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From: TSS ()
Section VII Prevention and control of waterborne zoonoses snip... 24.5 ARE TSES POTENTIAL WATERBORNE PATHOGENS? 24.5.1 Characteristics of TSEs TSEs are a group of infectious diseases characterized by slow and progressive degenerative changes in the central nervous system. TSEs affecting humans include Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome, kuru, and fatal familial insomnia; those affecting animals include scrapie in sheep and goats, feline spongiform encephalopathy, transmissible mink encephalopathy, chronic wasting disease (CWD) in elk and deer, and Control in animal reservoirs 395 bovine spongiform encephalopathy (BSE) (Dormont 2002). It is hypothesized that these unique infectious agents are aberrant forms of a normal host protein. Prusiner (1982) first proposed the existence of this self-propagating protein, which he termed a "prion," as the causative agent of TSEs. Although the theory that prions are responsible for TSEs is now accepted by the majority of the scientific community, some scientists are still not convinced and suggest that an infectious agent such as viruses or virinos may be responsible (Manuelidis 2003). The normal prion protein is found in neural as well as many other body tissues and is thought to be a membrane-bound glycoprotein involved in copper transport into host cells and protection of these cells against oxidative stress (Clarke et al. 2001; Collinge 2001). The infectious form of the prion is thought to occur when the -helical structure of the native protein is somehow converted to the -sheet isoform. The altered prion protein differs from the native form in three important respects. Firstly, it is highly resistant to proteases and other physical and chemical agents, such as heat, ultraviolet (UV) light, and oxidants (Dormont 2002). Secondly, it is postulated that it catalyses the transformation of native prion protein to the infectious form using the infectious form of prion as a template, perhaps with the addition of an accessory factor termed "protein X." Finally, the highly resistant form of the protein accumulates over time in the host tissues and in some way leads to the characteristic neural pathology associated with TSEs. It is possible that the accumulation of the aberrant form of the prion protein leads to a failure of the normal prion protein role in the protection of cells against oxidative stress and to calcium cytotoxicity (Hur et al. 2002), but this is not certain. BSE was first diagnosed in 1986 at the Central Veterinary Laboratory in Weybridge in the United Kingdom. It is thought that BSE may have originated spontaneously in cattle or as a rare type of scrapie present in sheep. Subsequently, cattle became infected as a result of feeding bovine- or ovinederived BSE-contaminated meat and bone meal (MBM) to cattle. Once cattle became infected, they in turn contributed further to the contamination of MBM with the BSE agent. The highly resistant nature of the prion protein is thought to have allowed it to survive an altered rendering process used at the time in the production of MBM. The protease and acid resistance of the prion may also allow it to pass through the stomach and into the intestinal tract. Once in the intestine, it is thought to be taken up by gut-associated lymphoid tissues and subsequently passed to lymphoid tissues such as the spleen and tonsils, where it enters the lymphoid-associated peripheral nervous system. It then makes its way to the central nervous system over the course of many months and years, depending on the TSE strain and the host species and genotype. The resistant nature of the protein may also be responsible for the ability of TSEs such as scrapie from 396 Waterborne Zoonoses sheep to persist in soils for more than 3 years (Brown and Gajdusek 1991). There is strong epidemiological evidence supporting lateral transfer of scrapie and CWD in sheep and deer, respectively. 24.5.2 Risks of acquiring BSE from drinking-water sources In 1997, evidence was presented that BSE was a zoonotic agent (Bruce et al. 1997). The BSE-associated disease in humans was termed "variant Creutzfeldt-Jakob disease" (vCJD) because of its similarity to the well recognized human TSE, CJD. It is assumed that humans with vCJD acquired the infection through the consumption of bovine nervous tissues (bovine offal, beefon- the-bone) containing high levels of the infectious BSE agent. Shortly after this finding, it was suggested that nearly a million cattle in the United Kingdom would have to be culled and disposed of to control the BSE and vCJD epidemics in cattle and humans, respectively. As a result of this impending action, concern was expressed that the BSE agent present in infected material from the cattle to be slaughtered could enter surface water and groundwater (from slaughterhouses, rendering plants, and landfills) and pose a public health risk. The following is a list of some of the key components of this risk assessment (Gale 1998, 2001; Gale et al. 1998): (1) Concentration of BSE agent in bovine neural tissue. It was assumed that the level of infectious material in the nervous tissues of cattle would be equivalent to that which occurred at the peak of the BSE outbreak as a worst-case scenario. (2) Infectious dose models for BSE. It can be postulated that a certain threshold dose level of the BSE agent is required to cause vCJD in humans and that this dose is much less likely to be achieved as a result of a single