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Abstract Background It is unknown if serum concentrations of cobalamin, folate, canine pancreatic lipase immunoreactivity (cPLI), and canine trypsin‐like immunoreactivity (cTLI) obtained postprandially are equivalent to measurements obtained after withholding food in dogs with suspected gastrointestinal disease. Hypothesis/Objectives Measurements of serum concentrations of cobalamin, folate, cPLI, and cTLI postprandially will be equivalent to measurements after 12 hours of withholding food in dogs with signs of chronic gastrointestinal disease. Changes observed will not alter clinical interpretation. Animals 51 client‐owned dogs with signs of gastrointestinal disease. Methods Prospective single arm clinical trial. Serum concentrations of cobalamin, folate, cPLI and cTLI 2, 4, and 8 hours postprandially were compared by equivalence testing to values after withholding food for 12 hours (baseline). Results Mean serum cobalamin concentrations 2 hours (498.1 ± 213.1 ng/L; P = 0.024) and 4 hours (501.9 ± 207.4 ng/L; P = 0.008) postprandial were equivalent to baseline (517.3 ± 211.5 ng/L). Mean serum cTLI 2 hours (31.3 ± 14 μg/L; P

Abstract Background Hypertriglyceridemia (HTG) is prevalent in Miniature Schnauzers, predisposing them to life‐threatening diseases. Varied responses to management strategies suggest the possibility of multiple subtypes. Hypothesis/Objective To identify and characterize HTG subtypes in Miniature Schnauzers through cluster analysis of lipoprotein profiles. We hypothesize that multiple phenotypes of primary HTG exist in this breed. Animals Twenty Miniature Schnauzers with normal serum triglyceride concentration (NTG), 25 with primary HTG, and 5 with secondary HTG. Methods Cross‐sectional study using archived samples. Lipoprotein profiles, generated using continuous lipoprotein density profiling, were clustered with hierarchical cluster analysis. Clinical data (age, sex, body condition score, and dietary fat content) was compared between clusters. Results Six clusters were identified. Dogs with primary HTG were dispersed among 4 clusters. One cluster showed the highest intensities for triglyceride‐rich lipoprotein (TRL) and low‐density lipoprotein (LDL) fractions and also included 4 dogs with secondary HTG. Two clusters had moderately high TRL fraction intensities and low‐to‐intermediate LDL intensities. The fourth cluster had high LDL but variable TRL fraction intensities with equal numbers of NTG and mild HTG dogs. The final 2 clusters comprised only NTG dogs with low TRL intensities and low‐to‐intermediate LDL intensities. The clusters did not appear to be driven by differences in the clinical data. Conclusions and Clinical Importance The results of this study support a spectrum of lipoprotein phenotypes within Miniature Schnauzers that cannot be predicted by triglyceride concentration alone. Lipoprotein profiling might be useful to determine if subtypes have different origins, clinical consequences, and response to treatment.

Background and Aim: Magnetic resonance imaging (MRI) has been widely used as a non-invasive modality to evaluate neurological organ structures. However, brain MRI studies in cats with neurological signs are limited. This study evaluated the association between patient characteristics, neurological signs, and brain lesion locations identified by MRI. Blood profiles of cats with presumptive inflammatory and structural brain lesions were also determined. Materials and Methods: Medical records of 114 cats that underwent brain MRI were retrospectively reviewed. Cats were categorized into five groups based on the location of their lesion: Cerebrum, brainstem, cerebellum, multifocal, and non-structural. Patient characteristics, neurological signs, and hematological profiles were obtained from their medical records. Disease classification was categorized based on their etiologies. Associations were determined using Fisher's exact test. Blood parameters were compared using the Kruskal-Wallis test. Results: A total of 114 cats met the inclusion criteria. Lesions were identified in the cerebrum (21.1%), brainstem (8.8%), cerebellum (6.1%), multifocal (39.5%), and non-structural (24.6%) of the cats. Common neurological signs included seizure activity (56.1%), cerebellar signs (41.2%), and anisocoria (25.4%). The most common brain abnormality was inflammation (40.4%). There was no significant difference in hematological profiles between cats with presumptive inflammatory and non-inflammatory brain lesions. Neutrophils, platelets, total protein, and globulin concentrations were higher in cats with structural brain lesions. Conclusion: The most common neurological signs and brain disease category were seizure activity and inflammation, respectively. However, the hematological profile did not predict inflammatory and structural brain lesions. Further studies with a large number of birds are required to molecularly characterize the circulating strains of this virus in this area.

Abstract Background A panel of IgA‐based serologic assays might aid in the diagnosis of chronic enteropathy (CE) in dogs, a syndrome encompassing conditions such as food‐responsive enteropathy, immunosuppressant‐responsive enteropathy, and inflammatory bowel disease (also referred to as chronic inflammatory enteropathy). However, it is unclear whether these biomarkers discriminate between CE and other types of primary intestinal disorders. Objectives To evaluate a diagnostic panel that measures serum concentrations of IgA directed against OmpC (ACA), canine calprotectin (ACNA), and gliadin‐derived peptides (AGA) in dogs with well‐characterized intestinal diseases. Animals Fifty‐five dogs with primary intestinal disease. Methods Serum ACA, ACNA, and AGA concentrations were measured in 30 dogs with CE and 25 dogs with other intestinal diseases (non‐CE population), including histoplasmosis, parasitism, E. coli‐associated granulomatous colitis, and lymphoma. Serum IgA concentrations were compared among populations, and sensitivities and specificities were calculated using laboratory‐provided cut‐points. Results Twenty‐six of 30 (87%) CE dogs and 21 of 25 (84%) non‐CE dogs had abnormal concentrations (intermediate or high) of at least 2 markers; these proportions were not significantly different (P = .99). A serum ACA concentration ≥15 EU/mL was 86.7% (95% confidence interval [CI], 69.3%‐96.2%) sensitive and 24.0% (95% CI, 9.4%‐45.1%) specific for CE diagnosis. High AGA concentrations were observed in 16 of 25 (64%) non‐CE dogs. Conclusions and Clinical Importance The evaluated serologic markers were poorly specific for CE diagnosis, which raises concerns that their use in clinical practice might lead to misdiagnoses and delayed or even detrimental treatments in dogs with non‐CE intestinal diseases.

Abstract Background Proton pump inhibitors are administered prophylactically in dogs treated surgically for acute thoracolumbar intervertebral disc extrusion (TL‐IVDE). However, their efficacy in decreasing gastrointestinal (GI) complications is unknown. Hypothesis Omeprazole does not decrease the frequency of GI complications compared to placebo in dogs treated surgically for acute TL‐IVDE. Animals Thirty‐seven client‐owned dogs undergoing hemilaminectomy for acute TL‐IVDE. Methods Randomized double‐blinded placebo‐controlled prospective clinical trial. Dogs received PO placebo or omeprazole at 1 mg/kg q12h for 5 days during hospitalization. Development of GI signs (e.g., diarrhea, vomiting, regurgitation, hematochezia, melena) was recorded daily. Clinicopathologic testing performed during hospitalization and at 2 and 4‐week re‐evaluations included: fecal occult blood, PCV, blood urea nitrogen/creatinine ratio, fecal calprotectin, canine pancreatic lipase immunoreactivity and fecal alpha‐1 proteinase inhibitor concentrations. Omeprazole and placebo groups were compared using chi‐squared or Fisher's exact tests. Results Gastrointestinal signs developed in 10/20 (50%) dogs in the omeprazole group and in 7/17 (41%) dogs in the placebo group (P = .59). Diarrhea was common (8/20 omeprazole, 5/17 placebo), hematochezia was rare (1/20 omeprazole, 1/17 placebo); melena was not observed. Clinicopathologic evidence suggestive of bleeding was present in 9/20 dogs treated with omeprazole and in 11/17 dogs that received placebo (P = .23). Fecal occult blood positivity was more common in dogs with GI signs (P = .03). Canine pancreatic lipase immunoreactivity was higher during hospitalization compared to re‐evaluations (P = .01). Conclusions and Clinical Importance Short‐term, prophylactic omeprazole treatment did not decrease clinically detectable GI complications in dogs with acute TL‐IVDE.

