A neurological locomotor disorder in sheep grazing Stachys arvensis

OBJECTIVE: To describe the clinical signs and pathology of a neurological locomotor disorder in sheep associated with ingestion of Stachys arvensis. DESIGN: Field observations and laboratory examinations. PROCEDURE: Clinical and pathological examinations were performed on sheep with suspected S arvensis intoxication. FIELD OBSERVATIONS: Merino sheep in a flock on the southwestern slopes of New South Wales developed a neurological disorder after grazing S arvensis. Affected animals had pelvic limb paresis and a proprioceptive deficit. When forced to exercise they stumbled and collapsed. Recovery following removal from the plant was slow. Many deaths were associated with the outbreak. RESULTS: Affected sheep developed a mild degenerative myelopathy and peripheral neuropathy. Deficiencies of vitamins A and E were also observed in the affected flock. CONCLUSION: Grazing S arvensis is sometimes associated with a neurological locomotor disorder in sheep.     

Neurological Manifestations of Niemann-Pick Disease Type C in Cats

Seven Domestic shorthair cats with a lysosomal storage disorder analogous to human Niemann-Pick disease type C, from a breeding colony were studied to characterize the neurological manifestations of this disorder. Affected cats were identified by means of liver biopsies at 4 to 6 weeks of age. Neurological examinations were performed at 2 week intervals from the onset of clinical signs. All cats displayed signs referrable to the cerebellum, with a subtle intention tremor noticed initially at 8 to 12 weeks of age; the disease was rapidly progressive. The tremor became more pronounced, menace response was lost, and severe dysmetria and ataxia developed. Three cats also had signs referrable to other areas of the central nervous system. Cats died or were euthanized between 12 and 43 weeks of age. Pathological findings included accumulation of substrate within neurons throughout the central nervous system, and axonal spheroid formation. The clinical and pathological findings in these cats are comparable to those in the human form of the disease.     

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.     

Trypanosomiasis by Trypanosoma vivax in cattle in the Brazilian semiarid: Description of an outbreak and lesions in the nervous system

An outbreak of trypanosomiasis by Trypanosoma vivax is reported in the semiarid of Paraíba, Northeastern Brazil from May to August 2002. Sixty-four cows out of 130 were affected; 11 died and the other recovered after treatment with diminazene aceturate. Affected animals had fever, anemia, weight loss, hypoglycemia, increased serum levels of aspartate aminotransferase and, in nine cows, nervous signs. All cows with nervous signs died; six of them recovered after treatment, but the disease relapsed. Six cows aborted and one delivered a calf that died immediately after parturition. Thirty-two out of 100 calves were affected and five died. Nervous signs were not observed in the calves. Gross lesions were thickening of the meninges, enlarged lymph nodes and prominent white pulp of the spleen. The main histological lesion was meningoencephalitis and malacia in the brain of cows with nervous signs. No antibodies against trypanosomes were found in 33 blood samples collected before the outbreak in the affected farm and in 29 samples collected at the same time in two other neighbor farms. Until January 2003, all 89 animals tested had antibodies against T. vivax, suggesting the occurrence of sub clinical infections in cattle without clinical signs. Only two out of 85 serum samples collected on April 2004 were positive for T. vivax antibodies. Data obtained suggested that the semiarid region is non-endemic for trypanosomiasis and that disease occurred due to introduction of the parasite in a susceptible population after an apparent rise in the Tabanus spp. population.     

Suspected dimethoate toxicity in cattle

Dimethoate, an organophosphorus insecticide, was the suspected cause of toxicosis in a group of young cattle grazing on pasture that had been sprayed 6 weeks before the onset of clinical signs. Affected animals had primarily nicotinic signs, such as muscle twitching, stiffness, weakness and paralysis, though muscarinic signs, such as diarrhea, salivation and pollakiuria, were also observed. Whole blood acetylcholinesterase activity was depressed in 3 animals. The atypical clinical syndrome and poor response to treatment with atropine and other anticholinergics may have been due to coexistent hypomagnesemia.     