consumption event of water rather than of bovine nervous tissue. This is because the agent is likely to be highly dispersed in water and concentrated in nervous tissues in beef. However, it is also possible that the threshold could be reached by a susceptible individual after years or months of low-level long-term exposure. However, even if this assumption is accepted, Gale et al. (1998) calculated that a threshold dose from the agent in water would be reached only after approximately 45 million years. Alternatively, it is possible that a specific threshold does not exist for the population and that a very low dose of the BSE agent could result in infection in a correspondingly small proportion of the population — i.e., those most susceptible would have a lower threshold dose. If this assumption is accepted and it is considered that the prion ID50 is divisible and cumulative, according to Gale et al. Control in animal reservoirs 397 (1998), one arrives at similar levels of risk for drinking water and eating beef-on-the-bone (10-8 versus 10-9 per person per year). (3) The interspecies barrier. Mice can be infected with BSE by feeding them infected bovine nervous tissue; however, the ID50 by the oral route for mice is approximately 1000 times greater on an equivalent-weight basis than it is for cattle. A large part of the interspecies difference in ID50 may be related to the ability of the prion material to pass through the gastrointestinal tract and then enter gut-associated lymphoid and nervous tissues. While pigs can be infected with BSE-infected nervous tissue by the combined intracranial, intravenous, and intraperitoneal routes, they appear to be completely refractory to infection with this TSE by the oral route (Wells et al. 2003). Martinsen et al. (2002) recently reported that the BSE ID50 in mice can be decreased by lowering concentrations of hydrochloric acid in the stomach of mice using ranitidine. It is therefore conceivable that some humans may be more susceptible to infection than others and that this susceptibility could change with the physiology of the gastrointestinal tract. (4) Susceptibility to TSEs based on genotype. It is known that there are differences in the genotype of prion proteins within sheep, mice, and human populations that make them resistant or susceptible to specific TSEs. Humans that are homozygous for methionine at codon 129 of the prion protein gene are more susceptible to CJD, and all cases of vCJD described thus far have this genotype (Will et al. 2000). (5) Dilution in water. As mentioned above, humans with vCJD are thought to have acquired the infection through the consumption of bovine nervous tissues containing high concentrations of the BSE agent. The human ID50 has been calculated to be equivalent to 1013 BSE prion proteins (Gale et al. 1998). As mentioned above, it is thought that in contrast to beef products, the BSE agent is likely to be highly dispersed in water. Therefore, the daily intake of infectious prions by consumers of water is likely to be very low by nature of dilution when compared with BSE-contaminated nervous tissue in beef-on-the-bone. (6) Transport and solubility in water. The prion protein is a typical membrane protein and has both hydrophilic and hydrophobic domains. This property limits its solubility in water and favours the formation of insoluble aggregates, promotes adhesion to hydrophobic particles, and would be predicted to limit its mobility in surface water or groundwater. Further, Brown and Gajdusek (1991) showed that a closely related TSE agent, scrapie, has very limited mobility in soils. Thus, risks of infectious prions entering groundwater or surface water from cattle carcasses buried for disposal are likely very low. 398 Waterborne Zoonoses In support of these risk assessments, Cousens et al. (2003) reported that vCJD cases in the United Kingdom have not been geographically clustered, as would be expected if the source of infection was from an environmental source such as soil or water. While much of the evidence suggests that the risks of infection with the BSE agent from drinking-water are negligible (Gale 2001), further research on our levels of exposure to TSEs in the environment and parameters affecting the infective dose in humans is required. A reasonable estimate of the ID50 for humans of BSE-infected material is required before a meaningful quantitative risk assessment can be conducted. However, essential elements necessary for this risk assessment model, such as the nature of the interspecies barrier for BSE infection in humans, are not known. In addition, a lack of understanding of the genotypic and physiological differences in susceptibility to this TSE within the human population has further complicated this task. 24.5.3 BSE eradication plan The epidemic in the United Kingdom has resulted in 180 121 cases of BSE in cattle (http://www.defra.gov.uk/animalh/bse/index.html). The BSE epidemic appears to have reached its peak in 1992, and the number of cases has declined since then. At the time of this writing, 137 deaths have been associated with vCJD in the United Kingdom, and the peak of the epidemic appears to have been in 2000 (http://www.doh.gov.uk/cjd/cjd_stat.htm). In the United Kingdom, a number of steps have been taken to control the BSE outbreak in cattle and the vCJD epidemic in humans. The MBM ban for ruminant feed and culling of animals from infected herds were likely to have been the most important steps in controlling these epidemics. Many other countries have adopted similar measures to combat and/or prevent the entry of BSE. The MBM ban has been expanded to include all food-producing animals in certain countries. Measures to protect the human population from vCJD have included removal of specified risk materials (offal, heads, and spines) of bovine origin from the food-chain, restriction of slaughter of animals for human consumption to those under 30 months of age, and banning the importation of cattle or beef from countries with BSE. Both BSE and vCJD cases have declined due to these measures. 