仔猪先天性震颤的病理组织学诊断

利用病理组织学方法对仔猪先天性震颠病病例进行诊断。病理组织学主要变化为大脑软脑膜血管充血,脑膜下水肿;大脑白质和脊髓部位的有髓神经髓鞘发育不全,横切面可见神经髓鞘相对数量少,疏密、大小不均,形态差别大。其他脏器见继发性细菌感染病变。     

Lesions in bovine progressive degenerative myeloencephalopathy ("Weaver") of Brown Swiss cattle

Gross changes and other necropsy findings in 36 purebred Brown Swiss cattle affected with bovine progressive degenerative myeloencephalopathy were nonspecific. Primary microscopic lesions were confined to the central nervous system, specifically the white matter of the spinal cord, axons in some brainstem nuclei, and Purkinje cells of the cerebellar cortex. Spinal cord lesions involved only the white matter and consisted of axonal degeneration, loss of axons and myelin, and status spongiosus. Axonal degeneration was characterized by swelling and fragmentation of the axoplasm or formation of large, discontinuous swellings referred to as spheroids. Lesions were qualitatively similar at all levels, but quantitatively dissimilar in the same funiculi at different levels. Both ascending and descending fibers were involved but correlation to specific fasciculi was not evident. Lesions always were most severe in thoracic spinal cord segments. Little or no astroglial response, no inflammatory response, and no involvement of gray matter were observed in the spinal cord. Cerebellar lesions were limited to selective degeneration and loss of Purkinje cells and occasional swelling of Purkinje cell axons (torpedos) in the granular layer of the cerebellar cortex. Brainstem lesions were inconsistent and limited to occasional axonal swelling in brainstem nuclei. The pathogenesis of bovine progressive degenerative myeloencephalopathy is unknown and possible mechanisms were discussed. The disease exhibits a familial pattern in Brown Swiss cattle and may be hereditary. Extraneural lesions were considered secondary to central nervous system lesions.     

Spongy degeneration of white matter in the central nervous system of silver foxes (Vulpes vulpes)

A disorder of central nervous white matter in Norwegian-bred silver foxes is described from the case histories of 21 clinically affected foxes. The main presenting sign of this disorder was caudal limb ataxia, which appeared between 2 1/2 and 4 months of age and progressed over the next 4-8 weeks. Only four affected foxes were allowed to live beyond this period, but they showed moderate to marked improvement. Light microscopic examination of specimens from 16 affected foxes necropsied between 3 1/2 and 6 1/2 months of age revealed lesions that were restricted to the white matter of brain and spinal cord. The lesions were characterized by a symmetrical spongy change with vacuoles of varying sizes and included significant myelin deficiency. There was a relative preservation of axons and nerve cells and no significant inflammation or vascular reaction. An astrocytic hypertrophy was usually associated with the spongy change. Ultrastructural examination of central nervous tissue from two, perfusion-fixed, 6-month-old foxes showed intramyelin vacuoles resulting from splitting of the myelin lamellae at the intraperiod line and was interpreted as indicating myelin edema. Expanded extracellular spaces and watery astrocytic processes also contributed to the vacuolar appearance. Astrocytic processes in affected areas were hypertrophic and contained abundant filaments. Although the 16 silver foxes had severe clinical signs, their lesions had features in common with the juvenile form of Canavan's disease in children and a spongy degeneration reported in Labrador Retrievers; however, the clinical course in the foxes was not uniformly progressive.     

Canine spinal cord neuron and axon myelin sheath morphometry

This inedited morphometric study has been developed from healthy canine spinal cord neuron cytoplasm and nucleus, and white matter axonal myelin sheath, from cervical, thoracic and lumbar regions. For the morphometric study, the parameters were area, perimeter, maximum and minimum diameters and roundness for neurons and myelin thickness for axon. For each parameter, 300 neurons were analysed. The results revealed that lumbar neurons had the highest mean values for the analysed parameters, indicating the presence of large neurons in this region, with large axons as a result of myelin thickness, which is proportional to axon calibre. We conclude that these morphometric results can contribute for the establishment of normal patterns, for canine spinal cord cervical, thoracic and lumbar segments.     

