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Biomedical subjects

B A Summers

Publications and source records attributed to B A Summers.

At least 19 recordsLinked to original sources

Epithelioid variant of hemangioma and hemangiosarcoma in the dog, horse, and cow.

Epithelioid hemangiomas, hemangioendotheliomas, and angiosarcomas are well recognized histologic variants of endothelial tumors in humans that in the past have been confused with neoplasms of epithelial or histiocytic origin. We describe 12 epithelioid endothelial vascular tumors in 8 dogs, 3 horses, and 1 cow that share microscopic features with these tumors in humans. Ten tumors were located within the dermis and subcutis, 1 in the gastrocnemius tendon, and 1 in the skeletal muscle of the thigh. Key histologic features were the plump, epithelioid appearance of neoplastic endothelial cells and occasional cytoplasmic vacuolation, which rarely contained a single erythrocyte. Patterns of epithelioid endothelial cell growth ranged from conventional vasoformative structures to glandlike acini and short ducts to solid, sheetlike arrangements. All tumors were positive for endothelial markers: 12/12 (100%) were positive for von Willebrand factor with variable intensity and distribution and 9/9 (100%) were positive for CD31. All 12 were negative for cytokeratin. We subdivided these tumors into epithelioid hemangiomas (n = 3) and hemangiosarcomas (n = 9) based on conventional morphologic criteria, growth pattern (invasive or not), and metastasis (known in 1 case at the time of biopsy). Additional follow-up information obtained by a written questionnaire was available for 6/12 (50%) animals and revealed local recurrence in 3 animals (1 epithelioid hemangioma and 2 epithelioid hemangiosarcoma) and regional metastasis in 3 animals (all epithelioid hemangiosarcomas). This series represents a novel group of vascular tumors in domestic animals of which there are only 3 previous cases reported in the veterinary literature.

Animals↗

CNS hypomyelination in Rat Terrier dogs with congenital goiter and a mutation in the thyroid peroxidase gene.

Arrested physical development and neurologic abnormalities were identified in 3 of 5 Rat Terrier puppies at 9 weeks of age. Bilaterally firm symmetrical masses were palpated in the region of the thyroid glands. Low serum total (T4) and free thyroxine (FT4, by equilibrium dialysis) and markedly elevated thyroid stimulating hormone (TSH) concentrations supported the diagnosis of hypothyroidism. At necropsy, the thyroid gland was grossly enlarged and histologically exhibited severe, diffuse hyperplasia of the follicular epithelium. Gross examination of the central nervous system revealed a myelin deficiency, most evident in the corpus callosum. Regional distribution of hypomyelination was confirmed histologically, affecting the corpus callosum and, to a lesser degree, the corona radiata, the longitudinal fibers of the pons, the pyramids, and the lateral funiculi of the spinal cord. Myelin reduction was paralleled by axon reduction, suggesting that hypomyelination was a consequence of reduced axonal formation. A homozygous nonsense mutation in the thyroid peroxidase gene was identified in the affected puppies. The dam and a clinically normal litter mate were heterozygous for this mutation, confirming simple autosomal recessive inheritance of the disease trait. The same mutation, causing congenital hypothyroidism with a goiter was previously described in the Toy Fox Terrier breed. Given the ongoing practice of introducing the Toy Fox Terrier genetic background into some Rat Terrier breeding programs to obtain a smaller stature and the apparent relative incidence of the disorder in the 2 breeds, it is likely that this mutation crossed into the Rat Terrier breed from Toy Fox Terriers fairly recently.

Animals↗

Impaired dimensional selection but intact use of reward feedback during visual discrimination learning in Parkinson's disease.

