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1.
Localized diseases of the bovine brain and spinal cord   总被引：1，自引：0，他引：1  
Localized lesions of the central nervous system do occur in cattle. Those affecting the cranial nerves and focal lesions of the spinal cord are most easily recognized by careful neurologic examination. Once the lesion has been anatomically localized, likely etiologic causes can be pursued. Probably the most common cause of cranial nerve deficits in cattle is listeriosis. Important differential diagnoses include brain and pituitary abscesses and extensions of ear infections. Other possible causes include PEM, TEME, hypovitaminosis A, and several rare, sporadic causes. In young cattle, spinal trauma and vertebral body abscesses are the most common causes of progressive paresis resulting from spinal cord lesions. Congenital abnormalities must be considered in the differential diagnoses for very young calves. Non-neurologic conditions, including fractures of the limbs and especially nutritional muscular dystrophy, must be ruled out. In older cattle, compressive neoplasms, most notably lymphosarcoma, are primarily responsible for progressive paresis. Differential diagnosis should include other neurologic conditions such as delayed organophosphate neurotoxicity; early progressive diffuse neurologic diseases such as rabies, pseudorabies, and botulism; plant toxicities; and non-neurologic conditions resulting in recumbency, such as hypocalcemia and musculoskeletal trauma.  相似文献   

2.
SUMMARY: Case records of 450 horses with signs of neurological disease are reviewed. One hundred and nineteen horses with neurological disease due to trauma were examined, of which 60 were due to spinal cord trauma, 47 to brain or cranial nerve trauma and 12 to peripheral nerve trauma. Cervical vertebral fractures/trauma were the most common injury. Basisphenold/basloccipital bone fractures were the most common form of cranial trauma and facial nerve paralysis the most common cranial nerve injury. Eighty-nine horses with neurological disease due to malformation were examined. Cervical vertebral malformation occurred in 83 horses and congenital defects in 6 foals. Neurological disease due to inflammation or infection occurred in 30 horses. The most common disease of this type was meningitis, which occurred in 11 horses and foals. Neoplasms in the CNS caused neurological disease in 8 horses. The final category was miscellaneous neurological disease, which was diagnosed in 204 horses. Diseases in this category included neonatal (28 cases), toxic/metabolic (27 cases), idiopathic (133 cases), degenerative (3 cases) and other neurological diseases (13 cases). The most common condition was idiopathic laryngeal hemiplegia (116 cases).
Where possible, diagnosis relied on a thorough neurological examination with use of ancillary tests in selected cases including rhinolaryngoscopy, radiography, myelography, ophthalmoscopy and cerebrospinal fluid analysis when indicated. In many cases necropsy and histopathological confirmation or diagnosis was necessary.  相似文献   

3.
Spinal trauma can originate from internal or external sources. Injuries to the spinal cord can be classified as either concussive or compressive and concussive. The pathophysiologic events surrounding spinal cord injury include the primary injury (compression, concussion) and numerous secondary injury mechanisms (vascular, biochemical, electrolyte), which are mediated by excessive oxygen free radicles, neurotransmitter and electrolyte alterations in cell membrane permeability, excitotoxic amino acids, and various other biochemical factors that collectively result in reduced SCBF, ischemia, and eventual necrosis of the gray and white matter. Management of acute spinal cord injuries includes the use of a high-dose corticosteroid regimen within the initial 8 hours after trauma. Sodium prednisolone and methylprednisolone, at recommended doses, act as oxygen radical scavengers and are anti-inflammatory. Additional considerations are the stability of the vertebral column, other conditions associated with trauma (i.e., pneumothorax), and the presence or absence of spinal cord compression, which may warrant surgical therapy. Vertebral fractures or luxations can occur in any area of the spine but most commonly occur at the junction of mobile and immobile segments. Dorsal and dorsolateral surgical approaches are applicable to the lumbosacral and thoracolumbar spine and dorsal and ventral approaches to the cervical spine. Indications for surgical intervention include spinal cord compression and vertebral instability. Instability can be determined from the type of fracture, how many of the three compartments of the vertebrae are disrupted, and on occasion, by carefully positioned stress studies of fluoroscopy. Decompression (dorsal laminectomy, hemilaminectomy, or ventral cervical slot) is employed when compression of the spinal cord exists. The hemilaminectomy (unilateral or bilateral) causes less instability than dorsal laminectomy and therefore should be used when practical. The preferred approach for atlantoaxial subluxation is ventral, and the cross pinning, vertebral fusion technique is used for stabilization. Fracture luxations of C-2 are repaired with small plates on the ventral vertebral body. The thoracic and upper lumbar spine is stabilized with dorsal fixation techniques or combined dorsal spinal plate/vertebral body plate fixation. Several methods of fixation can be used with lower lumbar or lumbosacral fractures, including the modified segmental technique and the combined dorsal spinal plate/Kirschner-Ehmer technique.  相似文献   

