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The impact of probiotics on dogs with acute hemorrhagic diarrhea syndrome (AHDS) has not been evaluated so far. The study aim was to assess the effect of probiotic treatment on the clinical course, intestinal microbiome, and toxigenic Clostridium perfringens in dogs with AHDS in a prospective, placebo-controlled, blinded trial. Twenty-five dogs with AHDS with no signs of sepsis were randomly divided into a probiotic (PRO; Visbiome, ExeGi Pharma) and placebo group (PLAC). Treatment was administered for 21 days without antibiotics. Clinical signs were evaluated daily from day 0 to day 8. Key bacterial taxa, C. perfringens encoding NetF toxin and enterotoxin were assessed on days 0, 7, 21. Both groups showed a rapid clinical improvement. In PRO a significant clinical recovery was observed on day 3 (p = 0.008), while in PLAC it was observed on day 4 (p = 0.002) compared to day 0. Abundance of Blautia (p<0.001) and Faecalibacterium (p = 0.035) was significantly higher in PRO on day 7 compared to day 0, while in PLAC the abundance of Faecalibacterium was not significantly higher on any study day and Blautia (p = 0.016) was only significantly higher on day 21 compared to day 0. Abundance of C. perfringens was significantly lower on day 7 (p = 0.011) compared to day 0 in PRO but not in PLAC. Enterotoxin genes were significantly lower in PRO on day 21 (p = 0.028) compared to PLAC. Fecal samples of 57% of all dogs were positive for netF toxin genes on day 0 and the abundance was significantly lower on day 7 compared to day 0 in PRO (p = 0.016) and PLAC (p = 0.031). The probiotic treatment was associated with an accelerated normalization of the intestinal microbiome. Dogs with aseptic AHDS showed a rapid decrease of netF toxin genes and fast clinical recovery in both groups under symptomatic treatment without antibiotics.

Background Diarrhea associated with parvovirus infection is common in dogs. Supportive care is the mainstay of treatment, but recovery may be prolonged and mortality rate can be high. Modification of the intestinal bacterial microbiota has been promising in human and veterinary medicine as an adjunctive treatment of various enteric diseases. Objectives To investigate the safety and efficacy of fecal microbiota transplantation (FMT) on the clinical recovery of puppies with acute hemorrhagic diarrhea syndrome. Animals Sixty‐six puppies with parvovirus infection were evaluated at 2 veterinary hospitals. Methods Randomized clinical trial. Puppies were randomly distributed into 2 groups: standard treatment (STD) and standard treatment + FMT (STD + FMT). The STD puppies (n = 33) received only treatment with IV fluids and antimicrobials and the STD + FMT puppies (n = 33) received FMT in addition to standard treatment. For FMT, 10 g of feces from a healthy dog diluted in 10 mL of saline were administered rectally 6‐12 hours post‐admission. Results Among survivors, treatment with FMT was associated with faster resolution of diarrhea (P < .001) and shorter hospitalization time (P = .001; median, 3 days in STD + FMT; median, 6 days in STD) compared to standard treatment. Mortality in STD was 36.4% (12/33) as compared to 21.2% (7/33) in puppies treated with FMT, but there was no statistical difference between groups (P = .174). Polymerase chain reaction indicated that all animals carried canine parvovirus, strain CPV‐2b. Conclusions Fecal microbiota transplantation in parvovirus‐infected puppies was associated with faster resolution of diarrhea.

Hemorrhagic abomasitis, also known as Salivary Abomasum Disease (SAD), is a largely under-researched condition affecting young lambs and kids, often leading to high mortality rates and significant economic losses. The disease’s etiopathogenesis, risk factors, and clinical features remain poorly understood. Existing studies have been limited and fragmented, leading to misdiagnoses and confusion about its true nature. Given the lack of a comprehensive investigation into SAD’s incidence, risk factors, and causative agents, this study aims to provide a thorough analysis through clinical, necropsy, histopathological, microbiological, and molecular examinations. This study involved 633 kids, with 323 in the SAD group and 310 in the control group. A multifaceted approach was utilized, encompassing clinical evaluations, necropsies, histopathological assessments, risk factors, and microbiological and molecular analyses, focusing on investigating virulence genes. During the kidding season, 323 deaths were linked to SAD, with a mean disease duration of 1.34 ± 0.54 days. The highest incidence occurred in the 8–14 day age group, accounting for 51.7% of cases ( p  < 0.05). The dominant clinical symptoms included weakness, lethargy, depression, failure to suckle, reluctance to move, significantly reduced mobility, unsteady gait, and a withdrawn demeanor. Necropsy findings consistently showed dark hemorrhagic content in the abomasum and characteristic “coffee grain” lesions, with no abnormalities in other organs. Escherichia coli was isolated in 63% of sampled kids, significantly more than in controls ( p  < 0.03), and confirmed through molecular analysis. Examination of virulence genes highlighted the presence of hlyA , stx1 , cnf1 , stx2 , and eaeA in complex combinations linked to severe abomasum damage. Poor bed and bottle hygiene were identified as the primary risk factors for SAD ( p  < 0.001), with risk escalating in the later stages of the kidding season as farm conditions deteriorated. This study thoroughly re-evaluates hemorrhagic abomasitis in young kids, delivering valuable and reliable insights into this fatal disease. Based on multifaceted analyses, it strongly indicates E. coli as the primary causative agent.