It has been suggested that Parkinson's disease (PD) impairs the ability to learn on the basis of reward or reinforcing feedback i.e., by trial-and-error. In many learning tasks, particular 'dimensions' of stimulus information are relevant whilst others are irrelevant; therefore, efficient performance depends on identifying the dimensions of these 'compound' stimuli and selecting the relevant dimension for further processing. We investigated the ability of patients with PD, as well as patients with Huntington's disease and patients with frontal or temporal lobe lesions, to learn visual discriminations which required either a number of associations to be learned concurrently (the 'eight-pair' task) or the selection of information from compound stimuli (the 'five-dimension' task), both tasks being learned by trial-and-error. None of the basal ganglia disorder patient groups was impaired on the eight-pair task, militating against a crucial role for these brain structures in trial-and-error learning per se. Patients with mild, medicated PD, but not unmedicated PD patients, were impaired at identifying all five feature dimensions in the five-dimension task, implying dopaminergic 'overdosing' of the ability to analyse compound stimuli in terms of their component dimensions. Temporal lobe lesion patients performed similarly, suggesting that the temporal lobe may be the site of the medication overdose effect. Patients with severe, medicated PD were impaired at compound discrimination learning on the five-dimension task in the absence of an underlying impairment in identifying component stimulus dimensions; this pattern resembled that seen in Huntington's disease and frontal lobe lesion patients, implying that fronto-striatal circuitry is involved in the formation of rules based upon selected stimulus dimensions.

Adult↗

Oligodendroglial dysplasia in two bullmastiff dogs.

Leukodystrophies are inherited neurological disorders involving central nervous system white matter. They are uncommon in animals but a few, breed-specific entities have been described. In 2002, two young-adult, purebred Bullmastiff dogs from central New York State presented to their referring veterinarians displaying moderate to severe ataxia of all limbs, spastic tetraparesis that was worse in the pelvic limbs, and a diffuse, action-related, whole-body tremor. Clinical signs were insidious in onset and slowly progressive. Anatomic diagnoses considered were a C1-C5 lesion or, based on the whole-body tremor, a diffuse central nervous system disorder. No gross lesions were apparent in the brain or spinal cord. Histopathologically, numerous, multifocal, sharply demarcated, small, ovoid to angular areas of myelin pallor (plaques) were present throughout the major white matter tracts of the brainstem and spinal cord. These plaques, which often were traversed by axons, did not stain with luxol fast blue for myelin and were associated with minimal astrocytosis. Ultrastructural findings include occasional hypertrophic glia in white matter, rare unmyelinated segments of axons, and focal proliferation of tubule-containing cytoplasmic glial cell processes (oligodendroglial). The described clinical and morphological findings and age of onset are similar to the well-characterized, presumably hereditary, bovine syndrome known as Charolais ataxia or oligodendroglial dysplasia. This article presents the first description of a leukodystrophy in the Bullmastiff breed and the first report of oligodendroglial dysplasia in animals other than Charolais cattle.

Animals↗

Neurohistologic and ultrastructural lesions in cattle experimentally intoxicated with the plant Prosopis juliflora.

Intoxication by pods of Prosopis juliflora (mesquite beans) causes an impairment of cranial nerve function in cattle and goats. In goats, vacuolation of neurons in the trigeminal motor nuclei has been reported. To study the lesions in cattle caused by consumption of P. juliflora pods and dry ground pods, eight 6- to 12-month-old male cattle were divided into 4 groups: group 1 was fed a ration containing 50% of pods; groups 2 and 3 received a ration containing 50 and 75% of dry ground pods, respectively; group 4 was the control. After 200 days, all cattle were killed and sampled for histologic evaluation. Samples of the trigeminal motor nucleus were examined by electron microscopy. All cattle from groups 1, 2, and 3 showed clinical signs resulting from impaired function of cranial nerves V, IX, X, and XII, starting 45-75 days after consumption of the plant. The main histologic lesions were vacuolation and loss of neurons in trigeminal motor nuclei and other motor cranial nerve nuclei with Wallerian-like degeneration in the cranial nerves. Mild denervation atrophy was observed in the masseter and other masticatory muscles. On electron microscopy, neurons of the trigeminal nuclei had markedly swollen mitochondria, with the mitochondrial cristae displaced peripherally, disoriented and disintegrating. Intoxication by P. juliflora seems to have a novel pathogenesis, characterized by a selective, primary, chronic, and progressive injury to mitochondria of neurons of the trigeminal and other cranial nerve nuclei. Cranial nerve degeneration and denervation atrophy of the muscles occurs as a consequence of the neuronal lesion.

Animals↗

Histopathological studies of experimental lyme disease in the dog.