24.5.4 Scrapie eradication plan Scrapie is a TSE endemic in sheep populations throughout most of the world (Australia and New Zealand are notable exceptions to this, with their sheep scrapie-free). It is often stated that scrapie has existed in sheep in the United Control in animal reservoirs 399 Kingdom for more than two centuries without an apparent public health impact (Baylis et al. 2002). However, as stated above, it has been hypothesized that BSE may be a rare strain of scrapie that has existed for some time at low levels in the sheep population in the United Kingdom prior to causing BSE in the cattle population. It is also certain that some sheep consumed MBM contaminated with the BSE agent before the MBM feed ban took place. It therefore seems likely that some sheep may have become infected with BSE through MBM and may pose a public health risk (Butler 1998). Further, there is concern that the public health risk from BSE in sheep could be potentially greater than is posed by BSE in cattle. Firstly, the scrapie agent is distributed more widely in body tissues of sheep than is BSE in the tissues of cattle. Therefore, BSE in sheep could present a greater risk for acquiring a TSE for human consumers of mutton. Secondly, the epidemiology of scrapie in sheep is quite different from that of BSE in cattle. Studies on BSE in cattle suggest that there is little or no spread of the agent horizontally to herd mates and vertically to offspring; in scrapie in sheep and CWD in cervids, however, there is both vertical and horizontal spread of the agent within flocks and herds, and these agents appear to persist in pastures and act as a source of infection for other susceptible animals (Baylis et al. 2002; Detwiler and Baylis 2003; Salman 2003). This raises the possibility that BSE not only could be transmitted by consumption of mutton but also could become more widely dispersed in the environment. In response to this potential public health threat, a National Scrapie Plan has been implemented in the United Kingdom with the aim of eradicating scrapie (and BSE, if it exists) from the national sheep flock. The plan will use selective breeding for the scrapie/BSE-resistant prion genotype of sheep ARR/ARR (Houston et al. 2003). 24.6 SUMMARY AND CONCLUSIONS The risk of zoonotic waterborne diseases can be resolved to some extent by minimizing the entry of animal wastes to source waters, by controlling animal movements, proper storage and disposal of farm animal wastes, using procedures that will minimize the survival of zoonotic pathogens, and limiting transport of these wastes in surface water runoff. Control and, in some cases, eradication of zoonotic agents in animal reservoirs may be an efficient and cost-effective means of controlling drinkingwater source and recreational water contamination with zoonotic pathogens. Most zoonotic pathogens are not uniformly distributed through animal populations but rather are present in specific animal species reservoirs. Further specific age classes or animals such as young calves may shed these organisms in much higher numbers than adults. 400 Waterborne Zoonoses Control measures for domestic animals centre around the issue of increased biosecurity. This can be brought about by measures such as limiting access of other animal species through physical barriers, limiting cross-contamination among animals by using good sanitation practices and raising susceptible animals away from animals that may be carriers of zoonotic agents, keeping "closed herds," "all-in all-out" procedures, quarantine of new animals and surveillance-based test and slaughter procedures, providing food and water free of zoonotic agents, competitive exclusion, bacteriophage therapy, other feed additives, and active and passive immunization. These strategies can be applied with success at the farm level but are more effective on a national level with economic incentives for compliance. Control of zoonotic diseases in domestic animal populations, while difficult, is more easily addressed than control of these diseases in wild animal populations. Wherever it is possible, there should be physical separation of wildlife from domestic animals; in addition, population control of wild species should be considered only in selected areas where there is a high rate of infection with a zoonotic agent in a reservoir population and there is a clear risk of contamination of surface water with pathogens and/or transfer of these pathogens to domestic livestock. Wildlife vaccination schemes to limit infection with specific zoonotic agents or for immunocontraception represent possible strategies for limiting certain zoonotic waterborne diseases. The sudden emergence of zoonotic pathogens responsible for the outbreak of BSE in cattle and vCJD in humans in the United Kingdom has been a cause of concern for most public health authorities. A ban on feeding MBM to food-producing animals and a rigorous test and slaughter policy have brought both the BSE epidemic in cattle and the vCJD epidemic in humans under control in the United Kingdom. The small size and extreme resistance of these TSE agents to proteases, heat, UV light, and chemical treatments suggest that current water treatment technologies would have little effect in controlling these zoonotic agents, and TSE agents have been shown to persist in soils for years. However, the insoluble nature of prions is likely to limit their movement into water systems. Further, it is felt that a relatively small quantity of prions would be released following slaughter or rendering of cattle and that these prions would be diluted in the environment and would be highly unlikely to constitute an infective dose for a human over a lifetime. 