Gastroenteritis of basenji dogs

Intestinal digestive and absorptive function and the gross and histologic appearance of the gastrointestinal tract were evaluated in Basenji dogs with chronic diarrhea, asymptomatic Basenji dogs, and healthy control dogs. Gastric rugal hypertrophy, lymphocytic gastritis, and gastric mucosal atrophy occurred in asymptomatic and affected Basenji dogs. All affected dogs had moderate or severe intestinal lesions characterized by villous clubbing and fusion, increased tortuosity of intestinal crypts, and diffuse infiltration of mononuclear inflammatory cells. Intestinal lesions in asymptomatic Basenji dogs invariably were less severe than those in affected dogs, but the small intestinal lamina propria of asymptomatic Basenji dogs consistently contained greater numbers of mononuclear inflammatory cells than did that of control dogs. The proportion of cells containing each immunoglobulin isotype (IgG, IgM, IgA) was similar among affected Basenji dogs, asymptomatic Basenji dogs, and control dogs. As compared to healthy beagle controls, intestinal function was abnormal in both affected and asymptomatic Basenji dogs evaluated by combined N-benzoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test, but malabsorption and maldigestion were most pronounced in affected Basenji dogs.     

ULTRASONOGRAPHIC AND CLINICOPATHOLOGIC FINDINGS IN 21 DOGS WITH INTESTINAL ADENOCARCINOMA

In a retrospective study of 21 dogs with intestinal adenocarcinoma, the signalment, clinical presentation, laboratory findings, ultrasonographic features, treatment, and outcome were reviewed. Anorexia (n = 16), vomiting (n = 15), diarrhea (n = 10), and weight loss (n = 9) were the most common clinical signs reported. Ultrasonographic features that were evaluated included location, length, wall thickness, echogenicity, regional motility, layering, regional lymphadenopathy, and fluid accumulation proximal to the lesion site. All lesions were transmural and associated with complete loss of wall layering. Maximum wall thickening at the lesion site ranged from 7 to 17 mm (median 12 mm, mean 11.9 mm). Most of the dogs had a lesion measuring from 23 to 63 mm in length, (median 40 mm, mean 42 mm). Most intestinal lesions were poorly echogenic and had an irregular lumen. Fluid accumulation proximal to the lesion site was identified in 17 of 21 dogs, and in 13 of 17 dogs the fluid accumulation was considered moderate to severe. Regional lymphadenopathy and/or nodular mesentery/omentum were noted in 12 of 21 dogs. The tumor was located in small intestine for 15 dogs and in the colon for the remaining 6 dogs. Fifteen dogs were treated by surgical resection of the intestinal mass. Their median survival time was 233 days. Only gender appeared to influence survival. Female dogs lived a median of 28 days, whereas male dogs lived a median of 272 days.     

Diarrhea associated with myenteric ganglionitis in a dog

Diarrhea in a Border Terrier was associated with inflammatory lesions of the myenteric plexus. This lesion has been documented rarely in dogs. It is speculated that the myenteric plexus lesions were responsible for an autonomic nervous system dysfunction, which resulted in extreme intestinal hypermotility and subsequent diarrhea. Suggested tests for dogs suspected to have autonomic dysfunction are given.     

Single and mixed infections of neonatal pigs with rotaviruses and enteroviruses: clinical signs and microscopic lesions.

Neonatal colostrum-deprived pigs were inoculated with cell-culture preparations of three rotaviruses and three enteroviruses, singly or in combination. The three enteroviruses established intestinal and systemic infection but did not induce diarrhea or intestinal lesions. The three rotaviruses produced severe enteric disease characterized by profuse watery diarrhea, dehydration and death. Villi were severely stunted. All three isolates were equally virulent. Inoculation with three different rotavirus-enterovirus combinations resulted in disease less severe than that produced by the rotaviruses alone. Intestinal lesions were less extensive and fewer pigs became moribund or died.     