Congenital erythropoietic protoporphyria in a Limousin calf

Bovine congenital erythropoietic protoporphyria is an uncommon genetic defect in Limousin and Blonde d'Aquitaine cattle that is characterized by severe photosensitization. Clinical signs include intense pruritus and exudative dermatitis involving the face, pinnae, and dorsal aspect of the thorax. Affected cattle have hematologic and serum biochemical values within reference ranges, and their teeth are normochromic. Definitive diagnosis of bovine congenital erythropoietic protoporphyria is accomplished by genetic testing. Affected cattle should be sent to a terminal market.     

Naturally occurring and experimental Stachys arvensis (staggerweed) toxicity in lambs in New Zealand

Stachys arvensis (staggerweed) is a common, widely distributed weed of cultivated and waste land with the potential to intoxicate sheep. Two naturally occurring outbreaks of suspected staggerweed toxicity in the lower North Island were investigated. Affected lambs had been recently moved onto staggerweed-contaminated Brassica spp. crops. In total, 150/1,200 (13%) lambs developed hindlimb paresis, a fine generalised muscular tremor, and hunched posture. When forced to move, many became recumbent. Most lambs recovered within 48 h of removal from staggerweed, although a few developed clinical signs again when transported 2–3 weeks later. Grossly, affected lambs had large amounts of staggerweed plant material and seeds within the rumen. Histopathology showed mild, multifocal degeneration of the white matter tracts of the central nervous system (CNS), most commonly in the ventral funiculi of the spinal cord, and acute, mild to moderate, multifocal degeneration of skeletal muscles. Creatine kinase (CK) activity in serum was mildly to markedly elevated in affected lambs. In a feeding trial, ten 10-month-old Romney lambs were randomly assigned to equal treatment and control groups. Treated lambs were drenched with a liquid extract of staggerweed once daily for 7 days. Three of five treated lambs developed mild exercise intolerance, and 1/5 displayed mild paresis of the hindlimbs, slightly crouched hindlimb stance, and shortened gait, on days 6 and 7. Histologically, 4/5 treated lambs had degeneration in white matter tracts of the CNS, indistinguishable from those seen in the lambs in the outbreak, and in 1/5 lambs there was scattered regeneration of skeletal muscle. CK activity in serum in treated lambs was not significantly higher than that in control lambs. None of the control lambs developed significant clinical signs, histological changes or increases in CK activity in serum. The clinical signs and lesions observed in both the outbreaks and feeding trial were similar to those previously described in studies in Australia, with the exception that myodegeneration was more prominent in the outbreaks in New Zealand. Further characterisation of the pathogenesis of staggerweed toxicity and its potential role as a food safety hazard will be facilitated through identification of the toxic principle(s).     

Neurotoxicity in calves induced by the plant, Nierembergia hippomanica Miers var. violacea Millán in South Africa

The plant Nierembergia hippomanica var. violacea has been incriminated in field outbreaks of neurotoxicity in calves in the Free State Province. Hepatotoxicity and electrocardiogram (ECG) deviations were induced in a sheep dosed with 5 g/kg dried plant material on four consecutive days. A calf dosed with 2.5 g/kg dried plant material, on two consecutive days, did not show overt clinical changes. Voluntary ingestion of approximately 30 g/kg fresh flowering plants by a second calf resulted in nervous signs characterized by chewing motions, protrusion of the tongue, dysphagia, hypermetria, ataxia, paresis and lateral recumbency. Salivation, dehydration and cardiac irregularities completed the clinical picture. Clinical chemistry changes revealed muscle damage and increased serum urea and creatinine concentrations indicative of kidney involvement. This is the first confirmed outbreak of Nierembergia hippomanica var. violacea intoxication of stock in South Africa.     

A Brief Review of Bovine Coccidiosis in Western Canada

Coccidiosis of beef cattle, in both its enteric and nervous forms, seen in feedlots in Western Canada is discussed. Cases of coccidiosis accompanied by nervous signs, occasionally up to 30% of those affected enterically, are most common during the coldest winter months. The pathogenesis of the nervous form of the disease is unknown. Clinical management of disease outbreaks using various chemotherapeutics is described. The importance of using anticoccidial drugs before the onset of clinical signs in cattle in contact with sick animals is discussed.     

Multifocal subacute necrotizing encephalomyelopathy in a Simmental calf

Multifocal subacute necrotizing encephalomyelopathy affects Simmental and Simmental-cross cattle. First clinical signs are ataxia and hind limb paresis. The characteristic gross lesion is bilaterally symmetrical, grey, depressed to cavitated foci involving nuclei in the brainstem. The caudal olivary nucleus is consistently involved. The etiology of the syndrome remains unknown.     