Experimental borrelia infection was induced in 62 specific--pathogen-free beagle dogs by exposure to Ixodes scapularis ticks harbouring the spirochaete Borrelia burgdorferi. Clinical signs of Lyme disease occurred in 39/62 dogs, the remaining 23 being subclinically infected. Clinical signs consisted of one to six episodes of transitory lameness with joint swelling and pain, most commonly affecting the elbow or shoulder joints. The polymerase chain reaction and culture demonstrated that the dogs remained infected for up to 581 days. At necropsy, gross findings consisted of lymphadenopathy in the area of tick attachment. Microscopical changes consisted of effusive fibrinosuppurative inflammation or nonsuppurative inflammation, or both, affecting synovial membranes, joint capsules and associated tendon sheaths. Plasma cells dominated areas of chronic inflammation, with CD3(+) T cells being present in lesser numbers. Microscopical signs of arthritis were polyarticular and more widespread than indicated by clinical signs, and most of the subclinically affected animals also had synovitis. In areas of tick attachment to the skin, hyperkeratosis and a mixture of suppurative and nonsuppurative dermatitis were encountered. Lymphadenopathy in superficial lymph nodes resulted from follicular and parafollicular hyperplasia. In 14/62 dogs, lymphoplasmacytic periarteritis and perineuritis were noted, resembling lesions found in human Lyme disease and syphilis, in which an underlying microangiopathy has been proposed.

Animals↗

Renal (uremic) encephalopathy in a goat.

Renal encephalopathy was diagnosed in a 2-year-old male boar goat with a history of chronic weight loss and ataxia. Histopathological examination of the brain revealed a striking myelin vacuolation distributed mainly in two patterns: (i) along the junction of the neocortex and corona radiata, and (ii) in the bundles of the internal capsule as it dissects through the basal nuclei. The kidneys had diffuse severe tubular and glomerular necrosis and degeneration. The neural lesions are consistent with renal (uremic) encephalopathy. To the authors' knowledge, this is the first report of renal encephalopathy in a goat.

Animals↗

West Nile virus encephalitis in a dog.

In November 2002, a 2-year-old, spayed Maltese Terrier in central Mississippi was presented for an acute illness characterized by uncontrolled hyperactivity that rapidly progressed to generalized tremors, ataxia, and intermittent hyperthermia. Postmortem examination after a 2-week course revealed mild, multifocal, nonsuppurative meningo encephalitis, with focal necrosis in the medulla. Reverse transcriptase-nested-polymerase chain reaction for West Nile virus (WNV) was positive on brain and negative on other tissues. Immunohistochemistry was negative on all tissues. The clinical, postmortem, and laboratory findings are consistent with acute encephalitis due to WNV infection. WNV infection should be considered in dogs showing signs of encephalitis when and where WNV and mosquito vectors occur.

Animals↗

Feline systemic reactive angioendotheliomatosis: eight cases and literature review.

A rare, multisystemic intravascular proliferative disorder was identified postmortem in eight cats. The majority of these cats died or were euthanized following episodes of dyspnea, lethargy, and anorexia. Microscopic examination revealed occlusive, intraluminal proliferations of spindle cells within small vessels. The heart was consistently involved, and myocardial dysfunction was the probable cause of illness in all cats. Immunohistochemically, the majority of intravascular cells expressed von Willebrand factor, and a smaller number expressed smooth muscle actin, compatible with a dual population of endothelial cells and pericytes, suggesting a reactive rather than a neoplastic process. Four cases of a similar feline vascular disorder from the veterinary literature are reviewed. The histopathology resembles reactive angioendotheliomatosis in humans, a benign cutaneous intravascular endothelial and pericytic proliferative condition. However, in contrast, this feline disease is multisystemic and fatal. We propose the name "feline systemic reactive angioendotheliomatosis" for this unique, idiopathic disorder of domestic cats.

Animals↗

Glioblastoma multiforme in three baboons (Papio spp).

