Hemorrhagic bowel syndrome in dairy cattle: Gross, histological, and microbiological characterization.

Hemorrhagic bowel syndrome (HBS) is a sporadic and fatal disease of predominantly lactating dairy cattle, characterized by segmental hemorrhage and luminal clot formation in the small intestine. Although, Clostridium perfringens and Aspergillus fumigatus have been associated with HBS, the pathogenesis and cause are currently unknown. In this study, 18 naturally occurring cases of HBS (7 necropsied immediately following euthanasia, 11 with 12-48 hour postmortem intervals) were investigated to characterize the pathology and the intestinal microbiome. Hemorrhagic bowel syndrome was characterized by a single small-intestinal, intramucosal hematoma with dissection of the lamina muscularis mucosae. In most cases necropsied immediately after euthanasia (4/7), the intestinal mucosa proximal to the hematoma contained 9 to 14, dispersed, solitary or clustered, erosions or lacerations measuring 4 to 45 mm. In 77% (37/48) of these mucosal lesions, microscopic splitting of the lamina muscularis mucosae comparable to the hematoma was present. These findings suggest the intramucosal hematoma to originate from small mucosal erosions through dissecting hemorrhage within the lamina muscularis mucosae. No invasive fungal growth was observed in any tissue. Bacteriological cultivation and nanopore sequencing showed a polymicrobial population at the hematoma and unaffected intestine, with mostly mild presence of C perfringens at selective culture. Gross and microscopic lesions, as well as the culture and sequencing results, were not in support of involvement of C perfringens or A fumigatus in the pathogenesis of HBS.

Retrospective evaluation of the incidence of gastrointestinal bleeding in dogs receiving ophthalmic nonsteroidal anti-inflammatory drugs.

OBJECTIVES: To report the incidence of gastrointestinal (GI) bleeding and associated risk factors in a population of dogs receiving ophthalmic nonsteroidal anti-inflammatory drugs (NSAIDs). ANIMAL STUDIED: Medical records of dogs prescribed ophthalmic NSAIDs (cases), dogs receiving systemic NSAIDs alone and dogs receiving systemic prednisone alone (controls). PROCEDURES: Data were collected retrospectively from the medical records of 204 dogs prescribed ophthalmic NSAIDs (diclofenac, ketorolac, or flurbiprofen), which were subdivided based on if they received any concurrent systemic NSAIDs or glucocorticoids, 136 dogs receiving a systemic NSAID (carprofen or meloxicam) alone, and 151 dogs receiving a systemic glucocorticoid (prednisone) alone at a referral hospital from 2015 to 2019. RESULTS: Gastrointestinal bleeds developed in 8/79 (10.1%) of topical NSAID-only cases, 10/136 (7.4%) of systemic NSAID controls, and 14/151 (9.3%) of systemic glucocorticoid controls, with no significant difference between the three groups (p = .6103). There were no significant differences in GI bleed rates between cases treated with ketorolac, diclofenac, or flurbiprofen (p = .160), although severe GI bleeding was only seen in ketorolac-treated dogs. Presence of a known concurrent risk factor for GI bleeding was significantly associated with the development of GI bleed in dogs on ophthalmic NSAIDs (p = .032). CONCLUSIONS: Dogs treated with ophthalmic NSAIDs developed GI bleeding at a frequency comparable to dogs receiving systemic NSAIDs or systemic glucocorticoids alone, suggesting that dogs receiving ophthalmic NSAIDs may be at increased risk of GI bleeding.

Life-threatening gastrointestinal bleeding caused by jejunal heterotopic gastric mucosa in an adult dog: a rare case report.

