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Saulo Petinatti Pavarini – One of the best experts on this subject based on the ideXlab platform.

  • Histiocytic Ulcerative Colitis in an American Staffordshire Terrier.
    Journal of comparative pathology, 2018
    Co-Authors: Fernando Froner Argenta, David Driemeier, S. O. De Souza, L.s. Meirelles, Gustavo Geraldo Medina Snel, C. De Lorenzo, J. Ienes-lima, F. Horn, Saulo Petinatti Pavarini

    Abstract:

    Summary A 9-year-old female American Staffordshire Terrier was presented to a veterinary hospital with diarrhoea, severe prostration, hypothermia, dehydration and anaemia. The dog died 6 days after the first consultation. At necropsy examination the serosa of the large intestine showed a granular appearance and the mucosa was thickened, ulcerated and red, with prominent folding. Histological examination revealed marked inflammatory infiltration of macrophages into the mucosa and submucosa of the large intestine. These cells stained positively by the periodic acid–Schiff reaction. Immunohistochemistry showed marked presence of intracytoplasmic Escherichia coli in the macrophages. Bacteriological examination of intestinal sections yielded E. coli growth and the isolate displayed atypical characteristics when compared with strains associated with previously published cases of histiocytic ulcerative colitis (HUC). The molecular characterization showed that the isolate harboured none of the genes associated with enterotoxigenic E. coli strains and harboured only a limited number of genes associated with extra-intestinal pathotypes. Adherent and invasive E. coli are unlikely to have been involved in the pathogenesis of HUC in the present case. HUC is a rare disease with a predisposition for boxer dogs; however, sporadic occurrence in other breeds may occur. This is the first reported case of HUC in an American Staffordshire Terrier.

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  • cerebellar abiotrophy in an American Staffordshire Terrier adult dog in brazil
    Acta Scientiae Veterinariae, 2014
    Co-Authors: Cristine Mari, Daniele Mariath Bassuino, Angélica Terezinha Barth Wouters, Marcele Bettim Bandinelli, David Driemeier, Saulo Petinatti Pavarini

    Abstract:

    Background: Cerebellar abiotrophy is a spontaneous, progressive degenerative disease of the cerebellum in which Purkinje cell loss and functional disorders occur secondary to an intrinsic metabolic defect. Clinically, all animals with cerebellar abiotrophy are normal at birth, and neurological signs become evident during development. This work aimed to report and describe a case of cerebellar cortical abiotrophy in an adult American Staffordshire Terrier in Brazil, highlighting the pathologic fi ndings of the cerebellar lesions. Case: A 10-year-old female American Staffordshire Terrier presented with a 3-year history of progressive neurological changes. These changes began with mild ataxia of the hind limbs that involved the forelimbs after 2 years. In the recent months prior to presentation, the patient spent most of her time lying down with a head tilt. When she stood with her head raised, she exhibited abasia and required a broad base of support. When she attempted to walk, she quickly fell and rolled over if not supported. She could not eat on her own because of intense intention tremors. Because of the severity of her condition, the decision was made to euthanize the animal. Necropsy examination revealed no signifi cant fi ndings. Various organ specimens were collected, fi xed in 10% formalin, and processed for routine histology. The tissue sections were stained with hematoxylin and eosin. Cerebellar specimens were subjected to immunohistochemistry (IHC). Two cerebellar specimens from two normal 8to 9-year-old American Staffordshire Terriers were used as positive controls for IHC and comparative evaluation of the lesions. Histologically, the main changes were observed in the cerebellum and were characterized by necrosis, degeneration, and marked segmental loss of Purkinje cells; moderate reduction in the granular cells of the cerebellar cortex; and thinning of the molecular layer. Cerebellar IHC in the affected canine showed a slight reduction in immunoreactivity for neurofi laments in both the molecular layer and white matter as well as a marked increase in immunostaining for glial fi brillary acidic protein, indicating astrogliosis, in the molecular layer, granular layer, and white matter. Discussion: The diagnosis of cerebellar abiotrophy in this canine patient was based on clinical, pathologic, and immunohistochemical fi ndings. The framework cerebellar syndrome in an adult dog, slowly progressive, as in this case (10 years old with a 3-year clinical progression) is compatible with abiotrophy in the American Staffordshire Terrier. The main gross lesions observed in the cerebellum of canines with abiotrophy are projected to decline; however, these changes can be subtle, as in this case. Histopathology revealed a primary loss of Purkinje cells and depletion of the molecular and granular layers. These characteristics have been identifi ed as hereditary in American Staffordshire Terriers and other breeds. The clinical signs observed in this patient, namely ataxia, intention tremors, and abasia, refl ect the loss of function of the inhibitory neurons of the cerebellar cortex. The fact that cerebellar abiotrophy is relatively common in purebred dogs and the great variety in the early clinical signs and progression suggests different genetic etiologies in different breeds. An association with breed is evidenced by the fact that the clinical manifestations of cerebellar abiotrophy in American Staffordshire Terriers start late and have been shown to be hereditary. This paper reports the occurrence of cerebellar cortex abiotrophy as a cause of neurological disease in an American Staffordshire Terrier in Brazil.

