Delayed phalaris grass toxicosis in sheep and cattle

A phalaris grass (Phalaris caroliniana) caused neurologic signs and lesions in cattle and sheep. The sheep were hyperexcitable and uncoordinated, with severe muscle twitching, stiff gait, and head nodding. The cattle were thin, nervous, and ataxic. One feature of chronic phalaris toxicosis in these cases was onset of signs weeks or months after removal of the animals from the forage.     

Experimental evidence that tryptamine alkaloids do not cause Phalaris aquatica sudden death syndrome in sheep

The acute toxicity for sheep of 3 alkaloids that occur in Phalaris acquatica was examined by intravenous and oral administration. The lowest tested dose rates that produced clinically observed signs were, for 5-methoxy dimethyltryptamine, 0.1 mg/kg body weight intravenously and 40 mg/kg orally; for gramine, 10 mg/kg intravenously and 500 mg/kg orally; and for hordenine, 20 mg/kg intravenously and 800 mg/kg orally. All induced the clinical signs observed in the nervous form of phalaris toxicity, but none induced the cardiac, sudden death, syndrome.     

Mechanisms underlying Phalaris aquatica "sudden death" syndrome in sheep

Twenty outbreaks of Phalaris aquatica "sudden death" syndrome in sheep were investigated between 1981 and 1991. Four were confirmed and one was suspected, to be a cardiac disorder; 5 were confirmed and 3 were suspected, to be a polioencephalomalacic disorder; the aetiology of the remaining 7 outbreaks could not be determined. Potentially toxic levels of hydrocyanic acid (20 to 36 mg/100 g) were measured in the 3 toxic phalaris pastures tested. The measurement of potentially toxic levels of nitrate nitrogen (2920 micrograms/g) in toxic phalaris pastures by others, was noted. It is suggested that phalaris "sudden death" syndrome could have as many as 4 different underlying mechanisms, and that these might reflect the presence in the plant of a cardio-respiratory toxin, a thiaminase and amine co-substate, cyanogenic compounds, and nitrate compounds.     

Tryptamine alkaloid toxicosis in feedlot sheep

Tryptamine alkaloid toxicosis (Phalaris staggers) was diagnosed in feedlot sheep. Clinical signs of toxicosis, which were exacerbated by excitement, included gait abnormalities, muscular tremors, nystagmus, and convulsions. An estimated 8% of the most severely affected lambs had clinical signs of toxicosis. Gross lesions detected in the brain of affected lambs consisted of focal gray-green discoloration in the brain stem and thalamus; these areas had microscopic evidence of intraneuronal pigment accumulation. Brain specimens obtained at slaughter indicated that 60% of the lambs had lesions consistent with tryptamine alkaloid toxicosis. Tryptamine alkaloids were found in low concentrations in the feed. Lambs exposed to these feeds had higher death losses than those that were not exposed to the feeds. Cobalt concentration in the feed was higher than that previously reported to be associated with Phalaris staggers.     

Abnormal turning behaviour, GABAergic inhibition and the degeneration of astrocytes in ovine Tribulus terrestris motor neuron disease

OBJECTIVE: To observe the clinical signs of sheep affected by Tribulus terrestris motor neuron disease, to ascertain their response to striatal dopamine reducing drugs, and to examine their brains and spinal cords for microscopic changes. PROCEDURES: Twenty-eight sheep displaying well developed clinical signs of the disorder were observed. Twenty-two of these and 22 normal sheep were then randomly allocated to three groups and treated with diazepam, chlorpromazine, or xylazine. The time that it took an animal to return to a standing position following drug administration was recorded. The brain and complete spinal cord were removed from each of the other six affected sheep and fixed in formalin. Brains were sectioned throughout at 5 mm intervals and spinal cords at 10 mm intervals. All tissues were paraffin embedded and examined by light microscopy. A few samples were examined by electron microscopy. RESULTS: Clinical signs included postural asymmetry with a right:left body-side dominance within the group of 50:50, unequal flaccid paresis in the pelvic limbs, extensor muscle atrophy and adduction of the weaker pelvic limb, and concurrent abduction of the stronger. Forward motion followed either a fixed left or right hand curved trajectory, the sheep no longer being able to choose which. Twelve animals intermittently displayed rotational behaviour that involved loss of postural balance without locomotor activation. The administration of diazepam, chlorpromazine, or xylazine caused limb paresis and sedation, with affected sheep being slower than normal sheep by factors of 8, 3 and 2 respectively, to return to a standing position. There were scattered areas of mild Wallerian degeneration throughout the spinal cord, and in both the brain and the cord there were small numbers of degenerate astrocytes containing novel cytoplasmic pigment granules. CONCLUSIONS: Affected sheep had a dysfunction in the control of directional change and this provides a new insight into the normal mechanism for 'turning' in quadrupeds. Directional change requires a functional asymmetry or lateralisation within the upper motor neuron to accommodate a difference in the rate of forward progression of each body side and, simultaneously, a lateral shift of the centre of gravity. The sensitivity of affected sheep to diazepam is consistent with a pre-existing elevation in GABAergic neuronal inhibition, probably as a result of a reduction in glutamatergic neuronal excitation. The cytoplasmic pigment found in degenerate astrocytes was novel and its presence in the brain nuclei known to contribute to turning behaviour could have aetiological significance. The motor output of the basal ganglia in Tribulus neurotoxicity appeared to be excessively inhibitory to the pelvic limb extensor muscles and was asymmetric, causing fixation of the turning posture but not locomotor activation. An intoxication of specific purine sensitive, glutamate releasing astrocytes, located in nuclei controlling turning, was suspected.     

