Sunday, November 9, 2025

Feline and Canine Spongiform Encephalopathy TSE Prion Disease, Pet Food, and the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD, what if?

 Feline and Canine Spongiform Encephalopathy TSE Prion Disease, Pet Food, and the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD, what if?


Since the TSE Prion can survive the digestive track of the coyote and many other species, would it not seem prudent to eliminate those risk factor feed for animals and humans food chain?

I believe with great urgency, once again, that the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD, should be reevaluated and changed immediately to 2025 real world risk factors that would include all these species…terry

Distribution of chronic wasting disease (CWD) prions in tissues from experimentally exposed coyotes (Canis latrans) 

Published: July 9, 2025

Abstract

Cervids susceptible to chronic wasting disease (CWD) are sympatric with multiple other animal species that can interact with infectious prions. Several reports have described the susceptibility of other species to CWD prions, or their potential to transport them. One of these species is the coyote (Canis latrans), which has been previously shown to pass transmission-relevant prion titers in their feces for at least three days after ingesting prion-positive brain material. The current study followed up on these findings and evaluated the distribution of prions in multiple tissues from the same coyotes. Our results show that prions persist in the digestive tract of prion-exposed coyotes five days after exposure. Moreover, prion seeding activity was identified in other tissues, including lymph nodes and lungs. These results provide additional information about the dynamics of CWD prions in the environment and show the initial fate of prions after ingestion by a canid species that is a carnivorous predator and scavenger.

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Despite the strong species barriers, predators and scavengers may still be relevant as spreaders of infectious prion particles. In fact, both experimental research and natural observations indicate that insects, parasites, and various wild and domestic animals that co-exist with cervids can act as passive carriers of CWD prions [16–23]. For example, coyotes (Canis latrans) are relevant deer predators and scavengers. Previous studies showed that coyotes fed with an elk brain infected with CWD passed prions through their feces for at least three days after ingestion [23]. Similar observations were reported for cougars (Puma concolor) [21]. In contrast, crows (Corvus brachyrhynchos) passed prions for only few hours after ingesting infected materials [22]. Importantly, previous research in coyotes and cougars suggest that excreted prions contain decreased infectivity titers compared with the ingested material, suggesting that infectious particles are being retained in tissues within these animals, or degraded. In natural settings, prions have been identified in scat from multiple species of sympatric animals [20]. Overall, data indicates that predators and scavengers can excrete infectious prions after ingesting contaminated tissues. This, in turn, may contribute to the environmental spread of prions.

Snip…

Discussion

Here, we confirmed previous findings [23] demonstrating that predators and scavengers can spread CWD prions via feces while retaining some infectious prions in their bodies. As previously suggested, these animals may act in a dual manner, by sequestering a low proportion of the infectious particles in their bodies while also disseminating transmission-relevant titers into the environment. We explored the fate of CWD prions after entering the coyotes’ bodies by testing multiple tissues five days after ingestion. We effectively found that a number of the tissues contained in vitro (PMCA) prion seeding activities, demonstrating that some of the ingested infectious particles are retained in these animals [21]. Although some studies show that prions can be degraded by elements of the digestive tract [31], others demonstrate that their binding to other particles such as soils protects them from this degradation [32]. Further studies should explore the potential role of gastrointestinal retention and degradation in the prion infectivity titers present in excreta and whether this varies in different animal species (specifically focused in ruminants and carnivore predators).

The role of wildlife species that share environments with cervids in the translocation of CWD via feces has been experimentally explored, as well as their ability to become infected by CWD prions. The latter creates a worrisome scenario as prions adapted in a new species may generate new prion strains of unknown infectivity and host ranges [7–9]. This possibility was not explored here, due to the short post-exposure periods of this study. Previous reports suggesting that canids are resistant to prion infection [33,34] makes this possibility unlikely. Regardless, our data demonstrate that a fraction of CWD prions ingested by coyotes are incorporated in their tissues, while larger levels are released in feces. The presumable reduction of prion titers after crossing the gastrointestinal tract of predators [23] suggest that the presence of coyotes in specific environments may be beneficial in reducing CWD prions. Along this line, the expanding geographic range of coyotes in North America [35] may result in additional benefits. However, the fact that infectious relevant levels of prions are released in coyotes’ feces several days post ingestion suggest that they might promote the environmental spreading of CWD. Considering this, evaluating the dual implications of the CWD-coyote interactions in the spread and prevalence of CWD will need substantial epidemiological and molecular research efforts.

It is important to clarify certain discrepancies between the findings found in the present study compared to those communicated in the original report [23]. First, the previous article by Nichols et al. used different PMCA settings compared to those used in the current study. Specifically, the current PMCA protocol results in a considerable higher sensitivity. This explains the fact that here we detected CWD-prions in feces for additional days after prion exposure compared to the first publication.

The results presented here provide additional information on the fate of CWD prions consumed by a canid mesopredator and sheds additional light on the potential role of cervid sympatric species, specifically predators, in the ecology of CWD.


For to long, we’ve heard time and time again, Canine are resistant to Transmissible Spongiform Encephalopathy, but how many TSE Prion transmission studies have actually been done to make such a claim? How many TSE prion strains and from how many different species with TSE prion, have actually been performed on the canine? Seems Canine Cognitive Dysfunction Syndrome (CCDS), or Hound Ataxia, or Canine Spongiform Encephalopathy, is increasing. We know natural Feline Spongiform Encephalopathy exist in the field from the early days of BSE aka Mad Cow outbreak in the UK. We know that Chronic Wasting Disease CWD is highly transmissible by oral route to domestic cats. I have been very concerned with FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD, excluding CWD TSE Prion from this regulation, and Pet foods. With new transmission studies now confirming that indeed CWD will transmit by oral routes to Cattle, Sheep, Pigs, and to Cervid, oh, not to forget Camel Prion Disease. it is past time to reevaluate the FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD, and to enhance it to include theses species, immediately…terry

Feline and Canine Spongiform Encephalopathy, Pet Food, and the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD, what if?

“The publication stipulates requirements for animal ingredients, production conditions, manufacturing facilities and quarantine inspection by the exporting country for pet food imported into the Republic of Korea, in accordance with the Act on the Prevention of Contagious Animal Diseases. The IHRs apply to pet food intended for dogs, cats, ferrets, and hamsters. (Note: As these companion animals are omnivores, their pet food typically contains animal ingredients.)”

Voluntary Report – Voluntary - Public Distribution Date: February 19, 2025

Report Number: KS2025-0007

Report Name: Korea's New Import Health Requirements for Pet Food Country: Korea - Republic of

Post: Seoul

Report Category: Export Accomplishments - Market Access

Livestock and Products, Sanitary/Phytosanitary/Food Safety, MISC-Commodity, Prepared By: Shoshana Griffith

Approved By: Mark Dries

Report Highlights:

On January 14, 2025, Korea’s Ministry of Agriculture, Food and Rural Affairs (MAFRA) published new import health requirements (IHRs) for pet food, which are effective immediately. With the new IHRs, there is now a pathway to approve U.S. pet food products containing ruminant ingredients, which had been banned since 2003. Pet food products that have been exported to Korea within the last year may continue to use their existing health certificates until December 31, 2025. New-to-market products or those that have not been imported into Korea within the last year, should comply with the new IHRs.

THIS REPORT CONTAINS ASSESSMENTS OF COMMODITY AND TRADE ISSUES MADE BY USDA STAFF AND NOT NECESSARILY STATEMENTS OF OFFICIAL U.S. GOVERNMENT POLICY

Korea Publishes Import Health Requirements for Pet Food

Korea’s Ministry of Agriculture, Food, and Rural Affairs (MAFRA) published the final import health requirements (IHRs) for pet food on January 14, 2025. The new requirements are effective immediately, but there is a grace period until the end of the calendar year 2025 for products that have been imported into Korea during the year prior to publication.

The publication stipulates requirements for animal ingredients, production conditions, manufacturing facilities and quarantine inspection by the exporting country for pet food imported into the Republic of Korea, in accordance with the Act on the Prevention of Contagious Animal Diseases. The IHRs apply to pet food intended for dogs, cats, ferrets, and hamsters. (Note: As these companion animals are omnivores, their pet food typically contains animal ingredients.) Pet food manufacturing facilities must undergo inspection by the exporting country’s government to assure compliance with Korea’s requirements. The competent authority of the exporting country will work with the Korean government veterinary quarantine authority to notify inspection results and obtain approval of pet food manufacturing facilities through on-site inspections or other methods. For the United States, the competent authority is the USDA’s Animal and Plant Health Inspection Service (APHIS). Korea’s competent authority is the Animal and Plant Quarantine Agency (APQA) of MAFRA.

The full Korean text of the IHRs is available through the National Legislation Information Center and the MAFRA Announcement from January 14. A side-by-side English translation provided by MAFRA is attached to this report. This is an unofficial translation. The original Korean text takes precedence over the English translation.

Implementation Timeline

Although the notice went into effect January 14, 2025, MAFRA outlined interim measures to minimize trade disruption.

Pet food that has been imported into Korea within the past year from the date of enforcement (January 14, 2025) may be imported using the existing health certificate format until December 31, 2025, even if APQA has not yet approved the health certificate format as described in the IHRs.

Manufacturing facilities that have exported pet food to Korea within the past year from the date of enforcement and have no quarantine violations may be approved through a document review. Korea’s APQA may conduct on-site inspections if necessary. The quarantine authorities of the

THIS REPORT CONTAINS ASSESSMENTS OF COMMODITY AND TRADE ISSUES MADE BY USDA STAFF AND NOT NECESSARILY STATEMENTS OF OFFICIAL U.S. GOVERNMENT POLICY

exporting country shall provide information requested by the Korean government to verify the export performance of the manufacturing facility.

Pathway for Pet Food Containing Ruminant Ingredients

With these IHRs, Korea has created a process to allow importation of U.S. pet food containing ruminant ingredients, which had been banned since 2003 following the first U.S. bovine spongiform encephalopathy (BSE) case. Pet food products containing ruminant ingredients will be considered a new-to-market product under the new IHRs. As these products do not have an existing health certificate and have not been exported to Korea in the last year, they must follow the new process outlined in the IHRs, including having the manufacturing facility approved by MAFRA. Even if the same facility already exports non-ruminant product to Korea, MAFRA needs to approve the facility for the new product.

The United States originally requested resumption of market access for pet food containing ruminant ingredients in 2006. Although U.S. beef access had resumed, ruminant ingredients remained prohibited in U.S. pet food exports to Korea. In 2018, the United States submitted an expanded market access request for pet food containing U.S.-origin ruminant ingredients, as well as any ruminant ingredients imported from BSE-negligible risk countries. Since 2018, APQA has been drafting the new IHRs to reflect Korea’s updated assessment of the potential risk for BSE in imported pet food.

Support for U.S. Exporters

New-to-market products, including those with ruminant ingredients, or those that have not been imported into Korea within the last year, must comply with the new IHRs. Interested companies may begin the process to have their products and facilities registered by contacting the USDA Korea offices at AgSeoul@usda.gov.

For more information on Korea’s pet food market and practical considerations for exporters, please refer to the 2024 South Korea Pet Food Report.

Attachments: Import Health Requirements for Pet Food (MAFRA translation 02.07.25).pdf

https://apps.fas.usda.gov/newgainapi/api/Report/DownloadReportByFileName?fileName=Korea%27s%20New%20Import%20Health%20Requirements%20for%20Pet%20Food_Seoul_Korea%20-%20Republic%20of_KS2025-0007.pdf

Thursday, February 27, 2025

South Korea: Korea's New Import Health Requirements for Pet Food

February 19, 2025 | Attaché Report (GAIN) | KS2025-0007

https://fdabse589.blogspot.com/2025/02/south-korea-koreas-new-import-health.html

Canine Spongiform Encephalopathy CSE TSE Prion

ORIGINAL RESEARCH article Front. Vet. Sci., 28 October 2025 Sec. Veterinary Neurology and Neurosurgery Volume 12 - 2025 | https://doi.org/10.3389/fvets.2025.1685430

Current practices for diagnosis and management of Canine Cognitive Dysfunction Syndrome in the United States

Katherine E. SimonKatherine E. SimonMargaret E. Gruen&#x;Margaret E. Gruen†Natasha J. Olby &#x;Natasha J. Olby*† Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, United States Introduction:

There are currently no accepted guidelines for the diagnosis and management of Canine Cognitive Dysfunction Syndrome (CCDS). The objective of this study was to describe the current diagnostic and management practices regarding CCDS by veterinarians in the United States (US).

Methods: An anonymous online survey was distributed to veterinary practitioners from January to May 2025. The survey included questions regarding patient population, CCDS diagnosis and treatment and client interactions.

Results: A total of 318 survey responses were obtained from veterinarians who saw companion dogs regularly. Nearly all (97.2%) had made a diagnosis of CCDS in their career, citing patient history and clinical signs/ behavioral changes as the tools they use to make a diagnosis. Most veterinarians (approximately 80%) rarely or never referred their potential CCDS cases to a veterinary specialist. When managing their CCDS patients, pharmaceuticals are most often recommended, specifically selegiline. Selegilline was also considered most effective in managing CCDS, however this view was held by only about 30% of veterinarians. Responses reflected uncertainty regarding best practices and treatment efficacies, with veterinarians citing lack of knowledge and owner-related barriers such as lack of interest or financial constraints as factors which hinder treatment recommendations.

Discussion: Results from this survey underscore there are still significant gaps in knowledge as to best practices for the diagnosis and management of CCDS. Clear CCDS diagnostic and management guidelines are needed to support veterinarians and address the therapeutic needs of patients.

