Leukoencephalomyelopathy of mature captive cheetahs and other large felids: a novel neurodegenerative disease that came and went?

A novel leukoencephalomyelopathy was identified in 73 mature male and female large captive felids between 1994 and 2005. While the majority of identified cases occurred in cheetahs (Acinonyx jubatus), the disease was also found in members of 2 other subfamilies of Felidae: 1 generic tiger (Panthera tigris) and 2 Florida panthers (Puma concolor coryi). The median age at time of death was 12 years, and all but 1 cheetah were housed in the United States. Characteristic clinical history included progressive loss of vision leading to blindness, disorientation, and/or difficulty eating. Neurologic deficits progressed at a variable rate over days to years. Mild to severe bilateral degenerative lesions were present in the cerebral white matter and variably and to a lesser degree in the white matter of the brain stem and spinal cord. Astrocytosis and swelling of myelin sheaths progressed to total white matter degeneration and cavitation. Large, bizarre reactive astrocytes are a consistent histopathologic feature of this condition. The cause of the severe white matter degeneration in these captive felids remains unknown; the lesions were not typical of any known neurotoxicoses, direct effects of or reactions to infectious diseases, or nutritional deficiencies. Leukoencephalomyelopathy was identified in 70 cheetahs, 1 tiger, and 2 panthers over an 11-year period, and to our knowledge, cases have ceased without planned intervention. Given what is known about the epidemiology of the disease and morphology of the lesions, an environmental or husbandry-associated source of neurotoxicity is suspected.

Congenital hepatic fibrosis in 5 dogs.

Congenital hepatic fibrosis is a disorder of biliary system development histologically characterized by diffuse periportal to bridging fibrosis with numerous small often-irregular bile ducts and reduction in the number of portal vein branches. The condition results from abnormal development of the ductal plate, the embryonic precursor to the interlobular bile ducts. It has rarely been reported in veterinary species, and it has never been reported in dogs. This article describes 5 cases of a ductal plate malformation in dogs consistent with congenital hepatic fibrosis. On light microscopy, all 5 livers had severe bridging fibrosis with a marked increase in the number of small bile ducts, which often had irregular, dilated profiles reminiscent of the developing ductal plate. In addition, 80% (4 of 5) of cases lacked typical portal vein profiles. Cytokeratin 7 and proliferating cell nuclear antigen immunohistochemistry was performed on the 3 cases for which paraffin-embedded tissue was available. The bile duct profiles were strongly positive for cytokeratin 7 in all 3 cases, and they were negative for proliferating cell nuclear antigen or only had rare positive cells. All 5 dogs presented with clinical signs of portal hypertension. Congenital hepatic fibrosis should be considered in the differential diagnosis in young dogs that present with portal hypertension and lesions that may have been interpreted as bridging biliary hyperplasia or extrahepatic biliary obstruction.

IL-4(-/-) mice with lethal Mesocestoides corti infections--reduced Th2 cytokines and alternatively activated macrophages.

Protection against Mesocestoides corti, a cestode that invades vital organs, is dependent on the production of IL-4, as IL-4(-/-) mice were found to have higher parasite burdens when compared with wild-type mice. The goal of this study was to investigate the role of IL-4 in immunity to M. corti, focusing on the immunological profile and on potential mediators of pathology. IL-4(-/-) mice infected with M. corti showed 100% mortality by 32 days, whereas wild-type mice survived for approximately 1 year. Parasite burdens were significantly increased in the liver, peritoneal, and thoracic cavities of IL-4(-/-) mice, associated with impaired recruitment of inflammatory cells and a reduction in monocytes and macrophages. IL-5 production by splenocytes and expression in liver tissue was decreased in infected IL-4(-/-) mice compared with wild-type mice. In contrast, IL-4(-/-) mice produced increased amounts of IFNgamma and TNFalpha. Alternatively activated macrophages were a major feature of liver granulomas in wild-type mice evidenced by Arginase I expression, while livers from infected IL-4(-/-) mice showed impaired alternative macrophage activation without increased classical macrophage activation. Thus, lethality during M. corti infection of IL-4(-/-) mice is associated with decreased Th2 cytokines, increased Th1 cytokines and impairment of alternatively activated macrophages.

