Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
Greetings, I wish to submit some new and old data for the ones interested in reading about CWD and CJD. This study and others should warrant strict safety guidelines while field dressing your kill. I am not kidding you, inoculation is the most effective mode of transmission (route). A simple cut and or scratch while field dressing a kill (if infected with CWD/TSE), could very well transmit the agent to a human, and a pair of those cheap rubber gloves will not protect you very well. AND if you are exposed to the agent, you will never know it until years later, by that time, how many have you exposed through various other routes (dental, surgery, just to name a few)? I am not trying to scare anyone, just to enlighten you on TSEs (all of them), and to simply warn you of the potential for transmission from various routes and sources. Recently a study came out and I posted the abstract, but over the weekend I received the full text, and I think every hunter out there should have the opportunity to read it. Whether you do or not is your business; Occupational risk factors for the sporadic form of Creutzfeldt-Jakob disease (FULL TEXT snip... Among occupations and industries, for which previous reports suggested potential exposure to a transmissible spongiform encephalopathy (TSE) agent, the OR for CJD was significantly increased among butchers (OR=6.8, 95% C.I. 1.5, 30.1, based on 4 cases and 3 controls), and persons working in offices of physicians (OR=4.6, 95% C.I. 1.2, 17.6 based on 5 cases and 4 controls). snip... http://www.vegsource.com/talk/madcow...ges/91447.html some old data to reference too; ANOTHER FARMER KILLED BY CJD !!! snip... 20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19 year old died from sCJD in France in 1985. There is no evidence of an iatrogenic cause for those cases.... http://www.bseinquiry.gov.uk/files/y...0/04004001.pdf cover-up of 4th farm worker ??? http://www.bseinquiry.gov.uk/files/y...0/23006001.pdf http://www.bseinquiry.gov.uk/files/y...0/20006001.pdf CONFIRMATION OF CJD IN FOURTH FARMER http://www.bseinquiry.gov.uk/files/y...1/03008001.pdf now story changes from; SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms. to; This is not unexpected... was another farmer expected? http://www.bseinquiry.gov.uk/files/y...1/13010001.pdf 4th farmer, and 1st teenager http://www.bseinquiry.gov.uk/files/y...2/27003001.pdf 2. snip... Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES. 3. You will recall that the advice provided by Professor Smith in 1993 and by Dr. Gore this month used the sub-population of dairy farm workers who had had a case of BSE on their farms - 63,000, which is approximately half the number of dairy farm workers - as a denominator. If the above sums are repeated using this denominator population, taking an annual incidence in the general population of 1 per million the observed rate in this sub-population is 10 TIMES, and taking an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general population... http://www.bseinquiry.gov.uk/files/y...1/31004001.pdf snip... http://www.vegsource.com/talk/madcow...s/9912501.html http://www.vegsource.com/talk/madcow...ges/91448.html THOSE HEALTHY LOOKING DEER/ELK ''SUB-CLINICAL'' INFECTION DEAD DEER WALKING Issued: Monday, 28 August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a 'sub-clinical' form of BSE in mice which was unknown until now. The scientists took a closer look at what is known as the 'species barrier' - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a 'sub-clinical' form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases. Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain. In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters. The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust. Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE. "This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures." ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL. http://www.mrc.ac.uk/index/public_in...-mrc-43-00.htm OPINION OF THE SCIENTIFIC COMMITTEE ON MEDICINAL PRODUCTS AND MEDICAL DEVICES ON “THE PROTECTION OFFERED BY NATURAL RUBBER LATEX MEDICAL DEVICES (MEDICAL GLOVES AND CONDOMS) AGAINST TRANSMISSIBLE DISEASES” Adopted by the SCMPMD during the 24th plenary meeting of 16 October 2003 snip... 1. Introduction to the problem The changing characteristics of the risk of infection by blood borne pathogens with respect to clinical procedures has resulted in a number of discussions about the effectiveness of protective equipment and materials, including natural rubber latex products such as medical gloves, designed to have this barrier function (Anonymous 1987, CDC 1988, Fay and Dooher1992, Fay 1996, FDA 1999, Gerberding et al 1995, Rabussay and Korniewicz 1997, Stringer et al 2001). In addition, the low quality of some surgical and examination gloves, considering the importance of the barrier effectiveness, has been a concern in the past (Fay and Dooher 1992). This was particularly so in the 1980’s when the increased use of gloves placed an increased demand on industry, resulting in some low quality gloves on the market (Fay and Dooher1992). The perception of additional risks of infectivity with respect to the Transmissible Spongiform Encephalopathies (TSE) such as Bovine Spongiform Encephalopathy (BSE) and variant Creutzfeld-Jacob-Disease (vCJD) have also raised the level of concern. In addition, a series of alternative materials have been made available to clinicians, arising from the apparent increased levels of allergies to latex products. Similar concerns exist for these alternatives, leading to a greater degree of uncertainty over barrier effectiveness from one product to another. snip... 7. Risk assessment including populations at risk The risk of health care workers for blood borne exposure and infection is highest in operating room settings, the most likely means of transmission being percutaneous injuries (Fay and Dooher 1992, Stringer et al 2001, Wright et al 1991). Prevention is mainly provided by the use of the so-called universal precautions (CDC 1988). Glove use should reduce the incidence of contamination of hands, but they cannot prevent penetrating injuries due to needle or other sharp instruments. It should be noted that there is an increase in glove leakage during surgical and dental procedures (Albin et al 1992, Douglas et al 1997, Driever et al 2001, Fay and Dooher 1992, Fiehn and Westergaard 1989, Korniewicz et al 1990, Kotilainen et al 1989, Rego and Roley 1999). For example Driever et al (2001) found during an examination of 953 gloves worn during cardiac surgery, 26% of those worn by the operator were punctured, as were 38 % of those worn by the theatre nurses. Limiting the time of the surgical procedure reduces glove barrier failure, as glove failure increases in time (Fay and Dooher 1992, Gerberding et al 1990, Quebbeman et al 1991). The use of the double glove method in surgery gives an additional level of protection against blood borne infections and greatly reduces the risk of glove penetration, as discussed by Gerberding et al (1990) and Quebbeman et al (1992) a number of years ago. Recently there have been a number of studies published that strongly support and advocate the use of double gloving as the major risk management factor in the control of the transmission of disease in a clinical setting. In gynaecological surgery, Murta et al (2003) found that 10.4 % of single gloves perforated during use, as did 9.8 % of the outer double gloves whereas there was no perforation of any inner double glove. In general surgery Laine and Aarnio (2001) found a 6.2 % incidence of puncture of the inner of a double glove compared to an overall 18.3% of total operations resulting in perforation. In open lung surgery, Hollaus et al (1999) reported a 78 % incidence of perforation of gloves, but the inner glove only perforated in 1.1%, double gloving effectively protecting against cutaneous blood contact. It is recognised that double gloving may not always bring benefits (Avery et al 1999), that many surgeons are not in favour of it (St Germaine et al, 2003) and that care has to be taken not to reduce manual dexterity and increase discomfort (Alrawi et al, 2002), but a recent major systematic review of the evidence (Tanner and Parkinson 2002) makes it very clear that wearing two pairs of latex gloves significantly reduces the number of perforations of the glove in contact with the skin and reduces the risk of surgical cross infection. Although the risk for infection with TSE is largely unknown, certain assumptions for the possibility of infection can be established. The United