24.7 RECOMMENDATIONS Many zoonotic agents associated with waterborne disease are also associated with foodborne disease in humans. However, they frequently do not cause overt clinical disease in domestic animal populations. National and international agencies with health mandates that address control of waterborne and foodborne diseases should coordinate their activities and share resources to accomplish specific zoonotic Control in animal reservoirs 401 pathogen reduction targets. Programme objectives can be accomplished only by working with agricultural and conservation stakeholder groups and veterinary authorities that have experience in disease control in animal populations. Agencies with health mandates that encompass control of waterborne diseases should also coordinate their activities and share resources to control contamination of water with animal wastes by working with agricultural and environmental stakeholder groups and agencies. Control of waterborne zoonotic pathogens depends on the use of tools such as HACCP in water safety plans and risk assessments. Cost/benefit analyses must be performed before strategies are implemented, and the solutions proposed to limit waterborne disease must be communicated and found to be acceptable by stakeholders. The most important component of any water treatment strategy is likely to be source protection. This can best be accomplished by taking steps to control zoonotic pathogens in animal populations (as outlined above), proper storage and disposal of animal wastes, and limiting physical access of animals to source waters. Efforts should be focused on improving water treatment in rural areas and in small communities and improving the safety of water used in the irrigation of crops, in particular raw edible field crops. Members of communities that are most at risk of waterborne diseases need to be identified and protected from waterborne disease. Those most at risk include the very young, the aged, the immunocompromised, individuals who are genetically most susceptible, and those with increased occupational or recreational exposure to waterborne pathogens. 24.8 REFERENCES snip... http://www.who.int/water_sanitation_health/diseases/zoonosessect7.pdf National Renderers Association Public Response to USDA-APHIS ANPR “Risk Reduction Strategies for Potential BSE Pathways Involving Downer Cattle and Dead Sock of Cattle and Other Species” Docket No. 01-68-1, Federal Register, Vol.68, No.13: 2703 – 2711, 01/21/2003 APPENDICES I - III APPENDIX I snip... In spite of the concerted efforts by all participants in animal production, there are, and always will be, a significant number of on-farm mortalities. While the vast majority of livestock enter the food chain, a small portion die due to various non-infectious (accidents, injuries, etc.) causes and infectious, including major zoonotic, conditions or is condemned at time of slaughter. Add to these the already huge amounts of animal material derived from normal processing. Animals that succumb to either disease or accident prior to slaughter, making them unfit for human consumption, and living animals in a condition that doesn’t meet certain minimum standards are diverted away from the food chain. The data in Tables 3 – 12, gathered by the Sparks Companies (ref.36) on behalf of NRA, are revealing. In the year 2000 for example, the combined poultry and livestock mortalities in the U.S. amounted to 105,345,700 heads, with a total weight of more than 3.3 billion pounds. There is also a significant volume of animal by- products coming from various sectors of food processing, retail and catering business, as well as from free-roaming wildlife. The effective and safe utilization of these by-products is important to the overall food animal production, processing and consumption cycle. snip... Table 12: Estimated Number of Dead Stock Rendered in the United States in 2000 (Source: ref.36) ------------------------------------------------------------------------------------------------------------ Species Dead Stock (lbs) % of Deaths Meat and Bone Meal (lbs)1 Cattle 869,480,910 45.0 241,715,690 Pre-weaned Hogs 35,261,690 53.1 9,802,750 Weaned Hogs 622,369,300 68.0 173,018,700 Sheep, Lamb & Goats 32,052,800 45.0 8,910,680 ------------------------------------------------------------------------------------------------ Total 1,559,164,800 lbs 52.4% 433,447,790 lbs ------------------------------------------------------------------------------------------------------------ 1 assumes MBM yield of 27% http://www.rendermagazine.com/news/USDA-ANPRDownersApendices.doc ONE OTHER THING i must comment on. WITH all the open pit pyres and even down to say bones (spinal cord) surgery and grinding and the plume that is caused by that. It would be nice to see more studies