scholarly journals Spontaneous poisoning by Sida carpinifolia (Malvaceae) in horses

2017 ◽  
Vol 37 (9) ◽  
pp. 926-930 ◽  
Author(s):  
Daniele M. Bassuino ◽  
Guilherme Konradt ◽  
Matheus V. Bianchi ◽  
Matheus O. Reis ◽  
Saulo P. Pavarini ◽  
...  
Keyword(s):  
Neurodegenerative Disorder ◽  
Neurological Diseases ◽  
Clinical Signs ◽  
Lectin Histochemistry ◽  
Lysosomal Storage ◽  
Con A ◽  
Indolizidine Alkaloids ◽  
The Central Nervous System ◽  
Progressive Weight Loss ◽  
Gross Lesions

ABSTRACT: Sida carpinifolia poisoning causes a chronic neurodegenerative disorder associated with lysosomal storage by indolizidine alkaloids (swainsonine). The epidemiological, clinical, pathological and lectin histochemistry findings of an outbreak of natural poisoning by S. carpinifolia in horses in Rio Grande do Sul state, Brazil, are described. Five horses from a total of 15 that were kept on native pasture with large amounts of S. carpinifolia presented during 90 days clinical signs of progressive weight loss, incoordination, stiff gait and ramble, in addition to exacerbated reactions and locomotion difficulty after induced movement. Four horses died, and one of them was submitted for necropsy. At necropsy, no significant gross lesions were observed. Histological findings observed in the central nervous system were characterized by swollen neurons with cytoplasm containing multiple microvacuoles; these abnormalities were more severe in the thalamus, hippocampus, cerebellum and pons. Using lectin histochemistry, the pons and hippocampus sections stained positive for commercial lectin Con-A, sWGA and WGA. This study aimed to detail S. carpinifolia poisoning in horses to be included in the differential diagnoses of neurological diseases of horses.

scholarly journals Pathological findings in fetuses of goats and cattle poisoned by Sida carpinifolia (Malvaceae)

2012 ◽  
Vol 32 (3) ◽  
pp. 227-230 ◽  
Author(s):  
Pedro M.O. Pedroso ◽  
Edson Moleta Colodel ◽  
Anderson Luiz Seitz ◽  
Gabriel L.F. Correa ◽  
Mauro Pereira Soares ◽  
...  
Keyword(s):  
Neurological Diseases ◽  
Clinical Signs ◽  
Lectin Histochemistry ◽  
Purkinje Neurons ◽  
Pancreatic Acinar Cells ◽  
Renal Tubules ◽  
Pathological Findings ◽  
Lysosomal Storage ◽  
Follicular Cells ◽  
Thyroid Follicular Cells

In Brazil, the consumption of Sida carpinifolia by livestock has been associated with neurological diseases linked to lysosomal storage disorders. This paper describes the pathological findings in two caprine fetuses from dams that were experimentally poisoned with S. carpinifolia. The goats were orally dosed with 10 and 13g/kg of a paste of green chopped S. carpinifolia for 30 days and were observed for an additional 15 days period after the last dosage with the plant; thereafter they were euthanized and necropsied. The dams showed only slight clinical signs. The study also includes the findings in one bovine fetus from a naturally S. carpinifolia poisoned cow which showed mild incoordination, generalized tremors, staggering, and frequent falls. The cow was euthanized and necropsied. While there were no significant histopathological changes in the goats, in the cow vacuolation of Purkinje neurons of the cerebellum, pancreatic acinar cells, and thyroid follicular cells were observed. The main microscopic changes observed in the caprine and bovine fetuses were vacuolation in the epithelium of renal tubules, thyroid follicular cells, and Purkinje neurons of the cerebellum. Transmission electron microscopy of sections from CNS of the cow and its fetus revealed vacuoles containing fine granular material surrounded by membrane. Lectin-histochemistry of CNS sections from goat fetuses marked lightly to sWGA lectins, WGA, and Con-A.