Kingdom (UK) is at this moment the only country with a major infected population. Up to August 2003, 133 people have died of definite or probable vCJD in the UK, the total number of patients diagnosed being 137. In France 6 people were diagnosed with vCJD, while in some other countries only single cases were noted so far. A major difficulty here is that people may be infected and unknowingly be in the incubation phase of the disease at the time of a clinical procedure, this phase possibly lasting several years. This necessitates rather severe prophylactic measures. The route of infection is not known, but could be ingestion of BSE contaminated food. 11 Health care workers are one of the populations at risk, of which those working in the operating theatre (surgeons, nurses) have the highest risk, especially when surgery on the brain is performed. Considering the rather limited number of patients with TSE, and the professional measures which can be used to avoid contamination/infection, the actual risk to anyone is very limited. For those patients with a known TSE infection (CJD, vCJD) proper measures can be instigated to protect the health care workers. The use of natural rubber latex medical gloves is one of them. In view of the limited number of humans infected with vCJD, the general risk for health care workers for infection with vCJD even in the UK is marginal at most. As stated for specific cases, specific measures can be instigated to reduce the risk of infection. The risk for infection with vCJD (or BSE) by food consumption is unknown, and is largely reduced by various EU regulations, but is probably higher than the risk introduced by patient contact. For viral infections (HIV, Hepatitis) the situation is quite different. The risk especially for health care workers for infection with a viral infection can be rather high. However, this risk can be reduced to almost zero by proper preventive measures such as using protective clothing and natural rubber latex medical or examination gloves. An overview of the estimated risks for transmission of infectious agents through natural rubber latex medical devices i.e. gloves and condoms, along with risk management procedures is presented in Table 2. 8. Conclusions/recommendations For TSE it is unknown whether the agents can pass through an intact latex membrane. The estimated size of these agents lies below that of viral simulants which cannot pass the latex membranes, so, theoretically, TSE passage cannot be excluded. However, in view of the known physical and chemical characteristics of TSE agents and natural rubber latex, it seems unlikely that TSE can actually pass through intact latex. This is probably also true for alternative materials. So far, no infections with TSE in health care settings could be attributed to the barrier failure of latex medical gloves. Moreover, the population at risk for TSE infection in health care settings is very low, even in the UK. For condoms there is no indication of risk for TSE infection as there are no indications for sexual transmission of TSE’s. Both natural rubber latex medical gloves and condoms offer good protection against transmission of viral infections including HIV. However, the protection may diminish during use, especially when the glove material is aged or damaged. By far the greatest risk for transmission of infectious agents, is encountered when a glove is torn or punctured during a medical procedure. In order to prevent this, more detailed instructions on use of latex medical gloves would be warranted in terms of factors such as the duration of use and the use of double gloves. It should be emphasized that medical gloves and condoms are single use devices. It is known that some chemicals can penetrate natural rubber latex and affect the physical properties of the product. It is, however, unknown as to whether this process can influence transmission of infectious agents, either positively or negatively. In general, in terms of leakage properties, no alternative material has been found to be superior to natural rubber latex. 9. References snip... http://europa.eu.int/comm/food/fs/sc/scmp/out48_en.pdf TSS http://www.ngpc.state.ne.us/cgi-shl/...&f=12&t=000319 |
RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
Most of what you type will fall on death eyes Mad C. Unless its in their backyard, they think its no big deal. You have mail.
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RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
Ah, good ol' anti-hunter scare tactics. If you antis want to get people to read your posts, you should probably cut them off around the 500 word mark. Reading a few paragraphs of garbage is one thing, but I doubt many here have the patience to sift through this.
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RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
wrong, i am not anti-anything, but pro-truth. my grandfather was a great
hunter, i used to hunt the saddle back in Llano Texas. I use to love to hunt, but am disabled now with a damn neck injury. i really don't care if you believe me or not, it will not change anything. love guns, and love to fish. still eat meat occassionally. i only seek the truth, and i only wish to pass that to everyone. i do not want anyone to go through what my mother went through. 10 weeks from 1st of symptoms to death. she did everything Linda Blair did in the exorcists movie except spin here head 360 degrees. it took 3 of us to hold her down at times from the jerking. it will be 6 years Dec 14. there are always people like you that want to stick your head in the sand and ignore problems, and this is fine, i only hope to teach you what you don't know about. if i succeed in only convincing a few, then i have succeeded. but again, don't shoot the messenger..... 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. PMID: 6997404 http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. PMID: 8006664 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/q...&dopt=Abstract Lancet Infectious Disease Journal August 2003 issue Issue 8, 01 August 2003 http://infection.thelancet.com/journ.../iss8/contents Tracking spongiform encephalopathies in North America [Full Text] [PDF] Xavier Bosch Newsdesk 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 hunters—two of whom were friends—who 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”. http://infection.thelancet.com/journal/journal.isa Greetings, >>>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.<<< actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article. regardless, i said it and meant it...TSS Full Text Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/cgi/content...urnalcode=jama Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: [email protected] 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? http://www.neurology.org/cgi/eletters/60/2/176#535 Gerald Wells: Report of the Visit to USA, April-May 1989 snip... The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised... snip... It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US... snip... 3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_... snip... http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988 Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle R.F. Marsh* and G.R. Hartsough ⬢Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092 ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England. INTRODUCTION Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source. OBSERVATIONS AND RESULTS A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed. Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months. DISCUSSION These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy. We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed. ACKNOWLEDGEMENTS These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations. REFERENCES Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420. MARSH http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf Docket Management Docket: 02N-0273 - Substances Prohibited From Use in Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed Comment Number: EC -10 Accepted - Volume 2 http://www.fda.gov/ohrms/dockets/dai.../8004be07.html PART 2 http://www.fda.gov/ohrms/dockets/dai.../8004be09.html with kindest regards, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, TEXAS USA 77518 |
RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
i really dont have the time to read through all this. do you think maybe you could sum it up in a few sentences?
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RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
Let me guess 06. No CWD in your back yard. How do you know?
