Risk of oral infection with bovine spongiform encephalopathy agent in primates

Lasmézas, Corinne Ida; Comoy, Emmanuel; Hawkins, S. A. C.; Herzog, Christian; Mouthon, Franck; Konold, Timm; Auvré, Frédéric; Correia, Evelyne; Lescoutra-Etchegaray, Nathalie; Salès, Nicole; Wells, G. A. H.; Brown, Paul; Deslys, Jean‐Philippe

doi:10.1016/s0140-6736(05)17985-9

Cited by 79 publications

(68 citation statements)

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“…We infected nonhuman primates (Macaca fascicularis) with the agents of bovine spongiform encephalopathy (BSE), sCJD, iCJD (linked to growth hormone administration), and vCJD. Previous studies have shown that this animal model, which is closely related to humans, faithfully reproduces the main characteristics of vCJD, i.e., the clinical presentation, the typical neuropathology, and the possibility of oral transmission (23,24). sCJD and iCJD can be readily distinguished from vCJD and from each other in these animals on the basis of the clinical signs and the neuropathology (unpublished data).…”

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confidence: 56%

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PrP ^TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease

Herzog

Rivière

Lescoutra-Etchegaray

et al. 2005

J Virol

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Human prion diseases, such as Creutzfeldt-Jakob disease (CJD), are neurodegenerative and fatal. Sporadic CJD (sCJD) can be transmitted between humans through medical procedures involving highly infected organs, such as the central nervous system. However, in variant CJD (vCJD), which is due to human contamination with the bovine spongiform encephalopathy (BSE) agent, lymphoreticular tissue also harbors the transmissible spongiform encephalopathy-associated prion protein (PrP TSE ), which poses a particularly acute risk for iatrogenic transmission. Two blood transfusion-related cases are already documented. In addition, the recent observation of PrP TSE in spleen and muscle in sCJD raised the possibility that peripheral PrP TSE is not limited to vCJD cases. We aimed to clarify the peripheral pathogenesis of human TSEs by using a nonhuman primate model which mimics human diseases. A highly sensitive enzyme-linked immunosorbent assay was adapted to the detection of extraneural PrP TSE . We show that affected organs can be divided into two groups. The first is peripheral organs accumulating large amounts of PrP TSE , which represent a high risk of iatrogenic transmission. This category comprises only lymphoreticular organs in the vCJD/BSE model. The second is organs with small amounts of PrP TSE associated with nervous structures. These are the muscles, adrenal glands, and enteric nervous system in the sporadic, iatrogenic, and variant CJD models. In contrast to the first set of organs, this low level of tissue contamination is not strain restricted and seems to be linked to secondary centrifugal spread of the agent through nerves. It might represent a risk for iatrogenic transmission, formerly underestimated despite previous reports of low rates of transmission from peripheral organs of humans to nonhuman primates (5, 10). This study provides an additional experimental basis for the classification of human organs into different risk categories and a rational re-evaluation of current risk management measures.Prion diseases are fatal disorders of both humans and animals and can be acquired, spontaneous, or genetic in origin (28). All forms of Creutzfeldt-Jakob disease (CJD) are infectious (5, 12), and transmission of sporadic CJD (sCJD) has occurred through cross-contamination from neurosurgical devices or through therapeutic usage of human central nervous system (CNS) tissues, causing over 267 iatrogenic CJD (iCJD) cases worldwide (6). With the appearance of variant CJD (vCJD), a new risk of iatrogenic transmission emerged, since the misfolded form of the prion protein which accumulates in transmissible spongiform encephalopathies (PrP TSE ) was found in peripheral organs, including lymphoid tissues and the rectum (32). Therefore, leukoreduction of blood units was implemented in 1999, and precautions have been recommended for gastrointestinal endoscopies (4). However, interhuman transmission of vCJD has probably already happened twice through blood transfusion from persons with preclinical vCJD (25,27). This demonst...

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“…All cynomolgus macaques are M/M at codon 129 of the PrP gene. The macaque model displays the same human "strain-specific" electrophoretic pattern of PrP TSE in sCJD and vCJD (23). In this way we could explore the "strain"-specific PrP TSE distribution in controlled inoculation conditions.…”

Section: Discussionmentioning

confidence: 97%

PrP ^TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease

Herzog

Rivière

Lescoutra-Etchegaray

et al. 2005

J Virol

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“…Classical BSE is efficiently transmitted to 50% of animals challenged orally with as little as 0.15 g of high titre BSE brain (95% confidence interval) 22) . Oral challenges with classical BSE have also been successful to transmit disease to other species including cynamologous macaques 23,24) , sheep and goats 25,26) . Proof of oral transmissibility of classical BSE has resulted in ruminant to ruminant feed bans and specified risk material removal to prevent intra-and interspecies transmission by consumption of contaminated food or feed.…”