BACKGROUND: Heterotopic gastric mucosa has been scarcely reported in the veterinary literature. Its presence can be asymptomatic or associated with various clinical signs ranging from apathy, vomiting, to abdominal pain. This report illustrates the presence of heterotopic gastric mucosa in the jejunum of an adult dog. It is the first to describe severe anemia, requiring acute blood transfusion, following intestinal hemorrhage caused by heterotopic gastric mucosa. CASE PRESENTATION: A twelve-year-old, intact male Maltese dog was presented with a history of apathy, vomiting and anemia. The dog was on a strict diet for recurrent diarrhea, food intolerance and skin allergy. Clinical examination revealed severe anemic mucous membranes and painful abdominal palpation. Blood examination confirmed severe regenerative anemia. Ultrasonography showed an intestinal neoplasm, gall bladder sludge and non-homogeneous liver parenchyma. Three-view thoracic radiographs failed to show any metastatic lesions or enlarged lymph nodes. After initial stabilization and blood transfusion, a midline exploratory laparotomy was performed. Three different masses were found in the jejunum. Resection and anastomosis of approximately 40 cm of jejunum was performed, followed by liver and lymph node biopsy and placement of an esophagostomy tube. Two days after surgery the dog started to clinically improve and was discharged from the hospital on the sixth day after surgery. Histopathology revealed the intestinal masses to be heterotopic gastric mucosa associated with intramural cystic distensions, multifocal ulceration and bleeding into the intestinal lumen. Two years after surgery, the dog did not have a recurrence of anemia or gastrointestinal signs. CONCLUSIONS: This case demonstrates that heterotopic gastric mucosa can be considered one of the differential diagnoses in case of severe anemia due to gastrointestinal hemorrhage and suspected intestinal tumors. Although in most described cases in literature the finding seems to be incidental on necropsy, our report shows that heterotopic gastric mucosa can be the etiology of life-threatening signs. In addition, because no recurrent diarrhea episodes occurred after surgical resection of the ectopic tissue, it is likely that the heterotopic gastric mucosa was the cause of the food intolerance signs in this dog.

Eimeria ninakohlyakimovae casts NOX-independent NETosis and induces enhanced IL-12, TNF-α, IL-6, CCL2 and iNOS gene transcription in caprine PMN.

Eimeria ninakohlyakimovae represents a highly pathogenic coccidian parasite causing severe haemorrhagic typhlocolitis in goat kids worldwide. NETosis was recently described as an efficient defense mechanism of polymorphonuclear neutrophils (PMN) acting against different parasites in vitro and in vivo. In vitro interactions of caprine PMN with parasitic stages of E. ninakohlyakimovae (i. e. oocysts and sporozoites) as well as soluble oocyst antigens (SOA) were analyzed at different ratios, concentrations and time spans. Extracellular DNA staining was used to illustrate classical molecules induced during caprine NETosis [i. e. histones (H3) and neutrophil elastase (NE)] via antibody-based immunofluorescence analyses. Functional inhibitor treatments with DPI and DNase I were applied to unveil role of NADPH oxidase (NOX) and characterize DNA-backbone composition of E. ninakohlyakimovae-triggered caprine NETosis. Scanning electron microscopy (SEM)- and immunofluorescence-analyses demonstrated that caprine PMN underwent NETosis upon contact with sporozoites and oocysts of E. ninakohlyakimovae, ensnaring filaments which firmly entrapped parasites. Detailed co-localization studies of E. ninakohlyakimovae-induced caprine NETosis revealed presence of PMN-derived DNA being adorned with nuclear H3 and NE corroborating molecular characteristics of NETosis. E. ninakohlyakoimovae-induced caprine NETosis was found to be NOX-independent since DPI inhibition led to a slight decrease of NETosis. Exposure of caprine PMN to vital E. ninakohlyakimovae sporozoites as well as SOA resulted in up-regulation of IL-12, TNF-α, IL-6, CCL2 and iNOS gene transcription in stimulated PMN. Since vital E. ninakohlyakimovae-sporozoites induced caprine NETosis, this effective entrapment mechanism might reduce initial sporozoite epithelial host cell invasion during goat coccidiosis ultimately resulting in less macromeront formation and reduced merozoites I production.

Evaluation of the guaiac fecal occult blood test for detection of gastrointestinal bleeding in the rhesus macaque (Macaca mulatta).