Unless its in their backyard, they think its no big deal. |
RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
hunters are not about to stop hunting because of cwd
we take the risk of carrying a loaded gun through the woods, climbing trees and often times sitting still for hours in freezing weather. until the chance of killing a cwd deer and actually having it transfer to a human becomes anywhere near the other risks hunters take, i wont even worry about it |
RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
i am not anti-anything I've read about all of these diseases myself. I'm not about to give up hunting over any of it. I'd rather die doing what I enjoy than live not doing what I love. Regarding "my backyard", no, there have been no reported cases of CWD in Virginia. I'm not interested in sifting through this crap. I've already read up on it, and I've taken note. End of story. |
RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
A final greetings and Happy Holidays to all, for now,
> i really dont have the time to read through all this. you have _no_ idea, and this is all i do, neither do i, so this is my last post. the data is here, read it, delete it and stick your head back in the sand. have a great hunt. > we take the risk of carrying a loaded gun through the woods, climbing trees ah yes, the same mentality with AIDS, the old 'only a gay thing' or 'it will not transmit by blood myth', and look at the mess we are in now. only difference is the incubation period, and it's catchen up, we have floundered much too long. mark my word here and now, once the USA, Canada and Mexico convince the OIE to change there BSE guidelines (and i believe they will because too many other countries are in the same boat, but if you look at the known BSE countries to date, the same ones that followed those same _very weak_ guidelines, once they get the game down pat, with the case study they are doing with CWD population, once they start rapid TSE testing the USA bovine population in sufficient numbers to find (not only 57,000 to date in 13 years), then the price of poker will go up, and the truth will be known. the deer and elk industry were pawns in a sea of politics, something they ignored for decades, but they knew, that's the difference. the mad cow scare pre-2001 in the USA, a year later was changed to CWD. concindence you ask, make your own mind up, you will have to do that eventually with all this, maybe not now, but sooner or later. > do you think maybe you could sum it up in a few sentences? > yes and no, the short verse first; you've been lied too. and or told only half truths. my personal opinion of research over the last 6 years and through confidential data (most of which is not so confidential anymore) I recieved through the FOIA (pre this administration, FACT, both parties to blame), from both the UK and the USA. CWD is only a small part of a much larger problem. But for now, we will speak of the topic at hand, but if you don't think some strain of BSE/TSE whether atypical or not is in the USA cattle herd, then again, find that same hole in the sand, or just go hunting or fishing, some youngster caught a 10 pound flatty a few weeks ago, i could see that sucker stuffed and baken in the oven. I am NO Doctor, I have NO PhDs, and am President of NOTHING, I only seek the truth... NOW, since I am through here for now, the _long version_, or the 'other side of the story'...later...TSS ########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############ Subject: CWD testing in Texas Date: Sun, 25 Aug 2002 19:45:14 -0500 From To: [email protected] CC: Dear Dr. Singletary, In Fiscal Year 2001, seven deer from Texas were tested by the National Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer). During these two years, an additional six elk and one white-tailed deer were tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least eight other white-tailed deer have been tested at TVMDL. One elk has been tested at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke of the Texas Parks and Wildlife Department also has records of 601 clinically ill white-tailed deer which were necropsied at Texas A&M during the late 1960's and early 1970's, and no spongiform encepalopathies were noted. Thank you for your consideration. xxxxxxxx, DVM, PhD Texas Animal Health Commission ================================= Dr. Jerry Cooke of the Texas Parks and Wildlife Department also has records of 601 clinically ill white-tailed deer which were necropsied at Texas A&M during the late 1960's and early 1970's, and no spongiform encepalopathies were noted. were they even looking for a SE and would they have even known what it was if they had seen it back in 1960-70 ?...TSS ================================================== =================== APPENDIX A: Results of CWD Sampling Sampling and testing results for CWD from June, 2002 to April 1, 2003 are presented below: Sampling and testing results for CWD from June, 2002 to April 1, 2003 TPWD TAHC Private Sector 1349 CWD Negative Deer 335 CWD Negative Deer 336 CWD Negative Deer 23 CWD Negative Exotics No Exotics No Exotics 1372 Total 335 Total 336 Total The Grand Total of all samples collected and known 4/1/03 is 2043 of which 2020 deer and 23 exotics were found CWD negative. Samples were collected from 143 of 254 counties in Texas, and seven counties had 50 or more samples collected. Five ecoregions had 160 or more samples collected (150 samples from each ecoregion was the goal). The geographic distribution of sampling is currently not considered adequate for determining whether or not CWD exists in Texas (see map pg. 15). The goal is to improve upon distribution of samples collected within ecoregions and within counties. The goal of 2003-2004 and the next three to five years, is to collect 5000 samples (500 from each ecoregion) each sample year. The increased sampling is to have a 99 per-cent confidence level in detecting CWD if only one per-cent of the population is infected. Long-term surveillance sampling for CWD is required, as little is known about the incubation and infectious periods of the disease. http://www.tpwd.state.tx.us/hunt/chr...an/appendix_a/ another coincidence, why no sampling in the obvious place, WHITE SANDS NM BORDER? compare sampling maps to NW and then look at TEXAS, they simply ignore the most obvious plase to sample? Date: Mon, 21 Apr 2003 11:53:45 -0500 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Subject: Chronic Wasting Disease (CWD) Gaining status: TEXAS Chronic Wasting Disease (CWD) Gaining status: An annual inventory of the cervids in the herd must be verified by the TAHC, USDA or an accredited veterinarian. Animals over one year must have an approved identification device, and animals less than a year are identified at change of ownership. Appropriate samples must be collected and submitted from cervids over 16 months of age that die or are hunter-harvested. Slaughtered animals are exempt, if they are examined by state or federal meat inspectors. Herd status depends on the total years of participating in the plan. http://www.tahc.state.tx.us/news/bro...ain_status.pdf Greetings, i am curious as to how a slaughtered animal can gain exempt status, and claimed to be CWD free, simply by being examined by state or federal meat inspectors. how do they claim CWD free of a dead animal already slaughtered without CWD/TSE testing of that animal? what about sub-clinical TSE? NEGATIVE CWD SAMPLING IN TEXAS ECO REGION (MAP) JUNE 1, 2002 TO PRESENT http://www.tahc.state.tx.us/animal_h...mar21-2003.gif With approximately 4 million animals, Texas has the nation's largest white-tailed deer population. In addition, about 19,000 white-tailed deer and 17,000 elk are held in private facilities.... April 16, 2003 USDA Provides Funding for Chronic Wasting Disease Monitoring in Texas AUSTIN, Texas -- Texas is likely to get a share of $4 million in new federal funding to help detect the presence of chronic wasting disease, a fatal deer and elk brain illness. The U.S. Department of Agriculture, Animal and Plant Health Inspection Service this week announced it is providing $4 million nationwide for CWD surveillance. $1 million of that is available to be split among 14 states, including Texas. Last year, the International Association of Fish and Wildlife Agencies provided about $6,700 to support Texas CWD monitoring. As of April 1 in Texas, samples from 2,043 wild white-tailed deer and mule deer had been tested, all with negative results. Even though the disease has not been detected in Texas, authorities say sampling is incomplete. They plan to use USDA funding to continue testing this fall when hunting season begins. The illness has infected deer in 12 U.S. states and two Canadian provinces. Last year, it was detected for the first time in southern New Mexico, where seven deer have tested positive. CWD is in the family of diseases called transmissible spongiform encephalopathies (TSE). The disease is detected in infected animals' neural tissue such as brains and spinal cords, as