microbiota in scrapie-infected sheep.
- Scrapie-infected sheep showed increased abundance of Cyanobacteria and Lentisphaerae phyla.
Conclusions:
- Classical scrapie infection in sheep is associated with an altered gut microbiota.
- Increased abundance of Cyanobacteria and Lentisphaerae may play a role in scrapie pathogenesis.
- These findings advance the understanding of prion disease mechanisms and the gut-brain axis.
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