Abstract Background The prevalence and clinical importance of cardiac abnormalities in dogs with acute pancreatitis (AP) is unknown. Animals Twelve dogs with AP and 60 archived serum samples from dogs with suspected AP. Methods Two‐phase study. Phase I: Analysis of archived serum samples from dogs with clinical signs of AP and high Spec cPL concentrations. High sensitivity troponin I (TnIH) and N‐terminal pro‐B‐type natriuretic peptide (NT‐proBNP) concentrations were measured in achieved serum samples. Phase II: Prospective observational study. Dogs with AP underwent echocardiography and Holter monitoring. Serum cardiac troponin I (cTnI) and plasma NT‐proBNP concentrations were measured. Previously described disease severity indices were calculated for each dog. Results Phase I: 41 of 60 dogs suspected of having AP had abnormally high TnIH concentrations and 13 of 60 had abnormally high serum NT‐proBNP concentrations. Higher TnIH concentrations were observed in dogs with Spec cPL concentration >2000 μg/L as compared to those with concentrations of 1000‐2000 μg/L. Phase II: 11 of 12 dogs diagnosed with pancreatitis had abnormal cTnI concentrations (median: 0.384 ng/mL, range: 0.041‐2.966 ng/mL, RI: ≤0.06 ng/mL) and 7 of 12 dogs had plasma NT‐proBNP concentrations above the reference interval (median: 971 pmol/L, range: 250‐2215 pmol/L, RI: ≤900 pmol/L). Supraventricular and ventricular ectopic beats occurred in 3 dogs. Echocardiographic abnormalities were detected in 5 dogs. Cardiovascular variables were not associated with indices of disease severity. Conclusions and Clinical Importance Myocardial injury is common in dogs with AP, but clinical consequences appeared to be uncommon in our small cohort. Cardiac biomarkers should be interpreted with caution in dogs with AP.

Abstract While most cases of pancreatitis in dogs are thought to be idiopathic, potential risk factors are identified. In this article we provide a state‐of‐the‐art overview of suspected risk factors for pancreatitis in dogs, allowing for improved awareness and detection of potential dog‐specific risk factors, which might guide the development of disease prevention strategies. Additionally, we review important advances in our understanding of the pathophysiology of pancreatitis and potential areas for therapeutic manipulation based thereof. The outcome of pathophysiologic mechanisms and the development of clinical disease is dependent on the balance between stressors and protective mechanisms, which can be evaluated using the critical threshold theory.

Abstract Background Miniature Schnauzers (MS) commonly have idiopathic hypertriglyceridemia (HTGL), which is associated with insulin resistance (IR) and a subclinical inflammatory phenotype. Objectives Determine the association between indicators of IR and inflammatory biomarkers in MS with and without HTGL and identify how indicators of IR are affected by dietary intervention in MS with HTGL. Animals Seventy MS with HTGL and 79 MS without HTGL. In addition, 15 MS with HTGL were placed on a low‐fat diet. Methods Serum concentrations of triglycerides, cholesterol, calprotectin, insulin, and glucose were compared between groups. Results Serum glucose and calprotectin concentrations (shown to be higher in MS with HTGL than in MS without HTGL) were inversely correlated (ρ = −.28; P

Hyperadrenocorticism (HAC) often leads to vacuolar hepatopathy. The impact of trilostane treatment on serum total bile acids (SBAs) concentrations in dogs with HAC remains unknown. This study investigated SBAs concentrations in healthy dogs and those with HAC following trilostane therapy. Ten healthy dogs and fifteen dogs with HAC were prospectively enrolled. A biochemistry profile and pre- and post-prandial SBAs concentrations were determined in each dog. Dogs with HAC were reassessed at 1 and 3 months after the initiation of trilostane treatment. Dogs with HAC had significantly higher serum ALT, ALP, and GGT activities, and cholesterol, triglyceride, and pre-prandial SBAs concentrations compared to healthy dogs. After 3 months of trilostane treatment, polyuria/polydipsia and polyphagia were completely resolved in 42.8% and 35.7%, respectively. Significant improvements in serum ALT and ALP activities and cholesterol concentrations were observed within 1–3 months of trilostane treatment. However, pre- and post-prandial SBAs concentrations did not significantly decrease. These findings suggest that treatment with low-dose trilostane for 3 months appears to reduce serum liver enzyme activities, but not SBAs concentrations. Further investigation is warranted to explore the effects of low-dose trilostane treatment on SBAs concentrations for a longer duration or after achieving appropriate post-ACTH cortisol levels.

Chronic inflammatory enteropathies (CIEs) in dogs involve the infiltration of gastrointestinal tissue with inflammatory cells. This study aimed to assess the sensitivity of serum and fecal 3-bromotyrosine (3-BrY) concentrations in dogs with CIE. The difference in 3-BrY concentrations in dogs with different gastrointestinal (GI) pathological changes was also assessed. In total, 68 dogs with CIE were enrolled in the study. The median serum 3-BrY concentration was 3.3 µmol/L, while the median 3-day mean and maximum fecal 3-BrY concentrations were 38.9 and 63.2 mmol/g of feces, respectively. The median serum C-reactive protein concentration was 45.0 mg/L. The median 3-day mean and maximum fecal α1-proteinase inhibitor concentrations were 6.1 and 9 µg/g of feces, respectively. Increased 3-BrY concentrations were observed in 90.9% of CIE dogs based on serum concentrations, 75.8% based on mean fecal concentrations, and 69.4% based on maximum fecal concentrations. A weak correlation (ρ = 0.31, p < 0.0118) was found between serum CRP and serum 3-BrY concentrations. There was no correlation between the canine chronic enteropathy clinical activity index and serum or fecal 3-BrY concentrations (p > 0.05). Additionally, no significant difference in serum or fecal 3-BrY concentrations was found among CIE dogs with different GI pathological changes (p > 0.05). In conclusion, dogs with CIE have increased 3-BrY concentrations in serum and fecal samples. However, 3-BrY concentrations may not accurately indicate the severity of gastrointestinal inflammation.