well as eyes and lymph nodes. The TSE in domestic sheep is called scrapie, and in cattle it's bovine spongiform encephalopathy (BSE). Similar diseases in humans include Creuzfeldt-Jacobs disease (CJD) and its new variant, kuru, and fatal familial insomnia. CWD should not be confused with BSE, scrapie or CJD. The World Health Organization has said there is no scientific evidence CWD can infect humans. (After more than 16 years of monitoring in the affected area in Colorado, no disease has been detected in people or cattle living there.) However, the organization also says no people or animals should consume any part of potentially CWD-infected deer or elk. Hunters are advised to wear latex gloves when field dressing game, to de-bone all meat and avoid consuming any neural tissue, such as brain or spinal cords of animals. With approximately 4 million animals, Texas has the nation's largest white-tailed deer population. In addition, about 19,000 white-tailed deer and 17,000 elk are held in private facilities. To determine if CWD is present in captive herds, Texas Parks and Wildlife Department and Texas Animal Health Commission are working with breeders to monitor their herds. http://www.tpwd.state.tx.us/news/news/030416a.htm Media Contacts: Steve Lightfoot: (512) 389-4701, [email protected] Business Hours (512) 389-8046 E-mail [email protected] Public Information: (800) 792-1112 April 18, 2003 Public Invited To Comment on Mule Deer Permit Proposal AUSTIN, Texas -- The Texas Parks and Wildlife Department will hold public hearings to take public comments on a proposed wildlife regulation change that would expand the Managed Lands Deer (MLD) permit program for white-tailed deer to include mule deer. The MLD permit program is incentive-based and habitat-driven and is designed to facilitate deer herd management goals of landowners and land managers by having a more flexible season. The public is invited to attend any of the following hearings and provide comment. All meetings are set for 7 p.m. * Morton, April 28, County Room Downtown * Turkey, April 29, Senior Citizens Room at City Hall * Dumas, April 30, County Annex Room * Alpine, May 6, Brewster County Courthouse Annex * Fort Stockton, May 7, Small Community Building * Van Horn, May 8, Van Horn Convention Center * Iraan, May 12, Community Bldg. (6th Street) Questions about the meetings or the proposed wildlife regulation change can be directed to TPWD staff at the Wildlife District office in Alpine (915) 837-2051, Kerrville (830) 896-2500, or Canyon (806) 655-3782. Individuals who cannot attend local public hearings can send their comments on the proposed regulation change to Robert Macdonald, TPWD, 4200 Smith School Road, Austin, TX, 78744; phone (512) 389-4775; email [email protected] or by voicing comments at the TPW Commission meeting May 29 in Austin at TPWD Headquarters. If approved the TPW Commission, the proposed program will take effect September 1, 2003. http://www.tpwd.state.tx.us/news/news/030418a.htm Texas Chronic Wasting Disease Management Plan Draft (February 10, 2003) Texas Chronic Wasting Disease Management Plan Links: * Executive Summary * Purpose * Problem * Introduction * Texas Chronic Wasting Disease Status * Plan for Management of the Disease in Texas * Components of the Plan * Education and Information * Ongoing Targeted Surveillance * Implementation of Geographically-Focused Surveillance * Actions Should a CWD Positive Be Detected * Appendix A. CWD Status of Current Knowledge * Appendix B. Importation of Cervids * Appendix C. Response Plan for CWD If Discovered * Appendix C2. USDA-APHIS, Regulatory Statistics * Appendix E. Media Response Plan http://www.tpwd.state.tx.us/hunt/chr...nagement_plan/ MRC-43-00 [ ] [Text only version of this site] [Print this page] Issued: Monday, 28 August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a 'sub-clinical' form of BSE in mice which was unknown until now. The scientists took a closer look at what is known as the 'species barrier' - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a 'sub-clinical' form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases. Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain. In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters. The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust. Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE. "This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures." ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL. FOR FURTHER INFORMATION CONTACT THE MRC PRESS OFFICE ON 020 7637 6011 (OFFICE HOURS) OR 07818 428297 OR 0385 774357 (OUT-OF-OFFICE-HOURS) OR PROFESSOR JOHN COLLINGE ON 020 7594 3760. PLEASE NOTE THAT OWING TO TRAVEL COMMITMENTS PROFESSOR COLLINGE WILL ONLY BE AVAILABLE UNTIL 16.30 ON FRIDAY 25 AUGUST AND CONTACTABLE AGAIN ON MONDAY 28 AUGUST VIA THE MRC PRESS OFFICE. DR ANDREW HILL (A CO-AUTHOR ON THE PAPER) FROM THE DEPARTMENT OF PATHOLOGY AT THE UNIVERSITY OF MELBOURNE WILL BE AVAILABLE ON 00 61 3 8344 3995 (DURING OFFICE HOURS) OR 00 61 3 9443 0009 (OUT-OF-OFFICE HOURS). PLEASE NOTE THAT AUSTRALIA IS TEN HOURS AHEAD OF UK TIME. NOTES FOR EDITORS Professor Collinge is a consultant neurologist and Director of the newly formed MRC Prion Unit based at The Imperial College School of Medicine at St Mary's Hospital. He is also a member of the UK Government's Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in 1999, and its work includes molecular genetic studies of human prion disease and transgenic modelling of human prion diseases. Prions are unique infectious agents that cause fatal brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease) in animals. In some circumstances prions from one species of animals can infect another and it is clear that BSE has done this to cause the disease variant CJD in the UK and France. It remains unclear how large an epidemic of variant CJD will occur over the years ahead. The strain of prion used here to infect the mice is the Sc237 strain (also known as 263K) which infects hamsters, and until now was assumed not to infect mice. This research was funded by the Medical Research Council and Wellcome Trust. The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRC's expenditure of £345 million is invested in over 50 of its Institutes and Units, where it employs its own research staff. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools. The Wellcome Trust is the world's largest medical research charity with a spend of some £600 million in the current financial year 1999/2000. The Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42 different countries to promote and foster research with the aim of improving human and animal health. As well as funding major initiatives in the public understanding of science, the Wellcome Trust is the country's leading supporter of research into the history of medicine. ©2002 Medical Research Council Data Protection policy | Contact the MRC ========================================= TSS Getting a gauge on CWD in Texas http://www.vegsource.com/talk/madcow/messages/1138.html Chronic Wasting Disease (CWD) Gaining status: TEXAS http://pub70.ezboard.com/fwolftracks...icID=189.topic Wildlife policies http://pub70.ezboard.com/fwolftracks...opicID=6.topic SEWING THE SEEDS OF MAD COW (CWD) THROUGH ANIMAL PROTEIN $ http://www.americansportsman.com/mes...nting&post=642 http://www.deerfarms.com/messages/189.shtml 5TH COW AND 1 SHEEP GO DOWN WITH CWD IN TESTING http://www.stopcwd.org/discussion/showPost.cfm?post=49 Subject: CWD SAMPLING IN TEXAS NOT CONSIDERED ADEQUATE FOR DETERMINING EXISTANCE OF CWD Date: October 28, 2003 at 1:55 pm PST Samples were collected from 143 of the states 254 counties, and seven counties had 50 or more samples collected. However, the geographic distribution of sampling was not considered adequate for determining whether or not CWD exists in Texas, Edwards said, so a minimum of 5,000 samples are scheduled to be collection statewide during the next three to five years. http://www.empiretribune.com/EMPIRET...25&PubID=14513 Subject: BSE/TSE RAPID TESTING EU/USA (why does USA not rapid Test$) Date: December 9, 2003 at 7:16 pm PST http://www.vegsource.com/talk/madcow...ges/91483.html Re: BSE/TSE RAPID TESTING EU/USA (why does USA not rapid Test$) TSS 12/09/03 (0) http://www.vegsource.com/talk/madcow...ges/91484.html Gerald Wells: Report of the Visit to USA, April-May 1989 snip... The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised... snip... It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US... snip... 3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_... snip... http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988 Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle R.F. Marsh* and G.R. Hartsough "Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092 ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England. INTRODUCTION snip... Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed. MARSH http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf just what is sporadic CJD ??? It apparently arises from a one-in-a-million spontaneous conversion of a normal cellular protein (encoded by a gene on chromosome 20) into an abnormal 3-dimensional shape, or configuration. WRONG, THIS HAS NEVER BEEN PROVEN !!! 85% OF ALL CJDs, ''SPORADIC'' DO NOT JUST HAPPEN WITHOUT ROUTE AND SOURCE, THIS IS ONLY A MYTH. please read the data below, if you are seeking the truth. there are new findings that dispute this. why does the USA ignore these findings? i thought i might share this with you. please see below; Asante/Collinge et al, 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; http://www.fda.gov/ohrms/dockets/ac/...3923s1_OPH.htm Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Terry S. Singeltary Neurology Online, 27 Jan 2003 [Full text] RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 26 March 2003 Next Post-Publication Peer Review Top Terry S. Singeltary, retired (medically) CJD WATCH Send Post-Publication Peer Review to journal: Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: [email protected] 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? http://www.neurology.org/cgi/eletters/60/2/176#535 RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States IN the reply from Dr. Maddox to Terry S. Singeltary Sr., he states; snip... If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication)... snip... http://www.neurology.org/cgi/eletters/60/2/176#535 THERE seems to be some difference of opinion; Mouse model sheds new light on human prion disease snip... Professor John Collinge said We are not saying that all or even most cases of sporadic CJD are as a result of BSE exposure, but some more recent cases may be the incidence of sporadic CJD has shown an upward trend in the UK over the last decade. While most of this apparent increase may be because doctors are now more aware of CJD and better at diagnosing it, serious consideration should be given to a proportion of this rise being BSE-related. Switzerland, which has had a substantial BSE epidemic, has noted a sharp recent increase in sporadic CJD. snip... http://www.mrc.ac.uk/txt/index/publi...oradic_cjd.htm ALSO, Dr. Maddox states; make routine mortality surveillance a useful surrogate for ongoing CJD surveillance... THIS has proven not very useful in the U.K.; THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES) snip... One reason for this was the _inaccuracy_ in coding of cases correctly certified as CJD Coding is carried out by staff who are not medically qualified and it is not surprising that coding errors occur in the processing of large numbers of certificates. In 1982, 12,000 certificates per week were processed at the office of population censuses and surveys bu 15 coders and 6 checkers (Alderson et al., 1983). The occurrence of both inter- and intra-observer coding errors has been described (Curb et al., 1983) and the _inaccuracies_ of BOTH certification and coding discovered in this study _support_ the introduction of a more accurate system of death certificates and a more detailed and specific coding system... snip... http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf 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... http://www.bseinquiry.gov.uk/files/y...1/04004001.pdf DR. Maddox states here; In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions. HOWEVER in a recent article in the UPI out of Washington; CJD screening may miss thousands of cases By Steve Mitchell UPI Medical Correspondent Published 7/21/2003 3:00 PM snip... In addition, the NPDPSC sees less than half of all the CJD cases each year, so the CDC's investigational system not only is missing many of the misdiagnosed CJD cases, it also is not conducting autopsies on most of the detected cases. snip... http://www.upi.com/view.cfm?StoryID=...1-102924-4786r ALSO in Philip Yams book 'The Pathological Protein'; ''Answering critics like Terry Singeltary, who feels that the US undercounts CJD, Schonberger _conceded_ that the current surveillance system has errors but stated that most of the errors will be confined to the older population''.... http://www.thepathologicalprotein.com/ THERE has been a _documented_ case of nv/v CJD in a 74 year old, so the errors Schonberger speaks of (above) would be of significant importance, if one believes in the nv/v CJD 'only' theory. NOW we have _documented_ cases of very young CJD victims in the USA continuing to appear in several different states. HOW does Dr. Maddox explain this, and does he still believe that a National CJD surveillance program with a CJD questionnaire to every victims family is still not warranted? WITH CWD and Scrapie running rampant in the USA, with BSE now _documented_ in North America, with the feeding of ruminant-to-ruminant animal protein still happening in the USA in 2003 even though there has been a partial voluntary ban on ruminant feeding since 8/4/97, with only 48,000 BSE/TSE tests done on USA cattle in some 14 years of surveillance, when in any given year there are 100 million cattle in the USA, with all this, i think refusing to make CJD/TSEs reportable Nationally in the USA is not ONLY a grave mistake, but in my opinion, should be looked at with great suspicion... PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr. [[email protected]] Monday, January 08,200l 3:03 PM freas ... http://www.fda.gov/ohrms/dockets/ac/.../3681s2_09.pdf PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat - Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary Sr. [[email protected]] Monday, January 08,200l 3:03 PM freas ... http://www.fda.gov/ohrms/dockets/ac/.../3681s2_09.pdf BRITISH MEDICAL JOURNAL SOMETHING TO CHEW ON BMJ http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2 BMJ http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1 Subject: The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases by Philip Yam Date: Sun, 1 Jun 2003 00:17:59 -0500 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: [email protected] May 2003 A bizarre misshapen protein The story of the mysterious, devastating prion in a new book from Springer In the space of 12 months, Stephen Churchill lost his focus, his memory, most of his speech, then even the ability to dress, feed, and clean himself. He developed an excessive fear of water and sharp objects and refused to bathe or shave. And before long, with his unsteady gait and his tendency to fall, he spent his days slumped in a wheelchair or confined to a bed. To the staff of the nursing home where Stephen lived, the relentless decline was depressingly familiar-it had the earmarks of Alzheimer's disease. But something in the picture did not fit. The patient, when he died, was only 19 years old. Doctors later discovered that Stephen had succumbed to a new kind of killer, the prion, now known to be the cause of mad cow disease in cattle, chronic wasting disease in American deer and elk, Creutzfeldt-Jakob disease and fatal insomnia in humans, among other exotic ailments. Doctors and researchers have been aware of some of these diseases for a century and more, but only in the last two decades have scientists even begun to understand just how the pathological protein spreads to new species and kills its victims. In The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases, Philip Yam describes the history of the scientific effort to track down and understand the prion, and the medical effort, still underway, to devise treatments for those who suffer from its ravages. Philip Yam has been writing and editing for Scientific American since 1989 and is currently the magazine's news editor. This is his first book. Detailed information and order possibility: Philip Yam The Pathological Protein Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases 2003. Hardcover, 285 pp. Euro 29.95 (net price); ã21.00; $27.50; sFr 51.50 ISBN 0-387-95508-9 Contact and review copies: Joan Robinson Springer-Verlag Press and Public Relations Tel.: +49- (0) 6221-487-8130, Fax: +49- (0) 6221-487-8141, E-mail: [email protected] http://www.springer.de/press/newbooks/protein.html The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases Philip Yam List Price: $27.50 Our Price: $19.25 You Save: $8.25 (30%) Availability: Usually ships within 24 hours. http://www.target.com/gp/detail.html...sin=0387955089 Greetings, got this book in the mail and just about fell out of the chair. Mr. Yam mentions my endevours and sporadic CJD. and even a bit where schonberger states; ''Answering critics like Terry Singeltary, who feels that the US undercounts CJD, Schonberger _conceded_ that the current surveillance system has errors but stated that most of the errors will be confined to the older population''.... got a phone call a year or so ago and Mr. Yam interviewed me for about 2 hours, then i passed mountains of data to him. never thought i would hear from him again, much less a mention of me seeking the truth about what killed my mother and many more. most media take the data and run, never to be heard from again. then i got a signed book in the mail with a nice note. gonna sit back and read it. here is a bit about sporadic CJD and surveillance (or the lack of) from his book; CHAPTER 14 Laying Odds Are prion diseases more prevalent than we thought? Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongifbrm encephalopathy was a zoonosisan animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is? Revisiting Sporadic CJD It's not hard to get Terry Singeltary going. "I have my conspiracy theo- ries," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.mad- cow.orgWeb site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that 223 224 CHAPTER 14 prions represent more of a threat than people realize, and that the gov- ernment has responded poorly to the dangers because it is more con- cerned about protecting the beef industry than people's health. Singeltary has similar inclinations, but unlike these men, he doesn't have the professional credentials behind him. He is an 11-grade dropout, a machinist who retired because of a neck injury sustained at work. But you might not know that from the vast stores of information in his mind and on his hard drive. Over the years, he has provided unac- knowledged help to reporters around the globe, passing on files to such big-time players as The New Tork Times, Newsweek, and USA Today. His networking with journalists, activists, and concerned citizens has helped medical authorities make contact with suspected CJD victims. He has kept scientists informed with his almost daily posting of news items and research abstracts on electronic newsgroups, including the bulletin board on www.vegsource.com and the BSE-listserv run out of the University of Karlsruhe, Germany. His combative, blunt, opinion- ated style sometimes borders on obsessive ranting that earns praise from some officials and researchers but infuriates othersespecially when he repeats his conviction that "the government has lied to us, the feed industry has lied to usall over a buck." As evidence, Singeltary cites the USDA's testing approach, which targets downer cows and examined 19,900 of them in 2002. To him, the USDA should test 1 mil- lion cattle, because the incidence of BSE may be as low as one in a mil- lion, as it was in some European countries. That the U.S. does not, he thinks, is a sign that the government is really not interested in finding mad cows because of fears of an economic disaster. Singeltary got into the field of transmissible spongiform encepha- lopathy in 1997, just after his mother died of sporadic CJD. She had an especially aggressive versionthe Heidenhain variantthat first causes the patient to go blind and then to deteriorate rapidly She died just ten weeks after her symptoms began. Singeltary, who said he had watched his grandparents die of cancer, considered her death by CJD to be much, much worse: "It's something you never forget." Her uncon- trollable muscle twitching became so bad "that it took three of us to hold her one time," Singeltary recalled. "She did everything but levitate in bed and spin her head." Doctors originally diagnosed Alzheimer's disease, but a postmortem neuropathological exam demanded by Singeltary revealed the true nature other death. Laying Odds 225 Classifying a disease as "sporadic" is another way for doctors to say they don't know the cause. Normal prion proteins just turn rogue in the brain for no apparent reason. The term "sporadic" is often particularly hard for the victims' families to accept, especially when the patient was previously in robust health. Maybe it was something in the water, they wonder, or in the air, or something they atethe same questions CJD researchers tried to answer decades ago. The names "sporadic CJD" and "variant CJD" also confuse the public and raise suspicions that U.S. authorities are hiding something when they say there have been no native variant CJD cases in the country. Singeltary suspected an environmental cause in his mother's demise a feeling reinforced a year later when a neighbor died of spo- radic CJD. For years, the neighbor had been taking nutritional supple- ments that contained cow brain extracts. Researchers from the National Institutes of Health collected samples of the supplement, Singeltary recounted, and inoculated suspensions into mice. The mice remained healthywhich only means that those supplement samples tested were prion-free. Scientists have made several attempts during the past few decades to find a connection between sporadic CJD and the environment. Often, these studies take the form of asking family members about CJD vic- timstheir diet, occupation, medical history, hobbies, pets, and so forthand comparing them with non-CJD subjects. Such case-control CJD studies have produced some intriguingand sometimes contra- dictoryresults. In 1985, Carleton Gajdusek and his NIH colleagues reported a correlation between CJD and eating a lot of roast pork, ham, hot dogs, and lamb, as well as rare meats and raw oysters.2 Yet they also recognized that the findings were preliminary and that more studies were needed. Following up, Robert Will of the U.K. National CJD Surveillance Unit and others pooled this data with those from two other case-con- trol studies on CJD (one from Japan and one from the U.K.). In particu- lar, they figured the so-called odds ratiocalculated by dividing the fre- quency of a possible factor in the patient group by the frequency of the factor in the control group. An odds ratio greater than I means that the factor may be significant. In their study, Will and his collaborators found an increase of CJD in people who have worked as health profes- sionals (odds ratio of 1.5) and people who have had contact with cows 226 CHAPTER 14 (1.7) and sheep (1.6). Unfortunately, those connections were not statisti- cally significant: The numbers of pooled patients (117) and control sub- jects (333) were so small that the researchers felt the odds ratios needed to reach 2.5 to 8 (depending on the assumptions) before they could be deemed statistically significant. The only statistically significant corre- lations they found were between CJD and a family history of either CJD (19.1) or other psychotic disease (9.9), although the latter might simply be correlated because psychotic disease may be an early symp- tom of undiagnosed CJD.3 In contrast with earlier findings, the team concluded that there was no association between sporadic CJD and the consumption of organ meats, including brains (0.6). Although these case-control studies shed a certain amount of light on potential risk factors for CJD, it's impossible to draw firm conclu- sions. Obtaining data that produces statistically meaningful results can be difficult because of the rarity of CJD and hence the shortage of sub- jects. Human memory is quite fragile, too, so patients' families may not accurately recall the lifestyle and dietary habits of their loved ones over the course of a decade or more. Consequently, researchers must cope with data that probably contain significant biases. In a review paper on CJD, Joe Gibbs of the NIH and Richard T.Johnson of Johns Hopkins University concluded that "the absence of geographic differences in incidence is more convincing evidence against major dietary factors, since large populations eschew pork and some consume no meat or meat products."A CJD study of lifelong vegetarians, they proposed, could produce some interesting data.4 The inconclusive results of case-control studies do not completely rule out the environment as a possible cause of CJD. "Dr. Prusiner's theory does fit much of the data of spontaneous generation of [mal- formed] PrP somewhere in the brain," Will remarkedthat is, the idea that sporadic CJD just happens by itself falls within the realm of the prion theory. Still, "it's very odd, if you look at all the forms of human prion diseases there are, all of them are transmissible in the laboratory and could be due to some sort of infectious agent."5 One of the great difficulties, he explained, is that "given that this is a disease of an extraordinarily long incubation period, are we really confident that we can exclude childhood exposure that is transmitted from person to person, as people move around? It's difficult to be sure about that." There might a "carrier state" that leaves people healthy yet still able to Laying Odds 227 infect others. If so, "you would never be able to identify what's causing the spread of the disease," concluded Will, who hasn't stopped looking for a possible environmental link. He has some preliminary data based on studies that trace CJD victims' lives well before the time symptoms beganup to 70 years; they suggest some degree of geographic cluster- ing, but no obvious candidates for a source of infection. A Case for Undercounting The difficulty in establishing causal links in sporadic prion diseasesif there are any in the first placeunderlines the importance of thorough surveillance. The U.K. has an active program, and when a victim of CJD is reported, one of Robert Will's colleagues visits and questions the victim's family. "No one has looked for CJD systematically