Infectivity, reproductive capacity and distribution of Trichinella spiralis and T. pseudospiralis larvae in experimentally infected sheep

Twelve Merino sheep were experimentally shown to be susceptible to infection with Trichinella spiralis or T. pseudospiralis by feeding on infected carcasses of mice or by oral intubation with recovered muscle larvae. The larvae recovered from the sheep showed variable tissue distribution. The diaphragm and tongue were most affected. The viability of the recovered larvae was confirmed by successful passage in mice. The reproductive capacity of T. spiralis in sheep was higher than that of T. pseudospiralis, and also higher than its reproductive capacity in C57BL/6J mice. The reproductive capacity of T. pseudospiralis in sheep at a lower dose was higher than that observed in mice. However at higher doses, it was significantly lower than that in mice. Therefore, it may be concluded that the sheep may be considered a suitable host for both species of Trichinella.     

Recovery of Mycobacterium avium subsp. paratuberculosis from nematode larvae cultured from the faeces of sheep with Johne's disease

A study was conducted to determine whether trichostrongylid nematode larvae become contaminated with Mycobacterium avium subsp. paratuberculosis when they develop in the faeces of sheep with Johne's disease. Nematode larvae were hatched from ova in the faecal samples of affected sheep. Larval sheaths were removed and these as well as exsheathed larvae were subjected to radiometric culture for M. paratuberculosis. The organism was recovered from washing water used to prepare the larvae, third stage larvae and larval sheaths, but not from exsheathed larvae. The recovery of M. paratuberculosis from larvae was associated with the severity of the histological lesions in affected sheep and with the results of culture of the organism from intestinal tissues and faeces. Nematode parasites of sheep might be able to act as mechanical vectors for M. paratuberculosis as the organism associates with infective third stage larvae when these develop in the faeces of sheep with Johne's disease.     

HUMPY BACK OF SHEEP. CLINICAL AND PATHOLOGICAL OBSERVATIONS

Humpy back, a disease of Merino sheep in western Queesland, occurs during mustering for shearing. It is usually seen in summer 6-10 weeks after substantial rainfall and is thought to be caused by the ingestion of a toxic plant. The disease is characterised clinically by a short-stepping, stilted gait of the hind limbs, followed by lowering of the head, arching of the back and inability to continue walking. Histopathological examination of 8 cases from 5 properties revealed a Wallerian degeneration of the white matter throughout the length of the spinal cord with the ventral and lateral columns most severely affected. A similar degenerative change was seen in the posterior cerebellar peduncles of 3 of the sheep. A more severe hind limb incoordination with more extensive degeneration of the white matter of the spinal cord, medulla and cerebellum was seen in a case of humpy back of two years duration. Similar, but much milder, spinal cord lesions were found in apparently unaffected sheep from the same group as the sheep affected with humpy back on 2 properties. Severe myodegeneration of hind limb muscle groups was seen in 3 affected sheep. It was thought to be associated with the long rail journey (1500 km) to the laboratory after the sheep were affected in the field.     

Parasitism of Toxocara canis larvae in Japanese quails by inoculation of the ascarid eggs.

The distribution of T. canis larvae and pathological changes caused by them were studied in Japanese quails orally inoculated with 1,500, 4,000 or 15,000 embryonated eggs. Larvae were distributed mainly in the liver and, to lesser extent, in the muscles, brain, eyes and other organs. The number of larvae varied from 7 to 3,346, and from 1 to 288 in the liver and muscles (breast and legs), respectively. A small number of larvae were also recovered from the heart, gizzard, brain and eyes. In the groups of quails inoculated with 4,000 or 15,000 eggs, small white foci were observed on the surface of the liver 6 or 12 hr after inoculation. Histopathological examinations revealed necrotic lesions, leukocytic infiltration, granuloma and nodular lesions. The pathological changes became more serious with the large size of inoculum and days after inoculation.     