Introduction Canine Cognitive Dysfunction Syndrome (CCDS) is a canine analog of Alzheimer’s Disease (AD), characterized by behavioral changes which develop with advanced age (1–3). These include changes in social interactions (reduced responsiveness to familiar people/objects, aversion to petting), loss of spatial orientation (disorientation, wandering), disturbance of sleep–wake cycles, development of house soiling (urination or defecation in an unusual location), and development of anxiety and/or aggression (4, 5). Several studies have characterized AD-like neuropathology in elderly dogs, with findings such as amyloid beta accumulation, oxidative damage and neuroinflammation correlating with performance on cognitive assessments and/or behavioral questionnaires (6–9).

In human medicine, diagnosis of AD has evolved over the last 50 years, now encompassing different stages of disease (preclinical, mild cognitive impairment (MCI) and dementia) (10–12). In 2024, the National Institute on Aging and the Alzheimer’s Association (NIA-AA) released updated guidelines to inform diagnosis and staging of AD (13). These guidelines emphasize a biological definition of disease, relying heavily on biomarkers and diagnostic imaging, including blood-based markers, cerebrospinal fluid and positron emission tomography (PET) to achieve this. Biomarkers can be categorized as core, non-specific, or non-AD, and different types may offer differing utility to diagnosis, staging or prognosis (13). Given that biomarker abnormalities often precede clinical symptoms, they are critical to identifying individuals in the earliest phases of disease (14–16). In addition to biomarkers, accurate diagnosis relies upon clinical and functional evaluation including thorough history, physical examination, cognitive testing, advanced imaging, and laboratory tests (17). However, diagnostic workups are inconsistent due to differing individual presentations/trajectories, clinician preference, cost, or limited access to diagnostic resources (18–20). This inconsistency, even with formally established guidelines, has posed a significant barrier to understanding and treating AD (21, 22).

In dogs, the absence of formal diagnostic criteria for CCDS makes consistent and standardized clinical evaluation even more difficult. The behavioral abnormalities associated with CCDS can be captured using validated caregiver questionnaires (4, 5, 23). However, these are not specific diagnostic tests, and many of the behaviors described can be caused by other medical conditions such as (but not limited to) sensory decline (vision or hearing loss), chronic pain, renal disease, or intracranial neoplasia (24, 25). As such, a thorough diagnostic workup including signalment, detailed patient history, physical and neurological examination, laboratory testing and advanced imaging (radiographs, MRI) is indicated to exclude other differential diagnoses (3, 24, 26). While a few studies have suggested circulating biomarkers to be indicative of CCDS based on either caregiver questionnaires or cognitive assessments, they are not yet considered to be diagnostic (7, 27–31). As such, they have yet to employed in a point-of-care setting (32).

Diagnostic challenges are compounded by limited agreement on best therapeutic approaches. Currently, selegiline is the only drug in the United States approved by the Food and Drug Administration for treatment of canine cognitive dysfunction (33). However, there are many supplements and specialized diets formulated to promote cognitive improvement in aging dogs (34–38). Despite the availability of these products, the evidence supporting their efficacy remains variable. Further, it can be difficult to compare management options given the varying study designs, cognitive outcomes, and populations in which each was investigated. This makes selecting an appropriate intervention to recommend to patients challenging.

Little research has been performed to explore the perspectives of veterinarians regarding the diagnostics and treatments they perceive are most helpful and effective in clinical practice. The objective of this study was to describe the current practices of veterinarians in the United States (US) when making a diagnosis and management plan in a patient with CCDS. We hoped to identify gaps in practice which may be addressed through intentional educational and research efforts.

Materials and methods

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Results We obtained 471 survey responses, of which 319 were from veterinarians practicing in the US and completed in entirety. One respondent reported that they did not see dogs in their routine patient population and was therefore excluded from our analysis. Therefore, the final number of survey responses included in the descriptive analysis was 318; however, the number of responses included in subsequent analyses vary based on question-specific inclusion criteria.

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Discussion In this study, we set out to describe how veterinarians are currently diagnosing and managing CCDS in clinical practice. We obtained 318 responses from veterinary clinicians in the US who see dogs in their routine patient population, the majority of whom were general practitioners. While nearly all respondents had diagnosed CCDS at some point in their careers, the frequency of diagnosis appeared lower than expected, with most veterinarians reporting relatively few (1–15) cases diagnosed per year. These diagnoses are most often happening in dogs aged 13–15 years old. To establish a diagnosis, all but two veterinarians reported relying on patient history and clinical signs or behavioral changes. However, no single clinical sign emerged as the most common indicator. Over 80% of veterinarians reported recommending supplements or pharmaceuticals when managing patients with CCDS. When asked to identify the most effective intervention, the majority cited pharmaceuticals, most commonly selegiline, as the most effective treatment option. These data can serve as a guide to better establish practical consensus as to which diagnostic tools and treatments are most relevant to primary care practice.

We found that most veterinarians (over 90%) reported prior exposure to educational content on CCDS, either during veterinary school or through specialized continuing education training. Despite this, approximately half of respondents still reported a lack of knowledge regarding available treatment options, suggesting a disconnect between education and clinical confidence or application. Expansion of curriculum specific to geriatric medicine and CCDS may enhance the knowledge bases of future veterinarians. Another potential contributor to this gap may be the underutilization of key diagnostic tools. For example, only about half (~49%) of veterinarians reported performing a neurological examination when assessing a CCDS patient and less than 2% perform imaging. Given that CCDS is a diagnosis of exclusion, a neurological exam and/or imaging may be essential to ensure the rule-out of other conditions that could account for similar age-related behavioral changes (30). While imaging is expensive and not always available in all clinical settings, a neurological examination is relatively accessible and easy to perform. However, its limited use may reflect a phenomenon known as neurophobia, which has been documented in both human and veterinary medicine and refers to an aversion toward clinical neurology and the neurosciences among clinicians (40–42). A similar trend has been observed in veterinary behavioral medicine, where many clinicians report feeling underprepared to manage behavioral cases (43). Despite this, the majority of veterinarians in our study appear to be managing CCDS cases themselves, rather than referring to veterinary specialists (neurologists, behaviorists or internists), consistent with a recent study by Haake et al. (44). These findings highlight the prominent role of general practitioners in diagnosing CCDS. Therefore, efforts should be made to improve education and confidence in these skills, especially among general practitioners, to appropriately identify and manage CCDS.

When asked directly if there was anything that would improve their diagnostic confidence, only 2.5% of respondents selected no options, indicating that the vast majority of veterinarians felt as though additional aids could enhance their confidence. Approximately 64% indicated that they would like standardized diagnostic criteria and guidelines for discriminating CCDS from other differentials. In human medicine, there exist several guidelines for AD (across different working groups) which incorporate clinical cognitive changes, biomarker evidence and rule-out of non-dementia differentials (10–12, 17). However, even with these formally defined guidelines, many patients still go undiagnosed (45–47). This highlights the inherent difficulty of diagnosing a syndrome with gradual onset and variable progression in elderly individuals, even in well-resourced settings. Similarly, while CCDS is thought to affect a substantial proportion of senior dogs, it has been reported that a much smaller proportion gets formally diagnosed by a veterinarian (44, 48). It remains unclear whether this underdiagnosis reflects a true failure to identify symptomatic cases, whether some dogs die before cognitive signs become apparent, or whether diagnosis is deprioritized in the context of more pressing comorbidities, caregiver burden, or limited treatment options. These discrepancies may also reflect a disconnect between the veterinarian communicating the diagnosis and an owner understanding or accepting the diagnosis to the extent they are able to report it in a survey. Still, there exist resources to aid in CCDS screening which are appearing to be under-utilized, with only about a third of veterinarians using a screening questionnaire, similar to that reported in a recent Australian survey (49). Until the field establishes specific guidelines, these questionnaires offer a validated framework for linking observed behavioral changes with probable diagnosis of CCDS once systemic conditions have been ruled out (4, 5, 29, 50).

When considering all interventions, about 90% of veterinarians felt that current treatment strategies were only slightly or moderately effective. Over 80% of veterinarians recommend using pharmaceuticals or supplements, with selegiline being the most frequently recommended product. This is consistent with a recent study performed in Australia which determined that CCDS was most commonly managed by medications (selegiline, propentofylline), environmental modifications, and anti-anxiety treatments (49). After selegiline, the most recommended products in our survey were Purina ProPlan NeuroCare® and melatonin. Both selegiline and diets enriched with medium-chain triglycerides have shown some efficacy in supporting cognitive function in senior dogs (36, 51, 52). Conversely, while there has been some evidence that melatonin attenuates cognitive impairments in humans, this has yet to be specifically studied in dogs with CCDS (53). This aligns with ~25% of respondents who indicated that a lack of testing in clinical trials was a barrier to them recommending specific products, underscoring the need for both expanded clinical research and improved dissemination of existing evidence. However, almost half of respondents (~47%) cited lack of knowledge as a barrier to recommendation, consistent with the discordance observed between specific products recommendations and management strategies selected by respondents. For example, some veterinarians, selected pharmaceuticals as most effective overall strategy and then selected a supplement as the single most effective product or vice versa. This may reflect either lack of clarity between which products meet the definition of a supplement versus a pharmaceutical or, more likely, reflect a broader ambiguity as to what is effective (whether based on anecdotal evidence or limited testing in clinical trials). Further, 39 respondents indicated that they do not find any commercially available products to be effective, despite indicating that they recommend at least one of the products listed in the survey, reflective of a discrepancy between products being recommended and those perceived as effective. Broader discordance is additionally supported by the frequency of write-in responses describing use of non-specific therapies, generalized uncertainty, and/or emphasizing patient/owner specific factors which dictate selection of treatment and its impact. All together, these inconsistencies underscore the uncertainty and varying opinions surrounding efficacy of these products.

While we did not specifically list any anxiolytics in our questions surrounding the treatment of CCDS, many respondents used the “other” selection to identify their use. Given the established connection between dementia and anxiety across both humans and dogs (54–56), future studies could investigate the utility of anti-anxiety medication in the treatment of CCDS. However, a few veterinarians expressed caution with polypharmacy, citing concern for drug interactions, particularly between selegiline and fluoxetine. In humans, co-administration of an SSRI (selective serotonin reuptake inhibitors, ex: fluoxetine) and an MAO-B (monoamine oxidase B inhibitor, ex: selegiline) have been reported, though rarely, to be associated with cases of serotonin syndrome (57–59). This potential risk has been extrapolated to veterinary patients, although direct evidence of this interaction in dogs remains limited. The risks of polypharmacy in elderly patient populations are also well-documented in human medicine but require further exploration in elderly veterinary patients (60–62).

Another incidental finding from our survey was that the majority of respondents’ practices (~68%) do not have specified senior visits, despite large proportions of patient populations being senior (majority between 21 and 60%). Therefore, clients and veterinarians may not have the opportunity to proactively discuss CCDS and other age-related conditions in an efficient and comprehensive way. Further, there is a disparity between veterinarians, who reported strong to moderate concern for CCDS in their senior dog patients, as opposed to their perception of the level of concern held by clients (only moderate to slight). Effective client communication is essential to bridge this gap, however, based on our survey, these conversations are not always led by the veterinarian, and often wait until specific symptoms are mentioned or until the client initiates the conversation. Given that the single most significant risk factor for CCDS is age (48, 63), providing designated visits for all patients above a certain age, which incorporate CCDS screening, may help both the veterinarian and the client to address these concerns before they become unmanageable.

Our study has some limitations. While our findings were consistent with the recent Australian survey, we ultimately did screen for respondents who were practicing veterinarians in the US which may limit extrapolation to other populations. Another limitation is that given this was a voluntary online survey without incentive, it is highly susceptible to response bias. Likely, practitioners who are especially motivated toward senior patients or interested in CCDS were more motivated to respond to the survey. This is further supported by most respondents (approximately 47%) considering themselves to have a special interest in geriatric medicine. Further, individuals with greater technological proficiency may have been more likely to encounter and complete the survey. This is supported by majority of respondents having graduated in the past decade making them presumably younger and more comfortable with digital platforms. However, the COVID-19 pandemic did rapidly increase technological competence across more demographics, especially those who are considered health professionals (64–66).

While we sought to collect responses from all over the country (based on distribution by several state-related Veterinary Medical Associations) (reported in Supplementary Data Sheet 2), the anonymity of the survey precludes our ability to confirm geographic diversity. Future studies including specific analyses of geographic differences (i.e., by state or urban vs. rural) in diagnostic and management practices could provide insight into factors contributing to practice variation. Moreover, increased participation would strengthen the study as we were unable to reach our goal of 385 responses. Therefore, this study is likely underpowered. Additionally, the sample size estimated in the power analysis was based on a conservative estimate of all veterinarians in the US, rather than specifically only those who routinely see dogs, which may affect the precision of the power analysis. Nevertheless, the diversified distribution and targeted screening strategy support the representativeness of the collected sample for the population of interest. Finally, in this study we focused on the perspectives of veterinarians, but evidence demonstrates that veterinarians and dog owners disagree in their opinions of veterinary care for elderly patients (67). Future studies should examine owner perspectives on the identification and management of CCDS in their pets.

