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Biomedical subjects

B A Summers

Publications and source records attributed to B A Summers.

At least 55 records · Page 3Linked to original sources
PubMed1998

Progressive tetraparesis and laryngeal paralysis in a young rottweiler with neuronal vacuolation and axonal degeneration: an Australian case.

A 5-month-old female Rottweiler dog was diagnosed to have a neurodegenerative disease that has been recently reported in Rottweilers from North America and Europe. The dog was presented with progressive signs of ataxia, tetraparesis and inspiratory stridor. The clinical investigation included analysis of CSF, radiography, myelography and electrophysiological testing. No evidence of vertebral malformation or inflammatory CNS disease was identified. Bilateral laryngeal paralysis was identified in the lightly anaesthetised dog. Electromyography showed abnormal spontaneous activity from the intrinsic musculature of the larynx. At necropsy there were no gross abnormalities of the nervous system but there was atrophy of the dorsal cricoarytenoid muscles of the larynx. There were widespread histological abnormalities throughout the nervous system including neuronal vacuolation, spongiform changes in the neuropil and axonal degeneration which was most prominent in the spinal cord. These clinical and pathological findings are consistent with the diagnosis of a new neurodegenerative disease reported from North America and Europe. This diagnosis is of particular significance in Australia where transmissible spongiform encephalopathies have not been identified.

Animals↗
PubMed1998

Borrelia burgdorferi induces the production and release of proinflammatory cytokines in canine synovial explant cultures.

Canine synovial membrane explants were exposed to high- or low-passage Borrelia burgdorferi for 3, 6, 12, and 24 h. Spirochetes received no treatment, were UV light irradiated for 16 h, or were sonicated prior to addition to synovial explant cultures. In explant tissues, mRNA levels for the proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin-1alpha (IL-1alpha), IL-1beta, and IL-8 were surveyed semiquantitatively by reverse transcription-PCR. Culture supernatants were examined for numbers of total and motile (i.e., viable) spirochetes, TNF-like and IL-1-like activities, polymorphonuclear neutrophil (PMN) chemotaxis-inducing activities, and IL-8. During exposure to synovial explant tissues, the total number of spirochetes in the supernatants decreased gradually by approximately 30%, and the viability also declined. mRNAs for TNF-alpha, IL-1alpha, IL-1beta, and IL-8 were up-regulated in synovial explant tissues within 3 h after infection with untreated or UV light-irradiated B. burgdorferi, and mRNA levels corresponded to the results obtained with bioassays. During 24 h of coincubation, cultures challenged with untreated or UV light-irradiated spirochetes produced similar levels of TNF-like and IL-1-like activities. In contrast, explant tissues exposed to untreated B. burgdorferi generated significantly higher levels of chemotactic factors after 24 h of incubation than did explant tissues exposed to UV light-treated spirochetes. In identical samples, a specific signal for IL-8 was identified by Western blot analysis. High- and low-passage borreliae did not differ in their abilities to induce proinflammatory cytokines. No difference in cytokine induction between untreated and sonicated high-passage spirochetes was observed, suggesting that fractions of the organism can trigger the production and release of inflammatory mediators. The titration of spirochetes revealed a dose-independent cytokine response, where 10(3) to 10(7) B. burgdorferi organisms induced similar TNF-like activities but only 10(7) spirochetes induced measurable IL-1-like activities. The release of chemotactic factors was dose dependent and was initiated when tissues were infected with at least 10(5) organisms. We conclude that intact B. burgdorferi or fractions of the bacterium can induce the local up-regulation of TNF-alpha, IL-1alpha, and IL-1beta in the synovium but that the interaction of viable spirochetes with synovial cells leads to the release of IL-8, which probably is a prime initiator of PMN migration during acute Lyme arthritis.

Animals↗
PubMed1998

Axonal spheroids in the cochlear nucleus of normal beagle dogs.

In the course of drug evaluation studies, sporadic axonal spheroids were identified in the cochlear nucleus of 8-15-month-old Beagle dogs. These structures were identified by Bielschowski histochemical and anti-neurofilament immunohistochemical stains and by ultrastructural examination. No cellular reaction or significant neuropil alterations were associated with the presence of the spheroids. Their presence was unrelated to treatment and were considered to be an incidental background finding.