Background and Aim: Although cats are not natural hosts for heartworm infections (Dirofilaria immitis), evidence suggests that feline heartworm disease can be detrimental because of a severe inflammatory response. Recent studies have found that infection with bacteria of the genus Wolbachia is the principal cause of acute inflammatory filaria disease; nonetheless, the prevalence of cats naturally infected with heartworms and Wolbachia remains unclear. This study aimed to estimate the prevalence and current distribution of feline heartworm disease and its association with Wolbachia infection in pet and semi-domesticated cats in Bangkok, Thailand. Materials and Methods: A total of 260 cats (130 pet cats and 130 semi-domesticated cats) were enrolled in this study. Blood samples were placed into ethylenediaminetetraacetic acid tubes for hematological analysis and DNA extraction. A polymerase chain reaction (PCR) was performed to analyze samples for the presence of D. immitis and Wolbachia infections. Results: The prevalence (95% confidence interval [CI]) of D. immitis infection in pet, semi-domesticated, and all cats were 3.9% (1.3-8.8%), 27.7% (20.2-36.2%), and 19.6% (15.0-25.0%), respectively. The prevalence (95% CI) of Wolbachia infection in pet, semi-domesticated, and all cats were 18.5% (12.2-26.2%), 31.5% (23.7-40.3%), and 25.0% (19.9-30.7%), respectively. The prevalence of D. immitis and Wolbachia infections in semi-domesticated cats was significantly higher than in pet cats (p=0.002 and p=0.022, respectively). There was a significant association between D. immitis and Wolbachia infections (p

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

Abstract In the last 20 years, the diagnosis of pancreatitis has become more frequent as a result of improved diagnostic modalities such as abdominal ultrasound examination, advanced imaging, and immunoassays for the measurement of pancreatic lipase. Our aim is to provide a state‐of‐the‐art overview of the clinical diagnosis of acute pancreatitis (AP) in dogs with a particular focus on pancreatic lipase assay validation and clinical performance, in addition to advanced imaging modalities. We also discuss the potential indications for cytology and histopathology in dogs with suspected AP.

Abstract Background Cats with moderate to advanced chronic kidney disease (CKD) often display clinical signs such as vomiting and decreased appetite, and frequently receive omeprazole or other acid suppressants despite a lack of evidence to support their use. Hypothesis/Objectives To evaluate the effect of once‐daily PO omeprazole on appetite in cats with CKD. We hypothesized that omeprazole would improve subjective appetite assessments in cats with CKD. Animals Fourteen client‐owned cats with International Renal Interest Society (IRIS) stage 2 or 3 CKD and hyporexia. Methods Cats were prospectively enrolled in a multi‐institutional, double‐blinded, randomized, crossover study to evaluate the effect of a 14‐day trial of once‐daily PO omeprazole (1 mg/kg) or placebo (lactose gel capsule) on vomiting frequency and appetite. A daily log was completed by the owner during all treatment and rest periods to assess appetite using a subjective, qualitative, and 5‐point scoring system. Mixed model analyses of variance were performed to determine if average daily percentage food consumed or appetite score, as measured by subjective owner assessment, differed between treatments. Results Compared to placebo, a negligible but statistically significant difference in percentage of food consumed was observed between treatments (P = .04) with once‐daily omeprazole treatment resulting in a 2.7% increase in food consumption compared to placebo. No significant difference, however, was found in appetite score, body weight, or serum creatinine concentration between treatments. Conclusions and Clinical Importance Once‐daily omeprazole does not markedly increase appetite in cats with CKD and should not be used as a first‐line treatment in the absence of evidence of gastrointestinal ulceration.

Abstract Background Serum feline pancreatic lipase immunoreactivity (fPLI) and trypsin‐like immunoreactivity (fTLI) concentrations are commonly used in cats for the evaluation of pancreatic disease. The effect of kidney disease on these tests in cats are unknown. Objective To investigate the effect of experimentally induced chronic kidney disease (CKD) on serum fPLI and fTLI concentrations. Animals Surplus serum samples from 20 cats with CKD experimentally induced for an unrelated project and a group of healthy control cats. Methods Serum fTLI and fPLI concentrations were compared between groups. Results Mean (±SD) serum fTLI concentrations in 20 cats with CKD (117.8 ± 63.6 μg/L) were significantly higher than those in healthy cats (n = 32; 46.9 ± 17.5 μg/L; P

Miniature Schnauzers are predisposed to develop pancreatitis, with familial hypertriglyceridemia (HTG) described as a potential risk factor. Diagnosing pancreatitis in dogs is based on the integration of serum canine-specific pancreatic lipase (cPLI) concentration, clinical presentation, and diagnostic imaging findings. However, markers of systemic inflammation and antiprotease activity have not been extensively investigated in the characterization and prognostication of pancreatitis in dogs. Serum concentrations of alpha1-proteinase inhibitor (α1PI; as a marker of systemic antiprotease response) and calprotectin and S100A12 (as markers of systemic inflammation) were measured in serum samples from 35 Miniature Schnauzers diagnosed with pancreatitis (serum cPLI concentration >400 μg/L, clinical signs, abdominal imaging findings). These markers were evaluated for possible associations with patient characteristics, clinical presentation, risk factors for pancreatitis, and outcome. The study showed that biomarkers of systemic inflammation and antiprotease activity are commonly increased in Miniature Schnauzers with pancreatitis. Whereas serum calprotectin and S100A12 concentrations were found to have limited utility in differentiating pancreatitis presentations, serum α1PI concentrations and potentially also the serum calprotectin-to-S100A12 ratio might be non-invasive surrogate markers of disease severity in dogs with pancreatitis.

Abstract Diabetes mellitus (DM) is associated with a dysfunctional intestinal barrier and an increased risk for systemic infection and inflammation in people, though the pathogenic mechanisms leading to this are poorly understood. Using a canine model of DM, we showed that the peroxisomal proliferator-activated receptor-α agonist fenofibrate modulates plasma lipid profiles and markers of intestinal barrier function. A 3-week course of fenofibrate reduced fasting interstitial glucose and inflammatory cytokine IL-8 and TNF-α concentrations, which correlated with reduced triglyceride levels. The lipidomic profile exhibited significantly lower levels of triacylglycerols, phosphatidylethanolamines, diacylglycerols, and ceramides following fenofibrate administration. On histopathological analysis, we observed an aberrant amount of intraepithelial CD3+ T lymphocytes (IEL) in the small intestine of dogs with spontaneous and induced-DM. Fenofibrate reduced IEL density in the duodenum of dogs with DM and enhanced markers of intestinal barrier function in vivo and in vitro. There were minimal changes in the intestinal microbial composition following fenofibrate administration, suggesting that repair of intestinal barriers can be achieved independently of the resident microbiota. Our findings indicate that lipid metabolism is critical to functionality of the intestinal epithelium, which can be rescued by PPARα activation in dogs with DM.

Abstract Background Established treatment protocols for schistosomiasis (Heterobilharzia americana) in dogs are expensive. Anecdotal reports suggest that lower doses of praziquantel, combined with fenbendazole, may eliminate asymptomatic infections. Objectives Evaluate the efficacy of a low‐dose praziquantel and fenbendazole protocol to manage asymptomatic schistosomiasis in dogs and compare fecal saline sedimentation (FSS) and fecal PCR (FPCR) for therapeutic monitoring. Animals Twelve asymptomatic dogs with positive FPCR and FSS results for schistosomiasis. Methods Prospective observational study. On day 0, dogs received praziquantel at a median dose of 5 mg/kg PO q8h for 2 days, with fenbendazole at 24 mg/kg PO q24h for 7 days. Fecal PCR and FSS were repeated in all dogs on days 30, 60, and 90. Results By day 30, 10 of 12 dogs were negative by FSS, but only 3 of 12 were negative by FPCR. By day 60, all 12 dogs were negative by FSS, and 8 of 12 had become negative by FPCR. By day 90, all 12 dogs remained negative by FSS, but 5 of 12 were positive by FPCR (including 2 that were negative by FPCR on day 60). Three dogs that were positive by FPCR on day 60 were re‐treated and subsequently became both FPCR and FSS negative. One FPCR‐positive dog developed a mild increase in serum ALP activity, another developed mild hypercalcemia, and a third developed diarrhea. Conclusions and Clinical Importance A low‐dose praziquantel/fenbendazole protocol may be effective for asymptomatic schistosomiasis in some dogs, but monitoring to ensure treatment success is recommended. Fecal saline sedimentation and FPCR may demonstrate discrepant results, with FPCR being positive more frequently.