Polymicrogyria in standard poodles.

BACKGROUND: Polymicrogyria is a disorder of cerebrocortical migration resulting in increased numbers of small, disorganized gyri. This disorder occurs in Standard Poodles and in cattle. OBJECTIVES: To describe the clinical, electroencephalographic, imaging, and histopathologic features in poodles with polymicrogyria. ANIMALS: Five Standard Poodles with histologically confirmed polymicrogyria. METHODS: Retrospective case series. Cases were obtained by personal communication with 1 of 2 authors (TJVW, DPO). RESULTS: All dogs had cortical blindness and other neurologic abnormalities including gait and behavioral changes. Magnetic resonance imaging of 3 dogs showed multiple disorganized gyri, which were especially apparent on T2-weighted dorsal plane images. Electroencephalogram (EEG) of 1 dog revealed epileptiform discharges, including both spike and spike and wave discharges with voltage maximum potentials over the parietal/occipital region. The EEG supported that the repetitive behavior displayed by the dog was a complex partial motor seizure. One dog had concurrent hydrocephalus. All dogs had occipital lobe involvement and 2 dogs had involvement of other lobes. CLINICAL IMPORTANCE: The cases presented here demonstrate a larger age range (7 weeks to 5 years) and a decreased frequency of associated hydrocephalus when compared with the previous report.

Secondary intracranial neoplasia in the dog: 177 cases (1986-2003).

BACKGROUND: This study investigates the frequency, location, and clinical findings associated with 177 secondary brain tumors in dogs. HYPOTHESIS: Secondary intracranial neoplasia is more common than primary intracranial neoplasia in dogs during the time period studied, and hemangiosarcoma (HSA) is the most common secondary intracranial tumor. ANIMALS: One hundred and seventy-seven client-owned dogs presented to the Matthew J. Ryan Veterinary Hospital between 1986 and 2003. METHODS: Medical records were searched for a diagnosis of intracranial neoplasia in dogs who underwent complete postmortem examination. Of these dogs, those with a diagnosis of primary intracranial neoplasia were excluded. RESULTS: Of the 177 secondary brain tumors, 51 (29%) were HSAs, 44 (25%) were pituitary tumors, 21 (12%) were lymphosarcomas, and 21 (12%) were metastatic carcinomas. The average age at diagnosis was 9.6 +/- 3.0 years. Most tumors were located in the cerebrum, and a mentation change was the most common presenting clinical sign. On postmortem examination, the same tumor that was in the brain was also present in the lung in 84 cases (47%), in the kidney in 62 cases (35%), and in the heart in 55 cases (31%). CONCLUSIONS AND CLINICAL IMPORTANCE: Secondary intracranial neoplasia in dogs was more common than primary intracranial neoplasia during the time period studied. Many of these dogs had related disease in other body systems that was apparent on diagnostic tests such as thoracic radiography.

Interobserver Agreement Using Histological Scoring of the Canine Liver.

BACKGROUND: Grading schemes for the assessment of hepatic fibrosis and necroinflammatory activity in humans previously have been applied to dogs with chronic hepatitis. Interobserver agreement is a desirable characteristic for any histological scoring scheme. HYPOTHESIS/OBJECTIVES: To assess interobserver agreement associated with pathologists using a previously published histological scoring scheme to assess hepatic fibrosis and necroinflammatory activity in dogs and to compare fibrosis scores assigned to serial sections stained with hematoxylin & eosin (H&E) and picrosirius red. ANIMALS: Histological sections of liver from 50 dogs with variable degrees of hepatic fibrosis and necroinflammatory activity were selected from institutional tissue archives. METHODS: Six board-certified veterinary anatomic pathologists assigned fibrosis and necroinflammatory activity scores to the histological sections. The multiuser kappa statistic was calculated to assess interobserver agreement. Fibrosis stage assigned to serial sections stained with picrosirius red and H&E was compared using the Wilcoxon signed-rank test. RESULTS: Multiuser kappa statistics for assessment of fibrosis and necroinflammatory activity from H&E-stained sections were 0.35 and 0.16, respectively. There was no difference in median fibrosis scores assigned to serial section stained with H&E and picrosirius red (P = .248). CONCLUSIONS AND CLINICAL IMPORTANCE: There was fair interobserver agreement when pathologists assessed fibrosis and poor agreement when they assessed necroinflammatory activity. This suboptimal agreement must be taken into account by clinicians making decisions based on histology reports of the liver and in the design of studies evaluating these findings. To decrease this variability, ideally >1 pathologist should evaluate each section.

