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A de Lahunta

Publications and source records attributed to A de Lahunta.

At least 19 recordsLinked to original sources
PubMed2007

Verminous encephalitis in a horse produced by nematodes in the family protostrongylidae.

Parasitic granulomatous eosinophilic inflammation was observed in the central nervous system (CNS) of a 6-month-old Arabian colt from New York state. Inflammation was associated with eggs, larvae, and adult nematodes in the cerebellum. Nematodes had histological characteristics of the superfamily Metastrongyloidea. The presence of dorsal-spined larvae in the CNS was further indicative of infection with a nematode in the family Protostrongylidae. Infections were most compatible with Parelaphostrongylus tenuis but specific diagnosis was not possible. This is the first definitive report of a protostrongylid nematode infection in a horse.

Animals↗
PubMed2004

Intracranial fusariosis: a novel cause of fungal meningoencephalitis in a dog.

The Fusarium species are a group of saprophytic fungal organisms that are occasionally the cause of opportunistic infections in humans and animals. Central nervous system disease associated with a Fusarium species is most commonly described in horse, resulting in equine leukoencephalomalacia. This report describes a 2-year-old, spayed, female German Shepherd Dog with meningoencephalitis secondary to infection with Fusarium spp. Meningoencephalitis in dogs secondary to a species of Fusarium has not been previously reported. The diagnosis was made based on the histopathologic examination of brain tissues postmortem and special immunohistochemical stains specific for Fusarium solani. The clinical signs in this dog were indicative of multifocal brain disease and included seizures and a paradoxical vestibular syndrome. The clinical findings, diagnostic and histopathologic test results, and the comparative characterizations of other disseminated fungal diseases, especially aspergillosis, are described.

Animals↗
PubMed2004

Evaluation of decision criteria for detection of spinal cord compression based on cervical myelography in horses: 38 cases (1981-2001).

REASONS FOR PERFORMING STUDY: Different criteria have been described based on height reduction of the total myelographic contrast column and components of it as tests for compression of the spinal cord due to cervical stenotic myelopathy (CSM). Fifty percent height reduction of the dorsal myelographic column (DMC), <2 mm empiric height of the DMC and a 40% reduction of the ratio of stenosis calculated based on the height reduction of the entire dural diameter (DD) have been described as decision criteria for considering the test result positive. The reasons for selecting these decision criteria or their accuracies have rarely been reported. OBJECTIVES: To evaluate the accuracy of diagnostic criteria based on reduced height of the total myelographic column and components of it for diagnosing extradural spinal cord compression using different decision criteria, and make recommendations for consistent myelographic interpretation in horses suspected of having CSM. METHODS: Four measurements were obtained by 2 readers in a retrospective sample population of 38 horses in which both cervical myelography and histopathological examination of the cervical spinal cord were performed. The prevalence of CSM in the sample was 50%. At intervertebral sites, the minimum heights of the DD and DMC were measured. At intravertebral sites, the maximum heights of the entire DD and DMC were obtained. Percent height reductions of the DMC and DD were determined as the ratio of minimum intervertebral height to maximum intravertebral height within the next cranial vertebra. Histological examination was used as the gold standard for determining the actual site of spinal cord compression. Sensitivity and specificity for the diagnostic criteria were estimated at each site in neutral and flexed neck positions using several different decision criteria. CONCLUSIONS: At C6-C7, in neutral or flexed neck position and using 20% reduction of DD, the test was highly sensitive and specific for CSM. At other sites, reduced height of the myelographic column generally was not accurate for diagnosing extradural spinal cord compression. Using 20% reduction of DD in neutral position at the mid-cervical sites, the test had only low sensitivity and high specificity. Flexion of the neck appeared to increase detection of spinal cord compression in the mid-cervical region, but also substantially increased the frequency of false-positive diagnoses. POTENTIAL RELEVANCE: By using the reported sensitivity and specificity estimates, readers may decide on a decision criterion for diagnosis of extradural spinal cord compression due to CSM. However, in planning a surgical correction, it is difficult to define a decision criterion that combines acceptable sensitivity and specificity, especially at the mid-cervical sites.

Animals↗
PubMed2003

Gliomatosis cerebri in six dogs.