Animals↗
PubMed1998

Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy.

Over the past 10 years, 10 cats with primary central nervous system infection by larvae of Cuterebra flies have been documented at Cornell University. Clinical abnormalities noted in all cats were progressive and most commonly consisted of depression (6/10), blindness (6/10), and behavior changes (2/10). Affected cats presented most commonly in July (2/10) and August (7/10); one cat was presented in September. The diverse histopathologic changes are unique to this aberrant migration and consist of a combination of five characteristic features: 1) parasitic track lesion (7/10), 2) superficial laminar cerebrocortical necrosis (10/10), 3) cerebral infarction (8/10), 4) subependymal rarefaction and astrogliosis with or without ependymal cell loss (7/10), and 5) subpial astrogliosis (7/10). Changes 2-5 occurred throughout the parenchyma unassociated with the track lesion or the parasite in the affected tissue. The larvae have been recovered most commonly in the region of the olfactory bulbs and peduncles, optic nerves, and cribriform plate, suggesting entry from the nasal cavity. Many of the changes noted are suggestive of a toxic factor elaborated by the parasite and borne within the cerebrospinal fluid, as well as vascular compromise as a component in those cats with brain infarction. Because of the prevalence of infarction associated with this syndrome and the lack of reported cases of such lesions in regions of the world devoid of the fly, we propose that aberrant cuterebral larval migration in the brain is the cause of feline ischemic encephalopathy.

Animals↗
PubMed1997

Intrinsic, management, and nutritional factors associated with equine motor neuron disease.

OBJECTIVE: To identify intrinsic, management, nutritional, and environmental risk factors associated with equine motor neuron disease (EMND) and to determine whether epidemiologic evidence supports oxidative stress as a risk factor for developing EMND. DESIGN: Case-control study. ANIMALS: 87 horses with EMND and 259 control horses. PROCEDURE: Information concerning each horse's history of exposure to multiple environmental factors prior to developing EMND was obtained by means of a questionnaire or personal interview. Exposure histories of horses with EMND and control horses were compared, and the association of each risk factor with EMND was evaluated, using logistic regression analysis. RESULTS: Factors significantly associated with risk of developing EMND included age, breed of horse, duration of residence at the farm, not vaccinating against rabies, and certain feeding practices. Horses that were exercised on green pasture or in grass paddocks were less likely to develop EMND, compared with horses that were exercised in dirt pad-docks. Feeding complete pelleted feed as the only source of concentrate or combined with sweet feed was associated with a significant increase in the risk of EMND. Supplementary feeding of vitamin and mineral mixtures not formulated to provide vitamin E or selenium was associated with increased risk of EMND. Horses with a history of cribbing or coprophagia were also at higher risk of developing EMND. CLINICAL IMPLICATIONS: Several husbandry practices and intrinsic characteristics of horses appear to modify the risk of EMND. The relationship of specific nutritional factors to EMND supports the hypothesis that a deficiency of vitamin E contributes to the disease.

Aging↗
PubMed1997

Hereditary polioencephalomyelopathy of the Australian cattle dog.

A vacuolar degeneration affecting primarily the gray matter in the central nervous system (CNS) of young Australian Cattle Dogs is described. An initial presentation of seizures was followed by a progressive spastic tetraparesis. Grossly evident bilateral and symmetrical foci of malacia were in the nuclei of the cerebellum and brain stem and the gray matter of the spinal cord. Microscopically, vacuolation of glial cells, dilation of the myelin sheaths and reactive astrocytosis characterized mild CNS changes. More advanced lesions displayed progressive dissolution of the neuropil, prominent vacuolation of reactive astrocytes, numerous glial fibrillary acidic protein-positive coiled astrocytic processes, neuronal vacuolation and loss with relative sparing of large neurons. Ultrastructurally marked mitochondrial accumulation and swelling were seen in astrocytes. In the appendicular muscles, changes interpreted as long-term denervation atrophy accompanied by widespread expression of the neonatal isoform of myosin were observed. The character of the neurological sings, the nature and the distribution of the lesions within the neuroaxis have not been reported in domestic animals. An inherited biochemical defect, possibly mitochondrial, is proposed as the cause. Selected conditions with a bilateral and symmetrical distribution affecting the gray matter of domestic animals are summarized.

