An outbreak of spinal neuronopathy of goat kids in Fiji

A newly recognised caprine neuropathy is described in which goat kids developed rapidly progressive neurologic signs in association with widespread demyelination, spinal cord neuronal degeneration and active demyelination.     

Anaplastic astrocytoma in the spinal cord of an African pygmy hedgehog (Atelerix albiventris)

A 2-year-old, female hedgehog presented with an 8-month history of progressive, ascending paresis/paralysis and was tentatively diagnosed with wobbly hedgehog syndrome. She died awaiting further diagnostic tests, and the owners consented to postmortem examination. Grossly, the bladder was large and flaccid and the cervical and lumbar spinal cord were regionally enlarged, light grey, and friable with multifocal hemorrhages. The thoracic spinal cord was grossly normal. Microscopically all regions of the spinal cord had similar changes, although the cervical and lumbar sections were most severely affected. These regions were completely effaced by a moderately cellular infiltration of highly pleomorphic polygonal to spindle shaped cells, mineralization, and necrosis, which were most consistent with anaplastic astrocytoma. The thoracic spinal cord white matter was similarly infiltrated by the neoplastic cells, with perivascular extension into the otherwise normal grey matter. A diagnosis of anaplastic astrocytoma was confirmed using immunohistochemical stains that were positive for glial fibrillary acidic protein and S100.     

Posterior paralysis due to fibrocartilaginous embolism in two weaner pigs.

Acute posterior paralysis in two weaner pigs was attributed to ischemic infarction of the lumbar spinal cord due to fibrocartilaginous emboli. These arterial and venous emboli were assumed to have originated from the nucleus pulposus of one or more intervertebral discs. There was no indication of an initiating factor in either instance, although some form of trauma may have been involved. Lesions were not grossly evident and were limited to one or two lumbar segments. Although it appears to be a rare occurrence, fibrocartilaginous embolism of the spinal cord should be considered in cases of acute paralysis in pigs particularly when gross lesions are absent.     

Pathology of listerial encephalitis in chickens in Japan

Neural signs (torticollis, drowsiness) and mortality were observed in five chickens of a native chicken flock (reared for meat) that included 450 male birds on a farm that had 2300 native chickens and 1120 layers. Histologic lesions were observed in the medulla oblongata, optic lobe, cerebellum, and spinal cord of the affected birds. The lesions, which were most severe in the medulla oblongata, were massive abscesses with rarefaction (demyelination and malacia) of the parenchyma with gram-positive bacteria. The degenerative and necrotic areas were characterized by fibrin thrombosis, hemorrhages, and congestion in the blood vessels. Immunohistochemically, the bacteria positive for L. monocytogenes antigen were observed in the medulla oblongata, cerebellum, and spinal cord. Ultrastructurally, the small rod-shaped and thin-cell-walled bacteria were observed in the parenchyma of the medulla oblongata. Listeria monocytogenes (serotype 4b) was isolated from the medulla oblongata and spinal cord. The pathogenesis of listerial encephalitis in chickens was discussed.     

An outbreak of spinal neuronopathy of goat kids in Fiji

A newly recognised caprine neuropathy is described in which goat kids developed rapidly progressive neurologic signs in association with widespread spinal cord neuronal degeneration and active demyelination.     

California goats with a disease resembling enzootic ataxia or swayback

In a retrospective study typical signs and lesions of enzootic ataxia or swayback were found in 16 young dairy goats from eight widely scattered herds in California. In addition to the constant appearance of chromatolytic neurons in brainstem and spinal cord, and myelin deficiency in certain tracts of the cord, cerebellar hypoplasia was found frequently. Liver copper was subnormal in six of nine kids tested. The disease is viewed as a developmental defect in which failure of neuronal perikaryon metabolism leads to distal axonopathy with secondary demyelination.     

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.     

A case report: encephalitis in lions. Pathological and virological findings

An acute outbreak of encephalomyelitis in lions from a safari-park was investigated. Three moribund lions were euthanatized and a post mortem examination was performed. A disseminated non-suppurative polioencephalomyelitis with demyelination in the spinal cord was the only pathological finding. From tonsil material of one lion feline herpesvirus type 1 was isolated. Canine distemper virus, pseudorabies virus, feline infectious peritonitis virus and rabies were excluded as cause of the disease. The possible role of FHV-1 in etiology of the disease is discussed.     

