Prekallikrein deficiency in a dog

A 15-year-old male dog with chronic hematuria was found to have prolonged activated partial thromboplastin time. Results of plasma coagulation assays indicated a deficiency of prekallikrein, a plasma protein that modulates the rate of activation of factors XI and XII in the intrinsic clotting system. Patients with prekallikrein deficiency rarely have manifestations of hemorrhage. The hematuria was the result of a renal transitional cell carcinoma.     

A combined deficiency of factor VIII and contact activation defect in a family of cats

The coagulation parameters of a litter of kittens born to an obligate carrier of haemophilia A (classical haemophilia, factor VIII deficiency) are described. Three of four kittens were found to have an intrinsic coagulation defect, but only one was haemophilic. Factor XII deficiency was confirmed in one female, the other female and the dam being carriers of the defect. A confirmed haemophilic male from a previous litter was also found to be a factor XII deficient carrier.     

Septic peritonitis in a dog caused by Anaerobiospirillum succiniproducens

This is the first reported case of septic peritonitis caused by Anaerobiospirillum succiniproducens in a dog. The infection was associated with marked exfoliation of reactive mesothelial cells into the abdominal fluid mimicking neoplasia. The source of the infection was not determined but was presumed to be of gastrointestinal origin as A succiniproducens is part of the normal gastrointestinal flora of dogs. Anaerobiospirillum spp. have been previously reported as causing diarrhea and bacteremia in people, particularly if immunocompromised; however, there were no indicators for a compromised immune system in this dog.     

Eosinophilic granulomatous gastroenterocolitis and hepatitis in a 1-year-old male Siberian Husky

A case of eosinophilic granulomatous gastroenterocolitis and hepatitis in a 1-year-old male Siberian Husky is described. The dog presented with a history of diarrhea, weakness, lethargy, and anorexia of several months' duration. Hematologic and biochemical examinations, abdominal ultrasonography, computer tomography, and exploratory laparotomy were performed. Histopathologic examination of full-thickness biopsies from the gastrointestinal tract and liver revealed the presence of eosinophilic granulomatous lesions in the submucosa and tunica muscularis of stomach, jejunum, ileum, colon, and liver. Infectious agents were not detected by light microscopic and electron microscopic examination or by immunohistochemistry. On the basis of the findings, it is concluded that the disease in this dog represents an unusual manifestation of chronic idiopathic inflammatory bowel disease.     

Experimentally induced bluetongue virus infection in white-tailed deer: coagulation, clinical pathologic, and gross pathologic changes

Ten yearling white-tailed deer (Odocoileus virginianus) were inoculated with bluetongue virus serotype 17. Two yearling white-tailed deer were inoculated with sonicated heparinized noninfected blood and served as controls. Clinical signs of bluetongue virus infection included increased rectal temperature, erythema, facial edema, coronitis, and stomatitis. By postinoculation day (PID) 8, excessive bleeding and hematoma formation at venipuncture sites, dehydration, and diarrhea developed. At necropsy, the most consistent findings were oral lesions and widespread hemorrhage, which ranged from petechia to massive hematoma formation. Bluetongue virus caused progressive prolongation of activated partial thromboplastin time and prothrombin time, and progressive reduction of Factors VIII and XII plasma activities beginning on PID 6. A progressive decrease in platelet numbers also developed on PID 6. Changes in platelet size were not detected. Mean thrombin time was shortened, but prolongation developed in 1 deer. Mean fibrinogen concentration and Factor V plasma activity initially increased and then decreased, but remained above preinoculation values. Factor V activity was low in a few deer. Results of screening tests for inhibitors of the intrinsic coagulation system were positive in 2 deer. High concentrations of fibrin(ogen) degradation products were first detected between PID 3 and 6. Hematologic changes included leukopenia, lymphopenia, neutrophilia, and low total plasma protein concentration. Differences in PCV, hemoglobin concentration, or RBC counts were not detected between infected and control deer. Serum total bilirubin concentration increased by PID 6, primarily because of increased unconjugated bilirubin concentration. Mild to severe increases in serum aspartate transaminase activity were accompanied by more marked increases in creatine kinase activity. Indirect Coombs test results were negative in all deer.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hemangiosarcoma in a geriatric Labrador retriever

A geriatric Labrador retriever dog was presented for acute collapse. The dog was conscious but lethargic, tachypneic, tachycardic with weak femoral pulses, occasional pulse deficits, and pale mucous membranes. Radiography, ultrasonography, quick assessment tests, and a complete blood (cell) count (CBC)/biochemistry panel indicated internal hemorrhage and potential problems with hemostasis. The dog was euthanized. A necropsy, histopathology, and immunohistochemistry for CD31 and Factor VIII-related antigen cell markers supported a diagnosis of splenic hemangiosarcoma.     

