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.

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.

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.

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.

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.

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.

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.

Esophageal varices in dogs: A retrospective case series.

BACKGROUND: Esophageal varices (EV) are abnormally dilated veins in the esophagus caused by alterations of blood flow or pressure. Esophageal variceal hemorrhage is a major complication of hepatic disease in humans, but a lack of information exists regarding associated adverse events in dogs. OBJECTIVE: To describe the clinical manifestations and associated etiologies and outcomes of dogs with EV. ANIMALS: Twenty-five client-owned dogs with EV diagnosed via computed tomography (CT), endoscopy, or fluoroscopy. METHODS: Retrospective case series. Cases were identified by review of the hospital imaging records database between 2010 and 2020. Signalment, clinical signs, and outcomes were documented. When present, additional collateral vasculature was also recorded. Cases were subcategorized into suspected etiology based upon the anatomic location or absence of an attributable underlying disease process, as well as the direction of blood flow. RESULTS: Twenty-four of 25 cases were identified via CT, with a prevalence of 0.012% (24/1950 total studies). Presenting clinical signs were nonspecific, and more likely because of the underlying cause as opposed to complications secondary to EV themselves. Etiologic anatomic locations were similar in occurrence between the abdomen (N = 14) and thorax (N = 11). All cases with an abdominal etiologic location had presumed or confirmed portal hypertension and 9/11 cases with a thoracic etiologic location had pulmonary, caval, or systemic hypertension. No cases died or were euthanized as a direct result of EV or associated hemorrhage. CONCLUSIONS AND CLINICAL IMPORTANCE: Esophageal varices are rarely reported in dogs and commonly identified concurrently with portal, pulmonary, and caval hypertension. Hemorrhage is not a common clinical manifestation of EV.

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.

Feasibility, complications, and quality of visualization using video capsule endoscopy in 40 dogs with overt or questionable gastrointestinal bleeding.

BACKGROUND: Prospective studies describing video capsule endoscopy (VCE), its feasibility, and complications in dogs are limited. OBJECTIVE: To assess VCE, quality of visualization, complications, and risk factors for incomplete studies in dogs with overt or questionable gastrointestinal bleeding (GIB). ANIMALS: Forty dogs with overt or questionable GIB. METHODS: Prospective, multicenter, interventional study. From August 2017 to March 2020, dogs were examined by VCE (ALICAM) because of overt or questionable GIB. Reported outcomes included diagnostic results of VCE study, quality of visualization, and complications. Risk factors for incomplete studies were evaluated using logistic regression. RESULTS: In total, 40 dogs (13 overt, 27 questionable GIB) were included. The capsules were administered PO in 29 and endoscopically in 11 dogs (6 duodenum, 5 stomach). One capsule was not retrieved. In 24 of 39 recordings, bleeding lesions were identified (10 overt GIB, 14 questionable GIB). Overall, the quality of visualization was poor to limited in the stomach and colon, and adequate to good in the small intestine. The most common complication was an incomplete study in 15/39 studies, particularly after oral administration (13/28). Risk factors for incomplete study after oral administration included administration of simethicone or opioids, chronic enteropathy, and capsule gastric transit time >6 hours. CONCLUSIONS AND CLINICAL IMPORTANCE: Video capsule endoscopy can be used to diagnose a variety of lesions causing bleeding in the gastrointestinal tract of dogs with questionable GIB. Incomplete studies are the most common complications in dogs after oral administration of capsules.

One dog's waste is another dog's wealth: A pilot study of fecal microbiota transplantation in dogs with acute hemorrhagic diarrhea syndrome.