in the U.S.," the NIH's Paul Brown noted. "Ever."6 The U.S., through the Centers for Disease Control and Prevention, has generally maintained a more passive system, collecting information from death certificates from the National Center for Health Statistics. Because CJD is invariably fatal, mortality data is considered to be an effective means of tabulating cases. The CDC assessed the accuracy of such data by comparing the numbers with figures garnered through an active search in 1996: Teams covering five regions of the U.S. contacted the specialists involved and reviewed medical records for CJD cases between 1991 and 1995. Comparing the actively garnered data with the death certificate infor- mation showed that "we miss about 14 percent," said CDC epidemiolo- gist Lawrence Schonberger. "That's improving. Doctors are becoming more knowledgeable," thanks to increased scientific and media atten- tion given to prion diseases.7 The active surveillance study of 1996, however, only looked at cases in which physicians attributed the deaths to CJD. Misdiagnosed patients or patients who never saw a neurologist were not tabulated thus CJD may be grossly underreported. Many neurological ailments share symptoms, especially early on. According to various studies, autopsies have found that CJD is misdiagnosed as other ills, such as dementia or Alzheimer's disease, 5 to 13 percent of the time. The CDC finds that around 50,000 Americans die from Alzheimer's each year 228 CHAPTER 14 (about 4 million have the disease, according to the Alzheimer's Association). Therefore, one could argue that thousands of CJD cases are being missed. (On the flip side, CJD could be mistakenly diagnosed as Alzheimer's disease or dementia, but the number of CJD patients is so small that they wouldn't dramatically skew the statistics for other neurological ills.) In part to address the issue of misdiagnosis, CJD families have asked the CDC to place the disease on the national list of officially notifiable illnesses, which tends to include more contagious conditions such as AIDS, tuberculosis, hepatitis, and viral forms of encephalitis. Currently, only some states impose this requirement. CDC officials have discounted the utility of such an approach, arguing that it would duplicate the mortality data, which is more accurate than early diag- noses of CJD, anyway. Moreover, mandatory reporting of CJD cases does not necessarily guarantee the end to missed cases.8 One clue suggests that the passive system is undercounting CJD in the U.S.: racial difference. The number of black CJD victims is about 38 percent that of white victims. Rather than sporadic CJD being a one- in-a-million lottery, it's more like one-in-2.5-million for African- Americans. Access to medical care might be one reason. Schonberger recounted that the CDC had asked other countries with substantial black populations to submit CJD figures for comparison but found that the surveillance in those countries was inadequate. "We haven't been able to find any comparable literature on this issue, so it's still up in the air," Schonberger said. On the other hand, Alzheimer's disease is more common among black people than whites, with an estimated higher prevalence ranging from 14 percent to almost 100 percent, according to a February 2002 report by the Alzheimer's Association. Are some black CJD cases being misdiagnosed as Alzheimer's? Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population. As Schonberger pointed out, no doctor would misdiagnose a 30-year-old CJD patient as having Alzheimer's. The average age of the first 100 variant CJD victims was 29; should the epidemiology of vCJD changeif older people start coming down with itthen there would be problems. "The adequacy of our overall CJD surveillance would be Laying Odds 229 greatly reduced should the proportion of older individuals affected by variant CJD substantially increase," Schonberger explained.9 To date, only brain autopsies can confirm CJD. To encourage the necessary neuropathological studies, in 1997 the CDC helped establish the National Prion Disease Pathology Surveillance Center at Case Western Reserve University, under the directorship of Pierluigi Gambetti. But the number of brains examined has fallen far short of the number of CJD cases in the U.S.: Gambetti's lab, which receives brains based on referrals from local physicians and families, looked at only 99 sporadic CJD cases in 2000 and 138 in 2001, when about 300 each year are expected. "I'm very unhappy with the numbers," Gambetti lamented. "European countries see 100 or 90 percent of all the cases suspected. We see 30 to 40 percent."10 Most families don't think about having an autopsy done (which can cost upward of $1,500 if the hospitals don't pick up the tab), and mem- bers of the support group CJD Voice have said they were too distraught to think of shipping a loved one's brain by Federal Express to Gambetti's lab. (For accurate analyses of brain tissue, the autopsy must be performed within 72 hours of death, assuming the body has been kept refrigerated.) Moreover, physicians often do not suggest an autopsy, perhaps because of liability fears should the postmortem reveal that the original diagnosis was wrong. Gambetti has been work- ing on establishing a network that would enable postmortems to be done near where the deceased person lived and without cost to the family. He is also working on advertising the existence of his surveil- lance center, via meetings and letters to neurologists, pathologists, and other specialists. Gambetti is also attempting to combat what he termed "hysteria" over the potential for infection that has pathologists irrationally shunning CJD cases while they willingly conduct arguably riskier AIDS autopsies. "In order to make people aware, you have to keep informing them over and over and over," he said. Money is the main reason why the U.S. lags behind Europe in terms of surveillance. To adequately survey the 290 U.S. million residents, "you need a lot of money," Robert Will explained. "There was a CJD meeting of families in America in which poor old Larry {Schonberger] got attacked fairly vigorously because there wasn't proper surveillance. You could only do proper surveillance if you have adequate resources. 230 CHAPTER 14 That's the bottom line. We're very fortunate in the U.K.; we have very generous resources for CJD surveillance." Moreover, the U.K. makes feline spongifbrm encephalopathy an offi- cially notifiable disease. Domestic cats proved to be good sentinel ani- mals because they dine on the meat not fit for human consumption the parts more likely to harbor prion infectivity. In the U.S., FSE isn't federally notifiable. And while the USDA says it has sent educational material to private veterinarians and works with vet schools,21 it's not clear just how many vets can spot FSE, which has never been reported in the U.S. Certainly, not many cat postmortems are done. The only active portion of the U.S. CJD surveillance system are the follow-up investigations conducted for victims of CJD under 55 years of age. It began in 1996, when young people in the U.K. started succumb- ing to variant CJD. Victims under 30 years of age especially arouse interest, because such cases could indicate an infection from the envi- ronment. Except for the variant CJD case in Florida, the CDC has clas- sified all of these more youthful cases of CJD as having either sporadic or familial origins. One such age cluster involved the three venison eaters that the CDC tried unsuccessfully to link to the deer-and-elk borne chronic wasting disease. A second grouping occurred in 2002 in a pair of Michigan men. The twoone 26 years old, the other 28 did not know each other but lived in neighboring counties in Michigan and went to the same hospi- tal for diagnosis.12 The CDC's investigation turned up nothing that suggested a new form of CJD had emerged. But the increased frequency of young CJD cases is disturbing. In the 18-year period between 1979 and 1996, the U.S. had 12 cases in patients under 30, and only one of them had the sporadic form of CJD. (The other cases resulted from heredity or from transmission via contami- nated growth hormone or dura mater grafts.13) Between 1997 and 2001, five people under 30 died of sporadic CJD: the three venison eaters and the two Michigan patients. That represents a substantial blip of five young cases in five years, as opposed to only one case in 18 years. Physicians at the University of Michigan Health System who examined the two Michigan men concluded: As a result of our findings, we feel that sporadic CJD may be more common than previously thought, that it may occur in younger indi- Laying Odds 231 viduals than currently perceived, and that some cases may go undiag- nosed due to insufficient testing. . . . We recommend that physicians everywhere begin to consider CJD in rapidly progressive neurological decline of unknown causes in people under 30 years of age, and that brain biopsy and autopsy with genetic and prion analysis be performed