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Biomedical subjects

A De Lahunta

Publications and source records attributed to A De Lahunta.

At least 19 recordsLinked to original sources
PubMed2006

Oligodendroglial dysplasia in two bullmastiff dogs.

Leukodystrophies are inherited neurological disorders involving central nervous system white matter. They are uncommon in animals but a few, breed-specific entities have been described. In 2002, two young-adult, purebred Bullmastiff dogs from central New York State presented to their referring veterinarians displaying moderate to severe ataxia of all limbs, spastic tetraparesis that was worse in the pelvic limbs, and a diffuse, action-related, whole-body tremor. Clinical signs were insidious in onset and slowly progressive. Anatomic diagnoses considered were a C1-C5 lesion or, based on the whole-body tremor, a diffuse central nervous system disorder. No gross lesions were apparent in the brain or spinal cord. Histopathologically, numerous, multifocal, sharply demarcated, small, ovoid to angular areas of myelin pallor (plaques) were present throughout the major white matter tracts of the brainstem and spinal cord. These plaques, which often were traversed by axons, did not stain with luxol fast blue for myelin and were associated with minimal astrocytosis. Ultrastructural findings include occasional hypertrophic glia in white matter, rare unmyelinated segments of axons, and focal proliferation of tubule-containing cytoplasmic glial cell processes (oligodendroglial). The described clinical and morphological findings and age of onset are similar to the well-characterized, presumably hereditary, bovine syndrome known as Charolais ataxia or oligodendroglial dysplasia. This article presents the first description of a leukodystrophy in the Bullmastiff breed and the first report of oligodendroglial dysplasia in animals other than Charolais cattle.

Animals↗
PubMed1999

Encephalopathy with idiopathic hyperammonaemia and Alzheimer type II astrocytes in equidae.

In 3 mature female horses of varying breeds, episodes of colic and depression for 14 days preceded an encephalopathic disorder with maniacal behaviour, anxiety, profuse sweating and, in one case, terminal opisthotonus. Blood ammonia levels were elevated approximately 10-fold. At necropsy, there were gastrointestinal serosal and mesenteric haemorrhages. Histologically, all 3 cases revealed diffuse Alzheimer type II astrocytes in the cerebral grey matter. Alzheimer type II astrocytes were glial fibrillary acidic protein (GFAP) negative or only weakly positive, weakly S-100 positive, and vimentin negative. In the absence of primary hepatic and/or renal lesions, an increase in intestinal ammonia absorption due to ileus or increased ammonia production by colonic bacteria is hypothesised.

Alzheimer Disease↗
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↗
PubMed1994

Equine motor neuron disease: findings in 28 horses and proposal of a pathophysiological mechanism for the disease.

Over a three and one-half year period, 28 adult horses were diagnosed with equine motor neuron disease (EMND). The most commonly identified environmental risk factors for a horse having EMND were absence of grazing for more than a year and provision of poor quality hay. Quarter Horses were 5.4 times more at risk than other breeds but this was thought to be an epiphenomenon related to the frequency of Quarter Horses at boarding stables. Weight loss, excessive recumbency and/or trembling were the first signs noted. Other clinical diagnostic signs included: constant shifting of the weight in the rear limbs, abnormally low head carriage and muscle fasciculations. Excellent to ravenous appetites were present in all cases and marked coprophagia in some cases. Abnormally high serum concentration of muscle-derived enzymes was the only consistent serum chemistry abnormality found. Abnormal glucose absorption, increased cerebrospinal fluid total protein and intrathecal production of IgG were identified in a number of cases. Euthanasia was performed on 5 horses within 4 days of hospital admission, because of inability to stand or respiratory distress, and on 18 horses after the diagnosis had been completed. Five affected horses were maintained for observational purposes for periods of 9 months to over 2 years after the onset of clinical signs. They were given access to pasture and 2 were given supplemental vitamin E as the only therapy. Marked clinical improvement occurred in the 4 more acutely affected horses. Pathological findings, preference of type 1 muscle fibre atrophy and lipopigment accumulation within the capillary endothelium of the spinal cord of all cases, supported the hypothesis of EMND being an oxidative disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗
PubMed1993

Brain abscess in a goat.

A young goat was presented with a left spastic hemiparesis and general proprioceptive ataxia with postural reaction deficits, a right head tilt and positional nystagmus. Seizure-like activity was elicited by rapid changes in the position of the animal's head. The neurological signs and quality of the seizure activity suggested a lesion involving the medulla and possibly the cerebellum. A focal lesion at the level of the left cerebellar peduncles could explain the left hemiparesis and right paradoxical vestibular signs. A large encapsulated abscess was found at the confluence of the left cerebellar peduncles. The morphology and staining characteristics of the organisms within the abscess were consistent with Corynebacterium pseudotuberculosis.