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  • abiotrofi a cerebelar em um canino American staff ordshire Terrier adulto no brasil cerebellar abiotrophy in an American staff ordshire Terrier adult dog in brazil
    , 2014
    Co-Authors: Cristine Mari, Daniele Mariath Bassuino, Marcele Bettim Bandinelli, David Driemeier, Angelica Terezinha, Barth Wouters, Saulo Petinatti Pavarini

    Abstract:

    Background: Cerebellar abiotrophy is a spontaneous, progressive degenerative disease of the cerebellum in which Purkinje cell loss and functional disorders occur secondary to an intrinsic metabolic defect. Clinically, all animals with cerebellar abiotrophy are normal at birth, and neurological signs become evident during development. This work aimed to report and describe a case of cerebellar cortical abiotrophy in an adult American Staffordshire Terrier in Brazil, highlighting the pathologic fi ndings of the cerebellar lesions. Case: A 10-year-old female American Staffordshire Terrier presented with a 3-year history of progressive neurological changes. These changes began with mild ataxia of the hind limbs that involved the forelimbs after 2 years. In the recent months prior to presentation, the patient spent most of her time lying down with a head tilt. When she stood with her head raised, she exhibited abasia and required a broad base of support. When she attempted to walk, she quickly fell and rolled over if not supported. She could not eat on her own because of intense intention tremors. Because of the severity of her condition, the decision was made to euthanize the animal. Necropsy examination revealed no signifi cant fi ndings. Various organ specimens were collected, fi xed in 10% formalin, and processed for routine histology. The tissue sections were stained with hematoxylin and eosin. Cerebellar specimens were subjected to immunohistochemistry (IHC). Two cerebellar specimens from two normal 8- to 9-year-old American Staffordshire Terriers were used as positive controls for IHC and comparative evaluation of the lesions. Histologically, the main changes were observed in the cerebellum and were characterized by necrosis, degeneration, and marked segmental loss of Purkinje cells; moderate reduction in the granular cells of the cerebellar cortex; and thinning of the molecular layer. Cerebellar IHC in the affected canine showed a slight reduction in immunoreactivity for neurofi laments in both the molecular layer and white matter as well as a marked increase in immunostaining for glial fi brillary acidic protein, indicating astrogliosis, in the molecular layer, granular layer, and white matter. Discussion: The diagnosis of cerebellar abiotrophy in this canine patient was based on clinical, pathologic, and immunohistochemical fi ndings. The framework cerebellar syndrome in an adult dog, slowly progressive, as in this case (10 years old with a 3-year clinical progression) is compatible with abiotrophy in the American Staffordshire Terrier. The main gross lesions observed in the cerebellum of canines with abiotrophy are projected to decline; however, these changes can be subtle, as in this case. Histopathology revealed a primary loss of Purkinje cells and depletion of the molecular and granular layers. These characteristics have been identifi ed as hereditary in American Staffordshire Terriers and other breeds. The clinical signs observed in this patient, namely ataxia, intention tremors, and abasia, refl ect the loss of function of the inhibitory neurons of the cerebellar cortex. The fact that cerebellar abiotrophy is relatively common in purebred dogs and the great variety in the early clinical signs and progression suggests different genetic etiologies in different breeds. An association with breed is evidenced by the fact that the clinical manifestations of cerebellar abiotrophy in American Staffordshire Terriers start late and have been shown to be hereditary. This paper reports the occurrence of cerebellar cortex abiotrophy as a cause of neurological disease in an American Staffordshire Terrier in Brazil.

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Natasha J. Olby – One of the best experts on this subject based on the ideXlab platform.