Tamoxifen induces hypoxia in MCF-7 xenografts.

Tamoxifen is widely used as an adjunct therapy for breast cancer. We hypothesized that hypoxia develops in tumors as a result of tamoxifen treatment because tamoxifen has been reported to be antiangiogenic and thrombogenic. MCF-7 breast tumors were grown under estrogenic stimulation in 4-6-week-old CD-1 nu/nu female mice. When the tumors were approximately 5 mm in diameter, 17beta-estradiol pellets were replaced with either placebo or tamoxifen-containing pellets. Two days later, tissue oxygenation was measured using immunohistochemical detection of binding of the 2-nitroimidazole EF5. Intravascular oxygen partial pressures were measured noninvasively by oxygen-dependent quenching of phosphorescence of an injected dye that is excited by light pulses. Tamoxifen treatment increased hypoxia in the tumors, as measured by EF5 binding (P = 0.01 by Mann-Whitney test). This observation was not dependent on the presence of tamoxifen-induced necrosis. Intravascular oxygen partial pressures were lower in tumors relative to surrounding normal tissue in tamoxifen-treated tumors as compared to placebo-treated tumors. In vitro, tamoxifen did not modify the oxygen-dependent metabolism of EF5, indicating that the increased EF5 binding in tamoxifen-treated tumors reflects a physiological decrease in tissue oxygenation. The clinical significance of these observations is discussed in the context of the sequencing of tamoxifen with other therapies, and in light of recent data suggesting that hypoxia may be associated with genetic changes resulting in a more aggressive tumor phenotype.

Creatinine kinase kinetics studied by phosphorus-31 nuclear magnetic resonance in a canine model of chronic hypertension-induced cardiac hypertrophy.

To determine whether cardiac hypertrophy secondary to chronic renovascular hypertension is associated with altered in vivo myocardial metabolism, phosphorus-31 nuclear magnetic resonance saturation transfer techniques were used to study creatine kinase (CK) kinetics in six chronically hypertensive dogs with moderate cardiac hypertrophy and eight control dogs. The forward rate constant of CK and the flux of phosphocreatine to adenosine triphosphate were determined in both groups of dogs before and during norepinephrine administration (1 microgram/kg per min), used to increase heart rate x systolic blood pressure (rate-pressure product), cardiac output and oxygen consumption. Baseline and norepinephrine-induced changes in rate-pressure product, cardiac output and oxygen consumption were similar in both groups of dogs, as were baseline forward rate constant and flux of phosphocreatine to adenosine triphosphate. However, the norepinephrine-induced changes in forward rate constant and flux were significantly less in hypertensive than in control dogs (p less than 0.05) even though changes in hemodynamic and functional variables were similar in both groups. These data demonstrate that moderate myocardial hypertrophy is associated with altered CK kinetics, which do not appear to affect the heart's ability for global mechanical recruitment at this stage in the hypertensive process. It is possible that the changes in myocardial enzyme kinetics may contribute to diastolic dysfunction previously reported in this model and may be a precursor for ultimate development of heart failure if hypertension is maintained for prolonged periods.(ABSTRACT TRUNCATED AT 250 WORDS)

The efferent connections of the feline nucleus cuneatus.