Veterinarians play a key role in identifying age-related disease in companion animals (68–70). In this study, we found that while most veterinarians have diagnosed a dog with CCDS at some point in their career, not many diagnose these cases regularly. To make a diagnosis, veterinarians are using a combination of tools, but most commonly rely on patient history and clinical signs. To treat CCDS, most veterinarians use pharmaceuticals and supplements, and many find selegiline to be the most effective treatment option. However, current treatment strategies were collectively described as only slightly or moderately effective at best. When asked what is preventing their recommendation of currently available treatments, respondents reported a lack of knowledge with almost all respondents desiring more information on CCDS. Together, this highlights the need for increased education and consensus surrounding the diagnosis and management of CCDS. Veterinarians would benefit from clear guidelines which are based on scientific evidence. Efforts should aim to increase veterinarian’s knowledge and familiarization of CCDS in order to fully address any needs and concerns of both patients their owners.

Data availability statement The original contributions presented in the study are included in the article/Supplementary material, further inquiries can be directed to the corresponding author.


“There are currently no accepted guidelines for the diagnosis and management of Canine Cognitive Dysfunction Syndrome (CCDS).”

I remember what MAFF DEFRA told me way back in earl BSE nvCJD days about THE HOUND STUDY…

*** DEFRA TO SINGELTARY ON HOUND STUDY AND BSE 2001 ***

DEFRA Department for Environment, Food & Rural Affairs Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk GTN: FAX: 

Mr T S Singeltary P.O. Box Bacliff Texas USA 77518 

21 November 2001

Dear Mr Singeltary

TSE IN HOUNDS Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding. As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to peer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less critical.

For more details see- http://www.bseinquiry.gov.uk/files/yb/1995/06/21005001.pdf

new url;


As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address. Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

I hope this is helpful Yours sincerely

HUGH MCDONAGH BSE CORRESPONDENCE SECTION

======================================

HOUND SURVEY I am sorry, but I really could have been a co-signatory of Gerald's minute. I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding. If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service. J W WILESMITH Epidemiology Unit 18 October 1991 Mr. R Bradley cc: Mr. G A H Wells

http://collections.europarchive.org/tna/20081106102318/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf

see new url;


3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.

http://collections.europarchive.org/tna/20080103034308/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf

see new url;


TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS

http://www.mad-cow.org/00/aug00_late_news.html#ggg


TSE & HOUNDS GAH WELLS (very important statement here...TSS)

HOUND STUDY AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease. snip...


76 pages on hound study; snip...


The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.

38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.

40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.

41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished. Histopathological support to various other published MAFF experiments

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).


It was thought likely that at least some, and probably all, of the cases in zoo animals were caused by the BSE agent. Strong support for this hypothesis came from the findings of Bruce and others (1994) ( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. & Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and scrapie to mice: strain variation and species barrier. Philosophical Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405 ), who demonstrated that the pattern of variation in incubation period and lesion profile in six strains of mice inoculated with brain homogenates from an affected kudu and the nyala, was similar to that seen when this panel of mouse strains was inoculated with brain from cattle with BSE. The affected zoo bovids were all from herds that were exposed to feeds that were likely to have contained contaminated ruminant-derived protein and the zoo felids had been exposed, if only occasionally in some cases, to tissues from cattle unfit for human consumption.

snip...

10. The case of SE in a cheetah that occurred during the period, involved a 7 year-old female which had been born and lived all her life at Whipsnade (except for the final stages when she was moved to the Animal Hospital at Regent’s Park for diagnosis and treatment). This animal, which died in December 1993, had been fed on cuts of meat and bone from carcases of cattle unfit for human consumption and it was thought likely that she had been exposed to spinal cord (Kirkwood, J.K., Cunningham, A.A., Flach, E.J., Thornton, S.M. & Wells, G.A.H. (1995) Spongiform encephalopathy in another captive cheetah (Acinonyx jubatus): evidence for variation in susceptibility or incubation periods between species. Journal of Zoo and Wildlife Medicine 26, 577-582: J/ZWM/26/577).

11. During the period we also collated information on cases of SE that occurred in wild animals at or from other zoos in the British Isles. The total number of cases of which I was aware in June 1996, when I presented a review on occurrence of spongiform encephalopathies in zoo animals (at the Royal College of Pathologists’ Symposium on Transmitting prions: BSE, CJD, and other TSEs, The Royal Society, London, 4th July 1996), was 25, involving 10 species. The animals involved were all from the families Bovidae and Felidae, and comprised:

1 Nyala Tragelaphus angasi,

5 Eland Taurotragus oryx,

6 greater kudu Tragelaphus strepsiceros,

1 Gemsbok Oryx gazella,

1 Arabian oryx Oryx leucoryx,

1 Scimitar-horned oryx Oryx dammah,

4 Cheetah Acinonyx jubatus,

3 Puma Felis concolor

2 Ocelot Felis pardalis,

and 1 Tiger Panthera tigris.

(A spongiform encephalopathy, which was thought probably to have a different aetiology, had also been reported in 3 ostriches Struthio camelus in Germany). This list did not include cases of BSE in domesticated species in zoos (ie BSE in Ankole or other cattle, or SEs, assumed to be scrapie, in mouflon sheep Ovis musimon).


PRION 2016 TOKYO http://prion2016.org/

OR-09: Canine spongiform encephalopathy—A new form of animal prion disease

Monique David, Mourad Tayebi UT Health; Houston, TX USA

It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8

Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.

Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.

In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.

If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).

References

http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf



=======================================

2013 Strain characteristics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibility of rabbits and dogs to prion infections should not alter their zoonotic potential if these animals became infected with BSE.

=======================================

Neurobiology of Disease Bovine Spongiform Encephalopathy Induces Misfolding of Alleged Prion-Resistant Species Cellular Prion Protein without Altering Its Pathobiological Features

Enric Vidal3, Natalia Fernández-Borges1, Belén Pintado4, Montserrat Ordóñez3, Mercedes Márquez6, Dolors Fondevila5,6, Juan María Torres7, Martí Pumarola5,6, and Joaquín Castilla1,2 + Author Affiliations 1CIC bioGUNE, 48160 Derio, Bizkaia, Spain, 2IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Bizkaia, Spain, 3Centre de Recerca en Sanitat Animal, Campus de la Universitat Autònoma de Barcelona (UAB)-IRTA, 08193 Bellaterra, Barcelona, Spain, 4Centro Nacional de Biotecnología, Campus de Cantoblanco, 28049 Cantoblanco, Madrid, Spain, 5Department of Animal Medicine and Surgery, Veterinary Faculty, UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, 6Murine Pathology Unit, Centre de Biotecnologia Animal i Teràpia Gènica, UAB, 08193 Bellaterra (Cerdanyola del Vallès), Barcelona, Spain, and 7Centro de Investigación en Sanidad Animal-Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, 28130 Valdeolmos, Madrid, Spain Author contributions: E.V., N.F.-B., and J.C. designed research; E.V., N.F.-B., B.P., M.O., M.M., D.F., and J.C. performed research; E.V., N.F.-B., B.P., and J.C. contributed unpublished reagents/analytic tools; E.V., N.F.-B., B.P., M.O., M.M., D.F., J.M.T., M.P., and J.C. analyzed data; E.V. and J.C. wrote the paper.

Abstract

Bovine spongiform encephalopathy (BSE) prions were responsible for an unforeseen epizootic in cattle which had a vast social, economic, and public health impact. This was primarily because BSE prions were found to be transmissible to humans. Other species were also susceptible to BSE either by natural infection (e.g., felids, caprids) or in experimental settings (e.g., sheep, mice). However, certain species closely related to humans, such as canids and leporids, were apparently resistant to BSE. In vitro prion amplification techniques (saPMCA) were used to successfully misfold the cellular prion protein (PrPc) of these allegedly resistant species into a BSE-type prion protein. The biochemical and biological properties of the new prions generated in vitro after seeding rabbit and dog brain homogenates with classical BSE were studied. Pathobiological features of the resultant prion strains were determined after their inoculation into transgenic mice expressing bovine and human PrPC. Strain characteristics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibility of rabbits and dogs to prion infections should not alter their zoonotic potential if these animals became infected with BSE. This study provides a sound basis for risk assessment regarding prion diseases in purportedly resistant species.

Received January 18, 2013. Revision received March 7, 2013. Accepted March 23, 2013. Copyright © 2013 the authors 0270-6474/13/337778-09$15.00/0


Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY

From: Steve Dealler <deal@AIRTIME.CO.UK>

Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>

Date: Fri, 18 Oct 2002 23:12:22 +0100

Content-Type: text/plain Parts/Attachments: text/plain (126 lines)

######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########

Dear Terry, An excellent piece of review as this literature is desperately difficult to get back from Government sites.

What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currently then you wont find any!

Steve Dealler

"Terry S. Singeltary Sr." wrote:

######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########

Greetings BSE-L,

is there any other CWD surveys/testing in the UK on their deer?

what sort of testing has been done to date on UK/EU deer?

any input would be helpful... thank you

DEER SPONGIFORM ENCEPHALOPATHY SURVEY

http://www.bse.org.uk/files/yb/1991/11/20004001.pdf


Mr P Gayford V I Section MAFF Tolworth (TJ) Your relerene Our refcrence Date 4 Noveaber 1992 RJH/ASB

DEER SPONGIFOR ENCEPHALOPATHY SURVEY

Date 4 Norember 1992 f.JH/ASB

DEER SPONGIFORM ENCEPHALOPATHY SURVEY

Dear Paul

I have now found time to review the 10 deer brains collected fron Mr. Walker' farm via Winchester VIC. In answer to your specific question was there sufficien difference in preservation of brain tissue to warrant the extra effort involved i rapid brain removal on the farm, the answer is definitely "Yes." The origina rive brains (Winchester ref M487/11) showed varying degrees of autolytic vacuolation affecting both white and grey matter throughout the brain, vacuolation and separation of Purkinje cells and marked perivascular spaces. These artifacts made interpretation of subtle, specific pathological vacuolation more difficult.

By contrast the second submission (Winchester reference M736/2) showed excellent preservation of white and grey matter. Any vacuolar change present could be confidently interpreted as pathological, albeit of unknown pathogenesis. I can only reiterate the comments made by Gerald Wells and myself at the preliminary discussion at Weybridge in Autumn 1991. If the survey's purpose is an accurate histopathological interpretation of brain tissue, the material must br collected in a pristine state. This is particularly valid when looking for ar unrecognised and undefined spongiform encephalopathy in a new species. Deer brains are very large structures which take a lot of fixation and therefore mut be handled sympathetically from the start. We have already seen the problem: encountered in comparatively smaller hound brains where delayed fixation was a major limitation on interpretation of true pathological change. The bottom line must be that if a pathologist's expertise is to be used, it is critical to collect artefact free brain material . If the politics or economics do not allow this, then I would suggest that an electron microscopy survey involving detection of scrapie associated fibrils would be much more appropriate. Best wishes Yours sincerely R J HIGGINS VIO

http://www.bse.org.uk/files/yb/1992/11/04002001.pdf


Hound Study

I am sorry, but I really could have been a co-signatory of Gerald's minute.

I do not think that we can justify devoting any resources to this study. especially as larger and more important projects such as the pathogenesis study will be quite demanding.

If there is a political need to continue with the examination of hound brains then it should be passed entirely to the VI Service.

http://www.bse.org.uk/files/yb/1991/10/18001001.pdf


3.3 Mr RJ Iliggins in conjunction with Mr G A Wells and Mr A C Scott would, by the and of the year, identify the three brains that were from the "positive"end of the lesion spectrum. These would need to be SAF inconclusive (fibrils observed) and histopathologicaly unresolved. They would also identify the best site of the brain to sample for the survey. These would be likely to be a portion of the medulla near the obex and a portion of spinal cord. Very little (less than a gram) of tissue was required. At the same time three "negative" brains from the negative end of the lesion spectrum would siso be identified. These "negative" brains would be held pending the work on the "positive" brains. The kennels from which the hound brains were derived should be geographically well seperated.

http://www.bse.org.uk/files/yb/1993/12/06001001.pdf


37.Putative TSE in hounds - work started 1990 -(see para 41)

Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.

38.I reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.

40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.

41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished.

Histopathological support to various other published MAFF experiments

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).

http://www.bse.org.uk/witness/htm/stat067.htm


See hound survey histopath


Annex 67


maddogs and Englishman

http://www.bse.org.uk/files/yb/1990/11/28001001.pdf


kind regards,

terry

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

snip...

''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

Table 9 presents the results of an analysis of these data.

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;




Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk

BSE Inquiry Steve Dealler

Management In Confidence

BSE: Private Submission of Bovine Brain Dealler

snip...end

########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

BSE INQUIRY

CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane

BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.


TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..

see references:

DEER BRAIN SURVEY


CONFIDENTIAL AND IN CONFIDENCE TRANSMISSION TO CHIMPANZEES AND PIGS

IN CONFIDENCE

TRANSMISSION TO CHIMPANZEES

Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.

We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, i/p and i/v).

I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.

In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.

A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans ‘susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday's meeting.

R Bradley

CVO (+ Mr Wells’ commenters 23 September 1990 Dr T W A Little Dr B J Shreeve

90/9.23/1.1


########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############

------- Original Message --------

Subject: Cognitive Dysfunction Syndrome (CDS) or MAD DOG DISEASE

Date: Mon, 4 Apr 2005 13:14:12 -0500

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@KALIV.UNI-KARLSRUHE.DE

##################### Bovine Spongiform Encephalopathy #####################

Greetings,

THIS is a hoot from purina, as to why your dog might be acting a bit strangely. nothing mentioned about the decades of feeding those dogs the same thing we been feeding humans, potentially tainted feed, tainted with TSEs. dog food (like cat food) is loaded with SRMs. new regulations are suppose to go into effect, but that will not help all the animals exposed over the decades. some data on dogs, cats and TSE.

