Tuesday, March 25, 2014

Transmission of Chronic Wasting Disease in Wisconsin White-Tailed Deer: Implications for Disease Spread and Management

Transmission of Chronic Wasting Disease in Wisconsin White-Tailed Deer: Implications for Disease Spread and Management


Christopher S. Jennelle mail,

Viviane Henaux,

Gideon Wasserberg,

Bala Thiagarajan,

Robert E. Rolley,

Michael D. Samuel


Published: March 21, 2014 •DOI: 10.1371/journal.pone.0091043





Few studies have evaluated the rate of infection or mode of transmission for wildlife diseases, and the implications of alternative management strategies. We used hunter harvest data from 2002 to 2013 to investigate chronic wasting disease (CWD) infection rate and transmission modes, and address how alternative management approaches affect disease dynamics in a Wisconsin white-tailed deer population. Uncertainty regarding demographic impacts of CWD on cervid populations, human and domestic animal health concerns, and potential economic consequences underscore the need for strategies to control CWD distribution and prevalence. Using maximum-likelihood methods to evaluate alternative multi-state deterministic models of CWD transmission, harvest data strongly supports a frequency-dependent transmission structure with sex-specific infection rates that are two times higher in males than females. As transmissible spongiform encephalopathies are an important and difficult-to-study class of diseases with major economic and ecological implications, our work supports the hypothesis of frequency-dependent transmission in wild deer at a broad spatial scale and indicates that effective harvest management can be implemented to control CWD prevalence. Specifically, we show that harvest focused on the greater-affected sex (males) can result in stable population dynamics and control of CWD within the next 50 years, given the constraints of the model. We also provide a quantitative estimate of geographic disease spread in southern Wisconsin, validating qualitative assessments that CWD spreads relatively slowly. Given increased discovery and distribution of CWD throughout North America, insights from our study are valuable to management agencies and to the general public concerned about the impacts of CWD on white-tailed deer populations.






CWD Transmission


Using white-tailed deer harvest data from south-central Wisconsin, we show that FD CWD transmission is the best supported model for both sexes (with higher infection rates for males) at a broad spatial scale, whereas our earlier efforts to model this system could not discriminate between FD and DD transmission [18]. It has been suspected that FD was a dominant transmission mechanism in mule deer [5], [17]; [ but see 6], and more recently in white-tailed deer [28], [46]. Furthermore, our modeling results suggest a more recent and biologically plausible time since CWD introduction in south-central Wisconsin compared with earlier analysis [18]. As demonstrated in previous work in this CWD system [21], [22], [25] and in Colorado [7], [47], adult males have higher CWD infection rates than females. Although the mechanism for higher CWD infection and prevalence in males is unknown, these differences may be driven by sex-specific social behavior [7], [21]. Males typically have larger home ranges, longer dispersal distances, interactions with other males, or rut-related behavior [48] that could result in more contacts with infectious deer. In contrast, females generally interact within a much smaller matrilineal group [27], [28], [49], and only briefly with males during rut [47].


Given the simplicity of our model, our estimated infection coefficients are likely a function of several different (and largely unknown) mechanisms that may vary between/among sexes, seasons, and the environment. These infection rates represent a weighted average of many potential drivers as summarized by Potapov et al. [39]. Our models do not account explicitly for indirect transmission from the environment where prions can persist for years [50], [51], although our infection rates implicitly subsume both direct and indirect routes of infection. The importance of environmental transmission has been demonstrated in captive mule deer [52], [53] and theoretical modeling indicates that population impacts can be driven by the length of time that prions remain infectious in the environment [54]. In the long term, the potential accumulation of an environmental reservoir of infectious prions may become an increasingly important component of CWD transmission; however, the relative contribution of direct and indirect transmission in wild deer populations remains unknown and requires further research. Although we expect infectious contact likely varies by sex and season, harvest data were insufficient to account for intra-annual complexity in sex-specific transmission. Additional insights for CWD management given directional sex-specific transmission (i.e., female-to-male, female-to-female) may require focal research studies that determine differences in infectious contact between and among sexes [49], [55]–[57] and how these influence the risk of disease transmission [28]. In particular, understanding the mechanisms that lead to rates of male infection twice as high as females could provide crucial insights on management strategies designed to reduce male CWD prevalence as an alternative to high male harvest.


