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Background: In humans, absorption and tissue retention rates of intramuscularly administered hydroxocobalamin (OH‐Cbl) are superior compared to cyanocobalamin (CN‐Cbl). Supplementation with OH‐Cbl has not been described in cats. Objectives: To evaluate effects of parenteral OH‐Cbl supplementation on clinical signs, serum Cbl and methylmalonic acid (MMA) concentrations in hypocobalaminemic cats with gastrointestinal disease. Animals: Twenty‐three client‐owned cats. Methods: Prospective study. Serum Cbl and MMA concentrations were determined at enrollment (t0), immediately before the 4th OH‐Cbl IM injection (300 μg, given q2 weeks) (t1), and 4 weeks after the 4th injection (t2). Severity of clinical signs (activity, appetite, vomiting, diarrhea, body weight) was graded at each time point and expressed as clinical disease activity score. Results: Median clinical disease activity score decreased significantly from t0 (6; range, 2‐10) to t1 (1; range, 0‐6) and t2 (1; range, 0‐9). Median serum Cbl concentration increased significantly from 111 pmol/L (range, 111‐218; reference range, 225‐1451 pmol/L) at t0 to 1612 pmol/L (range, 526‐14 756) (P

OBJECTIVE To evaluate the effects of storage conditions and duration on cobalamin concentration in serum samples from dogs and cats. DESIGN Experiment. SAMPLE Serum samples from 9 client-owned cats and 9 client-owned dogs. PROCEDURES Serum harvested from freshly obtained blood samples was separated into 11 aliquots/animal. One aliquot (baseline sample) was routinely transported in light-protected tubes to the laboratory for cobalamin assay; each of the remaining aliquots was stored in a refrigerator (6°C; n = 5) or at room temperature (20°C) with exposure to daylight (5) for 24, 48, 72, 96, or 120 hours. Aliquots were subsequently wrapped in aluminum foil, frozen (−20°C), and then transported to the laboratory for measurement of cobalamin concentration, all in the same run. Percentage decrease in cobalamin concentration from baseline was analyzed by means of linear mixed modeling. RESULTS No differences in cobalamin values were identified between cats and dogs; therefore, data for both species were analyzed together. Median baseline serum cobalamin concentration was 424 ng/L (range, 178 to 1,880 ng/L). Values for serum samples stored with daylight exposure at room temperature were significantly lower over time than were values for refrigerated samples. Although values for refrigerated samples did not decrease significantly from baseline values over time, values for the other storage condition did; however, the mean percentage decrease for serum samples stored at room temperature was small (0.14%/h; 95% confidence interval, 0.07% to 0.21%/h). CONCLUSIONS AND CLINICAL RELEVANCE Overall, serum cobalamin concentration appeared stable for 5 days when feline and canine serum samples were refrigerated at 6°C. The effect of light and room temperature on serum cobalamin concentration, although significant, was quite small for samples stored with these exposures for the same 5-day period.

BACKGROUND: Effects and duration of commonly used protocols for cobalamin (Cbl) supplementation on cellular Cbl deficiency have not been determined in hypocobalaminemic cats. HYPOTHESIS/OBJECTIVES: To evaluate effect of Cbl supplementation on clinical signs, serum and urine methylmalonic acid (MMA) concentrations over 16 weeks. ANIMALS: Twenty client-owned hypocobalaminemic cats with enteropathy. METHODS: Prospective study. Serum Cbl and serum and urine MMA concentrations were determined prospectively in cats at enrollment (t0), immediately before (t6), and 4 (t10) and 10 weeks (t16) after 6th Cbl injection (250 μg, IM q 7 days). Clinical signs severity (activity, appetite, vomiting, diarrhea, body weight) graded at each time point and expressed as clinical disease activity score. RESULTS: Clinical disease activity score decreased during supplementation and increased after treatment discontinuation. Median serum Cbl concentration increased significantly from t0 (111 pmol/L, range 111-212) to t6 (2,332.5 pmol/L, range 123-22,730) (P < 0.01). Values at t10 were 610.5 pmol/L (range, 111-2,527) and 180.5 pmol/L (range, 111-2,262) at t16 (P < 0.01). Median baseline serum MMA concentration (372 μmol/L, range 0.39-147,000) decreased significantly to 1.62 μmol/L (range, 0.18-806) at t6 (P < 0.01) and gradually increased to 5.34 μmol/L (range, 0.13-1,730) at t10 and 189 μmol/L (range, 0.4-983) at t16. Similar, nonsignificant, pattern observed for urine MMA concentration. Serum and urine MMA concentrations had not normalized in 12 and 6 cats, respectively, at t6. CONCLUSION AND CLINICAL IMPORTANCE: The Cbl supplementation protocol used here did not lead to complete normalization of cellular Cbl deficiency in all examined cats, and biochemical improvements were transient.

An 11-month-old Border collie presented collapsed and continued to deteriorate rapidly despite supportive treatment. The dog had a history of failure to thrive and recurring respiratory infection. Laboratory abnormalities included neutrophilic leucocytosis, Heinz body anaemia, hyperammonaemia, hyperbilirubinaemia, proteinuria and hypocobalaminaemia. Post-mortem examination revealed multi-focal necrosis within the heart, kidneys, pancreas, liver, meninges and cerebral cortex. Fungal hyphae in lesions were identified as Scedosporium prolificans following culture. Subsequent genotyping confirmed that the dog carried the CUBN:c.8392delC mutation in a homozygous state, verifying hereditary cobalamin deficiency (a.k.a. Imerslund-Grasbeck syndrome). Cobalamin deficiency may have been a predisposing factor for the development of systemic fungal infection in this dog.

This report describes the clinical and histologic recovery of a 2‐year‐old mixed‐breed dog presented with hypovolemic shock, markedly increased serum alanine amino transferase activity, and hemoabdomen. Emergency exploratory surgery revealed a friable liver with multiple capsule hemorrhages necessitating removal of the left lateral lobe. Histologic evaluation showed acute massive hepatic necrosis with centrilobular and midzonal distribution. The dog survived, and all monitored laboratory values normalized within 7 weeks. A liver biopsy taken 8 weeks after presentation revealed normal hepatic architecture with a few, randomly distributed neutrophilic foci. Follow‐up included intermittent determination of liver variables including liver function tests for a period of 7 years. The dog's health status, and all test results remained normal during this time. Complete recovery and good long‐term quality of life after life‐threatening acute liver failure secondary to massive hepatic necrosis is possible in dogs.