Glioblastoma multiforme is the most malignant astrocytic neoplasm and the most common brain neoplasm of humans. Spontaneous neoplasms of the brain are rare in nonhuman primates. This report describes three glioblastomas in adult captive-reared baboons. The animals exhibited a range of clinical signs, including depression, weight loss, weakness, and blindness. All three neoplasms were located in the cerebrum, with extension into the pons in one case. Histologically, the tumors were similar and were characterized by cellular pleomorphism, multinucleated cells, areas of necrosis, microvascular proliferation (glomeruloid bodies), and palisading of neoplastic cells around blood vessels and areas of necrosis. Two baboons exhibited gemistocytic differentiation, and in one baboon, the neoplastic cells were predominantly spindle shaped with a fascicular growth pattern. Immunohistochemical staining for glial fibrillary acidic protein, vimentin, and S-100 protein was positive, whereas immunostaining for synaptophysin and chromogranin A was negative. Positive staining for the cell proliferation marker Ki67 ranged from 8.2% to 13.9%. Terminal deoxynucleotidyl transferase mediated dVTPnick end labeling (TUNEL) staining ranged from 1.8% to 5.7%. These baboon glioblastomas share many features with those of humans.

Animals↗

Mixed germ cell tumour of the spinal cord in a young dog.

A spinal cord mixed germ cell tumour was identified in a two-year-old, female Airedale terrier with a history of progressive paraplegia. At necropsy, a discrete pale pink spinal cord mass was identified at the L5 vertebra, which extensively invaded the associated spinal cord segments L6 and L7. Histologically, the tumour was located within the subarachnoid space and invaded the spinal cord. It was composed of three different types of cells: small round cells, forming clusters or islands, similar to germ cells identified in testicular germinomas; large cells with eosinophilic or amphophilic cytoplasm, forming trabeculae; and a third, rarer type of well differentiated epithelial cells, forming acinar or tubular structures. Immunohistochemical examination revealed reactivity to antibodies against alpha-fetoprotein and broad spectrum cytokeratins. The composition, cytological features and immunohistochemical staining of this neoplasm are similar to germ cell tumours previously reported in the suprasellar region and in the eye of dogs.

Animals↗

Vasculitis in a dog resembling isolated angiitis of the central nervous system in humans.

An 1-year-old dog succumbed to a seizure disorder of 18 days duration. At necropsy, an area of hemorrhage and discolored parenchyma was identified in the left pyriform lobe of the brain. Microscopic examination revealed a localized, necrotizing vasculitis with associated cerebral necrosis. Vasculitis was not present in other organs. This presentation is consistent with isolated central nervous system (CNS) angiitis, a rare form of vasculitis in humans.

Animals↗

Symmetric focal degeneration in the cerebellar and vestibular nuclei in swine caused by ingestion of Aeschynomene indica seeds.

A vestibulocerebellar disorder was observed in 2- to 4-month-old swine after consumption of broken rice contaminated with 13% Aeschynomene indica seeds. Affected animals recovered in 2-14 days after removal of the contaminated food. To reproduce the syndrome, 10 pigs were fed 13% A. indica seeds in commercial pig ration or rice. They showed clinical signs similar to those observed in the spontaneous cases, 1 hour to 6 days after ingestion. Three pigs recovered after the withdrawal of the contaminated food. The others were killed. Two pigs that were fed for 25 days with food containing 3% and 6% seeds and two control pigs did not show clinical signs. Histologic lesions were characterized by symmetric focal degeneration in the cerebellar and vestibular nuclei. The initial lesion, observed 24 hours after the first ingestion, was characterized by vacuolation of the neuropil. Subsequently, there was progressive loss of parenchyma, vascular reaction, a few small spheroids, astrocytosis, and accumulation of gitter cells. The brains from four pigs were perfused with a buffered solution of glutaraldehyde-paraformaldehyde 12-48 hours after they started to ingest the seeds. No ultrastructural lesions were observed in the cerebellar nuclei after 12 hours of seed consumption. At 24 hours, endothelial cells and pericytes were separated by empty spaces from astrocyte foot processes, suggesting perivascular edema. The astrocytes were enlarged, consistent with intracellular fluid accumulation. These results suggest that A. indica seeds are toxic, causing functional derangement of the vestibulocerebellar system, followed by alterations in the microvasculature in the cerebellar and vestibular nuclei.

Animals↗

Postanaesthetic cerebral necrosis in five horses.