Disseminated sarcocystosis in a cat with lymphosarcoma

Cysts of the protozoan Sarcocystis sp were found in skeletal and cardiac musculature in a 1.5-year-old cat with lymphosarcoma. The cat was FeLV-positive and had grossly visible neoplastic involvement of the spinal cord, mediastinum, bone marrow, and kidneys. Ultrastructural examination of the parasitic cyst wall suggested that the species in this case was different from that described in the only other reported case. It was hypothesized that immunosuppression from FeLV infection permitted an aberrant life cycle with encystment of Sarcocystis sp in this cat.     

Myelopathy and Reactive Microgliosis and Astrogliosis in Equine Back Pain

Equine chronic back pain (CBP) has been linked to different pathologic processes, which directly or indirectly involve spinal structures. Thus, making diagnosis and management very challenging with most horses with the condition recommended for early retirement from athletic activity. This study described the spinal cord lesions and the development of reactive microgliosis and astrocytosis in the spinal cords of horse with CBP. Thoracolumbar spinal cord segments from three horses euthanized because of unresolved CBP were dissected and grossly and histopathologically examined. The expression of activated microglia and astrocytes were demonstrated immunohistochemically using polyclonal rabbit anti-Iba-1 and anti-glial fibrillary acidic protein antibodies, respectively. All horses had radiological evidence of varying degrees of kissing spine involving six to nine vertebrae with the majority of the lesions graded between 2 and 5. Grossly, there was myelomalacia with intramedullary hemorrhages. The gray matters of the spinal cords were characterized by hemorrhagic malacic lesions with medullary disintegration. Reactive microgliosis and astrocytosis were evident in the spinal dorsal horns. White matter lesions include axonal swollen and/or loss, satellitosis, and varying degrees of dilation of myelin sheaths with some containing macrophages. In conclusion, the presence of reactive microgliosis and astrogliosis in the spinal dorsal horn indicates that they are possible precipitating factors in the development of equine CBP.     

Chronic cervical compressive myelopathy in horses: clinical correlations with spinal cord alterations

Histological examination was performed on the cervical spinal cord from 13 horses with chronic cervical compressive myelopathy of 4 to 29 months duration. Structural alterations were correlated with clinical features. At the level of compression, the spinal cord was grossly deformed. Histological alterations included nerve fibre swelling and degeneration, occasional spheroids, astrocytic gliosis, increased macrophage activity and increased perivascular collagen. Myelin degeneration or loss at the level of the compressive lesion was greatest in the ventral and lateral funiculi and less consistently present in the dorsal funiculi. Asymmetry of lesions in the dorsal funiculi was associated with asymmetry of clinical signs in 5 horses. Histological alterations in areas of Wallerian degeneration were similar to that at the level of spinal cord compression, except that perivascular collagen was not increased. Wallerian degeneration was present cranial to the compressed site in the superficial portions of the lateral funiculi and in the middle of the dorsal funiculi. Caudal to the compressed site it was present in the ventral funiculi adjacent to the ventral median fissure and in the middle of the lateral funiculi. Deformation of the spinal cord did not correlate with the severity or duration of clinical signs but was positively correlated with the amount of perivascular collagen increase. The amount of nerve fibre swelling was not correlated with the severity of clinical signs but was negatively correlated with their duration. A rapid loss of nerve fibres apparently occurred early in the course of compression, since there was a marked decrease in the amount of nerve fibre swelling and Marchi stained degenerating myelin with increasing clinical duration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postural and neurological deficits in broiler chicks after cervical vaccination with live vaccine.