Gliomatosis cerebri is a well-recognized entity in human medicine characterized by unusually widespread infiltration of the neuraxis by neoplastic glial cells with relative preservation of brain architecture. This report describes the pathologic features of the disease in six dogs. The dogs ranged from 3 to 9 years of age (mean 6.1 years) without evidence of breed predilection; five of the six dogs were neutered or intact males. The clinical findings were mixed (including depression, circling, cranial nerve deficits), reflecting the diffuse nature of the disease. Histologically, there was remarkably diffuse infiltration of the white and gray matter of the brain by small numbers of elongated neoplastic cells. Areas of greater cellularity formed grossly visible lesions in four cases. Anisocytosis and pleomorphism were greater in areas of higher cellularity. Other features of tumor growth included subpial accumulation, neuronal satellitosis, perivascular cuffing, and tropism for cranial nerve and brain stem nuclei. Neoplastic cells were negative on immunohistochemical stains for glial fibrillary acid protein (GFAP) and leukocyte markers, reflecting the uncertain histogenesis of these unusual neoplasms.

Animals↗
PubMed2002

Ganglioradiculitis (sensory neuronopathy) in a dog: clinical, morphologic, and immunohistochemical findings.

A 9-year-old Labrador Retriever was diagnosed with ganglioradiculitis (sensory neuronopathy). This idiopathic disease of mature dogs is characterized by a profound loss of sensory nerve function due to mononuclear inflammatory infiltration of peripheral ganglia and spinal nerve roots, with destruction of sensory neurons. Immunohistochemistry demonstrates that the infiltrating cells are primarily T lymphocytes and that immunoglobulins are not present on the cell membranes of affected neurons. The pathogenesis of ganglioradiculitis remains unclear, but the evidence points to a cell-mediated immune mechanism.

Adrenal Cortex Hormones↗
PubMed2001

Central neuropathology of equine grass sickness.

Equine grass sickness (EGS) is an acquired disease of unknown aetiology affecting horses kept at grass. The disease is characterised by postganglionic sympathetic and parasympathetic neuronal pathology and is categorised as a dysautonomia. This study undertook a systematic examination of brain stem cranial nerve nuclei in 59 cases of EGS. Pathology consisting of neuronal chromatolysis was most consistently noted in the lower motor neurons of the general visceral efferent nucleus of CN III and X and the general somatic efferent nuclei of CN III, V, VII and XII. The prevalence of chromatolysis differed significantly between the diagnostic categories and was inversely related to the age of the animal. Duration of disease had a small but significant negative effect on the proportion of nuclei with chromatolytic neurons in chronic cases. The distribution of chromatolytic neurons is unlike that reported in any other equine or human disease; however, it appears to be equivalent to that in other animals with primary dysautonomias. EGS should be classified as a multisystem disease.

Age Factors↗
PubMed2000

Cerebellar degeneration in Old English Sheepdogs.

OBJECTIVE: To evaluate related and unrelated Old English Sheepdogs (OESD) by clinical examination, histologic evaluation, and pedigree analysis to determine whether cerebellar degeneration develops in this breed and whether there are genetic implications. DESIGN: Case study and pedigree analysis. ANIMALS: 24 clinically normal or affected OESD; brain tissue specimens from 25 unaffected or affected OESD. PROCEDURE: Twenty-four OESD that were chosen because of a family history of gait abnormalities were given physical and neurologic examinations to determine whether they had clinical signs of cerebellar degeneration. Tissue specimens from 25 brains of OESD were examined histologically. Nine OESD that were determined to have cerebellar degeneration histologically as well as 2 clinically affected littermates of the histologically confirmed affected OESD were included in the pedigree analysis. Standard statistical evaluation of pedigrees for hereditary conclusions was used. RESULTS: Twelve of the 24 OESD evaluated by neurologic examination had a progressive gait abnormality. Clinical signs of cerebellar degeneration typically started later in life in OESD, compared with description for other dog breeds, and progressed ore slowly. Results of pedigree analysis revealed that 11 of 49 dogs were affected in 9 litters, providing an affected-to-total ratio of 22.49%. CONCLUSIONS AND CLINICAL RELEVANCE: Results of our study indicate that a slowly progressing late-onset form of cerebellar degeneration develops in OESD, and the mode of inheritance is by an autosomal recessive gene.

Animals↗
PubMed2000

Alaskan Husky encephalopathy--a canine neurodegenerative disorder resembling subacute necrotizing encephalomyelopathy (Leigh syndrome).