THE reason of bringing this up again, there was a small write-UP in question to a Dr. Michael Fox about this in the Houston Chronicle 'Easing Life of older dogs' ; 'My black Lab is 12 years old and has entered his ''Alzheimer's'' phase ... 'it's called canine cognitive dysfunction disorder ...

snip... end

SO, went to see what the feed sellers say about this ; Does your dog suffer from Cognitive Dysfunction Syndrome? Find out how to cope with dog dementia. Typically, an elderly dog tends to sleep longer hours and slow down in comparison to his or her younger or middle-aged years. But some older dogs exhibit behaviour changes that appear abnormal. Until recently, such changes had been attributed to normal aging, for which little could be done. However, behaviour changes in elderly dogs may be due to a disorder called Cognitive Dysfunction Syndrome. Cognitive Dysfunction Syndrome (CDS) is associated with a number of clinical signs. The diagnosis is made when dogs exhibit multiple signs which develop in old age, and which are not completely due to other medical or physical problems. Dogs with CDS may appear disoriented in familiar surroundings such as their own homes, wandering aimlessly and perhaps appearing to 'forget' to back out of corners.

Those that were flawlessly housetrained throughout their lives may start to have 'accidents'. They may no longer greet their owners at the door, bring them balls to throw, or appear to care about being petted. And while they may sleep throughout the day, the night may bring restlessness and increased wandering, as though their biological clocks were reversed. Because aging dogs are increasingly susceptible to medical problems (see 'The Elderly Dog'), regular examinations by a vet are important. Only a veterinary surgeon can determine whether your dog's behaviour changes are due to CDS (rather than, for example, liver, heart, or kidney disease). If a diagnosis of CDS is made, your vet may recommend treatment. Behaviour changes in aging dogs may be responsive to treatment. Whatever, happens, after a lifetime of unconditional love and companionship, our older dogs deserve every consideration we can give them.

http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=71


Is your dog elderly? If so, you'll have to ease their way. Here's how...

Often dogs are older than we think they are. It's hard to guess-timate how old a dog is as there are considerable breed differences between dogs. Generally speaking, small dogs live the longest (a Yorkshire Terrier is considered 'old' at 10 years), while large breeds have relatively short lifespans (a Great Dane is considered 'old' at six years). Here we help you tell if your dog is old and then advise you on how to make your elderly dog's life easier& The physical signs:

Physical inactivity- Difficulty getting up after lying down for a while or after a long walk can be a sign of deteriorating joints due to wear and tear through life. Some dogs may be less keen to go for walks and prefer to curl up in a warm bed. Others may be initially keen to go out but as the joints ease with gentle exercise may be tempted to do a little too much with dire consequences later in the day as joints stiffen up and become even worse.

Hair loss- The skin may appear dry and scaly while the coat texture may be harsher, thinner with bald patches or white hairs. Often the coat is dull and the colour may be less vivid.

Dog breath- Bad teeth or gum infections may cause bad breath or inability to eat. A common sign is of food being dropped or excessive salivation and pawing at the mouth. Swellings appearing below the eye may be signs of tooth root abscesses and need veterinary attention.

Lumps and bumps- Warts, fatty lumps and even tumours may appear in old age. Check these out with your vet as early detection may save your dog's life.

Loss of bladder control- Incontinence: this is sometimes associated with changes in thirst but sometimes it's associated with sore joints, which make posturing difficult.

Mental alertness- Many older dogs become confused and fail to recognise their surroundings, their name or their owner! They may become less interested in food or what is happening around them. Some dogs appear dull and depressed while others become disobedient or destructive. Many older dogs get anxious if left alone for any length of time.

Sleep- Many older dogs sleep more during the day but sleep less at night. Some may prowl around the house at night because of sore joints, senility or even loneliness.

Ways to make your dog's life easier If your dog shows these signs, consider the following to make your dog's life easier:

* Install ramps to allow your dog to get back into the house from the garden.

* Dry your dog well if you've been walking in the rain.

* Arthritic dogs may have trouble standing up after lying down for a period of time so gently rub the muscles to warm them up and relieve some of the stiffness.

* Understand that changes in oxygen flow to the brain in old age mean dogs are likely to remember events from the past much better than if they happened yesterday. They get confused. Another change experienced by some dogs, cognitive dysfunction syndrome, may affect behaviour in more general ways, similar to the changes caused by senile dementia in humans.

* Some retraining may be necessary. Often using treats is a particularly good way to retrain the older dog. Food is a great motivator but beware of obesity in a less active older dog.

* Perhaps amounts at mealtimes need adjusting as elderly dogs usually become less active and require fewer calories. But conversely in some dogs, particularly the very old, more calories are needed. The main thing is to keep an eye on the dog's weight, however.

* Deteriorating vision and hearing may reduce a dog's ability to respond to his environment. He/she may not greet you immediately only because he/she isn't aware that you've arrived. Take a look at how to cope with blindness and deafness.

* Older dogs may also develop a fear of thunderstorms. The booming sounds of thunder may be exaggerated because of a loss of high-frequency hearing.

* Ensure their bed is in a warm draught-free place to make sleep time that bit more comfortable.

http://www.purina.co.uk/index.asp?frame=/dog/article.asp&id=69


Feline Spongiform Encephalopathy FSE TSE Prion Disease

Oral.29: Susceptibility of Domestic Cats to CWD Infection

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†

Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf



DIA-45

FELINE SPONGIFORM ENCEPHALOPATHY: FIRST CONFIRMED CASE REPORTED IN PORTUGAL

J.F. Silva1, J.J. Correia, 1 J. Ribeiro2, S. Carmo2 and L.Orge31 Faculdade de Medicina Veterinária (UTL), Lisbon, Portugal 2 Clínica Veterinária Ani+, Queluz, Portugal 3 Laboratório Nacional de Investigação Veterinária, Unidade de BSE, Lisbon, Portugal

Feline spongiform encephalopathy (FSE), affecting domestic and captive feline species, is a prion disease considered to be related to bovine spongiform encephalopathy (BSE). Here we report the first case diagnosed in Portugal, highlighting the neuroapthological findings. In 2004 a 9-year old intact female Siamese cat was referred with chronic progressive behavioural changes, polydipsia, gait abnormalities and episodes of hypersalivation. Clinical signs progressed to tetraparesis and dementia and euthanasia was performed. At necropsy, brain and spinal cord had no significative changes. Tissue samples from brain, cerebellum, brainstem and spinal cord were collected for histopathology and immunohistochemistry for detection of PrPres. Histology revealed neuropil and neuronal perikarion vacuolation in several areas of the central nervous system together with gliosis and cell rarefaction at the granular layer of the cerebellum. Immunohistochemical detection of PrPres showed a strong and widespread PrPres accumulation as granular and linear deposits as well as associated with some neurons. These findings are supportive of FSE. To the authors knowledge this is the first confirmed case of FSE reported in Portugal.


Research article

Immunohistochemical study of PrPSc distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy

Monika M Hilbe , Guido G Soldati , Kati K Zlinszky , Sabina S Wunderlin and Felix F Ehrensperger

BMC Veterinary Research 2009, 5:11doi:10.1186/1746-6148-5-11

Published: 31 March 2009

Abstract (provisional) Background Two domestic shorthair cats presenting with progressive hind-limb ataxia and increased aggressiveness were necropsied and a post mortem diagnosis of Feline Spongiform Encephalopathy (FSE) was made. A wide spectrum of tissue samples was collected and evaluated histologically and immunohistologically for the presence of PrPSc. Result Histopathological examination revealed a diffuse vacuolation of the grey matter neuropil with the following areas being most severely affected: corpus geniculatum medialis, thalamus, gyrus dentatus of the hippocampus, corpus striatum, and deep layers of the cerebral and cerebellar cortex as well as in the brain stem. In addition, a diffuse glial reaction involving astrocytes and microglia and intraneuronal vacuolation in a few neurons in the brain stem was present. Heavy PrPSc immunostaining was detected in brain, retina, optic nerve, pars nervosa of the pituitary gland, trigeminal ganglia and small amounts in the myenteric plexus of the small intestine (duodenum, jejunum) and slightly in the medulla of the adrenal gland.

Conclusions The PrPSc distribution within the brain was consistent with that described in other FSE-affected cats. The pattern of abnormal PrP in the retina corresponded to that found in a captive cheetah with FSE, in sheep with scrapie and was similar to nvCJD in humans.

snip...

In cattle orally infected with BSE immunostaining in the follicles of the distal ileum was observed only after the onset of clinical disease at 36, 38 and 40 months after exposure [27]. Neurons in the enteric nervous system were positive in only one animal from each of the groups killed 38 and 40 months after exposure, but even then the staining was sparse and confined to the myenteric plexus. In contrast none of the follicles in the distal ileum showed evidence of immunostaining for PrPSc and only a few animals showed sparse staining in the myenteric plexus in naturally affected cattle with BSE. The mesenteric lymph nodes were negative 6 months after exposure in the experimental animals. Some authors concluded that the restricted distribution of the BSE agent in the lymphoreticular system of cattle contrasts with the distribution of the scrapie agent in sheep which, in most cases, spreads rapidly after the initial early involvement of the system [27]. The restricted distribution of BSE appears to be also true for FSE. Mice inoculated intraperitoneally or intracerebrally with brain material from cats with FSE had progressive neurological signs similar to those seen in mice affected with scrapie or BSE. Moreover some authors postulate, that the distribution of vacuolar degeneration was identical to that seen in mice terminally infected with primary sources of BSE and the lesion profile in mice 12 inoculated with FSE resembles that observed in BSE, rather than scrapie. It was postulated, therefore, that BSE and FSE probably arose from a common source [10]. The source of infection at least in one cat presented here could have been canned food contaminated with nervous tissue of BSE infected cattle before the ban.

Conclusions In conclusion, the two FSE cases described here had essentially the same histological lesions and PrPSc distribution in the brain and the peripheral tissues as reported in earlier FSE cases. In addition we were able to demonstrate PrPSc accumulation in the retina, the neurohypophysis, trigeminal ganglion and in the adrenal medulla, but not in lymphatic tissues nor in the bone marrow. The kidneys showed random immunohistochemical staining in the mesangial glomerular tufts. This was seen in the kidneys of one FSE as well as in the control cats. Even though in experimentally infected Syrian hamsters and in scrapie infected sheep a possible prionuria and infectivity of urine is postulated, our findings confirm previously reported observations in the kidney of FSE cases, showing that immunohistochemical labelling of glomerular structures has to be regarded as unspecific. In summary, the distribution of PrPSc in FSE is similar to BSE but different from classical scrapie. In analogy, horizontal PrPSc transmission in FSE appears to be unlikely.

see full text ;


Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK in 1990. Most cases have been reported in the UK, where the epidemic has been consistent with that of the BSE epidemic. Some other countries (e.g. Norway, Liechtenstein and France) have also reported cases.

Most cases have been reported in domestic cats but there have also been cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot, Puma and Tiger). The disease is characterised by progressive nervous signs, including ataxia, hyper-reactivity and behavioural changes and is fatal.The chemical and biological properties of the infectious agent are identical to those of the BSE and vCJD agents. These findings support the hypothesis that the FSE epidemic resulted from the consumption of food contaminated with the BSE agent.The FSE epidemic has declined as a result of tight controls on the disposal of specified risk material and other animal by-products.References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a cat.

Veterinary Record. 127. 586-588Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat. Veterinary Record. 129. 320Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy to mice. Veterinary Record 134. 449.Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in Norway. Veterinary Record 136. 444Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in France. Veterinary Record 141. 270-271Zanusso, G et al. (1998) Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp 1116-1117.Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy. Veterinary Record 146. 437-441Kelly, D.F. et al. (2005) Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy. Veterinary Record 156. 472-477.TSEs in Exotic Ruminants

TSEs have been detected in exotic ruminants in UK zoos since 1986. These include antelopes (Eland, Gemsbok, Arabian and Scimitar oryx, Nyala and Kudu), Ankole cattle and Bison. With hindsight the 1986 case in a Nyala was diagnosed before the first case of BSE was identified. The TSE cases in exotic ruminants had a younger onset age and a shorter clinical duration compared to that in cattle with BSE. All the cases appear to be linked to the BSE epidemic via the consumption of feed contaminated with the BSE agent. The epidemic has declined as a result of tight controls on feeding mammalian meat and bone meal to susceptible animals, particularly from August 1996.References: Jeffrey, M. and Wells, G.A.H, (1988) Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet.Path. 25. 398-399Kirkwood, J.K. et al (1990) Spongiform encephalopathy in an Arabian oryx (Oryx leucoryx) and a Greater kudu (Tragelaphus strepsiceros) Veterinary Record 127. 418-429.Kirkwood, J.K. (1993) Spongiform encephalopathy in a herd of Greater kudu (Tragelaphus strepsiceros): epidemiological observations. Veterinary Record 133. 360-364Kirkwood, J. K. and Cunningham, A.A. (1994) Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Veterinary Record. 135. 296-303.Food and Agriculture Organisation (1998) Manual on Bovine Spongiform Encephalopathy.


Feline Spongiform Encephalopathy (FSE)

FSE was first identified in Britain in 1990. Since then there have been 87 cases in Great Britain, one in Northern Ireland, one in Norway and one in Liechtenstein. FSE is not an easy disease to study. Although Britain has a large cat population they would not normally have been subjected to close neurological examination in the past. Nevertheless, sufficient numbers of FSE cases have been seen and investigated to permit an association with BSE to be made. Obtaining lifetime feeding history for cats is not easy, so although all have eaten foods that would be expected to contain specified bovine offals, no particular type of food can be implicated.

The epidemic in cats is often thought to be a useful model for past human exposure to BSE. The number of feline cases has declined dramatically.

