Post by Terry S. Singeltary Sr. on Feb 10, 2023 15:20:50 GMT -6
OIE WAHIS SPAIN BOVINE SPONGIFORM ENCEPHALOPATHY BSE Atypical H-Type
Spain - Bovine spongiform encephalopathy - Immediate notification
GENERAL INFORMATION
COUNTRY/TERRITORY OR ZONE
ZONE
ANIMAL TYPE
TERRESTRIAL
DISEASE CATEGORY
OIE-listed
EVENT ID
4888
DISEASE
Bovine spongiform encephalopathy
CAUSAL AGENT
Bovine spongiform encephalopathy prion, atypical strain, H-type
GENOTYPE / SEROTYPE / SUBTYPE
START DATE
2023/01/21
REASON FOR NOTIFICATION
Recurrence of an eradicated disease
DATE OF LAST OCCURRENCE
2021/04/16
CONFIRMATION DATE
2023/02/03
EVENT STATUS
Resolved
END DATE
2023/02/06
SELF-DECLARATION
NO
REPORT INFORMATION
REPORT NUMBER
Immediate notification
REPORT ID
IN_159183
REPORT REFERENCE
REPORT DATE
2023/02/07
REPORT STATUS
Validated
NO EVOLUTION REPORT
EPIDEMIOLOGY
SOURCE OF EVENT OR ORIGIN OF INFECTION
Unknown or inconclusive
EPIDEMIOLOGICAL COMMENTS
Point 1 of paragraph 2, Chapter B (Measures following confirmation of a TSE in cattle) of ANNEX VII - CONTROL AND ERADICATION OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES of Regulation (EC) 999/2001 establishes that in case of confirmation of BSE in a bovine animal, all cattle identified in the following cases must be killed and completely destroyed: - in cases where the disease has been confirmed in a female, all her offspring born within two years before or after the clinical onset of the disease, - all animals in the age group of the animal in which the disease has been confirmed, - other animals present on the holding of the animal in which the disease was confirmed, or on other holdings, which may have been infected by the TSE agent or exposed to the same feed or source of contamination. Based on investigations of the two cattle identified on the case farm, they are NOT: - descendants of the affected animal, - cattle that, during their first year of life, were raised with the case so that in their first year of life they have not consumed the same feed, - cattle born during the twelve months before or after the birth of the affected animal, - nor have had access to the same feed while on the farm. So that their slaughter is not considered necessary. However, and as required by European legislation, they were identified for epidemiological investigation as in all cases of BSE.
QUANTITATIVE DATA SUMMARY
MEASURING UNIT
Animal
Species Susceptible Cases Deaths Killed and Disposed of Slaughtered/ Killed for commercial use Vaccinated Cattle (DOMESTIC)NEW11-1--TOTAL11-1--
DIAGNOSTIC DETAILS
CLINICAL SIGNS
NO
METHOD OF DIAGNOSTIC
Diagnostic test
Test name Laboratory Species sampled Outbreaks Result date Result
Antigen detection Western blot (Ag Western blot) Laboratorio Central de Veterinaria de Algete Cattle Pontevedra 2023/02/03 Positive
Immunohistochemistry (IHC) Laboratorio Central de Veterinaria de Algete Cattle Pontevedra 2023/02/03 Positive
CONTROL MEASURES AT EVENT LEVEL
CONTROL MEASURES AT EVENT LEVEL
DOMESTIC ANIMALS
WILD ANIMALS
Traceability
Applied
Official disposal of carcasses, by-products and waste
Applied
wahis.woah.org/#/in-review/4888
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.
see full report;
REPORT OF THE MEETING OF THE OIE AD HOC GROUP ON BOVINE SPONGIFORM ENCEPHALOPATHY RISK ASSESSMENT AND SURVEILLANCE
Paris, 18-21 March 2019
snip...
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.
snip...
In contrast, there have not been any substantiated reports of the successful oral transmission of H-BSE in cattle. Initial reports from Dudas et al., 2014 based on RT-QuIC pointed to the possibility of oral transmission following a very high dose (100 grams of brain material), although the individual did not display clinical signs and the findings from standard molecular or immunohistochemical assays were all negative. Investigations are ongoing in an attempt to clarify these findings.
Although significant uncertainty remains regarding the origin of C-BSE, several studies involving the serial passage of H-BSE and L-BSE in transgenic and wild-type mice have revealed their potential to lead to the emergence of a C-BSE-like phenotype (Baron et al., 2011; Torres et al., 2011; Bencsik et al., 2013) or other novel strains (Masujin et al., 2016). Whether or not one or both of these atypical strains led to the emergence of C-BSE remains speculative; however, the similarities between transmissible mink encephalopathy (TME), first reported in the USA in 1947 (Hartsough and Burger, 1965), and L-BSE indicate that TME may have been a surrogate indicator for the presence of L-BSE in cattle populations in those countries such as the USA, Canada, Germany, Finland and Russia where outbreaks of TME had been reported decades before C-BSE was first recognised in the United Kingdom in 1986 (Hadlow and Karstad, 1968; Marsh et al., 1991; McKenzie et al., 1996; Baron et al., 2007!
; Comoy et al., 2013). Although TME was originally thought to have occurred as a result of feeding mink with scrapie infected sheep carcases, oral challenge studies did not confirm this (Marsh et al., 1991). Importantly, in an outbreak reported in the USA in 1985, mink had never been fed sheep products; instead they had been fed on products derived from dead and sick dairy cattle (March et al., 1991). Similarly, from an outbreak in Canada in 1963, mink had reportedly been fed with products derived from cattle but not sheep (Hadlow and Karstad, 1968).
Although, as discussed above, the passage of H-BSE or L-BSE has been proposed as a possible explanation for the origin of C-BSE, transformation of L-BSE or H-BSE to C-BSE has not been observed so far in transmission studies in cattle. That being said, it is likely that, compared to various rodent models, an insufficient number of passages have been undertaken.
It is worth noting that sheep and goats are susceptible to L-BSE following intracerebral inoculation without lymphoid involvement in most individuals (Simmons et al., 2016; Gielbert et al., 2018; Vallino-Costassa et al., 2018). As discussed by Houston and Andreoletti (2018), C-BSE appears to increase in virulence for humans if it is first passaged in sheep. Whether or not this is the same for atypical strains remains to be determined.
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.
www.oie.int/fileadmin/SST/adhocreports/Bovine%20spongiform%20encephalopathy/AN/A_AhG_BSEsurv_RiskAss_Mar2019.pdf
***> Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
***> 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.
***> 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.
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
Hiroyuki Okada, corresponding author Yoshifumi Iwamaru, Morikazu Imamura, Kohtaro Miyazawa, Yuichi Matsuura, Kentaro Masujin, Yuichi Murayama, and Takashi Yokoyama Author information Copyright and License information Disclaimer This article has been cited by other articles in PMC. Go to: Abstract To determine oral transmissibility of the L-type bovine spongiform encephalopathy (BSE) prion, we orally inoculated 16 calves with brain homogenates of the agent. Only 1 animal, given a high dose, showed signs and died at 88 months. These results suggest low risk for oral transmission of the L-BSE agent among cattle.
Keywords: atypical bovine spongiform encephalopathy, cattle, L-type, prion, oral transmission, L-BSE, prions and related diseases, zoonoses The epidemic of bovine spongiform encephalopathy (BSE) in cattle is thought to be caused by oral infection through consumption of feed containing the BSE agent (prion). Since 2003, different neuropathologic and molecular phenotypes of BSE have been identified as causing ≈110 cases of atypical BSE worldwide, mainly in aged cattle. Although the etiology and pathogenesis of atypical BSE are not yet fully understood, atypical BSE prions possibly cause sporadic cases of BSE (1).
The L-type BSE (L-BSE) prion has been experimentally transmitted to cattle by intracerebral challenge, and the incubation period was is shorter than that for classical BSE (C-BSE) prions (2–6). The origin of transmissible mink encephalopathy in ranch-raised mink is thought to be caused by ingestion of L-BSE–infected material (7). Although L-BSE has been orally transmitted to mouse lemurs (8), it remains to be established whether L-BSE can be transmitted to cattle by oral infection. We therefore investigated the transmissibility of L-BSE by the oral route and tissue distribution of disease-associated prion protein (PrPSc) in cattle. All experiments involving animals were performed with the approval of the Animal Ethical Committee and the Animal Care and Use Committee of the National Institute of Animal Health (approval nos. 07–88 and 08–010).
snip...
The neuroanatomical PrPSc distribution pattern of orally challenged cattle differed somewhat from that described in cattle naturally and intracerebrally challenged with L-BSE (2–6,11,13,14), The conspicuous differences between the case we report and cases of natural and experimental infection are 1) higher amounts of PrPSc in the caudal medulla oblongata and the spinal cord coupled with that in the thalamus and the more rostral brainstem and 2) relatively low amounts of PrPSc in the cerebral cortices and the olfactory bulb. Furthermore, fewer PrPSc deposits in the dorsal motor nucleus of the vagus nerve may indicate that the parasympathetic retrogressive neuroinvasion pathway does not contribute to transport of the L-BSE prion from the gut to the brain, which is in contrast to the vagus-associated transport of the agent in C-BSE (15). PrPSc accumulation in the extracerebral tissues may be a result of centrifugal trafficking of the L-BSE prion from the central nervous syste!
m along somatic or autonomic nerve fibers rather than centripetal propagation of the agent (4,6,9). Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/
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.
www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/
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
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.
www.ars.usda.gov/research/publications/publication/?seqNo115=353094
see full text and more history of SPAIN CJD and BSE;
Friday, February 10, 2023
OIE WAHIS SPAIN BOVINE SPONGIFORM ENCEPHALOPATHY BSE Atypical H-Type
woahoie.blogspot.com/2023/02/oie-wahis-spain-bovine-spongiform.html
terry
Spain - Bovine spongiform encephalopathy - Immediate notification
GENERAL INFORMATION
COUNTRY/TERRITORY OR ZONE
ZONE
ANIMAL TYPE
TERRESTRIAL
DISEASE CATEGORY
OIE-listed
EVENT ID
4888
DISEASE
Bovine spongiform encephalopathy
CAUSAL AGENT
Bovine spongiform encephalopathy prion, atypical strain, H-type
GENOTYPE / SEROTYPE / SUBTYPE
START DATE
2023/01/21
REASON FOR NOTIFICATION
Recurrence of an eradicated disease
DATE OF LAST OCCURRENCE
2021/04/16
CONFIRMATION DATE
2023/02/03
EVENT STATUS
Resolved
END DATE
2023/02/06
SELF-DECLARATION
NO
REPORT INFORMATION
REPORT NUMBER
Immediate notification
REPORT ID
IN_159183
REPORT REFERENCE
REPORT DATE
2023/02/07
REPORT STATUS
Validated
NO EVOLUTION REPORT
EPIDEMIOLOGY
SOURCE OF EVENT OR ORIGIN OF INFECTION
Unknown or inconclusive
EPIDEMIOLOGICAL COMMENTS
Point 1 of paragraph 2, Chapter B (Measures following confirmation of a TSE in cattle) of ANNEX VII - CONTROL AND ERADICATION OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES of Regulation (EC) 999/2001 establishes that in case of confirmation of BSE in a bovine animal, all cattle identified in the following cases must be killed and completely destroyed: - in cases where the disease has been confirmed in a female, all her offspring born within two years before or after the clinical onset of the disease, - all animals in the age group of the animal in which the disease has been confirmed, - other animals present on the holding of the animal in which the disease was confirmed, or on other holdings, which may have been infected by the TSE agent or exposed to the same feed or source of contamination. Based on investigations of the two cattle identified on the case farm, they are NOT: - descendants of the affected animal, - cattle that, during their first year of life, were raised with the case so that in their first year of life they have not consumed the same feed, - cattle born during the twelve months before or after the birth of the affected animal, - nor have had access to the same feed while on the farm. So that their slaughter is not considered necessary. However, and as required by European legislation, they were identified for epidemiological investigation as in all cases of BSE.
QUANTITATIVE DATA SUMMARY
MEASURING UNIT
Animal
Species Susceptible Cases Deaths Killed and Disposed of Slaughtered/ Killed for commercial use Vaccinated Cattle (DOMESTIC)NEW11-1--TOTAL11-1--
DIAGNOSTIC DETAILS
CLINICAL SIGNS
NO
METHOD OF DIAGNOSTIC
Diagnostic test
Test name Laboratory Species sampled Outbreaks Result date Result
Antigen detection Western blot (Ag Western blot) Laboratorio Central de Veterinaria de Algete Cattle Pontevedra 2023/02/03 Positive
Immunohistochemistry (IHC) Laboratorio Central de Veterinaria de Algete Cattle Pontevedra 2023/02/03 Positive
CONTROL MEASURES AT EVENT LEVEL
CONTROL MEASURES AT EVENT LEVEL
DOMESTIC ANIMALS
WILD ANIMALS
Traceability
Applied
Official disposal of carcasses, by-products and waste
Applied
wahis.woah.org/#/in-review/4888
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.
see full report;
REPORT OF THE MEETING OF THE OIE AD HOC GROUP ON BOVINE SPONGIFORM ENCEPHALOPATHY RISK ASSESSMENT AND SURVEILLANCE
Paris, 18-21 March 2019
snip...
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.
snip...
In contrast, there have not been any substantiated reports of the successful oral transmission of H-BSE in cattle. Initial reports from Dudas et al., 2014 based on RT-QuIC pointed to the possibility of oral transmission following a very high dose (100 grams of brain material), although the individual did not display clinical signs and the findings from standard molecular or immunohistochemical assays were all negative. Investigations are ongoing in an attempt to clarify these findings.
Although significant uncertainty remains regarding the origin of C-BSE, several studies involving the serial passage of H-BSE and L-BSE in transgenic and wild-type mice have revealed their potential to lead to the emergence of a C-BSE-like phenotype (Baron et al., 2011; Torres et al., 2011; Bencsik et al., 2013) or other novel strains (Masujin et al., 2016). Whether or not one or both of these atypical strains led to the emergence of C-BSE remains speculative; however, the similarities between transmissible mink encephalopathy (TME), first reported in the USA in 1947 (Hartsough and Burger, 1965), and L-BSE indicate that TME may have been a surrogate indicator for the presence of L-BSE in cattle populations in those countries such as the USA, Canada, Germany, Finland and Russia where outbreaks of TME had been reported decades before C-BSE was first recognised in the United Kingdom in 1986 (Hadlow and Karstad, 1968; Marsh et al., 1991; McKenzie et al., 1996; Baron et al., 2007!
; Comoy et al., 2013). Although TME was originally thought to have occurred as a result of feeding mink with scrapie infected sheep carcases, oral challenge studies did not confirm this (Marsh et al., 1991). Importantly, in an outbreak reported in the USA in 1985, mink had never been fed sheep products; instead they had been fed on products derived from dead and sick dairy cattle (March et al., 1991). Similarly, from an outbreak in Canada in 1963, mink had reportedly been fed with products derived from cattle but not sheep (Hadlow and Karstad, 1968).
Although, as discussed above, the passage of H-BSE or L-BSE has been proposed as a possible explanation for the origin of C-BSE, transformation of L-BSE or H-BSE to C-BSE has not been observed so far in transmission studies in cattle. That being said, it is likely that, compared to various rodent models, an insufficient number of passages have been undertaken.