4.
Spinal cord injury causes obvious clinical deficits early in the course of lesion evolution, but it is commonly observed that recovery can occur spontaneously during a period of days, weeks or even months afterwards. Spinal cord dysfunction arises after injury because of a combination of reversible alterations in the concentration of intra- and extracellular ionic constituents and irreversible tissue destruction. Recovery can therefore occur through re-establishment of the normal microenvironment of the spinal cord, which occurs soon after injury induction, and also by formation of new patterns of central nervous system circuitry. Alterations in circuitry, termed 'plasticity', can occur during the immediate period after injury but apparently continue for many weeks or months. There are differences in the extent and nature of recovery between complete and incomplete experimental spinal cord injuries that illustrate the roles played by reorganisation of intra- and suprasegmental circuitry. Information that is available on mechanisms of spontaneous recovery may aid development of novel therapies for clinical spinal cord injury.  相似文献   

5.
The conventional slaughtering of cattle includes some critical process stages where a carry over of BSE-risk material (brain, spinal cord) on the meat can occur. These processes are captive bolt stunning, cut off the head and first of all sawing the spine lengthways. Alternative stunning methods like electrical stunning or concussion stunning are under investigation, nevertheless they are in the moment no useful alternatives for most of the slaughter houses. The most promising methods available at present for minimising the risk appear to be in manual cattle slaughtering boning the entire carcass, either still warm or refrigerated and in industrial beef cattle slaughtering extraction of the spinal cord by vacuum from the whole carcass followed by conventional sawing or completely sawing out the spine including spinal ganglia. Working processes, including the cutting or exposure of risk material, are a risk for the employer's too. Special protective measures must be taken.  相似文献   

6.
Management of persistent lower urinary tract dysfunction resulting from severe thoracolumbar spinal cord injury can be challenging. Severe suprasacral spinal cord injury releases the spinal cord segmental micturition reflex from supraspinal modulation and increases nerve growth factor concentration in the bladder wall, lumbosacral spinal cord, and dorsal root ganglion, which subsequently activates hypermechanosensitive C‐fiber bladder wall afferents. Hyperexcitability of bladder afferents and detrusor overactivity can cause urine leaking during the storage phase. During urine voiding, the loss of supraspinal control that normally coordinates detrusor contraction with sphincter relaxation can lead to spinal cord segmental reflex‐mediated simultaneous detrusor and sphincter contractions or detrusor‐sphincter dyssynergia, resulting in inefficient urine voiding and high residual volume. These disease‐associated changes can impact on the quality of life and life expectancy of spinal‐injured animals. Here, we discuss the pathophysiology and management considerations of lower urinary tract dysfunction as the result of severe, acute, suprasacral spinal cord injury. In addition, drawing from experimental, preclinical, and clinical medicine, we introduce some treatment options for neurogenic lower urinary tract dysfunction that are designed to: (1) prevent urine leakage arising because of detrusor overactivity during bladder filling, (2) preserve upper urinary tract integrity and function by reducing intravesical pressure and subsequent vesicoureteral reflux, and (3) prevent urinary tract and systemic complications by treating and preventing urinary tract infections.  相似文献   

