Poisoning by Indigofera lespedezioides in horses.

Poisoning by Indigofera lespedezioides is reported in horses in the state of Roraima, northern Brazil. The main clinical signs are anorexia, sleepiness, unsteady gait, severe ataxia, weakness, stumbling, and progressive weight loss. To induce the disease experimentally, a 7-year-old horse was introduced in a small paddock invaded by the plant. The first nervous signs were observed 44 days from the start of grazing. The animal was euthanized on day 59. No significant gross lesions were observed upon necropsies of the experimental horse as well as one spontaneously affected horse. Upon histologic examination neuronal lipofuscinosis was observed in the brain, cerebellum, and spinal cord. Wallerian-type degeneration was observed on some mesencephalic tracts. Neuronal and axonal degeneration and lipofuscinosis were observed on electron microscopy examination. Indospicine was detected in four samples of I. lespedezioides with concentrations ranging from 63 to 1178 µg/g whereas nitro toxins could be detected in only one of the samples at a concentration of 2.5 mg/g. In conclusion, poisoning by I. lespedezioides is very similar to those poisonings by Indigofera linnaei and Indigofera hendecaphylla. Based on the preponderance of indospince and lack of nitro toxins in the samples it is proposed that indospicine is the toxic compound responsible for the poisoning.

Histopathological investigation of syringomyelia in the Cavalier King Charles spaniel.

Syringomyelia (SM) in Cavalier King Charles spaniels (CKCSs) is identified commonly on magnetic resonance images and is sometimes associated with clinical signs of pain and cervical hyperaesthesia. However, the mechanism by which SM develops in this breed has not been fully elucidated and the associated effects on spinal cord structure have not been reported previously. The aims of this study were to describe changes found in the spinal cord of CKCSs, to compare findings between symptomatic and asymptomatic dogs and to determine whether syrinx formation was associated with tissue destruction. Anomalies of the central canal were found in all specimens and many dogs had grossly visible fluid-filled cavities within the spinal cord. Prominent microscopical findings were spongy degenerative changes associated with neuronal necrosis and Wallerian degeneration. The ependyma was discontinuous in many specimens, notably in symptomatic individuals, and there was evidence of angiogenesis and fibrous tissue proliferation around blood vessels adjacent to syrinx cavities. Compared with two different samples of the normal dog population, dogs with syrinxes had significantly less grey matter, although this decrease was associated with generalized loss of spinal cord area. Therefore, SM is associated with degenerative changes in the spinal cord and may develop through primary disruption of ependymal integrity followed by vascular hypertrophy and proliferation. Glial and fibrous proliferation appears to be associated with expression of clinical signs.

The experimental induction of leukoencephalomyelopathy in cats.

Leukoencephalomyelopathy of undetermined etiology has been described in specific pathogen-free cats. A study was established to assess if the long-term feeding of a gamma-irradiated diet could induce this disease. Cats fed exclusively on diet irradiated at 25.7-38.1 kGy ("typical" dose) and 38.1-53.6 kGy (high-end dose), respectively, developed typical lesions with attendant, progressively severe ataxia between study days 140 and 174. The onset of ataxia at day 140 and the number of animals affected at this time were similar in animals fed each ration. A maximum ataxia "score" was first reached by an animal on the high-end dose diet on day 167 and by 2 cats fed the "typical-end" dose diet 21 days later. Ataxic cats and 1 animal euthanized on day 93 prior to the onset of ataxia exhibited varying degrees of Wallerian degeneration in the spinal cord and brain, similar to the spontaneous disease. The elevated total antioxidant status of spinal cord segments and hepatic superoxide dismutase concentration of cats fed typical and high-end treated diets suggested free-radical involvement in the pathogenesis. The significantly elevated peroxide concentrations of the irradiated diets (1,040% and 6,440% of untreated values) may have resulted in increased oxidative insult, a factor possibly exacerbated by the treated diets' reduced vitamin A content. This study has reproduced leukoencephalomyelopathy in cats similar to spontaneous outbreaks by feeding a gamma-irradiated dry diet with elevated peroxide and reduced vitamin A concentrations.

Degenerative myelopathy and vitamin A deficiency in a young black-maned lion (Panthera leo).

Degenerative myelopathy and vitamin A deficiency were diagnosed in a 1-year-old, female, black-maned lion (Panthera leo). Diffuse white matter degeneration characterized by dilated myelin sheaths, Wallerian degeneration, and reactive astrocytosis was present at all levels of the spinal cord. With luxol fast blue-resyl echt violet stain, bilaterally symmetrical demyelination was observed in the fasciculus cuneatus of the cervical spinal cord and in peripheral white matter of cervical, thoracic, and lumbar segments. Additionally, the ventral gray columns and brain stem nuclei contained rare chromatolytic neurons with abnormal neurofilament accumulation. Leptomeninges of the cervical spinal cord were focally adhered to the dura and thickened by fibrosis and osseous metaplasia. Vitamin A deficiency was diagnosed based on hepatic vitamin A concentration of 1.71 microg/g dry weight. Adequate hepatic vitamin A concentration for yearling to adult domestic animals ranges between 150 and 1000 microg/g dry weight. Lesions were distinct from those previously described in young captive lions with vitamin A deficiency, which had thickened skull bones and cerebellar herniation. The pathogenesis of vitamin A-associated myelopathy in this lion may be similar to that described in adult cattle, which is believed to result from spinal cord compression secondary to elevated pressure of cerebrospinal fluid.