Cobalamin deficiency is a common sequela of chronic enteropathies (CE) in dogs. Studies comparing the intestinal microbiome of CE dogs with cobalamin deficiency to those that are normocobalaminemic are lacking. Therefore, our aim was to describe the fecal microbiome in a prospective, comparative study evaluating 29 dogs with CE and cobalamin deficiency, 18 dogs with CE and normocobalaminemia, and 10 healthy control dogs. Dogs with cobalamin deficiency were also analyzed after oral or parenteral cobalamin supplementation. Overall microbiome composition (beta diversity) at baseline was significantly different in CE dogs with cobalamin deficiency when compared to those with normocobalaminemia (p = 0.001, R = 0.257) and to healthy controls (p = 0.001, R = 0.363). Abundances of Firmicutes and Actinobacteria were significantly increased (q = 0.010 and 0.049), while those of Bacteroidetes and Fusobacteria were significantly decreased (q = 0.002 and 0.014) in CE dogs with cobalamin deficiency when compared to healthy controls. Overall microbiome composition in follow-up samples remained significantly different after 3 months in both dogs receiving parenteral (R = 0.420, p = 0.013) or oral cobalamin supplementation (R = 0.251, p = 0.007). Because cobalamin supplementation, in combination with appropriate therapy, failed to restore the microbiome composition in the dogs in our study, cobalamin is unlikely to be the cause of those microbiome changes but rather an indicator of differences in underlying pathophysiology that do not influence clinical severity but result in a significant aggravation of dysbiosis.

Abstract Background Culture‐based assessment of the fecal microbiome using fecal culture profiles frequently is performed in dogs with chronic diarrhea, but the diagnostic value of this approach has not been determined. Objectives To compare the reported results of fecal culture profiles and the polymerase chain reaction‐based dysbiosis index (DI) between dogs with chronic diarrhea and healthy dogs; to assess interlaboratory variability in bacterial and fungal cultures among 3 veterinary diagnostic laboratories (diagnostic laboratory 1 [L1], diagnostic laboratory 2 [L2], diagnostic laboratory 3 [L3]); and to compare the reported interpretation of culture profiles (normobiosis versus dysbiosis) with those of the DI. Animals Eighteen dogs with chronic diarrhea (CDG) and 18 healthy control dogs (HG). Methods In this prospective, case‐control study, fecal samples were submitted to 3 commercial laboratories for fecal culture. The microbiota was assessed using PCR assays. Dogs receiving antimicrobials were excluded. Results Dysbiosis index was significantly increased in CDG (mean, 0.9; SD, 3.8; 95% confidence interval [CI], −1.0; 2.8) compared to HG (mean, −3.0; SD, 2.8; CI, −4.3; −1.6; P = .0002), whereas cultures from all laboratories failed to detect significant differences (P = .66, .18, and .66, respectively). Hemolytic Escherichia coli was the only potential enteropathogen on culture, but no significant difference was found between CDG and HG. For diagnosis of dysbiosis, culture showed no agreement with DI (L1, κ = −0.21; CI, −0.44; −0.02; L2, κ = −0.33; CI, −0.58; −0.08; L3, κ = −0.25; CI, −0.39; −0.11). Furthermore, variability among the 3 laboratories was high (L1/L2, κ = 0.15; CI, −0.05; 0.35; L1/L3, κ = −0.08; CI, −0.01; −0.16; L2/L3, κ = −0.06; CI, −0.33; −0.20). Conclusions and clinical importance Fecal cultures failed to distinguish between diseased and healthy dogs, and a high level of interlaboratory variation for culture was found.

Abstract Background Integrating immunohistochemistry (IHC) and clonality testing with histopathology may improve the ability to differentiate inflammatory bowel disease (IBD) and alimentary small cell lymphoma (LSA) in cats. Hypothesis/Objectives To evaluate the utility of histopathology, IHC, and clonality testing to differentiate between IBD and LSA and agreement of diagnostic results for endoscopic biopsy (EB) samples from the upper (USI) and lower small intestine (LSI). Animals Fifty‐seven cats with IBD or LSA. Methods All cases were categorized as definitive IBD (DefIBD), possible LSA (PossLSA), probable LSA (ProbLSA), or definitive LSA (DefLSA) based on histopathology alone. Results from IHC and clonality testing were integrated. Results Based on histopathology alone, 24/57 (42.1%), 15/57 (26.3%), and 18/57 (31.6%) cats were diagnosed with DefIBD, PossLSA or ProbLSA, and DefLSA, respectively. After integrating IHC and clonality testing, 11/24 cases (45.8%) and 15/15 cases (100%) previously categorized as DefIBD and PossLSA or ProbLSA, respectively, were reclassified as LSA. A final diagnosis of IBD and LSA was reported in 13/57 (22.8%) and 44/57 (77.2%) cats, respectively. Agreement between USI and LSI samples was moderate based on histopathology alone (κ = 0.66) and after integrating IHC and clonality testing (κ = 0.70). However, only 1/44 (2.3%) of the LSA cases was diagnosed based on LSI biopsy alone. Conclusions and Clinical Importance Integrating IHC and clonality testing increased the number of cases diagnosed with LSA, but the consequence for patient outcome is unclear. There was moderate agreement between USI and LSI samples. Samples from the LSI rarely changed the diagnosis.

Abstract Background Current tests for diagnosis and differentiation of lymphoplasmacytic enteritis (LPE) and small cell lymphoma (SCL) in cats are expensive, invasive, and lack specificity. The identification of less invasive, more reliable biomarkers would facilitate diagnosis. Objectives To characterize the mucosal proteome in endoscopically obtained, small intestinal tissue biopsy specimens. We hypothesized that differentially expressed proteins could be identified and serve as biomarker candidates for the differentiation of LPE and SCL in cats. Animals Six healthy control cats, 6 cats with LPE, and 8 cats with SCL. Methods The mucosal proteome was analyzed using 2‐dimensional fluorescence difference gel electrophoresis (2D DIGE) and nanoflow liquid chromatography tandem mass spectrometry. For 5 proteins, results were verified by Western blot analysis. Results A total of 2349 spots were identified, of which 9 were differentially expressed with a ≥2‐fold change between healthy cats and cats with LPE and SCL (.01 < P

Abstract Background Metronidazole has a substantial impact on the gut microbiome. However, the recovery of the microbiome after discontinuation of administration, and the metabolic consequences of such alterations have not been investigated to date. Objectives To describe the impact of 14‐day metronidazole administration, alone or in combination with a hydrolyzed protein diet, on fecal microbiome, metabolome, bile acids (BAs), and lactate production, and on serum metabolome in healthy dogs. Animals Twenty‐four healthy pet dogs. Methods Prospective, nonrandomized controlled study. Dogs fed various commercial diets were divided in 3 groups: control group (no intervention, G1); group receiving hydrolyzed protein diet, followed by metronidazole administration (G2); and group receiving metronidazole only (G3). Microbiome composition was evaluated with sequencing of 16S rRNA genes and quantitative polymerase chain reaction (qPCR)‐based dysbiosis index. Untargeted metabolomics analysis of fecal and serum samples was performed, followed by targeted assays for fecal BAs and lactate. Results No changes were observed in G1, or G2 during diet change. Metronidazole significantly changed microbiome composition in G2 and G3, including decreases in richness (P