Compressive cervical myelopathy in young Texel and Beltex sheep

BACKGROUND: This investigation was prompted by the referral of increasing numbers of young Texel and Beltex rams with ataxia and weakness, or wobbler syndrome. HYPOTHESIS: The study aims were to describe the clinical and pathologic findings in affected sheep. ANIMALS: The animals evaluated in this study included 7 Texel sheep (6 male and 1 female) and 3 Beltex sheep (2 male and 1 female) referred from pedigree flocks. Typically, the sheep were 15-18 months of age at referral. METHODS: Diagnostic investigations included radiographic and computed tomographic (CT) myelography followed by gross postmortem and histopathologic examinations. RESULTS: Clinical findings typical of cervical spinal cord compression were present in all sheep but varied in severity. Myelography confirmed dorsal spinal cord compression in the region of C6-C7. No bony abnormalities were identified as described in cases of canine and equine wobbler syndrome. Postmortem examinations revealed discrete, smooth, nodular to polypoid projections of adipose tissue apparently prolapsing through the dorsolateral intervertebral space at C6-C7 and causing localized spinal cord compression. Histopathology of the nodules confirmed that they were composed of well-differentiated adipocytes typical of fatty tissue. Spinal cord lesions were similar in all sheep with marked Wallerian degeneration at the site of compression and mild Wallerian degeneration present cranial and caudal to the lesion. CONCLUSIONS AND CLINICAL IMPORTANCE: The findings of this study suggest a novel cervical myelopathy in these sheep breeds caused by the presence of fatty nodules encroaching into the dorsal vertebral canal at C6-C7. Additional investigations are required to establish the etiology and possible hereditary risk factors for this unique clinicopathologic syndrome.     

Cerebellar abiotrophy and segmental axonopathy: two syndromes of progressive ataxia of Merino sheep

Findings of a study of 39 sheep with progressive ataxia from 14 farms in the Yass district of New South Wales are described. Microscopic lesions in 25 sheep, 3.5 to 6 years of age, diagnosed as having clinical cerebellar disease, consisted of an apparent primary loss of cerebellar Purkinje neurons, and glial cell accumulation. It is suggested that this previously unreported disorder may be an hereditary cerebellar abiotrophy of Merino sheep. A further 14 sheep, 1 to 4 years of age, had distinguishable clinical signs referable to a spinal cord lesion with widespread segmental axonal ballooning, or "spheroids", in the white matter of the brain and spinal cord. It is suggested that these sheep have a unique form of neuroaxonal dystrophy, described here as segmental axonopathy, and that this is likely to be the same condition described previously as Murrurindi disease (Hartley and Loomis 1981).     

Chronic cervical compressive myelopathy in horses: patterns of astrocytosis in the spinal cord

The distribution and morphology of fibrous astrocytes in the cervical spinal cord of normal horses and horses with chronic compressive myelopathy were demonstrated using immunohistochemical staining for glial fibrillary acidic protein. In the spinal cord from normal horses, astrocytes with stellate cell bodies and short processes were irregularly distributed in grey matter. In the white matter, their cell bodies were small and angular in areas adjacent to grey matter and larger and more stellate-shaped in the subpial area. Astrocyte processes were fine, and evenly distributed in a predominantly radial pattern in transverse sections of cord. Gliosis was marked in the spinal cords of horses with cervical compressive myelopathy. In the grey matter at the level of compression astrocytes were often enlarged and rounded, with short, blunt processes, but the gliosis was generally mild. In the white matter, gliosis was obvious in areas of nerve fibre swelling and degeneration at the level of compression and in areas of ascending and descending Wallerian degeneration. The fine radial pattern of astrocyte fibres was replaced by a dense, irregular arrangement. Gliosis persisted in the cords of chronically affected horses after active nerve fibre degeneration had subsided. The areas of gliosis coincided with the areas of Marchi staining for degenerating myelin and with areas of myelin loss in osmium tetroxide post-fixed tissue. Histological observations were consistent with astrocytes replacing areas of extracellular space that remained after nerve fibre degeneration. it is concluded that astrocytic gliosis is a prominent and persistent alteration of the spinal cord of horses with chronic cervical compressive myelopathy.     