Background Efficacy of PO cobalamin (Cbl) supplementation in dogs with hereditary Cbl malabsorption (Imerslund-Grasbeck syndrome, IGS) is unknown. Objectives To evaluate PO Cbl supplementation in Beagles with IGS previously treated parenterally. We hypothesized that 1 mg cyano-Cbl daily PO would maintain clinical and metabolic remission. Animals Three client-owned Beagles with IGS and 48 healthy control dogs. Methods Prospective study. Daily PO cyanocobalamin (cyano-Cbl; 1 mg) supplementation was monitored for 13 (2 dogs) and 8 months (1 dog). Health status was assessed by owner observations. Methylmalonic acid (MMA)-to-creatinine concentrations were measured using an ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-TMS) method on urine samples collected monthly. Concurrent measurements of serum MMA concentration (n = 7; UPLC-TMS) were available for 1 dog. Results All dogs remained in excellent health during PO supplementation. Urine MMA remained consistently low in 2 dogs (median, 2.5 mmol/mol creatinine; range, 1.2-9; healthy dogs [n = 30], median, 2.9 mmol/mol creatinine; range, 1.3-76.5). Urine MMA ranged from 38.9-84.9 mmol/mol creatinine during the first 6 months in 1 dog already known to excrete comparable amounts when supplemented parenterally. Brief antibiotic treatment for an unrelated condition after 6 months resulted in low urine MMA (median, 2.8 mmol/mol creatinine; range, 1.9-4.8) for the next 7 months. All concurrent serum MMA concentrations (median, 651 nmol/L; range, 399-919) before and after month 6 were within the established reference interval (393-1476 nmol/L; n = 48). Conclusions and clinical importance One milligram of cyano-Cbl daily PO appears efficacious for maintaining normal clinical status and normal cellular markers of Cbl metabolism in Beagles with IGS.

BACKGROUND: Prospective studies on maintenance treatment for Beagles with hereditary selective cobalamin (Cbl) malabsorption (Imerslund‐Grasbeck syndrome, IGS) are lacking. In our experience, measurement of methylmalonic acid (MMA), a Cbl‐dependent metabolite, seems more helpful to monitor Cbl status as compared with serum Cbl concentrations. OBJECTIVES: To evaluate a standardized Cbl supplementation scheme in Beagles with IGS. We hypothesized that a single parenteral dose of 1 mg hydroxocobalamin (OH‐Cbl) would maintain clinical and metabolic remission for up to 2 months. ANIMALS: Six client‐owned juvenile Beagles with genetically confirmed IGS and 28 healthy control dogs. METHODS: Prospective study. Monthly IM OH‐Cbl (1 mg) supplementation was done over a median of 9 months (range, 6‐13) in 6 dogs, followed by bimonthly (every 2 months) injections in 5 dogs over a median of 6 months (range, 3‐10). Health status was assessed by routine clinical examinations at injection time points and owner observations. Voided urine samples were collected immediately before OH‐Cbl injections for measurement of MMA‐to‐creatinine concentrations using a gas‐liquid chromatography‐tandem mass spectrometry (GC‐MS) method. RESULTS: All dogs were clinically healthy while receiving monthly and bimonthly OH‐Cbl supplementation. Urinary MMA results in healthy dogs ranged from 1.3 to 76.5 mmol/mol creatinine (median, 2.9). Median urinary MMA concentrations did not differ between dogs with IGS receiving monthly (n = 49; 5.3 mmol/mol creatinine; range, 2.3‐50.4) and bimonthly (n = 31; 5.3 mmol/mol creatinine; range, 1.6‐50) injections. CONCLUSIONS AND CLINICAL IMPORTANCE: A maintenance parenteral dose of 1 mg OH‐Cbl monthly or bimonthly appears adequate in Beagles with IGS monitored by metabolic testing.

ZusammenfassungHypothese der Studie war, dass sich typische Kriterien einer hyperregeneratorischen Ösophagopathie (HRÖ) des Menschen wie Hyperplasie der Basalzellschicht und Verlängerung der Stromapapillen im Epithel des kaninen Ösophagus nachweisen lassen und dass diese Veränderungen assoziiert sind mit auf gastroösophagealen Reflux (GÖR) hinweisenden Symptome und endoskopischen Läsionen.Bei 65 adulten Hunden mit klinischen Anzeichen einer Speiseröhrenerkrankung erfolgten Ösophagoskopien und Biopsien. Auf GÖR hinweisende Symptome (Regurgitieren, Ptyalismus, schmerzhaftes Unwohlsein) wurden prospektiv über einen Fragebogen ermittelt. Mittels Videoendoskopie wurden auf GÖR hinweisende minimale Veränderungen und deutliche Mukosaschäden erfasst. Neben einer histologischen Untersuchung der Ösophagusbioptate wurden Strukturen des ösophagealen Plattenepithels mikroskopisch morphometrisch quantifiziert.Das ösophageale Plattenepithel zeigte sich histologisch bei 48 Hunden unauffällig und bei 17 Hunden bestand eine HRÖ mit Vorliegen beider pathognomonischer Veränderungen (Hyperplasie der Basalzellschicht, Verlängerung der Stromapapillen). Die Basalzellschicht und die Stromapapillen waren morphometrisch bei den 17 Hunden mit HRÖ signifikant (jeweils p < 0,0001) breiter und länger als bei den 48 Hunden ohne HRÖ. Symptome von GÖR insgesamt sowie Regurgitieren fanden sich signifikant (p = 0,02 bzw. p = 0,009) häufiger bei den 17 Hunden mit HRÖ als bei den 48 Hunden ohne HRÖ. Ebenso wurden endoskopische Läsionen insgesamt sowie minimale auf GÖR hinweisende endoskopische Veränderungen signifikant (p = 0,002 bzw. p = 0,004) häufiger bei den 17 Hunden mit HRÖ festgestellt als bei den 48 Hunden ohne HRÖ.Typische Merkmale der hyperregeneratorischen Ösophagopathie des Menschen lassen sich auch im kaninen Speiseröhrenepithel nachweisen. Die histologischen Veränderungen sind assoziiert mit Symptomen und endoskopischen Läsionen, die auf einen gastroösophagealen Reflux hinweisen.

