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Meat and bone meal back into feed

Dick Ziggers
It has been ten years now since the European Commission has banned the use of meat and bone meal (mbm) in animal feeds. There are enough reasons for lifting this ban, but decision making in Brussels is slow. Too long the feed industry has been withheld from a cheap and valuable feed ingredient.

Europe, and mainly the United Kingdom, in the nineties of the last century were facing a crisis when mad cow disease paralysed the animal industry. Cattle were fed ruminant remains that contained a protein (prion) that caused Bovine Spongiform Encephalopathy (BSE) or mad cow disease. The big problem is that people can get the BSE related and lethal Creutzfeld-Jacob disease, if they eat infected beef.

So, with the knowledge of the nineties it was logic to ban all animal remains from all animal feed. Since then a lot of research has taken place and we now know that only ruminants are affected by the prions. Pigs and poultry could never be related to the disease. Still, these sectors have to suffer from the ban on mbm in feed the EU imposed ten years ago.

 
Valuable product
Meat and bone meal is a valuable raw material providing energy, protein, vitamins and minerals, which vary in levels, but that are very well digested by the animals. There is considerable variation in nutrient specifications from company to company. In a recent survey the National Renderers' Association questioned several US feed manufacturers. Twenty-seven feed companies responded and the range in nutrient values for meat and bone meal was as follows:

Moisture
3.0 - 11.2%
Crude protein
49.0 - 52.8%
Crude fat
8.5 - 14.8%
Calcium
6.0 - 12.0%
Total phosphorus
3.5 - 5.0%
Lysine
2.2 - 3.0%
Metabolizable energy for poultry
1,770 – 2,420 MCal/kg
 
Saving the rainforest
When mbm had to be taken out of the feed it was merely replaced by soybean products, which needed to be imported from Brazil. Because of the vast demand from Europe large areas were cultivated to satisfy the European demand. In his PhD thesis Emiel Elferink at the University of Groningen in the Netherlands calculated that because of the ban in Europe annually 16 million tonnes of mbm is replaced by 23 million tonnes of soybeans. Since the ban on mbm was installed the area planted with soybeans has increased from 10 million hectares in the eighties to more than 20 million hectares at the beginning of this century.
So, apart from the nutritional benefits putting mbm back into the feed this would also have an enormous environmental benefit as it would put less pressure on the rainforest in South America.
 
Omnivores
Another very strong argument is that pigs and poultry are omnivores, meaning they eat everything and if they have a choice, they do not restrict themselves to a vegetarian diet. Poultry in the wild, for example, peck for grubs and beetles to supplement their protein needs.
And with limited and ending sources of phosphorous mbm can contribute to the phosphorous supply in the feed reducing the need for rock phosphate.
Until today there are no signs that poultry and pigs are susceptible to BSE-like diseases. Scientists therefore assume that meat and bone meal from poultry and pigs can be used in feeds without any risks. Advocacy groups for agriculture lobby in Brussels to have mbm back in animal feed, but this is a slow and arduous route. Installing a law seems far more easy than to get rid of one.
 
Emotions
The poorly informed general public, however, is worried about the return of mbm in feeds. Cannibalism is the hot word. From a theoretical standpoint I can understand the resistance of feeding animal remains to cattle, since these are herbivorous. Strangely enough these questions are not asked when fish meal is fed to fish.
 
But there is no ground to refrain pigs and poultry from eating meat and bone meal. To satisfy the general public politicians first want to ensure that only pig-mbm is fed to poultry and poultry-mbm to pigs. DNA test kits are already available to distinguish the differences. So this cannot be a reason for upholding the release of mbm again.
 
Cost benefit
These DNA-limitations could dampen down the euphoria on the return of mbm in animal feeds. It would require a strict logistic organisation with separate channels for feeds with pig-mbm and feeds with poultry-mbm.
 
At present every feed for every livestock specie can be manufactured in one mill. With mbm returning separate production lines would be needed to make pig and poultry feed with mbm and ruminant feeds. Meat and bone meal is a cheap raw material, but when it may return in feeds under the above mentioned restrictions it can be questioned if these benefits result in cheaper feed.
 