Observations of the sheath extension of the third stage, infective larvae of Trichostrongylus rugatus

The length of the sheath extension of third stage (L(3)), infective larvae of Trichostrongylus rugatus is reported. The total length and length of the sheath extension of L(3) recovered from the faeces of sheep originating from two localities in South Australia were measured. The total length of larvae was 615-722 microm and the length of the sheath extension was 46-56 microm (mean 51.5). The larvae of T. rugatus comprised up to 72% of the larvae recovered. Worm free sheep were infected with larvae from the two localities and L(3) were recovered following culture of faeces from these experimentally infected animals. L(3) measured 640-746 microm in total length with a sheath extension of 46-56 microm (mean 51.4). Adult nematodes recovered from gastro-intestinal tracts were identified as T. rugatus. The length of the sheath extension used in conjunction with the total length is a characteristic that enables confident differentiation of infective larvae of T. rugatus from other Trichostrongylus species infecting sheep in southern Australia and Haemonchus contortus.     

Cutaneous habronemiasis in horses and domestic donkeys (Equus asinus asinus)

Cutaneous habronemiasis in 15 horses and 5 donkeys is described. The lesions were distributed in many parts of the body involving the medial canthus, shoulder and pectoral regions, knee and fetlock joints, abdominal wall and prepuce. Some animals had more than one lesion. The lesions were ulcerative and filled with soft light red granulation tissue. When curretted, the deeper layers revealed a dense fibrous tissue with calcified foci. Close examination of the lesions showed that the superficial layer of this dense fibrous tissue contained small caseated and necrotic foci. The same features prevailed in lesions involving the muscular areas, but the deeper layers consisted of a dense granuloma with no evidence of cicatrization. Curretted material digested in potassium hydroxide revealed fragments of larvae of the nematode suggestive of Draschia or Habronema. The histopathological changes were severe and comprised: necrotic foci in a dense fibrous stroma infiltrated with eosinophils, macrophages and few giant cells. Sections of the larvae surrounded by eosinophils were encountered in lesions of the muscular areas. Curretting and excision of the lesion were effective and produced complete healing of the wound by scar tissue formation.     

Structural and biochemical changes in a spinal myelinopathy in twelve English foxhounds and two harriers

Degenerative lesions in the spinal cord white matter of 12 English Foxhounds and two Harriers between 3 and 6 years old were associated with a diet composed mainly of ruminant stomachs. Lesions were present throughout the length of the spinal cord and were more severe in ventral and lateral columns than in dorsal columns. Degenerate fibers were accompanied by astrocytic proliferation. Changes suggestive of a primary myelinopathy included vacuolated myelin sheaths around apparently intact axons and thick-thin transitions in myelin sheath thickness. Mixed sensory and motor peripheral nerves and muscle histochemical fiber type profiles appeared normal. Similarities were noted with the changes described in subacute combined degeneration of the spinal cord in human beings, a neuropathy caused by methionine and methylation deficiency in patients with vitamin B12 deficiency. Mean serum methionine levels were significantly lower (P greater than 0.01) and mean liver methionine synthetase levels were significantly greater (P greater than 0.01) in affected dogs restored to a balanced diet than in age-matched controls maintained on the balanced diet. The elevated methionine synthetase levels possibly reflected compensatory reactions to the associated dietary change.     

Susceptibility of Rocky Mountain bighorn sheep and domestic sheep to pneumonia induced by bighorn and domestic livestock strains of Pasteurella haemolytica.

Bighorn sheep were inoculated intratracheally with suspensions of nonhemolytic Pasteurella haemolytica biotype T (10(12) organisms) unique to wild bighorns, with beta-hemolytic P. haemolytica biotype T (10(12) organisms) isolated from clinically normal domestic sheep or intradermally with half a dose of a cattle vaccine containing P. haemolytica biotype A (10(5) organisms). The bighorn strain caused lobar necrotizing bronchopneumonia whereas both domestic livestock strains precipitated fatal septicemia and fibrinous bronchopneumonia. The serotypes given were T3, T4, T15 and A1 and these were recovered from lung lesions and other organs. In three trials, domestic sheep were inoculated intratracheally with suspensions of bighorn sheep pneumonic lungs, and two concentrations of the P. haemolytica bighorn strain (10(4) and 10(12) organisms). One of these sheep was inoculated intrabronchially. The domestic sheep experienced a transient fever and elevated white blood cell counts. After six days, none of the sheep had lung lesions and inoculated organisms could not be recovered. It is suggested that bighorn sheep are very susceptible to P. haemolytica from domestic livestock and should not be allowed in contact with sheep or cattle.     