Abstract Background Sensitivity and specificity for commercial and in‐house pancreatic lipase immunoreactivity (cPLI) assays have been reported, but repeatability under routine clinical conditions is unknown. Objectives To determine: Coefficient of variation (CV) between replicates of a commercial assay (Spec cPL) and 2 in‐house assays (VetScan cPL, Vcheck cPL) under routine conditions. Effects of sample condition or personnel on results. Potential directional bias between assays. Animals Serum from 12 canine clinical patients. Methods Prospective study. Serum Spec cPL, VetScan cPL, and Vcheck cPL (6 aliquots each) were measured, and CVs were calculated, effects of sample condition and personnel were assessed using a linear mixed model, and direction of bias was assessed using least square mean cPLI concentration. Results Mean %CVs for Spec cPL, VetScan cPL, and Vcheck cPL were 5.5, 17.0, and 23.7%. Three of 6 VetScan cPL samples and 5/9 Vcheck cPL samples had an unacceptably high %CV (>20%). Transportation (Spec cPL) and sample condition or personnel (VetScan cPL, Vcheck cPL) did not affect repeatability. Least square mean cPL was higher for Spec cPL (807.9 μg/L) than for VetScan cPL (558.5 μg/L) or Vcheck cPL (399.8 μg/L). Conclusions and Clinical Importance For clinical use, the commercial Spec cPL has the highest repeatability, and Vcheck cPL has significantly lower repeatability. Both in‐house assays evaluated may provide discrepant categorical results (“pancreatitis” versus “equivocal” versus “not pancreatitis”) for the same sample. In‐house pancreatic lipase concentrations may be lower than those determined by the Spec cPL assay.

Abstract Background Despite limited evidence of efficacy, antibiotic treatment is still frequently prescribed in dogs with uncomplicated acute diarrhea (AD). Objective To assess whether amoxicillin‐clavulanic acid has a clinical benefit, an effect on the fecal microbiome, and the proportion of amoxicillin‐resistant Escherichia coli in dogs with AD. Animals Sixteen dogs with AD of .99). All dogs gained normal clinical scores (CADS index ≤3) after 1 to 6 days (median 2 days) after presentation. There was no significant difference in the fecal dysbiosis index (during treatment: AG mean −2.6 (SD 3.0; CI [−5.1; 0.0]); PG mean −0.8 (SD 4.0; CI [−4.2; 2.5]; P > .99) or its bacterial taxa. The proportion of resistant fecal E. coli increased (to median: 100%; range: 35%‐100%) during treatment with amoxicillin‐clavulanic acid and was still increased (median: 10%; range 2%‐67%) 3 weeks after treatment, both of which were significantly higher proportions than in the placebo group for both time points (during treatment AG median 100% versus PG median 0.2% (P

Abstract Background Previous studies have reported an association between hyperlipidemia and pancreatitis in dogs, but details of this association remain poorly defined. Hypothesis/Objectives To compare serum triglyceride and cholesterol concentrations and lipoprotein profiles between dogs with naturally occurring pancreatitis and healthy dogs. Animals Seventeen dogs with a clinical diagnosis of pancreatitis (Group 1) and 53 healthy control dogs (Group 2). Methods Prospective case‐control study. Results In Group 1, 3/17 dogs (18%) had hypertriglyceridemia whereas in Group 2, 4/53 dogs (7.5%) had hypertriglyceridemia (odds ratio [OR], 2.63; 95% confidence interval [CI], 0.52‐13.14; P = .35). A significant difference was found in serum triglyceride concentrations between Group 1 (median, 67 mg/dL) and Group 2 (median, 54 mg/dL; P = .002). In Group 1, 4/17 dogs (24%) had hypercholesterolemia, whereas 1/53 (1.9%) dogs in Group 2 had hypercholesterolemia (OR, 16; 95% CI, 1.64‐155.5; P = .01). No significant difference was found in serum cholesterol concentrations between Group 1 (median, 209 mg/dL) and Group 2 (median, 227 mg/dL; P = .56). Lipoprotein profiles were significantly different between Group 1 and Group 2 dogs (Eigenvalues, 0.6719; R2 = 1.0; P = .001). Conclusions and Clinical Importance Most dogs with pancreatitis (>70%) had serum triglyceride and cholesterol concentrations within reference intervals. In the small percentage of dogs that had hypertriglyceridemia, hypercholesterolemia, or both, increases were mild. Important differences were identified in lipoprotein profiles between dogs with pancreatitis and healthy control dogs. Dogs with pancreatitis had higher low‐density lipoprotein fractions and lower triglyceride‐rich lipoprotein and high‐density lipoprotein fractions than healthy dogs.

Abstract Background Differentiation of lymphocytic‐plasmacytic enteropathy (LPE) from small cell lymphoma (SCL) in cats can be challenging. Hypothesis/Objective Histology‐guided mass spectrometry (HGMS) is a suitable method for the differentiation of LPE from SCL in cats. Animals Forty‐one cats with LPE and 52 cats with SCL. Methods This is a retrospective clinicopathologic study. Duodenal tissue samples of 17 cats with LPE and 22 cats with SCL were subjected to HGMS, and the acquired data were used to develop a linear discriminate analysis (LDA) machine learning algorithm. The algorithm was subsequently validated using a separate set of 24 cats with LPE and 30 cats with SCL. Cases were classified as LPE or SCL based on a consensus by an expert panel consisting of 5‐7 board‐certified veterinary specialists. Histopathology, immunohistochemistry, and clonality testing were available for all cats. The panel consensus classification served as a reference for the calculation of test performance parameters. Results Relative sensitivity, specificity, and accuracy of HGMS were 86.7% (95% confidence interval [CI]: 74.5%‐98.8%), 91.7% (95% CI: 80.6%‐100%), and 88.9% (95% CI: 80.5%‐97.3%), respectively. Comparatively, the clonality testing had a sensitivity, specificity, and accuracy of 85.7% (95% CI: 72.8%‐98.7%), 33.3% (95% CI: 14.5%‐52.2%), and 61.5% (95% CI: 48.3%‐74.8%) relative to the panel decision. Conclusions and Clinical Importance Histology‐guided mass spectrometry was a reliable technique for the differentiation of LPE from SCL in duodenal formalin‐fixed paraffin‐embedded samples of cats and might have advantages over tests currently considered state of the art.

Isoprostanes are stable end products of lipid peroxidation that can be used as markers of oxidative stress. It was previously reported that a cohort of dogs with various liver diseases had increased urinary isoprostane concentrations compared to healthy control (HC) dogs. The aim of this study was to measure and report urinary isoprostane concentrations in dogs with different types of liver diseases. Urine was collected from 21 HC dogs and from 40 dogs with liver disease, including 25 with chronic hepatitis (CH), 7 with steroid hepatopathy (SH), and 8 with a congenital portosystemic shunt (CPSS). In this prospective, observational study, urinary 15-F2t-isoprostane (F2-IsoP) concentrations were measured by liquid chromatography/mass spectrometry and normalized to urinary creatinine concentrations. Concentrations were compared between groups using a Kruskal–Wallis test followed by Dunn’s multiple comparisons tests. Significance was set at p < 0.05. The median (range) urinary F2-IsoP to creatinine ratios (ng/mg UCr) were 3.6 (2.2–12.4) for HC dogs, 5.7 (2.4–11.3) for dogs with CH, 4.8 (2.4–8.6) for dogs with SH, and 12.5 (2.9–22.9) for dogs with CPSS. CPSS dogs had significantly higher urinary F2-IsoP concentrations than HC dogs (p = 0.004), suggesting increased oxidative stress among this cohort.