Pathology of Angiostrongylus cantonensis infection in two model avian hosts

Parasitology ◽  
2020 ◽  
pp. 1-4
Author(s):  
Barbora Fecková ◽  
Priyanka Djoehana ◽  
Barbora Putnová ◽  
Michaela Valašťanová ◽  
Michaela Petríková ◽  
...  
Keyword(s):  
Low Dose ◽  
Natural Infection ◽  
Clinical Signs ◽  
French Polynesia ◽  
Angiostrongylus Cantonensis ◽  
High Dose ◽  
Wide Range ◽  
The Central Nervous System ◽  
Gross Lesions ◽  
Natural Pest Control

Abstract Angiostrongylus cantonensis causes severe neurological disorders in a wide range of warm-blooded animals, including several avian species. A laboratory isolate of A. cantonensis originating from French Polynesia, genotyped as clade 2, was used to assess the effect of experimental infection in chicken and Japanese quail. Low dose groups of birds were infected orally by 100 L3 larvae, high dose groups by 1500 L3 larvae and the birds in the third group were fed three infected snails, mimicking a natural infection. Clinical signs during the first week after infection, haematology, biochemistry, gross lesions and histology findings were used to assess the pathology of the infection. Some of the infected birds showed peripheral eosinophilia, while mild neurological signs were seen in others. No larvae were observed in serial sections of the central nervous system of infected birds 1 week after infection and no major gross lesions were observed during necropsy; histopathology did not reveal lesions directly attributable to A. cantonensis infection. Our results suggest that galliform birds are not highly susceptible to A. cantonensis infection and open a question of the importance of Galliformes in endemic areas as natural pest control, lowering the number of hosts carrying the infective larvae.

scholarly journals Mannosidosis in Galloway Calves

1985 ◽  
Vol 22 (6) ◽  
pp. 548-551 ◽  
Author(s):  
D. H. Embury ◽  
I. V. Jerrett
Keyword(s):  
Lysosomal Enzyme ◽  
Lysosomal Enzymes ◽  
Lysosomal Storage ◽  
Normal Tissues ◽  
Liver And Kidney ◽  
The Central Nervous System ◽  
Gross Lesions ◽  
Renal Tubular ◽  
Histologic Changes ◽  
The Brain

Mannosidosis was diagnosed in four stillborn Galloway calves and an autolyzed full-term fetus from experimental matings of carrier animals. Gross lesions were moderate internal hydrocephalus, and pallor and enlargement of the liver and kidneys and arthrogryposis. Histologic changes in the central nervous system of each calf were marked foamy vacuolation of the cytoplasm of neurones in the cerebral cortex, thalamus and brainstem, and vacuolation of the Purkinje cells of the cerebellum. Spheroids were common throughout the brain and there was also consistent severe foamy cytoplasmic vacuolation of renal tubular epithelial cells and hepatocytes. The activities of α-mannosidase, the lysosomal enzyme whose activity is deficient in mannosidosis, and activities of five other lysosomal enzymes were compared in brain, liver, and kidney tissues of three mannosidosis-affected calves and normal calf tissues. Tissues from the affected calves had a marked deficiency of α-mannosidase activity compared with the normal tissues; the greatest deficiency was in the liver (99%) and brain (98%). Activities of the other lysosomal enzymes were elevated in the affected tissues compared with normal. Mannosidosis is a lysosomal storage disease that results from a defect in glycoprotein metabolism and affects man,18 Angus and Angus-related breeds of cattle, such as Murray greys,12,21 and the cat.4 The congenital disease is caused by an inherited deficiency of the lysosomal enzyme α-mannosidase,14 and is inherited in an autosomal recessive manner. Mannosidosis was recently reported in a number of aborted and stillborn Australian Galloway calves3 from an experimental breeding trial. This is more detailed account of the histological and biochemical results obtained during the trial.

scholarly journals Intoxication by Astragalus garbancillo var. garbancillo in llamas

2020 ◽  
Vol 32 (3) ◽  
pp. 467-470
Author(s):  
Raul E. Marin ◽  
Juan F Micheloud ◽  
Nilda D. Vignale ◽  
Eduardo J. Gimeno ◽  
Donal O’Toole ◽  
...  
Keyword(s):  
High Performance ◽  
Storage Disease ◽  
Clinical Signs ◽  
Lysosomal Storage Diseases ◽  
Clinical History ◽  
Lysosomal Storage ◽  
Cell Degeneration ◽  
Nervous Disease ◽  
Indolizidine Alkaloids ◽  
Axonal Spheroids

