Biomedical subjects

B A Summers

Publications and source records attributed to B A Summers.

At least 91 records · Page 5Linked to original sources

PubMed1992

A survey of epithelial odontogenic tumors and cysts in dogs and cats.

A retrospective histologic study of 12 canine and eight feline epithelial odontogenic tumors and cysts was conducted from oral masses (n = 3,917) obtained between 1980 and 1990. No sex or breed predilection was identified. Ameloblastoma was observed in two dogs (case Nos. 1, 2) 6 and 8 months of age. Calcifying epithelial odontogenic tumors were seen in a dog (case No. 3) and in two cats (case Nos. 4, 5) between 8 and 16 years of age. Ameloblastic fibroma (or fibroameloblastoma) was observed in cats (case Nos. 6-10) only. Inductive fibroameloblastoma was observed in four cats (case Nos. 6-9) up to 1 year of age, whereas ameloblastic fibroma was seen in a 14-year-old cat (case No. 10). A single ameloblastic odontoma was identified in a 20-month-old dog (case No. 11). Two complex odontomas occurred in a 6-month-old (case No. 12) and a 4-year-old (case No. 13) dog. Odontogenic cysts were identified in five dogs (case Nos. 14-18) aged 4.5 months to 16 years and in a 1-year-old cat (case No. 19) and have not been previously reported in these species. These cysts were lined by a stratified epithelium reminiscent of the appearance of ameloblastic epithelium. An odontogenic keratocyst with prominent central parakeratotic keratinization was identified in one 9-year-old female dog (case No. 20). Almost all epithelial odontogenic tumors were circumscribed, benign tumors that warranted a good prognosis for survival, although local recurrence may have followed (or may follow) incomplete excision. Calcifying epithelial odontogenic tumors may be locally invasive. Of six odontogenic cysts (case Nos. 14-19), two (case Nos. 15, 18) gave rise to basi-squamous carcinomas. The classification and behavior of epithelial odontogenic tumors and cysts in human beings, dogs, and cats are discussed.

Animals↗

PubMed1992

Dog lymphocyte cultures facilitate the isolation and growth of virulent canine distemper virus.

Optimal conditions for the isolation and growth of virulent canine distemper virus (CDV) in canine thymic and peripheral blood lymphocyte cultures were determined. Peak virus titers were seen from 3 to 6 days postinoculation of lymphocytes and depended on the multiplicity of infection. Dog lymphocytes were at least as susceptible as canine macrophages to infection with virulent CDV. Virus replication in lymphocytes resulted in higher virus titers than in dog lung macrophages. Peripheral blood lymphocytes (PBL) from CDV-immune dogs were as susceptible to CDV as were PBL from susceptible dogs.

Animals↗

PubMed1991

Virulent and attenuated canine distemper virus infects multiple dog brain cell types in vitro.

Canine Distemper Virus (CDV) produces an encephalitis in dogs that varies with viral strain. We have studied the cell tropisms of two virulent strains (CDV-SH and CDV A75-17) and an attenuated strain, Rockborn (CDV-RO), in cultured canine brain cells. Infected cell types were identified by double immunofluorescent labeling of specific cell markers and viral antigens. All viral strains studied produced infection in astrocytes, fibroblasts, and macrophages. Neurons were not infected by CDV A75-17 but were rapidly infected by CDV-SH and CDV-RO. Multipolar oligodendrocytes were very rarely infected by any of the virus strains. In contrast, a morphologically distinct subset of bipolar oligodendrocytes were commonly infected by CDV-SH and CDV-RO. The kinetics of infection in the astrocytes, oligodendrocytes, neurons, and macrophages varied between strains. Both CDV-SH and CDV-RO rapidly infected bipolar oligodendrocytes, astrocytes, neurons, and macrophages by 14 days post infection while infection by CDV A75-17 was delayed until after 28-35 days post infection. The differences in the growth kinetics and cell tropisms for some brain cells, exhibited by the three viral strains examined in this in vitro study, may relate to the different CNS symptoms that these strains produce in vivo.