As Defra has not historically held responsibility for investigating disease, other than rabies, in domestic pets, most of the information gathered about FSE in domestic cats and zoo animals has been provided through the good will of owners and veterinary practitioners. Laboratory diagnosis of a spongiform encephalopathy in any species has however been notifiable since November 1994, thus ensuring that cases would not be missed.

Interestingly, when brain tissue from some of the early cats identified as having FSE, was inoculated into mice, the pattern of incubation periods and lesion profiles in the mice was indistinguishable from that produced by BSE.

In exotic cats there have now been nine cases in cheetahs (three were diagnosed abroad but originated in Britain), three in pumas, three in ocelots, two in tigers and two in lions.

In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.

References:

Zanusso-G, Nardelli-E Rosati-A Fabrizi-G-M Ferrari-S Carteri-A Desimone-F Rizutto-N Monaco-S. Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. LANCET, 1998 V352, N9134, OCT 3, Pp 1116-1117.

Pearson G. R. et al. 1992. Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.

Wyatt. J. M. et al. 1991. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.

Gruffydd-Jones T. J. et al. 1991. Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.

Willoughby K. 1992. Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.

https://webarchive.nationalarchives.gov.uk/ukgwa/20130822074033/http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html

In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.

http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html




Image] Research letters Volume 352, Number 9134 [Image] 3 October1998[Previous] [Next] [Image][Image]

Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy

[Image] Gianluigi Zanusso, Ettore Nardelli, Anna Rosati, Gian Maria Fabrizi, Sergio Ferrari, Antonella Carteri, Franco De Simone, Nicola Rizzuto, Salvatore Monaco

Transmissible spongiform encephalopathies (TSE) encompass inherited, acquired, and sporadic mammalian neurological disorders, and are characterised by the conversion of the cellular prion protein (PrP) in an insoluble and protease-resistant isoform (PrPres). In human TSE, four types of PrPres have been identified according to size and glycoform ratios, which may represent different prion strains. Type-1 and type-2 PrPres are associated with sporadic Creutzfeldt-Jakob disease (CJD), type 3 with iatrogenic CJD, and type 4 with variant CJD.1,2 There is evidence that variant CJD is caused by the bovine spongiform encephalopathy (BSE)-prionstrain.2-4 The BSE strain has been identified in three cats with feline spongiform encephalopathy (FSE), a prion disease which appeared in 1990 in the UK.5

We report the simultaneous occurrence of sporadic CJD in a man and a new variety of FSE in his cat.

A 60-year-old man, with no unusual dietary habits, was admitted in November,1993, because of dysarthria, cerebellar ataxic gait, visual agnosia, and myoclonus. An electroencephalogram (EEG) showed diffuse theta-delta activity. A brain magnetic resonance imaging scan was unremarkable. 10 days later, he was speechless and able to follow only simple commands. Repeat EEGs showed periodic triphasic complexes. 2 weeks after admission, he was mute, akinetic, and unable to swallow. He died in early January, 1994. His 7-year-old, neutered, female shorthaired cat presented in November,1993, with episodes of frenzy, twitching of its body, and hyperaesthesia. The cat was usually fed on canned food and slept on its owner's bed. No bites from the cat were recalled. In the next few days, the cat became ataxic, with hindquarter locomotor dysfunction; the ataxia got worse and there was diffuse myoclonus. The cat was killed in mid-January, 1994. No pathogenic mutations in the patient's PrP gene were found. The patient and the cat were methionine homozygous at codon 129. Histology of the patient's brain showed neocortical and cerebellar neuronal loss, astrocytosis, and spongiosis (figure A). PrP immunoreactivity showed a punctate pattern and paralleled spongiform changes (figure B). The cat's brain showed mild and focal spongiosis in deeper cortical layers of all four lobes (figure C), vacuolated cortical neurons (figure D), and mild astrogliosis. The cerebellar cortex and the dentate nucleus were gliosed. Immunoreactive PrP showed a punctate pattern in neocortex, allocortex, and caudate nucleus (figure E). Western blot analysis of control and affected human and cat brain homogenates showed 3 PrP bands of 27-35 kDa. After digestion with proteinase K and deglycosylation, only samples from the affected patient and cat showed type-1 PrPres, with PrP glycoform ratios comparable to those observed in sporadic CJD1 (details available from author). [Image] Microscopic sections of patient and cat brains A: Occipital cortex of the patient showing moderate spongiform degeneration and neuronal loss (haematoxylin and eosin) and B: punctate perineuronal pattern of PrP immunoreactivity; peroxidase immunohistochemistry with monoclonal antibody 3F4. C: cat parietal cortex showing mild spongiform degeneration (haematoxylin and eosin). D:vacuolated neurons (arrow, haematoxylin and eosin), E: peroxidase immunohistochemistry with antibody 3F4 shows punctate perineuronal deposition of PrP in temporal cortex. This study shows a spatio-temporal association between human and feline prion diseases. The clinical features of the cat were different from previously reported cases of FSE which were characterised by gradual onset of behavioural changes preceding locomotor dysfunction and ataxia.5Neuropathological changes were also at variance with the diffuse spongiosis and vacuolation of brainstem neurons, seen in FSE.5 The synaptic pattern of PrP deposition, similar in the cat and in the patient, was atypical for a BSE-related condition. Evidence of a new type of FSE was further provided by the detection of a type-1 PrPres, other than the BSE-associated type 4.2

Taken together, our data suggest that the same agent strain of sporadic CJD as involved in the patient and in his cat. It is unknown whether these TSE occurred as the result of horizontal transmission in either direction, infection from an unknown common source, or the chance occurrence of two sporadic forms.

1 Parchi P, Castellani R, Capellari S, et al. Molecular basis of phenotypic variablity in sporadic Creutzfeldt-Jakob disease. Ann Neurol 1996; 39:767-78 [PubMed]. 2 Collinge J, Sidle KCL, Meads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996;383: 685-90 [PubMed]. 3 Bruce ME, Will RG, Ironside JW, et al. Transmissions to mice indicate that' new variant' CJD is caused by the BSE agent. Nature 1997; 389: 498-501[PubMed]. 4 Hill AF, Desbruslais M, Joiner S, et al. The same prion strain causes vCJD and BSE. Nature 1997; 389: 448-50 [PubMed]. 5 Pearson GR, Wyatt JM, Henderson JP, Gruffydd-Jones TJ. Feline spongiform encephalopathy: a review. Vet Annual 1993; 33: 1-10.

------------------------------------------------------------------------

Sezione di Neurologie Clinica, Dipartimento di Scienze Neurologiche e dellaVisione, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy(S Monaco; e mail rizzuto@Gorgorna.univr.it); and Istituto Zooprofilattico Sperimentale della Lombardia e dell' Emilia, Brescia


indeed there have been 4 documented cases of TSE in Lions to date. Lion 32 December 98 Born November 86 Lion 33 May 1999 (euthanased) Born November 81. Lion 36 Euthanased August 2000 Born July 87. Deteriorating hind limb ataxia. Lion 37 Euthanased November 2001 Male, 14 years. Deteriorating hind limb ataxia since September 2001. (Litter mate to Ref. 36.) http://www.defra.gov.uk/animalh/bse/index.html go to the url above, on the bar at the top, click on _statistics_, then in middle of next page, click on_other TSEs_. or go here;

http://www.defra.gov.uk/animalh/bse/bse-statistics/level-3-tsestat.html


http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html


SPONGIFORM ENCEPHALOPATHY IN A CAPTIVE PUMA

1. Mr TayloI's minute of 6 November refers.

2. The Minister and the Minister of State were concerned to see an article in yesterday's Times (attached) which suggested that the puma concerned had never "eaten any part cow or sheep which, in the opinion of Government scientists, could transmit the species to a different species.

3. You explained to me that this was incorrect.

The position was as set out in the briefing for Prime Minister's questions attached to Mr Taylor's note. The puma had probably been fed low guality beef meat in the form of split carcasses. Prior to the Specified Bovine Offal ban, these would have contained spinal cord, which is one of the tissues most likely to contain the BSE agent.

http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf





***> 5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis. snip... R. BRADLEY


Saturday, September 5, 2009

Possible Case of Maternal Transmission of Feline Spongiform Encephalopathy in a Captive Cheetah


Tuesday, September 02, 2008

Fecal transmission of AA amyloidosis in the cheetah contributes to high incidence of disease



FOR IMMEDIATE RELEASE

P01-05

January 30, 2001

Print Media: 301-827-6242

Broadcast Media: 301-827-3434

Consumer Inquiries: 888-INFO-FDA

FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT

Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.

FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.

It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.

According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."

Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.

FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.

This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.

FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.

http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html


“FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.”

*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****

Monday, November 13, 2023

Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023 Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023

The infamous 1997 mad cow feed ban i.e. Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

***>However, this recommendation is guidance and not a requirement by law.

WITH GREAT URGENCY, THE Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) MUST BE ENHANCED AND UPDATED TO INCLUDE CERVID, PIGS, AND SHEEP, SINCE RECENT SCIENCE AND TRANSMISSION STUDIES ALL, INCLUDING CATTLE, HAVE SHOWN ORAL TSE PrP TRANSMISSIONS BETWEEN THE SPECIES, AND THIS SHOULD BE DONE WITH THE UTMOST URGENCY, REASONS AS FOLLOW.

First off I will start with a single BSE feed breach 10 years after 1997 partial ban. If you got to the archived link, all the way down to bottom…THE NEXT YEAR I RECALL ONE WITH 10,000,000+ banned products recall…see this records at the bottom…terry

2016

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed

PUBLIC SUBMISSION

Comment from Terry Singeltary Sr.

Posted by the Food and Drug Administration on May 17, 2016 Comment

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission



How in the hell do you make a complete recall of 27,694,240 lbs of feed that was manufactured from materials that may have been contaminated with mammalian protein, in one state, 2006? Wonder how much was fed out?

RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II

______________________________

PRODUCT

a) CO-OP 32% Sinking Catfish, Recall # V-100-6;

b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;

c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;

d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;

e) "Big Jim’s" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;

f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;

g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;

h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;

i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;

j) CO-OP LAYING CRUMBLES, Recall # V-109-6;

k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;

l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;

m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6

CODE Product manufactured from 02/01/2005 until 06/06/2006

RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006.

FDA initiated recall is complete.

REASON

Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".

VOLUME OF PRODUCT IN COMMERCE

125 tons

DISTRIBUTION

AL and FL

______________________________

PRODUCT

Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6 CODE All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.

RECALLING FIRM/MANUFACTURER Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006.

Firm initiated recall is complete.

REASON

The feed was manufactured from materials that may have been contaminated with mammalian protein.

VOLUME OF PRODUCT IN COMMERCE

27,694,240 lbs

DISTRIBUTION

MI

______________________________

PRODUCT

Bulk custom made dairy feed, Recall # V-114-6

CODE None

RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.

REASON

Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.

VOLUME OF PRODUCT IN COMMERCE

???

DISTRIBUTION

KY

END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006

###


***>However, this recommendation is guidance and not a requirement by law.

“Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent.”

THIS MUST CHANGE ASAP!

“Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent.”

“For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.”

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

snip.....

In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.

It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip.....


“Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent.”

PLoS One. 2020 Aug 20;15(8):e0237410. doi: 10.1371/journal.pone.0237410. eCollection 2020.

Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease

Nathaniel D Denkers 1 , Clare E Hoover 2 , Kristen A Davenport 3 , Davin M Henderson 1 , Erin E McNulty 1 , Amy V Nalls 1 , Candace K Mathiason 1 , Edward A Hoover 1

PMID: 32817706 PMCID: PMC7446902 DOI: 10.1371/journal.pone.0237410

Abstract

The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.

Snip…

Discussion

As CWD expands across North America and Scandinavia, how this disease is transmitted so efficiently remains unclear, given the low concentrations of prions shed in secretions and excretions [13, 14]. The present studies demonstrated that a single oral exposure to as little as 300nmg of CWD-positive brain or equivalent saliva can initiate infection in 100% of exposed white-tailed deer. However, distributing this dose as 10, 30 ng exposures failed to induce infection. Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent. These dynamics also invite speculation as to whether potential infection co-factors, such as particle binding [46, 47] or compromises in mucosal integrity may influence infection susceptibility, as suggested from two studies in rodent models [48, 49].


PRION 2023 CONTINUED;


Prion 2023 

Experimental Oronasal Inoculation of the Chronic Wasting Disease Agent into White Tailed Deer

Author list: Sarah Zurbuchena,b , S. Jo Moorea,b , Jifeng Biana , Eric D. Cassmanna , and Justin J. Greenleea . a. Virus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, US b. Oak Ridge Institute for Science and Education (ORISE), U.S. Department of Energy, Oak Ridge, TN, United States

Aims: The purpose of this experiment was to determine whether white-tailed deer (WTD) are susceptible to inoculation of chronic wasting disease (CWD) via oronasal exposure.

Materials and methods: Six male, neutered WTD were oronasally inoculated with brainstem material (10% w/v) from a CWD-positive wild-type WTD. The genotypes of five inoculated deer were Q95/G96 (wild-type). One inoculated deer was homozygous S at codon 96 (96SS). Cervidized (Tg12; M132 elk PrP) mice were inoculated with 1% w/v brainstem homogenate from either a 96GG WTD (n=10) or the 96SS WTD (n=10).