Lysosomal storage diseases are inherited and acquired disorders characterized by dysfunctional lysosomes. Intracytoplasmic accumulation of undegraded substrates leads to impaired cellular function and death. Several plant species are toxic to livestock because of the presence of indolizidine alkaloids, including swainsonine, which cause a storage disease. Swainsonine-induced nervous disease (i.e., locoism) of sheep and cattle is well recognized in several parts of the world, particularly in the western United States and in parts of Australia. Spontaneous intoxication by Astragalus garbancillo var. garbancillo was suspected in a group of 70 llamas ( Lama glama) in Jujuy Province, northwestern Argentina. The animals grazed an area dominated by stands of A. garbancillo var. garbancillo. Clinical signs were staggering, ataxia, hypermetria, and progressive weight loss. The clinical course in individual animals was ~50 d. The main microscopic changes were Purkinje cell degeneration, necrosis, and loss, associated with intracytoplasmic vacuolation, meganeurite formation, and Wallerian degeneration. Specific positive labeling for ubiquitin was observed in axonal spheroids. Composite leaf and stem samples of A. garbancillo var. garbancillo analyzed by high-performance liquid chromatography contained 0.03% swainsonine. Based on the microscopic lesions, clinical history, and plant analysis, a diagnosis was made of storage disease caused by consumption of swainsonine-containing A. garbancillo var. garbancillo.

scholarly journals Streptococclcs Suis Infection in Swine: A Retrospective Study of 256 Cases. Part II. Clinical Signs, Gross and Microscopic Lesions, and Coexisting Microorganisms

1994 ◽  
Vol 6 (3) ◽  
pp. 326-334 ◽  
Author(s):  
Rachel Y. Reams ◽  
Lawrence T. Glickman ◽  
Daniel D. Harrington ◽  
H. Leon Thacker ◽  
Terry L. Bowersock
Keyword(s):  
Escherichia Coli ◽  
Retrospective Study ◽  
Pasteurella Multocida ◽  
Bacterial Culture ◽  
Clinical Signs ◽  
Animal Disease ◽  
Diagnostic Laboratory ◽  
Serotype 1 ◽  
The Central Nervous System ◽  
Gross Lesions

A retrospective study of 256 cases of naturally acquired Streptococcus suis infections in swine submitted to the Indiana Animal Disease Diagnostic Laboratory from 1985 to 1989 was undertaken to describe the clinical signs, lesions, and coexisting organisms associated with S. suis serotypes 1–8 and 1/2. Infected pigs generally had clinical signs and gross lesions referable to either the respiratory system or to the central nervous system (CNS), but not both. Neurologic signs were inversely related to gross lesions in the respiratory tract ( R2 = −0.19, P = 0.003), as were respiratory signs and gross lesions in the CNS ( R2 = −0.19, P = 0.003). Suppurative bronchopneumonia was the most common gross lesion observed (55.2%, overall). Fibrinous and/or suppurative pleuritis, epicarditis, pericarditis, arthritis, peritonitis, and polyserositis were also reported. In 68% of the pigs, other bacteria in addition to S. suis were isolated. Escherichia coli (35.0%) and Pasteurella multocida (30.0%) were the most commonly recovered bacterial agents. Mycoplasma and viral agents were identified less often, and their role in the development of streptococcosis was difficult to assess. In pigs infected with serotypes 2–5, 7, 8, and 1/2, suppurative meningitis with suppurative or nonsuppurative encephalitis, suppurative bronchopneumonia, fibrinopurulent epicarditis, multifocal myocarditis, and cardiac vasculitis were the most common microscopic lesions observed, whereas pigs infected with serotype 1 generally presented with suppurative meningitis and interstitial pneumonia. Microscopic lesions were morphologically similar among serotypes and were also similar to those reported with other pyogenic bacteria. The distribution of clinical signs and the gross and microscopic lesions in pigs infected with S. suis varied among serotypes. However, these differences were not statistically significant and could not be used to distinguish between the various serotypes. These findings suggest that in pigs infected with S. suis, suppurative or fibrinopurulent inflammation in brain, heart, lungs, and serosae predominates and that bacterial culture is needed to confirm a diagnosis of streptococcosis in swine and to differentiate this disease from those caused by other pyogenic bacteria.

Palliative care in non-malignant neurological disease

2019 ◽  
pp. 619-636
Keyword(s):  
Parkinson’S Disease ◽  
Palliative Care ◽  
Parkinson's Disease ◽  
Multiple System Atrophy ◽  
Neurodegenerative Disorder ◽  
Neurological Diseases ◽  
Urogenital Dysfunction ◽  
Jakob Disease ◽  
The Central Nervous System ◽  
Incomplete Bladder Emptying

This chapter covers the palliative care aspects of non-malignant neurological diseases, including multiple sclerosis, Parkinson’s disease, motor neurone disease, multiple system atrophy, progressive supranuclear palsy, and Creutzfeldt–Jakob disease. MS is a disease characterized by inflammation and demyelination affecting the central nervous system and ultimately injury and gliosis. Parkinson’s disease (PD) is the commonest neurodegenerative disease after Alzheimer’s disease, with an estimated incidence of 2/1000. It affects just under 1% of people over the age of 65 years. PD is probably not one disease but several with common clinical features. Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by Parkinsonian features, plus autonomic dysfunction in the form of orthostatic hypotension, and/or urogenital dysfunction in the form of incontinence and incomplete bladder emptying. At times it can also include cerebellar symptoms. It is not hereditary, and affects adults usually in the fourth or fifth decade. Post-mortem studies of patients diagnosed with PD indicate that 10–25% had multiple system atrophy.

scholarly journals Wobbly syndrome in an Africa pygmy hedgehog (Atelerix albiventris): neuropathological and immunohistochemical studies

2019 ◽  
Vol 49 (1) ◽  
Author(s):  
Letícia Batelli de Oliveira ◽  
Matheus Vilardo Lóes Moreira ◽  
Willian Henrique de Magalhães Santos ◽  
Líslie Caroline Oliveira Stuart ◽  
Maria Dolors Pi Castro ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous Tissue ◽  
Axonal Degeneration ◽  
Clinical Signs ◽  
Proteolipid Protein ◽  
Genetic Origin ◽  
The Central Nervous System ◽  
Gross Lesions ◽  
Immunohistochemical Studies ◽  
Myelin Proteolipid

ABSTRACT: A three-year-old female African pygmy hedgehog (Atelerix albiventris), born and domiciled in Brazil, presented apathy, prostration, and difficulty to stay standing. Its parents were siblings but did not present clinical signs related to this condition. As its clinical condition worsened, the animal was euthanized and referred for necropsy. No gross lesions were found in the central nervous system (CNS). Histologically, there was vacuolation with axonal degeneration in the white matter of the CNS and in peripheral nervous tissue. The Kluver-Barrera (KB) stain confirmed demyelination in vacuolated areas. Immunohistochemistry using several neural markers confirmed astrocytosis and microgliosis associated with vacuolated areas. In addition, there was a mild decrease in the immuno intensity of myelin proteolipid protein (PLP) in these areas. These results suggest a genetic origin of the present demyelination, which resulted in the wobbly syndrome described in this report.

scholarly journals Spontaneous poisoning of goats by the plant Ipomoea sericophylla (Convolvulaceae) in Brazil – a case report

2011 ◽  
Vol 80 (2) ◽  
pp. 235-239 ◽  
Author(s):  
Fábio de S. Mendonça ◽  
Joaquim Evêncio-Neto ◽  
Raquel F. de Albuquerque ◽  
David Driemeir ◽  
Lázaro M. Camargo ◽  
...  
Keyword(s):  
Clinical Signs ◽  
Acinar Cells ◽  
Lectin Histochemistry ◽  
Pancreatic Acinar Cells ◽  
Positive Staining ◽  
Lysosomal Storage ◽  
Thyroid Cells ◽  
Axonal Spheroids ◽  
Renal Tubular Cells ◽  
Semi Arid Region

The aim of this study was to report a neurological disease in goats caused by the plant I. sericophylla. The epidemiology, clinical signs, histological findings and the results of the lectin histochemistry analysis of a nervous cells and epithelial cells are also reported. Five goats that remained with neurological signs were examined in more detail. Two goats were necropsied. Histological lesions consisted of neurons with thin cytoplasm vacuolation, presence of axonal spheroids and vacuolation in pancreatic acinar cells, thyroid folliculars cells, hepatocytes and renal tubular cells. On lectin-histochemical analysis, cerebellar cells, pancreatic acinar cells and follicular thyroid cells showed positive staining for Concanavalia ensiformis, Triticum vulgaris, succinylated Triticum vulgaris and Lens culinares, which indicate the storage of α-D-mannose, α-D-glucose, β-D-N-acetyl-glucosamine, and acetyl-neuraminic acid. It is concluded that I. sericophylla is an important toxic plant that causes lysosomal storage disease in goats at semi-arid region of Pernambuco, Brazil.

scholarly journals Experimental poisoning of goats by Ipomoea carnea subsp. fistulosa in Argentina: a clinic and pathological correlation with special consideration on the central nervous system

