2017 ACVIM Forum Research Abstract Program

This study showed that fecal composition is altered in dogs with naturally occurring EPI even when managed with enzyme supplementation. Larger prospective clinical studies are necessary to elucidate the mechanisms leading to this altered fecal composition despite enzyme replacement therapy. The aim of the present study was to identify single nucleotide polymorphisms using a genome wide association study (GWAS) which may confer genetic susceptibility or resistance to IBD. Genomic DNA was extracted from EDTA blood or saliva samples of 96 cases and 98 controls. Genotyping of cases and controls was performed on the Canine Illumina HD SNP array and data generated were analyzed using PLINK. Using Fst and logistic association analyses, we identified 16 candidate genes that have been previously reported to be associated with human IBD or are involved in the pathways that are linked to the disease. Eight of these genes, one (PTPRC; Protein Tyrosine Phosphatase, Receptor Type C) on chromosome 7 and seven (IL4, IL5, IL13, CSF2; Colony Stimulating Factor 2, SLC22A4 and A5; Solute Carrier Fami-ly22 member 4 and 5, IRF1; Interferon Regulatory Factor 1) on chromosome 11 have been identified in both approaches. In conclusion we identified 16 genes associated with IBD in GSDs. Our results suggest that Th2 cytokines could be implicated in the pathogenesis of IBD in GSDs. Targeted re-sequencing of the genes identified in our study will help to identify causative SNPs and consequently functional analysis of the causal SNPs reveal insights into mechanisms involved in pathogenesis on canine IBD. The purpose of this study was to analyze capsule endoscopy (CE) findings in hypoalbuminemic dogs. The records of 178 dogs given ALICAM for gastrointestinal signs and/or laboratory abnormalities were retrospectively assessed. Seventeen dogs were hypoalbuminemic and had complete studies. The mean AE SD albumin was 1.9 AE 0.4 g/dL, mean AE SD age was 7.5 AE 2.8 years, and mean AE SD weight was 20.5 AE 11.4 kg. Eight of 17 dogs had concurrent anemia. Prior to CE, 15 of 17 dogs had ultrasound examinations. The gastrointestinal tract (stomach, small intestine [SI], and colon) was normal (n = 8) or characterized by nonspecific wall thickening (n = 7). Seventeen of 17 CE studies were abnormal. Findings consisted of irregular/thickened mucosa with or without erosions (n = 6), numerous dilated lacteals (n = 4), severe erosions or ulcers with active bleeding (n = 2), mass (n = 2), hookworms (n = 1), SI nodules (n = 1), and lesions consistent with colonic vascular ectasia (n = 1). Lesions seen on CE (dilated lacteals, colonic vascular ectasia) were confirmed in two dogs that subsequently underwent traditional endoscopy. A third dog had gastroduodenoscopy prior to CE, which showed SI hemorrhage, but missed the SI nodules later identified with CE. A diagnosis of Strongyloides was made based on endoscopic biopsies and fecal Baermann test. A fourth dog with severe melena had a negative gastroduodenoscopy and laparoscopy, yet CE subsequently identified severe gastrointestinal erosions and ulcers thought to be secondary to NSAID administration. CE can be informative in dogs with hypoalbuminemia even when lesions are not identified with traditional endoscopy, surgery, or ultrasound. Severe acute pancreatitis (SAP) is associated with systemic complications and high mortality rate in dogs. Mesenchymal stem cells (MSCs) have been investigated for their therapeutic potential in several inf