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Biomedical subjects

Alexander de Lahunta

Publications and source records attributed to Alexander de Lahunta.

17 recordsLinked to original sources

Evaluation of the risk of motor neuron disease in horses fed a diet low in vitamin E and high in copper and iron.

OBJECTIVE: To determine whether equine motor neuron disease (EMND) could be induced in adult horses fed a diet low in vitamin E and high in copper and iron. ANIMALS: 59 healthy adult horses. PROCEDURE: Horses in the experimental group (n = 8) were confined to a dirt lot and fed a concentrate low in vitamin E and high in iron and copper in addition to free-choice grass hay that had been stored for 1 year. Control horses (n = 51) were fed a concentrate containing National Research Council-recommended amounts of copper, iron, and vitamin E. The hay fed to control horses was the same as that fed to experimental horses, but it had not been subjected to prolonged storage. Control horses had seasonal access to pasture, whereas experimental horses had no access to pasture. Horses that developed clinical signs of EMND were euthanatized along with an age-matched control horse to determine differences in hepatic concentrations of vitamin E, vitamin A, copper, iron, and selenium. RESULTS: 4 experimental horses developed clinical signs of EMND. Plasma concentrations of vitamin E decreased in all 8 experimental horses. There were no significant changes in plasma concentrations of vitamin A, selenium, and copper or serum concentrations of ferritin. There were no significant differences in those analytes between experimental horses with EMND and experimental horses that did not develop EMND. No control horses developed EMND. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that lack of access to pasture, dietary deficiency of vitamin E, or excessive dietary copper are likely risk factors for EMND.

Animals↗

Bilateral, hypertrophic neuritis of the brachial plexus in a cat: magnetic resonance imaging and pathological findings.

A 9-year-old Burmese cat was presented for investigation of a subacute onset of bilateral forelimb paresis. Magnetic resonance imaging of the cervico-thoracic vertebral column and brachial plexus revealed a bilaterally symmetrical, severe and diffuse swelling of the spinal nerves forming the caudal part of the brachial plexus. Histopathology of the abnormal nerve roots, spinal nerves and brachial plexi showed inflammatory and marked proliferative changes with similar features to that of hypertrophic neuritis of man. Hypertrophic neuritis in man is a rare, tumor-like, chronic inflammatory peripheral nerve disorder of unknown origin most frequently involving the brachial plexus.

Animals↗

A degenerative encephalomyelopathy in 7 Kuvasz puppies.

Seven Kuvasz puppies from 2 same-parentage litters developed weakness and ataxia. Six necropsied dogs had lesions in caudate nucleus, cerebellar nuclei and folia, and spinal cord. Lesions seen were felt to be familial or due to the effects of an amprolium-induced thiamine deficiency on the developing brains of these puppies.

Amprolium↗

Parastrongylus cantonensis in a nonhuman primate, Florida.

Parastrongylus (= Angiostrongylus) cantonensis is a parasitic nematode of Norway rats throughout tropical regions. This parasite is neurotropic and causes disease and death in humans and other mammals. We report the first identification of P. cantonensis as the cause of a debilitating neurologic disease in a captive primate in Florida.

Angiostrongylus cantonensis↗

Neurologic disease putatively associated with ingestion of Solanum viarum in goats.

Several Nubian-cross goats were evaluated because of chronic progressive neurologic disease. Physical and neurologic examination revealed signs consistent with diffuse cerebellar disease. Neurologic signs included generalized hyperresponsiveness, fine head tremors, wide-based posture, dysmetria, weakness, and horizontal nystagmus. No clinical improvement was noted after removing goats from affected enclosures. Histologic examination of cerebellar tissues revealed extensive vacuolation within the cytoplasm of Purkinje cells. The clinical and histologic lesions resembled closely findings that were associated with ingestion of Solanum spp in cattle and goats. Examination of enclosures revealed Solanum viarum (tropical soda apple) that had been heavily consumed by the goat herd. We hypothesized that ingestion of S. viarum caused the neurologic disorder.

Animals↗

Magnetic resonance imaging features of lissencephaly in 2 Lhasa Apsos.