there. a new study, a small abstract; EM 47 The study of a lab-scale contaminant plume Helen Rees1, Steven Banwart1, Sascha Oswald2, Roger Pickup3 & David Lerner1 1Groundwater Protection & Restoration Group, Dept of Civil & Structural Engineering, University of Sheffield, Mappin Street, S1 3JD; 2Centre for Environmental Research, Permoserstraße 15, D-04318 Leipzig, Germany; 3Centre for Ecology and Hydrology, Lancaster Environment Centre, Library Avenue, Bailrigg, Lancaster LA1 4AP see full text of ; Microbiology s o c i e t y f o r g e n e r a l 156th Meeting 4–7 April 2005 Heriot-Watt University, Edinburgh http://www.socgenmicrobiol.org.uk/meetings/pdfabstracts/hw2005abs.pdf SEEMS THEY HAVE BEEN WRONG about a lot of things ; The implications remain however disquieting, since it is clear that cases of BSE were not detected initially and have entered the human and animal food chain. Milk and milk products are considered safe. Tallow and gelatin are considered safe if prepared by a manufacturing process which has been shown experimentally to inactivate the transmissible agent. No infectivity has yet been detected in skeletal muscle tissue. Reassurance can be provided by removal of visible nervous and lymphatic tissue from meat. . Human and veterinary vaccines prepared from bovine materials may carry the risk of transmission of animal TSE agents. The pharmaceutical industry should ideally avoid the use of bovine materials and materials from other animal species in which TSEs naturally occur. If absolutely necessary, bovine materials should be obtained from countries which have a surveillance system for BSE in place and which report either zero or only sporadic cases of BSE. These precautions apply to the manufacture of cosmetics as well. . vCJD has never been known to have developed in a recipient of vCJD patient’s blood, but studies are limited in scope and should continue. Blood donation should not be taken from donors treated with human pituitary gland extracts, donors with family history of CJD, GSS or FFI, or donors receiving a human dura mater graft. http://www.who.dk/document/eehc/eurobulletinmay2001.pdf THEY would not listen to there own concerns and kept there concerns SECRET from the public...TSS -------- Original Message -------- Subject: Re: MMR vaccine http://www.bseinquiry.gov.uk/files/yb/1989/02/14010001.pdf http://www.bseinquiry.gov.uk/report/volume7/chapted2.htm http://www.bseinquiry.gov.uk/files/yb/1989/02/14011001.pdf although 176 products do _not_ conform to the CSM/VPC http://www.bseinquiry.gov.uk/files/yb/1989/09/06011001.pdf 5.23 This alerted Sir Donald Acheson to the fact that concerns about the http://www.bseinquiry.gov.uk/report/volume7/chapted2.htm WHO/CDS/CSR/APH/2000.2 3.5 Animal vaccine-related Transmissible Spongiform Encephalopathy risks: Scrapie outbreak in Italy Maurizio Pocchiari: Historically, Italy has had a low incidence of scrapie; however, in 1997 snip... 7.6 Could vaccines prepared from animal brain tissue pose a risk of Over 40,000 deaths due to rabies are reported annually worldwide and WHO/CDS/CSR/APH/2000.2 34 WHO Consultation on Public Health and Animal TSEs publication strongly suggests that scrapie was transmitted to sheep and snip... Recommendation 25 Human vaccines prepared from whole ruminant brains may carry the risk of "The (Expert) Committee reiterated, as stated in its 1983 report, its Recommendation 26 The use of veterinary vaccines prepared from whole ruminant brains, for snip... http://www.who.int/emc-documents/tse/docs/whocdscsraph20002.pdf http://216.239.37.100/search?q=cache:ha1lZiMaWG4C:www.who.int/emc-documents/tse/docs/whocdscsraph20002.pdf+Acquisition+of+spongiform+encephalopathies+in+India+through+sheep-brain+rabies+vaccination.&hl=en&ie=UTF-8 55 III.3.1 VACCINES III.3.2.OTHER MEDICINAL PRODUCTS DERIVED FROM TSE-SUSCEPTIBLE SPECIES http://europa.eu.int/comm/food/fs/sc/ssc/out236_en.pdf Indian J Pediatr 1991 Sep-Oct;58(5):563-5 Arya SC. Centre for Logistical Research and Innovation, Greater Kailash, New Delhi. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1813404&dopt=Abstract BMJ 1996 Nov 30;313(7069):1405 Comment on: * BMJ. 1996 Aug 24;313(7055):441. Arya SC. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8956737&dopt=Abstract BMJ 1996;313:1405 (30 November) In many countries in Asia and Africa limited supplies of imported rabies Before accepting blood donations from immigrants it would be desirable Clinical microbiologist Centre for Logistical Research and Innovation, Subhash C Arya http://bmj.com/cgi/content/full/313/7069/1405/a : Neuroepidemiology 1991;10(1):27-32 Creutzfeldt-Jakob disease in India (1971-1990). Satishchandra P, Shankar SK. Department of Neurology, National Institute of Mental Health and Thirty cases including 20 definite and 10 probable cases of http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2062414&dopt=Abstract i recieved the 1947 report of the Louping-ill vaccine Louping-ill vaccine (scrapie transmission by vaccine) THE VETERINARY RECORD NATIONAL VETERINARY MEDICAL ASSOCIATION OF GREAT BRITAIN AND IRELAND ANNUAL CONGRESS, 1946 snip... The enquiry made the position clear. Scrapie was developing in (1) the infective agent of scrapie was present in the brain, spinal Two Frenchmen, Cuille & Chelle (1939) as the result of experiments As a result of this experience a large-scale transmision experiment The prolonged incubative period of the disease and the remarkable http://www.vegsource.com/talk/lyman/messages/7634.html USA IMPORTS VACCINE PRODUCTS FROM