Peer-reviewed veterinary case report
Faecal IgA deficiency and genetics in German Shepherd dogs
By Grützner, Niels et al.·Published in Veterinary medicine and science·2021·Department of Small Animal Clinical Sciences, United States·View original on PubMed →
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Original publication title: Genomic association and further characterisation of faecal immunoglobulin A deficiency in German Shepherd dogs.
- Species:
- dog
Plain-English summary
A group of German Shepherds was studied to understand a condition called faecal immunoglobulin A deficiency (IgAD), which can affect their gut health. Researchers found that while only a small percentage of these dogs had this deficiency, it might be linked to other health issues like exocrine pancreatic insufficiency (EPI). They looked at genetic markers to see if there was a connection, but the results were inconclusive. Overall, the study suggests that faecal IgAD in German Shepherds is not very common and may not be a permanent issue.
People also search for: German Shepherd faecal IgA deficiency · dog EPI treatment · German Shepherd gut health issues
Abstract
BACKGROUND: Immunoglobulin A (IgA) deficiency, chronic enteropathies and exocrine pancreatic insufficiency (EPI) have a high prevalence in German Shepherd dogs (GSD). This prospective study determined the prevalence of faecal IgA deficiency (IgAD) in GSD and investigated several candidate genes and the canine genome for a region or locus co-segregating with IgAD in GSD. Faecal IgA concentrations were quantified and genomic DNA was extracted from 8 GSD with an undetectable faecal IgA (classified as IgAD) and 80 non-IgAD GSD. The canine minimal screening set II microsatellite markers were genotyped, with evidence of an association at p < 1.0 × 10. Faecal IgA concentrations were also tested for an association with patient clinical and biochemical variables. RESULTS: Allele frequencies observed using the candidate gene approach were not associated with faecal IgAD in GSD. In the genome-wide association study (GWAS), the microsatellite marker FH2361 on canine chromosome 33 approached statistical significance for a link with IgAD in GSD (p = 1.2 × 10). A subsequent GWAS in 11 GSD with EPI and 80 control GSD revealed a significant association between EPI and FH2361 (p = 8.2 × 10). CONCLUSIONS: The lack of an association with the phenotype of faecal IgAD in GSD using the candidate gene approach and GWAS might suggests that faecal IgAD in GSD is a relative or transient state of deficiency. However, the prevalence of faecal IgAD in GSD appears to be low (<3%). The relationship between faecal IgAD, EPI and loci close to FH2361 on canine chromosome 33 in GSD warrants further investigation.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/34390535/