After being anaesthetised for between one hour 40 minutes and seven hours, five adult horses developed acute neurological signs and extensive cerebrocortical necrosis. Four of them had had abdominal surgery for colic and one had had repeated orthopaedic interventions. Between five hours and seven days after the surgery, all five horses suddenly developed severe signs of a predominantly prosencephalic disturbance: bilateral blindness with normal pupillary light responses, abnormal behaviour varying from propulsive pacing to head pressing profound lethargy and generalised seizures. They were euthanased between 24 hours and three weeks after the onset of these signs. In three of the cases a gross examination of the brain revealed patchy malacia of the cerebral grey matter and some discolouration of the adjacent white matter. Microscopical examination revealed lesions that varied from laminar neuronal necrosis in the grey matter of the cerebral cortex to more diffuse necrosis of the cortex and underlying white matter. Four of the five cases had had a period of hypercapnea while anaesthetised, and two of them (and possibly a third) had also had hypoxaemia.

Anesthesia↗

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.

Animals↗

Necrotising encephalitis in the Yorkshire terrier: a case report and literature review.

A four-year-old, spayed female Yorkshire terrier was presented with a two-month history of lameness in the left forelimb, circling and falling. A magnetic resonance imaging (MRI) examination 11 days after presentation revealed dilation of the right lateral ventricle. Following euthanasia, which was performed about 10 months after the onset of clinical signs, there was gross evidence of degeneration and cavitation of the cerebrum and dilation of the lateral ventricle on the right side. Microscopically, cavitation and necrosis were observed in the white and grey matter of the right cerebrum and there was abundant gemistocytic and fibrillary astrocytosis. Haemorrhage and marked perivascular cuffing with mononuclear cells were found in the mesencephalon. Inflammatory lesions consisting of lymphocytic infiltration and glial proliferation were also present in the dorsal funiculus of the cervical spinal cord. This case was diagnosed as necrotising encephalitis in the Yorkshire terrier (NEYT) with involvement of the spinal cord. NEYT is a chronic progressive neurological disorder, resulting from widespread, destructive non-suppurative inflammation of the central nervous system of unknown cause. In the past decade, 12 cases have been documented in adult to aged Yorkshire terriers. Computed tomography and MRI can detect the characteristic multifocal cavitations and ventriculomegaly, facilitating premortem diagnosis.

Animals↗

Mitochondriopathy with regional encephalic mineralization in a Jack Russell Terrier.

A 10-month-old female Parson Jack Russell Terrier was euthanatized because of therapy-resistant ataxia, hypermetria, and deafness that had first been observed at 10 weeks of age. Severe, bilateral, symmetrical neuronal degeneration and mineralization of the brain were found in the cochlear and cerebellar nuclei, dorsal areas of the medulla oblongata, the vestibulocochlear nerve, plexus choroideus, and within the granule cell layer of the ventral cerebellar hemispheres. The mineralized deposits were located free in the parenchyma, around intact or degenerate neurons, in myocytes of small- and medium-sized arteries, and around capillaries. Hepatocytes and cardiac myocytes showed oncocytotic change with increased numbers of enlarged or misshapen mitochondria filled with densely packed cristae and electron-dense inclusions. Skeletal myocytes had only minor increases in the number of mitochondria. The microscopic and ultrastructural lesions were consistent with mitochondrial encephalopathy with similarities to mitochondrial encephalomyopathy with lactic acidosis and strokelike episodes in humans.

Animals↗

Protection against tick-transmitted Lyme disease in dogs vaccinated with a multiantigenic vaccine.

In an effort to develop a safe and effective vaccine for the prevention of Lyme borreliosis that addresses concerns raised over currently available vaccines, dogs were vaccinated twice with a multiantigenic preparation of Borrelia burgdorferi, strain N40, on days 0 and 20 of the experiment. About 70 and 154 days after the first immunization, dogs were challenged by exposing them to field-collected Ixodes scapularis ticks harboring B. burgdorferi. Vaccinated dogs were completely protected from infection by all criteria utilized to assess infection, developed high-titer anti-B. burgdorferi serum antibodies and growth inhibitory activity which persisted for over 200 days, and did not demonstrate any untoward consequence of vaccination. Serum absorption experiments revealed that borreliacidal and most likely protective antibodies in dogs receiving the multiantigenic preparation were not only elicited against the OspA antigen, but were also produced against additional yet to be determined targets on B. burgdorferi organisms. These data demonstrate that a multiantigenic vaccine is effective in preventing Lyme disease transmitted via the natural vector.

Animals↗