PubMed Health⌕ Search

Biomedical subjects

A de Lahunta

Publications and source records attributed to A de Lahunta.

At least 37 records · Page 2Linked to original sources
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↗
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

Incidence and risk factors of equine motor neuron disease: an ambidirectional study.

We have conducted an ambidirectional study to estimate the incidence of equine motor neuron disease (EMND) in the northeastern US. The clinical and pathological features of EMND are similar to those described in human motor neuron disease. We have also collected data on all EMND cases reported in the US and described the geographic distribution of the disease. To identify factors associated with the risk of EMND, the authors assembled 163 control horses from the population in which cases were identified. The significance of association between the hypothesized factors and the risk of EMND was evaluated using the logistic regression analysis and the risk was estimated using the odds ratio. Seventy-eight horses in North America were diagnosed with EMND between the period of January 1985 and November 1993. Most of the cases were identified in the Northeast of the US and the incidence of EMND appears to be increasing in this area. Factors found to be significantly associated with EMND were breed and the age of the horse. Quarter horses were the only breed with a significantly higher risk of EMND (odds ratio = 2.3). The risk of EMND increased with age, reached a peak around 16 years of age and then declined. The sex of the horse was not associated with the risk of the disease.

Age Distribution↗
PubMed1995

Trypanosoma cruzi infection in Walker hounds from Virginia.

Trypanosomiasis has been reported in dogs from Texas, Oklahoma, Louisiana, and South Carolina. We describe the first isolation and characterization of Trypanosoma cruzi from a Walker Hound pup in Virginia that also had postvaccinal distemper. The mother of the pup and 7 of its 8 siblings also were found to be infected with T cruzi, suggesting that the parasite had been transmitted transplacentally or through lactation. Parasitologic, serologic, histologic, and molecular methods were used to establish the diagnosis of T cruzi infection in these dogs. In a serologic survey of 12 dogs (including the sire of the pups) from the area in which the index case occurred, none were found to have antibodies to T cruzi. However, 2 of a further 52 dogs from different areas (to the index case), but in the same county, were seropositive to T cruzi. These findings indicate that canine trypanosomiasis is present in an area of the United States not previously known to be enzootic.

Animals↗
PubMed1994

Microglossia in three littermate puppies.

Three of five two-day-old Miniature Schnauzer puppies were diagnosed as having 'bird-tongue,' a microglossia that prevents normal nursing. With intensive nursing care, the puppies survived to seven weeks of age, then deteriorated and were euthanized. From clinical and pathological examinations, a multi-system defect is suspected, though no primary neuromuscular abnormality could be determined.

Abnormalities, Multiple↗
PubMed1993

Motor neuron degeneration in a horse.

A 9-year-old Quarter Horse mare was examined because of progressive weight loss, weakness, muscle atrophy and tremors, and behavioral change. Selenium and glutathione peroxidase assays, blood lead analysis, erythrocyte transketolase analysis, pseudorabies and Borrelia burgdorferi serology, electromyography, and CSF analysis were performed. Motor neuron degeneration was diagnosed by microscopic examination of neural tissues. The cause of the disease was not substantiated, but several possibilities were excluded via diagnostic testing. Diagnosis of motor neuron degeneration in horses may be made from an accurate history, thorough neurologic examination, and ancillary testing. In particular, antemortem diagnosis may be based on finding scattered angular atrophy of predominantly type-1 or of type-1 and -2 skeletal muscle fibers in frozen sections of muscle biopsy specimens.

Animals↗
PubMed1993

Eosinophilic cytoplasmic inclusions in sporadic equine motor neuron disease: an electron microscopic study.

Equine motor neuron disease (EMND) is a sporadic, progressive neurodegenerative disorder that has been identified recently in horses of different breeds in North America. The cause is unknown. Pathologic changes which occur in spinal and certain brain stem motor neurons include chromatolysis, swelling, neurofilamentous accumulation, and development of eosinophilic cytoplasmic inclusions. Punctate eosinophilic inclusions, the type usually encountered in degenerating neurons, resembled Bunina bodies at the light microscopic level, but differed in their ultrastructural composition. These and less common but larger juxtanuclear inclusions appeared to be aggregated vesicular residues of membranous organelle degradation. The third kind of eosinophilic inclusion was a marginated derivative of endoplasmic reticulum and consisted of large membrane-bound accumulations of finely granular material. It was concluded that, although the distribution and nature of the lesions in EMND appeared similar to those of human motor neuron disease, none of the equine eosinophilic inclusions duplicated the ultrastructure of Bunina bodies.