7.
Tissues from sequential-kill time course studies of bovine spongiform encephalopathy (BSE) were examined to define PrP immunohistochemical labeling forms and map disease-specific labeling over the disease course after oral exposure to the BSE agent at two dose levels. Study was confined to brainstem, spinal cord, and certain peripheral nervous system ganglia-tissues implicated in pathogenesis and diagnosis or disease control strategies. Disease-specific labeling in the brainstem in 39 of 220 test animals showed the forms and patterns observed in natural disease and invariably preceded spongiform changes. A precise temporal pattern of increase in labeling was not apparent, but labeling was generally most widespread in clinical cases, and it always involved neuroanatomic locations in the medulla oblongata. In two cases, sparse labeling was confined to one or more neuroanatomic nuclei of the medulla oblongata. When involved, the spinal cord was affected at all levels, providing no indication of temporal spread within the cord axis or relative to the brainstem. Where minimal PrP labeling occurred in the thoracic spinal cord, it was consistent with initial involvement of general visceral efferent neurons. Labeling of ganglia involved only sensory ganglia and only when PrP was present in the brainstem and spinal cord. These experimental transmissions mimicked the neuropathologic findings in BSE-C field cases, independent of dose of agent or stage of disease. The model supports current diagnostic sampling approaches and control measures for the removal and destruction of nervous system tissues in slaughtered cattle.  相似文献   

8.
Abstract: The diagnosis of neuromuscular diseases can be challenging. The first step is recognition that the disease involves the neuromuscular system (muscle, neuromuscular junction, peripheral nerve, and ventral horn cells of the spinal cord). Many neuromuscular diseases share clinical signs and cannot be distinguished based on clinical examination. Routine laboratory screening, including a CBC, biochemical profile, and urinalysis, can identify some of the most common systemic abnormalities that cause muscle weakness and myalgia, such as hypo‐ and hyperglycemia, electrolyte disorders, or thyroid abnormalities, and may suggest a specific diagnosis, such as diabetes mellitus, hypo‐ or hyperadrenocorticism, renal failure, or hypothyroidism. Increased creatine kinase activity, increased cardiac troponin I concentration, and myoglobinuria are useful in detecting skeletal and cardiac muscle damage. Identification of acetylcholine receptor antibodies is diagnostic for acquired myasthenia gravis. For primary muscle or peripheral nerve diseases, tissue biopsy is the most direct way to determine specific pathology, correctly classify the disease, and determine the course of additional laboratory testing. For example, inflammatory, necrotizing, dystrophic, metabolic, or congenital myopathies require different laboratory testing procedures for further characterization. Many neuromuscular diseases are inherited or breed‐associated, and DNA‐based tests may already be established or may be feasible to develop after the disorder has been accurately characterized. This review focuses on both routine and specialized laboratory testing necessary to reach a definitive diagnosis and determine an accurate prognosis for neuromuscular diseases.  相似文献   

9.
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.  相似文献   

10.
The toxicity of ochratoxin to ruminants.   总被引：1，自引：0，他引：1       下载免费PDF全文
Among the mold toxins the most toxic ochratoxin, ochratoxin A, commonly occurs in many grains, other feedstuffs, and in soil but in low concentrations. The amount required to produce acute toxicity in ruminants makes such occurrences unlikely. Toxic effects are more likely to occur in chronic low-level intoxication. The lethal single oral dose in cattle is high, probably being a few milligrams more than 13 mg/kg. The lethal level produced by repeated feeding to goats was 3 mg/kg. Ochratoxin A occurred in cows milk and urine but only when massive doses were ingested. Abortion or fetal death, though occurring in rodents, are unlikely to be induced in cattle.  相似文献   