Nucleus cuneatus projections to nucleus ventralis posterolarteralis pars medialis (VPLm) and other thalamic as well as midbrain and medullary nuclei were studied in cats using the Fink-Heimer I silver technique. Single electrolytic lesions of very small size were made stereotaxically in different zones of nucleus cuneatus under electrophysiological control. All zones studied projected to contralateral VPLm in a pattern of discrete terminal arborizations or clusters, which were organized in onionskin-like dorso-ventral laminae. The clusters of degeneration varied in size and density according to their dorsoventral location within VPLm. Those in dorsal areas were smaller in diameter (50-125 mu) and contained less dense amounts of degeneration than clusters (150-300 mu) in more ventral regions. The clustered terminal arborizations mirrored the organization of the VPLm neuronal clusters, themselves. Terminations within VPLm were topographically organized, but were completely inverted, i.e. dorsal nucleus cuneatus projected to ventral VPLm and ventral to dorsal, lateral to medial, and medial to lateral VPLm. A ventral zone of nucleus cuneatus, which contained "deep" units, projected to a separate dorsal zone of VPLm. In addition to its classical connection with VPLm, nucleus cuneatus projected to the following contralateral brainstem or thalamic nuclei: medial and dorsal accessory olives, external nucleus of the inferior colliculus, ventrolateral part of the superior colliculus, nucleus ruber, medial geniculate nucleus pars magnocellularis, suprageniculatus, medial and lateral divisions of the posterior thalamic nuclear group, zona incerta, and Fields of Forel. Very sparse amounts of degeneration were also present within nuclei ventralis posteromedialis (caudal pole) and ventralis posterolateralis pars lateralis. The brain-stem and thalamic projections of the dorsocaudal part (cell nest region) of the cuneate nucleus were more restricted than those of its rostral and ventral regions. The clusters of both the VPLm neurons and cuneate terminations within VPLm provides an anatomical basis for the functional characteristics of synaptic security, fine grain somatotopia and modality specificity so prominent in the dorsal column nuclei-medial lemniscal system.

Protection against metastasis of radiation-induced thymic lymphosarcoma and weight loss in C57Bl/6NCr1BR mice by an autoclave-resistant factor present in soybeans.

We have investigated the ability of Bowman-Birk inhibitor, a protease (trypsin and chymotrypsin) inhibitor, to protect against radiation-induced thymic lymphosarcoma in C57Bl/6NCr1BR mice. Fifty-five 7-week-old male mice were randomized into 11 groups and gavaged 5 days per week with purified Bowman-Birk inhibitor, Bowman-Birk inhibitor concentrate, and autoclaved Bowman-Birk inhibitor concentrate. Following 7 days of gavage, those mice undergoing total-body or sham total-body irradiation received 1.7 Gy weekly for 4 weeks. At 6 months following the radiation exposure, all mice were sacrificed and examined histopathologically. Samples of Bowman-Birk inhibitor concentrate, purified Bowman-Birk inhibitor, and autoclaved Bowman-Birk inhibitor concentrate were evaluated with thin-layer chromatography. The mice treated with total-body irradiation and autoclaved Bowman-Birk inhibitor had significantly (P < 0.05) fewer deaths, lower average grade of lymphosarcoma, and larger fat stores compared to those treated with total-body irradiation and water gavage. The results for the total-body-irradiated mice receiving Bowman-Birk inhibitor concentrate suggested an effect midway between these two groups. Thin-layer chromatography analysis indicated that sterols and the phospholipids varied in the three different samples in a way that approximately corresponded with the observed effects. We have observed that an autoclave-resistant factor in soybeans is capable of reducing metastasis of radiation-induced lymphosarcoma and weight loss in C57Bl/6NCr1BR mice, presumably by preventing the extension and metastasis of cancer cells. Thus, in addition to the anticarcinogenic Bowman-Birk inhibitor, there appears to be another anticarcinogenic agent in soybeans which is capable of inhibiting the later stages of cancer cell development.

Magnetic resonance imaging observations of blood-brain-barrier permeability in an animal model of brain injury.