BSE COUNTRIES http://www.mad-cow.org/00/may00_news.html Furthermore, we showed that http://www.pnas.org/cgi/content/full/041490898v1 Human vaccine prepared in animal brains http://www.mad-cow.org/00/nov00_late_news.html#fff http://www.whale.to/v/singeltary7.html http://www.mad-cow.org/00/may00_news.html http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh STUDY DESIGN AND METHODS: BSE was passaged through macaque monkeys and RESULTS: All three inoculated microcebes became ill after incubation CONCLUSION: Buffy coat from a symptomatic microcebe infected 17 months http://www.blackwell-synergy.com/servlet/useragent?func=synergy&synergyAction=showAbstract&doi=10.1046/j.1537-2995.2002.00098.x Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001 snip... [host Richard Barns] [TSS] [no answer, you could hear in the back ground, [host Richard] [TSS] [not sure whom ask this] [TSS] [not sure who is speaking] [TSS] [not sure whom speaking] snip... http://vegancowboy.org/TSS-part1of8.htm Meanwhile, health officials with the Food and Drug Administration say "The MRC-5 line was developed & from lung tissue taken from a 14-week http://www.worldnetdaily.com/news/article.asp?ARTICLE_ID=25362 SMALLPOX VACCINE, Dried, Calf Lymph Type Dryvax, Wyeth Laboratories, Marietta, PA (1960) Ingredients calf lymph chloriatracycline hydrochloride; http://www.vaccineawareness.org/IllinoisIssues/SmallpoxInsert.htm TSS ########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############ -------- Original Message -------- Subject: CJD AND BLOOD PRODUCTS DATA In what follows, Chapter 2 begins by summarizing the regional markets for imported and exported human blood, prepared animal blood, toxins, cultures of micro-organisms, and similar products excluding yeasts. The total level of imports and exports on a worldwide basis, and those for each region, is based on a model which aggregates across country markets and projects these to the current year. From there, each country represents a percent of the world market. This market is served from a number of competitive countries of origin. Based on both demand- and supply-side dynamics, market shares by country of origin are then calculated across each country market destination. These shares lead to a volume of import and export values for each country and are aggregated to regional and world totals. In doing so, we are able to obtain maximum likelihood estimates of both the value of each market and the shares that countries are likely to receive this year. From these figures, rankings are calculated to allow managers to prioritize markets. In this way, all the figures provided in this report are forecasts that can be combined with internal information for strategic planning purposes. U.S. $795.00 [sorry, can't help you there...TSS) http://www.marketresearch.com/researchindex/918108.html BLOOD PRODUCTS ADVISORY COMMITTEE SIXTYSIXTH Thursday, June 15, 2000 snip... They looked at estimates of possible human http://www.fda.gov/ohrms/dockets/ac/00/transcripts/3620t1.pdf Variant Creutzfeldt-Jakob Disease and Haemophilia snip... The following table includes European countries that contribute plasma to products available full text; http://www.wfh.org/Content_Documents/Blood_Safety/vCJD_Bulletin2_revised.pdf ACTION TAKEN BY THE UK MEDICINES CONTROL 6.1 Information is held on a especial data base from the initial BSE http://www.bseinquiry.gov.uk/files/yb/1994/09/01003001.pdf RESTRICTED-COMMERCIAL..............CSM/BIOLS/94/6th Meeting NOT FOR PUBLICATION COMMITTEE ON SAFETY OF MEDICINES SUB-COMMITTEE ON BIOLOGICALS snip... 1.1 The chairman reminded the Sub-Committee that the papers and snip... 4.6 BOVINE SERA 4.6.1 There was a discussion of the problem of the paper trail audit, http://www.bseinquiry.gov.uk/files/yb/1994/09/14003001.pdf RESTRICTED-COMMERCIAL CSM/94/8th Meeting NOT FOR PUBLICATION COMMITTEE ON SAFETY OF MEDICINES (7 blank pages to follow...TSS) http://www.bseinquiry.gov.uk/files/yb/1994/09/22006001.pdf http://www.bseinquiry.gov.uk/files/yb/1994/09/22007001.pdf Variant CJD and BPL Plasma Products February 1, 2001 Dr. P.L.F. Giangrande The World Federation of Hemophilia has received several enquiries about a recent problem which has arisen in the United Kingdom. As a physician working in the UK, I have been very closely involved in this matter and am writing this to set out the facts. A volunteer donor in the UK who gave blood in 1996 and 1997 has recently died of variant CJD (vCJD). The plasma from this donor was used by Bio-Products Laboratory (BPL) in the manufacture of several batches of various factor VIII and IX concentrates, including 8Y, Replenate and Replenine. These products were used in the UK in 1997 and 1998. All patients who were treated with the implicated batches have already been traced, and will be notified of this problem which has arisen. The Haemophilia Society in the UK has also issued a statement, which has been circulated to members. Of course, I recognise that this news may generate some anxiety amongst the haemophilia community, particularly in the UK. However, it must be emphasised that there is no evidence that vCJD is transmitted by blood products and no person with haemophilia in the world has ever been reported to have developed either the classical or variant form of CJD. Furthermore, BPL has assured me that none of the implicated batches have been exported from the UK for use abroad. Although BPL continues to export a number of blood products (including coagulation factor concentrates), it must be