Leukoencephalomyelopathy in specific pathogen-free cats

Investigations were carried out on 8 specific pathogen-free cats (5 male and 3 female) from a colony experiencing "outbreaks" of progressive hind limb ataxia in 190 of 540 at-risk animals ranging from 3 months to 3 years old. These studies identified moderate to severe bilateral axonal degeneration within white matter regions of the cervical, thoracic, and lumbar spinal cord and in the white matter of the cerebral internal capsule and peduncle, in the roof of the fourth ventricle and inferior cerebellar peduncle, and in the external arcuate and pyramidal fibres of the medulla. There were varying degrees of accompanying microgliosis, astrocytosis, and capillary hyperplasia. Such a clinicopathologic syndrome, termed feline leukoencephalomyelopathy, has previously been described in cat colonies in Britain and New Zealand, although its etiology has not been determined. The degenerative nature of the lesions and their bilateral distribution suggest possible nutritional, metabolic, or toxic causes. Although these findings provide circumstantial evidence that the exclusive feeding of a gamma-irradiated diet of reduced vitamin A content is associated with the development of the neuronal lesions, further tissue micronutrient and antioxidant analysis will be required to support this hypothesis.     

Hepatic lesions caused by migrating larvae of Ascaris suum in chickens

Group A consisted of chickens infected with a single dose of Ascaris suum and group B of chickens infected with two successive doses. At days 1, 3, 7, 14 and 21 after the first or second infection dose, six chickens from each group were sacrificed. In both groups, larvae were recovered from the livers on days 1, 3, and 7 and lungs on days 3 and 7. No larvae were detected in chickens on day 14. Clear white lesions were noticed only on the livers from chickens of group B at day 7 but had disappeared at day 14. A comparison with group B showed mild histological changes that developed relative to the livers from group A.     

Equine herpesvirus type 1 (EHV-1) myeloencephalopathy: a case report

An outbreak of neurological disease occurred in a well-managed riding school. Ataxia and paresis were observed in several horses, five of which became recumbent and were euthanized. Post-mortem analysis revealed scattered haemorrhages along the spinal cord, that were reflected by multiple haemorrhagic foci on formalin-fixed sections, with the thoracic and lumbar segments being the most affected. Pathohistologically, perivascular mononuclear cuffing and axonal swelling, especially in the white matter, were evident. Parallel to the course of disease, alterations in myelin sheets and activation of astrocytes and microglial cells were also observed. Virological findings confirmed an acute equine herpesvirus type 1 infection and virus was isolated from the spinal cord of a 26-year-old mare.     

Unusual manifestation of hepatic encephalopathy in two Irish wolfhound siblings

In hepatic encephalopathy the brain lesions are usually characterised by polymicrocavitation, preferentially in the white matter, and the occurrence of Alzheimer type II cells. This paper describes an unusual manifestation of hepatic encephalopathy in two Irish wolfhound siblings in which the white matter was not involved predominantly. Both puppies had developed progressive neurological disturbances and signs of blindness. Histologically, there were widespread spongiform changes in the neuropil and fibre bundles interspersed within the grey matter, and there were some neuronal vacuoles. In both animals, the regions of the brain mainly affected were the nucleus caudatus, amygdala, cerebellar nuclei, mesencephalon, thalamus, hypothalamus and medulla oblongata. An astrogliosis characterised by Alzheimer type II-like cells was also observed. Electron microscopy revealed a splitting of the myelin sheath. No infectious agents such as rabies virus, canine distemper virus or prion proteins were detected. The main findings in the portal regions of the liver consisted of a dilatation of the lymphatic vessels and increased numbers of small arteries, indicating that a portosystemic shunt was the probable cause of the spongiform brain lesions.