FSIS Issues Public Health Alert for Ineligible Imported Meat and Poultry Products from China, what about BSE?
NAIS, COOL, FROM FARM TO FORK, MAD COW DISEASE BSE TSE PrP?
FSIS Issues Public Health Alert for Ineligible Imported Meat and Poultry Products from China
FSIS Announcement
WASHINGTON, Dec. 29, 2021 - The U.S. Department of Agriculture’s Food Safety and Inspection Service (FSIS) is issuing a public health alert for an undetermined amount of imported meat and poultry products from China. A recall was not requested because FSIS has been unable to identify and contact the importers. The total amount of ineligible product is undetermined because the investigation is ongoing.
The products subject to the public health alert and labels are listed here.
The meat and poultry products do not identify an eligible establishment number on their packaging and were not presented to FSIS for import reinspection. These products are ineligible to import into the U.S., making them unfit for human consumption.
The problem was identified through an investigation with U.S. Customs and Border Protection (CBP) and USDA’s Animal and Plant Health Inspection Service (APHIS). FSIS will continue working with CBP and APHIS on the ongoing investigation.
Retailers who have purchased the products are urged not to sell them. Consumers who purchased the products should not consume them and need to dispose of them properly. Consumers are asked to dispose of the products by double bagging them to reduce the possibility of animals accessing the products. USDA cannot confirm whether the products were properly heated to control pathogens that affect domestic livestock.
There have been no confirmed reports of adverse reactions due to consumption of these products. Anyone concerned about an illness should contact a health care provider.
Consumers with food safety questions can call the toll-free USDA Meat and Poultry Hotline at 1-888-MPHotline (1-888-674-6854) or live chat via Ask USDA from 10 a.m. to 6 p.m. (Eastern Time) Monday through Friday.
Consumers can also browse food safety messages at Ask USDA or send a question via email to MPHotline@usda.gov. For consumers that need to report a problem with a meat, poultry, or egg product, the online Electronic Consumer Complaint Monitoring System can be accessed 24 hours a day at https://foodcomplaint.fsis.usda.gov/eCCF/.
***> It is evident from Table 1 that China reacted to the outbreak of BSE by placing various bans such as feed ban, MBM ban and making BSE a notifiable disease in 1990. <***
(3) (PDF) Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease risk management strategies in the People's Republic of China. Available from: https://www.researchgate.net/.../264815349_Bovine...[accessed Dec 29 2021].
The Scientific Steering Committee (SSC) of European Union established a qualitative indicator − the geographical BSE risk (GBR) − of the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, at a given point in time, in a country (Scientific Steering Committee, 2002b). This system was further expanded by the European Food Safety Authority (EFSA) to include countries participating in the import and export of cattle and cattle by-products. The previous GBR classifications have been phased out and as of 2007 WOFAH took the responsibility of classifying countries for their BSE risk under a new categorization system. The categories under the new system are negligible BSE risk, controlled BSE risk and undetermined BSE risk (Official Journal of the European Union, 2007). However, a GBR risk assessment was not conducted for China by any of the above mentioned agencies.
As of 2008, the World Organization for Animal Health recognizes Chinese Taipei as a ‘controlled BSE risk region’ (Office of International des Epizooties, 2008).
An internal risk analysis was performed by the Chinese Government in 2000 entitled, Risk Analysis and Assessment of BSE in China. Some key highlights from this analysis for China have been reported by Ozawa (2003) (Table 1) as well as for Hong Kong and Chinese Taipei (Table 2). It is evident from Table 1 that China reacted to the outbreak of BSE by placing various bans such as feed ban, MBM ban and making BSE a notifiable disease in 1990. China has been carrying out passive surveillance since 1997 and made it more comprehensive by including an active surveillance stream in the year 2000.