  • a de novo mutation in the ext2 gene associated with osteochondromatosis in a litter of American Staffordshire Terriers
    Journal of Veterinary Internal Medicine, 2018
    Co-Authors: Steven G. Friedenberg, Daniella Vansteenkiste, Oriana Yost, Amy E Treeful, Kathryn M. Meurs, Debra A Tokarz, Natasha J. Olby

    Abstract:

    BACKGROUND: We aimed to identify mutations associated with osteochondromatosis in a litter of American Staffordshire Terrier puppies. HYPOTHESIS: We hypothesized that the associated mutation would be located in a gene that causes osteochondromatosis in humans. ANIMALS: A litter of 9 American Staffordshire puppies, their sire and dam, 3 of 4 grandparents, 26 healthy unrelated American Staffordshire Terriers, and 154 dogs of 27 different breeds. METHODS: Whole genome sequencing was performed on the proband, and variants were compared against polymorphisms derived from 154 additional dogs across 27 breeds, as well as single nucleotide polymorphism database 146. One variant was selected for follow-up sequencing. Parentage and genetic mosaicism were evaluated across the litter. RESULTS: We found 56,301 genetic variants unique to the proband. Eleven variants were located in or near the gene exostosin 2 (EXT2), which is strongly associated with osteochondromatosis in humans. One heterozygous variant (c.969C > A) is predicted to result in a stop codon in exon 5 of the gene. Sanger sequencing identified the identical mutation in all affected offspring. The mutation was absent in the unaffected offspring, both parents, all available grandparents, and 26 healthy unrelated American Staffordshire Terriers. CONCLUSIONS AND CLINICAL IMPORTANCE: These findings represent the first reported mutation associated with osteochondromatosis in dogs. Because this mutation arose de novo, the identical mutation is unlikely to be the cause of osteochondromatosis in other dogs. However, de novo mutations in EXT2 are common in humans with osteochondromatosis, and by extension, it is possible that dogs with osteochondromatosis could be identified by sequencing the entire EXT2 gene.

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  • a canine arylsulfatase g arsg mutation leading to a sulfatase deficiency is associated with neuronal ceroid lipofuscinosis
    Proceedings of the National Academy of Sciences of the United States of America, 2010
    Co-Authors: Marie Abitbol, Natasha J. Olby, Jeanlaurent Thibaud, Christophe Hitte, Jeanphilippe Puech, Marie Maurer, Fanny Pilotstorck, Benoit Hedan, Stephane Dreano, Sandra Brahimi

    Abstract:

    Neuronal ceroid lipofuscinoses (NCLs) represent the most common group of inherited progressive encephalopathies in children. They are characterized by progressive loss of vision, mental and motor deterioration, epileptic seizures, and premature death. Rare adult forms of NCL with late onset are known as Kufs’ disease. Loci underlying these adult forms remain unknown due to the small number of patients and genetic heterogeneity. Here we confirm that a late-onset form of NCL recessively segregates in US and French pedigrees of American Staffordshire Terrier (AST) dogs. Through combined association, linkage, and haplotype analyses, we mapped the disease locus to a single region of canine chromosome 9. We eventually identified a worldwide breed-specific variant in exon 2 of the Arylsulfatase G (ARSG) gene, which causes a p.R99H substitution in the vicinity of the catalytic domain of the enzyme. In transfected cells or leukocytes from affected dogs, the missense change leads to a 75% decrease in sulfatase activity, providing a functional confirmation that the variant might be the NCL-causing mutation. Our results uncover a protein involved in neuronal homeostasis, identify a family of candidate genes to be screened in patients with Kufs’ disease, and suggest that a deficiency in sulfatase is part of the NCL pathogenesis.

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Cristine Mari – One of the best experts on this subject based on the ideXlab platform.

  • cerebellar abiotrophy in an American Staffordshire Terrier adult dog in brazil
    Acta Scientiae Veterinariae, 2014
    Co-Authors: Cristine Mari, Daniele Mariath Bassuino, Angélica Terezinha Barth Wouters, Marcele Bettim Bandinelli, David Driemeier, Saulo Petinatti Pavarini

    Abstract:

    Background: Cerebellar abiotrophy is a spontaneous, progressive degenerative disease of the cerebellum in which Purkinje cell loss and functional disorders occur secondary to an intrinsic metabolic defect. Clinically, all animals with cerebellar abiotrophy are normal at birth, and neurological signs become evident during development. This work aimed to report and describe a case of cerebellar cortical abiotrophy in an adult American Staffordshire Terrier in Brazil, highlighting the pathologic fi ndings of the cerebellar lesions. Case: A 10-year-old female American Staffordshire Terrier presented with a 3-year history of progressive neurological changes. These changes began with mild ataxia of the hind limbs that involved the forelimbs after 2 years. In the recent months prior to presentation, the patient spent most of her time lying down with a head tilt. When she stood with her head raised, she exhibited abasia and required a broad base of support. When she attempted to walk, she quickly fell and rolled over if not supported. She could not eat on her own because of intense intention tremors. Because of the severity of her condition, the decision was made to euthanize the animal. Necropsy examination revealed no signifi cant fi ndings. Various organ specimens were collected, fi xed in 10% formalin, and processed for routine histology. The tissue sections were stained with hematoxylin and eosin. Cerebellar specimens were subjected to immunohistochemistry (IHC). Two cerebellar specimens from two normal 8to 9-year-old American Staffordshire Terriers were used as positive controls for IHC and comparative evaluation of the lesions. Histologically, the main changes were observed in the cerebellum and were characterized by necrosis, degeneration, and marked segmental loss of Purkinje cells; moderate reduction in the granular cells of the cerebellar cortex; and thinning of the molecular layer. Cerebellar IHC in the affected canine showed a slight reduction in immunoreactivity for neurofi laments in both the molecular layer and white matter as well as a marked increase in immunostaining for glial fi brillary acidic protein, indicating astrogliosis, in the molecular layer, granular layer, and white matter. Discussion: The diagnosis of cerebellar abiotrophy in this canine patient was based on clinical, pathologic, and immunohistochemical fi ndings. The framework cerebellar syndrome in an adult dog, slowly progressive, as in this case (10 years old with a 3-year clinical progression) is compatible with abiotrophy in the American Staffordshire Terrier. The main gross lesions observed in the cerebellum of canines with abiotrophy are projected to decline; however, these changes can be subtle, as in this case. Histopathology revealed a primary loss of Purkinje cells and depletion of the molecular and granular layers. These characteristics have been identifi ed as hereditary in American Staffordshire Terriers and other breeds. The clinical signs observed in this patient, namely ataxia, intention tremors, and abasia, refl ect the loss of function of the inhibitory neurons of the cerebellar cortex. The fact that cerebellar abiotrophy is relatively common in purebred dogs and the great variety in the early clinical signs and progression suggests different genetic etiologies in different breeds. An association with breed is evidenced by the fact that the clinical manifestations of cerebellar abiotrophy in American Staffordshire Terriers start late and have been shown to be hereditary. This paper reports the occurrence of cerebellar cortex abiotrophy as a cause of neurological disease in an American Staffordshire Terrier in Brazil.

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  • abiotrofi a cerebelar em um canino American staff ordshire Terrier adulto no brasil cerebellar abiotrophy in an American staff ordshire Terrier adult dog in brazil
    , 2014
    Co-Authors: Cristine Mari, Daniele Mariath Bassuino, Marcele Bettim Bandinelli, David Driemeier, Angelica Terezinha, Barth Wouters, Saulo Petinatti Pavarini

    Abstract:

    Background: Cerebellar abiotrophy is a spontaneous, progressive degenerative disease of the cerebellum in which Purkinje cell loss and functional disorders occur secondary to an intrinsic metabolic defect. Clinically, all animals with cerebellar abiotrophy are normal at birth, and neurological signs become evident during development. This work aimed to report and describe a case of cerebellar cortical abiotrophy in an adult American Staffordshire Terrier in Brazil, highlighting the pathologic fi ndings of the cerebellar lesions. Case: A 10-year-old female American Staffordshire Terrier presented with a 3-year history of progressive neurological changes. These changes began with mild ataxia of the hind limbs that involved the forelimbs after 2 years. In the recent months prior to presentation, the patient spent most of her time lying down with a head tilt. When she stood with her head raised, she exhibited abasia and required a broad base of support. When she attempted to walk, she quickly fell and rolled over if not supported. She could not eat on her own because of intense intention tremors. Because of the severity of her condition, the decision was made to euthanize the animal. Necropsy examination revealed no signifi cant fi ndings. Various organ specimens were collected, fi xed in 10% formalin, and processed for routine histology. The tissue sections were stained with hematoxylin and eosin. Cerebellar specimens were subjected to immunohistochemistry (IHC). Two cerebellar specimens from two normal 8- to 9-year-old American Staffordshire Terriers were used as positive controls for IHC and comparative evaluation of the lesions. Histologically, the main changes were observed in the cerebellum and were characterized by necrosis, degeneration, and marked segmental loss of Purkinje cells; moderate reduction in the granular cells of the cerebellar cortex; and thinning of the molecular layer. Cerebellar IHC in the affected canine showed a slight reduction in immunoreactivity for neurofi laments in both the molecular layer and white matter as well as a marked increase in immunostaining for glial fi brillary acidic protein, indicating astrogliosis, in the molecular layer, granular layer, and white matter. Discussion: The diagnosis of cerebellar abiotrophy in this canine patient was based on clinical, pathologic, and immunohistochemical fi ndings. The framework cerebellar syndrome in an adult dog, slowly progressive, as in this case (10 years old with a 3-year clinical progression) is compatible with abiotrophy in the American Staffordshire Terrier. The main gross lesions observed in the cerebellum of canines with abiotrophy are projected to decline; however, these changes can be subtle, as in this case. Histopathology revealed a primary loss of Purkinje cells and depletion of the molecular and granular layers. These characteristics have been identifi ed as hereditary in American Staffordshire Terriers and other breeds. The clinical signs observed in this patient, namely ataxia, intention tremors, and abasia, refl ect the loss of function of the inhibitory neurons of the cerebellar cortex. The fact that cerebellar abiotrophy is relatively common in purebred dogs and the great variety in the early clinical signs and progression suggests different genetic etiologies in different breeds. An association with breed is evidenced by the fact that the clinical manifestations of cerebellar abiotrophy in American Staffordshire Terriers start late and have been shown to be hereditary. This paper reports the occurrence of cerebellar cortex abiotrophy as a cause of neurological disease in an American Staffordshire Terrier in Brazil.