Nervous disease associated with coccidiosis in young cattle

Four cases are described of nervous disease associated with coccidiosis in young cattle. Prodromal nystagmus, ventromedial strabismus, sternal or lateral recumbency with contortions of the head and neck, near normal interictal periods and palpable proctitis were common findings. Differentiation from other nervous disorders in young cattle and the pathogenesis of the nervous signs associated with coccidiosis are discussed. It is suggested that the clinical picture is sufficiently distinctive to allow a diagnosis to be made on clinical grounds alone.     

Hereditary encephalomyelopathy and polyneuropathy in an Alaskan husky

An Alaskan husky puppy was examined for a neurologic disease which began at six weeks of age with generalised paresis that progressed resulting in recumbency by 18 weeks. Thoracic limbs primarily exhibited lower motor neuron signs that included distal muscle atrophy and persistent elbow and carpal flexion that resisted manual extension. Pelvic limb signs primarily exhibited upper motor neuron and general proprioceptive deficits, but also included lower motor neuron signs. Abnormal vocalisation suggested a laryngeal paresis. Histopathologic lesions included a diffuse axonopathy and secondary demyelination in the nerves of the limbs and larynx and a similar bilaterally symmetrical degeneration in the spinal cord white matter suggestive of a dying back axonopathy. In addition, a degenerative process was present in nuclei in the brain stem and cerebellum. Recognition of this disease through clinical and pathologic examination in other related Alaskan Huskies suggested an autosomal recessive inherited disorder.     

Performance of clinical signs to detect bluetongue virus serotype 8 outbreaks in cattle and sheep during the 2006-epidemic in The Netherlands

The performance of clinical signs as a diagnostic test for the detection of BTV-8 outbreaks during the 2006-epidemic in The Netherlands was evaluated by constructing and analysing receiver operating characteristic (ROC) curves. The area under the ROC curve of the BT-associated clinical signs in cattle was 0.77. An optimal efficient test (maximising both sensitivity and specificity) in cattle herds combined a sensitivity (Se) of 67% with a specificity (Sp) of 72%, comprising the following clinical signs: ulcerations and/or erosions of oral mucosa or erosions of lips/crusts in or around nostrils or oedema of the nose or hyperaemic/purple coloration of tongue, tongue protrusion or coronitis or apathy/tiredness or muscle necrosis, stiffness of limbs or loathing or refusal to move, prostration or torticollis or anoestrus. The area under the ROC curve of the BT-associated clinical signs in sheep was 0.81. The optimal efficient test in sheep flocks combined a Se of 76% with a Sp of 72%, comprising the following clinical signs: ulcerations of oral mucosa or serous nasal discharge or erosions/ulceration of tongue mucosa or hypersensitivity of the skin or muscle necrosis, stiffness of limbs or coronitis or grinding of teeth or salivation or weakness/paresis.     

Locomotor effects in sheep of alkaloids identified in Australian Tribulus terrestris

Fresh, mature, ungrazed Tribulus terrestris plant material was subjected to a standard alkaloid extraction procedure. The extract was fractionated by thin layer chromatography (TLC) and high performance liquid chromatography (HPLC). Two major alkaloid fractions were demonstrated. These fractions were identified by means of TLC, ultraviolet spectrofluorimetry (UVS) and HPLC, as the beta-carboline indoleamines harmane and norharmane. The extractable alkaloid content was determined to be 44 mg/kg dry matter. Synthetic harmane and norharmane were administered subcutaneously to sheep at a dose rate of 54 mg/kg. Both compounds caused similar nervous effects. The main effect observed was limb paresis, which in some sheep was body side blased. The clinical signs observed in the experimental sheep were consistent with those described for naturally occurring cases of Tribulus terrestris staggers. It was proposed that harmane and norharmane accumulate in tryptamine-associated neurones of the central nervous system, during months of tribulus ingestion, and gradually interact irreversibly with a specific neuronal gene DNA sequence.     

Localized diseases of the bovine brain and spinal cord

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.     

Pathology of velogenic Newcastle Disease virus infection in turkeys.