RATIONALE AND OBJECTIVES: Knowledge of the in vivo relaxivity of paramagnetic contrast agents is important in the accurate measurement of the permeability of the blood-brain barrier (BBB). This study was aimed at developing an animal model for the magnetic resonance (MR) imaging investigation of injuries to the BBB. METHODS: MR imaging (1.9 T) was performed in 18 rats with acute, stable injuries to the brain caused by freezing. After injection of gadodiamide (0.05-0.20 mmol/kg), estimates were made of BBB permeability, leakage space, and relaxivity (also measured in saline). RESULTS: The BBB was always disrupted at the injured site (permeability = 0.038 min-1 +/- 0.0006). The central area of necrosis and the periphery of edema showed substantial differences in leakage space and relaxivity. The relaxivity of gadodiamide was much greater at the injured site than in saline. CONCLUSION: The in vivo relaxivity at a site of pathologic change in the brain may be substantially greater than that measured in aquo.

Retrovirus-like activity in an immunosuppressed dog: pathological and immunological findings.

A putative retrovirus was isolated from a dog with a severe, acquired immunodeficiency-like syndrome. The haematological abnormalities and immunological deficiencies included anaemia, leucopenia (lymphopenia and neutropenia), thrombocytopenia, decreased humoral immunity, and ineffective T-cell responses in-vitro. The necropsy findings included generalized lymphoid depletion, severe bone marrow hypoplasia, plasmacytic infiltrates in lymphoid and non-lymphoid organs, and severe secondary infections. Supernates of peripheral blood mononuclear cell cultures from the affected dog contained an agent with manganese-dependent reverse transcriptase (RT) activity that sedimented at a density of 1.122 g/ml. RT activity was also found post-mortem in extracts prepared from the bone marrow, lymph nodes, and small intestine. The lymph nodes and small intestine expressed a 3.8 kb mRNA that was recognized by a bovine leukaemia virus (BLV) pol DNA probe by Northern blotting. DNA isolated from the lymph nodes and small intestine from the affected dog showed distinct band patterns by Southern analysis, suggesting an exogenous retrovirus. The retrovirus could be propagated in normal canine peripheral blood mononuclear cells or short-term canine lymphocyte cell lines in-vitro, and was cytopathogenic for cells of canine, but not human, origin. These results suggest the existence of a pathogenic canine retrovirus capable of producing disease of the type associated with retroviruses in other species.

Clinicopathological and immunophenotypical features of canine intravascular lymphoma (malignant angioendotheliomatosis).

Intravascular lymphoma (IVL) is a rare angiotropic large-cell lymphoma in which neoplastic lymphocytes proliferate within the lumina of blood vessels in the absence of a primary extravascular mass or leukaemia. A retrospective review of veterinary medical records identified 17 cases of canine IVL. Spinal cord ataxia (seven dogs), posterior paralysis (one dog), seizures (four dogs) and vestibular disease (three dogs) dominated the clinical presentation. Haemorrhage, ischaemia, and occasional foci of vascular proliferation were found in tissue sections from affected dogs. Vessels, predominantly veins, throughout the body were frequently filled with neoplastic lymphocytes. Splenic involvement occurred in only one of 10 cases examined and bone marrow involvement was absent in four cases examined. Formalin-fixed paraffin wax-embedded tissues from 15 cases were examined immunohistochemically with streptavidin-biotin-horseradish peroxidase and a catalysed signal amplification system. The neoplastic cells were classified in eight cases as T cells (CD3+/IgG-/CD79a-), in one case as B cells (CD3-/CD79a.dim/IgG+), and in the remaining six cases as non-T, non-B (CD3-/IgG-/CD79a-). The clinical and pathological features of canine IVL closely resembled those of the human disease. In striking contrast to human cases, which are most often B-cell lymphomas, the immunophenotypes of the canine IVLs in this series were heterogeneous. The canine IVLs were derived primarily from T cells and non-T, non-B lymphocytes, B cells being found in only a single instance.

Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976-1989).