Results: All deer developed characteristic clinical signs of CWD including weight loss, regurgitation, and ataxia. The 96SS individual had a prolonged disease course and incubation period compared to the other deer. Western blots of the brainstem on all deer yielded similar molecular profiles. All deer had widespread lymphoid distribution of PrPCWD and neuropathologic lesions associated with transmissible spongiform encephalopathies. Both groups of mice had a 100% attack rate and developed clinical signs, including loss of body condition, ataxia, and loss of righting reflex. Mice inoculated with material from the 96SS deer had a significantly shorter incubation period than mice inoculated with material from 96GG deer (Welch two sample T-test, P<0.05). Serial dilutions of each inocula suggests that differences in incubation period were not due to a greater concentration of PrPCWD in the 96SS inoculum. Molecular profiles from western blot of brain homogenates from mice appeared similar regardless of inoculum and appear similar to those of deer used for inoculum.

Conclusions: This study characterizes the lesions and clinical course of CWD in WTD inoculated in a similar manner to natural conditions. It supports previous findings that 96SS deer have a prolonged disease course. Further, it describes a first pass of inoculum from a 96SS deer in cervidized mice which shortened the incubation period.

Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection, analysis, decision to publish, or preparation of the manuscript.

Acknowledgement: We thank Ami Frank and Kevin Hassall for their technical contributions to this project.

=====end

PRION 2023 CONTINUED;


***> Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry <***

“While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle.”

Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure

Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA

Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.

Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).

Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.

Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.

Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.

*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****

=====end

Strain characterization of chronic wasting disease in bovine-PrP transgenic mice

Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada.

Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context.

Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer).

Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology.

Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.

Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR

Grant number: PCI2020-120680-2 ICRAD

"Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study."

=====end


*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****

***> Porcine Spongiform Encephalopathy <***

Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States

Volume 31, Number 1—January 2025

Abstract

Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.

Snip…

Conclusions

In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.


“While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle.”

Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.

2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.





Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.


CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...


we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.


May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...


3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...


But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...


Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....


It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.


4.303 The minutes of the meeting record that:

It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17


IN CONFIENCE

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;


IN CONFIDENCE

So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...


we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.


May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...


3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...


But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...


Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....


BSE TO PIGS NEWS RELEASE


CONFIDENTIAL

BSE: PRESS PRESENTATION






INDUSTRY RESPONSE TYPICAL


DEFENSIVE BRIEFING


CONFIDENTIAL

pigs & pharmaceuticals





COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP

There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............


snip...

7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;

1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,

The neuropathology of experimental bovine spongiform encephalopathy in the pig.

Ryder SJ, Hawkins SA, Dawson M, Wells GA.

Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.

In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.

PMID: 10684682 [PubMed - indexed for MEDLINE]


Susceptibility of Beavers to Chronic Wasting Disease

by Allen Herbst 1,2,3,Serene Wohlgemuth 2,4,Jing Yang 2,4,Andrew R. Castle 2,4ORCID,Diana Martinez Moreno 2,5,Alicia Otero 6ORCID,Judd M. Aiken 2,3,David Westaway 2,4 andDebbie McKenzie 2,5,*

1 U.S. Geological Survey National Wildlife Health Center, Madison, WI 53711, USA 2 Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton, AB T6G 2R3, Canada 3 Department of Agricultural, Food and Nutritional Sciences, University of Alberta, Edmonton, AB T6G 2R3, Canada 4 Department of Medicine, University of Alberta, Edmonton, AB T6G 2R3, Canada 5 Department of Biological Sciences, University of Alberta, Edmonton, AB T6G 2R3, Canada 6 Centro de Encefalopatias y Enfermedades Transmisibles Emergentes, University of Zaragoza, 50009 Zaragoza, Spain * Author to whom correspondence should be addressed. Academic Editor: Walker Jackson

Biology 2022, 11(5), 667; https://doi.org/10.3390/biology11050667 (registering DOI)

Received: 18 March 2022 / Revised: 16 April 2022 / Accepted: 20 April 2022 / Published: 26 April 2022

(This article belongs to the Special Issue Selective Vulnerability in Neurodegenerative Diseases)

Download PDF Citation Export

Simple Summary

Chronic wasting disease is increasing across the landscape, and this is threatening other wildlife species in addition to cervids. Our objective was to evaluate the possibility that chronic wasting disease could transmit to beavers. Our results indicate that beavers are susceptible to multiple types of prion diseases, including chronic wasting disease.

Intracranial infection is a gold-standard laboratory method to measure the molecular barrier between a recipient PrPC and an invading prion strain; however, this approach alone cannot determine the risk of pathogen transfer, which also requires exposure. CWD is geographically expanding, increasing its prevalence within endemic regions, and increasing CWD prion environmental contamination [55]. These factors are increasing the exposure of all sympatric species to CWD prions, including beavers, and driving the risk of interspecies transmission of CWD. High levels of exposure can override even strong species barriers, as was shown by the transmission of bovine spongiform encephalopathy to humans. CWD prion transfer to beavers may result in pathogen spillover facilitated by long beaver lifespans (>20 years) that would enable CWD adaptation and shedding and social interactions that would facilitate transmission.

Transmission studies demonstrate that CWD prions can infect a variety of other species including cattle, sheep, pigs, ferrets, hamsters, red-backed and bank voles, and whitefooted mice. Our data indicate that beavers also are expected to be susceptible to CWD and at risk for pathogen transfer and spillover. We are unaware of any attempt to perform surveillance for prion disease in wild beavers. Targeted or opportunistic surveillance of wild beavers in areas where CWD, in cervids, has reached high prevalence would further clarify the risk of CWD to beavers.



The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons


so, this is what we leave our children and grandchildren?

WHERE we know that .1 gram is lethal and the 8/4/97 partial and voluntary ruminant feed ban was nothing more than ink on paper, nobody adhered to it, others did not even know about it for pete's sake. YOU know, we now have some 4.5 MILLION people in the USA with alzheimers, i read some other 19 million taking care of them, and by 2050 there will be a projected 14 MILLION with Alzheimer's in the USA. Mad cows, mad sheep, mad goats, mad deer, mad elk, mad mink, mad cats, mad people, NO mad dogs?

***> DEER, CAT and DOG SPONGIFORM ENCEPHALOPATHY SURVEY <***

This an excellent review by Terry Singletary: see message on 1.3.5 concerning pet food manufacture and rulings.

38. Terry Singletary reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

http://www.priondata.org/data/A_deerdog.html


Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.

------------------------------------------------------------------------

TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..see references:

http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf


http://www.bseinquiry.gov.uk/files/yb/1992/11/04002001.pdf


TSEs (Transmissible Spongiform Encephalopathies) in deer - Advisory notes for farmers

http://www.defra.gov.uk/animalh/bse/bse-publications/adv-TSEs-deer.pdf


------------------------------------------------------------------------

TSE in zoo ungulates (hoofed animals) In parallel to the first BSE cases, sporadic cases of spongiform encephalopathy in hoofed zoo species were diagnosed in British zoos. Strain typing indicates that all these TSEs are caused by the same strain that had caused cttle BSE. Until April 2002, 6 kudus, 5 elands, 2 Arabian orynx, 2 ankole cows and one nyala, Gemsbock and bison were affected (DEFRA). The animals showed a range of clinical symptoms that, depending on the species, were distinctly different from those of cattle BSE or sheep scrapie. Incubation time and duration of clinical disease seemed to be shorter in the zoo ungulates, which could be a reflection of the generally shorter lifespan of those species in comparison to that of domestic cattle. In the majority of those TSE cases in zoos, exposure to animal feed produced with animal protein (and therefore potentially containing BSE infectivity) was either documented, or at least could not be excluded. The fact that the nyala case was so early was simply showing just how quickly an animal that was exposed early in life could incubate the disease. Also the suggestion has always been that BSE had been in small quantities in bovine feed early in the 1970s. Kirkwood JK, Cunningham AA . Epidemiological observations on spongiform encephalopathies in captive wild animals in the British Isles. Vet Rec. 1994 Sep 24;135(13):296-303. Since 1986, scrapie-like spongiform encephalopathy has been diagnosed in 19 captive wild animals of eight species at or from eight zoological collections in the British Isles. The affected animals have comprised members of the family Bovidae: one nyala (Tragelaphus angasi), four eland (Taurotragus oryx), and six greater kudu (Tragelaphus strepsiceros), one gemsbok (Oryx gazella), one Arabian oryx (Oryx leucoryx), and one scimitar-horned oryx (Oryx dammah), and members of the family Felidae: four cheetah (Acinonyx jubatus) and one puma (Felis concolor). In addition, three cases of a spongiform encephalopathy of unknown aetiology have been reported in ostriches (Struthio camellus) from two zoos in north west Germany. Three features suggest that some of these cases may have been caused by the agent of bovine spongiform encephalopathy (BSE). First, they have been temporally and geographically coincident with the BSE epidemic. Secondly, in all the ungulates for which details are available, it is possible that either the affected animal itself, or the herd into which it was born or moved, had been exposed to proprietary feeds containing ruminant-derived protein or other potentially contaminated material, and all the carnivores had been fed parts of cattle carcases judged unfit for human consumption. Thirdly, the pathological results of inoculating mice with a homogenate of fixed brain tissue from the nyala and from one greater kudu were similar to the results of inoculating mice with BSE brain tissue. (notably a few cases of this type of disease are still appearing in UK zoos)

------------------------------------------------------------------------

TSE in cervidae (deer and elk) A chronic wasting condition (Chronic Wasting Disease, CWD) in captive and free-roaming North-American deer and elk has been described since approx. 1980. Initially, cases were only reported from captive cervidae in Colorado, but now also from both captive and free roaming animals in Colorado, Wyoming, Wisconsin, South Dakota and Nebraska. In addition, several captive herds in Canada that had imported animals from affected farms in the USA have diagnosed CWD cases. In an increased surveillance (screening) of hunted deer and elk and animals killed in car accidents, in some regions in Northern Colorado (Larimer County) and Southern Wyoming 8% (hunted animals) and 11% (car accidents) of the tested brains were CWD-positive in histology and/or immunhistochemistry (IHC). Recent reports of 50% CWD prevalence in hunted cervidae in one geographically defined region in the USA still need to be validated. Until now cervidae are the only known free-roaming species with a spontaneous (naturally transmitted?) TSE. The origin of CWD is still unknown. There was some contact to sheep reported. However, sheep scrapie was not observed in the sheep flocks in the regions where CWD was initially observed, and in general is a rarely observed condition in Colorado and Wyoming. Close contact to cattle did not occur. One hypothesis is that the disease was introduced into the captive herds with subclinically infected captured wildlife, and that it spread in the captive population due to higher animal density. However, even recent studies were not able to answer the question whether CWD started in the captive or the free-roaming deer and elk population, and they also were not able to determine the mode of transmission among free-roaming cervidae. The clinical picture of the disease is characterized by a chronic wasting with loss of condition and untidy coat, behavioural disorders, polydipsia and polyuria, lowered head and hanging ears. Feed intake is reduced, and affected animals loose weight and die within a few months after the onset of clinical symptoms. In Switzerland, until April 2002 approx. 80 brain samples of captive elk have been examined for CWD, all with a negative result.

The full list details are on 


(by rights this is up to date) also see the internal reference on this site and 


------------------------------------------------------------------------

Hound studies This largely started after it was found that dogs were being reported with a spongiform encephalopathy and ataxia. The condition seemed to take place in older dogs and was being reported from various parts of the UK. There was never any proof that it was caused by a TSE. One of the most difficult prblems to get around in all this was the outbreak of the disease that was seen in a large pack of game dogs. It was as if all the animals developed the disease concurrently..as would be expected if an infection was involved. The animals were not very young and no specific infective cause or toxic cause was found. The documents below became clear during the Phillips Inquiry and represent documents passed around in the UK Ministry of Agriculture and Central Veterinary Laboratory:

http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf


http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf


From these various documents:

37. Putative TSE in hounds - work started 1990 -(see para 41) Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been working on a hound survey in 1990. Gerald Wells and I myself received histological sections from this survey along with the accompanying letter (YB90/11.28/1.1) dated November 1990. This letter details spongiform changes found in brains from hunt hounds failing to keep up with the rest of the pack, along with the results of SAF extractions from fresh brain material from these same animals. SAFs were not found in brains unless spongiform changes were also present. The spongiform changes were not pathognomonic (ie. conclusive proof) for prion disease, as they were atypical, being largely present in white matter rather than grey matter in the brain and spinal cord. However, Tony Scott, then head of electron microscopy work on TSEs, had no doubt that these SAFs were genuine and that these hounds therefore must have had a scrapie-like disease. I reviewed all the sections myself (original notes appended) and although the pathology was not typical, I could not exclude the possibility that this was a scrapie-like disorder, as white matter vacuolation is seen in TSEs and Wallerian degeneration was also present in the white matter of the hounds, another feature of scrapie.

38. Terry Singletary reviewed the literature on hound neuropathology, and discovered that micrographs and descriptive neuropathology from papers on 'hound ataxia' mirrored those in material from Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had done much of this work, and I obtained original sections from hound ataxia cases from him. This enabled me provisionally to conclude that Robert Higgins had in all probability detected hound ataxia, but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed in 'blind' examination of single restricted microscopic fields that there was no distinction between the white matter vacuolation present in BSE and scrapie cases, and that occurring in hound ataxia and the hound survey cases.

39.Hound ataxia had reportedly been occurring since the 1930's, and a known risk factor for its development was the feeding to hounds of downer cows, and particularly bovine offal. Circumstantial evidence suggests that bovine offal may also be causal in FSE, and TME in mink. Despite the inconclusive nature of the neuropathology, it was clearly evident that this putative canine spongiform encephalopathy merited further investigation.

40.The inconclusive results in hounds were never confirmed, nor was the link with hound ataxia pursued. I telephoned Robert Higgins six years after he first sent the slides to CVL. I was informed that despite his submitting a yearly report to the CVO including the suggestion that the hound work be continued, no further work had been done since 1991. This was surprising, to say the very least.