Abstract Background Tylosin is commonly prescribed to dogs with diarrhea. Orally administered antibiotics may alter the intestinal microbiota, which is responsible for crucial key bile acid (BA) biotransformation reactions. Objectives To prospectively evaluate the impact of tylosin administration on fecal microbiota and unconjugated bile acids (UBAs) over time. Animals Sixteen healthy adult dogs. Methods Prospective, randomized controlled clinical trial. Dogs were randomized to receive 20 mg/kg of tylosin or a placebo capsule PO q12h for 7 days while undergoing daily fecal scoring. Fecal samples were collected on days 0, 7, 21, and 63. The microbiota was assessed using quantitative PCR and 16S rRNA gene sequencing. Unconjugated BAs were assessed using gas chromatography‐mass spectrometry (GC‐MS). Results Fecal scores were unchanged during placebo and tylosin administration. In the placebo group, no significant changes were observed in fecal microbiota or UBA concentrations. Day 7 samples from tylosin‐exposed dogs exhibited decreased bacterial diversity (observed species, Chao1, Shannon, P

Abstract Background Accumulating evidence shows an important relationship between the gastrointestinal (GI) microbiota and host health. Microbial metabolites are believed to play a critical role in host‐microbial interactions. Short‐chain fatty acids (SCFAs) are major end products of bacterial carbohydrate fermentation in the intestinal tract. Decreased concentrations of SCFAs have been observed in humans with GI disease. However, large‐scale clinical data in dogs are lacking. Hypothesis/Objective To evaluate fecal concentrations of SCFAs and the fecal microbiota in healthy control (HC) dogs and dogs with chronic enteropathy (CE). Animals Forty‐nine privately owned HC dogs and 73 dogs with CE. Methods Prospective cohort study. Fecal concentrations of SCFAs were measured using gas chromatography/mass spectrometry. Illumina sequencing and quantitative real‐time polymerase chain reaction were utilized to evaluate the fecal microbiota. Results Fecal concentrations (median [range] μmol/g of dry matter) of acetate were lower (P = .03) in dogs with CE (185.8 [20.1‐1042.1]) than in HC dogs (224.0 [87.7‐672.8]). Propionate were also lower (P

Abstract Background Chronic hepatopathies present a diagnostic challenge, with different diseases being associated with similar clinical and laboratory findings. Characterization of dogs with chronic hepatopathies can be difficult and require costly diagnostic procedures such as acquisition of a liver biopsy specimen. Noninvasive and inexpensive biomarkers that reliably characterize chronic hepatopathies such as chronic hepatitis or a congenital portosystemic vascular anomaly may decrease the need for costly or invasive diagnostic testing and guide novel therapeutic interventions. Objective To investigate differences in the serum metabolome among healthy dogs, dogs with congenital portosystemic shunts, and dogs with chronic hepatitis. Animals Stored serum samples from 12 healthy dogs, 10 dogs with congenital portosystemic shunts, and 6 dogs with chronic hepatitis were analyzed. Methods The serum metabolome was analyzed with an untargeted metabolomics approach using gas chromatography–quadrupole time of flight mass spectrometry. Results Principal component analysis and heat dendrogram plots of the metabolomics data showed clustering among individuals in each group. Random forest analysis showed differences in the abundance of various metabolites including increased aromatic amino acids and xylitol in dogs with congenital portosystemic shunts. Based on the univariate statistics, 50 metabolites were significantly different among groups. Conclusions and Clinical Importance The serum metabolome varies among healthy dogs, dogs with congenital portosystemic shunts, and dogs with chronic hepatitis. Statistical analysis identified several metabolites that differentiated healthy dogs from dogs with vascular or parenchymal liver disease. Further targeted assessment of these metabolites is needed to confirm their diagnostic reliability.

Serum concentrations of feline pancreatic lipase immunoreactivity (fPLI), feline trypsin-like immunoreactivity (fTLI), and cobalamin are commonly used for the diagnostic investigation of cats with gastrointestinal signs. No information on these parameters in healthy cats less than 1 year of age exists. We aimed to evaluate serum concentrations of fPLI, fTLI, and cobalamin in healthy cats at different time-points during their first 12 months of life. Fourteen healthy 2-month-old kittens were included. Blood was collected at 2, 3, 4, 6, and 12 months of age, and serum concentrations of fPLI, fTLI, and cobalamin were measured. While there was a statistically significant difference in serum fPLI concentrations over time, there was no statistically significant difference between individual time-points. There was no significant difference in serum fTLI concentrations over time. Serum cobalamin concentrations were below the reference interval in 3/13 cats at 2 months of age and were significantly lower by 3 months, when 13/14 had hypocobalaminemia. By 12 months, serum cobalamin had significantly increased, yet 4/12 cats still had hypocobalaminemia. Serum fPLI and fTLI concentrations did not show any statistically or clinically significant differences in young kittens. In contrast, serum cobalamin concentrations were commonly below the reference interval in kittens. Serum fPLI and fTLI concentrations are not practically affected by age in kittens as young as 2 months of age and could be used for the investigation of pancreatic diseases.

Limited data exist regarding the full array of clinical signs seen in dogs with pancreatitis and potential risk factors for the disease. Laboratory submissions from the Gastrointestinal Laboratory at Texas A&M University were retrospectively reviewed for dogs with an increased serum pancreatic lipase immunoreactivity (cPLI) concentration (≥400 µg/L), and an internet-based survey was distributed to the attending veterinarian and/or technician on each case. The survey contained questions related to (i) clinical signs, (ii) prior gastrointestinal upset, (iii) comorbidities, (iv) pre-existing medical therapies, and (v) dietary history. One hundred and seventy (170) survey responses were recorded. The top three clinical signs reported were inappetence (62%), diarrhea (53%), and vomiting (49%). Abdominal pain was noted in only 32% of dogs, likely associated with poor pain detection. Additionally, the majority of dogs (71%) had prior episodes of gastrointestinal upset within the past 12 months, lending support for the commonality of recurrent acute pancreatitis, or acute on chronic disease. Hepatobiliary abnormalities (24%) were the most common concurrent disease, and endocrine disorders were seen in a low proportion of respondents (5–8%). Adult maintenance diets (65%), dog treats (40%), and human foods (29%) were commonly consumed by dogs prior to the discovery of increased cPLI concentration.

The aim was to characterize differences in fecal consistency, and fecal microbiota and metabolome profiles in dogs with acute diarrhea (AD) treated with either fecal microbiota transplantation as enema (FMT; n = 11) or oral metronidazole (MET; n = 7) for 7 days. On days 0, 7, and 28 fecal samples were obtained. Fecal samples from healthy dogs (HC; n = 14) were used for comparison. Samples were analyzed by the previously validated qPCR based canine Dysbiosis Index (DI; increased values indicate microbiota dysbiosis) and 16S rRNA gene sequencing. The fecal metabolome was analyzed using a previously validated targeted canine assay for fecal unconjugated bile acids, and untargeted metabolomics. Fecal consistency improved significantly in dogs treated with FMT and MET by day 7 and day 28 (p < 0.01) compared to day 0. However, on day 28 fecal consistency was significantly better in FMT compared to MET (p = 0.040). At day 0, dogs with AD had an altered microbiota indicated by significantly increased DI, decreased alpha-diversity, and altered beta-diversity. In the FMT group, the DI decreased over time, while MET led to a significant increase in the dysbiosis index at day 7 and 28 compared to FMT. Sequencing data revealed that in FMT microbial diversity and beta-diversity was similar to HC at day 28, while in MET these parameters were still significantly different from HC. In dogs treated with FMT, a decrease in cholic acid and the percentage of primary bile acids was observed, whereas treatment with metronidazole led to an increase in cholic acid at day 7 and an increase in percentage of primary bile acids over time. Based on untargeted metabolomics, dogs with AD had an altered fecal metabolome compared to HC. Dogs treated with FMT clustered closer to HC at day 28, while dogs treated with MET did not. In this pilot study, dogs with AD had significant differences in fecal microbiota and metabolome profiles. Dogs treated with MET still had altered microbial and metabolic profiles at day 28 compared to dogs treated with FMT or healthy dogs.