appreciated that these are now manufactured with plasma imported from North America. -------------------------------------------------------------------------------- http://www.wfh.org/ShowDoc.asp?Rubrique=30&Document=110 7.4 The Committee was informed that, since the publication of Hunter et al. CJD: Transmission Lord Lucas asked Her Majesty's Government: The Parliamentary Under-Secretary of State, Department of Health (Lord Hunt of Kings Heath): The following, peer reviewed articles, relate to this subject and will be placed in the Library: T F G Esmonde et al, 1993, Creutzfeldt-Jakob disease and blood transfusion, Lancet 341; 205-207; 11 Apr 2000 : Column WA32 Ricketts MN et al: Is Creutzfeldt-Jakob Disease transmitted in blood?, Energ Infect Dids 1997:3, 155-166; and These studies cover all types of CJD. Sporadic (classic) CJD, however, accounts for some 85 per cent of non-variant cases. The European Committee for Proprietory Medicinal Products (CPMP) reviewed the evidence in December 1995 and advised that there was no experimental or epidemiological evidence that classical CJD is transmitted by blood transfusions or plasma-derived products. A recall policy was not considered justified for plasma derived products from plasma pools incorporating a donation implicated for classical CJD. It reaffirmed that advice in March 1997. CPMP concluded on the basis of currently available information from epidemiological and experimental studies that there is no scientific justification for changing from the current CPMP position on classical CJD. CPMP further stated there to be no evidence that classical CJD is transmitted via blood or plasma derived products. This issue was also subsequently considered by the US Food and Drugs Administration, which came to the same conclusion. New-variant CJD Lord Lucas asked Her Majesty's Government: (b) the status of codons 26, 56 and 174 of doppel; (c) the dates of onset and confirmation for those patients diagnosed with new-variant CJD but still living; (d) the definition of "onset"; and (e) the age of the patients at onset to the nearest month.[HL1807] Confirmation of a diagnosis of vCJD is currently obtained by postmortem neuropathology. There are therefore no "confirmed" patients still living. The dates of onset for patients still living and defined as "probable" to the nearest month are as follows: Bovine Embryos and Live Cattle: Imports from North America The Earl of Caithness asked her Majesty's Government: The European Parliament and European Council introduced legislation in May last year laying down rules for the prevention, control and eradication of certain transmissible spongiform encephalopathies (TSEs). The legislation was introduced in response to the recommendations of the Office International des Epizooties (OIE—the international animal health organisation) and advice from the Commission's scientific comittees. The legislation (and the transitional measures which came into effect in October last year) includes requirement that imports into the EU of bovine embryos and live cattle must be accompanied by certification confirming that the feeding of ruminants with protein derived from mammals has been banned and that the ban has been effectively enforced. Some exporting countries, such as Canada and the USA, are currently unable to meet these new requirements. http://www.publications.parliament.uk/pa/ld199900/ldhansrd/pdvn/lds02/text/20425w04.htm BSE: US Export of Specified Risk Material Lord Kennet asked Her Majesty's Government: Lord Donoughue: Yes. But their position on the Specified Risk Material legislation is based on the assumption that the United States can safely be regarded as a "BSE free" country. Their case for such treatment has not been accepted by the EU Commission's Scientific Veterinary Committee. http://www.publications.parliament.uk/pa/ld199798/ldhansrd/vo971215/text/71215w02.htm Baroness Masham of Ilton: My Lords, as blood products which infected haemophiliacs with HIV came from the USA, is the Minister confident that something else nasty may not come again from imported blood from the USA? Is he aware that there are ways of cleaning blood to make it safer? I know that that is done in Vienna, in Austria. Will the Minister look into that? Following the question asked by the noble Lord, Lord Clement-Jones, about people using their own blood, I am sure that, when this Statement goes out into the wider community, people will want to know that information. http://www.publications.parliament.uk/pa/ld199900/ldhansrd/pdvn/lds03/text/31217-09.htm However, the Bio Products Laboratory who produce plasma products did export surplus products, under the Income Generation Regulations for the NHS, and used the income for the benefit of the health service.[21] http://www.publications.parliament.uk/pa/cm200001/cmselect/cmpubacc/207/20703.htm#n21 43. Do you sell any of it abroad at all? http://www.publications.parliament.uk/pa/cm200001/cmselect/cmpubacc/207/1012904.htm Blood and Blood Products Mr. Hinchliffe: To ask the Secretary of State for Health what estimate he has made of the number of persons who have been inoculated with blood or blood products over the past three years in the United Kingdom. [61681] Ms Jowell [holding answer 2 December 1998]: It is estimated that about one million people in the United Kingdom receive blood and blood products every year. http://www.parliament.the-stationery-office.co.uk/pa/cm199899/cmhansrd/vo990210/text/90210w02.htm Although hospitals have been advised to return the product, used in X-ray screenings to detect lung disease, so far only 15 per cent has been recovered. There is no order obliging hospitals to return it and some clinicians may go on using up stocks on the basis that patients are far more likely to die from infections or cancer that can be diagnosed with the product than from CJD. Another 268 patients in Ireland are known to have been given injections from the same batch of the product. The Irish Health Ministry has decided to notify all the patients concerned. Even though the identity of all those who have been given an injection of the product is known, it was decided not to tell them because there is no evidence that the illness can be transmitted through the blood or the serum derived from it to make the product and the risk of developing CJD is regarded as negligible. "You are putting an enormous burden on people by telling them they have a remote risk of contracting the disease," the department said last night. "The ethics committee which advises us on these matters decided it was just not appropriate to tell them." Many were exported but 210 of the 50ml bottles remained in Britain and were sent to eight different hospitals and companies. Some of the bottles were used intravenously to rehydrate burn victims. One bottle was sent to Nycomed Amersham which used it to produce 14,000 vials of Amerscan Pulmonate II, an agent which is injected into the lungs so that infections and cancer show up under X-ray. The company sent almost 3,700 vials to 100 British hospitals. At the end of October the European Committee on Proprietary Medicinal Products called for the withdrawal of blood products derived from donors who were confirmed CJD cases. On November 1 the Blood Transfusion Service was notified that one of its donors had died from the disease so the Amersham company was told. In turn the company got in touch with the Medicines Control Agency which informed the Health Department and it recommended withdrawal of the product on November 17. Despite regular alarms, there has never been any convincing evidence that blood or blood products can transmit CJD (Nigel Hawkes writes). Unless new variant CJD, the human form of "mad cow" disease, is more easily transmitted than classic CJD via blood or blood products, there does not appear to be any cause for concern. [This is no medical basis for this statement -- webmaster] For classic CJD the risk seems negligible. About 50 people a year die of the disease, so it is certain that every year some of them give blood after they have the infection but before its symptoms appear. Studies show that classic CJD can be passed on in human tissue, but not - so far as we know - in blood. [This is not an accurate summary of current scientific knowledge -- webmaster] The Sunday Times report said that Austrian officials have investigated two British companies, based in Guernsey and Berkshire. Police are still trying to find out where the companies' plasma products were used. Johann Kurz, head of unit for biologicals with the federal Ministry of Social Security & Generation in Vienna, Austria, told The Lancet, "We suspect that in 1996 and earlier, some products coming from South Africa were transferred to India, China, and Hong Kong, among other countries". The products were albumin and intravenous immunoglobulins. Nevertheless, Luc Noel, Coordinator of Blood Safety with the WHO in Geneva, Switzerland, emphasised that: "There should not be any confusion of the transfusion services in South Africa--which are now world class--with these criminal activities". While it is important that this trafficking is exposed, the public can be confident in their blood services, Noel added. Sanjay Kumar Kirsten Myhr, MScPharm, MPH Bygdøy alle 58B 0265 Oslo, Norway Tel.: +47 22 56 05 85, fax: +47 22 24 90 17 myhr@online.no http://www.freerepublic.com/focus/f-news/889385/posts WITH the amount of diseased dead stock downer livestock that is being disposed in the USA and other countries in various ways, the potential amplification and transmission to humans and animals of this agent via a multitude of routes and sources is enormous. to flounder and continue to insist on finding reasons why we should NOT impliment this or that rule for human/animal safety due to economic consequenses, with an agent that is so unusual and deadly as the TSE agent, and with an agent with an incubation period as long as the TSE agent, would be the most inhumane and immoral thing any governing body could do for there human and animal population, especially with the science documented to date. sadly, it will be politics as usual. the agent will continue to spread, while we find ourselves with a new cause for all of these TSE agents now, the cause, spontaneous TSE. it's nobody's fault, there is no route and source for any of this, ignore all transmission studies, just happens. right$ i have yet to hear from any of these spontaneous folks, a figure of what they call spontaneous VS a figure of the other multitude of proven routes and sources? like, how much of the 85%+ of all CJD 'sporadic', is this so called spontaneous TSE? 1%, 2%, or 80%? another odd thing that most are refusing to see, the 'spontaneous' TSE to date that stan proved to be infectious, looked like no other TSE he had seen in human or animal documented to date. SO could someone please show me this data that shows that any natural TSE has ever been proven spontaneous? show me the data... TSS Terry S. Singeltary Sr.
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