Histopathological features of canine spontaneous non-neoplastic gastric polyps - a retrospective study of 15 cases.

Fifteen cases of canine gastric polyps, collected over a 4-year period, were investigated using gross inspection, histological procedures and immunohistochemical techniques for Helicobacter infection. No breed or sex predisposition was found for gastric polyps, although they occurred mainly in elderly animals. There were 9 pedunculated and 6 sessile polypoid growths, between 5 to 30 mm in diameter developed mainly in the pyloric region of the stomach. The most common type of gastric polyps was the hyperplastic one. The inflammatory type was identified in three cases. Foci of AB/PAS Goblet positive cells resembling intestinal metaplasia, mild dysplasia of gastric epithelium, well delimited calcified areas, islands of osteoid matrix and nematodes were present in some of these lesions. Histological examination of the adjacent gastric polyp (surrounding gastric mucosa) revealed a severe chronic inflammation in 13 cases and a high grade of Helicobacter species colonization in all cases, but Kendall test analysis showed no correlation between Helicobacter spp. colonization degree and gastritis scores (τ = 0289; p = 0.204). A significant correlation was found between Helicobacter spp. location and gastritis scores (τ = 0.497; p = 0.035). Immunohistochemistry performed with a polyclonal antibody confirmed Helicobacter spp. infection in all cases. Based on their morphology, Helicobacter pylori - like organisms were described in 3 of 15 cases. No high degree of dysplasia nor neoplasia were identified in these lesions. The etiology and pathogenesis of gastric polyps in dogs are still unknown, although a severe chronic antral gastritis may be a predisposing condition for development of gastric polyps in dogs.

Pathological changes associated with white striping in broiler breast muscles.

White striping is a condition in broiler chickens characterized grossly by the occurrence of white striations, seen parallel to the direction of muscle fibers, on broiler breast fillets and thighs. Based on visual evaluation of the intensity of white striping, breast fillets can be categorized into normal (NORM), moderate (MOD), and severe (SEV) categories. This study was undertaken to evaluate the details of changes in histology as well as proximate composition occurring in the fillets with respect to the 3 degrees of white striping. In experiment 1, representative breast fillets for each degree of white striping (n = 20) were collected from 45-d-old broilers, approximately 2 h postmortem. From each fillet, 2 skeletal muscle samples were obtained and fixed in 10% neutral buffered formalin. To identify and differentiate the histological changes, slides were prepared and stained using hematoxylin and eosin, Masson's Trichrome, and Oil Red O stains. In experiment 2, samples with 3 degrees of white striping were collected from 57-d-old birds for conducting proximate analysis. Major histopathological changes observed in the MOD and SEV samples consisted of loss of cross striations, variability in fiber size, floccular/vacuolar degeneration and lysis of fibers, mild mineralization, occasional regeneration (nuclear rowing and multinucleated cells), mononuclear cell infiltration, lipidosis, and interstitial inflammation and fibrosis. Microscopic lesions were visually scored for degeneration and necrosis, fibrosis, and lipidosis. The scale used to score the samples ranged from 0 (normal) to 3 (severe). There was an increase (P < 0.05) in mean scores for degenerative or necrotic lesions, fibrosis, and lipidosis as the degree of white striping increased from NORM to SEV. The results from the histopathological study were supported by the findings from proximate analysis confirming that the fat and protein contents of muscle increased (P < 0.05) and decreased (P < 0.05), respectively, as the degree of white striping increased. In conclusion, the histopathological changes occurring in white striping indicate a degenerative myopathy that could be associated with increased growth rate in birds.

Acute respiratory distress in an alpaca.

An alpaca was presented with a history of respiratory difficulty and death. Histology of the phrenic nerves and diaphragm revealed degenerative changes consistent with denervation atrophy, and a diagnosis of diaphragmatic paralysis was established. No gross or histological abnormalities were observed in the spinal cord or other organs. The etiology of the phrenic nerve neuropathy could not be determined. The need to examine phrenic nerves and diaphragm in camelids with respiratory distress is emphasized, as failure to examine these samples will preclude a diagnosis of diaphragmatic paralysis.

Lymphadenopathy associated with a thyroid carcinoma in a dog.

Angiomatoid lesions in a lymph node associated with a thyroid carcinoma of a dog were restricted to the subcapsular and medullary sinuses. Lymphoid atrophy was present, but nodal architecture was not distorted and normal structures were not invaded. Immunohistochemical staining indicated that the vascular spaces formed by spindloid cells were lined by endothelium with a low mitotic index. The spindloid cells were positive for smooth muscle actin, vimentin, and desmin and thus were likely to be fibroblasts, myofibroblasts, smooth muscle cells, and/or pericytes. These features are comparable to vascular transformation of lymph node sinuses in humans (nodal angiomatosis), a nonneoplastic condition often associated with mechanical or functional blockage of efferent lymphatics and veins.