Necrotizing enterotyphlocolitis in dogs treated with a potent antimuscarinic

To assess the safety of a potent muscarinic receptor antagonist (antimuscarinic) for human clinical testing, repeat-dose oral toxicity studies were conducted in the Beagle dog. Treatment resulted in unexpected gastrointestinal system effects that were likely mediated by the exaggerated pharmacologic effects of the antimuscarinic on intestinal motility. Dogs developed profound anorexia followed by severe bloody diarrhea, and at necropsy, the intestinal tract was distended, filled with red-tinged fluid, and the mucosa was reddened. Histologically, intestinal lesions consisted of severe epithelial necrosis and mucosal atrophy localized predominantly to the ileum and large intestine. Feces from dogs with diarrhea were culture-positive for Clostridium perfringens (CP), suggesting that CP might be the etiologic agent; however, the intestinal lesions were not consistent with histologic findings reported in dogs with hemorrhagic canine enteritis.     

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.     

Rectal ganglioneuroma in a dog

An 18-month-old, spayed female Australian terrier cross was presented with a 10-month history of chronic large bowel diarrhea. Ulceration and two proliferative masses in the rectum were seen on colonoscopy. Surgical resection was performed to remove the masses, and the dog recovered without complications related to surgery. Histopathology was consistent with the diagnosis of ganglioneuroma. The dog had no clinical signs of disease within three months of surgery and was completely normal 2.5 years after diagnosis. This is the first report providing follow-up and successful outcome of a ganglioneuroma in the gastrointestinal tract of a dog.     

Hepatic emphysema associated with ultrasound-guided liver biopsy in a dog

An eleven-year-old Chinese Crested Powder Puff dog presented with polydipsia/polyuria, inappetence, diarrhea and vomiting underwent an ultrasound-guided percutaneous liver biopsy. Two days post-biopsy the clinical condition of the dog acutely deteriorated with fever, dyspnea, ataxia and subcutaneous emphysema. Radiographs and ultrasound showed focal severe hepatic emphysema in the region of the previous liver biopsy. Post-mortem examination revealed chronic hepatitis with dissecting fibrosis, acute hepatitis with hemorrhage and in the hindlimb musculature extensive hemorrhage and necrosis. Pure cultures of the gas producing bacteria Clostridium perfringens were isolated in samples from the hind limb musculature. We propose that the hepatic emphysema in the region of the biopsy site was a result of a clostridial infection.     

Nonsurgical resolution of gallbladder mucocele in two dogs

CASE DESCRIPTION: A gallbladder mucocele was diagnosed in 2 dogs. In both dogs, the mucocele resolved with medical treatment but without the need for surgical intervention. CLINICAL FINDINGS: A 12-year-old spayed female Miniature Schnauzer had a history of signs of gastrointestinal tract disease and high serum liver enzyme activities. Gallbladder mucocele and hypothyroidism were diagnosed. A 6-year-old neutered mixed-breed dog had chronic intermittent diarrhea and recurrent otitis; gallbladder mucocele and hypothyroidism were diagnosed. TREATMENT AND OUTCOME: The first dog was treated with S-adenosyl-methionine, omega-3 fatty acids, famotidine, ursodiol, and levothyroxine. Substantial improvement in the gastrointestinal tract condition and complete resolution of the gallbladder mucocele within 3 months were evident, but the dog was not available for further follow-up monitoring. The second dog was treated with fenbendazole, ursodiol, and levothyroxine and fed a hypoallergenic diet. One month after evaluation, abdominal ultrasonography revealed that the gallbladder mucocele was resolving, and treatment was continued. Ultrasonographic evaluation 2 and 4 months later revealed complete resolution of the mucocele. CLINICAL RELEVANCE: Review of the clinical course of 2 dogs in which there was nonsurgical resolution of gallbladder mucocele revealed that surgery is not necessary in all dogs with gallbladder mucocele. Hypothyroidism may have resulted in delayed gallbladder emptying, and its role in the pathogenesis of gallbladder mucocele merits investigation. Despite this information, until further prospective trials with a control group and standardized treatments and follow-up monitoring can be performed, the authors recommend surgical intervention for treatment of dogs with gallbladder mucocele.     

Coinfection with multiple tick-borne and intestinal parasites in a 6-week-old dog

Coinfection with Ehrlichia canis, Babesia canis, Hepatozoon canis, Isospora spp., Giardia spp., and Dipylidium caninum were detected in a 6-week-old dog. The effect of multi-pathogen infection was a fatal combination of gastrointestinal and hematologic abnormalities, including diarrhea, vomiting, anorexia, distended painful abdomen, intussusception, severe thrombocytopenia, anemia, and hypoproteinemia.     

Gastrointestinal pythiosis in 10 dogs from California

BACKGROUND: Pythium insidiosum is an aquatic oomycete that causes severe segmental thickening of the canine gastrointestinal (GI) tract, resulting in weight loss, vomiting, diarrhea, and death. Infection in dogs previously has been observed primarily in the southeastern United States. OBJECTIVE: To describe the clinicopathologic and epidemiologic findings associated with GI pythiosis in 10 dogs from California. METHODS: Dogs were initially identified on the basis of supportive clinical findings and routine histology. Pythiosis was confirmed in each dog with at least one of the following: immunoblot serology, enzyme-linked immunosorbent assay serology, immunohistochemistry, and culture followed by species-specific polymerase chain reaction, rRNA gene sequencing, or both. RESULTS: Between September 2003 and December 2006, GI pythiosis was confirmed in 1 dog from central California and 9 dogs that lived within a 30-mile radius of Davis, CA. Seven of 8 dogs for which environmental data were available had frequent access to flooded rice fields or other water sources. Esophageal lesions were present in 2 of 10 dogs. Common laboratory findings included eosinophilia (7/9), hypoalbuminemia (9/9), and hyperglobulinemia (8/9). Median survival time was 26.5 days (range, 0-122 days), and the disease was ultimately fatal in all 10 dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: The geographic distribution of pythiosis has widened in recent years to include the western United States. Factors that may have contributed to this change include altered rice-farming practices and landscape irrigation. Veterinarians in California should be familiar with the clinicopathologic features associated with GI pythiosis to aid in early diagnosis and effective treatment.     

New findings on animal diseases published since 2003. 1. Dogs

This is the first article of a series of papers reviewing "new findings" on animal diseases. The articles are arranged in order of animal species. This article reviews seven publications on new findings on or directly related to dog diseases. The following seven cases are discussed: Canine sarcocystosis in Central America. Copper accumulation in a Skye terrier: Antemortem diagnosis and cytoprotective bile acid therapy. Keratinocyte culture and use of a cultured epidermal autograft. Line 1 insertion mutation in Factor IX of dogs with hemophilia B. Not previously described localization of the lesions in stifle osteochondritis dissecans. Panniculitis associated with pancreatitis: Antemortem diagnosis. Primary polydipsia associated with (and induced by?) gastrointestinal disease. After a short introduction, the bibliographical data, the abstract of the author(s) and some additional information derived from the article are given.     

Intestinal malabsorption and cryptosporidiosis in an adult dog

Chronic intestinal cryptosporidiosis was diagnosed as the cause of chronic diarrhea and weight loss in an adult dog without obvious signs of immunosuppression. Results of tests for digestive function suggested that the dog had impaired intestinal absorption or bacterial overgrowth. The nutrient malabsorption might have resulted in or have been caused by the cryptosporidiosis. Temporary clinical improvement without reduction in fecal oocyst concentration was noticed following treatment with clindamycin. The dog was euthanatized. At necropsy, the dog was found to have chronic lymphoplasmacytic enteritis and cryptosporidiosis. A veterinary student that worked in the ward where the dog was kept developed cryptosporidal diarrhea.     

What is your diagnosis? Rectal scraping from a dog with diarrhea

Abstract: A 3‐year‐old, spayed female, mixed‐breed dog was evaluated for chronic diarrhea, vomiting, and weight loss. A marked inflammatory leukogram, mild regenerative anemia, and marked hypoalbuminemia were noted. Cytologic evaluation of a rectal scraping revealed numerous round to ovoid protozoal cysts, 5–25 μm in diameter, with small to moderate amounts of pale blue cytoplasm and round eosinophilic nuclei. A distinct, variably sized, round to oval vacuole was often seen within the cytoplasm and frequently displaced the nucleus. The cysts were morphologically similar to Blastocystis sp., an amoeba‐like protozoal parasite found in both diseased and asymptomatic humans and animals. Histologic findings in endoscopic biopsies from the stomach, duodenum, ileum, and colon were unremarkable and protozoal organisms were not observed. The dog was diagnosed with exocrine pancreatic insufficiency based on markedly decreased serum levels of trypsin‐like immunoreactivity. Alteration of gastrointestinal flora secondary to the underlying pancreatic disease likely allowed overgrowth of the protozoa, which were considered an incidental finding. Their identification was important in avoiding an incorrect diagnosis and unwarranted treatment.     

Citrobacter freundii septicemia in two dogs.

A 4-month-old Maltese puppy and a 7.5-year-old Collie were diagnosed with septicemia associated with Citrobacter freundii. The puppy died soon, after developing weakness and mucohemorragic diarrhea. The Collie had immune-mediated hemolytic anemia and thrombocytopenia and was treated with immunosuppressive drugs before being euthanized. Gross examination of the puppy revealed mucohemorrhagic intestinal contents. Focal necrotic hepatitis, fibrinous peritonitis, interstitial pneumonia, and hemorrhagic gastrointestinal contents were observed in the older dog. Histologically, there was a diffuse, moderate, histiocytic meningitis in the puppy and a focal fibrinonecrotic hepatitis in the adult dog. Lesions in both dogs contained numerous gram-negative rods. Citrobacter freudii is a potential cause of monomicrobic bacteraemia-septicemia in puppies or immunocompromized adult dogs.The gastrointestinal tract is probably the main site of entry.     

IMAGING DIAGNOSIS—HETEROBILHARZIA AMERICANA INFECTION IN A DOG

An approximately three‐year‐old mixed breed female dog was evaluated for peritoneal effusion, anorexia, intermittent vomiting, and diarrhea. Radiographically, there was mineralization of the wall of small intestinal segments. Sonographic findings were consistent with multisystemic mineralization of liver, small intestinal wall, and pancreas. Multifocal granulomas containing schistosome eggs (Heterobilharzia americana) were identified histologically. The mineralization pattern described herein is an uncommon presentation of severe diffuse heterobilharziasis in a dog.     

Rauwolfia serpentina toxicity in a dog

Objective– To describe the clinical manifestations and treatment of Rauwolfia serpentina toxicity in a dog. Case Summary– A 9‐month‐old intact male mixed breed dog was presented following ingestion of an antihypertensive medication containing alkaloids from R. serpentina. R. serpentina alkaloids cause depletion of the biologic amines: norepinephrine, dopamine, and serotonin. The dog experienced hypotension, mental depression, bradycardia, diarrhea, bronchoconstriction, and gastrointestinal ulceration similar to the adverse effects reported in humans. The dog was released from the hospital after 4 days of supportive care. New Information Provided– This is the first case of accidental R. serpentina toxicity in a dog reported in the literature. This case had a good clinical outcome with supportive care and monitoring of all the subsequent adverse effects.     

Cytomegalovirus-associated discrete gastrointestinal masses in macaques infected with the simian immunodeficiency virus

Cytomegalovirus (CMV)-associated gastrointestinal masses have been reported in human acquired immune deficiency syndrome patients. This is the first report on CMV-associated gastrointestinal masses in simian immunodeficiency virus (SIV)-infected macaques. Two SIV-infected macaques presented at necropsy with multiple nodular or umbilicated masses within the gastrointestinal tract. In one animal, the masses were located throughout the gastrointestinal tract, whereas in the other, the masses were restricted to the proximal small intestine. Grossly, the masses were indistinguishable from those caused by neoplastic conditions such as lymphoma and, histologically, were composed of hyperplastic glandular tissue, dense neutrophilic infiltrates within the lamina propria, and multifocal proprial hemorrhage. Frequent cytomegalic cells with basophilic intranuclear inclusions were found in affected regions. Immunohistochemistry for CMV demonstrated frequent immunopositive cells within affected areas. Furthermore, immunohistochemistry for the proliferation marker Ki-67 demonstrated increased proliferation in hyperplastic glands and crypts. CMV should be considered a cause of discrete mass lesions in the gastrointestinal tract of SIV-infected macaques.