Section: Atypical Bse Transmissionmentioning

confidence: 99%

Atypical BSE: Current Knowledge and Knowledge Gaps

Dudas

Czub

2017

Food Safety

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Atypical BSE is an invariably fatal neurologic disease of cattle caused by misfolded prion proteins with different conformations than those associated with classical BSE. Evidence suggests that these atypical BSE types are sporadic or genetic prion diseases of cattle and the relevance of these diseases, as far as natural transmissibility, is still unknown. Different misfolded prion protein conformations also result in unique biochemical characteristics. This raised concerns about detection of atypical BSE on rapid test platforms designed and validated for classical BSE prions. Despite the differences in the misfolded prion protein characteristics, studies have shown that the tests also work well for detecting the known types of atypical BSE. A new question that has recently emerged is related to the possibility of additional forms of atypical BSE. Initially reactive bovine brain samples on certain rapid surveillance tests have sparked debate about the true BSE status of these samples. Work is currently underway to determine if these samples are infectious and if they eventually result in neurologic disease in cattle. Results of these studies could impact future BSE diagnostic testing programs as well as human and animal health policies.Key words: atypical BSE, bovine spongiform encephalopathy, neurologic disease, prion, PrP Atypical BSEBovine spongiform encephalopathy (BSE) is a prion disease of cattle that is invariably fatal and zoonotic. Three type of BSE have been detected in a number of countries around the world. Classical BSE is the most common types of BSE and the cause of the BSE epidemic in the United Kingdom 1) . In 2004, two additional types of BSE were identified mostly in older animals 2,3) and were named according to the electrophoretic migration of their protease resistant prion protein or PrP RES . High or H type BSE PrP RES is slightly larger, migrates slower and is detected in a position higher than classical BSE, while low or L type BSE PrP RES is smaller, migrates faster and is detected in a lower position than classical BSE during electrophoresis. Along with these differences in size, H and L type atypical BSE also have different biochemical and transmission characteristics, PrP RES distribution and pose different challenges for detection and diagnosis.

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“…Clinical and pathological similarities between those experimentally induced diseases in primates and corresponding natural diseases in human on the other hand have been described. C-BSE transmission has been demonstrated in different primate species, including marmosets (Baker et al, 1993), cynomolgus macaques (Lasmezas et al, 1996(Lasmezas et al, , 2005, lemurs (Bons et al, 1999) and squirrel monkeys (Williams et al, 2007). The secondary transmission of both macaque BSE and human vCJD to the same host, i.e.…”

Section: Overexpressing Transgenic Micementioning

confidence: 99%

Scientific Opinion on a request for a review of a scientific publication concerning the zoonotic potential of ovine scrapie prions

2015

EFSA Journal

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The factors that modulate the transmissibility of Transmissible Spongiform Encephalopathies (TSE) and the approaches for the study of their zoonotic potential are reviewed. The paper 'Evidence for zoonotic potential of ovine scrapie prions' by Cassard et al. (2014) is scientifically appraised, focussing on the experimental design, the results and the conclusions. The paper provides evidence in a laboratory experiment that some Classical scrapie isolates can propagate in humanised transgenic mice and produce prions that on second passage are similar to those causing one form of sporadic Creutzfeldt-Jakob disease (sCJD). It is concluded that the results from the study raise the possibility that scrapie prions have the potential to be zoonotic, but do not provide evidence that transmission can or does take place under field conditions. The conclusions of the 2011 ECDC-EFSA 'Joint Scientific Opinion on any possible epidemiological or molecular association between TSEs in animals and humans' are reviewed in the light of the new scientific evidence available since its publication. This supports and strengthens the conclusions of that opinion with regard to the potential for some animal TSE to be zoonotic, but does not provide evidence of a causal link between Classical or Atypical scrapie and human TSE. Current evidence does not establish this link, and no consistent risk factors have been identified for sCJD. The possibility of scrapie-related public health risks from the consumption of ovine products cannot be assessed. Recommendations are formulated on further studies and data that are needed to investigate the zoonotic potential of animal TSE and to estimate the amount of infectivity from TSE-infected products sourced from small ruminants and entering the food chain in the European Union. © European Food Safety Authority, 2015Keywords: Atypical scrapie, Classical scrapie, Creutzfeldt-Jakob disease, transmissible spongiform encephalopathy, zoonosis Amendment: An amendment has been made to the following sentence on p. 31: 'In this regard the emergence of sCJD is not so surprising, and has been described after inoculation of tgHu mice with cattle BSE and human vCJD (Asante et al., 2002;Beringue et al., 2008b)'. This was carried out to clarify that one of the references reported emergence of sporadic CJD after experimental inoculation of humanised transgenic mice with vCJD, which was not correctly stated in the published opinion. An amendment has been made on p. 28, to add the word 'OR' between two search terms within the literature search string reported. Reproduction is authorised provided the source is acknowledged. Requestor: European CommissionThe EFSA Journal is a publication of the European Food Safety Authority, an agency of the European Union. SummaryFollowing a request from the European Commission (EC), the EFSA Panel on Biological Hazards (BIOHAZ Panel) was asked to deliver a scientific opinion on the review of a scientific publication concerning the zoonotic potential of ovine scrapie prions.T...

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Risk of oral infection with bovine spongiform encephalopathy agent in primates

Cited by 79 publications

References 8 publications

PrP ^TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease

PrP ^TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease

Atypical BSE: Current Knowledge and Knowledge Gaps

Scientific Opinion on a request for a review of a scientific publication concerning the zoonotic potential of ovine scrapie prions

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Risk of oral infection with bovine spongiform encephalopathy agent in primates

Cited by 79 publications

References 8 publications

PrP TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease

PrP TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease

Atypical BSE: Current Knowledge and Knowledge Gaps

Scientific Opinion on a request for a review of a scientific publication concerning the zoonotic potential of ovine scrapie prions

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Product

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PrP ^TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease

PrP ^TSE Distribution in a Primate Model of Variant, Sporadic, and Iatrogenic Creutzfeldt-Jakob Disease