[Suckling calves with symptoms of swayback]. / Het beeld van swayback bij zoogkalveren.

Within a 1-year period, three calves from the same herd developed ataxia of the hind limbs and urinary incontinence at about 6 months of age. Signs progressed and the calves were slaughtered 1-8 months after the onset of signs. The calves belonged to a suckling beef herd of 35 cattle. Blood samples from 11 cattle of different ages were collected and glutathione peroxidase and copper levels were measured. Glutathione peroxidase levels were below the normal range in all cattle and copper levels were below the normal range in 7 of ll cattle. Pathological examination of an affected calf revealed a Wallerian type of degeneration of myelinated nerve fibres in the lateral and ventral spinal cord tracts. In addition, the hepatic copper content was very low. Copper deficiency is a well-known cause of swayback in young sheep and goats. To our knowledge, this is the first report of a possible association between a swayback-like syndrome and copper deficiency in calves.

Acute paraplegia in a young adult long-evans rat resulting from T-cell lymphoma.

We describe an unusual case of acute paraplegia in a young adult (7.5-month-old) Long-Evans rat that resulted from a spontaneous T-cell lymphoma. At presentation, a neurologic exam revealed normal pelvic limb flexor reflexes, the absence of an anal reflex, and deep pain recognition. Radiographs did not identify any obvious spinal abnormality or osseous trauma, although the liver and spleen were prominent. Hematologic analysis disclosed leukocytosis with atypical lymphocytes. At necropsy, red, friable to gelatinous masses were found associated with the ventral aspect of the vertebral column at the levels of the thoracic and lumbar vertebrae. Impression smears of the mass revealed a monocytic cell population with cells averaging 7 to 10 microm in diameter and having scant cytoplasm and pleomorphic nuclei, characteristics consistent with a lymphoid neoplasm. Histologically, the neoplasm was unencapsulated, poorly demarcated and highly infiltrative, invading and effacing the bone marrow and epidural space of the vertebral column. Neoplastic cells also were identified in the femoral bone marrow, spleen, liver, iliac and sacral lymph nodes, and lung. Immunophenotyping showed the neoplasm to be of T-cell origin. Although the lymphoma did not invade the meninges of the spinal cord, its impingement on the central and peripheral nervous systems resulted in foci of Wallerian degeneration that contributed to the paraplegia. This case report highlights the importance of having lymphoma and leukemia among the differential diagnoses in cases of acute paralysis in rodents.

Progressive encephalomyelopathy and cerebellar degeneration in 10 captive-bred cheetahs.

Progressive ataxia, with head tremor, developed in 10 captive-born cheetah cubs under six months of age. The condition was usually preceded by coryza and an ocular discharge. Initially the ataxia and weakness affected the hindquarters, then the forelegs, and head tremor developed later. Significant pathological changes were confined to the central nervous system. There was widespread Wallerian degeneration in the funiculi of the spinal cord (except those in the dorsal columns), in the medulla and in the cerebellum. In the cerebellum there was degeneration of Purkinje cells and of the molecular and granular cell layers. There was chromatolysis in the Purkinje cells, the ventral horn cells of the spinal cord and in the neurons of the lateral vestibular nucleus. The olivary nucleus was necrotic. There were foci of inflammatory cells in the molecular layer of the cerebellum and in the medulla. The cause of the disease remains unknown.

Peripheral nerve lesions in a case of equine motor neuron disease.

A male 14-year-old Arab horse was pathologically diagnosed as equine motor neuron disease (EMND), which was kept as a breeding horse on a farm in Tokachi district of Hokkaido in Japan. On examination of the peripheral nerves, the most characteristic feature was Wallerian-type degeneration revealed by myelinoclasis associated with myelin ovoids which were sometimes infiltrated by macrophages. The other abnormalities were axonal swellings which were surrounded by thin myelin sheaths. Ultrastructurally, the axonal swelling was due to an accumulation of neurofilaments, and was accompanied by a thin and degenerating myelin sheaths. In teased nerve fiber preparations, the most conspicuous change was myelinoclasis represented by segmentation into myelin ovoids or balls. Occasionally, segmental demyelination and axonal degeneration characterized by multifocal axonal swelling were observed.

[Acute blindness due to trauma in a Welsh pony-colt]. / Acute blindheid ten gevolge van trauma bij een Welsh ponyveulen.

A healthy, 10-day-old Welsh A pony colt was totally blind 1 day after arrival at a studfarm. Both eyes appeared normal on external inspection. The young animal had been very distressed during the 40-km journey to the studfarm. Intravenous corticosteroids were administered for 2 days, but did not result in any observable improvement. The animal was euthanized at the owner's request. Both eyes with the optic nerves were removed for histological examination. Both optic nerves showed Wallerian degeneration, a well-known response of peripheral nerves to trauma. The foal, which was not tethered during transportation, probably sustained a blunt trauma in the trailer. This case highlights the importance of taking adequate measures to prevent young animals from sustaining blunt trauma during transport.