Neurological disorder in dairy cattle associated with consumption of beer residues contaminated with Aspergillus clavatus.

A neurological syndrome in dairy cattle associated with consumption of moldy beer residues is described. The disease occurred on 1 farm in late June 2001, during winter. Six heifers and 1 cow out of 45 cattle were affected during a 3-week period. The affected animals died spontaneously or were euthanized approximately 2-14 days after the onset of clinical signs. The clinical signs were characterized by flaccid paralysis and gait abnormalities. Clinical signs were more pronounced after exercise and included stiff and unsteady gait, knuckling at the fetlocks of the hind limbs, frequent falling, inability to rise, muscular tremors, especially of the head and the hindquarters, and drooling. Main necropsy findings included degenerative and necrotic changes of the larger medial muscle groups of the hindquarters, i.e., adductor, pectineus, quadriceps femoris, rectus femuris, sartorius, semimembranosus, semitendinosus, and vastus medialis, and of the forequarters, including pectoralis descendens, pectoralis ascendens, and transversus pectoralis. The main histologic findings consisted of degenerative and necrotic neuronal changes (chromatolysis) of varying severity and extent affecting selected nuclei of the brainstem and neurons of the ventral horns of the spinal cord. Similar microscopic lesions were observed in the neurons of the spinal cord of 1 experimental sheep force-fed for 35 days with 1 kg/day of the same batch of foodstuff that was originally fed to the cattle. Coarse white or gray lumps, interpreted as mycelia, were observed in the beer by-product. Aspergillus clavatus was the dominant fungus isolated. Deaths ceased after the consumption of beer residue was discontinued. Recovery from illness was observed in 1 animal. The diagnosis was based on epidemiological data, clinical signs, necropsy findings, histological lesions, dosing trial, and mycology. A similar condition caused by consumption of barley by-products, sprouted wheat, corn sprouts, and beetroot screenings contaminated with A. clavatus has been reported in cattle and sheep worldwide.     

Staggers in sheep associated with the ingestion of Tributes terrestris

The history of an unusual locomotory disturbance of sheep is traced from its first recognition in 1937 through to the most recent outbreak in 1981-83. The condition occurred only at certain times and in restricted areas of the central and northern slopes districts of New South Wales. Outbreaks were repeatedly associated with drought periods during which sheep grazed large areas of Tribulus terrestris for many months at a time. Many thousands of sheep were affected, but the prevalence varied greatly between flocks. The course of the disease was characterised by a slowly developing, irreversible, asymmetrical, weakness of the hindlimbs. The clinical signs suggested that a lesion of the thoraco-lumbar spinal cord region was present. The macroscopic and microscopic examination of the nervous and musculoskeletal systems failed to demonstrate abnormalities which would account for the clinical signs. Haematological, biochemical and toxicological test results supported the concept of a neuromuscular disease process being present, but failed to indicate its aetiology.     

