One dog’s waste is another dog’s wealth: A pilot study of fecal microbiota transplantation in dogs with acute hemorrhagic diarrhea syndrome

Canine acute hemorrhagic diarrhea syndrome (AHDS) hasbeen associated insome studies with Clostridioides perfringens overgrowth and toxin-mediated necrosis of the intestinal mucosa. Weaimedtodetermine the effect of a single fecal microbiota transplantation (FMT) onclinical scores and fecal microbiomes of 1 and 7 dogs with AHDS from New Zealand and South Africa. We hypothesized that FMT would improve AHDS clinical scores and increase microbiota alpha-diversity and short-chain fatty acid (SCFA)-producing microbial communities’ abundances in dogs with AHDS after FMT. Wesequenced theV3-V4 region of the 16S-rRNA genein the feces of AHDSFMT-recipients andsham-treated control dogs, andtheir healthy donors at admission, discharge, and 30 days post-discharge. There were no significant differences in median AHDS clinical scores between FMT-recipients and sham-treated controls at admission or discharge (P = 0.22, P = 0.41). At admission, the Shannon diversity index (SDI) was lower in AHDS dogs than healthy donors (P = 0.002). TheSDIdidnotchange from admission to 30daysin sham-treated dogs yet increased in FMT-recipients from admission to discharge (P = 0.04) to levels not different than donors (P =0.33) but significantly higher than sham-treated controls (P = 0.002). At 30 days, the SDI did not differ between FMT recipients, sham-treated controls, and donors (P = 0.88). Principal coordinate analysis of the Bray-Curtis index separated post-FMT and donor dogs from pre-FMT andsham-treated dogs (P =0.009) because of increased SCFA-producing genera’s abundances after FMT. A single co-abundance subnetwork contained many of the sameOTUsfoundtobedifferentially abundant in FMT-recipients, and the abundance of this module was increased in FMT-recipients at discharge and 30 days, compared to shamtreated controls. We conclude in this small pilot study FMT did not have any clinical benefit.

PLoS ONE

PLoS ONE

16

1932-6203

N/A

4

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