Medical records and histologic sections of 40 cats with acute pancreatitis were reviewed. Two distinct groups of cats with pancreatitis were established by histologic analysis of tissue. Group 1 (32 cats) had acute pancreatic necrosis (APN). Group 2 (8 cats) had suppurative pancreatitis. Ages of affected cats ranged from 3 weeks to 16 years. The majority consisted of indoor cats of the Domestic Short-Haired breed but Siamese cats were over-represented relative to the general population (P < 0.05). Twenty-two percent of cats were obese and 57% were underweight. Thirty-eight percent of cats had acute disease. In the other cats, two stages in the progression of the disease were evident: (1) anorexia, weight loss, and lethargy, followed by (2) acute deterioration, development of shock, and a moribund state, despite fluid therapy. The most common clinical signs were severe lethargy (100%), reduced appetite (97%), dehydration (92%), and hypothermia (68%). The initial hemogram occasionally showed a neutrophilia (30%) and anemia (26%) but packed cell volume (PCV) decreased markedly to the extent that 55% of cats were anemic terminally. Serum biochemical abnormalities included increased activities of ALT (68%) and ALP (50%), and increased concentrations of bilirubin (64%) and cholesterol (64%). Cats with APN were hyperglycemic (64%), glycosuric (60%) and ketonuric (20%), whereas cats with suppurative pancreatitis tended to be hypoglycemic (75%). Renal failure and electrolyte abnormalities were mild or infrequent except for hypokalemia (56%). This study characterizes a severe necrotizing pancreatitis in the cat similar to that reported in other species, and a histologically distinct suppurative pancreatitis.

Cerebellar Purkinje's cell degeneration and coat color dilution in a family of Rhodesian Ridgeback dogs.

A syndrome of cerebellar Purkinje's cell degeneration and coat color dilution was diagnosed in a family of Rhodesian Ridgeback dogs. One male and 1 female from the same litter and 1 female from a different litter were evaluated for growth retardation, inability to ambulate, and progressive ataxia. On physical examination, lateral recumbency, severe ataxia, tremors, and diluted coat color were identified. Littermates with nondiluted coat color were neurologically normal. Results of routine laboratory tests, urine metabolic screenings, and karyotype analyses were normal. Histopathologic abnormalities at necropsy included cerebellar Purkinje's cell degeneration, reduced granular cell layer thickness, and uneven distribution of macromelanosomes within hair shafts. Pedigree analysis suggested an autosomal recessive mode of inheritance. This is the first description of a genetic syndrome affecting the central nervous system and associated with coat color dilution in dogs.

Study of long-term survival after transsphenoidal hypophysectomy in clinically normal dogs.

Experimental hypophysectomies were performed in 7 clinically normal dogs, using a new modification of the transsphenoidal approach. This approach facilitated centering of the sphenoid bone trephination and allowed safe exposure of the hypophysis regardless of the size or shape of a dog's skull. Complications did not occur during surgery and all dogs recovered well from surgery. Growth hormone secretory capacity was measured over a 3-month period to assess completeness of hypophysectomies. One dog was euthanatized 2 months after surgery, 4 dogs were euthanatized at 3 months after surgery, and 2 dogs were allowed to survive and their progress was followed for 2.5 years. Soft palate dehiscence and keratoconjunctivitis sicca developed in 2 of the dogs. The technical deficiencies responsible for these complications were corrected shortly after the beginning of the study. In 4 of the 5 necropsied dogs, minute remnants of adenohypophyseal tissue were found in the sellae turcica. Measurement of in vivo growth hormone secretory capacity revealed that these remnants had an altered stage of functional activity. Although complete hypophysectomy was not achieved consistently, the main technical obstacle of hypophysectomy, the reliable identification and the avoidance of the vascular structures surrounding the hypophysis, has seemingly been overcome. The surgical technique proved to enhance the safety of hypophysectomy, and the procedure can be recommended to treat clinical cases of canine pituitary-dependent hyperadrenocorticism. The clinical significance of potential subtotal hypophysectomy remains yet to be evaluated.

Cryptosporidiosis in young artiodactyls.

