Lesion profiles and gliosis in the brainstem of 135 Swiss Cows with Bovine Spongiform Encephalopathy (BSE)

Gubler, E.; Hilbe, Monika; Ehrensperger, F

doi:10.1024/0036-7281.149.3.111

Cited by 7 publications

(8 citation statements)

References 37 publications

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“…Taken additionally into account that we found a similar obex topography of PrP d types (Fig. 2) as that found in Italian and British classical BSE cattle [8], our data strengthen former studies on clinically BSE aVected Swiss cattle that revealed a histopathological BSE phenotype similar to British BSE cases [17,18] and extend this conclusion to asymptomatic BSE cattle identiWed in frame of active surveillance in Switzerland.…”

Section: Discussionsupporting

confidence: 90%

Neuropathological and molecular comparison between clinical and asymptomatic bovine spongiform encephalopathy cases

et al. 2007

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Interest in the proper neuropathological and molecular characterization of bovine spongiform encephalopathy (BSE) has increased since asymptomatic and atypical cases were detected in the cattle population by active disease surveillance. In this respect we investigated a total of 95 confirmed BSE cases originating from different active and passive surveillance categories (clinical suspects, emergency-slaughter, fallen stock and routinely slaughter) in Switzerland for their neuropathological and molecular phenotype. We looked for measurable differences between these categories in lesion profile, severity of spongiform change, degree of astrocytosis as well as immunohistochemical and molecular patterns of the disease-associated isoform of the prion protein (PrPd) in the caudal brainstem. Our results indicate significantly higher intensities of spongiform change in clinically affected compared to asymptomatic BSE cases. Similar effects were in trend observed for the intensities of PrPd deposition and astrocytosis, whereas the frequencies of morphological PrPd types and the molecular patterns in Western immunoblot were not different. Importantly, none of the animals included in this study revealed features of atypical BSE. Taken together, this study suggests that both clinically affected as well as asymptomatic Swiss BSE cases in cattle share the neuropathological and molecular phenotype of classical BSE and that asymptomatic classical BSE cases are at a pre-clinical stage of the disease rather than representing a true sub-clinical form of BSE.

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Section: Discussionsupporting

confidence: 90%

Neuropathological and molecular comparison between clinical and asymptomatic bovine spongiform encephalopathy cases

et al. 2007

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“…The authors hypothesised that this may also apply to larger animals although the range of tests that can be performed on sheep and cattle is obviously limited by the size and cooperation of the animals. BSE in cattle (C-type) is a neurological disease with a fairly uniform clinical presentation characterised by changes in behaviour, sensation and locomotion [ 31 ] and thought to be caused by a uniform strain based on a similarly uniform distribution and severity of vacuolar changes in cattle [ 32 - 34 ] and mice [ 35 , 36 ]. If strains predominantly dictate the clinical presentation, infection of sheep with the BSE agent should equally result in a relatively uniform clinical disease, regardless of breed and genotype, since the pathological phenotype, including the intracellular truncation pattern, remains constant when BSE is transmitted to sheep with different genotypes and by different routes [ 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

