Inflammatory bowel disease (IBD) is considered to be the most common cause of vomiting and diarrhoea in dogs, and the German shepherd dog (GSD) is particularly susceptible. The exact aetiology of IBD is unknown, however associations have been identified between specific single-nucleotide polymorphisms (SNPs) in Toll-like receptors (TLRs) and human IBD. However, to date, no genetic studies have been undertaken in canine IBD. The aim of this study was to investigate whether polymorphisms in canine TLR 2, 4 and 5 genes are associated with IBD in GSDs. Mutational analysis of TLR2, TLR4 and TLR5 was performed in 10 unrelated GSDs with IBD. Four non-synonymous SNPs (T23C, G1039A, A1571T and G1807A) were identified in the TLR4 gene, and three non-synonymous SNPs (G22A, C100T and T1844C) were identified in the TLR5 gene. The non-synonymous SNPs identified in TLR4 and TLR5 were evaluated further in a case-control study using a SNaPSHOT multiplex reaction. Sequencing information from 55 unrelated GSDs with IBD were compared to a control group consisting of 61 unrelated GSDs. The G22A SNP in TLR5 was significantly associated with IBD in GSDs, whereas the remaining two SNPs were found to be significantly protective for IBD. Furthermore, the two SNPs in TLR4 (A1571T and G1807A) were in complete linkage disequilibrium, and were also significantly associated with IBD. The TLR5 risk haplotype (ACC) without the two associated TLR4 SNP alleles was significantly associated with IBD, however the presence of the two TLR4 SNP risk alleles without the TLR5 risk haplotype was not statistically associated with IBD. Our study suggests that the three TLR5 SNPs and two TLR4 SNPs; A1571T and G1807A could play a role in the pathogenesis of IBD in GSDs. Further studies are required to confirm the functional importance of these polymorphisms in the pathogenesis of this disease.

Background Certain amino acids are decreased in humans with inflammatory bowel disease (IBD) and supplementation with the same amino acids has shown beneficial effects in animal models of IBD. Currently, the amino acid status of dogs with protein-losing enteropathy (PLE) is unknown. Hypothesis/Objective To determine if serum amino acid concentrations are abnormal in dogs with PLE and correlated with clinical and laboratory variables and outcome. Animals Thirty client-owned dogs diagnosed with PLE and 12 apparently healthy dogs seen at Bristol Veterinary School. Methods Retrospective study using stored residual serum from fasted dogs with PLE, collected at the time of diagnostic investigation and from apparently healthy dogs. Serum was analyzed for 30 amino acids using an automated high-performance liquid chromatography amino acid analyzer. Results Serum tryptophan concentrations were significantly decreased in dogs with PLE (median, 22 nmol/mL; range, 1–80 nmol/mL) compared with apparently healthy control dogs (median, 77.5 nmol/mL; range, 42–135 nmol/mL, P < .001). There were no significant differences in the remaining 29 serum amino acids between dogs with PLE and apparently healthy. Serum tryptophan concentrations were also significantly correlated with serum albumin concentrations in dogs with PLE (P = .001, R² = 0.506). Conclusions and Clinical Importance Decreased serum tryptophan concentration might play a role in the pathogenesis of canine PLE or be a consequence of the disease.

Background: Gall bladder mucoceles (GBM) are a leading cause of biliary disease in dogs with several breeds, including the Shetland Sheepdog, American Cocker Spaniel, Chihuahua, Pomeranian, and Miniature Schnauzer apparently predisposed. Objective: To determine risk factors, clinical features, and response to treatment of GBM in Border terriers (BT). Animals: Medical records of 99 dogs (including 51 BT) with an ultrasonographic (±histopathologic) diagnosis of GBM from three referral centers in the United Kingdom were collected. A control group of 87 similar-aged BT with no ultrasonographic evidence of gall bladder disease was selected for comparison. Method: Retrospective case-control study. Odds ratios were calculated to establish breed predisposition. Signalment, presence of endocrine disease, clinicopathologic results, and outcome were compared between the BT, other breeds, and control BTs. Results: The odds of identifying a GBM in a BT in this hospital population was 85 times that of all other breeds (95% confidence interval 56.9-126.8). BT had similar clinical signs and clinicopathologic changes to other breeds with GBM. There was no evidence that endocrinopathies were associated with GBM in BT. Clinical Significance: A robust breed predisposition to GBM is established for the BT.

Background Malnutrition is associated with increased risk of premature death in humans with inflammatory bowel disease. Hypothesis/Objective To determine if historical, clinical, and laboratory markers of malnutrition in dogs at the time of histologic diagnosis of protein‐losing enteropathy (PLE) caused by chronic enteropathy (CE) or lymphangiectasia are associated with increased risk of death. Animals Seventy‐one client‐owned dogs diagnosed with PLE. Methods The medical records were retrospectively searched for cases of PLE, diagnosed with CE or lymphangiectasia on the basis of histopathology of intestinal biopsies at a referral hospital. For each case, various variables at the time of diagnostic investigation were recorded and follow‐up obtained by telephone contact with the referring veterinarian. Results A multivariable cox model indicated that canine chronic enteropathy activity index (CCEAI) and blood urea concentration were significantly associated with death (P values <.01). For each unit increase in CCEAI, the hazard of death increased by 22.9% (confidence interval [CI]: 6.9%‐41.2%). Dogs with a CCEAI of ≤8 and dogs with urea ≤7 mmol/L survived 256 days longer (P = .001, CI: 106.7‐405.4 days) and 279 days longer (P = .009, CI: 70.0‐488.7 days) than those with a CCEAI of >8 and urea >7 mmol/L on average, respectively, when followed up for 647 days. Conclusions and Clinical Importance Increased CCEAI and blood urea concentration at the time of diagnosis might be predictive of death in dogs with PLE caused by CE or lymphangiectasia.

Background Serum feline pancreatic lipase immunoreactivity (fPL) commonly is used in the assessment of sick cats suspected to have pancreatitis but its diagnostic utility is debated. Objectives To evaluate the diagnostic utility of the Spec fPL test and selected serum biochemistry tests in the diagnosis of pancreatitis in cats. Animals Two hundred seventy‐four client‐owned cats presented to a university teaching hospital in the United Kingdom, from April 2013 to May 2017, in which Spec fPL was measured. Methods Cats were classified into 1 of 4 groups based on clinical signs (all cats), ultrasonographic findings (all cats) and histopathological or cytological assessment of the pancreas where available (9 cats) regardless of Spec fPL concentration. The groups were (a) definite pancreatitis (n = 9), (b) probable pancreatitis (n = 49), (c) possible pancreatitis (n = 139), and (d) unlikely pancreatitis (n = 77). Spec fPL and selected serum biochemistry test results were compared among groups. Results Serum fPL concentrations >5.3 μg/L were classified as positive and concentrations <3.5 μg/L were classified as negative. There was a significantly (P = .03) lower proportion of false‐positive results (cats unlikely to have pancreatitis, n = 77, with a positive fPL, n = 8, 10%) than false‐negative results (cats with definite or probable pancreatitis, n = 58, with a negative fPL result, n = 14, 24%). None of the selected biochemical tests were helpful diagnostically. Conclusion and Clinical Importance A positive Spec fPL result indicates that pancreatitis is a probable diagnosis, but the test cannot be used to rule the diagnosis out.