BACKGROUND: Gastrointestinal (GI) hemorrhage accompanies several common diseases of rhesus macaques (Macaca mulatta). Guaiac fecal occult blood testing (gFOBT) is a non-invasive means to detect such bleeding in several species; however, there are currently no data indicating reliability of this test to detect GI hemorrhage in macaques. METHODS: We evaluated sensitivity and specificity of gFOBT to detect simulated and biopsy-associated bleeding in the stomach, duodenum, and colon of 15 rhesus macaques. Fecal samples were analyzed via gFOBT for 72 hours. RESULTS: Guaiac fecal occult blood testing was more sensitive to detect lower vs upper GI bleeding; sensitivity was volume-dependent in the upper GI tract. Single-test specificity was 95.2%. Repeated fecal collections increased gFOBT sensitivity without affecting specificity. CONCLUSIONS: Guaiac fecal occult blood testing is a useful screening test for both upper and lower GI bleeding in rhesus macaques. For highest sensitivity, gFOBT should be performed on three fecal samples collected 24 hours apart.

Jejunal Lesion Identified at a Previous Anastomosis Site in a Dog Using Capsule Endoscopy.

A 3 yr old spayed female French bulldog was evaluated for a progressive regenerative anemia of unknown origin that was unresponsive to empiric immunosuppressive and gastroprotective therapy. The patient had a history of previous resection and anastomosis of a small intestinal diverticulum ∼2 yr prior to evaluation for her anemia. Capsule endoscopy revealed a focal abnormality in the distal jejunum at the site of a previous bowel resection and anastomosis. This lesion was suspected to be the cause of ongoing gastrointestinal bleeding and anemia. Exploratory laparotomy combined with endoscopy was performed to further investigate and localize the jejunal lesion. The lesion was resected, and a primary end-to-end jejunal anastomosis was performed. Histopathology of the specimen revealed jejunal suture granulomas with focal ulceration. The patient recovered well from surgery with significant improvement of the anemia and resolution of clinical signs at recheck examinations 1 and 2 wk postoperatively. Complete resolution of the anemia was noted at a 6 wk follow-up. The case report demonstrates how, in cases of unknown causes of anemia, capsule endoscopy is a noninvasive method of identifying the presence of gastrointestinal bleeding as a result of lesions that might otherwise not be detectable with abdominal ultrasound or conventional endoscopy. The report also documents a long-term complication to a resection and anastomosis surgery.

FIRST REPORT OF ADENOVIRAL HEMORRHAGIC DISEASE IN THREE MULE DEER (ODOCOILEUS HEMIONUS) IN ARIZONA.

This study presents the gross and histopathological findings of adenoviral hemorrhagic disease (AHD) in two yearling and one adult mule deer (Odocoileus hemionus). These cases represent the first known outbreak of deer adenovirus (Odocoileus adenovirus 1) in Arizona. Over the span of a month, three female captive mule deer were submitted to Midwestern University's Animal Health Institute for postmortem examination. All of these deer were from the same deer farm and historical findings were similar, consisting of acute presentation of hemorrhagic diarrhea and sudden death. Grossly and histopathologically, all cases had severe pulmonary edema and hemorrhagic enteritis. Additionally, two of the three cases had low numbers of large amphophilic intranuclear inclusions expanding endothelial cells within the small intestine and lungs. Viral PCR of pooled small intestine, lung, and spleen from each of the three cases were positive for deer adenovirus and negative for blue tongue and epizootic hemorrhagic disease.

Characterization of a Vesivirus Associated with an Outbreak of Acute Hemorrhagic Gastroenteritis in Domestic Dogs.