A disease characterized by paresis and paralysis was seen in 7-9-day-old broiler chicks after vaccination in the neck area at day-of-age with a live virus vaccine containing viruses of Marek's disease, fowl pox, and infectious bursal disease. Affected birds presented with variable signs of ataxia, lateral recumbency, leg paralysis, and twisting or S-shaped flexure of the neck. Gross lesions noted at necropsy included swelling and edema of the subcutaneous tissues and muscles of the neck at the injection site area. A heavy mononuclear inflammatory cell infiltration was seen in the subcutaneous tissues, connective tissues, and muscles of the neck at the injection site. In some cases, the inflammatory process extended along fascial planes to involve the epidural spaces surrounding the spinal cord. Fatty changes with possible demyelination of nerve fibers were noted in some sections of the spinal cord adjacent to the inflammatory lesions. Clusters of poxviruses were found within some inflammatory lesions on transmission electron photomicrographs.     

Lesions in the cat spinal cord following local injections of 6-aminonicotinamide.

Lesions were made in the spinal cord of cats by means of local injections of 6-aminonicotinamide. The concentration needed to induce primary demyelination also caused extensive axonal death. In the early stages following injection there was evidence of astrocyte and oligodendrocyte destruction and with longer survival times most of the surviving demyelinated axons were remyelinated by Schwann cells. This experimental system indicates that Schwann cell remyelination of central axons follows astrocyte destruction, but it was not considered a suitable model system for the study of cellular relationships in remyelination because of the extensive concomitant axonal damage.     

Healing Characteristics of Free and Pedicle Fat Grafts after Dorsal Laminectomy and Durotomy in Dogs

Dorsal laminectomy and durotomy were performed at thoracic vertebrae 12 and 13 (T12-T13) and lumbar vertebrae 1 and 2 (L1-L2) in 12 normal dogs. A free fat graft harvested from subcutaneous tissue adjacent to the incision was placed over the T12-T13 laminectomy site. A 75 X 25 X 5 mm pedicle fat graft harvested from a similar location was placed over the L1-L2 laminectomy site. Three dogs each were euthanatized at weeks 2, 4, 8, and 16. With both types of fat grafts, an initial inflammatory stage reduced the size of the graft approximately 50%. Axonal degeneration and demyelination of the spinal cord resolved by week 16. At week 16, the durotomy sites had healed, but the dura mater was adhered to the spinal cord. No difference between the grafts could be demonstrated by antemortem myelography and cerebrospinal fluid analysis. There was no demonstrable advantage to the use of pedicle fat grafts.     

Leukoencephalitis and vasculitis with perivascular demyelination in a Weimaraner dog

Aseptic and noninfectious diseases of the central nervous system are being recognized with increasing frequency. After multiple episodes of neurologic illness, this 7-year-old Weimaraner dog was euthanatized and submitted for postmortem examination. Lesions in the central nervous system were found mainly in the white matter of the cerebral cortex and cervical spinal cord and represented acute and more chronic injury. Necrotizing vasculitis with fibrinoid change and a marked neutrophilic infiltrate dominated the acute lesions. More chronic changes consisted of perivascular demyelination and accumulation of foamy macrophages with positive staining for myelin. An immune-complex (Arthus-type) vasculitis is suspected.     

Lesions in the central nervous system of DBA/2 mice infected with the D variant of encephalomyocarditis virus (EMC-D).

The central nervous system (CNS) of DBA/2 mice inoculated i.p. with the D variant of encephalomyocarditis virus (EMC-D) (10(3) PFU/head) was examined up to 28 days postinoculation (28 DPI). The virus titer of CNS reached a maximum level at 4 DPI, and infectious viruses became undetectable by 28 DPI. Histopathologically, degeneration of neurons with virus antigens was observed in St. pyramidale hippocampi, Nuc. amigdaloideus corticalis and St. granulosum cerebelli of the brain and in Cornu ventrale of the thoracic to lumbar spinal cord at 6 DPI. In addition, in the spinal cord, demyelination was found in Funiculus ventralis and Funiculus lateralis at 6 DPI and it progressed to form spongiosis at 10 DPI. In correspondence with these virological and histopathological findings, hind limb paralysis developed in some mice at 6 DPI, and its incidence increased markedly to about 60% at 10 DPI.     

Lightning injury in an outdoor swine herd.