Animals↗
PubMed1993

Risk factors associated with equine motor neuron disease: a possible model for human MND.

Equine motor neuron disease (EMND), a newly described neurodegenerative disease, bears a striking resemblance to progressive muscular atrophy (PMA) in humans. We present a comparison of the equine and human diseases and the results of a case-control study conducted to identify intrinsic factors associated with EMND. Cases included all horses with a confirmed diagnosis of EMND diagnosed in the United States since 1985 (32 cases). Controls included horses diagnosed with either cervical stenotic myelopathy, equine degenerative myeloencephalopathy, or protozoan myelitis at the Veterinary Teaching Hospital at the College of Veterinary Medicine, Cornell University (153 controls). Logistic regression analysis identified factors associated with the risk of EMND. Risk factors considered were age, sex, and breed of the horse. Most cases of EMND (30 of 32) have been sporadic. There was a breed association with the risk of EMND. Quarter horses were at a high risk for developing EMND (odds ratio [OR] = 12.7; 95% confidence interval, 3.3 to 49.6); thoroughbred horses were at increased risk (OR = 2.9, 0.8 to 10.4). There was also an age association with the risk of EMND. The risk increased with age, peaked at 16 years, and then declined, a pattern similar to that for amyotrophic lateral sclerosis in humans. There was no sex association with the disease. Despite the breed association, equine lymphocyte antigen studies have not revealed a systematic pattern, suggesting that genetic factors influencing susceptibility to EMND may be outside the major histocompatibility complex.

Animals↗
PubMed1992

Cervical fibrotic stenosis in a young Rottweiler.

An 18-month-old neutered male Rottweiler was examined because of slowly progressive spastic tetraparesis and ataxia. Signalment and clinical signs were suggestive of 2 neuronal degenerative diseases presumed to be inherited in young Rottweilers: leukoencephalomyelopathy and neuroaxonal dystrophy. Myelography revealed an extradural compression at the articulation of the second and third cervical vertebrae. At surgery, focal hypertrophy of the yellow ligament was observed to compress the spinal cord ventrally at that site.

Animals↗
PubMed1992

Tibetan terrier model of canine ceroid lipofuscinosis.

Over a 10-year period, we have studied the Tibetan terrier's visual electrophysiology, light and electron microscopic (EM) retinal characteristics of a slowly evolving inherited ceroid lipofuscinosis (CL). The retinal degeneration with CL inclusions (rdi) in the inner nuclear layer (bipolar cells) and nerve fiber layer (ganglion cells) has been called "rdi" to differentiate the visual abnormality from typical early retinal degeneration (erd) reported also in the Tibetan terrier. The unique "rdi" electroretinogram (ERG) gives a predominant P III wave at age 7 weeks but becomes more characteristically depressed in all phases over several years. Nyctalopia is the only functional abnormality for the first 5 to 6 year of life. Signs are remarkably few considering the pathology. Microscopic studies of the retina show accumulations, increasing with age, of autofluorescent dense inclusion particles which stain intensely by Luxol fast blue, PAS, and acid-fast procedures. Ultrastructural studies of the retina show the dense particles to be lamellar membranes repeating every 2 to 4 nm, consistent with ceroid lipofuscin. The inner retinal layers were always the target layer to be affected first and most severely. The ganglion cells were most frequently involved. The photoreceptors eventually degenerated but relatively few particles were found in this layer. The cytosomes in the cerebral cortex and brainstem neurons resemble lipofuscin, containing granular, lamellar, and globular components. Different pigment bodies were present in the cerebellar Purkinje cells. Neuronal loss which was moderate in the cerebellum and mild in the cerebrum was accompanied by astrogliosis and a striking presence of macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