Four of eleven affected dogs died despite aggressive treatment during a 2015 focal outbreak of hemorrhagic gastroenteritis following a stay in a pet housing facility. Routine diagnostic investigations failed to identify a specific cause. Virus isolation from fresh necropsy tissues yielded a calicivirus with sequence homology to a vesivirus within the group colloquially known as the vesivirus 2117 strains that were originally identified as contaminants in CHO cell bioreactors. In situ hybridization and reverse transcription-PCR assays of tissues from the four deceased dogs confirmed the presence of canine vesivirus (CaVV) nucleic acids that localized to endothelial cells of arterial and capillary blood vessels. CaVV nucleic acid corresponded to areas of necrosis and hemorrhage primarily in the intestinal tract, but also in the brain of one dog with nonsuppurative meningoencephalitis. This is the first report of an atypical disease association with a putative hypervirulent vesivirus strain in dogs, as all other known strains of CaVV appear to cause nonclinical infections or relatively mild disease. After identification of the CU-296 vesivirus strain from this outbreak, four additional CaVV strains were amplified from unrelated fecal specimens and archived stocks provided by other laboratories. Broader questions include the origins, reservoir(s), and potential for reemergence and spread of these related CaVVs.

COLONIC DIVERTICULOSIS AND DIVERTICULAR HEMORRHAGE IN A GERIATRIC FEMALE ORANGUTAN ( PONGO ABELII).

A 57-yr-old female Sumatran orangutan ( Pongo abelii) presented with signs of intermittent lethargy and inappetence, then subsequently developed profuse hemorrhagic diarrhea. Colonoscopy under anesthesia revealed diverticulosis of the descending colon, with multiple large diverticula containing fecoliths. There was no evidence of diverticulitis, but a regenerative anemia had developed following an acute diverticular bleed. The orangutan recovered with conservative therapy. Colonic diverticulosis has been reported in nonhuman primates and appears to have a similar clinical presentation to the condition as it occurs in humans. This is the first published report of colonic diverticulosis in a great ape.

Aberrant heartworm migration to the abdominal aorta and systemic arteriolitis in a dog presenting with vomiting and hemorrhagic diarrhea.

A 2-year-old Dachshund was presented for vomiting and diarrhea. Abdominal ultrasound revealed Dirofilaria immitis in the abdominal aorta and an avascular segment of small intestine. The dog was euthanized. Necropsy revealed D. immitis in the abdominal aorta and widespread necrotizing arteriolitis. This is a unique presentation of aberrant migration of D. immitis.

Migration aberrante du ver du cœur vers l'aorte abdominale et artériolite systémique chez un chien présentant des vomissements et une diarrhée hémorragique. Un Dachshund âgé de 2 ans a été présenté pour des vomissements et de la diarrhée. Une échographie de l'abdomen a révélé Dirofilaria immitis dans l'aorte abdominale et un segment avasculaire du petit intestin. Le chien a été euthanasié. La nécropsie a révélé D. immitis dans l'aorte abdominale et une artériolite nécrosante généralisée. Il s'agit d'une présentation unique de la migration aberrante de D. immitis.(Traduit par Isabelle Vallières).

Colonic gastrointestinal stromal tumor resulting in recurrent colic and hematochezia in a warmblood gelding.

A 14-year-old Trakehner gelding was evaluated for recurrent colic, with episodes occurring over 1 year. Signs were consistent with intermittent ascending colon obstruction and hematochezia. Necropsy examination revealed an ulcerated mass extending into the lumen of the right dorsal ascending colon. Gross and histologic appearance and immunoreactivity to c-kit (CD117), desmin, vimentin, and smooth muscle actin, were consistent with a diagnosis of gastrointestinal stromal tumor.

Tumeur ventrale gastro-intestinale du côlon produisant des coliques et de l'hématochézie et des coliques récurrentes chez un hongre à sang chaud. Un hongre Trakehner âgé de 14 ans a été évalué pour des coliques récurrentes et les épisodes duraient depuis 1 an. Les signes étaient conformes à une obstruction intermittente du côlon ascendant et à l'hématochézie. La nécropsie a révélé une masse ulcéreuse s'étendant dans la lumière du côlon ascendant dorsal droit. L'apparence brute et histologique et l'immunoréactivité à c-kit (CD117), à la desmine, à la vimentine et à l'actine des muscles lisses étaient conformes au diagnostic de tumeur ventrale gastro-intestinale.(Traduit par Isabelle Vallières).