41.The hound work could have provided valuable evidence that a scrapie-like agent may have been present in cattle offal long before the BSE epidemic was recognised. The MAFF hound survey remains unpublished. Histopathological support to various other published MAFF experiments

42.These included neuropathological examination of material from experiments studying the attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice (RVC 1994).

http://www.bseinquiry.gov.uk/files/ws/s067.pdf


Annex 


My views have not changed, namely as the survey is designed, has little to offer scientifically;

http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf


maddogs and Englishman

http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf


Editorial: Things are really not as clear with dogs and TSE as you might think. The first thing was that the MAFF in the UK decided to do no scientific work investigating the cases (e.g. by inoculating them into animals), and that they were really not happy about discussing this with the public. I was contacted by an Member of the UK Parliament in 1994 concerning the possibility that a series of dogs near Doncaster had gone down with a similar condition that sounded very similar to BSE. The animals were roughly the same age, and had been fed collectively by the owner. The other main possibility was that the condition was due to a poisoning element present in the food. A second group was in contact in around 1995 in which the animals were considered to have been poisoned with heavy metals but no proof (or even investigation) seems to have taken place. This determination by MAFF not to carry out any studies of inoculating BSE into dogs was indeed strange at the time. The reason for this being so odd is that dogs are commonly available for experimental animals and it would be looked on as being a low cost experiment. However politically it is always extremely bad to do experiments with loveable domestic dogs by inoculating them with a disease that could, to some degree be blamed on the incompitence of the government of the time.

------------------------------------------------------------------------

Cats Only four years after initial BSE cases had been diagnosed in cattle in the UK, first reports of a new spontaneous spongiform encephalopathy in domestic cats were published. Epidemiological research and strain typing indicated that cattle BSE and this new disease in domestic cats, called Feline Spongiform Encephalopathy (FSE), are linked. All but four of the approx. 100 FSE cases diagnosed worldwide until April 2002 have been seen in the UK (DEFRA). One of the four non-UK cases was diagnosed in Northern Ireland, one in Norway, one in Liechtenstein, and one in 2001 in Switzerland. The most widely accepted hypothesis, although not proven, is that the affected domestic cats were exposed to BSE infectivity through contaminated commercial cat feed or fresh slaughter offal that contained brain or spinal cord from cattle BSE cases. An interesting observation is that in addition to domestic cats, several large cats kept in zoos were diagnosed with FSE. Based on data provided by the British ministry (DEFRA) until April 2002 5 cheetahs, 4 lions and 3 ocelots, pumas and tigers were affected. The large cats that were diagnosed with FSE outside of the UK all originated from UK zoos. It is suspected that these large cats acquired the infection by being fed meat and bones of BSE-infected cattle. There is a parallel development in the significant reduction in clinical BSE cases in the UK (peak in 1992) and the course of the FSE epidemic. This can be seen as additional evidence for the feed-related association between cattle BSE and FSE. Until April 2002, only adult cats around 4-6 years of age have been diagnosed with clinical FSE. Reports on the clinical symptoms presented by these cats give a relatively homogeneous picture: Affected cats show a lack of coordination with an ataxia mainly of the hind limbs, they often fall and miss their target when jumping. Fear and increased aggressiveness against the owner and also other animals is often seen. They do not longer tolerate to be touched (stroked) and start hiding. These behavioural chances might be the result of a hypersensibility to touch and noise, but also to increased fear. Excessive salivation is another more frequently seen symptom. Cats with FSE in general show severe behavioural disturbances, restlessness and depression, and a lack of coat cleaning. Symptoms in large cats in general are comparable to those in domestic cats. A report on FSE (in german) has been presented in 2001 in the Swiss FVO Magazin. A paper on the first FSE case in a domestic cat in Switzerland is currently in press in the Journal Schweizer Archiv für Tierheilkunde Various things appeared in the Phillips Inquiry:

* imported crushed heads were extensively used in the petfood industry...

http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf


* it was clear that vets in the MAFF did not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed...

http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf 


and 

http://www.bseinquiry.gov.uk/files/yb/1989/04/25001001.pdf


* some 100+ _documented_ TSE cats of all types later. .on occassions, materials obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture...

BSE IN PETFOOD

1. The Secretary asked on 19 April whether I was content the advice in para 3 of the record of the meeting 17 March with the Parliamentary Secretary (Mr Thompson). simple answer is "not entirely”.

2. On accasions, material obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture. Some of this material must be classified as high risk since it contains brain, spinal cord, spleen or lymphatic glands. 

3. The above material will be exposed to a low processing temperature in the preparation of dry petfood (as against canned petfood) which will be insufficient to destroy the agent of scrapie/BSE. Thus, on occasions, domestic pets will be the agent. This was recognized by Southwood who said “domestic pets may well be susceptible to BSE were the agent to reach them in an adequate dose by an appropriate route.” He went on to say that it seemed “unlikely but possible that pre-clinical infection exists but is not revealed because of an incubation period longer than the natural lifespan.”
Southwood went on to comment that "hounds that are often fed uncooked carcases would be particularly appropriate for study".

4. Views on this issue may take more shape after the meeting with…on 19 May.

http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf


BSE and Pedigree Pet Foods

* Meldrum's notes on pet foods and materials used

http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf 


http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf 


* In confidence 

* concerning passing CJD to cats....

"Officials have recently had a very useful exploratory meeting with ‘redacted’. The company is sufficiently concerned about BSE to employ a consultant to advise them on the risk to slaughterhouse meat and offal. It should be noted that under experimental conditions cats succumb to an encephalopathy intracerebral inoculation of material derived from patients affected with Creutzfeldt-Jakob Disease. The consultant is doing a very thorough job and is attempting to classify the relative risk from a variety of materials and to assess how these risks are reduced by canning and other forms of heat treatment. Since none of the treatments will destroy all the agent in the raw material pet animals will be exposed through feed although does appear that the load of the agent in the final food would be fairly low. The company will be taking steps to reduce this load even further when the risk assessment exercise is completed. In the meantime we have been asked to maintain confidentiality on the work that ‘redacted’, are doing.”

http://www.bseinquiry.gov.uk/files/yb/1989/05/18002001.pdf


CONFIDENTIAL 

* BSE and ‘redacted’.

3. I have thought very hard about whether the Branch should carry out a similar execise with meat and meat products for human foods. On balance I do not think we should undertake but a final decision has not been taken and you may wish to discuss this further. The reason for my reluctance is that I would have to use the same data as ‘redacted’ who has used as his basis, infectivity titres of different organs rom sheep and goats with scrapie. The infectivity levels ere determined by intercerebral injection into mice…

http://www.bseinquiry.gov.uk/files/yb/1989/05/22012001.pdf


* 1st case natural FSE....

NATURAL SPONGIFORM ENCEPHALOPATHY IN A DOMESTIC CAT 

We have heard from MAFF that a domestic Siamese cat from the Bristol area has had spongiform encephalopathy confirmed. Although there are previous instances of experimental infection in cats, there have been no previous natural infections reported. The assumption must be the cat became infections infected by scrapie/BSE agent in its food.

http://www.bseinquiry.gov.uk/files/yb/1990/05/09002001.pdf


* FSE and pharmaceuticals

IN CONFIDENCE

FELINE MATERIAL IN VETERINARY MEDICINES

Snip…

When the BSE questionnaires were sent to holders of veterinary product licences, the covering letter asked for information on substances of bovine, ovine or caprine origin. However, many of the returns included information on all substances of animal origin used in the product. From these returns and from information from licence applications, we know that feline cell lines are used in the manufacture of a few products. 

Most of these cell lines originated in the United States of America and have been established for a number of years. One feline cell line is of UK origin. It was established more than 10 years ago.

Dr A M T LEE Veterinary Medicines Directorate June 1990

90/06.00/17.


* CONFIDENTIAL 

cats/dogs and unsatisfactory posture MAFFs failure to assure key research!

http://www.bseinquiry.gov.uk/files/yb/1990/06/14006001.pdf 


Deaths of CJD man and cat linked http://news.bbc.co.uk/1/hi/health/184558.stm

In October 1998 the simultaneous occurrence of spongiform encephalopathy in a man and his pet cat was reported. The report from Italy noted that the cat did not display the same clinical features as FSE cases previously seen. Indeed, the presence of a new type of FSE was suggested. The man was diagnosed as having sporadic CJD, and neither case (man nor cat) appeared to be affected by a BSE-related condition.

http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html


Editorial: At the time of BSE first being isolated and identified at the CVL in Weybridge it was realised quite quickly by the staff that the disease was probably the case of the illness in the zoo animals, and that it may well represent a risk to domestic cats and dogs. At that point Richard Kimberlin was both sitting on the committee that advised the Government and also advised the manufacturers of pet food in the UK. As you will realise if you read the (many volumes!) Phillips Inquiry, you will realise that on the Government Committee they were only really listened to their advice when the Government had asked for it, and any other advice could be simply ignored. As it was all being done in private and no information could be released to the public, it was possible for the MAFF to simply decide that there was no risk to humans....whereas Kimberlin had already told the pet food manufacturers association in the UK to stop all bovine offal in pet food. They did this immediately as far as I can tell. One company (this must be looked on as simply heresay), however decided to check up whether BSE was a risk to cats at all. They fed a large number (?80) of cats with infected bovine brain and when cats started to produce the symptoms and it seemed that all of them were likely to die of the disease, the experiment was stopped and the as yet asymptomatic cats were slaughtered! The reason for the simultaneous appearance of the FSE in the cat and the CJD in the Italian man....has not come to light.

------------------------------------------------------------------------

Zoo Cats 

Only four years after initial BSE cases had been diagnosed in cattle in the UK, first reports of a new spontaneous spongiform encephalopathy in domestic cats were published. Epidemiological research and strain typing indicated that cattle BSE and this new disease in domestic cats, called Feline Spongiform Encephalopathy (FSE), are linked. All but four of the approx. 100 FSE cases diagnosed worldwide until April 2002 have been seen in the UK (DEFRA). One of the four non-UK cases was diagnosed in Northern Ireland, one in Norway, one in Liechtenstein, and one in 2001 in Switzerland. The most widely accepted hypothesis, although not proven, is that the affected domestic cats were exposed to BSE infectivity through contaminated commercial cat feed or fresh slaughter offal that contained brain or spinal cord from cattle BSE cases. An interesting observation is that in addition to domestic cats, several large cats kept in zoos were diagnosed with FSE. Based on data provided by the British ministry (DEFRA) until April 2002 5 cheetahs, 4 lions and 3 ocelots, pumas and tigers were affected. The large cats that were diagnosed with FSE outside of the UK all originated from UK zoos. It is suspected that these large cats acquired the infection by being fed meat and bones of BSE-infected cattle. Reports on the clinical symptoms presented by these cats give a relatively homogeneous picture: Affected cats show a lack of coordination with an ataxia mainly of the hind limbs, they often fall and miss their target when jumping. Fear and increased aggressiveness against the owner and also other animals is often seen. They do not longer tolerate to be touched (stroked) and start hiding. These behavioural chances might be the result of a hypersensibility to touch and noise, but also to increased fear. Excessive salivation is another more frequently seen symptom. Cats with FSE in general show severe behavioural disturbances,restlessnessand depression, and a lack of coat cleaning. Symptoms in large cats in general are comparable to those in domestic cats. A report on FSE (in german) has been presented in 2001 in the Swiss FVO Magazin. A paper on the first FSE case in a domestic cat in Switzerland is currently in press in the Journal Schweizer Archiv für Tierheilkunde (SAT).

see: http://www.neurocenter-bern.ch/tse_e.shtml



There is a lot more information about each individual case of disease. For example there have been 4 documented cases of TSE in Lions to date: * Lion 32 December 98 Born November 86 * Lion 33 May 1999 (euthanased) Born November 81. * Lion 36 Euthanased August 2000 Born July 87. Deteriorating hind limb ataxia. * Lion 37 Euthanased November 2001 Male, 14 years. Deteriorating hind limb ataxia since September 2001. (Litter mate to Ref. 36.)

http://www.defra.gov.uk/animalh/bse/index.html


http://www.defra.gov.uk/animalh/bse/bse-science/level-4-othertses.html 


Spongiform Encephalopathy in a Captive Puma

http://www.bseinquiry.gov.uk/files/yb/1992/11/13001001.pdf


It now seems clear that all of the cases of zoo cats (as felidiae) that have been reported either were directly found in the UK or were exported from the UK to the country in which the disease was reported. It is not so much an export of animal food, but more of the animal exported itself. The age of infection is not clear but seems to have been relatively young because of this i.e. they could be exported when less than a year old.