Objective—To evaluate the effects of cisapride and metoclopramide hydrochloride administered orally on the lower esophageal sphincter (LES) resting pressure in awake healthy dogs. Animals—6 adult Beagles. Procedures—Each dog was evaluated after administration of a single dose of cisapride (0.5 mg/kg), metoclopramide (0.5 mg/kg), or placebo (empty gelatin-free capsule) in 3 experiments performed at 3-week intervals. To measure LES pressure, a high-resolution manometry catheter equipped with 40 pressure sensors spaced 10 mm apart was used. For each experiment, LES pressure was recorded during a 20-minute period with a virtual electronic sleeve emulation before treatment (baseline) and at 1, 4, and 7 hours after drug or placebo administration. A linear mixed-effects model was used to test whether the 3 treatments affected LES pressure differently. Results—In the cisapride, metoclopramide, and placebo experiments, median baseline LES pressures were 29.1, 30.5, and 29.0 mm Hg, respectively. For the cisapride, metoclopramide, and placebo treatments, median LES pressures at 1 hour after administration were 44.4, 37.8, and 36.6 mm Hg, respectively; median LES pressures at 4 hours after administration were 50.7, 30.6, and 31.1 mm Hg, respectively; and median LES pressures at 7 hours after administration were 44.3, 28.5, and 33.3 mm Hg, respectively. The LES pressures differed significantly only between the placebo and cisapride treatments. Conclusions and Clinical Relevance—Results suggested that orally administered cisapride may be of benefit in canine patients for which an increase in LES pressure is desirable, whereas orally administered metoclopramide did not affect LES resting pressures in dogs.

Background Spec cPL is the most sensitive and specific test for diagnosing pancreatitis in dogs. Its results have not been compared to those of the 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) lipase assay or those of abdominal ultrasonography. Objectives To investigate agreement of Spec cPL with DGGR lipase activity and pancreatic ultrasonography in dogs with suspected pancreatitis. Animals One hundred and forty-two dogs. Methods DGGR lipase activity (reference range, 24–108 U/L) and Spec cPL were measured using the same sample. The time interval between ultrasonography and lipase determinations was 108, >216 U/L) and Spec cPL (>200 μg/L) had κ values of 0.79 (95% confidence interval [CI], 0.69–0.9) and 0.70 (CI, 0.58–0.82). DGGR lipase (>108, >216 U/L) and Spec cPL (>400 μg/L) had κ values of 0.55 (CI, 0.43–0.67) and κ of 0.80 (CI, 0.71–0.9). An ultrasonographic diagnosis of pancreatitis and DGGR lipase (>108, >216 U/L) had κ values of 0.29 (CI, 0.14–0.44) and 0.35 (CI, 0.18–0.52). Ultrasonographically diagnosed pancreatitis and Spec cPL (>200, >400 μg/L) had κ values of 0.25 (CI, 0.08–0.41) and 0.27 (CI, 0.09–0.45). Conclusions and Clinical Importance Although both lipase assays showed high agreement, agreement between ultrasonography and lipase assays results was only fair. Because lipase results are deemed more accurate, ultrasonography results should be interpreted carefully.

Juvenile cobalamin deficiency is a rare disease in border collies and its diagnosis requires a high level of clinical suspicion. The goal of this study was to increase awareness of this disease by describing the clinical and laboratory findings in four young border collies with inherited cobalamin deficiency. The median age of the dogs was 11.5 mo (range, 8–42 mo), and two of the four dogs were full siblings. Clinical signs included intermittent lethargy (n = 4), poor body condition (n = 4), odynophagia (n = 2), glossitis (n = 1), and bradyarrhythmia (n = 1). Pertinent laboratory abnormalities were mild to moderate normocytic nonregenerative anemia (n = 3), increased aspartate aminotransferase (AST) activity (n = 3), and mild proteinuria (n = 3). All of the dogs had serum cobalamin levels below the detection limit of the assay, marked methylmalonic aciduria, and hyperhomocysteinemia. Full clinical recovery was achieved in all dogs with regular parenteral cobalamin supplementation, and laboratory abnormalities resolved, except the proteinuria and elevated AST activity persisted. This case series demonstrates the diverse clinical picture of primary cobalamin deficiency in border collies. Young border collies presenting with ambiguous clinical signs should be screened for cobalamin deficiency.

Medical records of 261 cats presenting with gastrointestinal disease that had a serum cobalamin concentration measured were reviewed. In addition, a reference range for cobalamin (305 - 1.967ng/L) was established using 22 healthy adult cats with undetectable levels of urinary methylmalonic acid. A total of 108 of 261 cats (41.4 %) had hypocobalaminemia; 69 cats (26.4 %) had cobalamin concentrations below the detection limit of the assay (

Eine 3-jahrige, intakte Miniature Australian Shepherd-Hundin wurde nach Gabe von Milbemycinoxim in der empfohlenen Dosierung im Status epilepticus vorgestellt. Aufgrund einer Aspirationspneumonie-bedingten massiven Hypoxamie musste die Hundin zusatzlich zur kontinuierlichen intravenosen antiepileptischen Therapie wahrend 36 Stunden kunstlich beatmet werden. Nach Extubation lag der Patient weitere 96 Stunden im Koma; die kontinuierliche Propofolinfusion zur Kontrolle rezidivierend auftretender tonisch-klonischer Krampfe konnte am 5. Tag ausgeschlichen werden. Nach insgesamt 10 Tagen war der Patient vollstandig genesen. Im Vorfeld war bereits eine homozygote Mutation im MDR1-Gen (-/-) bekannt. Milbemycinoxim galt bisher bei MDR1-defizienten Hunden als sicher. Der vorliegende Bericht zeigt jedoch, dass Milbemycinoxim bei MDR1-defizienten Hunden moglichst tief dosiert und der Besitzer uber mogliche Komplikationen aufgeklart werden sollte.

BACKGROUND: Endoscopic ultrasound (EUS)-guided fine needle aspiration (EUS-FNA) has proven a useful and safe diagnostic tool for assessing pancreatic disease in human medicine. No information about pancreatic EUS-FNA is available in dogs. OBJECTIVES: To assess the feasibility and safety of pancreatic EUS-FNA in healthy dogs. ANIMALS: Thirteen beagles with a median body weight of 13.4 kg. METHODS: Experimental study. An ultrasound endoscope (insertion tube outer diameter 11.8 mm) was used, and FNA was carried out with 19 G needles. The optimal puncture site was chosen with the aid of Doppler imaging. Complete clinicopathologic assessments including pain scoring and pancreas-specific lipase measurements were obtained before EUS as well as on day 1 and day 2 after EUS-FNA. RESULTS: The pancreatic body was identified in all dogs, the left lobe was clearly identified in 9/13 and appeared indistinctly marginated in 4/13 dogs, and the distal third of the right lobe could not be identified in 7/13 dogs. EUS-FNA was carried out in 12/13 dogs. Cellularity of smears was adequate for evaluation in 8/12 cases, in which samples were obtained transgastrically (n = 4) or transduodenally (n = 4). All dogs recovered uneventfully and no clinical and laboratory abnormalities occurred during the 48 hour monitoring period after the procedure. CONCLUSION AND CLINICAL IMPORTANCE: Although the healthy canine pancreas is difficult to visualize in its entirety with EUS, pancreatic EUS-FNA with a 19 G needle is feasible in medium-sized dogs and can be considered a safe procedure. Its diagnostic usefulness should be evaluated in dogs with pancreatic disease.

Six dogs with lornoxicam induced severe gastrointestinal bleeding are described. The ingested dose ranged between 0.5 - 5.1 mg/kg BW (median 0.63 mg/kg BW). The severity of the bloodloss anemia was moderate to severe with PCV values ranging between 12 - 27 % (median 16 %) and serum albumin concentrations between 12 - 22 g/l (median 16 g/l). One dog had evidence of chronic thrombocytopathia over 13 days and clinicopathologic findings of gastrointestinal bleeding over 55 days. None of the dogs developed kidney injuries. The clinical condition required transfusion of blood products in 5 of 6 cases. One dog with a perforated duodenal ulcer and septic peritonitis survived until discharge but had to be euthanized later on due to recrudescent clinical signs (hematemesis, melena). The median length of hospitalisation was 12 days (5 - 14). No correlation was seen between the ingested dose and severity of clinical signs. Lornoxicam ingestion leads to severe and longlasting gastrointestinal bleeding in the dog and requires immediate intensive therapy.

Ein 10 Wochen alter Hovawartrude wurde aufgrund eines akuten Nierenversagens vorgestellt. Anhand klinischer und labordiagnostischer Parameter wurde die Diagnose akute Leptospirose gestellt. Neben der Azotamie wurde initial auch eine starke Erhohung des Kalzium-Serumspiegels festgestellt. Der Hund wurde erfolgreich behandelt, entwickelte jedoch unter Therapie ausgedehnte metastatische intestinale und kutane Verkalkungen. Infolge einer massiven Verkalkung des Pylorus kam es zu einer funktionellen Pylorusobstruktion, die durch eine Pyloromyotomie korrigiert werden konnte. Die Hautlasionen wurden topisch behandelt und bildeten sich innerhalb einiger Wochen zuruck. Nach Wissen der Autoren ist dies die erste Beschreibung einer generalisierten intestinalen und kutanen Kalzinosis im Zusammenhang mit einer Leptospirose-bedingten akuten Niereninsuffizienz.

Background: Urinary catecholamines and metanephrines are used for the diagnosis of pheochromocytoma (PHEO) in dogs. Hyperadrenocorticism (HAC) is an important differential diagnosis for PHEO. Objectives: To measure urinary catecholamines and metanephrines in dogs with HAC. Animals: Fourteen dogs with HAC, 7 dogs with PHEO, and 10 healthy dogs. Methods: Prospective clinical trial. Urine was collected during initial work-up in the hospital; in dogs with HAC an additional sample was taken at home 1 week after discharge. Parameters were measured using high-pressure liquid chromatography and expressed as ratios to urinary creatinine concentration. Results: Dogs with HAC had significantly higher urinary epinephrine, norepinephrine and normetanephrine to creatinine ratios than healthy dogs. Urinary epinephrine, norepinephrine, and metanephrine to creatinine ratios did not differ between dogs with HAC and dogs with PHEO, whereas the urinary normetanephrine to creatinine ratio was significantly higher (P= .011) in dogs with PHEO (414, 157.0–925.0, median, range versus (117.5, 53.0–323.0). Using a cut-off ratio of 4 times the highest normetanephrine to creatinine ratio measured in controls, there was no overlap between dogs with HAC and dogs with PHEO. The variables determined in urine samples collected at home did not differ from those collected in the hospital. Conclusion and Clinical Importance: Dogs with HAC might have increased concentrations of urinary catecholamines and normetanephrine. A high concentration of urinary normetanephrine (4 times normal), is highly suggestive of PHEO.

Urinary adrenaline (epinephrine), noradrenaline, dopamine, metadrenaline (metanephrine) and normetadrenaline to creatinine ratios were measured from spot samples of seven client-owned dogs with a histologically confirmed phaeochromocytoma. Urine was collected on day 0 in the hospital in six dogs, and additionally on days 2, 6 and 7 after discharge in two of these dogs. In one dog, urine was sampled on day 7 only. Samples were also collected from 10 healthy control dogs on days 0, 1 and 7. In dogs with phaeochromocytomas, normetadrenaline:creatinine ratios at all time points ranged from 103 to 6430 nmol/mmol. From day 0, ratios of samples taken at the hospital (range 157 to 925 nmol/mmol) were significantly higher (P

Background: In people, hypercortisolism (HC) has been associated with acalculous cholecystitis and biliary dyskinesia, which may potentiate ascending biliary infections. In dogs, an association between HC and gallbladder disease recently has been documented, although the role of bacteria remains controversial. Furthermore, there is no information on the gallbladder bile microbial flora in healthy dogs. Objectives: To investigate the microbial flora in gallbladder bile in healthy dogs, the relationship between iatrogenic hyperadrenocorticism and bactibilia and possible changes in biliary microbial flora after cortisol withdrawal in dogs. Animals: Six control dogs and 6 dogs treated with hydrocortisone. Methods: Gallbladder bile obtained by percutaneous ultrasound-guided cholecystocentesis was cultured aerobically and anaerobically and examined cytologically before (d0), during (d28, d56, d84), and after (d28p, d56p, d84p) administration of hydrocortisone (8 mg/kg PO q12h). Results: In the control group, 2/42 bile cultures yielded bacterial growth (Enterococcus sp.; Escherichia coli on d0) and 1/42 bile smears had cytological evidence of bacteria (d28). In the HC group, 2/42 bile cultures yielded bacterial growth (Enterococcus sp. on d28; Bacillus sp. on d28p) and 3/42 bile smears had cytological evidence of bacteria (d84, d84, d28p). All dogs remained healthy throughout the study period (168d). Conclusions and Clinical Importance: Based on the results of conventional bacterial culture techniques, gallbladder bile of healthy dogs periodically may harbor bacteria, which do not appear to be clinically relevant. A 3-month period of iatrogenic HC was not associated with bactibilia. A higher prevalence of bactibilia may be detected with micromolecular techniques.