But what is notable about China and Hong Kong is the absence of SRM ban whereas data on a similar ban was not available for Chinese Taipei. Ozawa (2003) also noted some disparities in the instituted prevention policies between China, Chinese Taipei, and Hong Kong (Table 1 and Table 2) namely a MBM ban and rendering conditions. Hong Kong relies on voluntary ban on feeding cattle ruminant derived meat and bone meal. Information on national rendering conditions could not be gathered for China. 3.1
Import of cattle and beef from BSE-affected countries China imports live cattle for breeding purposes. Importation of breeding cattle from EU countries (France and Germany), North America (the USA and Canada), and Japan continued until the first case of BSE was reported in these countries. As shown in Figure 1, a total of 6,720 live cattle were imported during the period 1990 to 2003 from countries that later reported BSE (United States Department of Agriculture, 2004a, 2005, 2007; Smith, 2001). Another source reported the country had imported 2,863 breeding cattle from Japan, Canada, the USA and Australia between 1992 to 1999 (China Daily, 2001). Regardless of the number, the fact remains that China did import a large number of live cattle during the 1990s from countries that later reported BSE.
BSE and vCJD risk management strategies in the People’s Republic of China 309 Table 2 Data on BSE preventive measures in Hong Kong and Chinese Taipei Cattle import Feed ban MBM ban SRM ban Surveillance and monitoring Rendering Public awareness programs Hong Kong None No official ban No official ban (rely on voluntary bans since 2001) No official ban BSE was not a notifiable disease until 2003 Ruminant material not rendered; sent to landfills None 1997 – Ban on use of ruminant derived MBM in feed Chinese Taipei None 2001 – ban on use of animal protein 1990 – Ban on import of MBM from BSE affected countries No data 1990 – BSE made notifiable Rendering at 133°C/3bar/ 20 minute 1990 – Programs in place Source: Data summarised from Ozawa (2003)
(3) (PDF) Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease risk management strategies in the People's Republic of China. Available from: https://www.researchgate.net/.../264815349_Bovine...[accessed Dec 29 2021].
***> However, a GBR risk assessment was not conducted for China by any of the above mentioned agencies.
Animal Health Status of Regions
Last Modified: Sep 22, 2021
Regions classified by APHIS as having either negligible risk or controlled risk for Bovine Spongiform Encephalopathy (BSE) 9 CFR 92.5
NO LISTING OF BSE RISK FACTOR FOR CHINA; SEE;
BSE RISK ASSESSMENT PEOPLES REPUBLIC OF CHINA ??? not listed!
Spongiform encephalopathies in mainland China
Chang-Kai Sun Xiao-Qin Chong Yuan-Gui Huang
Published:August 24, 1996DOI: https://doi.org/10.1016/S0140-6736(05)64699-5
Bovine spongiform encephalopathy (BSE) and a new variant of human Creutzfeldt-Jakob disease (CJD) in the UK have had international medical, economic, and political repercussions. 1 , 2 Not a single case of BSE or scrapie has been reported in the People's Republic of China. Yet more than 30 confirmed and probably naturally occurring, sporadic or family, cases of spongiform encephalopathy including more than 20 cases of CJD and five of the slower progressing Gerstmann-Straussler-Scheinker syndrome, have been described since 1980. None of the patients had a history of ever having received any probable contaminated medical treatment. Nor were they medical workers who had ever contacted any person with spongiform encephalopathy. The onset of progressive neuropsychiatric dysfunction at an early or late age is rare in these cases. However, there were six cases of spongy degeneration of the brain in infancy reported 12 years ago. 3
Published: 18 October 2008
Surveillance for Creutzfeldt-Jakob disease in China from 2006 to 2007
Qi Shi, Chen Gao, Wei Zhou, Bao-Yun Zhang, Jian-Ming Chen, Chan Tian, Hui-Ying Jiang, Jun Han, Ni-Juan Xiang, Xiao-Fang Wang, Yong-Jun Gao & Xiao-Ping Dong BMC Public Health volume 8, Article number: 360 (2008) Cite this article
Abstract Background Human transmissible spongiform encephalopathies (HTSE), or Creutzfeldt-Jakob disease (CJD), is a group of rare and fatal diseases in central nervous system. Since outbreak of bovine spongiform encephalopathy (BSE) and variant CJD, a worldwide CJD surveillance network has been established under the proposition of WHO. In China, a national CJD surveillance system has started since 2002. The data of CJD surveillance from 2006 to 2007 was analyzed.