Pruritus is a common feature in sheep infected with the BSE agent

et al. 2008

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BackgroundThe variability in the clinical or pathological presentation of transmissible spongiform encephalopathies (TSEs) in sheep, such as scrapie and bovine spongiform encephalopathy (BSE), has been attributed to prion protein genotype, strain, breed, clinical duration, dose, route and type of inoculum and the age at infection. The study aimed to describe the clinical signs in sheep infected with the BSE agent throughout its clinical course to determine whether the clinical signs were as variable as described for classical scrapie in sheep. The clinical signs were compared to BSE-negative sheep to assess if disease-specific clinical markers exist.ResultsForty-seven (34%) of 139 sheep, which comprised 123 challenged sheep and 16 undosed controls, were positive for BSE. Affected sheep belonged to five different breeds and three different genotypes (ARQ/ARQ, VRQ/VRQ and AHQ/AHQ). None of the controls or BSE exposed sheep with ARR alleles were positive. Pruritus was present in 41 (87%) BSE positive sheep; the remaining six were judged to be pre-clinically infected. Testing of the response to scratching along the dorsum of a sheep proved to be a good indicator of clinical disease with a test sensitivity of 85% and specificity of 98% and usually coincided with weight loss. Clinical signs that were displayed significantly earlier in BSE positive cases compared to negative cases were behavioural changes, pruritic behaviour, a positive scratch test, alopecia, skin lesions, teeth grinding, tremor, ataxia, loss of weight and loss of body condition. The frequency and severity of each specific clinical sign usually increased with the progression of disease over a period of 16–20 weeks.ConclusionOur results suggest that BSE in sheep presents with relatively uniform clinical signs, with pruritus of increased severity and abnormalities in behaviour or movement as the disease progressed. Based on the studied sheep, these clinical features appear to be independent of breed, affected genotype, dose, route of inoculation and whether BSE was passed into sheep from cattle or from other sheep, suggesting that the clinical phenotype of BSE is influenced by the TSE strain more than by other factors. The clinical phenotype of BSE in the genotypes and breed studied was indistinguishable from that described for classical scrapie cases.

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“…These diseases are characterised by the accumulation in the central nervous system of an abnormally folded version (PrP Sc ) of a normal cellular protein, PrP C . The related neurological lesions include spongiform changes in grey matter, intraneuronal vacuoles in particular nuclei of the brain stem, gliosis, and neuronal degeneration [1-5]. Although various mechanisms have been proposed to explain neuronal death in prion diseases, apoptosis and autophagy are the types of cell death considered most likely to be involved [6].…”

Section: Introductionmentioning

confidence: 99%

Changes in HSP gene and protein expression in natural scrapie with brain damage

Serrano

Bolea

Lyahyai

et al. 2011

Vet Res

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Heat shock proteins (Hsp) perform cytoprotective functions such as apoptosis regulation and inflammatory response control. These proteins can also be secreted to the extracellular medium, acting as inflammatory mediators, and their chaperone activity permits correct folding of proteins and avoids the aggregation of anomalous isoforms. Several studies have proposed the implication of Hsp in prion diseases. We analysed the gene expression and protein distribution of different members of the Hsp27, Hsp70, and Hsp90 families in the central nervous system of sheep naturally infected with scrapie. Different expression profiles were observed in the areas analysed. Whereas changes in transcript levels were not observed in the cerebellum or medulla oblongata, a significant decrease in HSP27 and HSP90 was detected in the prefrontal cortex. In contrast, HSP73 was over-expressed in diencephalons of scrapie animals. Western blotting did not reveal significant differences in Hsp90 and Hsp70 protein expression between scrapie and control animals. Expression rates identified by real-time RT-PCR and western blotting were compared with the extent of classical scrapie lesions using stepwise regression. Changes in Hsp gene and protein expression were associated with prion protein deposition, gliosis and spongiosis rather than with apoptosis. Finally, immunohistochemistry revealed intense Hsp70 and Hsp90 immunolabelling in Purkinje cells of scrapie sheep. In contrast, controls displayed little or no staining in these cells. The observed differences in gene expression and protein distribution suggest that the heat shock proteins analysed play a role in the natural form of the disease.

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Lesion profiles and gliosis in the brainstem of 135 Swiss Cows with Bovine Spongiform Encephalopathy (BSE)

Cited by 7 publications

References 37 publications

Neuropathological and molecular comparison between clinical and asymptomatic bovine spongiform encephalopathy cases

Neuropathological and molecular comparison between clinical and asymptomatic bovine spongiform encephalopathy cases

Pruritus is a common feature in sheep infected with the BSE agent

Changes in HSP gene and protein expression in natural scrapie with brain damage

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