Two Lhasa Apsos were diagnosed with lissencephaly based on MR imaging and clinical findings. Histologic confirmation of the diagnosis was obtained in one dog. The MR imaging appearance of the brain in 2 Lhasa Apsos with lissencephaly was of a smooth cerebral surface and a thick neocortex with an absence of the corona radiata. This correlated very well with the histopathologic findings in the dog. Our findings, together with the histopathologic features reported previously, are most consistent with Lhasa Apsos having the canine equivalent of human classical lissencephaly. MR is the imaging modality of choice for antemortem diagnosis of canine lissencephaly.

Animals↗

Choroid plexus cyst in a dog.

A 6-year-old male Doberman Pinscher had a 2-month history of dysequilibrium. Lesion localization was determined to be the cerebellomedullary pontine angle. In computed tomographic images, a well-defined, circular, hypoattenuating mass was visible at the cerebellomedullary pontine angle. The lesion, which was isoattenuating to cerebrospinal fluid, was 4 x 8 mm in diameter. Peripheral ring enhancement was evident after contrast medium administration. A choroid plexus cyst was diagnosed histopathologically.

Animals↗

Myelopathy in Holstein x Gir calves in Brazil.

This case report contains clinical and pathologic features of a degenerative myelopathy in Holstein X Gir crossbred calves in Brazil. The bilateral and symmetrical spinal cord white matter lesions were interpreted as a primary axonopathy that may be of the dying-back type.

Animals↗

A variant form of neuronal ceroid lipofuscinosis in American bulldogs.

Neuronal ceroid lipofuscinoses (NCLs) are inherited neurodegenerative diseases characterized by accumulations of autofluorescent lipopigments within cells of the nervous system. Nine related American Bulldogs demonstrated dysmetria in all limbs and paraparesis. Nonambulatory tetraparesis was observed only in the later stages of the disease. The clinical signs developed between 1 and 3 years of age and were slowly progressive over several years, which is inconsistent with most reports in other breeds. Results from blood tests for 8 different lysosomal storage diseases on 4 affected and 6 related but unaffected dogs were negative. Four affected dogs were euthanized and histopathologic examinations showed diffuse accumulations of periodic acid-Schiff-positive inclusions in neurons and axonal spheroids along the entire neuraxis and retinae. The most severe lesions were in the brainstem proprioceptive nuclei and spinal cord, consistent with clinical signs. The storage material was autofluorescent and immunohistochemically positive for products of lipid peroxidation. Ultrastructural analysis was consistent with NCL. Pedigree analysis supports an autosomal-recessive mode of inheritance. NCL has not been previously reported in the American Bulldog and these findings suggest a variant form of the canine disease.

Animals↗

Polymerase chain reaction screening for DNA viruses in paraffin-embedded brains from dogs with necrotizing meningoencephalitis, necrotizing leukoencephalitis, and granulomatous meningoencephalitis.

The objective of this investigation was to determine whether or not herpesvirus (herpes-), adenovirus (adeno-), or canine parvovirus DNA is present in the brains of dogs with necrotizing meningoencephalitis (NME), necrotizing leukoencephalitis (NLE), and granulomatous meningoencephalitis (GME). Paraffin-embedded brain specimens from 12 histopathologically confirmed dogs with NME, 3 with NLE, and 7 with GME were screened for viral DNA with degenerate herpes- and adenovirus polymerase chain reaction (PCR) and a canine parvovirus-specific PCR. Positive-control specimens included genomic viral DNA and paraffin-embedded tissues from dogs with confirmed herpes-, adeno-, or canine parvovirus infections. Herpes-, adeno-, or canine parvovirus DNA was amplified by PCR from the corresponding positive-control specimens. Negative controls included 7 dogs with various brain disorders and produced no viral amplicons. The 22 dogs with NME, NLE, and GME were negative for viral DNA. Additional studies testing for other viruses or inherited genetic mutations are warranted to gain insight into the etiologies of NME, NLE, and GME. We discuss potential etiologies and provide a clinical and histopathologic overview of these common canine encephalitides.

Animals↗

Cerebellar degeneration in a mature Staffordshire terrier.

A 5-year-old Staffordshire terrier exhibited slowly progressive signs of cerebellar disease, including nystagmus and dysmetria. After a 30-month course, the dog was euthanized. Grossly, the cerebellum was small and comprised only 5% of the brain weight. Histopathological examination of the brain documented diffuse degeneration. Purkinje cells were most depleted, but granular cells and the molecular layer of cerebellum were also depleted. The history and necropsy examination were evidence of late-onset primary cerebellar degeneration.

Animals↗