------------------------------------------------------------------------

References Br Med Bull. 2003;66:199-212. Other animal prion diseases. Sigurdson CJ, Miller MW. Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, Colorado, USA. In addition to bovine spongiform encephalopathy (BSE) of cattle and scrapie of sheep and goats, a few other animal prion diseases have been reported. These include feline spongiform encephalopathy of zoological and domestic cats (FSE) and transmissible spongiform encephalopathy (TSE) of zoological ruminants and non-human primates, as well as chronic wasting disease of deer and elk (CWD) and transmissible mink encephalopathy of farmed mink (TME). The origins of TSE in cats, zoo bovids, and non-human primates are clearly linked to the BSE epidemic; however, the origins of CWD and TME are less clear, but are not epidemiologically linked to the BSE epidemic. Here we review the epidemiology, transmission, clinical features and pathology of these other animal prion diseases. Schweiz Arch Tierheilkd. 2002 Dec;144(12):664-73. [Beyond BSE: Transmissible spongiform encephalopathies in other animal species] Heim D, Geiser F, Perler L, Wyss R. Bundesamt fur Veterinarwesen, Bern-Liebefeld. dagmar.heim@bvet.admin.ch There are several other diseases besides BSE which belong to the group of transmissible spongiform encephalopathies (TSE). Although most mammals can be experimentally infected with the agent of these diseases, generally only single representatives of the orders Artiodactyla (cloven-hoofed animals), Carnivora (carnivores) and Primates (humans and monkeys) are naturally infected in the field. An overview of the current state of knowledge on TSE in several species like exotic ruminants, deer, mink and cats is presented. Etiological, clinical, anatomic-pathological and epidemiological aspects are described. Gene. 1997 Oct 15;199(1-2):283-6. Sequencing analysis of prion genes from red deer and camel. Kaluz S, Kaluzova M, Flint AP.University of Nottingham, Sutton Bonington Campus, Loughborough, UK. virukalu@savba.sk An abnormal isoform of the prion protein (PrP) appears to be the agent responsible for transmissible spongiform encephalopathies (TSE). The normal isoform of PrP is host-encoded and expressed in the central nervous system. The recent bovine spongiform encephalopathy (BSE) epidemic in the UK and the incidence of prion-related diseases in other animals could indicate that ruminants are highly susceptible to infection via ingestion of prion-contaminated food. Sequence analysis of PrP gene open reading frames from red deer and camel was carried out to investigate sequence variability of these genes among ruminants. (this article merely shows that the PrP gene of the deer and camel are similar to those of sheep, cattle and humans...but this is not surprising!)

------------------------------------------------------------------------

This an excellent review by Terry Singletary: see message on 1.3.5 concerning pet food manufacture and rulings.

http://www.priondata.org/data/A_deerdog.html


Pet Food

EU Pet food Legislation

http://www.useu.be/agri/petfood.html


I just wonder with these new more sensitive TSE testing coming out, what they might find, IF a real study was funded and undertaken for TSEs in dogs? WELL heck, we can't even get an honest TSE study in cattle in the USA, so i guess one in dogs or cats would be way out of the question ... TSS

######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########

Friday, March 8, 2013

Dogs may have been used to make Petfood and animal feed


Monday, March 26, 2012

CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE


MONDAY, FEBRUARY 25, 2019

MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019


FRIDAY, NOVEMBER 3, 2017

BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW

''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''

IN CONFIDENCE


Camel Prion Disease

Friday, May 12, 2023

Camel prion disease, a new emerging disease in North Africa, Lymphoid Tropism, Neuropathological Characterization Update 2023

11th Iberian Congress on Prions Barcelona 2023



A Camelid Anti-PrP Antibody Abrogates PrPSc Replication in Prion-Permissive Neuroblastoma Cell Lines

Daryl Rhys Jones,William Alexander Taylor,Clive Bate,Monique David,Mourad Tayebi

Published: March 22, 2010



15 Apr 2018 23:13 GMT MOST RECENT

Prion Disease in Dromedary Camels, Algeria

Posted by flounder on 15 Apr 2018 at 23:13 GMT




Wednesday, May 24, 2023

***> WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification




SATURDAY, MAY 20, 2023

***> Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE



MAY 19, 2023


2 weeks before the announcement of this recent mad cow case in the USA, i submitted this to the APHIS et al;

***> APPRX. 2 weeks before the recent mad cow case was confirmed in the USA, in Tennessee, atypical L-Type BSE, I submitted this to the APHIS et al;

Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission May 2, 2023

''said 'burden' cost, will be a heavy burden to bear, if we fail with Bovine Spongiform Encephalopathy BSE TSE Prion disease, that is why this information collection is so critical''...



Chronic Wasting Disease CWD TSE Prion

i thought I should share with you Ranchers and Farmers. As most of you know, Chronic Wasting Disease CWD TSE Prion of Cervids is spreading across the US, with no stopping it to date, new transmission studies are showing that indeed CWD has the potential to jump species, oral transmission studies showing CWD can transmit to cattle, sheep, pigs, and to deer. But what concerns me is the way CWD can transmit both vertically and horizontally, and most concerning is the CWD TSE prion distribution in not only brains, eyes, CNS, but also MEATs as well, and the most disturbing of all, is the environmental spread of CWD TSE Prion. For these reasons, i thought some of you folks might should see the…kind regards, terry

Arkansas CWD Deer Study Final 2025

4. Objective 4 and 6 - Infection rates and population modeling

a. In 2024, CWD sample prevalence was 40% across the study area, with higher rates seen in males (65%) than in females (34%).

b. Approximately 50% of males tested positive for CWD by the age of 2.5.

c. White-tailed deer abundance in the study area declined, driven by reduced lifespans and lower lifetime reproduction.

d. If survival does not increase, this population is expected to continue to decline.


FRIDAY, OCTOBER 31, 2025

Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?

The economic burden of ignoring CWD would be far greater, imo, with time, if no cervid were left, or just a select few, if the environment/property was so exposed and saturated with CWD, that you couldn’t sell it, you couldn’t grow crops because of the soil saturation of the CWD, water tables saturated with CWD, saturation of hay, grains, from crops uptake on said property, cervid meat saturated from Cervid CWD, remember, You cannot cook the TSE prion disease out of meat, In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. So, what Do we do, how many humans and animals do we continue to expose, continue to saturate with the CWD TSE Prion, …



SUNDAY, MAY 04, 2025

Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?


Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer

Trying to legislate CWD is what got Texas in this CWD mess to begin with, how did that work out$$$ Legislators and Politicians need to stay away and let TPWD and TAHC et try and contain this mess that Legislators and Politicians got us in, called CWD TSE Prion…terry


THURSDAY, APRIL 10, 2025

CWD TSE Prion, Politics, Friendly Fire, Unforeseen Consequences, What If?


Friday, February 21, 2025

Deer don’t die from CWD, it’s the insurance companies, or it's a Government conspiracy?


THURSDAY, APRIL 24, 2025

***> US Captive CWD Positive Herds Update April 2025


Captive CHRONIC WASTING DISEASE CASES Update August 2025 


Porcine Spongiform Encephalopathy PSE TSE Prion Disease

Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States

Volume 31, Number 1—January 2025

Abstract

Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.

Snip…

Conclusions

In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.


Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.

2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.

The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP


Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.


Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.


This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.


Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure

Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA

Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.

Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).

Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.

Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.






Component 6: Transmissible Spongiform Encephalopathies

Sheep scrapie agent can infect white-tailed deer after oronasal exposure.

Virus and Prion Disease Research Unit, National Animal Disease Center, Ames, Iowa

The origin of chronic wasting disease (CWD) is not known, but it has many similarities to the sheep prion disease called scrapie. It has long been hypothesized that CWD arose through transmission of sheep scrapie to deer. ARS researchers in Ames, Iowa, conducted research to determine if scrapie derived from sheep could be transmitted to white-tailed deer. The deer inoculated with sheep scrapie developed clinical signs and the abnormal prion protein could be detected in a wide range of tissues. These results indicate that deer may be susceptible to sheep scrapie if exposed to the disease in natural or agricultural settings. In addition, several strong similarities between CWD in white-tailed deer and the experimental cases of scrapie in white-tailed deer suggests that it would be difficult to distinguish scrapie from CWD in deer or identify scrapie if a case occurs. This information should be considered by deer farmers for keeping their herds free from prion diseases.


Alzheimers a TSE prion disease?

O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?

Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)

snip...see full Singeltary Nature comment here;

Alzheimer's disease

let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...

Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Background

Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.

Methods

Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.

Results

I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.

Conclusions

There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.

end...tss

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT


Ann N Y Acad Sci. 1982;396:131-43.

Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).

Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.

Abstract

Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.


CJD1/9 0185 Ref: 1M51A

IN STRICT CONFIDENCE

Dr McGovern From: Dr A Wight Date: 5 January 1993 Copies: Dr Metters Dr Skinner Dr Pickles Dr Morris Mr Murray

TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES

1. CMO will wish to be aware that a meeting was held at DH yesterday, 4 January, to discuss the above findings. It was chaired by Professor Murray (Chairman of the MRC Co-ordinating Committee on Research in the Spongiform Encephalopathies in Man), and attended by relevant experts in the fields of Neurology, Neuropathology, molecular biology, amyloid biochemistry, and the spongiform encephalopathies, and by representatives of the MRC and AFRC. 2. Briefly, the meeting agreed that:

i) Dr Ridley et als findings of experimental induction of p amyloid in primates were valid, interesting and a significant advance in the understanding of neurodegenerative disorders;

ii) there were no immediate implications for the public health, and no further safeguards were thought to be necessary at present; and

iii) additional research was desirable, both epidemiological and at the molecular level. Possible avenues are being followed up by DH and the MRC, but the details will require further discussion. 93/01.05/4.1


BSE101/1 0136

IN CONFIDENCE

5 NOV 1992 CMO From: Dr J S Metters DCMO 4 November 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognized the public sensitivity of these findings and intend to report them in their proper context. This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.

2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed'. As the report emphasizes the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. What are the implications for public health?

3. The route of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.

92/11.4/1-1 BSE101/1 0137

4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required" before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.

JS METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 121/YdeS 92/11.4/1.2


''on the possible transmissibility of Alzheimer's''

9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly

(1) concerning a farmer with CJD who had BSE animals,

(2) on the possible transmissibility of Alzheimer's and

(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT




Singeltary 2001

Subject: CJD or Alzheimer's or the same ???

Date: Sun, 29 Apr 2001 12:45:28 -0700

From: "Terry S. Singeltary Sr."

Reply-To: Bovine Spongiform Encephalopathy

To: BSE-L@uni-karlsruhe.de

Bovine Spongiform Encephalopathy

Greetings List,

thought some might be interested in this. I have always wondered if CJD and or all TSEs and Alzheimer's could be linked. i have been of the opinion that Alzheimer's is a TSE for a long time, just at the low end of the titre of infectivity scale. i also believe in the accumulation theory. by dose, you could be killed by one sitting, or one injection, or one whatever, depending on the titre of infectivity of that whatever. on the other hand, if the dose is not a lethal dose, over a period of time, the accumulation will become lethal (if consumption continued), and i believe the route/source/titre of infectivity, will be a key roll to the incubation period, and symptoms.

just my opinion...snip…end

Human TSE Prion Creutzfeldt Jakob Disease CJD

2001 Singeltary on CJD, Journal of American Medical Association

February 14, 2001

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr

Author Affiliations

JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

February 14, 2001

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Terry S. Singeltary, Sr

Author Affiliations

JAMA. 2001;285(6):733-734. doi:10-1001/pubs.JAMA-ISSN-0098-7484-285-6-jlt0214


2023


Professor John Collinge on tackling prion diseases

Professor John Collinge is Director of the MRC Prion Unit and also directs the NHS National Prion Clinic at the adjacent National Hospital for Neurology and Neurosurgery.

What are prions, why are they important, and how might they help us develop treatments for neurodegenerative conditions like dementia?

Prions are lethal pathogens that cause neurodegenerative diseases of humans and other mammals.

The best-known human prion disease is sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia which accounts for around 1 in 5000 deaths worldwide. In sharp distinction to all other infectious agents, prions lack their own DNA or RNA genome and consist of polymers of a misfolded form of a normal cellular protein (the prion protein or PrP) which form amyloid fibrils.

These fibres grow by addition of PrP molecules at their ends and they eventually fragment producing more prion particles which continue this process and spread throughout the brain. The final proof of the once controversial “protein-only hypothesis” of prions came with the determination of the structure of infectious prions at near atomic resolution by cryogenic electron microscopy by ourselves and US colleagues in the last few years.

The normal cellular prion proteins are very similar between different species of mammals and therefore a prion infection from one species can sometimes infect another species. This is what happened with the prion disease of cattle, bovine spongiform encephalopathy (BSE) in the 1990’s which caused a new human prion disease known as variant Creutzfeldt-Jakob disease (vCJD) and led to the BSE crisis in the UK, EU and other countries.

While human prion diseases are thankfully rare, there are common prion diseases of other species, for example scrapie in sheep and goats worldwide and chronic wasting disease in deer in North America. While prions were first thought to be unique to these rare neurological diseases, it became clear that the molecular process was of far wider relevance with for example the recognition of several different proteins in yeast that could form prions.

Most importantly with respect to neurodegeneration and dementia in humans, it has been established that similar so-called “prion-like” mechanisms are involved in much commoner conditions including Alzheimer’s and Parkinson’s diseases. In Alzheimer’s disease (AD) for example, two proteins in the brain, amyloid-beta and tau can form self-propagating assemblies which spread in the brain. Indeed, we reported in two articles in Nature that the amyloid-beta pathology seen in AD can be transmissible between humans in rare circumstances causing the newly recognised condition iatrogenic cerebral amyloid angiopathy.

There is accumulating evidence also for iatrogenic AD. Understanding prion biology, and in particular how propagation of prions leads to neurodegeneration, is therefore of central research importance in medicine. Many years ago, we demonstrated that targeting the production of the normal cellular prion protein completely halted the progression of neurodegeneration (and indeed even reversed early pathological changes) in laboratory mice. This work has underpinned multiple efforts to develop rational treatments for prion and other neurodegenerative diseases…


WEDNESDAY, OCTOBER 15, 2025

US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT 2025


Terry S. Singeltary Sr.

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Feline and Canine Spongiform Encephalopathy TSE Prion Disease, Pet Food, and the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD, what if?

  Feline and Canine Spongiform Encephalopathy TSE Prion Disease, Pet Food, and the FDA PART 589 SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOO...