“Neuronopathy” and “pseudolipidosis” in Aberdeen‐Angus calves

Whittem, J. H.; Walker, D.

doi:10.1002/path.1700740205

Cited by 75 publications

(23 citation statements)

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“…These cellular changes were similar to those reported previously in cattle, 16 goats, 7,13,19 sheep, 33 and ponies 25 poisoned by S. carpinifolia. Similar lesions were also reported in cases of poisoning by plants that contain the alkaloid swainsonine, 1,3,4,9,10,12,20,22 as well as in cases of inherited alpha-mannosidosis in cattle, 21,39 humans, 29 domestic cats, 5,27 and the guinea pig. 28 As in the inherited disease, in the acquired form of alpha-mannosidosis, the alkaloid swainsonine inhibits lysosomal enzyme alpha-mannosidase, 6,8,11,14 resulting in the storage and excretion of partially impaired oligosaccharides.…”

Section: Discussionsupporting

confidence: 69%

Spontaneous Lysosomal Storage Disease Caused by Sida carpinifolia (Malvaceae) Poisoning in Cattle

Furlan

Lucioli

Veronezi

et al. 2009

Veterinary Pathology

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Abstract. Clinical and pathologic findings for the spontaneous poisoning by Sida carpinifolia in cattle are described in this study. A survey on field cases of S. carpinifolia in cattle was carried out on farms of Alto Vale do Itajaí, State of Santa Catarina, southern Brazil. Sixteen affected animals were clinically evaluated and 9 were subjected to postmortem examination. The main clinical signs consisted of marching gait, alert gaze, head tremors, and poor growth. Histologic and ultrastructural lesions consisted of vacuolization and distension of neuronal perikarya, mainly from Purkinje cells, and of the cytoplasm of acinar pancreatic and thyroid follicular cells. Clinical signs and lesions varied from mild to severe. Improvement of the clinical signs was observed in cattle after a period of up to 90 days without consuming the plant; however, residual lesions, mainly characterized by axonal spheroids and absence of Purkinje neurons in some areas of the cerebellum, were observed in these cases. It is concluded that the natural chronic consumption of S. carpinifolia was the etiologic cause of storage disease in cattle in this study.

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Section: Discussionsupporting

confidence: 69%

Spontaneous Lysosomal Storage Disease Caused by Sida carpinifolia (Malvaceae) Poisoning in Cattle

Furlan

Lucioli

Veronezi

et al. 2009

Veterinary Pathology

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“…About 10% of New Zealand stocks of Aberdeen Angus cattle are heterogeneous carriers of an abnormal MANB gene. Homozygous cattle have reduced levels of MANB activity and show a similar progressive ataxic disease to that seen in humans (Whittem and Walker, 1957).…”

Section: Animal Modelsmentioning

confidence: 99%

“…A deficiency of MANB causes the lysosomal storage disease, α-mannosidosis, which is an autosomal recessive disorder in humans (Ockerman, 1967), cattle (Whittem et al, 1957), domestic cats (Burditt et al, 1980) and guinea pigs (Crawley et al, 1999). The inherited disorder is characterized by massive accumulation of undegraded oligosaccharides, resulting in varied neural, skeletal and immune defects, and extension of the lysosomes in most cell types.…”

Section: α-Mannosidosismentioning

confidence: 99%

Recent progress in lysosomal α-mannosidase and its deficiency

Sun

Wolfe²

2001

Exp Mol Med

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Lysosomal α-mannosidase (EC 3.2.1.24) is a major exoglycosidase in the glycoprotein degradation pathway. A deficiency of this enzyme causes the lysosomal storage disease, α-mannosidosis, which has been described in humans, cattle, domestic cats and guinea pigs. Recently, great progress has been made in studying the enzyme and its deficiency. This includes cloning of the gene encoding the enzyme, characterization of mutations related to the disease, establishment of valuable animal models, and encouraging results from bone marrow transplantation experiments.

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“…23,24,27 Neuropathological findings include vacuolated neurons, glia, and endothelial cells throughout the brain and spinal cord; Purkinje cell loss; and myelin deficiency of the central and peripheral nervous systems. 27 Feline alpha-mannosidosis Spontaneously occurring AMD has been reported in cats, [28][29][30][31][32][33][34] cattle, [35][36][37][38][39][40][41][42] and guinea pigs, [43][44][45] and a knockout mouse has been created. 46 Interestingly, disease can also be induced by ingestion of the indolizidine alkaloid swainsonine, which is found in locoweed plants.…”

Section: Alpha-mannosidosismentioning

confidence: 99%

A review of gene therapy in canine and feline models of lysosomal storage disorders

Bradbury¹,

Gurda²,

Casal³

et al. 2015

Human Gene Therapy Clinical Development

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Lysosomal storage disorders (LSDs) are inherited diseases that result from the intracellular accumulation of incompletely degraded macromolecules. The majority of LSDs affect both the peripheral and central nervous systems and are not effectively treated by enzyme replacement therapy, substrate reduction therapy, or bone marrow transplantation. Advances in adeno-associated virus and retroviral vector development over the past decade have resurged gene therapy as a promising therapeutic intervention for these monogenic diseases. Animal models of LSDs provide a necessary intermediate to optimize gene therapy protocols and assess the safety and efficacy of treatment prior to initiating human clinical trials. Numerous LSDs are naturally occurring in large animal models and closely reiterate the lesions, biochemical defect, and clinical phenotype observed in human patients, and whose lifetime is sufficiently long to assess the effect on symptoms that develop later in life. Herein, we review that gene therapy in large animal models (dogs and cats) of LSDs improved many manifestations of disease, and may be used in patients in the near future.

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“Neuronopathy” and “pseudolipidosis” in Aberdeen‐Angus calves

Cited by 75 publications

References 0 publications

Spontaneous Lysosomal Storage Disease Caused by Sida carpinifolia (Malvaceae) Poisoning in Cattle

Spontaneous Lysosomal Storage Disease Caused by Sida carpinifolia (Malvaceae) Poisoning in Cattle

Recent progress in lysosomal α-mannosidase and its deficiency

A review of gene therapy in canine and feline models of lysosomal storage disorders

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