Effect of intestinal inflammation on fecal elastase concentration in dogs

BACKGROUND: A commercially available ELISA kit for fecal elastase measurement can be used in the diagnosis of exocrine pancreatic insufficiency (EPI) in dogs. However, other causes of diarrhea also may affect fecal elastase concentration. OBJECTIVE: This study was undertaken to determine whether intestinal inflammation alters fecal elastase concentration in dogs. METHODS: Fecal elastase concentration was measured with an ELISA kit in the following groups of dogs: group 1 (n=16), control dogs, without gastrointestinal disease; group 2 (n=14), dogs with diarrhea and no histopathologic evidence of intestinal inflammation; and group 3 (n=12), dogs with diarrhea and histopathologic evidence of intestinal inflammation. Serum trypsin-like immunoreactivity (TLI) was determined in dogs with diarrhea to rule out EPI. RESULTS: All dogs in groups 2 and 3 had serum TLI concentrations >5 microg/L, ruling out EPI. No statistically significant difference was found in fecal elastase concentration among the 3 groups of dogs (P=.969). CONCLUSIONS: The results indicate that intestinal inflammation does not affect fecal elastase concentration, such that test results may be used to exclude a diagnosis of EPI even in animals with inflammatory bowel disease.     

Hemolytic-uremic syndrome in a dog

A 3-year-old, spayed, female Boxer was presented because of acute onset of anorexia, vomiting, and hemorrhagic diarrhea. Microangiopathic hemolytic anemia with intravascular hemolysis, thrombocytopenia, and acute renal failure were detected. The dog was treated with fluids, antiemetics, antibiotics, and diuretics. Despite supportive therapy, the dog's condition worsened, and the owners elected euthanasia. Necropsy revealed disseminated petechiae on the parietal peritoneum and serosal surfaces of the intestinal tract. The histologic lesions were consistent with severe arteritis and microvascular thrombosis involving only the renal and intestinal arterioles. The final diagnosis was hemolytic-uremic syndrome (HUS), a rarely described disorder in dogs. The clinical presentation of primarily gastrointestinal clinical signs was similar to that of typical or diarrhea-associated HUS (D+ HUS) in humans (mainly children), which is caused by gastrointestinal proliferation of verocytotoxin-producing Escherichia coli. Bacterial toxins can be adsorbed and cause endothelial injury, activation of hemostasis, and thrombosis, with lesions confined primarily to the kidneys. Although rare, HUS should be considered in the differential diagnosis of dogs with microangiopathic hemolytic anemia.     

Protein-losing enteropathy in a dog with lymphangiectasia,lymphoplasmacytic enteritis and pancreatic exocrine insufficiency

This is a report of seven-year-old male Akita mixed dog, with protein-losing enteropathy (PLE). He had a history of chronic vomiting and diarrhea with anorexia/hyporexia. Previously he suffered acute abdomen about eight months prior to this visit. Our dog showed uncommon combination of diseases that could cause PLE since it was affected by inflammatory bowel disease (IBD), intestinal lymphangiectasia (IL), and exocrine pancreatic insufficiency (EPI). The dog had most of the abnormalities found in IL, as well as hypoalbuminemia, hyperglobulinemia, lymphopenia, hypocalcemia, and hypercholesterolemia. During endoscopy exam, we found changes characteristic of IL such as irregular small white spots. We took biopsies from stomach, duodenum, and cecum. These biopsies showed infiltration by lymphocytes and plasmatic cells in the lamina propria also, the duodenal biopsies showed moderate dilation of the lymphatic vessels. The patient had 2.1?µg/mL of TLI, this result was compatible with EPI. We assume that the first pathology in this animal was IBD, which caused chronic pancreatitis (CP) that in turn progressed to EPI. It is also possible that IL was secondary to IBD. We have reported for the first time the correlation of IBD and EPI in dogs. This should change our approach to treating chronic diarrhea in dogs. Therefore, we propose that dogs diagnosed with EPI should also be subjected to endoscopy and intestinal biopsy. Similarly, to rule out secondary EPI, TLI should be measured routinely in dogs with IBD.     

鸡源A型产气荚膜梭菌致病性及药物疗效分析

本研究旨在调查规模化养鸡场内鸡源产气荚膜梭菌（Clostridium perfringens，CP）的致病性和耐药性，并评价阿维拉霉素和磷酸泰乐菌素预防CP感染鸡群发生坏死性肠炎（necrotizing enteritis，NE）的效果，为鸡NE的防治提供指导。在河北、山西两地选择有CP引起NE发病史的规模化养鸡场，随机采集新鲜粪便，分离CP，并通过多重PCR测定其毒素型。选定3个不同养殖场分离到的A型CP，以10⁹CFU·只^-1的剂量，连续5 d经灌胃的方式感染14日龄SPF鸡，观察肠道病变和NE发生情况，评价分离菌株的致病力。使用微量肉汤稀释法测定分离到的CP对阿维拉霉素、林可霉素和磷酸泰乐菌素的最小抑菌浓度（minimal inhibitory concentration，MIC）。根据MIC结果，选择药物敏感性较好的两种药物对因CP引起NE发病的鸡群中未出现临床症状的鸡进行预防试验，观察精神食欲、腹泻症状、肠道病变情况，统计CP检出率和NE发生率，评价两种药物预防效果。结果显示：自753份鸡粪便样品分离到91株CP，且毒素型全部为A型。攻毒试验结果显示：A、B、C组攻毒组NE病变发生率均显著高于未攻毒组D组（P<0.05），攻毒组肠道病变评分均显著高于未攻毒组（P<0.05）。与未攻毒组相比，攻毒组出现明显的腹泻症状和肠道病变，差异显著（P<0.05），3株CP都可以引起鸡NE。MIC结果表明：阿维拉霉素、林可霉素和磷酸泰乐菌素的MIC范围分别是0.25～4、0.125～128和0.25～32 μg·mL^-1。药物疗效试验结果表明：通过拌料连续21 d给予阿维拉霉素预混剂，给药期间及停药后1周可保护鸡群，防止出现NE症状或防止病变恶化，显著降低NE发生率、NE病变评分以及CP检出率（P<0.05）。通过拌料连续7 d给予磷酸泰乐菌素预混剂，效果与阿维拉霉素预混剂相当，但停药14 d后，6只鸡（6/11）又出现NE症状。目前，河北、山西省部分规模化鸡养殖场内流行的CP多为A型，并且可以引起NE，同时，A型CP对阿维拉霉素和磷酸泰乐菌素仍较敏感，其预混剂用于发病鸡群的预防效果较好。     

Nosocomial diarrhea associated with enterotoxigenic Clostridium perfringens infection in dogs

A retrospective analysis of the medical records of 30 consecutive cases of diarrhea occurring in dogs that were hospitalized in a teaching hospital was performed. A prospective analysis of culture results for Clostridium perfringens of dogs with diarrhea were compared with those of a control nondiarrheal group. Hospital-acquired diarrhea in dogs was found to be associated with multiple serotypes of enterotoxigenic Clostridium perfringens. Other potential etiologic agents could not be isolated. Clinical signs were variable, and included mild depression, anorexia, and soft to watery diarrhea with or without frank blood, mucus, and tenesmus. Fever was not present. There were no hematologic or serum biochemical abnormalities, nor were there any consistent virologic or parasitologic findings. Salmonella spp or Campylobacter spp were not identified by fecal culture. No risk factors could be identified. A dog that was euthanatized on the day it developed diarrhea had intestinal histologic findings suggestive of clostridial enteritis. Dogs with diarrhea had significantly higher fecal clostridial counts than did dogs without diarrhea (mean log10 counts +/- SD = 6.34 +/- 1.79 vs 4.75 +/- 2.07). Enterotoxin was found in the feces of 41% of diarrheic dogs but in only 7% of dogs without diarrhea.     

Effects of flunixin meglumine in dogs following experimentally induced endotoxemia

Twelve dogs were randomly divided into three groups. Group 1 dogs were given Escherichia coli endotoxin and then treated with flunixin meglumine. Group 2 dogs were given endotoxin as group 1, but untreated. Group 3 dogs were given flunixin meglumine alone. The dogs were monitored clinically and urine and serum samples were collected at regular intervals for 72 hours. All surviving dogs were humanely killed after 72 hours and examined for gross and histologic lesions. Group 1 dogs all survived 72 hours, but showed prerenal azotemia, hepatocellular damage, hemorrhagic enteritis, and numerous gastric ulcerations. Three of the four dogs in group 2 died before 72 hours. Group 2 dogs showed many of the same chemical and hemodynamic changes as group 1. They had severe hemorrhage into the intestinal lumen; however, there were no gastric ulcerations. Group 3 dogs all survived and showed little physical or hematologic change. The study suggested the following: 1) flunixin meglumine was an effective drug in ameliorating the fatal effects of canine endotoxemia, 2) the effects of endotoxin in combination with flunixin meglumine, at 1.1 mg/kg body weight, caused gastric ulcerations, and 3) in normal dogs flunixin meglumine at 1.1 mg/kg body weight did not cause severe side effects or gross lesions.     

Scanning electron microscopy of intestine of gnotobiotic piglets infected with porcine rotavirus.

The development of intestinal lesions caused by the porcine rotavirus were studied in six day old gnotobiotic piglets by scanning electron microscopy. The onset of diarrhea followed an incubation period of 17 to 31 hr. The first detectable lesion was observed in the ileum at 12 hr postinfection, a few hours before the onset of diarrhea. At this time enterocytes appeared swollen and began to separate from each other. Seventeen hours after the onset of diarrhea, lesions were quite severe jejunum and ileum. Enterocytes were detaching from the lamina propria leaving denuded areas. Microvilli were sparse on the cell surfaces and there was marked villous atrophy. Regeneration of ileal mucosa was evident at 4.8 days after the onset of diarrhea. Nine days after recovery from diarrhea the intestinal villi had returned to near its normal structure but there remained some evidence of mucosal damage.     

Diagnosis and surgical management of vascular ectasia in a dog

CASE DESCRIPTION: An 8-year-old male Golden Retriever was evaluated because of an 8-week history of intermittent diarrhea with melena and hematochezia that were not responsive to medical treatment and resulted in severe anemia. CLINICAL FINDINGS: Exploratory celiotomy with intestinal and colonic biopsy revealed mild enterocolitis but did not result in diagnosis of the cause of melena and hematochezia. Endoscopy of the upper portion of the gastrointestinal tract and colonoscopy were performed. Multifocal areas of coalescing, tortuous mucosal blood vessels were observed in the cecum and all regions of the colon. A diagnosis of vascular ectasia (VE) was made on the basis of the endoscopic and histologic appearance of the lesions. TREATMENT AND OUTCOME: An ileorectal anastamosis was performed. Melena and hematochezia resolved within 3 days after surgery, and the anemia resolved within 6 weeks after surgery. Surgical resection of the cecum and colon and feeding of a highly digestible diet resulted in long-term (22 months) resolution of clinical signs. CLINICAL RELEVANCE: Initial exploratory celiotomy with intestinal and colonic biopsy failed to reveal the VE lesions responsible for the melena, hematochezia, and anemia. Endoscopic evaluation was necessary for detection of the colonic VE lesions. Surgical resection of the cecum and colon and feeding of a highly digestible diet may result in a favorable outcome in affected dogs.     

Pathogenesis of canine parvovirus enteritis: the importance of viremia

The clinical signs, hematologic changes, serum and fecal virus titers, specific antibody production and the occurrence of histologic lesions were studied in 22 nine-week-old seronegative beagle dogs inoculated by the oral and intravenous route with canine parvovirus. Approximately 30% of the dogs had clinical signs of pyrexia, depression, vomiting, and diarrhea irrespective of the route of inoculation. Events in the dogs inoculated intravenously preceded those in dogs inoculated orally by approximately two days. Only one dog died. Lymphopenia was the most consistent hematologic change. Viremia always preceded the initiation of fecal virus shedding. Viral titers in the serum and feces were significantly greater in symptomatic dogs compared to asymptomatic dogs. Termination of the plasma viremia coincided with the onset of the humoral immune response, but viremia persisted one day longer in symptomatic dogs. The severity of lymphoid tissue and intestinal infection, assessed by tissue immunofluorescence and histology, was also greater in symptomatic dogs. The severity of intestinal disease was highly correlated with the magnitude and duration of viremia.     

Clinical, clinicopathologic, radiographic, and ultrasonographic characteristics of intestinal lymphangiectasia in dogs: 17 cases (1996-1998)

OBJECTIVE: To characterize the clinical, clinicopathologic, and imaging findings in dogs with intestinal lymphangiectasia and to compare the histologic grade of lymphangiectasia with clinicopathologic and imaging abnormalities. DESIGN: Retrospective study. ANIMALS: 17 dogs with a histologic diagnosis of intestinal lymphangiectasia. PROCEDURE: Medical records of dogs with a histologic diagnosis of intestinal lymphangiectasia were reviewed for signalment, history, clinical signs, results of exploratory laparotomy, and clinicopathologic, radiographic, ultrasonographic, and histologic findings. RESULTS: Mean age of dogs was 8.3 years; the most common clinical signs were diarrhea, anorexia, lethargy, vomiting, and weight loss. Abnormal physical examination findings included dehydration, ascites, and signs of pain on palpation of the abdomen. The most notable clinicopathologic findings were low serum ionized calcium concentration and hypoalbuminemia. Abdominal ultrasonography was performed in 12 dogs and revealed intestinal abnormalities in 8 dogs and peritoneal effusion in 7 dogs. Exploratory laparotomy revealed abnormalities in 9 of 16 dogs including thickened small intestine, dilated lacteals, lymphadenopathy, and adhesions. On histologic examination of the small intestine, concurrent inflammation was observed in 15 of 17 dogs, crypt ectasia in 5 of 17, and lipogranulomas in 2 of 17. CONCLUSIONS AND CLINICAL RELEVANCE: Intestinal lymphangiectasia in dogs appears to be a heterogeneous disorder characterized by various degrees of panhypoproteinemia, hypocholesterolemia, lymphocytopenia, and imaging abnormalities. In most dogs, the severity of hypoalbuminemia appears to offer the best correlation with severity of histologic lesions of lymphangiectasia. Imaging abnormalities are common in dogs with intestinal lymphangiectasia but are not specific enough to differentiate this disorder from other gastrointestinal disorders, nor are they predictive of histologic severity.     

Pathogenesis of canine parvovirus enteritis: sequential virus distribution and passive immunization studies

After oral inoculation, the sequential distribution of canine parvovirus was studied in 14 nine-week-old seronegative beagle dogs. Two or three dogs were necropsied on days 1 through 6 after inoculation. Tissues were collected for virus isolation, immunofluorescence testing, and light microscopy. Virus was isolated from, and fluorescent cells were seen in the tonsil, retropharyngeal and mesenteric lymph nodes one and two days after inoculation. Virus infection of systemic and intestinal lymphoid tissues occurred as early as three days after inoculation and was associated with viremia. Intestinal epithelial infection was first seen four days after oral inoculation. All dogs were viremic before intestinal epithelial infection was found. Fecal virus excretion first occurred four days after oral virus inoculation. Intestinal virus infection and lesions became progressively more severe between four and six days after inoculation. The severity of intestinal lesions was variable and related to the severity of systemic lymphoid tissue lesions and the magnitude and duration of viremia. Four littermates of virus-infected dogs were passively immunized against canine parvovirus with convalescent canine serum 24 hours after oral virus inoculation. Neither clinical signs, lymphopenia, nor fecal virus excretion occurred in passively immunized dogs. Intestinal epithelial infection was not demonstrable by immunofluorescence testing when passively immunized dogs were necropsied four, five, and six days after virus inoculation.     

Observational study of 14 cases of chronic pancreatitis in dogs

This study reports the clinical, clinicopathological and ultrasonographic findings from dogs with chronic pancreatitis (CP). Fourteen dogs with clinical signs consistent with CP and histological confirmation of the disease were evaluated. Abdominal ultrasound and clinical pathology results were recorded. Sensitivities of pancreatic enzymes for diagnosis of CP were calculated with two different cut-off values. The mean age of affected dogs was 9.1 years. Spaniels were the most common breed with CP, representing seven of the 14 dogs in this study. CP was histologically severe in nine cases. Most dogs showed chronic low-grade gastrointestinal signs and abdominal pain. Five dogs had exocrine pancreatic insufficiency and five dogs had diabetes mellitus. The sensitivity of elevated trypsin-like immunoreactivity for CP was 17 per cent. The sensitivities of canine pancreatic lipase immunoreactivity, lipase and amylase for CP were 44 to 67 per cent or 14 to 28 per cent depending on the cut-off value used. Cholesterol was elevated in 58 per cent of samples. Liver enzymes were often elevated. The pancreas appeared abnormal on 56 per cent of ultrasound examinations. Ten dogs had died by the end of the study period; only one case was due to CP.     

Pathology of experimental CV777 coronavirus enteritis in piglets. I. Histological and histochemical study

Sixteen cesarean-derived colostrum-deprived piglets were infected oronasally with CV777 coronavirus on the second or third day of life. Two uninfected piglets were controls. They were killed at 96 and 120 hours after birth. After an incubation period of 22 to 36 hours, all principals showed severe diarrhea. The principals were killed between 12 and 120 hours after infection. Exfoliation of enterocytes were seen first in the piglet killed 24 hours after infection (two hours after the diarrhea began). From that time on, shortening and fusion of villi was present in all small intestinal parts. Affected cells showed vacuolation. The histochemical study showed that infected piglets had decreased activity of all four enzymes studied. The light microscope showed no lesions in the absorptive colonic epithelium. The significance of the lesions in relation to intestinal dysfunction is discussed, and lesions are compared to those of transmissible gastroenteritis and porcine rotavirus infection.     

Pulmonary thromboembolism during therapy of dirofilariasis with thiacetarsamide: modification with aspirin or prednisolone

The effects that 4 weeks of treatment of dirofilaria-infected dogs with either aspirin or prednisolone had on the pulmonary thromboembolism which occurs after they are given thiacetarsamide were determined, using light and electron microscopies. Pulmonary lesions in control dogs at 4 weeks after thiacetarsamide was given were compared with lesions in dogs which were treated with either aspirin (22 mg/kg daily) or prednisolone (1 mg/kg daily) during the 4-week period after adulticide was given. Pulmonary vascular and perivascular lesions were most severe in the prednisolone-treated dogs and least severe in the aspirin-treated dogs. The aspirin-treated dogs had greater resolution of pulmonary arterial proliferative disease, and prednisolone-treated dogs had the lesser resolution.     

Effects of Prednisone Alone or Prednisone with Ultralow-Dose Aspirin on the Gastroduodenal Mucosa of Healthy Dogs

Background: The coadministration of prednisone and ultralow-dose aspirin has been recommended for the management of various diseases, but the safety of this combination in dogs has not been studied.
Hypotheses: The gastroduodenal lesions associated with prednisone and ultralow-dose aspirin administration will be similar to those caused by prednisone alone, but both treatments will result in more severe lesions than placebo.
Animals: Eighteen healthy adult purpose-bred dogs.
Methods: Randomized, blinded, placebo-controlled study of 3 treatment groups for 27 days: placebo, prednisone, and prednisone and aspirin. Gastroduodenoscopy was performed before and on days 5, 14, and 27 of treatment and mucosal lesions scores were assigned. Mucosal lesion scores were compared by a Kruskal-Wallis test. Clinical signs were compared by the Friedman's chi-square test (significance at P < .05).
Results: There were no significant differences in the gastroduodenal lesion scores among groups, or within groups at any time during the study. Significantly more dog-days of diarrhea occurred in the prednisone and aspirin group during treatment, compared with baseline. No significant differences in clinical signs were found among any of the groups.
Conclusion: The concurrent use of prednisone and ultralow-dose aspirin did not increase the severity of gastroduodenal lesions compared with prednisone or placebo. Coadministration of prednisone and ultralow-dose aspirin increases the frequency of mild, self-limiting diarrhea in some dogs.     

Small Bowel Volvulus in Dogs Clinical Observations

Small bowel volvulus was diagnosed in six dogs. Peracute onset, hematochezia, and lack of vomition were the most prominent clinical features. All affected dogs exceeded 23 kg in body weight. Five of the six dogs were males and two were German shepherd dogs.
There were no diagnostic findings that were specific for intestinal volvulus. Abdominal radiographs in two dogs were interpreted as showing "pathologic" dilatation of bowel. However, it could not be determined whether the dilatation was caused by adynamic ileus or by mechanical obstruction. Results of hematological tests help to differentiate other causes of bloody diarrhea such as hemorrhagic gastroenteritis and parvovirus enteritis.
Prognosis for dogs with intestinal volvulus was poor: all six of the dogs in our series died.