Animals↗

PubMed1991

Canine distemper virus infection and encephalitis in javelinas (collared peccaries).

Canine distemper virus has been isolated in dog lymphocyte cultures from the brains of three javelinas that became moribund with signs of encephalitis. Canine distemper viral antigen was demonstrated predominantly in neurons and morbillivirus-like structures were seen by electron microscopy in brains of diseased animals. Serological studies suggest that CDV infection may be common in javelinas.

Animals↗

PubMed1991

Correlation between humoral immune responses and presence of virus in the CNS in dogs experimentally infected with canine distemper virus.

The role of the humoral immune response in clearance or prevention of canine distemper viral encephalitis of dogs infected with a virulent strain of canine distemper virus has been evaluated. Dogs that have demyelinating lesions, CDV proteins and infectious virus in their brains demonstrate an impaired humoral immune response. In dogs that recover from infection and contain no demyelinating lesions, viral proteins or infectious virus in the brain, antibodies to the internal proteins of CDV are observed early after infection. Later antibodies to primarily the H protein are detectable in sera of these dogs and the appearance of antibodies against the surface glycoprotein (H) correlates with the absence of lesions, CDV antigen and infectious virus in the brains of these dogs. Very late after infection immunoprecipitating antibody to all CDV antigens diminished rapidly so that at about ten weeks post infection antibodies that precipitate CDV antigens are barely detectable.

Animals↗

PubMed1991

Viral expression in experimental canine distemper demyelinating encephalitis.

We have characterized the relationship between the expression of canine distemper virus (CDV) and demyelinating lesions in the white matter of the cerebellum of experimentally infected dogs. In animals which had demyelinating lesions, CDV proteins (N, P, F and H) were expressed and infectious virus could be recovered from brain tissue. Viral proteins (N, P, F and H) were detected by monoclonal antibodies and immunocytochemistry within demyelinating lesions as well as in scattered glial cells in areas of the white matter which lacked detectable lesions. Many cell types, including astrocytes, neurons, ependymal cells, choroid plexus cells, meningeal cells and perivascular inflammatory cells were labelled for viral antigen. We conclude from our results that the mechanism of demyelination in canine distemper virus-induced encephalitis involves expression of viral gene products at the lesion site.

Animals↗

PubMed1990

Growth of canine distemper virus in cultured astrocytes: relationship to in vivo persistence and disease.

Canine distemper virus (CDV) causes an encephalomyelitis in dogs which varies with the viral strain. The CDV Cornell A75-17 strain produces a delayed, subacute to chronic, demyelinating CNS disease. In contrast, the Snyder Hill (CDV-SH) strain-associated neurological disease is more acute in onset, is usually non-demyelinating and primarily produces lesions in the gray matter. In these studies we describe the effects of these two virulent and one avirulent CDV strain, Rockborn (CDV-RO), on astrocytes in dissociated canine brain cell cultures. In multiple replicate experiments, astrocytes were infected most rapidly by CDV-RO [100% of astrocytes were infected by 14 days post-inoculation (p.i.)]. This strain caused severe cytopathic effect (CPE) and cytolysis. CDV-SH similarly produced a rapid infection of the astrocytes. In contrast, CDV A75-17 infected less than 25% of the astrocyte population during the first 28 days p.i. (+/- 7 days); after 28 days p.i., a rapid rise in astrocyte infection occurred. Both virulent viruses caused astrocytic syncytial formation but did not cause cytolysis of the astrocyte population as was observed with the attenuated virus. Titers of infectious virus, released into the supernatant fluid, reflected the degree of astrocyte infection. Virus released by the cultures late in CDV A75-17 infection showed enhanced ability to infect newly derived astrocytes; in contrast, brain cell passaged CDV-SH did not show increased growth in these cells. These results show that (1) there is a difference in growth rate, CPE and capacity for adaptation of three different CDV strains in astrocytes in vitro, and (2) some aspects of the disease (such as persistence in white matter) produced by the virulent strains in vivo may be related to the course of astrocyte infection observed in vitro.

Animals↗

PubMed1990

Equine motor neuron disease; a preliminary report.

A spontaneous motor neuron disease or neuronopathy was identified in 10 horses from the northeastern United States. Signs of generalized weakness, muscle fasciculations, muscle atrophy and weight loss progressed over 1 to several months in young and old horses of various breeds. Pathologic studies revealed that degeneration and loss of motor neurons in the spinal cord and brain stem resulted in axonal degeneration in the ventral roots and peripheral and cranial nerves and denervation atrophy of skeletal muscle. Many spinal neurons were swollen, chromatolytic and contained neurofilamentous accumulations. Other cell bodies were shrunken and undergoing neuronophagia and some were lost and replaced by glia. This fatal equine motor neuron disease has not been reported previously and its cause has not been determined. The progressive weakness and wasting and the neuronal degenerative changes in these horses were similar to those described in people with sporadic amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease.

Animals↗

PubMed1989

Evidence of oligodendrocyte infection and degeneration in canine distemper encephalomyelitis.

Canine distemper encephalomyelitis is an important neurological disease of the dog and is also of comparative medical interest. With some viral strains, demyelinating encephalomyelitis is seen; whether or not oligodendrocyte infection occurs has remained controversial. By examining very early white matter lesions unequivocal oligodendrocyte infection has been identified. Accordingly the direct effect of virus on oligodendrocyte viability must be weighed in considering the pathogenesis of this canine CNS infection.

Animals↗

PubMed1989

Lymphocyte-myelin sheath interactions in acute experimental allergic encephalomyelitis.

Using a passively transferred acute model of experimental allergic encephalomyelitis (EAE) in the rat, inflammatory central nervous system (CNS) lesions were shown to develop rapidly, peak and then resolve. An unusual feature of the lesions in the CNS was the presence of pyknotic cells within myelin sheaths. A sequence of observations indicated that such cells were lymphocytes which had insinuated themselves into the myelin sheath by passage along the interperiod line. The presence of lymphocytes within myelin sheaths, a process which did not lead to demyelination, was considered to represent a change which reflects the specificity of the immune response in this disease. The detection of this change in other CNS autoimmune diseases, notably those associated with virus infections, may be important as an indicator of pathogenetically relevant lymphocyte-myelin interactions.

Acute Disease↗

PubMed1988

Suprasellar germ cell tumors in the dog: a report of five cases and review of the literature.

Suprasellar germ cell tumors were identified in five young adult to middle-aged dogs. Clinical signs included depression, mydriasis, ptosis and visual deficit. At necropsy large extramedullary masses were found on the ventral surface of the rostral brain stem. Histologically four were characterized by sheets and nests of moderately pleomorphic round cells resembling seminoma, admixed with larger vacuolated cells, glandular formations with secretory material, and occasional foci of squamous differentiation. The fifth case was more homogeneous, with germinomatous elements predominating. Immunohistochemical examination of three tumors revealed positive staining for alpha fetoprotein. Although only one case showed intracranial metastasis, these tumors were considered malignant due to the marked local invasion and destruction. The veterinary literature is reviewed, and we propose that two tumors previously reported as craniopharyngioma be reclassified as germ cell tumors. One other tumor previously reported as an unclassified suprasellar tumor was identified, which also demonstrated features of a germ cell tumor.

Animals↗

PubMed1988

A novel intradural extramedullary spinal cord tumor in young dogs.

We have studied an unusual, spontaneous, intradural extramedullary spinal cord tumor in 12 dogs. Animals presented with paraparesis and ataxia early in life (11/12 ranged from 6 to 38 months of age) suggesting that these tumors may be congenital. Various breeds of dogs were represented with four cases in German Shepherds and three in retrievers; there was no sex predisposition. Post-mortem examinations revealed a single intradural mass consistently located between T10 and L2, which produced extensive compression of the spinal cord. Metastasis was never observed and significant pathological changes in other organs were lacking. Microscopic examination revealed solid sheets of ovoid to fusiform cells interspersed with areas of acinar and tubular differentiation. Some areas were rarified and focal squamous metaplasia was observed. Ultrastructural features included the presence of a continuous basal lamina, junctional complexes, microvilli and occasional cilia at the apices of acinar complexes. Immunocytochemical studies did not support a neurectodermal origin. At least 13 case reports of this entity have been previously published and have been designated ependymomas, medulloepitheliomas and neuroepitheliomas. A recent case was diagnosed as a nephroblastoma and we feel that this is an interesting and provocative diagnosis. These tumors could result from remnants of renal primordium which becomes trapped between the dura and the developing spinal cord. However, firm evidence of such a histogenesis is not yet at hand.

Age Factors↗

PubMed1988

Factor VIII-related antigen in canine endothelial neoplasms: an immunohistochemical study.

Canine vascular tumors (47 hemangiomas, 36 hemangiosarcomas) were investigated for the endothelial cell marker factor VIII-related antigen (F VIII RAg). The primary antibody was a commercial rabbit anti-human (r/h) F VIII RAg antiserum. All (100%) hemangiomas and 32 (89%) of 36 hemangiosarcomas stained for F VIII RAg. One hemangiosarcoma (3%) was negative, and three tumors (8%) were equivocal in staining. Rarely, the interpretation of stained immature endothelial cells was difficult. The r/h F VIII RAg antibody was a positive marker of normal, reactive, and neoplastic endothelial cells in the dog.

Animals↗

PubMed1987

Juvenile-onset bulbospinal muscular atrophy with deafness: Vialetta-van Laere syndrome or Madras-type motor neuron disease?

A girl with rapid-onset, bulbospinal muscular atrophy and deafness is described. The patient's mother and brother showed EMG features consistent with subclinical involvement. T is bulbospinal form of spinal muscular atrophy associated with deafness described by Vialetto and van Laere closely resembles the Madras type of motor neuron disease, also associated with deafness, described by Jagganathan and colleagues.

Adolescent↗

PubMed1987

Meningocerebral hemangiomatosis resembling Sturge-Weber disease in a horse.

A 3-year-old horse presented with intermittent generalized seizures of 2-month duration. During interictal periods, the horse appeared normal and a cause for the seizures could not be identified. Necropsy revealed opacity of the leptomeninges, covering most of one cerebral hemisphere along with thinning and collapse of the cortex in the ipsilateral pyriform lobe. Histopathology demonstrated leptomeningeal vascular proliferation and meningothelial hyperplasia. Prominent tortuous vessels of the gyri and sulci extended into some regions of the subjacent cortex, where there was neuronal loss, ectopia, and disorganization. Clusters of prominent arterioles were found in the sclerotic choroid plexus of the lateral and fourth ventricles. Milder vascular lesions were present in the leptomeninges of the ventral brain stem, right cerebrum, spinal cord, and in the eye. The left trigeminal nerve was distorted by swollen fasicles containing onion bulb-like structures. Most bulbs contained central axons surrounded by myelin sheaths of variable thickness. Electron microscopy demonstrated concentrically arranged cells with continuous basal laminae and rare pinocytotic vesicles. S-100 immunohistochemistry showed strong positive staining in these cells. This is an unusual combination of lesions to which analogies can be drawn with the human neuroectodermal dysplasias, specifically Sturge-Weber disease. The relationship of the neuropathy to the leptomeningeal hemangiomatosis is unclear, but a compound anomaly in embryological development resulting in dysplasia and neoplasia may be involved.

Angiomatosis↗

PubMed1987

Demyelination in canine distemper encephalomyelitis: an ultrastructural analysis.

A morphological study of selected white matter lesions was carried out in three dogs with canine distemper encephalomyelitis. Two dogs had experimental infections while the third was a spontaneous case. Two stages were identified in the process of demyelination. The earliest evidence of myelin injury was a ballooning change in myelin sheaths involving single or multiple axons. This was followed by a progressive stripping of compact sheaths by the cytoplasmic fingers of phagocytic cells which infiltrated and removed myelin lamellae. Some axonal necrosis also accompanied these changes. Where demyelination occurred, canine distemper viral nucleocapsids were found in astrocytes, macrophages, ependymal cells and infiltrating lymphocytes. In contrast, oligodendrocytes were conspicuous by their apparent lack of infection. Thus it seems that myelin loss cannot be ascribed to oligodendrocyte infection. Perturbed astrocyte function following canine distemper viral infection may cause oedema of myelin sheaths, leading to ballooning and primary demyelination. Cells which phagocytosed myelin were mainly identified as microglial cells with lesser involvement by astrocytes. Rarely, oligodendrocytes also acted as macrophages. Myelin debris was engulfed in bulk or as small droplets into coated pits. Remyelination was present in established plaques although not in great abundance, perhaps due to the diminished oligodendrocyte numbers and a relative increase in immature forms of these cells. These observations are compared to similar changes observed in other demyelinating diseases of animals and man.

Animals↗

PubMed1987

Demyelinating canine distemper encephalomyelitis: measurement of myelin basic protein in cerebrospinal fluid.

Beagle dogs were experimentally infected with the Cornell A75-17 strain of canine distemper virus. At three time points post-infection (PI), immunoreactive myelin basic protein (MBP) was measured in cerebrospinal fluid (CSF). Levels were correlated with neuropathological findings, interferon in CSF and virus isolation from the brain. CSF from animals inoculated with Cornell A75-17 strain often showed detectable immunoreactive MBP late in the disease course. As anticipated from earlier morphological studies, CSF drawn around day 20 PI lacked MBP while subsequent samples were positive. Dogs with severe demyelination had elevated values of immunoreactive MBP while dogs with only mild inflammation had little or none. Release of MBP or MBP peptides into CSF of dogs with canine distemper may be a valuable laboratory test in studies of the natural history of this disease and in assessing the response to treatment. Whether an immune response to MBP plays an immunopathogenic role in the chronic, demyelinating phase of canine distemper encephalitis remains to be determined.

Animals↗

PubMed1987

Immunocytochemistry of normal pancreatic islets and spontaneous islet cell tumors in dogs.

Immunocytochemical studies of the distribution of glucagon, gastrin, insulin, and somatostatin in normal canine pancreatic islets and 20 canine islet cell tumors were done using the peroxidase-anti-peroxidase (PAP) technique. In the normal adult canine pancreas, islets typically consisted of clusters of 20-30 cells, but smaller foci and even individual cells were identified. Alpha cells (glucagon) were often peripherally located, beta cells (insulin) were centrally located and most numerous, and delta cells (somatostatin) were the least numerous and randomly located. Both juvenile and adult canine pancreases did not stain for gastrin. Of the 20 tumors examined, 18 had positive immunoreactivity for insulin, nine for glucagon, 14 for somatostatin, and one for gastrin. Two tumors were uninterpretable due to autolysis. Three tumors were pure insulinomas, but no pure somatostatinomas, glucagonomas, or gastrinomas were identified. Most tumors and metastases had mixed positive immunoreactivity; one neoplastic cell type predominated with lesser numbers of other cell types. Metastatic sites (liver and lymph node) stained for insulin and somatostatin, only. Foci of non-neoplastic islet cell tissue (nesidioblastosis), often located at the pancreatic-mesenteric junction, stained strongly positive for insulin, glucagon, and somatostatin but not for gastrin. The tumor staining pattern did not consistently correlate with tumor function, as determined by blood glucose and serum insulin assays. The PAP technique works well on paraffin-embedded, formalin-fixed tissue using rabbit or guinea pig antisera as the primary antibody. Staining occurred on sections of paraffin blocks stored for up to 7 years.

Adenoma, Islet Cell↗