Cutaneous schwannomas in 22 horses.

Schwannomas are uncommonly recognized in horses. This study describes cutaneous schwannomas in 22 horses aged 8 to 25 years: 12 male, 7 female, and 3 of unknown sex. The horses had solitary cutaneous masses: 9 on the head, 3 on the neck, and the others on the shoulder, hip, thorax, abdomen, rump, extremities, or tail. The location of 1 tumor was unknown. The dermal tumors were well demarcated and expansile. Twelve had a multinodular pattern, whereas 10 formed a single nodule. Antoni A areas were observed in all tumors, and 10 tumors contained Antoni B areas. In Antoni A areas, the densely packed spindle-shaped neoplastic cells were arranged in short fascicles with nuclear palisading. In the hypocellular Antoni B areas, neoplastic cells were separated by abundant myxomatous stroma. Tumors commonly had hyalinization of stroma and vessel walls and ancient change. Cellular vacuolation was observed in 18 tumors. In all 22 cases, neoplastic cells were immunopositive for S100 protein. Expression of laminin and glial fibrillary acidic protein was observed in all 6 tumors evaluated by immunohistochemistry for these markers. One tumor was examined ultrastructurally: Neoplastic cells had branched cytoplasmic processes and were surrounded by an external lamina. Follow-up information was available 8 months to 10 years postexcision for 9 horses, for which surgical excision of the tumor was curative. The equine cutaneous schwannomas in this study had microscopic features like those of human schwannoma and had benign clinical behavior. Correct classification of equine cutaneous schwannoma will facilitate accurate prognosis and appropriate treatment.

Malignant round cell neoplasia in llamas and alpacas.

Malignant round cell neoplasia was identified in 12 llamas and 12 alpacas aged 0-23 years. Mean age of affected alpacas (3.1 years) was significantly less than that of affected llamas (8.0 years). Tumor cell morphology varied from large and often pleomorphic (11 tumors) to small and often homogeneous (13 tumors). Neoplastic lesions were multicentric in 12 cases. Other sites were gastric (5 cases), intra-abdominal (perirenal; 4 cases), intrathoracic (2 cases), and cervical (1 case). Immunohistochemistry with antibodies to CD79alpha, BLA36, and CD3 identified B-cell lymphoma (12 cases) and T-cell lymphoma (6 cases). Six tumors did not express any lymphoid marker and were further immunostained for neuron-specific enolase (NSE), synaptophysin, S-100, glial fibrillary acidic protein (GFAP), and chromogranin A. All 6 of these tumors were negative for GFAP and chromogranin A but expressed 1 or more of the neural markers NSE, synaptophysin, and S-100 and were classified as primitive malignant round cell tumors (PMRCT). Tumor types could not be distinguished on the basis of animal age, gross pathologic appearance, tumor morphology, or tumor location. All animals with lymphoma and 5 with PMRCT died or were euthanatized. One alpaca with a focal cervical PMRCT lived for at least 20 months after diagnosis. Results of this study indicate that malignant round cell tumors in llamas and alpacas are a heterogeneous group that cannot be distinguished on the basis of signalment, postmortem findings, or routine light microscopic findings. Immunohistochemistry is a valuable diagnostic procedure when evaluating malignant round cell neoplasia in llamas and alpacas.

An outbreak of fatal herpesvirus infection in domestic rabbits in Alaska.

A herpesvirus infection affecting mini Rex and crossbred meat rabbits was identified in a rabbitry in Alaska. Illness affected over half of the 55 rabbits on the premises, and 16 rabbits died or were euthanatized because of illness. Disease affected all ages from adults to nursing young and occurred over an approximately 2-month period. Clinical signs included conjunctivitis and periocular swelling, ulcerative dermatitis, progressive weakness, anorexia, respiratory distress, and abortion. Hemorrhagic dermatitis and panniculitis were associated with epidermal microvesicular degeneration, dermal and subcutaneous vascular necrosis, and thrombosis. Eosinophilic intranuclear inclusions consistent with herpesvirus were found within the epidermis and superficial follicular epithelium and within mesenchymal cells within the dermis and subcutis. Syncytial cells containing viral inclusions occurred within the epidermal and superficial follicular epithelium. Other findings were hemorrhagic necrosis of the myocardium with rare intranuclear inclusions within stromal cells, multifocal pulmonary hemorrhage, hemorrhage with sinus erythrophagocytosis in lymph nodes, and massive necrosis and fibrin deposition within red pulp of the spleen. A virus isolated from the skin produced syncytia, intranuclear inclusions, and cell lysis typical of herpesvirus in rabbit kidney cells in vitro. The viral isolate was characterized ultrastructurally as an enveloped virus with icosahedral nucleocapsids 100 nm diameter, consistent with a herpesvirus.