The gross and histopathological findings in the brain and spinal cord of five Alaskan Husky dogs with a novel incapacitating and ultimately fatal familial and presumed hereditary neurodegenerative disorder are described. Four dogs presented with neurological deficits before the age of 1 year (7-11 months) and one animal at 2.5 years old. Clinical signs in all dogs were of acute onset and included ataxia, seizures, behavioral abnormalities, blindness, facial hypalgesia and difficulties in prehension of food. In animals allowed to survive, the disease was static but with frequent recurrences. Pathological findings were limited to the central nervous system. Grossly visible bilateral and symmetrical cavitated foci were consistently present in the thalamus with variable extension into the caudal brain stem. Microscopic lesions were more widespread and included foci of bilateral and symmetrical degeneration in the basal nuclei, midbrain, pons and medulla, as well as multifocal lesions at the base of sulci in the cerebral cortex and in the gray matter of cerebellar folia in the ventral vermis. Neuronal loss with concomitant neuronal sparing, spongiosis, vascular hypertrophy and hyperplasia, gliosis, cavitation and transient mixed inflammatory infiltration were the main histopathological findings. In addition, a population of reactive gemistocytic astrocytes with prominent cytoplasmic vacuolation was noted in the thalamus. Lesions of this nature in this distribution within the neuroaxis have not been reported in dogs. The neuropathological findings resemble Leigh's disease/subacute necrotizing encephalomyelopathy of man. Neuronal sparing in conjunction with apparently transient astrocytic vacuolation point to the possible pathogenetic role of astrocytes in the evolution of these lesions. An inherited metabolic derangement of unknown nature is postulated as the cause of this breed-specific disorder.

Age Factors↗
PubMed2000

Possible intraspinal metastasis of a canine spinal cord nephroblastoma.

A 2-year-old Basset Hound was admitted to the University of Florida Veterinary Medical Teaching Hospital with progressive spastic paraparesis. At necropsy, intradural extramedullary tumors produced areas of spinal cord swelling and softening in spinal cord segments T11-T12 and L4-L6. Histologic examination of the masses revealed sheets of polygonal blastemal cells, epithelial cells forming tubules and rosettes, and embryonal glomeruloid-like structures in the thoracic mass. Cells in the lumbar mass were less differentiated, forming rare tubules and no glomeruloid-like structures. The occurrence of two tumors in the spinal cord along with the less differentiated appearance of the lumbar tumor raises the possibility that the lumbar mass arose as a result of intraspinal metastasis. To our knowledge, this is the first report of multifocal or metastatic canine spinal nephroblastoma. In addition, the vimentin and cytokeratin immunohistochemical staining characteristics of these spinal cord nephroblastomas are described.

Animals↗
PubMed2000

Marginal siderosis and degenerative myelopathy: a manifestation of chronic subarachnoid hemorrhage in a horse with a myxopapillary ependymoma.

Marginal siderosis is recognized in humans as an uncommon clinicopathologic entity characterized by degeneration of neural tissue at the surface of the brain and spinal cord, in association with the accumulation of hemosiderin, and resulting from chronic subarachnoid hemorrhage. The sources of hemorrhage are various and include neoplasms, malformations, cysts, and vasculopathy. Marginal siderosis of the spinal cord due to a myxopapillary ependymoma was diagnosed in a 19-year-old Dutch Warm Blood horse with clinical signs of myelopathy. There is only one previous report of marginal siderosis in the veterinary literature, also in a horse with clinical myelopathy.

Animals↗
PubMed1999

Clinical and pathologic findings in two draft horses with progressive muscle atrophy, neuromuscular weakness, and abnormal gait characteristic of shivers syndrome.

Two Belgian geldings, 4 and 14 years old, respectively, with muscle atrophy, weakness, and abnormal gait characteristic of severe advanced shivers were examined clinically and on necropsy. Neurologic examination revealed no evidence of ataxia, and the clinical diagnosis was neuromuscular weakness and shivers. Necropsies of both horses, including examination of pituitary, brain, spinal cord, spinal roots and ganglia, and peripheral nerves, revealed no gross or histologic abnormalities. Examination of multiple skeletal muscle specimens revealed chronic myopathic changes and periodic acid-Schiff positive, amylase-resistant inclusions within muscle fibers, characteristic of equine polysaccharide storage myopathy. It is suggested that underlying metabolic myopathy may be the cause of muscle weakness and cramping in horses with shivers.

Animal Feed↗
PubMed1999

Magnetic resonance imaging of the brain of a dog with hereditary polioencephalomyelopathy.