Characterization of early-stage lesions and investigation on the role of mucosal trauma in hemorrhagic bowel syndrome in cattle.

Hemorrhagic bowel syndrome (HBS) is characterized by a dissecting intramucosal hematoma at the small bowel, causing obstruction and severe hemorrhage in dairy cattle. Recent investigation revealed the presence of early-stage lesions in cows affected by HBS. These are presumed to be the initial stage of the hematoma, as both share unique dissection of the lamina muscularis mucosae (LMM) as histological hallmark. Early-stage lesions of HBS have not been characterized in greater detail, and neither has the hypothesis of mucosal abrasion as etiology been explored. Therefore, the first objective of the present study was to characterize the morphology of early-stage lesions, by gross examination, histochemistry, immunohistochemistry and transmission electron microscopy. The second objective was to determine the effect of mucosal abrasion to the small intestine in an ex vivo model. A total of 86 early-stage lesions from 10 cows with HBS were characterized. No underlying alterations at the LMM were evident which could explain their occurrence. However, degeneration at the ultrastructural level of the LMM smooth muscle cells was present in 3 of 4 lesions, it is however unclear whether this is primary or secondary. Bacteriological examination did not reveal any association with a specific bacterium. Experimental-induced and early-stage lesions were gross and histologically evaluated and scored in three cows with HBS and seven controls. Experimentally induced lesions in both affected cows and controls, were histologically very similar to the naturally occurring early-stage lesions. Altogether, the results are suggestive for mucosal trauma to play a role in the pathogenesis of HBS.

Circovirus in tissues of dogs with vasculitis and hemorrhage.

We characterized the complete genome of a novel dog circovirus (DogCV) from the liver of a dog with severe hemorrhagic gastroenteritis, vasculitis, and granulomatous lymphadenitis. DogCV was detected by PCR in fecal samples from 19/168 (11.3%) dogs with diarrhea and 14/204 (6.9%) healthy dogs and in blood from 19/409 (3.3%) of dogs with thrombocytopenia and neutropenia, fever of unknown origin, or past tick bite. Co-infection with other canine pathogens was detected for 13/19 (68%) DogCV-positive dogs with diarrhea. DogCV capsid proteins from different dogs varied by up to 8%. In situ hybridization and transmission electron microscopy detected DogCV in the lymph nodes and spleens of 4 dogs with vascular compromise and histiocytic inflammation. The detection of a circovirus in tissues of dogs expands the known tropism of these viruses to a second mammalian host. Our results indicate that circovirus, alone or in co-infection with other pathogens, might contribute to illness and death in dogs.

Clinicopathologic and gastrointestinal effects of administration of prednisone, prednisone with omeprazole, or prednisone with probiotics to dogs: A double-blind randomized trial.

BACKGROUND: The efffect of administering of probiotics or twice-daily omeprazole on glucocorticoid-induced gastric bleeding in dogs is unknown. HYPOTHESIS: Compare gastrointestinal bleeding among dogs administered placebo, prednisone (2 mg/kg q24h), prednisone with omeprazole (1 mg/kg q12h), or prednisone with probiotics (Visbiome, 11.2-22.5 billion CFU/kg q24h) for 28 days. ANIMALS: Twenty-four healthy research dogs. METHODS: Double-blinded, placebo-controlled randomized trial. Clinical signs and endoscopic gastrointestinal mucosal lesion scores at baseline (t1 ), day 14 (t2 ), and day 28 (t3 ) were compared using split-plot repeated-measures mixed-model ANOVAs. RESULTS: Fecal score differed by treatment-by-time (F[6,40] = 2.65, P < .03), with higher scores in groups receiving prednisone at t3 than t1 . Nineteen of thirty-three episodes of diarrhea occurred in the prednisone with omeprazole group. Gastric mucosal lesion scores differed by treatment-by-time (F[6,60] = 2.86, P = .05), among treatment groups (F[3,60] = 4.9, P = .004), and over time (F[2,60] = 16.5, P < .001). Post hoc analysis revealed lesion scores increased over time for all groups receiving prednisone. At t3 , scores for the prednisone (8.7 ± 4.9) and prednisone with probiotics (8.7 ± 4.9) groups differed significantly from placebo (1.8 ± 1.8; P ≤ .04), whereas scores for the prednisone with omeprazole (6.5 ± 5.5) group did not differ from placebo (P = .7). Ulcers occurred only in dogs receiving prednisone. CONCLUSIONS AND CLINICAL IMPORTANCE: Prednisone-induced gastric bleeding. Co-administration of omeprazole partially mitigated bleeding, but a similar protective benefit was not demonstrated by co-administration of the evaluated probiotic.