Canine acute hemorrhagic diarrhea syndrome (AHDS) has been associated in some studies with Clostridioides perfringens overgrowth and toxin-mediated necrosis of the intestinal mucosa. We aimed to determine the effect of a single fecal microbiota transplantation (FMT) on clinical scores and fecal microbiomes of 1 and 7 dogs with AHDS from New Zealand and South Africa. We hypothesized that FMT would improve AHDS clinical scores and increase microbiota alpha-diversity and short-chain fatty acid (SCFA)-producing microbial communities' abundances in dogs with AHDS after FMT. We sequenced the V3-V4 region of the 16S-rRNA gene in the feces of AHDS FMT-recipients and sham-treated control dogs, and their healthy donors at admission, discharge, and 30 days post-discharge. There were no significant differences in median AHDS clinical scores between FMT-recipients and sham-treated controls at admission or discharge (P = 0.22, P = 0.41). At admission, the Shannon diversity index (SDI) was lower in AHDS dogs than healthy donors (P = 0.002). The SDI did not change from admission to 30 days in sham-treated dogs yet increased in FMT-recipients from admission to discharge (P = 0.04) to levels not different than donors (P = 0.33) but significantly higher than sham-treated controls (P = 0.002). At 30 days, the SDI did not differ between FMT recipients, sham-treated controls, and donors (P = 0.88). Principal coordinate analysis of the Bray-Curtis index separated post-FMT and donor dogs from pre-FMT and sham-treated dogs (P = 0.009) because of increased SCFA-producing genera's abundances after FMT. A single co-abundance subnetwork contained many of the same OTUs found to be differentially abundant in FMT-recipients, and the abundance of this module was increased in FMT-recipients at discharge and 30 days, compared to sham-treated controls. We conclude in this small pilot study FMT did not have any clinical benefit. A single FMT procedure has the potential to increase bacterial communities of SCFA-producing genera important for intestinal health up to 30 days post-FMT.

[Use of antimicrobials in acute canine diarrhea - overview of potential risks, indications and alternatives]. / Antibiotikaeinsatz beim akuten Durchfall des Hundes ­ Übersicht potenzieller Risiken, Indikationen und Alternativen.

In Germany, antibiotics are frequently used in dogs with gastrointestinal disorders such as acute diarrhea. In line with global efforts to limit antibiotic use, this literature review aims to provide a guideline for the rational and judicious use of antibiotics in acute canine diarrhea. Antibiotics can lead to gastrointestinal side effects and may exert a negative influence on the intestinal microbiota in addition to increasing the occurrence of resistant bacteria. There is also evidence that chronic immunological diseases may be triggered by the administration of antibiotics. Therefore, these should not be administered in uncomplicated acute diarrhea without signs of sepsis or systemic inflammatory reaction. In addition, enteropathogenic bacteria usually do not play a role in the etiology of acute diarrhea. For select clinical entities such as acute hemorrhagic diarrhea syndrome, antibiotic therapy should only be recommended in cases displaying signs of bacterial translocation with subsequent sepsis. In the case of parvovirosis, on the other hand, the administration of antibiotics is unavoidable due to the immunological incompetence of the dog caused by the accompanying severe neutropenia.

Diagnostic evaluation of urea nitrogen/creatinine ratio in dogs with gastrointestinal bleeding.

BACKGROUND: Urea nitrogen/creatinine ratio (UCR) is a marker for upper gastrointestinal bleeding (GIB) in people. OBJECTIVES: To assess the usefulness of UCR to predict occult GIB and distinguish upper from lower GIB in dogs. ANIMALS: Eighty-nine dogs with GIB and 65 clinically healthy dogs. Dogs were grouped according to 65 overt GIB and 24 occult GIB, and based on lesion localization (37 upper, 13 lower, and 8 both). METHODS: Seventy-four dogs were included retrospectively and 15 dogs prospectively. Serum urea nitrogen and creatinine concentrations, UCR, hemoglobin concentration, hematocrit, mean corpuscular volume, and mean corpuscular hemoglobin concentration were compared between groups. Logistic regression models were fitted to assess if variables could distinguish occult GIB from being healthy and upper from lower GIB. RESULTS: The UCR was significantly higher in dogs with overt GIB compared to control dogs (P = .02) and dogs with occult GIB (P = .05). The UCR was not significantly associated with occult GIB vs being healthy, or upper vs lower GIB (P > .05 each). Dogs with higher hemoglobin concentration and hematocrit had significantly lower odds of having occult GIB than being healthy (P < .0001 each). CONCLUSIONS AND CLINICAL IMPORTANCE: The UCR does not seem to be a clinically useful marker of occult GIB and appears to have poor discriminatory ability between upper and lower GIB. An increased UCR in a dog without signs of overt GIB, especially if its hematocrit is within the middle or upper reference interval, does not appear to warrant prompt prescription of gastrointestinal protectants.

A retrospective study of 237 dogs hospitalized with suspected acute hemorrhagic diarrhea syndrome: Disease severity, treatment, and outcome.

BACKGROUND: Few studies have investigated management and outcome in dogs with acute hemorrhagic diarrhea syndrome (AHDS), and there is a paucity of data on dogs with concurrent signs of sepsis. OBJECTIVES: To report outcome in dogs with suspected AHDS according to disease severity and antimicrobial treatment, and to evaluate effect of fluid resuscitation on clinical criteria. ANIMALS: Two hundred thirty-seven dogs hospitalized with suspected AHDS. METHODS: Retrospective study based on medical records. Disease severity was evaluated using AHDS index, systemic inflammatory response syndrome (SIRS) criteria, and serum C-reactive protein (CRP) according to 3 treatment groups: No, 1, or 2 antimicrobials. RESULTS: Sixty-two percent received no antimicrobials, 31% received 1 antimicrobial, predominantly aminopenicillins, and 7% received 2 antimicrobials. At admission, median AHDS index was 13 (interquartile range, 11-15), which decreased significantly after the first day's hospitalization (P < .001) for all groups. Compared with no antimicrobials (7%), more dogs had ≥2 SIRS criteria in the antimicrobial groups (15% and 36%, respectively). C-reactive protein (CRP) correlated positively with AHDS index at hospitalization (P < .001). Across treatment groups, rehydration markedly reduced number of clinical SIRS criteria. Survival to discharge was 96%, lower for dogs receiving 2 antimicrobials (77%, P < .05). CONCLUSIONS AND CLINICAL IMPORTANCE: The majority of dogs hospitalized with suspected AHDS improve rapidly with symptomatic treatment only, despite signs of systemic disease on initial presentation. The often-used SIRS criteria might be a poor proxy for identifying dogs with AHDS in need of antimicrobial treatment, in particular when hypovolemic. The role of CRP in clinical decision-making or prognostication warrants further investigation.

Presumptive Lornoxicam Intoxication in Four Dogs.

Lornoxicam is a nonsteroidal anti-inflammatory drug extensively used in human medicine, which is not approved for canine use. Lornoxicam intoxication has been rarely reported in dogs. Four dogs of various breeds, aged 7 months to 10 years, were admitted with a recent history of melena, anorexia and depression, occurring 1-4 days after the ingestion of lornoxicam (dose range: 0.53-2.7 [median 1.17] mg/kg). No clinically relevant comorbidities were documented, but low doses of prednisolone had been given in 3 of the dogs, in close temporal association with lornoxicam. Major clinical and clinicopathologic findings on admission included mucosal pallor, melena, depression, severe anemia, neutrophilic leucocytosis, and panhypoproteinemia. Perforated pyloric and duodenal ulcers were documented in 3 dogs by exploratory celiotomy or postmortem. Prolonged hospitalization (5-20 days) with extensive supportive care and multiple blood transfusions was required in 3 of the 4 dogs who survived to discharge. Lornoxicam ingestion may cause protracted and severe gastrointestinal tract injury and bleeding, blood loss anemia, panhypoproteinemia, and perforated gastrointestinal ulcers, associated with significant morbidity and mortality in dogs.

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.