I am curious to hear what opinion you have on this issue….
 
Emmy Koeleman also wrote about this subject in 2007. Since then nothing has happened 
 

2 comments

  • no-profile-image

    Dr Jaydip Mulik

    Using the MBM from Pig & Poultry will help to reduce the Feed cost. But I don't understand why Poultry MBM should be used in Pig Feed & Pork MBM in Poultry feed. What will happen if used vis a vis?
    And if Europian Commission have confidence that they were successful to eradicate the BSE disease within past ten years then why should not use Beef-MBM?
    Due to Fear of Mad cow disease, is there any restrictions on Beef Eating in Europe? Please clarify the queries.

  • no-profile-image

    Josef Hlasny

    You wrote; Cattle were fed ruminant remains that contained a protein (prion) that caused Bovine Spongiform Encephalopathy (BSE) or mad cow disease. The big problem is that people can get the BSE related and lethal Creutzfeld-Jacob disease, if they eat infected beef...
    However, BSE can be a naturally occurring disease, so not an infectious disease. WHY? Because, about the BSE disease; this was never justified scientifically! It was pure, math-model-driven science fiction. But it was pushed very vigorously by the British science establishment, which has never confessed to its errors, and is therefore likely to make the same ones again.
    Indeed –really! See recently; the swine flu outbreak was a 'false pandemic'; said Wolfgang Wodarg, head of health at the Council of Europe (January 8, 2010). He has branded the H1N1 outbreak as 'one of the greatest medical scandals of the century'!
    However, the pandemic has started on May 1, 2009 when Roy Anderson was interviewed on the BBC's Today programme about the 2009 swine flu outbreak. He was a member of a group set up to give scientific advice to the British government over health issues relating to swine flu. However, swine flu is not the first time we have suffered this nonsense. See predictions about BSE/ vCJD by Roy M. Anderson. He has mathematically modelled the spread of new variant Creutzfeld- Jakob disease (v CJD), published in Nature (406, 583-584; 10 August 2000).
    There his team showed that the current mortality data are consistent with between 63 and 136,000 cases among the population known to have a susceptible genotype (about 40% of the total population), with on average less than two cases of vCJD arising from the consumption of one infected bovine. However, far fewer people are carrying the human form of mad cow disease than previously feared. There have been (to date) 168 definite or probable cases of vCJD since 1995, suggesting that the risk had been "overestimated".
    This led to an obscene GBP 5 billion campaign of British cattle destruction and compensation. And about the USA ? The International Trade Commission released a report estimating that trade restrictions resulting from BSE cost the cattle industry $11 billion from 2004 to 2007
    (www.beefusa.org/NEWSTradeRestrictionsCostCattlemen11BillioninLostSales36991.aspx). This could be "more greatest medical scandal"!
    See other relationships, according to my web www.bse-expert.c and recent presentation at 29th World Veterinary Congress in Vancouver; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors (www.bse-expert.cz/pdf/Veter_kongres.pdf).

    As I said; In Britain, much of the alarmism about Mad Cow disease was never justified scientifically. It was pure, math-model-driven science fiction...Indeed- Really ? There are some; "fifteen BSE/ vCJD mathematical examples", mostly headed by professor R.G.WILL (former director; National Creutzfeldt-Jakob Disease Surveillance Unit in Edinburgh) or by :
    Professor J. COLLINGE, former head of Department of Neurogenetics, Imperial College School of Medicine at St Mary's, London.
    This "BSE saga" it was initiated by R.G.Will; see : the introduction of the "Letter to Neurologists", on 21 March 1996; In the past few weeks we believe we may have identified a new clinico-pathological phenotype of CJD which may be unique to the United Kingdom. This raises the possibility of a causative link between BSE and CJD. These cases have been very difficult to diagnose clinically because the clinical phenotype is largely distinct from that previously seen in CJD...(www.cjd.ed.ac.uk/letter.htm). Findings from this letter were "immediately" published in Lancet. See also other journals about the mathematical BSE/vCJD models (abstracts only);