in all such cases.14 Pathologically, the recent bout of young casualties in the U.S. appears to be no different from CJD already seen in America. Yet theoretically it may have come from a new source of infection, based on an unex- pected result announced in late November 2002. John Collinge of the British Medical Research Council's Prion Unit found that not all trans- genic mice infected with BSE prions developed the neuropathological and molecular characteristics of variant CJD; some of the mice instead generated the molecular features of sporadic CJD. Therefore, some CJD cases classified as sporadic may have actually been caused by BSE prions, Collinge hypothesized.15 So far, the epidemiology of CJD in the U.K. does not bear out that suppositionthere has been no substantial uptick in sporadic CJD as would be expected if BSE could paint more than one pathological picture. But the preliminary study, taken at face value, could be seen as evidence that something infectious is happening in the cases of young, sporadic CJD victims in the U.S. Another mouse study, reported in March 2002, fueled concern that prion infections may be more common than previously thought.16 Stanley Prusiner's lab found that mice infected with mouse prions accu- mulated PrPSc in their skeletal muscles, mostly in those in the hind limbs. In some mice, each gram of muscle contained some 10 million infectious doseson par with that in the brain in other experiments involving intracerebral inoculation. To some CJD researchers, this find- ing suggested that muscle meat from cows might not be safe, after all, and that the measures taken in Europe to protect the food supply banning high-risk cow partsmay not be enough. Although this study may seem alarming, its implications are not as sweeping as they may appear. Only a minority of results in mouse stud- ies end up having a direct analog in humans. The skeletal muscle discov- ery warrants further examination, but it would be premature to alter food policies. Prions are different for each species, and accumulation of prions varies from species to species and from disease to disease. Furthermore, BSE cattle muscle has failed to sicken mice in bioassay 232 CHAPTER 14 work, suggesting that little or no infectious prions lurk there. What such findings truly reveal is that prion diseases are complicated and still mysterious, and trying to quantify the risks for human health is fraught with uncertainties...snip...284 pages...thanks Philip...TSS The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases, Philip Yam Philip Yam News Editor Scientific American www.sciam.com http://www.thepathologicalprotein.com/ CJD screening may miss thousands of cases By Steve Mitchell UPI Medical Correspondent Published 7/21/2003 3:00 PM View printer-friendly version <http://www.upi.com/print.cfm?StoryID...2924-4786r> WASHINGTON, July 21 (UPI) -- The federal government's monitoring system for cases of Creutzfeldt-Jakob disease, a fatal human brain illness, could be missing tens of thousands of victims, scientists and consumer advocates have told United Press International. Creutzfeldt-Jakob disease or CJD can be caused by eating beef contaminated with mad cow disease, but the critics assert without a better tracking system it might be impossible to determine whether any CJD cases are due to mad cow or obtain an accurate picture of the prevalence of the disorder in the United States. Beginning in the late 1990s, more than 100 people contracted CJD in the United Kingdom and several European countries after eating beef infected with bovine spongiform encephalopathy -- the clinical name for mad cow disease. No case of mad cow has ever been detected in U.S. cattle and the Centers for Disease Control and Prevention's monitoring system has never detected a case of CJD due to eating contaminated American beef. Nevertheless, critics say, the CDC's system misses many cases of the disease, which currently is untreatable and is always fatal. The first symptoms of CJD typically include memory loss and difficulty keeping balance and walking. As the disease destroys the brain, patients rapidly progress in a matter of months to difficulty with movement, an inability to talk and swallow and, finally, death. Spontaneously-occurring or sporadic CJD is a rare disorder. Only about 300 cases appear nationwide each year, but several studies have suggested the disorder might be more common than thought and as many as tens of thousands of cases might be going unrecognized. Clusters of CJD have been reported in various areas of the United States -- Pennsylvania in 1993, Florida in 1994, Oregon in 1996, New York in 1999-2000 and Texas in 1996. In addition, several people in New Jersey developed CJD in recent years, including a 56 year old woman who died on May 31, 2003. Although in some instances, a mad cow link was suspected, all of the cases ultimately were classified as sporadic. People who develop CJD from eating mad-cow-contaminated beef have been thought to develop a specific form of the disorder called variant CJD. But new research, released last December, indicates the mad cow pathogen can cause both sporadic CJD and the variant form. "Now people are beginning to realize that because something looks like sporadic CJD they can't necessarily conclude that it's not linked to (mad cow disease)," said Laura Manuelidis, section chief of surgery in the neuropathology department at Yale University, who conducted a 1989 study that found 13 percent of Alzheimer's patients actually had CJD. Several studies, including Manuelidis', have found that autopsies reveal 3 percent to 13 percent of patients diagnosed with Alzheimer's or dementia actually suffered from CJD. Those numbers might sound low, but there are 4 million Alzheimer's cases and hundreds of thousands of dementia cases in the United States. A small percentage of those cases could add up to 120,000 or more CJD victims going undetected and not included in official statistics. Experiences in England and Switzerland -- two countries that discovered mad cow disease in their cattle -- have heightened concerns about the possibility some cases of sporadic CJD are due to consuming mad-cow-tainted beef. Both countries have reported increases in sporadic CJD since mad cow was first detected in British herds in 1986. Switzerland discovered last year its CJD rate was twice that of any other country in the world. Switzerland had been seeing about eight to 11 cases per year from 1997 to 2000. Then the incidence more than doubled, to 19 cases in 2001 and 18 cases in 2002. The CDC says the annual rate of CJD in the United States is one case per million people, but the above studies suggest the true prevalence of CJD is not known, Manuelidis told UPI. Diagnosing CJD or Alzheimer's is difficult because no test exists that can identify either disease in a living patient with certainty. So physicians must rely on the patient's symptoms to determine which illness might be present. Sometimes, however, the symptoms of one disease can appear similar to the other disorder. The only way to determine the disease conclusively is to perform an autopsy on the brain after death. Unfortunately, although autopsies once were performed on approximately half of all corpses, the frequency has dropped to 15 percent or less in the United States. The National Center for Health Statistics -- a branch of the CDC -- stopped collecting autopsy data in 1995. "If we don't do autopsies and we don't look at people's brains ... we have no idea about what is the general prevalence of these kinds of infections and (whether) it is changing," Manuelidis said. At the same time autopsies have been declining, the number of deaths attributed to Alzheimer's has increased more than 50-fold since 1979, going from 857 deaths then to nearly 50,000 in 2000. Though it is unlikely the dramatic increase in Alzheimer's is due entirely to misdiagnosed CJD cases, it "could explain some of the increase we've seen," Manuelidis said. "Neurodegenerative disease and Alzheimer's disease have become a wastebasket" for mental illness in the elderly that is difficult to diagnose conclusively, she said. "In other words, what people call Alzheimer's now is more broad than what people used to call it, and that has the possibility of encompassing more diseases -- including CJD." The autopsy studies that found undiagnosed CJD cases raise the question of whether the United States "already has an undetected epidemic here," Jeff Nelson, director of vegsource.com, a vegetarian advocacy Web site, told UPI. "What's the source of that?" Nelson asked. "Could it be the same source of encephalitis we saw in minks?" Nelson referred to an outbreak of a mad-cow-type disorder in minks in Wisconsin in the 1980s. The origin was traced ba |
RE: Field Dressing Deer/elk CWD/TSEs aka MAD COW DISEASE
sorry, forgot to put the URL for the CWD sampling in NM up.
cannot hardly compare without that; http://www.gmfsh.state.nm.us/PageMil...ing/cwdmap.pdf TSS |
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