Diagnosis of the nervous form of Maedi-Visna infection with a high frequency in sheep in Castilla y Leon, Spain

Between 1997 and March 2004, the nervous form, or visna, of maedi-visna infection was diagnosed in 71 of 1631 sheep (4.35 per cent) examined in the Castilla y León region of Spain, of which 634 had shown nervous signs. The presence of the virus was confirmed by immunohistochemistry and in some cases by pcr on frozen-thawed or paraffin-embedded tissue samples. The main clinical signs were hindleg ataxia and paresis, but blindness or nystagmus were also observed. Thirty-three of the affected sheep (46.5 per cent) were two years old or younger. The affected sheep showed variable degrees of a non-suppurative meningoencephalitis, and immunohistochemistry identified positive cells in all cases, with no relation to the intensity of the inflammatory lesion.     

Spina bifida with associated malformations of the central nervous system in Dorper-cross sheep

Abstract

CASE HISTORY: In 2008, six lambs within a flock of Dorpercross sheep were born with musculoskeletal and neurological disease. Clinical signs included hindlimb weakness, and urinary incontinence.

CLINICAL FINDINGS: All lambs had focal, inverted areas of alopecic skin over the caudal sacrum, and short, often kinked tails. Four affected lambs were subject to euthanasia, and necropsied. On gross examination, the arches of sacral vertebrae were absent, and spinal nerves and meninges were adherent to the overlying subcutis. Other gross lesions included narrow, elongated skulls, herniation of the occipital lobes into the caudal fossas, hydrocephalus, and syringomyelia. One lamb had coning of the cerebellar vermis, but cerebellar herniation through the foramen magnum was not identified.

DIAGNOSIS: Spina bifida, with associated malformations of the central nervous system.

CLINICAL RELEVANCE: Examination of breeding records suggested either an autosomal recessive or partially penetrant autosomal dominant pattern of inheritance. Because of the associated tail lesions it is proposed that the pathogenesis of this syndrome involves a defect in development of the tail bud (secondary neurulation), that tethering of the spinal cord resulted in the clinical signs, and abnormal pressure of the cerebral spinal fluid resulted in the defects in the skull and brain.     

A variant form of neuronal ceroid lipofuscinosis in American bulldogs

Neuronal ceroid lipofuscinoses (NCLs) are inherited neurodegenerative diseases characterized by accumulations of autofluorescent lipopigments within cells of the nervous system. Nine related American Bulldogs demonstrated dysmetria in all limbs and paraparesis. Nonambulatory tetraparesis was observed only in the later stages of the disease. The clinical signs developed between 1 and 3 years of age and were slowly progressive over several years, which is inconsistent with most reports in other breeds. Results from blood tests for 8 different lysosomal storage diseases on 4 affected and 6 related but unaffected dogs were negative. Four affected dogs were euthanized and histopathologic examinations showed diffuse accumulations of periodic acid-Schiff-positive inclusions in neurons and axonal spheroids along the entire neuraxis and retinae. The most severe lesions were in the brainstem proprioceptive nuclei and spinal cord, consistent with clinical signs. The storage material was autofluorescent and immunohistochemically positive for products of lipid peroxidation. Ultrastructural analysis was consistent with NCL. Pedigree analysis supports an autosomal-recessive mode of inheritance. NCL has not been previously reported in the American Bulldog and these findings suggest a variant form of the canine disease.     

A survey of more than 11 years of neurologic diseases of ruminants with special reference to transmissible spongiform encephalopathies (TSEs) in Greece

The first cases of scrapie were detected in Greece in a flock of sheep in October 1986. All the animals of the affected flock and all sheep in two flocks that were in contact were killed and buried. A systematic investigation of all available cases with signs indicating a neurological disease started in sheep and goats in late 1986, as well as in cattle in 1989. The investigation was based on clinical examination, necropsy or macroscopical examination of the brain and viscera, and histological examination of the brain in all animals except those with coenurosis. Histological examinations of specimens from the spinal cord and other tissues, and if considered necessary bacteriological, toxicological and serological examinations were also carried out. In October 1997, scrapie was diagnosed in sheep of a second flock (a mixed flock of sheep and goats), grazing in a pasture close to the place where scrapie was initially detected. All animals of the second flock were also killed and buried. Diagnosis in the first flock was based on clinical signs and histological lesions, and in the second immunoblotting was also used. Distinctive lesions of scrapie were found in the brain and/or the spinal cord of eight sheep with clinical signs from the two flocks. The lesions were revealed in the brain stem and/or in the cervical spinal cord, and tended to be symmetrical. In one sheep, severe lesions in the cortex of cerebral hemispheres and of the cerebellum were also found. In the brain of two sheep from the second flock the pathological isoform of PrP protein was detected. Despite the eradication scheme applied, scrapie in sheep reappeared after 11 years in a place close to where it occurred initially. This may indicate that the effectiveness of the eradication scheme implemented was not adequate and additional approaches may be needed.     