Recent reports identified Tritrichomonas fetus, the causative agent of bovine trichomonosis, in cats with large-bowel diarrhea in the US. Between July 2007 and August 2008, a total of 105 Swiss cats were tested for T. fetus with the InPouchTM culture system and/or PCR, whereof 27 (26%) yielded positive results. All positive cats were pedigree cats, whereof 22 (81%) were less than 1 year of age (median 5 months). 25 (93%) of these cats lived in multi-cat households, and all but one were kept indoor. The clinical picture was dominated by large bowel diarrhea with increased frequency of defecation and fresh blood and mucus. Furthermore, inflamed anus and fecal incontinence was common. 52% of the T. fetus-positive cats were tested positive for Giardia before, but the treatment with fenbendazole or metronidazole only temporarily alleviated the clinical signs. The treatment with 30 mg/kg of ronidazole q12h p.o. was successful in all but 1 cat with only minor transient adverse effects in 3 cats. In conclusion, T. fetus has to be considered an important causative agent of large bowel diarrhea in cats in Switzerland, especially in young indoor pedigree cats.

BACKGROUND: Feline pancreas-specific lipase (Spec fPL) is considered a useful test for the antemortem diagnosis of pancreatitis in cats. A recent study found good agreement between the results of the Spec fPL and catalytic 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester (DGGR) lipase assay. Prospective studies evaluating their sensitivity and specificity are lacking. OBJECTIVES: To compare the results of the Spec fPL and the DGGR assays with a standardized histologic assessment of the pancreas. ANIMALS: Sixty client-owned cats presented for necropsy. METHODS: Prospective study: Spec fPL concentrations and serum DGGR lipase activity were measured from the same blood sample. The pancreas was removed within 3 hours after euthanasia; serial transverse sections were made every 0.5 cm throughout the entire pancreas and reviewed using a histologic grading scheme. Sensitivity and specificity for the Spec fPL and DGGR assay results were determined. RESULTS: The sensitivity and specificity for the Spec fPL assay (cutoff value ≥5.4 μg/L) was 42.1 [95% confidence interval (95% CI), 29.4-55.9%] and 100% (95% CI, 31.0-100.0%). The sensitivity and specificity for the DGGR assay (cutoff value >26 U/L) was 36.8 (95% CI, 24.7-50.7%) and 100% (95% CI, 31.0-100.0%). When lymphocytic inflammation up to 10% of a section was considered normal, the sensitivity and specificity for Spec fPL assay (cutoff value ≥5.4 μg/L) was 61.1 (95% CI, 36.1-81.7%) and 69.0% (95% CI, 52.8-81.9%) and the sensitivity and specificity for the DGGR assay (cutoff value >26 U/L) was 66.7 (95% CI, 41.2-85.6%) and 78.6% (95% CI, 62.8-89.2%). CONCLUSIONS AND CLINICAL IMPORTANCE: Both lipase assays performed similarly well, but their agreement with histologic pancreatic inflammation was limited.

BACKGROUND: Gastric acid suppressants frequently are used in cats with acid-related gastric disorders. However, it is not known if these drugs effectively increase intragastric pH in cats. OBJECTIVES: To examine the effects of PO administered ranitidine and omeprazole on intragastric pH in cats and to compare the efficacy of once-daily versus twice-daily dosage regimens for omeprazole. ANIMALS: Eight domestic shorthair cats. METHODS: Using a randomized 4-way cross-over design, cats were given enteric-coated omeprazole granules (1.1-1.3 mg/kg q24h and q12h), ranitidine (1.5-2.3 mg/kg q12h), and placebo. Intragastric pH was monitored continuously for 96 hours using the Bravo(™) system, starting on day 4 of treatment, followed by a median washout period of 12 days. Mean percentage of time pH was ≥3 and ≥4 was compared among groups using repeated measures ANOVA. RESULTS: Mean ± SD percentage of time intragastric pH was ≥3 and ≥4 was 67.0 ± 24.0% and 54.6 ± 26.4% for twice-daily omeprazole, 24.4 ± 22.8% and 16.8 ± 19.3% for once-daily omeprazole, 16.5 ± 9.0% and 9.6 ± 5.9% for ranitidine, and 9.4 ± 8.0% and 7.0 ± 6.6% for placebo administration. Twice-daily omeprazole treatment significantly increased intragastric pH, whereas pH after once-daily omeprazole and ranitidine treatments did not differ from that of placebo-treated cats. CONCLUSION AND CLINICAL IMPORTANCE: Only twice-daily PO administered omeprazole significantly suppressed gastric acidity in healthy cats, whereas once-daily omeprazole and standard dosages of ranitidine were not effective acid suppressants in cats.

Background Cats with diabetes mellitus can have subclinical pancreatitis but prospective studies to confirm this are lacking. Metabolic control of diabetic cats with pancreatitis is difficult. Hypothesis Subclinical pancreatitis occurs in diabetic cats at the time diabetes is diagnosed or might develop during the follow-up period, hampering diabetic remission. Animals Thirty cats with newly diagnosed diabetes without clinical signs of pancreatitis on admission. Methods Prospective study. On admission and 2 and 6 months later, serum Spec fPL and DGGR-lipase were measured and the pancreas underwent ultrasonographic examination. Pancreatitis was suspected if serum markers were increased or ≥2 ultrasonographic abnormalities were detected. Cats were treated with insulin glargine and diabetic remission was defined as euglycemia ≥4 weeks after discontinuation of insulin. Nonparametric statistical tests were used for analysis. Results Subclinical pancreatitis at the time of diagnosis was suspected in 33, 50, and 31% of cats based on Spec fPL, DGGR-lipase and ultrasonography, respectively; and in 60% when diagnostic criteria were combined. During the follow-up period, suspected pancreatitis developed in additional 17–30% cats. Only 1 cat had transient clinical signs compatible with pancreatitis. Seventeen of the 30 cats (57%) achieved remission. Frequency of abnormal Spec fPL and DGGR-lipase and abnormal ultrasonographic findings did not differ in cats achieving remission and those who did not. Cats achieving remission had significantly lower Spec fPL at 2 months (P

A 12-month-old beagle presented for anorexia, pyrexia and vomiting. The dog had been treated intermittently with antibiotics and corticosteroids for inappetence and lethargy since five months of age. Previous laboratory abnormalities included macrocytosis and neutropenia. At presentation, the dog was lethargic, febrile and thin. Laboratory examination findings included anaemia, a left shift, thrombocytopenia, hypoglycaemia and hyperbilirubinaemia. Multiple, small, hypoechoic, round hepatic lesions were observed on abdominal ultrasound. Cytological examination of hepatic fine needle aspirates revealed a fungal infection and associated pyogranulomatous inflammation. The dog's general condition deteriorated despite supportive measures and treatment with fluconazole, and owners opted for euthanasia before hypocobalaminaemia was identified. Subsequent genomic analysis revealed a CUBN:c.786delC mutation in a homozygous state, confirming hereditary cobalamin malabsorption (Imerslund-Grasbeck syndrome). Similar to human infants, dogs with Imerslund-Grasbeck syndrome may rarely be presented for infectious diseases, distracting focus from the underlying primary disorder.

Background Although gastroesophageal reflux (GER) often is assumed to be causative for upper gastrointestinal and respiratory signs in dogs, no attempts have been made to verify this assumption. Objectives To monitor esophageal pH with the Bravo pH system in healthy dogs and client-owned dogs displaying signs commonly attributed to GER. Animals Seven healthy and 22 client-owned dogs. Methods After routine esophagogastroduodenoscopy, radiotelemetric pH capsules were placed in distal esophagus for continuous pH recording. Reflux was defined as single pH measurement 5 minutes in duration was 1 (0–14), and 1 (0–4), duration of longest reflux (min) was 10 (0–65) and 8 (0–27), and fractional time pH

Objective—To investigate agreement of a feline pancreas–specific lipase assay and a colorimetric lipase assay with a 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) substrate with results of pancreatic ultrasonography in cats with suspicion of pancreatitis. Design—Retrospective case series. Animals—161 client-owned cats with suspicion of pancreatitis. Procedures—Feline pancreas–specific lipase concentration and DGGR lipase activity were measured from the same blood sample in cats undergoing investigation for pancreatitis, with < 24 hours between ultrasonography and lipase determinations. Ultrasonographic variables evaluated were ultrasonographic diagnosis of pancreatitis, enlargement, margins, echogenicity, mesenteric echogenicity, peripancreatic free fluid, cysts, masses, and common bile and pancreatic duct dilation. Agreement was assessed by use of the Cohen κ coefficient. Results—Agreement between the lipase assays was substantial (κ = 0.703). An ultrasonographic diagnosis of pancreatitis had fair agreement with feline pancreas–specific lipase concentration > 5.4 μg/L (κ = 0.264) and DGGR lipase activity > 26 U/L (κ = 0.221). The greatest agreement between feline pancreas–specific lipase concentration > 5.4 μg/L and DGGR lipase activity > 26 U/L was found for a hypoechoic and mixed-echoic (κ = 0.270 and 0.266, respectively), hypoechoic (κ = 0.261 and 0.181, respectively), and enlarged (κ = 0.218 and 0.223, respectively) pancreas. Conclusions and Clinical Relevance—Agreement between pancreatic ultrasonography and lipase assay results was only fair. It remains unknown whether lipase results or pancreatic ultrasonography constitutes the more accurate test for diagnosing pancreatitis; therefore, results of both tests need to be interpreted with caution.

Mammals are unable to synthesize cobalamin or vitamin B12 and rely on the uptake of dietary cobalamin. The cubam receptor expressed on the intestinal endothelium is required for the uptake of cobalamin from the gut. Cubam is composed of two protein subunits, amnionless and cubilin, which are encoded by the AMN and CUBN genes respectively. Loss-of-function mutations in either the AMN or the CUBN gene lead to hereditary selective cobalamin malabsorption or Imerslund-Gräsbeck syndrome (IGS). We investigated Beagles with IGS and resequenced the whole genome of one affected Beagle at 15× coverage. The analysis of the AMN and CUBN candidate genes revealed a homozygous deletion of a single cytosine in exon 8 of the CUBN gene (c.786delC). This deletion leads to a frameshift and early premature stop codon (p.Asp262Glufs*47) and is, thus, predicted to represent a complete loss-of-function allele. We tested three IGS-affected and 89 control Beagles and found perfect association between the IGS phenotype and the CUBN:c.786delC variant. Given the known role of cubilin in cobalamin transport, which has been firmly established in humans and dogs, our data strongly suggest that the CUBN:c.786delC variant is causing IGS in the investigated Beagles.

Objective—To evaluate the use of high-resolution manometry (HRM) in awake and sedated dogs and to assess potential effects of a standard sedation protocol. Animals—22 Beagles. Procedures—An HRM catheter with 36 pressure sensors was inserted intranasally in each dog. After an adaption period of 5 minutes, each set of measurements included 5 swallows of a liquid and 5 swallows of a solid bolus. Measurements were repeated 30 minutes after IM administration of buprenorphine and acepromazine. Results—HRM was successfully performed in 14 dogs. Data sets of 8 dogs were adequate for analysis. For the upper esophageal sphincter, median values of baseline pressure, residual pressure, relaxation time to nadir, and relaxation duration were determined for awake and sedated dogs for liquid and solid swallows. For the tubular portion of the esophagus, median values of peristaltic contractile integral, bolus transit time, and contractile front velocity were determined for awake and sedated dogs for liquid and solid swallows. For the lower esophageal sphincter, median values of baseline pressure and residual pressure were determined for awake and sedated dogs for liquid and solid swallows. Significant differences (awake vs sedated) were found for the upper esophageal sphincter residual pressure (liquid swallows), relaxation time to nadir (liquid swallows), bolus transit time (solid swallows), and contractile front velocity (solid swallows). Conclusions and Clinical Relevance—HRM was feasible for evaluation of esophageal function in most awake dogs. Although sedation in uncooperative patients may minimally influence results of some variables, an overall assessment of swallowing should be possible.