Three pigs, weighing 63 kg-70 kg each, from a group of 8 pigs in an outdoor pen that was struck by lightning were necropsied. All 3 pigs presented with hind limb paralysis. The only lesions identified were multiple fractures of the last (seventh) lumbar vertebral body and first sacral vertebral segment, with dorsal displacement of the sacrum and transection of the distal spinal cord and spinal nerves. Hemorrhages extended from the fracture sites into muscles immediately surrounding the lumbosacral junction and retroperitoneally into the pelvic cavity. These hemorrhages were not clearly visible until the pelvic region was dissected. Lesions commonly found in human lightning-strike victims were not present in these pigs. Because vertebral fractures may be the only lesions and may be grossly subtle in heavily muscled pigs, careful pelvic and vertebral dissection is recommended in cases of suspected lightning strike and electrocution.     

Gait deficits in liver disease: Hepatic encephalopathy and hepatic myelopathy

In this issue, the unusual clinical presentation of a horse diagnosed is described with severe liver cirrhosis and hepatic encephalopathy. The horse initially presented for thoracic and pelvic limb ataxia and weakness, and signs of forebrain disease were not apparent until later in the disease process. The typical pathology of central nervous system disease associated with liver disease is related to encephalopathy and forebrain disease; however, the spinal cord is occasionally also involved. Hepatic myelopathy is a rare syndrome usually associated with surgical or acquired portosystemic shunts, liver cirrhosis and/or portal hypertension in man. Where a gliopathy is the most prominent pathological feature seen in hepatic encephalopathy, in hepatic myelopathy the most remarkable feature is demyelination of the corticospinal tracts of the distal cervical and thoracic spinal cord with occasional axon loss. The clinical signs of hepatic myelopathy are spastic paresis/paralysis with normal sensory findings and preserved sphincter function. The prognosis for hepatic myelopathy is generally poor. In summary, in severe liver disease, motor deficits can occur secondary to the encephalopathy, but motor deficits can also occur as a result of spinal cord pathology such as seen in hepatic myelopathy. In examination of horses with myelopathies, liver disease as a cause of myelopathy should be included in our list of differentials.     

Cycad (zamia) poisoning in Australia

The Cycads belong to an ancient family of plants and were the cause of the first well documented plant poisoning in Australia when Captain Cook's men and their pigs were affected by eating them. Subsequent reports particularly by early explorers refer to toxicity of the seeds to man. One reason for this was the evidence that the natives ate them. Subsequent reports and experimental work established the toxicity to sheep and cattle. In sheep and cattle 2 syndromes occur, ataxia and liver damage. In cattle the former is the better known, the spinal cord lesion being mainly a demyelination of the sensory pathways. The liver damage is necrosis and fibrosis.     

Neurological diseases of rottweilers: Neuroaxonal dystrophy and leukoenceph- alomalacia

Neuroaxonal dystrophy (NAD) and leukoencephalomalacia (LEM) are two neurological disorders of the rottweiler that initially present as ataxia of all four limbs. Disorders to be included in the differential diagnosis are caudal cervical spondylomyelopathy, canine distemper virus meningoencephalomyelitis, other nervous system infections or inflammations and spinal cord neoplasia. All diagnostic tests including myelography, cerebrospinal fluid analysis, electrodiagnos-tic testing and serum and cerebrospinal fluid titres for canine distemper virus are normal in NAD and LEM. There is no treatment for either disease and neurological signs progressively deteriorate. Eventually neurological deficits develop besides ataxia and these help differentiate NAD from LEM. Dogs with NAD develop head tremors and nystagmus while dogs with LEM develop conscious proprioceptive deficits and quadriparesis; the short term prognosis for NAD is better than LEM. Most dogs with LEM are euthanased because of non-ambulatory tetraparesis within one year. The histopathological lesions associated with NAD include axonal spheroids in many spinal cord and caudal brainstem nuclei and reduced numbers of Purkinje cells in the cerebellum, while in LEM, multifocal areas of demyelination and malacia of the spinal cord and brainstem are the primary histopathological lesions. Both NAD and LEM are suspected to have an autosomal recessive genetic transmission.