Hereditary polioencephalomyelopathy was suspected in a young, female Australian Cattle Dog on the basis of clinical signs, including seizures, progressive ataxia, and weakness. Magnetic resonance imaging (MRI) of the brain revealed multiple ovoid, bilaterally symmetric signal abnormalities that were hypointense or isointense on T1-weighted images and hyperintense on T2-weighted images. On necropsy, these areas of signal abnormalities corresponded to areas of malacia in various brain and brain stem nuclei. In addition, poliomalacia was detected at the cervical intumescence of the spinal cord. Histologic examination revealed rarefaction of neuropil and vacuolation of glial cells in these areas, which are lesions consistent with hereditary polioencephalomyelopathy of Australian Cattle Dogs.

Animals↗
PubMed1999

Subacute necrotising encephalopathy in an Alaskan husky.

A 29-month-old female Alaskan husky was presented recumbent, tetraparetic and in a state of dementia, with blindness and cranial nerve deficits. The dog's progress was followed for over two months, as the signs resolved to an non-progressive mild hypermetria with slight proprioceptive ataxia, a diminished menace response and inability to prehend food. Magnetic resonance imaging (MRI) revealed bilateral cavitation extending from the thalamus to the medulla, with less pronounced degenerative lesions in the caudate nucleus, putamen and claustrum. Cerebrospinal fluid lactate and pyruvate concentrations were in their normal ranges. Necropsy and histological examination confirmed the MRI findings as well as neuronal degeneration of the cerebellar cortex in the vermis and degenerative changes in the neocortex at the depths of the cerebral sulci. In view of the similarity of lesions to subacute necrotising encephalomyelopathy, known as Leigh's disease in humans, a tentative diagnosis of a mitochondrial encephalopathy was made.

Animals↗
PubMed1999

Ocular manifestations of equine motor neuron disease.

The characteristics of the ocular manifestations of equine motor neuron disease (EMND) are described. Forty-two horses with histories, clinical signs and necropsies compatible with EMND were the subjects of this study. Ophthalmoscopic lesions that varied in severity were found in 40 of 42 horses and appeared as a distinct pigmented reticulated pattern at the tapetal-nontapetal junction or throughout the fundus, depending upon severity. The pattern colours ranged from yellow brown to black. Areas of hyperreflectivity formed mosaic patterns in the tapetal fundus. ERG B-wave amplitudes were usually at least 50% reduced and many animals showed extinguished amplitudes. None of the horses had apparent visual impairment. Histopathologically, all 42 horses had retinal pigment epithelial (RPE) congestion with ceroid-lipofuscin. Retinal degeneration was variable even within the eyes. Thin layer chromatography (TLC) analysis of the RPE and neural retina identified both green and orange emitting fluorescent compounds not found in normal horses. All unsupplemented horses had plasma vitamin E levels <1.0 microg/ml. The potential significance of this report is the pathognomonic role the ocular manifestations exhibit in helping to diagnose equine motor neuron disease.

Animals↗
PubMed1998

Adult-onset motor neuron disease in three cats.

Motor neuron diseases of domestic animals have rarely been described. Three cats with adult-onset, chronic, progressive generalized muscle weakness characterized initially by trembling on exertion and later by extreme difficulty in walking, cervical ventroflexion, dysphagia, and marked muscle atrophy were elevated. Spinal reflexes were evident early but were nondetectable as the disease progressed. Electromyography revealed fibrillation potentials, with nerve conduction velocities within the reference range. Histologic examination of muscle specimens revealed denervation. Marked neuron loss and gliosis were detected in the ventral horns of the spinal cord, with atrophy of ventral nerve rootlets. Less dramatic neuron loss was seen in brain stem motor nuclei. Electron microscopic examination of the ventral horns disclosed hypertrophied astrocytes, with densely arrayed intermediate filaments, swollen axons with large filamentous accumulations, and many macrophages with lipofuscin-like inclusions. Clinical and pathologic findings were consistent with a progressive neurodegenerative disease affecting spinal and some bulbar motor nuclei.

Age of Onset↗
PubMed1998

Quantitative assessment of motor neuron loss in equine motor neuron disease (EMND).

The mean number of motor neurons was assessed in the C7 spinal cord segment of 5 EMND and 5 control horses. Mean number per section in EMND horses was reduced significantly (P<0.001). The mean neuronal loss was estimated at 31%. Each of the 5 affected horses had a mean neuronal count below the 95% confidence interval for control horses. The statistically significant difference between the 2 groups was consistent in the cranial, middle and caudal thirds of the C7 segment (P<0.001). The results of regression analysis indicated an association between neuronal reduction in EMND horses and the duration of the disease when adjusted for age (P<0.001). This is the first quantitation of the neurodegenerative loss in EMND and it provides a clearer explanation for residual deficits in horses that survive EMND.

Animals↗