Thrombotic endocarditis in 10 alpacas.

BACKGROUND: A description of the clinical signs and necropsy findings in 10 alpacas with thrombotic endocarditis. ANIMALS: Clinical cases admitted to 2 veterinary referral hospitals between May 1998 and December 2006. METHODS: A retrospective study was performed by searching hospital records to identify alpacas diagnosed with endocarditis. RESULTS: Common clinical findings included sternal recumbency, tachycardia, tachypnea, and abdominal distension. Heart sounds were recorded as normal in 7 of 10 alpacas. Pleural and pericardial effusion and ascites were often present. Complete blood cell counts often suggested inflammation, and liver enzyme activity was often increased. When echocardiography was performed, a soft tissue density was imaged within the right ventricle. All alpacas died or were euthanized. Necropsy revealed mural endocarditis with right ventricular or biventricular fibrinous thrombi obliterating the ventricular lumina with no valvular involvement in 6 of 10 affected animals. Bacteria were not consistently identified as a cause for the endocarditic lesions. Eight of the 10 alpacas had evidence of hepatic fluke infestation. CONCLUSIONS AND CLINICAL IMPORTANCE: Valvular and mural thrombotic endocarditis should be included in the list of differential diagnoses for hepatomegaly, abdominal distension, and other signs of right-sided congestive heart failure in alpacas. The prognosis of this disease is grave.

Myonecrosis in three horses with colic: evidence for endotoxic injury.

Three horses with colic, clinical evidence of endotoxaemia and high serum activities of creatine kinase and aspartate aminotransferase were examined postmortem. The horses were diagnosed with severe ulcerative colitis, pyloric ulceration and stenosis with colonic sand impaction, and colonic obstruction due to faecaliths. There was no gross or histological evidence of muscle trauma. Their semimembranosus muscles had scattered acute to subacute segmental necrosis of the myofibres, suggestive of endotoxin-induced muscle injury.

Gastric adenocarcinoma in a horse with portal vein metastasis and thrombosis: a novel cause of hepatic encephalopathy.

A 17-year-old Quarter horse mare was referred to Cornell University for postmortem examination after 72 hours of encephalopathy that consisted of depression, mania, and blindness. A plasma sample and cerebral spinal fluid demonstrated hyperammonemia. Gross necropsy examination findings included the following: mild icterus, a transmural mass in the glandular portion of the gastric fundus, multiple masses throughout the liver, and a large tumor thrombus in the portal vein. Microscopically, the gastric mass, hepatic masses, and portal vein thrombus were composed of similar neoplastic epithelial cells that formed variably sized acini and branching cords separated by a dense desmoplastic stroma. Throughout the cerebral frontal cortex were numerous Alzheimer type II astrocytes. Hepatic encephalopathy was caused by gastric adenocarcinoma, with metastasis to the liver and the portal vein. The clinical and pathologic lesions from this unique case, as well as hyperammonemia and portal vein thrombosis in the pathogenesis of hepatic encephalopathy, are discussed.

Ubiquitin expression in muscle from horses with polysaccharide storage myopathy.

Serial sections of formalin-fixed, paraffin-embedded muscle biopsy specimens from 28 Quarter Horse, Paint, and draft-related breeds, aged 0.5-23 years, were treated with periodic acid-Schiff (PAS) stain for glycogen and were immunostained to detect ubiquitin expression. On the basis of findings in PAS-stained sections, a diagnosis of equine polysaccharide storage myopathy (EPSSM) was made in 22 horses aged 2-23 years (mean, 9.4 years); samples from 6 horses aged 0.5-15 years (mean, 7.3 years) had a normal PAS staining pattern, with no relevant lesions. Ubiquitin expression was detected in all but a 2-year-old EPSSM-affected horse and was not detected in the non-EPSSM-affected horses. Ubiquitin expression was greater than the degree of PAS-positive, amylase-resistant material, and ubiquitin was detected in aggregates of amylase-sensitive glycogen as well as in aggregates of amylase-resistant material. Results suggest that glycogen aggregates develop and are ubiquitinated prior to development of amylase-resistant inclusions. Ubiquitin immunostaining may be most useful for confirming the diagnosis of EPSSM in horses with only amylase-sensitive glycogen aggregates and in horses with early amylase-resistant inclusions. However, ubiquitin immunostaining is no more sensitive than is PAS staining for diagnosis of EPSSM.