Animals↗
PubMed1993

Neuroaxonal dystrophy in a Jack Russell terrier pup resembling human infantile neuroaxonal dystrophy.

A 9-week-old Jack Russell terrier with progressive ataxia had histopathological lesions consistent with neuroaxonal dystrophy. Gross observation revealed absence of the septum pellucidum, hypoplasia of the corpus callosum and marked bilateral hydrocephalus. Light microscopy of the CNS revealed extensive axonal swellings principally in the gray matter of the brain stem where the sensory nuclei were most affected. Ultrastructurally, spheroids were identified as axonal terminals and probably dystrophic boutons; they were characterized by accumulations of membrane bound bodies. Clinical and morphological findings are similar to those identified in human infantile neuroaxonal dystrophy (Seitelberger's disease).

Animals↗
PubMed1991

Encephalitic listeriosis in two adult llamas (Lama glama): clinical presentations, lesions and immunofluorescence of Listeria monocytogenes in brainstem lesions.

Encephalitic listeriosis was diagnosed in 2 adult llamas. Both had a multifocal suppurative encephalitis with mixed lymphocytic and neutrophilic perivascular infiltrates. Listeria monocytogenes was cultured from the brain stem of 1 llama using cold enrichment techniques; the other llama was culture negative. Formalin-fixed and paraffin embedded sections of brainstem lesions from both affected animals were labeled with a fluorescein-conjugated, anti-L. monocytogenes antibody. Using this technique, intralesional L. monocytogenes were identified in both llamas.

Animals↗
PubMed1990

Infarction of the pons and medulla oblongata caused by arteriolar thrombosis in a horse.

Infarction of the pons and rostral medulla secondary to arteriolar thrombosis was documented histologically in a 17-year-old mixed-Arabian female horse. Clinically, the animal experienced a sudden onset of a head tilt and subsequent non-controllable seizures. There was no historical, clinical or histological evidence to suggest the presence of infection of Equine Herpesvirus-1 or the feeding of corn contaminated by Fusarium moniliforme.

Animals↗
PubMed1988

Multisystemic chromatolytic neuronal degeneration in a Cairn terrier pup.

In a four-month-old female Cairn terrier with mild episodic paraparesis, a multisystemic chromatolytic degeneration affected widespread neuronal populations in the brain and spinal cord as well as spinal, autonomic, and enteric ganglia. There was little axon degeneration or cell body loss, and the latter findings may explain the mild clinical signs. Among affected perikarya the extent and distribution of chromatolysis varied. While peripheral lysis of Nissl substance occurred often in spinal motoneurons, central chromatolysis was frequent in brain stem nuclei, and patchy Nissl loss appeared in some neurons including those in the cerebral cortex and spinal dorsal horns. Although prior studies of various chromatolytic neurodegenerations often have demonstrated characteristic massings of neurofilaments, the major, and invariable ultrastructural finding in this study was dispersion and loss of ribosomes. Neurofilamentous accumulations were observed less consistently. The clinical and pathologic findings in this pup were compared and constrasted with those made in prior studies of chromatolytic neurodegenerations.

Animals↗
PubMed1986

Nemaline myopathy of cats.

An apparently inherited myopathy, characterized by the presence of large numbers of nemaline rods in skeletal muscle fibers, was investigated in five cats. Onset of signs varied from 6 months to 1.5 years of age and consisted of reluctance to move, jerky gait and muscle twitching, hyporeflexia, and muscle wasting, which was most prominent in the proximal muscles of the forelimbs. All of the cats, three males and two females, were from the same dam. In addition to the presence of rods, the myopathy was characterized by marked fiber size variation, with atrophy of type 1 and type 2a muscle fibers. In addition, there was infolding of the sarcolemma and fiber splitting. Ultrastructurally, the rods closely resembled those described in human nemaline myopathy.

Adenosine Triphosphatases↗
PubMed1978

Diagnosis of equine neurologic problems.

This is a review of the more common diseases of the spinal cord and various areas of the brain of horses. The results of a two and one-half year study of spinal cord disease are emphasized. After a description of the lesion the salient clinical signs are described and the features that differentiate them from other similar diseases. In the seminar, films of case and slides of lesions will be shown to document these diseases.

Animals↗