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  • Abiotrofia cerebelar em um canino American Staffordshire Terrier adulto no Brasil
    Acta Scientiae Veterinariae, 2014
    Co-Authors: Cristine Mari, Daniele Mariath Bassuino, Angélica Terezinha Barth Wouters, Marcele Bettim Bandinelli, David Driemeier, Saulo Petinatti Pavarini

    Abstract:

    Background: Cerebellar abiotrophy is a spontaneous, progressive degenerative disease of the cerebellum in which Purkinje cell loss and functional disorders occur secondary to an intrinsic metabolic defect. Clinically, all animals with cerebellar abiotrophy are normal at birth, and neurological signs become evident during development. This work aimed to report and describe a case of cerebellar cortical abiotrophy in an adult American Staffordshire Terrier in Brazil, highlighting the pathologic findings of the cerebellar lesions. Case: A 10-year-old female American Staffordshire Terrier presented with a 3-year history of progressive neurological changes. These changes began with mild ataxia of the hind limbs that involved the forelimbs after 2 years. In the recent months prior to presentation, the patient spent most of her time lying down with a head tilt. When she stood with her head raised, she exhibited abasia and required a broad base of support. When she attempted to walk, she quickly fell and rolled over if not supported. She could not eat on her own because of intense intention tremors. Because of the severity of her condition, the decision was made to euthanize the animal. Necropsy examination revealed no significant findings. Various organ specimens were collected, fixed in 10% formalin, and processed for routine histology. The tissue sections were stained with hematoxylin and eosin. Cerebellar specimens were subjected to immunohistochemistry (IHC). Two cerebellar specimens from two normal 8- to 9-year-old American Staffordshire Terriers were used as positive controls for IHC and comparative evaluation of the lesions. Histologically, the main changes were observed in the cerebellum and were characterized by necrosis, degeneration, and marked segmental loss of Purkinje cells; moderate reduction in the granular cells of the cerebellar cortex; and thinning of the molecular layer. Cerebellar IHC in the affected canine showed a slight reduction in immunoreactivity for neurofilaments in both the molecular layer and white matter as well as a marked increase in immunostaining for glial fibrillary acidic protein, indicating astrogliosis, in the molecular layer, granular layer, and white matter. Discussion: The diagnosis of cerebellar abiotrophy in this canine patient was based on clinical, pathologic, and immunohistochemical findings. The framework cerebellar syndrome in an adult dog, slowly progressive, as in this case (10 years old with a 3-year clinical progression) is compatible with abiotrophy in the American Staffordshire Terrier. The main gross lesions observed in the cerebellum of canines with abiotrophy are projected to decline; however, these changes can be subtle, as in this case. Histopathology revealed a primary loss of Purkinje cells and depletion of the molecular and granular layers. These characteristics have been identified as hereditary in American Staffordshire Terriers and other breeds. The clinical signs observed in this patient, namely ataxia, intention tremors, and abasia, reflect the loss of function of the inhibitory neurons of the cerebellar cortex. The fact that cerebellar abiotrophy is relatively common in purebred dogs and the great variety in the early clinical signs and progression suggests different genetic etiologies in different breeds. An association with breed is evidenced by the fact that the clinical manifestations of cerebellar abiotrophy in American Staffordshire Terriers start late and have been shown to be hereditary. This paper reports the occurrence of cerebellar cortex abiotrophy as a cause of neurological disease in an American Staffordshire Terrier in Brazil.

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