11.
Transmissible encephalopathies in animals.   总被引：1，自引：1，他引：0       下载免费PDF全文
Scrapie in sheep and goats is the best known of the transmissible encephalopathies of animals. The combination of maternal transmission of infection and long incubation periods effectively maintains the infection in flocks. A single sheep gene (Sip) controls both experimental and natural scrapie and the discovery of allelic markers could enable the use of sire selection in the control of the natural disease. Studies of experimental rodent scrapie show that neuroinvasion occurs by spread of infection from visceral lymphoreticular tissues along nerve fibers to mid-thoracic cord. The slowness of scrapie is due to restrictions on replication and cell-to-cell spread of infection affecting neuroinvasion and subsequent neuropathogenesis. Probably both stages in mice are controlled by Sinc gene, the murine equivalent of Sip. The glycoprotein PrP may be the normal product of Sinc gene. Posttranslationally modified PrP forms the disease specific "scrapie associated fibrils" and may also be a constituent of the infectious agent. Scrapie-like diseases have been reported in mink and several species of ruminants including cattle. All of them may be caused by the recycling of scrapie infected sheep material in animal feed. The human health implications are discussed.  相似文献   

12.
Animals presented with non-weight-bearing lameness are a diagnostic challenge for the veterinarian. It is extremely important to distinguish between orthopedic and neurologic causes of lameness, because the diagnostic and therapeutic plans can be quite different. Myopathies can be confused with orthopedic disease because of gait abnormalities and associated muscle pain. Common myopathies seen in companion animal medicine include polymyositis, muscular dystrophy, endocrine and infectious myopathies, and myasthenia gravis. Lameness caused by disease of the nerve root or nerve is confused with orthopedic disease because of the disturbances of a nerve's sensory distribution (nerve-root signature) or disruption of the motor innervation. The diseases of the nerve root or nerve discussed are lateralized intervertebral disk disease, spinal cord neoplasia, malignant peripheral nerve sheath tumors, and traumatic neuropathies. The diagnosis of these diseases requires careful attention to the signalment, a complete history, and a thorough physical examination focusing on the neurologic and orthopedic components. Ancillary testing should be selected based on these results and a minimum database. Electrodiagnostic testing, radiography, and advanced imaging may help to localize the lesion more precisely and sometimes to confirm the diagnosis. Surgical exploration and histopathology often provide the definitive diagnosis. These cases of non-weight-bearing lameness are a diagnostic challenge, but when successful resolution can be reached, it is gratifying to the clinician, client, and patient.  相似文献   

13.
Spinal disease in rabbits is most often the result of trauma; however, other causes have been reported including congenital defects and degenerative spinal diseases. Diagnosis of spinal disease is based on history, physical and neurologic examination findings, and imaging. Fractures and luxations of the spine are often apparent on plain radiographs; however, myelography is used to determine if the lesion is causing spinal cord compression that may be amenable to surgical decompression. Unless intervertebral discs are mineralized, they are not visible when viewing plain radiographic images; therefore, myelography may be useful to diagnose spinal cord compression from a herniated disc. Myelography can also define lesions that do not result in a disruption of the osseous vertebral architecture such as tumors and granulomas. In rabbits, myelography is performed when the animal is under general anesthesia and in lateral recumbency. A nonionic iodinated contrast agent is injected into the subarachnoid space, usually at the level of the lumbar spine, to outline the spinal cord and identify cord compressive or disruptive lesions.  相似文献   

14.
Paratuberculosis (Johne's disease) is a chronic infectious disease of ruminants, caused by Mycobacterium avium subspecies paratuberculosis (MAP). Because of its long incubation period, high economic losses, difficulties in diagnosis and possible links to Morbus Crohn in humans, paratuberculosis is one of the most important diseases of ruminants today. An abattoir-based nationwide survey on the occurrence of MAP in the Austrian cattle population was performed using serology (SVANOVIR-ELISA) as well as culture, ZN-stain and IS900-PCR on faeces and lymph node samples. A total of 756 Austrian slaughter cattle were serologically, bacteriologically and molecularbiologically tested for the occurrence of MAP and specific antibodies respectively. Samples were collected following a statistical plan to obtain balanced specimens from the whole country. Nineteen per cent of the animals tested were serological positive, 10.1% gave an inconclusive result and 70.9% showed no specific antibodies against MAP. Only in four individuals MAP could be detected by stain, bacteriology or Polymerase Chain Reaction. The calculated prevalence of 19.0% positive cattle, each representing one farm, showing specific antibodies against MAP is rather high in terms of animal-level but low in herd level prevalence compared with other countries. When this study is compared with a similar study performed in Austria 1999, a significant increase of positive cattle and farms could be seen in Austria.  相似文献   

15.
绵羊脑包虫病是由多头带绦虫（Taenia multiceps）的中绦期幼虫——脑多头蚴（Coenurus cerebralis）引起的一种严重危害羔羊的寄生虫病。脑多头蚴主要寄生于牛羊等反刍动物的脑和脊髓中,病畜出现一系列神经症状,最终导致死亡。介绍绵羊脑包虫病的病例情况、临床症状、病理剖解变化、诊断、手术治疗,分析发病原因,提出了针对脑包虫病的综合防控措施。  相似文献   

16.
Paratuberculosis (Johne's disease) is one of the most important diseases in ruminants today. Its contribution is worldwide and the disease is causing severe financial losses among cattle producers in some countries [Hasanova, L., Pavlik, I., 2006. Economic impact of paratuberculosis in dairy cattle herds: a review. Vet. Med.-Czech. 51, 193–211]. Paratuberculosis is untreatable; diagnosis limited to the early stages of the infection and control of the disease is difficult. The prevalence of serologically positive Austrian cattle farms rose significantly to 19.0% during the past years [Baumgartner, W., Damoser, J., Khol, J.L., 2005. Comparison of two studies concerning the prevalence of bovine paratuberculosis (Johne's disease) in Austrian cattle in the years 1995–1997 and 2002/2003 (Article in German with extended English summary). Vet. Med. Austria/Wien. Tierärztl. Mschr. 92, 274–277]. Based on these findings clinical paratuberculosis in ruminants was declared a notifiable disease in Austria in April 2006.

A survey of the current situation in Austria, the most important parts of the new compulsory measures and their practical implementation and impacts are presented in this short communication.  相似文献   


17.
A degenerative skeletal muscle disease with vascular, neurologic, and renal lesions and a probable familial distribution was identified in 4-20-month-old purebred Gelbvieh cattle. Thirteen affected animals were confirmed from 6 separate beef herds, with a mortality rate of 100%. Clinical signs in affected animals consisted of ataxia, weakness, and terminal recumbency. Gross and histologic muscle lesions were indicative of nutritional myopathy of ruminants, with a lack of myocardial lesions in most cases and only rare myocardial changes in a few animals. Acute to chronic lesions in most large skeletal muscle groups consisted of degeneration, necrosis, regeneration, fibrosis, and atrophy. Fibrinoid necrosis of arterioles was a common feature in multiple tissues. Lesions in the spinal cord white matter and peripheral nerves consisted of degeneration of the dorsal columns and axons, respectively. Changes in the kidneys consisted of chronic interstitial nephritis with fibrosis, hyaline droplet change and tubular epithelial vacuolar change and were most severe in the older calves. Intracytoplasmic myoglobin and iron were demonstrated within the hyaline droplets in degenerate renal cortical tubular epithelial cells. Vitamin E levels were deficient in most (6/7) of the animals tested. Investigation of the pedigree of affected animals revealed a common ancestry for all but 1 of the animals whose parentage could be traced. This investigation suggests that a hereditary metabolic defect, possibly involving antioxidant metabolism, could be responsible for this condition. Renal disease, possibly secondary to myoglobinuria, may be unique to this bovine condition.  相似文献   

18.
To anticipate improvement of a chronically affected animal may be expecting too much because reserve or functional spinal cord tissue may be minimal. An accurate prognosis is sometimes impossible to formulate because the extent of spinal cord damage is not known. Treatment may result only in halting progression of the disease, and even with total relief of spinal cord compression, recovery may be minimal. Animals with minimal neurologic deficits treated early in the course of the disease with adequate decompression and stabilization are more likely to return to function. The goals of treatment for cervical spinal cord compression are decompression and stabilization of the affected area. Adequate stabilization may result in atrophy of the soft tissues and further decompression once stabilization is achieved (see Fig. 3). If stabilization is not provided, adequate decompression of the spinal cord and the nerve roots is essential.  相似文献   

19.
Cartilage-derived retinoic acid-sensitive protein (CD-RAP)/melanoma inhibitory activity (MIA), which appears abundantly in hypertrophic cartilage at the stage of endochondral ossification, is also detected in cerebrospinal fluid (CSF) following spinal cord injury. In this study, the localization of the CD-RAP/MIA molecule in normal tissues of the spine and brain obtained from mice, rats, dogs, cattle and horses was examined using immunohistochemistry with a specific antibody. The positive signals of CD-RAP/MIA were found at nerve cells in the spinal cords of all species and were especially strong at cerebellar Purkinje cells. The results suggested that CD-RAP/MIA included in normal cerebrospinal tissues could be a biomarker associated with tissue injuries, as the molecules might flow into the CSF.  相似文献   

20.
Dogs are comparatively frequently affected by various spontaneously occurring inflammatory and degenerative central nervous system (CNS) conditions, and immunopathological processes are a hallmark of the associated neuropathology. Due to the low regenerative capacity of the CNS a sophisticated understanding of the underlying molecular basis for disease initiation, progression and remission in canine CNS diseases represents a prerequisite for the development of novel therapeutical approaches. In addition, as many spontaneous canine CNS diseases share striking similarities with their human counterpart, knowledge about the immune pathogenesis may in part be translated for a better understanding of certain human diseases. In addition to cytokine-driven differentiation of peripheral leukocytes including different subsets of T cells recent research suggests a pivotal role of these mediators also in phenotype polarization of resident glial cells. Cytokines thus represent the key mediators of the local and systemic immune response in CNS diseases and their orchestration significantly decides on either lesion progression or remission. The aim of the present review is to summarize the growing number of data focusing on the molecular basis of the immune response during spontaneous canine CNS diseases and to detail the effect of cytokines on the immune pathogenesis of selected idiopathic, infectious, and traumatic canine CNS diseases. Steroid-responsive meningitis arteritis (SRMA) represents a unique idiopathic disease of leptomeningeal blood vessels characterized by excessive IgA secretion into the cerebrospinal fluid. Recent reports have given sophisticated insights into the cytokine-driven, immune-mediated pathogenesis of SRMA that is characterized by a biased T helper 2 cell response. Canine distemper associated leukoencephalitis represents an important spontaneously occurring disease that allows investigations on the basic pathogenesis of immune-mediated myelin loss. It is characterized by an early virus-induced up-regulation of pro-inflammatory cytokines with chronic bystander immune-mediated demyelinating processes. Lastly, canine spinal cord injury (SCI) shares many similarities with the human counterpart and most commonly results from intervertebral disk disease. The knowledge of its pathogenesis is largely restricted to experimental studies in rodents, and the impact of immune processes that accompany secondary injury is discussed controversially. Recent investigations on canine SCI highlight the pivotal role of pro-inflammatory cytokine expression that is paralleled by a dominating reaction of microglia/macrophages potentially indicating a polarization of these immune cells into a neurotoxic and harmful phenotype. This report will review the role of cytokines in the immune processes of the mentioned representative canine CNS diseases and highlight the importance of cytokine/cytokine interaction as a useful therapeutic target in canine CNS diseases.  相似文献   

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