Imerslund-Grasbeck syndrome (IGS) or selective cobalamin malabsorption has been described in humans and dogs. IGS occurs in Border Collies and is inherited as a monogenic autosomal recessive trait in this breed. Using 7 IGS cases and 7 non-affected controls we mapped the causative mutation by genome-wide association and homozygosity mapping to a 3.53 Mb interval on chromosome 2. We re-sequenced the genome of one affected dog at ∼10× coverage and detected 17 non-synonymous variants in the critical interval. Two of these non-synonymous variants were in the cubilin gene (CUBN), which is known to play an essential role in cobalamin uptake from the ileum. We tested these two CUBN variants for association with IGS in larger cohorts of dogs and found that only one of them was perfectly associated with the phenotype. This variant, a single base pair deletion (c.8392delC), is predicted to cause a frameshift and premature stop codon in the CUBN gene. The resulting mutant open reading frame is 821 codons shorter than the wildtype open reading frame (p.Q2798Rfs*3). Interestingly, we observed an additional nonsense mutation in the MRC1 gene encoding the mannose receptor, C type 1, which was in perfect linkage disequilibrium with the CUBN frameshift mutation. Based on our genetic data and the known role of CUBN for cobalamin uptake we conclude that the identified CUBN frameshift mutation is most likely causative for IGS in Border Collies.

Objective—To characterize the ultrasonographic appearance of the canine esophagus. Animals—14 healthy Beagles. Procedures—Endoscopic ultrasonography (EUS) examinations were performed with a radial ultrasonographic gastrovideoscope in anesthetized dogs. Images were obtained at 3-cm intervals along the esophageal length to allow evaluation of the esophageal wall. Images were obtained with the probe in direct contact with the esophageal wall and with a water-filled balloon as a standoff. Results—Images were obtained with (12 dogs) and without (10) the water-filled balloon. Median thickness of the esophageal wall was 2.19 mm (range, 1.03 to 5.62 mm) in the proximal third of the esophagus, 2.15 mm (range, 1.10 to 4.45 mm) in the middle third, and 2.84 mm (range, 1.35 to 5.92 mm) in the distal third. Wall thickness differed significantly between proximal and distal thirds. Results were similar when the water-filled balloon was used. Esophageal wall layers appeared as 5 alternating hyperechoic and hypoechoic bands that could not be consistently identified in all dogs. All layers could be identified in 26 of 198 (13%) images, 3 layers could be identified in 67 of 198 (34%) images, and 105 of 198 (53%) images had no layers. Visual identification of layers in images obtained with and without the balloon did not differ significantly. Conclusions and Clinical Relevance—EUS appeared to be a useful technique for assessing esophageal wall integrity in dogs; however, complete evaluation of all layers could not be accomplished in all instances. Further studies with this technique in dogs are needed.

Background Serum lipase activities measured by catalytic assays are claimed to be of limited utility for diagnosing pancreatitis in cats. The Spec fPL assay currently is believed the most sensitive test; however, studies comparing different lipase assays are lacking. 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6′-methylresorufin) ester (DGGR) assay for the determination of lipase activity has been evaluated in dogs, but no information is available in cats. Objectives To investigate the agreement of DGGR-lipase activity and Spec fPL concentration in cats with clinical signs consistent with pancreatitis. Animals Two hundred fifty-one client-owned cats. Methods DGGR-lipase activity and Spec fPL concentration measured from the same blood sample in cats undergoing investigation for pancreatitis. The agreement between DGGR-lipase and Spec fPL at different cutoffs was assessed using Cohen's kappa coefficient (κ). Sensitivity and specificity were calculated for 31 cases where pancreatic histopathology was available. Results DGGR-lipase (cutoff, 26 U/L) and Spec fPL (cutoff, >5.3 μg/L) had a κ of 0.68 (standard error [SE] 0.046). DGGR-lipase (cutoff, 26 U/L) and Spec fPL (cutoff, >3.5 μg/L) had a κ of 0.60 (SE, 0.05). The maximum κ at a Spec fPL cutoff >5.3 μg/L was found when the DGGR-lipase cutoff was set >34 U/L and calculated as 0.755 (SE, 0.042). Sensitivity and specificity were 48% and 63% for DGGR-lipase (cut-off, 26 U/L) and 57% and 63% for Spec fPL (>5.3 μg/L), respectively. Conclusions and Clinical Importance Both lipase assays agreed substantially. DGGR assay seems a useful and cost-efficient method compared to the Spec fPL test.

A six-year-old Rottweiler with chronic ascites and moderate panhypoproteinaemia that had been treated with large volume paracentesis over several months duration was diagnosed with a large bi-atrial mass and hepatic fibrosis. For palliative treatment, a peritoneo-vesical automated fluid shunt system with an integrated chargeable battery and an integrated computer to control pump function and to transmit data transcutaneously was implanted by coeliotomy. The pump was left in place for 10 weeks, eliminating the need for further paracentesis during this time. At the end of this period, no ascites was discernible and serum protein concentrations had returned to their respective reference intervals. As a complication, decubitus with skin perforation had developed above the pump. Besides palliative treatment of chronic refractory ascites, this pump may have application in other conditions characterised by chronic cavity effusion or in peritoneal dialysis.

Objective—To determine reference ranges for serum cobalamin (Cbl), urine methylmalonic acid (uMMA), and plasma total homocysteine (tHcys) concentrations and to compare values for healthy control dogs with values for Border Collies (BCs), a breed in which hereditary cobalamin deficiency has been identified. Animals—113 BCs, 35 healthy control dogs fed a typical diet, and 12 healthy dogs fed a bone and raw food diet exclusively. Procedures—Urine and blood samples were obtained from each dog and Cbl, uMMA, and tHcys concentrations were determined. Results—Reference ranges for Cbl (261 to 1,001 ng/L), uMMA (0 to 4.2 mmol/mol of creatinine), and tHcys (4.3 to 18.4 μmol/L) concentrations were determined. Four BCs had a Cbl concentration lower than the assay detection limit (150 ng/L); median uMMA and tHcys concentrations in these dogs were 4,064 mmol/mol of creatinine and 51.5 μmol/L, respectively. Clinical abnormalities included stunted growth, lethargy, anemia, and proteinuria. Abnormalities improved after administration of cobalamin. Of the 109 healthy BCs with Cbl and tHcys concentrations within reference ranges, 41 (37.6%) had a high uMMA concentration (range, 5 to 360 mmol/mol). Results for dogs fed raw food were similar to those for control dogs. Conclusions and Clinical Relevance—Hereditary cobalamin deficiency is a rare disease with various clinical signs. The finding of methylmalonic aciduria in healthy eucobalaminemic BCs and BCs with clinical signs of Cbl deficiency was surprising and indicated these dogs may have defects in intracellular processing of Cbl or intestinal Cbl malabsorption, respectively. Studies investigating Cbl absorption and metabolic pathways are warranted.