Methods Total 12 provinces are included in CJD surveillance system. The surveillance unit in each province consists of one or two sentinel hospitals and the provincial CDC. All suspected CJD cases reported from CJD surveillance were diagnosed and subtyped based on the diagnostic criteria for CJD issued by WHO.
Results Total 192 suspected CJD cases were reported and 5 genetic CJD, 51 probable and 30 possible sporadic CJD (sCJD) cases were diagnosed. The collected sCJD cases distribute sporadically without geographical clustering and seasonal relativity and the highest incidences in both probable and possible sCJD cases appeared in the group of 60–69 year. The most common three foremost symptoms were progressive dementia, cerebellum and mental-related symptoms. The probable sCJD patients owning both typical EEG alteration and CSF protein 14-3-3 positive have more characteristic clinical syndromes than the ones having only one positive. The polymorphisms of codon 129 of all tested reported cases shows typical patterns of Han Chinese as previous reports, that M129M are predominant whereas M129V are seldom.
Conclusion Chinese CJD patients possessed similar epidemiological and clinical characteristics as worldwide.
SNIP...
Discussion Since German neurologists Creutzfeldt and Jakob firstly reported the cases with progressive cerebral dysfunction, the 'Creutzfeldt-Jakob disease' has been known for almost one century. Since the occurrence of vCJD in Europe was addressed, WHO consultation had recommended the establishment of worldwide CJD surveillance[14]. In 2002, China started to set up the national CJD surveillance and join into the worldwide surveillance system. It consists of twelve provinces now with about 440 millions inhabitants. In this paper, we propose the surveillance results from 2006 to 2007. Except five genetic CJD cases, all CJD cases are diagnosed as sCJD. No iCJD and vCJD has been identified. The collected sCJD cases distribute sporadically without geographical clustering. The mean onset ages of the probable sCJD and possible sCJD cases are almost the same, showing the highest incidence in the group of 60–69 years. There are more male cases than female ones in the past two years, probably reflecting only short-term surveillance.
Many symptoms have been described as the foremost clinical manifestations in sCJD patients. The first three common symptoms are progressive dementia, cerebellum and mental-related symptoms. Along with the progression of the disease, more neurological symptoms have been identified, among them progressive dementia has been observed sooner or later in all sCJD patients. No differences in the appearances and frequencies of other four main clinical manifestations have been notified in the groups of probable sCJD and possible sCJD.
EEG examination and CSF protein 14-3-3 test are the indexes for probable sCJD according to the diagnostic criteria recommended by WHO[9]. We find that the probable sCJD patients owning both typical EEG alteration and CSF protein 14-3-3 positive have more characteristic clinical syndromes than the ones having only one positive. Meanwhile, all cases with 14-3-3 positive and EEG altheration show myoclonus during their clinical courses. CSF 14-3-3 positive is believed as the marker of brain damage[15]. EEG abnormality represents early recognition of worsening brain function[16]. It might reflect that the patients owning two positive results have more pathological changes in brains.
In our surveillance system, the PRNP genes of all reported cases have been screened if available. The polymorphisms of codon 129 of all tested reported cases show typical patterns of Han Chinese as previous reports[13], that M129M are predominant whereas M129V are seldom. Additionally, analyses of a few biopsy and postmortem brain samples of sCJD cases collected previously show all type 1 PrPSc patterns in Western blots (unpublished data). All these patients have been confirmed to be M129M homozygous. Furthermore, five genetic CJD cases have been identified through CJD surveillance. Two cases, T188K and E200K, do not have detectable family histories, which are reported and primarily diagnosed as probable and possible sCJD, respectively. It emphasizes that PRNP gene sequencing is essential and unique for detection of gCJD without detectable family history.
Although CJD cases have been identified through our CJD surveillance, the reported and diagnosed cases is far from the expected one based on the numbers of inhabitants. Therefore, it is hard to line out the morbidity of CJD in China. Lack of knowledge of this rare disease in local clinicians in small town encumbers the sensitivity of surveillance system. Carefully designed training programs will help to improve this situation. Compared with the developed countries, the rate of postmortem is extremely lower in China, due to the traditional customs. Therefore, apart from the future legislation for brain autopsy of suspected CJD patient, enhancing follow-up will improve the quality of our CJD surveillance system.