Background Dogs with hypoadrenocorticism (HA) frequently show signs of gastrointestinal disease (SGD). The prevalence of dogs presented for chronic SGD with HA is unknown. Objectives The aims of this study were to determine the prevalence of HA in dogs with chronic SGD and to identify clinical and laboratory variables for HA in this population. Animals One hundred fifty‐one dogs with chronic SGD. Methods In this multicentered prevalence study a standardized workup was performed in prospectively enrolled dogs with SGD > 3 weeks duration. Basal serum cortisol concentration was measured in every dog with ACTH stimulation test (ACTHST) if basal serum cortisol concentration was <3 μg/dL. Results Basal serum cortisol concentration was <3 μg/dL in 80/151 (53%) dogs, <2 μg/dL in 42/151 (28%) dogs, and < 1 μg/dL in 9/151 (6%) dogs. In 6/151 dogs HA was diagnosed based on ACTHST (stimulated serum cortisol concentration < 2 μg/dL), a prevalence of 4%. There was no difference in history, physical examination, and laboratory variables between dogs with HA and those with other causes of chronic SGD. In 4/6 dogs with HA, there was melena or hematochezia indicating gastrointestinal blood loss. Hyperkalemia, hyponatremia, or both was not observed in any dog. Conclusion and Clinical Importance The prevalence of HA among dogs with chronic SGD is higher than in the general population. Based on these results, testing adrenal function should be performed as a standard screening test in dogs with chronic SGD to differentiate between HA and chronic enteropathies.

Background Recently, novel pore‐forming toxin genes designated netE and netF were identified in a Clostridium perfringens type A strain isolated from a dog with acute hemorrhagic diarrhea. Objectives Pore‐forming toxins could play an important role in the disease pattern of acute hemorrhagic diarrhea syndrome (AHDS) in dogs. Thus, we aimed to determine the prevalence of C. perfringens genes encoding for netE and netF in the feces of dogs with AHDS and to evaluate any association between selected clinical variables and the presence of these toxin genes. Animals In total, 174 dogs were included in the study. Methods Fecal samples of all dogs were tested by real‐time polymerase chain reaction for netE and netF genes. Time to recovery, hospitalization time, and selected laboratory variables were compared between dogs with AHDS that were positive or negative for the toxin genes. Results A significant difference was found among the 3 groups in the prevalence of the pore‐forming toxin genes netE and netF: dogs with AHDS: 26 of 54 (48.1%); dogs with canine parvovirus (CPV) infection: 0 of 54 (0%); and healthy dogs: 8 of 66 (12.1%; P < .001). In dogs with AHDS, no significant difference was detected in any variables evaluated between netE‐positive and netF‐positive and netE‐negative and netF‐negative dogs. Conclusions and Clinical Importance The prevalence of C. perfringens encoding for netE and netF is significantly higher in dogs with AHDS compared to control dogs. Further studies are warranted to evaluate whether these toxins are an inciting cause for AHDS in dogs.

Canine circovirus (CanineCV) has been detected in some dogs with severe haemorrhagic diarrhoea, but its pathogenic role is unclear. This study evaluated a suspected association between the presence of CanineCV and acute haemorrhagic diarrhoea syndrome (AHDS) in dogs. The prevalence of CanineCV in dogs with AHDS was compared with that in healthy dogs and those infected with canine parvovirus (CPV). Additionally, time to recovery and mortality rate were compared between CanineCV-positive and CanineCV-negative dogs. Faecal samples of dogs with AHDS (n=55), healthy dogs (n=66) and dogs infected with CPV (n=54) were examined by two real-time TaqMan PCR assays targeting the replicase and capsid genes of CanineCV. CanineCV was detected in faecal samples of two dogs with AHDS, three healthy controls and seven dogs infected with CPV. Among the three groups, there was no significant difference in prevalence of CanineCV. CPV-infected animals that were coinfected with CanineCV had a significantly higher mortality rate compared with those negative for CanineCV. CanineCV does not appear to be the primary causative agent of AHDS in dogs, but might play a role as a negative co-factor in disease outcome in dogs with CPV infection.

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.

Feline bocavirus-1 (FBoV-1) was identified in cats from different households with hemorrhagic enteritis during outbreaks of an unusual clinical presentation of feline panleukopenia virus (FPLV) in Thailand. Use of polymerase chain reaction revealed the presence of the FBoV-1 DNA in several tissues, suggesting hematogenous viremia, with the viral nucleic acid, detected by in situ hybridization (ISH), was localized in intestinal cells and vascular endothelium of intestinal mucosa and serosa, and in necrosis areas primarily in various lymph nodes while FPLV-immunohistochemical analysis revealed viral localization only in cryptal cells, neurons, and limited to leukocytes in the mesenteric lymph node. Full-length coding genome analysis of the Thai FBoV-1 strains isolated from moribund cats revealed three distinct strains with a high between-strain genetic diversity, while genetic recombination in one of the three FBoV-1 strains within the NS1 gene. This is the first report identifying natural genetic recombination of the FBoV-1 and describing the pathology and viral tropism of FBoV-1 infection in cats. Although the role of FBoV-1 associated with systemic infection of these cats remained undetermined, a contributory role of enteric infection of FBoV-1 is possible. Synergistic effects of dual infection with FPLV and FBoV-1 are hypothesized, suggesting more likely severe clinical presentations.

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.

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.