Incidence of polysaccharide storage myopathy: necropsy study of 225 horses.

Muscle samples were obtained at necropsy from 225 horses and ponies 1 year of age or older. Samples were processed in routine manner and were stained with hematoxylin and eosin and with periodic acid-Schiff for glycogen. Sections were examined for abnormal glycogen content and amylase-resistant complex polysaccharide and for chronic myopathic change (excessive fiber size variation, increase in number of internal nuclei). A total of 101 horses and ponies with lesions of polysaccharide storage myopathy were identified. Age of affected horses ranged from one to 30 years, with a mean of 14.7 years. Mean age of nonaffected horses was 12 years. Incidence of polysaccharide storage myopathy varied depending on breed; Thoroughbreds had the lowest (27%) and draft-related horses had the highest (86%) incidence. Chronic myopathic changes were more severe in polysaccharide storage myopathy-affected horses than in nonaffected horses. Results of this study indicate that polysaccharide storage myopathy is a common disorder of many breeds of horses and ponies.

Fatal paraquat poisoning in seven Portland, Oregon, dogs.

Paraquat is one of the few broad-spectrum herbicides available in the US; however, it is extremely toxic to companion animals when ingested. Despite its restricted use status, poisoning of dogs and cats remains relatively common. This clinical report documents a series of chronologically and geographically related cases of presumed malicious and fatal sub-acute paraquat poisoning in 7 dogs in Portland, OR. All animals developed acute gastrointestinal disturbance, renal compromise and insidiously progressive respiratory failure. Hyperlipasemia and moderate hypertension were notable featured in 5/7 cases. Trace levels of paraquat were demonstrated in the urine of 4/7 animals by gas-liquid chromatography/mass spectroscopy. Diagnosis in the remaining 3 cases was made through a combination of history or exposure, clinical signs and their progression, and pulmonary and renal histopathology.

Topical exposure to exogenous ultraviolet-irradiated urocanic acid enhances Mycobacterium ulcerans infection in a Crl:IAF(HA)-hrBR hairless guinea-pig model of Buruli ulcer disease.

BACKGROUND: Ultraviolet radiation (UVR) pre-exposure enhances Mycobacterium ulcerans infection in the Crl:IAF(HA)-hrBR hairless guinea-pig, possibly via a photoimmunosuppressive mechanism. The trans-cis photoisomerization of epidermal urocanic acid is an important initiator of the web of events leading to photoimmunosuppression. Thus, the hypothesis tested in this paper was that topical pre-exposure to UVR-irradiated urocanic acid mixture containing cis-urocanic acid (UVR-UCA) enhances the ulcerative form of M. ulcerans infection in the Crl:IAF(HA)-hrBR hairless guinea-pig model of human Buruli ulcer disease. METHODS: Groups of six animals were subjected to daily topical treatment with either 0 (vehicle only), 0.1, 0.5 or 1 mg of trans (tUCA) or UVR-UCA (contained a cis : trans urocanic acid isomer ratio of 1 : 9) for three consecutive days. A sham treatment group was also included in the experiment. Three days following their final treatment, the guinea-pigs were intradermally infected in the right dorsal flank with 1.5 x 107 CFU of M. ulcerans in 0.1 ml of phosphate-buffered saline (PBS) and sham infected with 0.1 ml of PBS in the left dorsal flank. The resultant skin lesions were then measured over the next 21 days. At day 21 postinfection, the animals were tested for delayed-type hypersensitivity (DTH) reactivity to M. ulcerans cell fragment antigens (MCF). RESULTS: Distinct, well-demarcated, dermally situated skin nodules were present at infected, but not sham-infected, skin sites by day 3 postinfection, and the lesions progressed to frank ulcers by day 5. Between days 5 and 21, the mean lesion diameters of the UVR-UCA-treated animals were significantly (P<0.001) greater than those of the sham, vehicle only or tUCA-treated groups. UVR-UCA-treated guinea-pigs also had significantly (P<0.001) suppressed DTH responses to MCF compared with the other treatment groups. There were no significant (P>0.4) differences between the lesion sizes and DTH responses of the tUCA, vehicle only or sham treatment groups. These results demonstrate that topical exposure to UVR-UCA promotes M. ulcerans infection and suppresses DTH responses to M. uclerans antigens in infected animals. These results lend credence to the hypothesis that UVR-mediated enhancement of Buruli ulcer disease in the Crl:IAF(HA)-hrBR hairless guinea-pig model occurs via modulation of cis-urocanic acid-susceptible immune pathways.