Anemia in canine chronic kidney disease is multifactorial and associated with decreased erythroid precursor cells, gastrointestinal bleeding, and systemic inflammation.

OBJECTIVE: Compare erythropoiesis-related factors between different stages of canine chronic kidney disease (CKD). ANIMALS: 8 healthy adult dogs (controls), and 24 dogs with CKD, equally divided into 3 groups based on International Renal Interest Society-CKD Guidelines (stage 2, 3, and 4) were recruited between December 2012 and December 2014. METHODS: The following were assessed in all dogs and then compared between groups: bone marrow cytology, CBC, reticulocyte count, urinalysis, serum biochemistry, blood pressure, occult gastrointestinal bleeding, and serum concentrations of parathyroid hormone (PTH), erythropoietin, interleukin-1ß, interleukin-3, tumor necrosis factor-α (TNFα), and interferon-γ. RESULTS: Erythropoiesis inducing and suppressing factors and the results of the bone marrow cytology of dogs in stage 2 CKD did not differ from the control group. The presence of reticulocytosis in CKD stage 2 suggests that blood loss or erythrocyte destruction might be contributing to developing anemia. Anemia in dogs with progressive CKD was associated with increasing PTH and TNFα and with elevation of the ratio of myeloid to erythroid precursor cells caused by hypoplasia of the erythroid series. The latter was represented mainly by a decrease in the population of polychromatophilic rubricytes and metarubricytes. CLINICAL RELEVANCE: Increased PTH and TNFα seem to contribute to the reduced percentage of polychromatophilic rubricytes and erythroid population, thereby aggravating the anemia of dogs with advanced CKD. Gastrointestinal blood loss contributes to anemia in all canine CKD stages.

Plasma urea:creatinine ratio as a biomarker of gastrointestinal bleeding in dogs with anaemia.

BACKGROUND: Gastrointestinal bleeding is a cause of anaemia in dogs. A reliable, non-invasive biomarker to differentiate gastrointestinal bleeding from other causes of anaemia would be advantageous to direct clinical decisions in anaemic patients. Plasma urea:creatinine ratio is an accepted biomarker of upper gastrointestinal bleeding in human medicine. OBJECTIVES: The objective of this study was to evaluate plasma urea:creatinine ratio as a biomarker of gastrointestinal bleeding in a population of dogs with anaemia. METHODS: This was a prospective cross-sectional study of dogs with anaemia presenting to referral centres for the investigation of anaemia. Cases were categorised as having overt gastrointestinal bleeding (melena on presentation), occult gastrointestinal bleeding (historical and diagnostic findings consistent with gastrointestinal bleeding without melena at presentation) or anaemia of other cause (confident diagnosis other than gastrointestinal bleeding reached, normal diagnostic imaging of gastrointestinal tract). Urea:creatinine ratio at presentation was calculated by dividing urea (mg/dL) by creatinine (mg/dL). RESULTS: Ninety-five dogs were included. Plasma urea:creatinine ratio was not significantly different between dogs with overt or occult gastrointestinal bleeding or those with anaemia of other cause (median urea:creatinine ratio 25.8, 20.7 and 22.5, respectively). No significant difference in urea:creatinine ratio was found between dogs with upper and lower gastrointestinal bleeding (median urea:creatinine ratio 19.4 and 24.6, respectively). CONCLUSIONS: Plasma urea:creatinine ratio was not helpful in differentiating between dogs with anaemia resulting from gastrointestinal bleeding (overt or occult) and those with other causes of anaemia.