Conclusion The results of the present study revealed the general epidemiology status of CJD in China from 2006 to 2007. Foremost clinical manifestations were different among the CJD patients, but along with the progression of the disease, progressive dementia was observed sooner or later in all cases. EEG examination, CSF protein 14-3-3 test and PRNP gene analyses were the main laboratory tools for the suspected patients without postmortem. M129M were the predominant genotype in Han Chinese. The morbidity of CJD in China still remained unsettled for the short-term surveillance. Due to the lower rate of postmortem, enhancing follow-up will improve the quality of the CJD surveillance system.
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
Officials and Industry can continue to post/quote that old BS junk science, but it's not true. for one thing, not a single case of the so called old age spontaneous atypical BSE cases have ever been proven to be spontaneous, and see what the OIE themselves state;
OIE Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
34 Scientific Commission/September 2019
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
The Group acknowledged the challenges in demonstrating the zoonotic transmission of atypical strains of BSE in natural exposure scenarios. Overall, the Group was of the opinion that, at this stage, it would be premature to reach a conclusion other than that atypical BSE poses a potential zoonotic risk that may be different between atypical strains.
4. Definitions of meat-and-bone meal (MBM) and greaves
snip...
REFERENCES
SNIP...END SEE FULL TEXT;
Atypical L-type BSE
Emerg Infect Dis. 2017 Feb; 23(2): 284–287. doi: 10.3201/eid2302.161416 PMCID: PMC5324790 PMID: 28098532
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
Our study clearly confirms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a first passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.
In most cases of naturally occurring atypical BSE identified so far, the animals were >8 years of age, except for 3 cases: 1 H-BSE and 1 L-BSE in Spain (1) and 1 H-BSE in Germany (12). Therefore, we cannot exclude the possibility that L-BSE developed sporadically/spontaneously.
Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
Atypical H-type BSE
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion
Research Title: The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies
Location: Virus and Prion Research
Title: The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Author item Greenlee, Justin item MOORE, S - Orise Fellow item WEST-GREENLEE, M - Iowa State University
Submitted to: Prion
Publication Type: Abstract Only
Publication Acceptance Date: 5/14/2018
Publication Date: 5/22/2018
Citation: Greenlee, J.J., Moore, S.J., West Greenlee, M.H. 2018. The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge. Prion 2018, May 22-25, 2018, Santiago de Compostela, Spain. Paper No. P98, page 116. Interpretive Summary:
Technical Abstract: In 2006, a case of H-type bovine spongiform encephalopathy (BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K). The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease. Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route. The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure. Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with either H-type BSE from the 2004 US H-type BSE case (n=3) or from the 2006 US H-type case associated with the E211K polymorphism (n=4) using 10% w/v brain homogenates. Cattle were observed daily throughout the course of the experiment for the development of clinical signs. At approximately 50 months post-inoculation, one steer (EK211 inoculated with E211K associated H-BSE) developed clinical signs including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and was euthanized. Enzyme immunoassay confirmed that abundant misfolded protein was present in the brainstem, and immunohistochemistry demonstrated PrPSc throughout the brain. Western blot analysis of brain tissue from the clinically affected steer was consistent with the E211K H-type BSE inoculum. With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States.
With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
PRION CONFERENCE 2018 CONFERENCE ABSTRACT
Published: 23 June 2011
Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits
The present study demonstrated successful intraspecies transmission of H-type BSE to cattle and the distribution and immunolabeling patterns of PrPSc in the brain of the H-type BSE-challenged cattle. TSE agent virulence can be minimally defined by oral transmission of different TSE agents (C-type, L-type, and H-type BSE agents) [59]. Oral transmission studies with H-type BSE-infected cattle have been initiated and are underway to provide information regarding the extent of similarity in the immunohistochemical and molecular features before and after transmission. In addition, the present data will support risk assessments in some peripheral tissues derived from cattle affected with H-type BSE.
References...END
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
PLEASE NOTE;
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author:
‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
3.2.1.2 Non‐cervid domestic species
The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD‐contaminated shared rangeland and subsequently developing a novel CWD‐related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.
For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).
In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post‐infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen‐Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen‐Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life‐long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).
A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low‐level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low‐level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low‐level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.
kind regards, terry
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