B-cell leukemia in a sheep.

Necropsy examination was performed on an 8.5-year-old Finnish ewe euthanatized because of progressive respiratory distress, cachexia, and weakness. Significant postmortem findings included a diffusely enlarged, dark-red friable liver, mild splenomegaly, and mild mesenteric lymphadenopathy. Examination of multiple tissue sections revealed intravascular atypical mononuclear cells in all tissues examined, with a leukemic pattern of infiltration of mesenteric lymph nodes, liver, lung, and spleen. Neoplastic cells were positive for CD79a and negative for CD-3, BLA.36, and CD68 leukocytic markers. The final diagnosis was B-cell leukemia.

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.

Cutaneous vasoproliferative lesions in goats.

Abstract. In a retrospective survey of caprine neoplastic disease, eight masses were diagnosed as cutaneous vascular tumors. The typical clinical presentation was a solitary raised, bleeding mass. No predilection with regard to age, breed, sex, or anatomic location was found. Reevaluation of the microscopic features of the masses resulted in diagnoses of hamartoma (2), hemangioma (4), and hemangiosarcoma (2). An endothelial cell origin was confirmed in all seven tumors tested immunohistochemically for factor VIII-related antigen. Although rarely reported, goats display a range of cutaneous vascular growth abnormalities similar to those observed in other domestic animals.

Complex polysaccharide inclusions in skeletal muscle adjacent to sarcomas in two dogs.

Inclusions of periodic acid-Schiff-positive, amylase resistant material were found within skeletal muscle fibers adjacent to an osteosarcoma in the proximal femur of an 8-year-old intact female Cocker Spaniel dog (dog No. 1) and adjacent to a synovial cell sarcoma of the stifle joint in a 7-year-old spayed female Bouvier des Flandres dog (dog No. 2). Inclusions were pale blue-gray with hematoxylin and eosin stain and formed irregular inclusions, replacing up to approximately 80% of the fiber diameter. Inclusions from dog No. 2 were of non-membrane-bound granular to filamentous material that occasionally formed discrete, elongate electron-dense masses. The features of these inclusions were similar to those of materials previously described as complex polysaccharide, polyglucosan bodies, amylopectin, and Lafora bodies. Evidence for a generalized metabolic disorder was not found in these two dogs, suggesting that storage of complex polysaccharide can occur as a relatively nonspecific response to metabolic alterations in skeletal muscle in a variety of conditions.

Congenital hypotrichosis in a Percheron draught horse.

A blue roan Percheron foal was born with poorly circumscribed patchy alopecia of the trunk and legs. Teeth and hoof development were normal. Alopecia was progressive, becoming almost complete by 1 year of age. Histopathological findings in a skin biopsy obtained at 7 months of age were consistent with severe follicular hypoplasia. Sebaceous glands, epitrichial sweat glands and arrector pilae muscles were normal. The horse is alive and otherwise well at 6 years of age, although adult stature is considered small for this breed. The clinical history and histopathological findings are most consistent with a form of congenital hypotrichosis.

Incidence of polysaccharide storage myopathy in draft horse-related breeds: a necropsy study of 37 horses and a mule.

Skeletal muscle samples from 38 draft horse-related animals 1-23 years of age were evaluated for evidence of aggregates of glycogen and complex polysaccharide characteristic of equine polysaccharide storage myopathy (EPSSM). Cardiac muscle from 12 of these horses was also examined. Antemortem serum levels of creatine kinase (CK) and aspartate aminotransferase (AST) from 9 horses with EPSSM and 5 horses without EPSSM were compared. Skeletal muscle from 17 horses contained inclusions of periodic acid-Schiff (PAS)-positive, amylase-resistant complex polysaccharide. Similar inclusions were also present in the cardiac muscle of 1 horse. A vacuolar myopathy with aggregates of PAS-positive, amylase-sensitive glycogen was seen in 8 other horses, and these findings are also considered diagnostic for EPSSM. Antemortem serum activities of CK and AST were often higher in EPSSM horses than in horses without EPSSM. Using the presence of amylase-resistant complex polysaccharide as the criterion for diagnosis of EPSSM, the incidence in this population was 45%. Inclusion of horses with aggregates of glycogen but no amylase-resistant complex polysaccharide as representative of the range of pathologic findings in horses with EPSSM resulted in a 66% incidence in this population.