Gastrointestinal angiodysplasias diagnosed using video capsule endoscopy in 15 dogs.

BACKGROUND: Angiodysplasia (AGD) is rarely diagnosed in dogs with gastrointestinal bleeding (GIB) and is reported in case reports in dogs. OBJECTIVE: Describe signalment, clinical and diagnostic features of dogs with gastrointestinal (GI) AGD diagnosed by video capsule endoscopy (VCE). ANIMALS: Dogs with overt or suspected GIB which underwent VCE. METHODS: Dogs for which a VCE was submitted for overt or suspected GIB from 2016 to 2021 were selected retrospectively. Medical records and full-length VCE recordings where AGDs were initially detected, were reviewed by 2 trained internists. AGD was considered definitive if 2 readers detected it. Signalment, clinical signs, blood work, medications, concurrent diseases, findings of previous conventional endoscopy, and surgical exploration (if applicable) of dogs with AGD were recorded. RESULTS: Definitive AGD was diagnosed in 15 of 291 (5%) dogs (12 males, 3 females). Twelve (80%) had overt GIB, 11 (73%) had hematochezia, and 6 (40%) had microcytic and hypochromic anemia. AGD was missed by conventional endoscopy in 9/9 dogs and exploratory surgery in 3/3 dogs. Thirteen capsules were administered by mouth (1 incomplete study), and 2 via endoscopy directly into the duodenum. AGD was visualized in the stomach of 3 dogs, in the small intestine of 4, and in the colon of 13 dogs. CONCLUSION AND CLINICAL IMPORTANCE: Although rare, AGD should be considered in dogs with suspected GIB after a negative conventional endoscopy or surgical exporation. Video capsuel endoscopy appears to be a sensitive test to identify AGD within the GI tract.

Double-blinded placebo-controlled clinical trial of prophylactic omeprazole in dogs treated surgically for acute thoracolumbar intervertebral disc extrusion.

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.

Clostridium perfringens type A fatal acute hemorrhagic gastroenteritis in a dog.

The morning after participating in a dog show, a 2-year-old Pomeranian dog was found dead in a pool of bloody feces. Necropsy revealed hemorrhagic gastroenteritis of the entire gastrointestinal tract, with many Gram-positive bacilli on the surface and in the lumen and crypts of the intestine. Enterotoxin-positive type A Clostridium perfringens were isolated in large numbers. This dramatic case of fatal C. perfringens gastroenteritis highlights the need to better understand the role of this bacterium in enteric disease of dogs.

Frequency of signs of chronic gastrointestinal disease in dogs after an episode of acute hemorrhagic diarrhea.

BACKGROUND: Acute enteropathy is a trigger of chronic gastrointestinal (GI) disease in humans. OBJECTIVE: To report the prevalence of and explore possible risk factors for signs of chronic GI disease in dogs after an episode of acute hemorrhagic diarrhea (AHD). ANIMALS: One hundred and fifty-one dogs, 80 dogs with a historical diagnosis of AHD, 71 control dogs with no history of AHD. METHODS: In this retrospective longitudinal study, data were collected from dogs with a historical diagnosis of AHD and healthy controls matched by breed, age and sex, aged between 1 year and 15 years of age, for which a follow-up of at least 12 months after enrolment was available. Dog owners responded to a questionnaire to determine the history of signs of chronic GI disease. RESULTS: There was a higher prevalence of signs of chronic GI disease in the dogs with a previous episode of AHD compared to control dogs (AHD 28%; controls 13%; P = .03; odds ratio = 2.57; confidence interval [CI] 95% 1.12-6.31) over a similar observation time (median 4 years; range, 1-12 years). CONCLUSIONS AND CLINICAL IMPORTANCE: Severe intestinal mucosal damage and associated barrier dysfunction might trigger chronic GI disease later in life.