2012 ◽  
Vol 32 (1) ◽  
pp. 37-42 ◽  
Author(s):  
Elvio E. Ríos ◽  
Luciana A. Cholich ◽  
Eduardo J. Gimeno ◽  
María G. Guidi ◽  
Ofelia C. Acosta de Pérez
Keyword(s):  
Clinical Signs ◽  
Head Movements ◽  
High Dose ◽  
Nociceptive Response ◽  
Lysosomal Storage ◽  
Ipomoea Carnea ◽  
Withdrawal Reflex ◽  
Abnormal Posture ◽  
The Central Nervous System ◽  
Incomplete Reaction

Ipomoea carnea subsp. fistulosa, aguapei or mandiyura, is responsible for lysosomal storage in goats. The shrub contains several alkaloids, mainly swansonine which inhibits lysosomal α-mannosidase and Golgi mannosidase II. Poisoning occurs by inhibition of these hydrolases. There is neuronal vacuolation, endocrine dysfunction, cardiovascular and gastrointestinal injury, and immune disorders. Clinical signs and pathology of the experimental poisoning of goats by Ipomoea carnea in Argentina are here described. Five goats received fresh leaves and stems of Ipomoea. At the beginning, the goats did not consume the plant, but later, it was preferred over any other forage. High dose induced rapid intoxication, whereas with low doses, the course of the toxicosis was more protracted. The goats were euthanized when they were recumbent. Cerebrum, cerebellum, medulla oblongata, pons and colliculi, were routinely processed for histology. In nine days, the following clinical signs developed: abnormal fascies, dilated nostrils and abnormal postures of the head, cephalic tremors and nystagmus, difficulty in standing. Subsequently, the goats had a tendency to fall, always to the left, with spastic convulsions. There was lack in coordination of voluntary movements due to Purkinje and deep nuclei neurons damage. The cochlear reflex originated hyperreflexia, abnormal posture, head movements and tremors. The withdrawal reflex produced flexor muscles hypersensitivity at the four legs, later depression and stupor. Abnormal responses to sounds were related to collicular lesions. Thalamic damage altered the withdrawal reflex, showing incomplete reaction. The observed cervical hair bristling was attributed to a thalamic regulated nociceptive response. Depression may be associated with agonists of lysergic acid contained in Ipomoea. These clinical signs were correlated with lesions in different parts of the CNS.

Lysosomal Storage Disease Caused by Sida carpinifolia Poisoning in Goats

2000 ◽  
Vol 37 (2) ◽  
pp. 153-159 ◽  
Author(s):  
D. Driemeier ◽  
E. M. Colodel ◽  
E. J. Gimeno ◽  
S. S. Barros
Keyword(s):  
Purkinje Cells ◽  
Granular Cell ◽  
Ultrastructural Changes ◽  
Lysosomal Storage ◽  
Histochemical Analysis ◽  
Pancreatic Cells ◽  
Liver And Pancreas ◽  
The Central Nervous System ◽  
Gross Lesions ◽  
Membrane Bound

A neurologic disease characterized by ataxia, hypermetria, hyperesthesia, and muscle tremors of the head and neck was observed for 2 years in a flock of 28 Anglo-Nubian and Saanen goats on a farm with 5 ha of pasture. Six newborns died during the first week of life, and five abortions were recorded. The predominant plant in the pasture was Sida carpinifolia. The disease was reproduced experimentally in two goats by administration of this plant. Three goats with spontaneous disease and the two experimental animals were euthanatized and necropsied. No significant gross lesions were observed. Fragments of several organs, including the central nervous system, were processed for histopathology. Small fragments of the cerebellar cortex, liver, and pancreas of two spontaneously poisoned goats and two experimentally poisoned goats were processed for electron microscopy. Multiple cytoplasm vacuoles in hepatocytes, acinar pancreatic cells, and neurons, especially Purkinje cells, were the most striking microscopic lesions in the five animals. Ultrastructural changes included membrane-bound vacuoles in hepatocytes, Kupffer cells, acinar pancreatic cells, Purkinje cells, and the small neurons of the granular cell layer of the cerebellum. Paraffin-embedded sections of the cerebellum and pancreas were submitted for lectin histochemical analysis. The vacuoles in different cerebellar and acinar pancreatic cells reacted strongly to the following lectins: Concanavalia ensiformis, Triticum vulgaris, and succinylated Triticum vulgaris. The pattern of staining, analyzed in Purkinje cells and acinar pancreatic cells coincides with results reported for both swainsonine toxicosis and inherited mannosidosis.

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