Cryptosporidium was found in the intestinal tract of 10 blackbuck, 2 scimitar-horned oryx, 2 fringe-eared oryx, 2 addax, and 1 sable antelope that had diarrhea. Cryptosporidia were most numerous in the small intestine, but also were found in the cecum, spiral colon, and colon. The small intestine had minimal inflammation in association with the cryptosporidia. Salmonella typhimurium was isolated from 10 of the 51 animals evaluated, with extensive inflammation of the cecum, spiral colon, and colon observed in these animals.

Clinical manifestations and associated disease syndromes in dogs with cranial vena cava thrombosis: 17 cases (1989-1996).

OBJECTIVE: To characterize cranial vena cava thrombosis in dogs with regard to signalment, clinical manifestation, potential inciting causes, treatment, and outcome. DESIGN: Retrospective study. ANIMALS: 17 dogs with a cranial vena cava thrombus. PROCEDURE: Medical and necropsy records were reviewed for signalment, potential causes of thrombus formation, diagnosis, clinicopathologic findings, treatment, and outcome. RESULTS: A signalment predisposition was not found. Ten dogs had cranial vena cava syndrome, and 10 had a pleural effusion. Ten dogs were dyspneic, and 5 had palpable jugular thrombi. Predisposing conditions identified were presumed immune-mediated hematologic disease and corticosteroid administration (6 dogs), sepsis (6), protein-losing nephropathy (2), neoplasia (2), and cardiac disease (1). Central venous catheterization was implicated as a contributing cause. Thrombocytopenia was the most consistent clinicopathologic finding, and ultrasonography was helpful in confirming the diagnosis. Treatment varied, but 15 of the 17 dogs died or were euthanatized within 20 days of clinical manifestation of the thrombus. At necropsy, thrombi were found in other organs, mainly the right atrium, jugular veins, and pulmonary arteries. CLINICAL IMPLICATIONS: Prognosis is poor for dogs with cranial vena cava thrombosis associated with clinical signs. Use of central venous catheters should be avoided in dogs with predisposing diseases such as immune-mediated disease, sepsis, protein-losing nephropathy, neoplasia, and cardiac disease.

Correlation between thoracic radiographs and postmortem findings in dogs with hemangiosarcoma: 77 cases (1984-1989).

Thoracic radiographic and postmortem findings were compared in dogs with histologically confirmed hemangiosarcoma (HSA). On the basis of results of radiography, a false-negative diagnosis was made for pulmonary HSA in 10 (21.7%) of 46 dogs, and in 26 (53.1%) of 49 dogs for cardiac HSA. The incidence of false-negative radiographic diagnosis for pulmonary HSA was lower in dogs when left and right lateral views were obtained. The radiographic sensitivity was 78%, and the negative-predictive value was 74% for pulmonary HSA. The radiographic sensitivity was 47%, and the negative-predictive value was 43% for cardiac HSA.

Evaluation of risk factors for fatal acute pancreatitis in dogs.

OBJECTIVE: To identify risk factors associated with fatal acute pancreatitis in dogs. DESIGN: Case-control study. ANIMALS: 70 case dogs with clinical evidence and histopathologic confirmation of fatal acute pancreatitis and 104 control dogs that had trauma, underwent necropsy, and did not have histologic evidence of acute pancreatitis. PROCEDURE: Information on signalment, weight, body condition, medical history, concurrent disease, and results of histopathologic examination was obtained by reviewing medical records. Logistic regression analysis included calculation of univariate and multivariate (adjusted) odds ratios and 95% confidence intervals. RESULTS AND CLINICAL IMPLICATIONS: Dogs with fatal acute pancreatitis were largely middle- to older-aged dogs. Risk of developing fatal acute pancreatitis was increased by overweight body condition, diabetes mellitus, hyperadrenocorticism, hypothyroidism, prior gastrointestinal tract disease, and epilepsy. Additionally, Yorkshire Terriers were at increased risk, and Labrador Retrievers and Miniature Poodles were at decreased risk, of developing fatal acute pancreatitis. Males and neutered females appeared to have an increased risk of developing fatal acute pancreatitis, compared with sexually intact females. Thrombus formation was more likely in dogs that developed fatal acute pancreatitis than in control dogs.