Assuming CWD originated in the core area and environmental accumulation of prions contributes significantly to transmission, we would expect higher infection rate estimates in the core compared with surrounding areas. We are uncertain why infection rate is apparently greater in males for some areas to the west and southwest of the core. These surrounding areas have similar habitat characteristics with the core, and we would not expect deer abundance to vary significantly prior to CWD discovery. Heterogeneous harvest management conducted among areas may be one potential explanation. However, this difference also suggests that unidentified environmental characteristics or management actions may influence the current and future trends in CWD prevalence. Regardless, these patterns suggest that our model predictions for the core area may underestimate the rate of CWD increase in other areas. Future research is needed to understand the drivers of CWD transmission, how these vary spatially, and their influence on future patterns of infection. The identification of potential environmental reservoirs (e.g., common feeding areas, mineral licks) and evaluation of the significance of indirect transmission in free-ranging deer populations would also enhance our ability to predict future trends in infection and allow a better evaluation of alternative control strategies.


In concept QAIC should help account for overdispersion in our data, which might result from missing covariates in the model and/or a lack of independence in the data (e.g., [58]). Such lack of independence may be due to spatial and/or temporal autocorrelation, and while we do not explicitly account for such effects, we rely on QAIC to generally accommodate a portion of these impacts. While we detected significant temporal autocorrelation in residuals for predicted female prevalence, other research in the same study area [44], [46] found no spatial autocorrelation in model residuals using a 93.6 km2 or 2.6 km2 spatial frame, respectively. We caution that despite use of QAIC, our model parameter estimates may still be overly precise.


Rate of spread


Several studies indicate that the southwestern core area of WI is the likely point of origin for CWD in our study area, with an inverse relationship between distance-to-core and prevalence as would be expected from an introduced disease spreading across the landscape [20], [22], [44]. To our knowledge, we present the first empirical estimate of CWD geographic spread, based on sex-specific FD transmission, which indicated a low average rate (1.13 km year−1) during initial phases of the epizootic. There is no current evidence to suggest that CWD spread in our study area was facilitated by humans (via movements of infectious animals between game farms or preserves); however, the anecdotal evidence of such events warrants further investigation. Though DD transmission was not supported by our data, the estimated rate of geographic spread was similar for this model structure. Our results suggest that in the south-central Wisconsin endemic area, CWD has slowly moved across the landscape and is probably not a recent development. Clearly this estimated rate of spread must be considered unique to the outbreak in south-central Wisconsin.


Rates of CWD spread in other regions are likely influenced by a number of factors including habitat features [44], [59], mode of disease transmission, host species (e.g., white-tailed or mule deer), population structure, host movements [60], dispersal [61], and possibly the environment [54]. For example, recent analyses [44] indicate that CWD may be spreading faster from the outbreak in eastern Wisconsin and northern Illinois than from south-central Wisconsin. Our simple estimate also assumes an average uniform diffusion from the point of origin and ignores potential disease movement via longer distance dispersal [60], although recent discovery of CWD in north-west Wisconsin does not appear to be linked to long-distance dispersal from southern Wisconsin based on genetic analysis (S. Robinson Pers. Comm.). In addition, our analysis does not account for habitat heterogeneity and physical barriers (natural or anthropogenic) that influence landscape scale movement and interaction of deer populations [62], [63] or CWD distribution [44], [63]. We also note that despite a highly significant R2 value, our simple regression utilizes only six data points (including the core, which we assume is the origin of the epizootic), with uncertainty that is not accounted for in the regression. As such, there is likely higher variance associated with our estimated rate of spread.


Despite these limitations, our estimate provides a starting place to conceptualize early CWD spread across the southern Wisconsin landscape. In the context of CWD, we believe the areas surrounding the core are currently in relatively early stages of the epizootic with low, but increasing prevalence. Under FD transmission and barring effective management efforts, CWD prevalence is predicted to increase over time, and we suspect that the rate of spread may also increase because more young males will become infected prior to dispersal [46]. As such, we consider our spread estimate as a lower bound that is likely to increase as the epizootic progresses.


Harvest strategies


As a consequence of FD transmission, our simulations predict that in the next decade CWD prevalence can increase to relatively high levels (25% in females and 50% in males) in the absence of significant management actions to reduce infection rates. Of the three harvest strategies we evaluated, only male-focused harvest succeeded in reducing CWD prevalence below current levels. Prevalence is reduced because this strategy removes animals from the highest prevalence class (reducing infection rates), while allowing dilution of population-level CWD prevalence by recruitment of more females [64]. In contrast, CWD increased under female-focused and herd-control harvest strategies. By focusing harvest on the portion of the population with highest prevalence and infection rates, our simulation suggests that harvest management can effectively reduce prevalence despite FD disease transmission. Although disease eradication may not be possible, prevalence reduction (especially in higher risk groups), which reduces force of infection, is the key to mediating disease impacts on host populations in the long term. Effective disease management by sex-specific differential harvest has also been explored for bovine tuberculosis in deer [55].


