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The Intestinal Microbiome in Dogs with Chronic Enteropathies and Cobalamin Deficiency or Normocobalaminemia-A
Linda Toresson1,2, Jan S Suchodolski3, Thomas Spillmann2
1Evidensia Specialist Animal Hospital Helsingborg, 254 66 Helsingborg, Sweden.
Cobalamin deficiency in dogs with chronic enteropathies is linked to significant fecal microbiome changes. Supplementation did not restore the microbiome, suggesting it indicates underlying issues rather than causing dysbiosis.
Area of Science:
- Veterinary Medicine
- Gastroenterology
- Microbiome Research
Background:
- Cobalamin (vitamin B12) deficiency is a frequent complication of chronic enteropathies (CE) in dogs.
- Limited research exists comparing the gut microbiome of CE dogs with and without cobalamin deficiency.
Purpose of the Study:
- To characterize and compare the fecal microbiome composition in dogs with CE and cobalamin deficiency versus those with CE and normal cobalamin levels, and healthy controls.
- To assess the impact of cobalamin supplementation on the fecal microbiome in CE dogs.
Main Methods:
- A prospective, comparative study included 29 dogs with CE and cobalamin deficiency, 18 dogs with CE and normocobalaminemia, and 10 healthy controls.
- Fecal samples were analyzed for microbiome composition (beta diversity) at baseline and after 3 months of cobalamin supplementation (oral or parenteral).
Main Results:
- Baseline fecal microbiome composition significantly differed between CE dogs with cobalamin deficiency compared to normocobalaminemic CE dogs and healthy controls.
- Dogs with cobalamin deficiency showed increased Firmicutes and Actinobacteria, and decreased Bacteroidetes and Fusobacteria relative to controls.
- Microbiome composition remained significantly altered 3 months post-supplementation in both oral and parenteral cobalamin groups.
Conclusions:
- Cobalamin deficiency in CE dogs is associated with significant gut dysbiosis.
- Cobalamin supplementation alone, even with other therapies, did not restore normal microbiome composition.
- Cobalamin deficiency likely serves as a marker for underlying pathophysiological differences contributing to dysbiosis, rather than being the direct cause.
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