Twenty-four 4-week-old poults, free from Mycoplasma meleagridis and M. gallisepticum, were inoculated with a velogenic viscerotropic strain of Newcastle disease virus. Clinical signs (gasping, coughing, and dyspnea) developed 4-5 days postinoculation, continued until nervous derangement appeared, and then (usually 3 days after initial clinical signs appeared) declined in severity. Prominent nervous signs were paresis and paralysis of the extremities, with pronounced head-shaking. The most constant gross lesions detected involved the airsacs. The abdominal sacs of a few poults contained a large accumulation of yellowish, cheesy exudate and there was cloudiness of the thoracic airsacs of all inoculated poults. A few turkeys had tracheitis with some catarrhal exudates and casts in the lower part of the tracheal lumen. Congestion of lepto-meningeal vessels usually correlated with the severity of the nervous signs. The histologic lesions were characterized by both degenerative and proliferative changes with predominantly mononuclear cell and heterophil infiltrations throughout the body. The obvious lesion seen in the recovery stage of the disease was proliferation of lymphofollicular nodules in the parenchymatous organs.     

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.     

Iatrogenic brainstem injury during cerebellomedullary cistern puncture

Cerebrospinal fluid collection is fundamental to the investigation of central nervous system disorders although it carries potential risks. Herein we report the clinical signs and magnetic resonance (MR) imaging findings associated with needle injury to the brainstem during cerebellomedullary cistern puncture in four dogs. Three dogs were nonambulatory tetraparetic with cranial nerve deficits and one dog had unexplained left thoracic limb paresis. In MR images, there were conspicuous T2 hyperintensities in the myelencephalon in all dogs. In T2* gradient echo images, the lesions were hypointense in two dogs with multiple cranial nerve deficits, and hyperintense in another dog. One dog was euthanized due to sudden neurologic deterioration 12 days later, one died shortly after MR imaging, and a third was euthanized due to concurrent cervical spondylomyelopathy. The fourth dog recovered gradually. Diagnosis was confirmed histopathologically in one dog and was presumptive based on clinical signs and MR findings in three dogs. None of the dogs with cranial nerve deficits recovered, only the one dog with left thoracic limb paresis and concurrent syringomyelia.     

Parturient paresis and hypocalcemia in ruminant livestock

Parturient paresis (hypocalcemia) is most likely to affect dairy cattle around the time of parturition. It causes progressive neuromuscular dysfunction and flaccid paralysis. Older dairy cows, cows with a history of parturient paresis during a previous lactation, high-producing cows, and cows from the Jersey and Guernsey breeds are at highest risk for developing parturient paresis. Nonparturient hypocalcemia may also occur and is related to events other than parturition, such as severe stress, that temporarily overwhelm the mechanisms of calcium homeostasis. Beef cattle, sheep, and goats are affected less frequently by hypocalcemia than are dairy cows. Because these species are not as stressed for milk production as dairy cattle, nonparturient hypocalcemia makes up a higher proportion of cases in nondairy ruminants. Clinical signs of hypocalcemia in beef cattle, sheep, and goats tend toward hyperesthesia and tetany rather than the classic flaccid paralysis that occurs in dairy cattle with parturient hypocalcemia. Prompt and effective treatment of hypocalcemia helps to reduce the incidence of secondary complications, such as muscle damage or mastitis. The standard treatment regimen of 500 ml of 23 per cent calcium gluconate, administered intravenously, will elicit a favorable response in approximately 75 per cent of recumbent cows within 2 hours of treatment. Relapses following successful initial therapy are common and may be prevented in part by supplementation of intravenous treatment with an additional 500 ml of 23 per cent calcium gluconate administered subcutaneously. Proper nursing care following treatment speeds recovery and reduces the incidence of secondary complications owing to hypocalcemia.     

GENERALISED GLYCOGENOSIS IN BRAHMAN CATTLE

Generalised glycogenosis was diagnosed in Brahman cattle on 4 Queensland properties on the basis of clinical observations and pathological and biochemical findings. The disease presented as a problem of ill-thrift and poor growth rate in calves which eventually showed nervous signs. Histologically there was vacuolation in the cells of the central nervous system, heart and muscular tissues. Biochemical assay of liver and blood mononuclear cells demonstrated a deficiency of alpha-glucosidase. Parents of affected calves had approximately half the alpha-glucosidase activity of that found in normal cattle.