It is worth noting that sheep and goats are susceptible to L-BSE following intracerebral inoculation without lymphoid involvement in most individuals (Simmons et al., 2016; Gielbert et al., 2018; Vallino-Costassa et al., 2018). As discussed by Houston and Andreoletti (2018), C-BSE appears to increase in virulence for humans if it is first passaged in sheep. Whether or not this is the same for atypical strains remains to be determined.
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.
www.oie.int/fileadmin/SST/adhocreports/Bovine%20spongiform%20encephalopathy/AN/A_AhG_BSEsurv_RiskAss_Mar2019.pdf
***> Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
***> 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.
***> 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.
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
Hiroyuki Okada, corresponding author Yoshifumi Iwamaru, Morikazu Imamura, Kohtaro Miyazawa, Yuichi Matsuura, Kentaro Masujin, Yuichi Murayama, and Takashi Yokoyama Author information Copyright and License information Disclaimer This article has been cited by other articles in PMC. Go to: Abstract To determine oral transmissibility of the L-type bovine spongiform encephalopathy (BSE) prion, we orally inoculated 16 calves with brain homogenates of the agent. Only 1 animal, given a high dose, showed signs and died at 88 months. These results suggest low risk for oral transmission of the L-BSE agent among cattle.
Keywords: atypical bovine spongiform encephalopathy, cattle, L-type, prion, oral transmission, L-BSE, prions and related diseases, zoonoses The epidemic of bovine spongiform encephalopathy (BSE) in cattle is thought to be caused by oral infection through consumption of feed containing the BSE agent (prion). Since 2003, different neuropathologic and molecular phenotypes of BSE have been identified as causing ≈110 cases of atypical BSE worldwide, mainly in aged cattle. Although the etiology and pathogenesis of atypical BSE are not yet fully understood, atypical BSE prions possibly cause sporadic cases of BSE (1).
The L-type BSE (L-BSE) prion has been experimentally transmitted to cattle by intracerebral challenge, and the incubation period was is shorter than that for classical BSE (C-BSE) prions (2–6). The origin of transmissible mink encephalopathy in ranch-raised mink is thought to be caused by ingestion of L-BSE–infected material (7). Although L-BSE has been orally transmitted to mouse lemurs (8), it remains to be established whether L-BSE can be transmitted to cattle by oral infection. We therefore investigated the transmissibility of L-BSE by the oral route and tissue distribution of disease-associated prion protein (PrPSc) in cattle. All experiments involving animals were performed with the approval of the Animal Ethical Committee and the Animal Care and Use Committee of the National Institute of Animal Health (approval nos. 07–88 and 08–010).
snip...
The neuroanatomical PrPSc distribution pattern of orally challenged cattle differed somewhat from that described in cattle naturally and intracerebrally challenged with L-BSE (2–6,11,13,14), The conspicuous differences between the case we report and cases of natural and experimental infection are 1) higher amounts of PrPSc in the caudal medulla oblongata and the spinal cord coupled with that in the thalamus and the more rostral brainstem and 2) relatively low amounts of PrPSc in the cerebral cortices and the olfactory bulb. Furthermore, fewer PrPSc deposits in the dorsal motor nucleus of the vagus nerve may indicate that the parasympathetic retrogressive neuroinvasion pathway does not contribute to transport of the L-BSE prion from the gut to the brain, which is in contrast to the vagus-associated transport of the agent in C-BSE (15). PrPSc accumulation in the extracerebral tissues may be a result of centrifugal trafficking of the L-BSE prion from the central nervous syste!
m along somatic or autonomic nerve fibers rather than centripetal propagation of the agent (4,6,9). Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
www.ncbi.nlm.nih.gov/pmc/articles/PMC5324790/
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.
www.ncbi.nlm.nih.gov/pmc/articles/PMC3310119/
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
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.
www.ars.usda.gov/research/publications/publication/?seqNo115=353094
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Friday, February 10, 2023
OIE WAHIS SPAIN BOVINE SPONGIFORM ENCEPHALOPATHY BSE Atypical H-Type
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