Key-Gaskell syndrome in a cat in Switzerland

As far as the authors know this is the first case of Key-Gaskell-syndrome being described in Switzerland. The clinical signs of megaoesophagus, anorexia, constipation, dryness of all mucous membranes, reduced tear production, protrusion of the membrana nictitans, mydriasis, regurgitation and bradycardia are pathognomonic and can't be mistaken by any other disease. The subject of the Key-Gaskell-syndrome is a dysfunction of the autonomic nervous system. Histopathological changes are exclusively related to the autonomic nervous system and to neurons of some nuclei in the cranial nerves. Less severe changes can be found in the neurons of the spinal cord or in the dorsal root ganglia. The etiology remains still unclear. There is a relationship to the grass sickness syndrome in horses and to dysautonomia of man and dog.     

Detection and clinical evolution of scrapie in sheep by 3rd eyelid biopsy

The goal of this article was to characterize the clinical evolution of scrapie in naturally affected sheep. Eighteen sheep with scrapie diagnosed by examination of 3rd eyelid biopsy and 12 control ewes were studied throughout the duration of their disease. Diagnosis was confirmed postmortem by histopathologic, immunohistochemical, and Western blot analysis of nervous tissue. Complete clinical examinations were performed every 2 weeks for each animal, of which 3 clinical examinations per animal are reported. Those clinical signs that showed a significant frequency within the corresponding clinical examination were considered representative of each stage of the disease (ie, early, middle, and late). The representative clinical signs for the early stage were hypoesthesia in the limbs, alteration of mental status, and a body condition score <3. Remarkably, hypoesthesia in the limbs was one of the 1st signs appearing during the early clinical stage in the affected animals, even before the appearance of other signs. For the middle stage, representative signs were the same as those for the early stage, together with hyporreflexia in the limbs, cardiac arrhythmia, pruritus/wool loss, and the appearance of the nibbling reflex. Representative clinical signs for the late stage were the same as those for the early and middle stage, together with head tremors, hyperexcitability to external stimuli, ataxia or gait abnormalities, and teeth grinding. On the basis of these results, we propose the calculation of an objective clinical index that allows the differentiation among clinical stages and that could be useful for further studies. The usefulness of 3rd eyelid lymphoid tissue biopsies for sequential clinical studies in naturally scrapie-affected sheep is demonstrated.     

Cerebellar ataxia in sheep grazing pastures infested with Romulea rosea (onion grass or Guildford grass)

There have been anecdotal reports since 1962 of 'staggers' in sheep grazing Romulea rosea infested pastures, but this is the first detailed account. In September 2005, a locomotor disorder developed in 12 of 120 Merino wethers that had grazed R. rosea infested pasture at Albury, New South Wales, over several months. Affected sheep displayed signs that included limb paresis, knuckling over in the fetlocks, fine head tremor, incoordination, and an equilibrium disturbance characterised by frequent falling. The microscopic examination of brain and spinal cord tissues from two affected sheep revealed mild vacuolation, occasional lymphocytic cuffing around blood vessels, mild Wallerian degeneration, and occasional glial cells that contained honey-brown cytoplasmic pigments. The most significant changes were found in the cerebellum, where there were decreased numbers of Purkinje cells, increased numbers of glial cells, scattered vacuoles and occasional swollen axons. Previous reports of cerebellar toxicoses in ruminants have involved goats and cattle and have been associated with the ingestion of six Solanum spp. The Purkinje cell loss in this type of disorder is ultimately extensive and consequently affected animals may survive, but will remain permanently disabled. Aust Vet J 2008;86:354 -356.     

Ovine congenital progressive muscular dystrophy: clinical syndrome and distribution of lesions

The distribution and severity of lesions in the skeletal muscles of 37 Merino sheep with congenital progressive muscular dystrophy (CPMD) are described. An explanation for the clinical signs is offered on the basis of functional defects in regional muscle groups. Lesions in the extensors of the hip, stifle and hock joints and flexors of the digits are primarily responsible for the progressive abnormality of hind limb gait that is characteristic of the clinical syndrome. Lesions in extensors of the elbow and flexors of the shoulder, carpus and digits affected fore limb function in advanced cases. The tendency for some affected sheep to develop ruminal tympany is probably caused by lesions in the diaphragmatic crus. Clinically affected sheep had higher resting and post-exercise concentrations of serum creatine phosphokinase and lactic dehydrogenase than unaffected control sheep. The rise in serum creatine phosphokinase after exercise was greater in affected sheep than in controls. Myotonia was not demonstrated in electromyographic studies in one sheep.     

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.     

脑多头蚴病研究进展

脑多头蚴病是由多头带绦虫的中绦期幼虫脑多头蚴寄生于绵羊、山羊、黄牛、牦牛等有蹄动物的脑及脊髓中引起的一种人兽共患寄生虫病,人可因误食虫卵而感染此病。该病在宿主出现典型临床症状后如果得不到治疗,多以死亡为转归,给畜牧业生产造成了巨大的经济损失。论文就脑多头蚴病的病原学、生活史、流行病学、临床症状、诊断、治疗及免疫预防等方面的研究进展进行了综述。     

An interesting neurologic case in a lovebird (Agapornis fisheri).

The pathogenic agent of proventricular dilatation disease causes a lymphoplasmacytic inflammation of the central peripheral nervous systems. Usually, the splanchnic nerves are affected, with resultant gastrointestinal dysfunction and clinical signs related to this. When the brain, spinal cord, and peripheral nerves are affected, neurologic signs may be present in various degrees. This case emphasizes the importance of necropsy and histopathologic examination in making a diagnosis and treatment.     

Nonsuppurative meningoencephalomyelitis of unknown etiology in mink

A central nervous system disease of mink occurred in three unrelated fur farms in Oregon in September, 1981. Only kits four to five months old were affected. Clinical signs consisted of posterior ataxia progressing to complete posterior paralysis with loss of motor control and sensation. Complete or partial recovery occurred in approximately 1.5 months in most mink. Microscopic lesions consisted of severe nonsuppurative meningoencephalitis and meningomyelitis with vacuolation of the white matter of the brain and spinal cord. Canine distemper virus infection and other recognized causes were ruled out on the basis of clinical signs, history, lesions, or laboratory findings. Experimental inoculations of mink with brain and spinal cord specimens from affected mink failed to reproduce the disease.     

The clinical differentiation of nervous and muscular locomotor disorders of sheep in Australia

SUMMARY Many of the nervous and muscular locomotor disorders that affect sheep throughout Australia are commonly referred to as ‘staggers’ syndromes. The range of clinical signs displayed by sheep suffering these disorders is sufficiently diverse to enable each syndrome to be graded into one of 5 progressive clinical groups. The first group, the limb paresis syndromes, includes the primary myopathies associated with the ingestion of Ixiolaena brevicompta, Malva parviflora, and Trachymene ochracea, as well as selenium and vitamin E disorders, Paroo virus staggers, congenital progressive muscular dystrophy, humpy back, hypocalcaemic muscle weakness, Tribulus terrestris staggers and tetanus . The second group is characterised by limb paresis with knuckling of the fetlocks, and includes the plant-associated toxicities of Romulea rosea, Stachys arvensis, Trachyandra divaricata, and Tribulus micrococcus, together with haloxon toxicity, enzootic ataxia (copper deficiency), and the probably genetic disorders of segmental axonopathy, neuroaxonal dystrophy, and degenerative thoracic myelopathy. Other locomotor disorders that fit more loosely into this group are listerial myelitis (post-dipping staggers), vitamin A deficiency, cervico-thoracic vertebral subluxation, Stypandra glauca toxicity, Ipomoea spp toxicity, ivermectin toxicity, and botulism . The third group, the falling syndromes, includes the probably genetic disorders of thalamic cerebellar neuropathy, cerebellar abiotrophy, and globoid cell leucodystrophy, together with Swainsona spp toxicity . The fourth group, the falling-with-tremors syndromes, includes the plant-associated toxicities of phalaris staggers, perennial rye grass staggers and nervous ergotism (Claviceps paspali) . The fifth group, the convulsive syndromes, includes the polioencephalomalacic entity nardoo fern (Marsilea drummondii) staggers, outbreaks of focal symmetrical encephalomalacia and the tunicaminyluracil toxicities known as annual ryegrass (Lolium rigidum) toxicity, annual beard grass (Polypogon monspeliensis) toxicity, blow away grass (Agrostis avenaceae) toxicity, and water damaged wheat (Triticum aestivum) toxicity . A dichotomous system is presented for the differential diagnosis of these groups of conditions .