The density-dependent harvest structure we imposed produced much lower average realized harvest (RH) rates for the female-focused and herd-control strategies, compared with male-focused harvest. High female harvest reduces population size, which requires lower realized harvest rates to maintain stable population goals (based on societal tolerance for deer). While this density-dependent harvest structure is artificial, it is intended to represent hunter effort in response to perceived deer densities. In the absence of such a mechanism, static harvest rates over the simulated time frame of 50 years resulted in host and disease extinction, as predicted in theoretical models of FD disease transmission [14]. In addition, our results show that deer demography and CWD dynamics are sensitive to changes in harvest. Estimation of unbiased harvest rates requires accurate information on both the distribution of harvested animals and the distribution of the underlying population. Although harvest-based estimates for deer populations have various limitations [9], [65], the importance of this parameter for monitoring the performance of CWD management programs suggests future research to improve estimation procedures should be considered.


The demographic implications of alternative harvest strategies for disease management are also important as they affect deer densities, recreational opportunities (e.g., hunting or observation), and potential disease spread. While male-focused harvest reduces CWD prevalence in the long term, it results in lower densities of adult males (compared with herd-control), which are usually of primary interest to deer hunters. For the herd-control harvest strategy (current deer management goals) nearly 50% of adult males and 25% of adult females are expected to become infected within another decade. Even worse, for female-focused harvest not only are deer densities expected to be low, but more than 50% of surviving adult males and 30% of adult females would be infected. In general, these harvest strategies are characterized by accelerating rates of infection in all deer, and higher prevalence, particularly in males. Considering the constraints of our model the tradeoff between strategies is clear; CWD can eventually be reduced with fewer opportunities to harvest healthy adult bucks, or more adult bucks may be available for harvest, but with higher rates of CWD infection. Given that quality deer management practices focus on production of older bucks with large antlers, management agencies could face difficult alternatives from these competing interests. However, if an efficacious CWD vaccine was available and cost-effectively distributed to broad segments of a deer population (particularly males), managers would have more flexibility to employ a disease control strategy combining harvest and vaccination to provide adequate recreational opportunities to harvest CWD-free deer.


The mechanism for density-dependent population regulation in deer is not well known, but one hypothesis is that deer reduce body size and maintain survival rates while lowering reproduction [66]. Therefore, we used density-dependent fecundity to regulate population size in our no-harvest simulations. The goal of these simulations was to illustrate the rapid increase in CWD prevalence and eventual impact on deer populations in the absence of harvest or other factors that remove infected animals prior to mortality from CWD. Such situations might be likely in high density urban deer populations, national parks, captive deer farms, or other areas where deer harvest or removal is limited. This simulation is not designed to represent current conditions in Wisconsin, and we consider this a worst-case disease scenario in areas without harvest.


*** However, we also note that CWD transmission rates and prevalence are much higher in captive deer farms than has been reported in wild populations [67].






Given our model structure and data, our results provide strong support for FD transmission of CWD with the force of infection driven by changes in prevalence, which we suggest is a vital metric for focused control efforts. Generally as prevalence increases, as found in Wisconsin, infection rate also increases in the absence of intervention, producing an accelerating pattern of infection. Assuming that frequency-dependent transmission predominates (as our evaluation indicates), management to reduce prevalence will mediate potential CWD population impacts. The higher rate of infection and prevalence in males, thus, provides the basis for effective CWD management using deer harvest focused on this sex. Management to reduce prevalence might be accomplished through the synergistic effects of targeted harvest and vaccination of males. Unfortunately, we know little about the mechanisms for male infection and further research is needed before alternative management strategies to reduce male infection rates can be developed. Spatial differences in CWD infection rates, despite similar habitat and pre-CWD deer abundance, suggest that unidentified environmental or management factors may also influence disease dynamics and future trends in prevalence. Future research to understand the drivers of CWD transmission, how these vary spatially, and the relative importance of environmental and direct transmission is critical to understanding future CWD dynamics in wild deer.


Our results also indicate that even with high deer densities CWD has been spreading at a relatively slow rate across the landscape; in agreement with larger scale spatial patterns for prevalence [44]. However, as disease prevalence continues to increase, the rate of infection in yearling bucks will also increase [46]. Because dispersing bucks may be an important source of disease spread, these patterns suggest that CWD prevalence outside the core area will continue to grow and the disease may spread at an increasing rate. Although the drivers of CWD spatial spread are not generally known (see [44] for identification of landscape features that affect spread), management efforts to reduce both local prevalence and deer abundance will likely reduce dispersal of infected yearling bucks. However, the relative impact of reducing deer abundance versus prevalence in lowering the number of infected yearling bucks likely depends on disease prevalence and deer density [46]. Further research is needed to determine the factors that affect spatial spread and develop effective management strategies.





WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$


Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013


*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***



Sunday, October 13, 2013


*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012



Sunday, March 09, 2014


A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease





Wednesday, December 11, 2013


*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease ***



Monday, February 10, 2014


18 Forsyth Medical Center patients exposed to CJD; apology issued...OOOPS, SORRY, TOO BAD $$$



Tuesday, February 11, 2014


Novant Health Forsyth Medical Center Information on potential CJD exposure



Monday, February 3, 2014


*** Evaluation of the zoonotic potential of transmissible mink encephalopathy TSE Prion disease





Sunday, March 23, 2014


APHIS USDA National Scrapie Eradication Program February 2014 Monthly Report Fiscal Year 2014



Monday, March 3, 2014


*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers to eat dead stock downers and whatever else the industry decides


see updated Rancho CLASS 1 HIGH RISK dead stock cancer downer recall for IDAHO






OAI 2012-2013


OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.


ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St. Newberry SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y


DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN 46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y


ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC 28163-7617 OPR FL, TH NP 7/17/2013 OAI N


NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007 OPR FR, OF NP 7/16/2013 OAI Y


DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N


CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y


*** DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N


Ruminant Feed Inspections Firms Inventory (excel format)



PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates posted, as in numerical order, you will have to sift through them for yourselves. ...tss


snip...see full text ;


Sunday, December 15, 2013





Saturday, December 15, 2012


Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012



Sunday, February 2, 2014


The Presence of Disease-Associated Prion Protein in Skeletal Muscle of Cattle Infected with Classical Bovine Spongiform Encephalopathy


NOTE Pathology



Saturday, December 21, 2013


**** Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle ****



Wednesday, December 4, 2013


*** Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products; Final Rule Federal Register / Vol. 78 , No. 233 /


Wednesday, December 4, 2013



Saturday, November 2, 2013


*** APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe





*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.







Friday, March 21, 2014


Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?


“As of March 20, 2014, FSIS has completed all checks (effectiveness checks and disposition verification checks) for recalls 002-2014 and 013-2014 regarding Rancho Feeding Corporation. FSIS has determined that based on the number of successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses were notified of the recall and removed affected products from commerce that the recall activities were effective.”


say what $$$



Monday, December 1, 2008


When Atypical Scrapie cross species barriers



why do we not want to do TSE transmission studies on chimpanzees $




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.







1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.


Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.


Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.




The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.


PMID: 6997404



Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"


Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.







Nature. 1972 Mar 10;236(5341):73-4.


Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis). Gibbs CJ Jr, Gajdusek DC.


Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0


Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)




National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland


SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).




 Re: vCJD in the USA * BSE in U.S. 15 November 1999 Terry S Singeltary, NA


CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997. So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie.


It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses.



U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...


2 January 2000 Terry S Singeltary


The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;


"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."


Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.


Something else I find odd, page 16;


"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."


A few more factors to consider, page 15;


"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."


"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."


"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."


Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow. Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.


To be continued...


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA


Competing interests: None declared





JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733


Diagnosis and Reporting of Creutzfeldt-Jakob Disease


Terry S. Singeltary, Sr Bacliff, Tex


Since this article does not have an abstract, we have provided the first 150 words of the full text.


KEYWORDS: creutzfeldt-jakob disease, diagnosis. 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.


References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.



Published March 26, 2003


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States


Terry S. Singeltary, retired (medically)


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?


Published March 26, 2003



14th ICID International Scientific Exchange Brochure - Final Abstract Number: ISE.114


Session: International Scientific Exchange


Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009


T. Singeltary Bacliff, TX, USA


Background: An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.


Methods: 12 years independent research of available data


Results: I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.


Conclusion: I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.



The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI


Tracking spongiform encephalopathies in North America




Xavier Bosch


“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...






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


Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003


Date: Tue, 29 Jul 2003 17:35:30 –0500


From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de


Volume 3, Number 8 01 August 2003








Tracking spongiform encephalopathies in North America


Xavier Bosch


My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.






Singeltary submission to PLOS ;


No competing interests declared.


see full text ;



Owens, Julie


From: Terry S. Singeltary Sr. [flounder9@verizon.net]


Sent: Monday, July 24, 2006 1:09 PM


To: FSIS RegulationsComments


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98






Sunday, August 09, 2009


CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009



Tuesday, August 18, 2009


* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009



Monday, March 10, 2014


Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014



Wednesday, May 16, 2012


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


Proposal ID: 29403




















never break a promise to your mom. DOD 12/14/97 CONFIRMED hvCJD...




Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net





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