Animals↗
PubMed1997

A canine encephalomyelopathy with morphological abnormalities in mitochondria.

A progressive encephalomyelopathy of insidious onset affecting a 16-month-old dog is described. Clinically, the dog was ataxic, stumbled into objects and showed mild behavioral abnormalities. Light microscopic findings included profound degeneration and astrogliosis of the optic pathways, loss of Purkinje neurons, focal bilateral and symmetrical brain stem spongiosis and diffuse neuroaxial astrogliosis with swollen and abnormally shaped nuclei. Ultrastructurally, there were giant and bizarre mitochondria within neuronal perikarya and axons as well as diffuse loosening of the cerebral and cerebellar neuropil. These neuropathological findings resemble the mitochondrial encephalomyopathies of man.

Animals↗
PubMed1997

Heterotopic neural tissue in the pharynx of a 7-week-old kitten.

A 7-week-old male kitten had a pharyngeal mass (1 x 2 cm) causing displacement of the tongue. The surgically resected tissue was seen to be a moderately discrete subepithelial mass comprising islands of neuroglia and neurons separated by dense collagenous connective tissue. It is not known whether this mass retained any connection with the brain. Histochemical and immunohistochemical examination confirmed the presence of neurons and a pleocellular glial population, supporting a diagnosis of heterotopic neural tissue. The cat remained well 20 months after surgical treatment. Heterotopic neural tissue is well-recognized in man but has not been described in animals.

Animals↗
PubMed1997

Spatial and non-spatial working memory at different stages of Parkinson's disease.

Groups of patients with Parkinson's disease, either medicated or unmedicated, were compared with a matched group of normal control subjects on a computerized battery of tests designed to assess spatial, verbal and visual working memory. In the spatial working memory task, subjects were required to search systematically through a number of boxes to find 'tokens' whilst avoiding those boxes in which tokens had previously been found. In the visual and verbal conditions, the subjects were required to search in exactly the same manner, but through a number of abstract designs or surnames, respectively, avoiding designs or names in which a token had previously been found. Medicated Parkinson's disease patients with severe clinical symptoms were impaired on all three tests of working memory. In contrast, medicated patients with mild clinical symptoms were impaired on the test of spatial working memory, but not on the verbal or visual working memory tasks. Non-medicated patients with mild clinical symptoms were unimpaired on all three tasks. These data are compared with the results of a previous study comparing groups of neurosurgical patients with frontal, temporal or amygdalo-hippocampectomy excisions on the same three tests of working memory. Taken together, the findings suggest that working memory deficits in Parkinson's disease emerge, and subsequently progress, according to a defined sequence, the evolution of which may be linked to the likely spatiotemporal progression of dopamine depletion within the striatum, in relation to the terminal distribution of its cortical afferents.

Antiparkinson Agents↗
PubMed1997

Association between plasma vitamin E concentration and the risk of equine motor neuron disease.

Equine motor neuron disease (EMND) is a neurodegenerative disorder of the somatic lower motor neurons that results in a syndrome of diffuse neuromuscular disease in the adult horse. The aetiology of this disorder is unknown, although prior studies have suggested that a deficiency in the lipid antioxidant vitamin E (alpha-tocopherol) contributes to the development of EMND. This paper describes a case-control study designed to investigate the association between plasma vitamin E levels and the risk of EMND for horses. Signalment, plasma vitamin E levels at the time of referral, and information relative to dietary and management practices were collected from 53 horses diagnosed with EMND and 69 controls. The mean plasma vitamin E concentration in EMND cases was significantly lower than that of control horses. After controlling for other risk factors of EMND, there was a statistically significant association between plasma vitamin E levels and EMND, with the likelihood of the disease increasing as the vitamin E concentration decreased. These findings support the reported role of vitamin E deficiency as one of the risk factors for EMND.

Animals↗
PubMed1997

Borrelia burgdorferi migrates into joint capsules and causes an up-regulation of interleukin-8 in synovial membranes of dogs experimentally infected with ticks.

Twenty 6-week-old specific-pathogen-free beagles were infected with Borrelia burgdorferi by tick challenge, and five uninfected dogs served as controls. During the study, all dogs were monitored for infection, clinical signs, and antibody response against B. burgdorferi. During episodes of lameness or postmortem, synovial fluids from each dog were examined for volume, cell number, polymorphonuclear leukocyte (PMN) content, cell viability, and chemotactic activity. Twenty-five tissues collected postmortem from each dog were tested for interleukin-8 (IL-8) mRNA, tumor necrosis factor alpha (TNF-alpha) mRNA, presence of live spirochetes, and histopathological changes. Thirteen infected dogs (group A), which seroconverted rapidly (maximum titers within 50 to 90 days), developed acute and severe mono- or oligoarthritis almost exclusively in the limb closest to the tick bite (median incubation period, 66 days). Synovial fluids of the arthritic joints collected during episodes of lameness had significantly elevated volume, cell count, PMN proportion, cell viability, and chemotactic activity for PMNs. The remaining joints of the same animals contained synovial fluids with elevated chemotactic activity and cell viability. Twelve dogs tested positive for IL-8 mRNA in multiple tissues (synovia, pericardium, and peritoneum), and 10 dogs expressed TNF-alpha mRNA, but only in the tributary lymph nodes of the inflamed joints. Histological examinations revealed severe poly- or oligoarthritis and moderate to severe cortical hyperplasia in draining lymph nodes of the inflamed joints in all 13 dogs. Seven infected dogs with mild or no clinical signs (group B) seroconverted slowly (peak titers after 90 days), and only some joint fluids showed chemotactic activity, which on average was lower than that in inflamed and noninflamed joints from dogs in group A. Four dogs expressed IL-8 mRNA (in the synovia and pericardium), and three dogs had TNF-alpha mRNA in tributary lymph nodes. Histologically, nonsuppurative arthritis was found in multiple joints, and mild to moderate cortical hyperplasia was found in draining lymph nodes. Five uninfected dogs without lameness (group C) had normal synovial fluids and tissues. In all infected dogs, live spirochetes were demonstrated more frequently in tissues of the somatic quadrant closest to the tick bite than in tissues further from the site of infection, suggesting that dissemination of B. burgdorferi occurs more by migration than by blood-borne spread. From these studies employing a canine model of B. burgdorferi infection, we conclude that IL-8 is involved in the pathogenesis of acute Lyme arthritis.

Animals↗
PubMed1997

Persistence of Borrelia burgdorferi in experimentally infected dogs after antibiotic treatment.

In specific-pathogen-free dogs experimentally infected with Borrelia burgdorferi by tick exposure, treatment with high doses of amoxicillin or doxycycline for 30 days diminished but failed to eliminate persistent infection. Although joint disease was prevented or cured in five of five amoxicillin- and five of six doxycycline-treated dogs, skin punch biopsies and multiple tissues from necropsy samples remained PCR positive and B. burgdorferi was isolated from one amoxicillin- and two doxycycline-treated dogs following antibiotic treatment. In contrast, B. burgdorferi was isolated from six of six untreated infected control dogs and joint lesions were found in four of these six dogs. Serum antibody levels to B. burgdorferi in all dogs declined after antibiotic treatment. Negative antibody levels were reached in four of six doxycycline- and four of six amoxicillin-treated dogs. However, in dogs that were kept in isolation for 6 months after antibiotic treatment was discontinued, antibody levels began to rise again, presumably in response to proliferation of the surviving pool of spirochetes. Antibody levels in untreated infected control dogs remained high.

Animals↗
PubMed1997

Arachidonic acid enhances contraction and intracellular Ca2+ transients in individual rat ventricular myocytes.

Modulation of intracellular free Ca2+ concentration ([Ca2+]i) by inotropic stimuli alters contractility in cardiac muscle. Arachidonic acid (AA), a precursor for eicosanoid formation, is released in response to receptor activation and myocardial ischemia and has been demonstrated to alter K+ and Ca2+ channel activity. We investigated the effects of AA on contractility by simultaneously measuring [Ca2+]i and shortening in single field-stimulated rat ventricular myocytes. [Ca2+]i transients were measured using fura 2, and myocyte shortening was assessed using video edge detection. AA stimulated a doubling in the amplitude of the [Ca2+]i transient and a twofold increase in myocyte shortening. In addition, AA stimulated a 30% increase in the time to 50% diastolic [Ca2+]i and a 35% increase in the time to 50% relengthening. These effects of AA were mediated by AA itself (56 +/- 5%) and by cyclooxygenase metabolites. Pretreatment with the protein kinase C inhibitors staurosporine and chelerythrine nearly abolished (> 90% inhibition) these AA-induced effects. Inhibition of voltagegated K+ channels with 4-aminopyridine mimicked the effects of AA. Addition of AA to the 4-aminopyridine-treated myocyte had no additional effect on parameters of contractile function. These data indicate that AA alters the amplitude and duration of Ca2- transients and myocyte shortening via protein kinase C-dependent inhibition of voltage-gated K+ channels. Release of AA by phospholipases in response to receptor activation by endogenous mediators or pathological stimuli may be involved in mediating inotropic responses in cardiac muscle.

4-Aminopyridine↗
PubMed1996

A canine distemper virus epidemic in Serengeti lions (Panthera leo).

Canine distemper virus (CDV) is thought to have caused several fatal epidemics in canids within the Serengeti-Mara ecosystem of East Africa, affecting silver-backed jackals (Canis mesomelas) and bat-eared foxes (Otocyon megalotis) in 1978 (ref. 1), and African wild dogs (Lycaon pictus) in 1991 (refs 2, 3). The large, closely monitored Serengeti lion population was not affected in these epidemics. However, an epidemic caused by a morbillivirus closely related to CDV emerged abruptly in the lion population of the Serengeti National Park, Tanzania, in early 1994, resulting in fatal neurological disease characterized by grand mal seizures and myoclonus; the lions that died had encephalitis and pneumonia. Here we report the identification of CDV from these lions, and the close phylogenetic relationship between CDV isolates from lions and domestic dogs. By August 1994, 85% of the Serengeti lion population had anti-CDV antibodies, and the epidemic spread north to lions in the Maasai Mara National reserve, Kenya, and uncounted hyaenas, bat-eared foxes, and leopards were also affected.

Amino Acid Sequence↗
PubMed1995

Endothelial lipopigment as an indicator of alpha-tocopherol deficiency in two equine neurodegenerative diseases.

Two spontaneous neurodegenerative diseases of the horse, equine motor neuron disease (EMND) and equine degenerative myeloencephalopathy (EDM), have been associated with alpha-tocopherol deficiency, and both were characterized by prominent accumulations of endothelial lipopigment in the small vessels of the spinal cord. These endothelial pigment deposits appear to be reversible. In EMND horses pasture-supplemented for 9 months or more after the progression of weakness and wasting had arrested, there was very little endothelial lipopigment. The origin and the potential effects of these endothelial lipopigment accumulations are discussed.

Animals↗
PubMed1995

Pathogenicity of morbilliviruses for terrestrial carnivores.

Many different species of the order Carnivora are susceptible to canine distemper and the mortality rate varies greatly between species. Ailuridae, Canidae, Hyaenidae, Mustelidae, Procyonidae, Ursidae, Viverridae and now Felidae have been reported to be susceptible to canine distemper virus infection. Although distemper outbreaks in dogs, fur farms and in zoo carnivores have been greatly reduced in recent years due to vaccination, there are still regular outbreaks in free-living carnivores. Unexpected outbreaks of canine distemper have occurred in exotic felids in a California wildlife park and in the Serengeti in Tanzania as well as in javelinas (collared peccaries, Tayassu tajacu) in Arizona. Although safe and efficacious in dogs, modified live canine distemper virus vaccines may be dangerous for a variety of zoo and wildlife carnivores, especially red pandas (Ailurus fulgens) and black footed ferrets (Mustela nigripes).

Animals↗