Primary hyperaldosteronism is a clinical syndrome characterized by an elevated aldosterone secretion by the adrenals. The present case series describes 7 cats with primary hyperaldosteronism, which were presented between 2002 and 2011. Common clinical symptoms were weakness, anorexia, cervical ventroflexion and blindness. All cats showed hypokalemia. In 6 cats, blood pressure was determined: 5 cats showed hypertension, of which 4 animals exhibited retinal detachment and blindness. In the ultrasonographic examination, unilateral adrenomegaly was present in 6 cats whereas one animal showed normal adrenals. In 4 cats, the serum aldosterone concentration was above the reference range. Five cats underwent unilateral adrenalectomy, which was accomplished uneventfully and returned the electrolytes back to normal. Histopathological examination of the adrenals revealed 2 carcinomas and 4 adenomas; one cat with ultrasonographic normal adrenals exhibited bilateral nodular hyperplasia.

Objective—To investigate the effects of twice-daily oral administration of hydrocortisone on the bile acids composition of gallbladder bile in dogs. Animals—6 placebo-treated control dogs and 6 hydrocortisone-treated dogs. Procedures—Dogs received hydrocortisone (median dose, 8.5 mg/kg) or a gelatin capsule (control group) orally every 12 hours for 84 days. Gallbladder bile samples were obtained via percutaneous ultrasound-guided cholecystocentesis from each dog before (day 0 [baseline]), during (days 28, 56, and 84), and after (days 28p, 56p, and 84p) treatment for differentiated quantification of unconjugated bile acids and taurine-conjugated and glycine-conjugated bile acids via high-performance liquid chromatography–tandem mass spectrometry. Results—Treatment with hydrocortisone for 84 days resulted in significant and reversible increases in the concentrations of unconjugated bile acids (ie, cholic, chenodeoxycholic, and deoxycholic acids) and a significant and reversible decrease in the concentration of total taurine-conjugated bile acids, compared with baseline or control group values. Treatment with hydrocortisone had no effect on bile concentrations of glycine-conjugated bile acids. Conclusions and Clinical Relevance—In dogs, hydrocortisone administration caused reversible shifts toward higher concentrations of the more hydrophobic unconjugated bile acids (chenodeoxycholic acid and deoxycholic acid) and toward lower concentrations of the amphipathic taurine-conjugated bile acids in gallbladder bile. These data suggest that similar bile acids changes could cause major alterations in gallbladder structure or function over time in hypercortisolemic dogs.

An association between gallbladder mucoceles and hypercortisolism (HC) was recently described in dogs. Because the formation of a mucocele from clear bile without the transitional formation of microprecipitates appears unlikely, the aim of this study was to investigate the effects of iatrogenic HC on sludge formation and changes in the biochemical composition of bile. Bile samples from 6 dogs obtained by percutaneous ultrasound-guided cholecystocentesis before (day 0), during (days 28, 56, and 84), and after (days 28p, 56p, and 84p) oral administration of hydrocortisone (8 mg/kg every 12 h) were analysed for calcium, cholesterol and bilirubin concentrations and pH. In addition the gallbladder was examined ultrasonographically for sludge. Six dogs receiving a placebo served as controls. Although gallbladder sludge was observed in all treated dogs at day 56, it was also noted in 50% of control dogs, and no significant differences were seen between groups at any sampling time. Bilirubin and cholesterol concentrations decreased significantly and reversibly during treatment, and calcium concentration showed a similar trend. Bile pH was consistently slightly alkaline during iatrogenic HC, whereas it was slightly acidic in control animals. A 3-month period of iatrogenic HC does not lead to ultrasonographically detectable gallbladder sludge or to an increase in bile constituents that are commonly implicated in sludge formation in humans.

Enteric duplication is a rare developmental malformation in people, dogs and cats. The purpose of the present report is to describe the first case of a rectal duplication cyst in a 7-year-old domestic shorthair cat presenting for acute constipation and tenesmus. On rectal palpation a spherical mass compressing the lumen of the rectum could be felt in the dorsal wall of the rectum. A computed tomography (CT) scan confirmed the presence of a well demarcated cystic lesion in the pelvic canal, dorsal to the rectum. The cyst was surgically removed via a perineal approach. No communication with the rectal lumen could be demonstrated. Histopathological examination was consistent with a rectal duplication cyst. Clinical signs resolved completely after excision of this conjoined non-communicating cystic rectal duplicate.

A 12-year-old Rottweiler cross Labrador was presented with anorexia and weakness. Adrenal insufficiency was diagnosed with hyponatraemia, hyperkalaemia and undetectable resting and post-ACTH cortisol and aldosterone concentrations. The only abnormal diagnostic imaging result was bilateral adrenomegaly. Cytologic findings of liver, spleen and peripheral lymph nodes were normal. The dog responded initially to standard replacement therapy but relapsed shortly afterwards. The owners opted for euthanasia and allowed only removal of both adrenal glands. Microscopically, infiltrative polymorphic proliferations of densely packed tumour cells arranged as nests, intermingled with multifocal areas of necrosis and inflammatory cells were found. Silver staining revealed a few non-neoplastic adrenomedullary cells, whereas neoplastic cells did not stain. Immunohistochemistry was negative for neuron-specific enolase, vimentin, cytokeratin, synaptophysin, chromogranin A, S-100 protein, CD 56, 79 and 3. The final diagnosis was highly anaplastic bilateral adrenal neoplasia. This is the first report of bilateral adrenal malignancy presenting as clinical hypoadrenocorticism in a dog.