The long-term impact of antibiotics on the serum and fecal metabolome of kittens has not yet been investigated. Therefore, the objective of this study was to evaluate the serum and fecal metabolome of kittens with an upper respiratory tract infection (URTI) before, during, and after antibiotic treatment and compare it with that of healthy control cats. Thirty 2-month-old cats with a URTI were randomly assigned to receive either amoxicillin/clavulanic acid for 20 days or doxycycline for 28 days, and 15 cats of similar age were enrolled as controls. Fecal samples were collected on days 0, 20/28, 60, 120, and 300, while serum was collected on days 0, 20/28, and 300. Untargeted and targeted metabolomic analyses were performed on both serum and fecal samples. Seven metabolites differed significantly in antibiotic-treated cats compared to controls on day 20/28, with two differing on day 60, and two on day 120. Alterations in the pattern of serum amino acids, antioxidants, purines, and pyrimidines, as well as fecal bile acids, sterols, and fatty acids, were observed in antibiotic-treated groups that were not observed in control cats. However, the alterations caused by either amoxicillin/clavulanic acid or doxycycline of the fecal and serum metabolome were only temporary and were resolved by 10 months after their withdrawal.

Abstract Background Previous data suggest that fecal S100A12 has clinical utility as a biomarker of chronic gastrointestinal inflammation (idiopathic inflammatory bowel disease) in both people and dogs, but the effect of gastrointestinal pathogens on fecal S100A12 concentrations is largely unknown. The role of S100A12 in parasite and viral infections is also difficult to study in traditional animal models due to the lack of S100A12 expression in rodents. Thus, the aim of this study was to evaluate fecal S100A12 concentrations in a cohort of puppies with intestinal parasites (Cystoisospora spp., Toxocara canis, Giardia sp.) and viral agents that are frequently encountered and known to cause gastrointestinal signs in dogs (coronavirus, parvovirus) as a comparative model. Methods Spot fecal samples were collected from 307 puppies [median age (range): 7 (4−13) weeks; 29 different breeds] in French breeding kennels, and fecal scores (semiquantitative system; scores 1−13) were assigned. Fecal samples were tested for Cystoisospora spp. (C. canis and C. ohioensis), Toxocara canis, Giardia sp., as well as canine coronavirus (CCV) and parvovirus (CPV). S100A12 concentrations were measured in all fecal samples using an in-house radioimmunoassay. Statistical analyses were performed using non-parametric 2-group or multiple-group comparisons, non-parametric correlation analysis, association testing between nominal variables, and construction of a multivariate mixed model. Results Fecal S100A12 concentrations ranged from < 24−14,363 ng/g. Univariate analysis only showed increased fecal S100A12 concentrations in dogs shedding Cystoisospora spp. (P = 0.0384) and in dogs infected with parvovirus (P = 0.0277), whereas dogs infected with coronavirus had decreased fecal S100A12 concentrations (P = 0.0345). However, shedding of any single enteropathogen did not affect fecal S100A12 concentrations in multivariate analysis (all P > 0.05) in this study. Only fecal score and breed size had an effect on fecal S100A12 concentrations in multivariate analysis (P < 0.0001). Conclusions An infection with any single enteropathogen tested in this study is unlikely to alter fecal S100A12 concentrations, and these preliminary data are important for further studies evaluating fecal S100A12 concentrations in dogs or when using fecal S100A12 concentrations as a biomarker in patients with chronic idiopathic gastrointestinal inflammation.

Abstract Background Intestinal mucosal S100A12 and myeloperoxidase (MPO) are inflammatory biomarkers in humans with inflammatory bowel disease (IBD). However, these biomarkers have not been studied in the intestinal mucosa of dogs with chronic enteropathies (CE), even though dogs with CE have increased S100A12 concentrations in feces and serum. This study investigated mucosal S100A12 concentrations and MPO activities in both dogs with CE and healthy Beagles. ELISA (S100A12 concentrations) and spectrophotometric methods (MPO activity) were used. The associations of both biomarkers with canine IBD activity index (CIBDAI), histopathologic findings, clinical outcome, and serum albumin concentrations were also investigated. We studied intestinal mucosal samples originating from different intestinal regions of 40 dogs with CE and 18 healthy Beagle dogs (duodenum, ileum, colon, and cecum). Results Compared with healthy Beagles, mucosal S100A12 concentrations in dogs with CE were significantly higher in the duodenum (p

Background Calprotectin is a marker of inflammation, but its clinical utility in dogs with chronic inflammatory enteropathies (CIE) is unknown. Objective Evaluation of fecal calprotectin in dogs with biopsy‐confirmed CIE. Animals 127 dogs. Methods Prospective case‐control study. Dogs were assigned a canine chronic enteropathy clinical activity index (CCECAI) score, and histologic lesions severity was assessed. Fecal calprotectin, fecal S100A12, and serum C‐reactive protein (CRP) were measured. Food‐ or antibiotic‐responsive cases (FRE/ARE, n = 13) were distinguished from steroid‐/immunosuppressant‐responsive or ‐refractory cases (SRE/IRE, n = 20). Clinical response to treatment in SRE/IRE dogs was classified as complete remission (CR), partial response (PR), or no response (NR). Results Fecal calprotectin correlated with CCECAI (ρ = 0.27, P = .0065) and fecal S100A12 (ρ = 0.90, P

Abstract Background Serum gastrin concentration can help diagnose gastrinomas in dogs if >3–10× the upper reference limit (URL), but antisecretory therapy and other conditions can also cause hypergastrinemia. Effects of antisecretory therapy (famotidine or ranitidine, omeprazole) on serum gastrin concentration in dogs with chronic enteropathy (CE) and its biological variation (BV) are unknown. Aim of the study was to evaluate serum gastrin in acid-suppressant-treated or -naïve CE dogs; test the association between serum gastrin and histopathologic findings in acid-suppressant-naïve CE dogs; and evaluate the BV of serum gastrin in dogs not receiving any gastric acid suppressive therapy. Samples from 231 dogs were used and serum gastrin was measured by chemiluminescence assay. Gastric and duodenal histologic lesions were evaluated and graded. BV of serum gastrin was evaluated in serial samples. Results Serum gastrin concentrations were significantly higher in acid-suppressant-treated than acid-suppressant-naïve dogs (P = 0.0245), with significantly higher concentrations in proton pump inhibitor (PPI)- than H2-antihistamine-treated patients (P = 0.0053). More PPI- than H2-antihistamine-treated dogs had gastrin concentrations above URL (P = 0.0205), but not >3× nor >10× the URL. Serum gastrin concentrations correlated with the severity of gastric antral epithelial injury (P = 0.0069) but not with any other lesions or the presence/numbers of spiral bacteria in gastric biopsies. Intra- and inter-individual BV were 43.4 and 21.6%, respectively, in acid-suppressant-naïve dogs, with a reciprocal individuality index of 0.49 and a critical difference of ≥29.5 ng/L. Conclusions Antisecretory (particularly PPI) treatment leads to hypergastrinemia in CE dogs, but the concentrations seen in this study are unlikely to compromise a diagnosis of gastrinoma. Use of a population-based URL for canine serum gastrin and a URL of ≤27.8 ng/L are appropriate.

Abstract Background Onset of canine transitional cell carcinoma (TCC) and prostatic carcinoma (PCA) is usually insidious with dogs presenting at an advanced stage of the disease. A biomarker that can facilitate early detection of TCC/PCA and improve patient survival would be useful. S100A8/A9 (calgranulin A/B or calprotectin) and S100A12 (calgranulin C) are expressed by cells of the innate immune system and are associated with several inflammatory disorders. S100A8/A9 is also expressed by epithelial cells after malignant transformation and is involved in the regulation of cell proliferation and metastasis. S100A8/A9 is up-regulated in human PCA and TCC, whereas the results for S100A12 have been ambiguous. Also, the urine S100A8/A9-to-S100A12 ratio (uCalR) may have potential as a marker for canine TCC/PCA. Aim of the study was to evaluate the diagnostic accuracy of the urinary S100/calgranulins to detect TCC/PCA in dogs by using data and urine samples from 164 dogs with TCC/PCA, non-neoplastic urinary tract disease, other neoplasms, or urinary tract infections, and 75 healthy controls (nested case-control study). Urine S100A8/A9 and S100A12 (measured by species-specific radioimmunoassays and normalized against urine specific gravity [S100A8/A9USG; S100A12USG], urine creatinine concentration, and urine protein concentration and the uCalR were compared among the groups of dogs. Results S100A8/A9USG had the highest sensitivity (96%) and specificity (66%) to detect TCC/PCA, with specificity reaching 75% after excluding dogs with a urinary tract infection. The uCalR best distinguished dogs with TCC/PCA from dogs with a urinary tract infection (sensitivity: 91%, specificity: 60%). Using a S100A8/A9USG ≥ 109.9 to screen dogs ≥6 years of age for TCC/PCA yielded a negative predictive value of 100%. Conclusions S100A8/A9USG and uCalR may have utility for diagnosing TCC/PCA in dogs, and S100A8/A9USG may be a good screening test for canine TCC/PCA.

Prebiotics are selectively fermentable dietary compounds that result in changes in the composition and/or activity of the intestinal microbiota, thus conferring benefits upon host health. In veterinary medicine, commercially available products containing prebiotics have not been well studied with regard to the changes they trigger on the composition of the gut microbiota. This study evaluated the effect of a commercially available nutraceutical containing fructo-oligosaccharides (FOS) and inulin on the fecal microbiota of healthy cats and dogs when administered for 16 days. Fecal samples were collected at two time points before and at two time points during prebiotic administration. Total genomic DNA was obtained from fecal samples and 454-pyrosequencing was used for 16S rRNA gene bacterial profiling. The linear discriminant analysis (LDA) effect size (LEfSe) method was used for detecting bacterial taxa that may respond (i.e., increase or decrease in its relative abundance) to prebiotic administration. Prebiotic administration was associated with a good acceptance and no side effects (e.g., diarrhea) were reported by the owners. A low dose of prebiotics (50 mL total regardless of body weight with the end product containing 0.45% of prebiotics) revealed a lower abundance of Gammaproteobacteria and a higher abundance of Veillonellaceae during prebiotic administration in cats, while Staphylococcaceae showed a higher abundance during prebiotic administration in dogs. These differences were not sufficient to separate bacterial communities as shown by analysis of weighted UniFrac distance metrics. A predictive approach of the fecal bacterial metagenome using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt) also did not reveal differences between the period before and during prebiotic administration. A second trial using a higher dose of prebiotics (3.2 mL/kg body weight with the end product containing 3.1% of prebiotics) was tested in dogs and revealed a lower abundance of Dorea (family Clostridiaceae) and a higher abundance of Megamonas and other (unknown) members of Veillonellaceae during prebiotic administration. Again, these changes were not sufficient to separate bacterial communities or predicted metabolic profiles according to treatment. A closer analysis of bacterial communities at all time-points revealed highly individualized patterns of variation. This study shows a high interindividual variation of fecal bacterial communities from pet cats and dogs, that these communities are relatively stable over time, and that some of this variation can be attributable to prebiotic administration, a phenomenon that may be affected by the amount of the prebiotic administered in the formulation. This study also provides insights into the response of gut bacterial communities in pet cats and dogs during administration of commercially available products containing prebiotics. More studies are needed to explore potentially beneficial effects on host health beyond changes in bacterial communities.

The prevalence and phylogenetic description of fungal organisms and their role as part of the intestinal ecosystem have not yet been studied extensively in dogs. This study evaluated the fungal microbiome of 19 dogs (12 healthy dogs and 7 dogs with acute diarrhea) using fungal tag-encoded FLX-Titanium amplicon pyrosequencing. Five distinct fungal phyla were identified, with Ascomycota (medians: 97.9% of obtained sequences in healthy dogs and 98.2% in diseased dogs) and Basidiomycota (median 1.0% in healthy dogs and median 0.5% in diseased dogs) being the most abundant fungal phyla. A total of 219 fungal genera were identified across all 19 dogs with a median (range) of 28 (4–69) genera per sample. Candida was the most abundant genus found in both the diseased dogs (median: 1.9%, range: 0.2%–38.5% of sequences) and healthy dogs (median: 5.2%, range: 0.0%–63.1% of sequences). Candida natalensis was the most frequently identified species. No significant differences were observed in the relative proportions of fungal communities between healthy and diseased dogs. In conclusion, fecal samples of healthy dogs and dogs with acute diarrhea harbor various fungal genera, and their role in gastrointestinal health and disease warrants further studies.

A 3-year-and-9-months old male neutered Bichon Frise was presented for a second opinion for diabetes mellitus, weight loss, pruritus, and loss of hair. During further work-up, the dog was diagnosed with uncontrolled diabetes mellitus and concurrent diagnoses of pancreatitis and atopy were also suspected. Multiple adjustments of insulin therapy did not improve control of diabetes mellitus. Also, a variety of different treatments failed to improve pruritus. The dog was seen by a veterinary dermatologist who further suspected atopy and started treatment with cyclosporine. Pruritus improved and coincidentally serum Spec cPL and fructosamine concentrations normalized after therapy, suggesting the possibility that cyclosporine may have controlled pancreatic inflammation and improved control of diabetes mellitus. This case report would suggest that further research into autoimmunity in dogs with chronic pancreatitis is warranted. Also, a controlled study is needed and in progress before the use of cyclosporine in dogs with chronic pancreatitis or a subgroup thereof can be advocated.

This study aimed to evaluate the variation associated with repeated measurement of gastrointestinal (GI) transit times and the effect of oral ranitidine on GI transit times in healthy dogs using a wireless motility capsule (WMC) system. Eight privately owned healthy adult dogs were enrolled, and one developed diarrhea and was removed from the study. For the first 3 repetitions, each dog was fed a standard meal followed by oral administration of a WMC. For the 4th repetition, each dog was given ranitidine hydrochloride (75 mg PO every 12 hours) prior to and during assessment of GI transit times. Mean between-subject coefficients of variation for gastric emptying time (GET), small and large bowel transit time (SLBTT), and total transit time (TTT) were 26.9%, 32.3%, and 19.6%, respectively. Mean within-subject coefficients of variation for GET, SLBTT, and TTT were 9.3%, 19.6%, and 15.9%, respectively. Median GET, SLBTT, and TTT without ranitidine were 719, 1,636, and 2,735 minutes, respectively. Median GET, SLBTT, and TTT with ranitidine were 757, 1,227, and 2,083 minutes, respectively. No significant differences in GI transit times were found between any of the 4 repetitions. Under these experimental conditions, no significant effects of oral ranitidine on GI transit times were observed.