    1. Lancet; April 7, 1996; 347: 921- 25
    A new variant of Creutzfeldt-Jakob disease in the UK
    R G Will, J W Ironside, M Zeidler, S N Cousens, K Estibeiro, A Alperovitch, S Poser, M Pocchiari, A Hofman, P G Smith
    See from summary; Findings and Interpretation;
    Findings; Ten cases of CJD have been identified in the UK in recent months with a new neuropathological profile. Other consistent features that are unusual include the young age of the cases, clinical findings, and the absence of the electroencephalogram features typical for CJD. Similar cases have not been identified in other countries in the European surveillance system.
    Interpretatlon; These cases appear to represent a new variant of CJD, which may be unique to the UK. This raises the possibility that they are causally linked to BSE. Although this may be the most plausible explanation for this cluster of cases, a link with BSE cannot be confirmed on the basis of this evidence alone. It is essential to obtain further information on the current and past clinical and neuropathological profiles of CJD in the UK and elsewhere.

    2. Dev Biol Stand. 1998;93:79-84.
    New variant Creutzfeldt-Jakob disease.
    Will RG..
    New variant Creutzfeldt-Jakob disease is a novel human spongiform encephalopathy with a consistent clinico-pathological phenotype. Epidemiological evidence indicates that this disease is occurring almost exclusively in the UK, where there has been an epidemic of spongiform encephalopathy in the cattle population. Current evidence strongly supports the hypothesis that there is a causal link between bovine spongiform encephalopathy and new variant Creutzfeldt-Jakob disease.

    3. Lancet, 1999 Jul 24;354(9175):317-23.
    Variant Creutzfeldt-Jakob disease.
    Collinge J.
    It is clear that the prion strain causing bovine spongiform encephalopathy (BSE) in cattle has infected human beings, manifesting itself as a novel human prion disease, variant Creutzfeldt-Jakob disease (CjD). Studies of the incubation periods seen in previous epidemics of human prion disease and of the effect of transmission barriers limiting spread of these diseases between species, suggest that the early variant CJD cases may have been exposed during the preclinical phase of the BSE epidemic. It must therefore be considered that many cases may follow from later exposure in an epidemic that would be expected to evolve over decades. Since the number of people currently incubating this disease is unknown, there are concerns that prions might be transmitted iatrogenically via blood transfusion, tissue donation, and, since prions resist routine sterilisation, contamination of surgical instruments. Such risks remain unquantified. Although variant CJD can be diagnosed during life by tonsil biopsy, a prion-specific blood test is needed to assess and manage this potential threat to public health. The theoretical possibility that BSE prions might have transferred to other species and continue to present a risk to human health cannot be excluded at present.

    4. Nature 406, 583-584 (10 August 2000) | doi:10.1038/35020688
    Predicted vCJD mortality in Great Britain
    Azra C. Ghani1, Neil M. Ferguson1, Christl A. Donnelly1 & Roy M. Anderson1
    Modelling the latest data puts a ceiling on the likely number of vCJD cases;
    There is continued speculation about the likely number of cases of variant Creutzfeldt–Jakob disease (vCJD) that will occur in Great Britain in the wake of the BSE epidemic in cattle and in light of a recent cluster of vCJD cases in Leicestershire, England. We show here that the current mortality data are consistent with between 63 and 136,000 cases among the population known to have a susceptible genotype (about 40% of the total population), with on average less than two cases of vCJD arising from the consumption of one infected bovine.

    5. Lancet. 2000 Aug 5;356(9228):481-2.
    Incidence of variant Creutzfeldt-Jakob disease in the UK.
    Andrews NJ, Farrington CP, Cousens SN, Smith PG, Ward H, Knight RS, Ironside JW, Will RG.
    The number of deaths from variant CJD (vCJD) in the UK increased in the last quarter of 1998, although numbers were lower in subsequent quarters. We analysed the numbers of definite and probable (living and dead) vCJD cases since 1994 to assess trends in incidence. We estimated that the number of onsets increased by 23% per year for 1994-2000 (p=0.004), and that deaths increased by 33% for 1995-2000 (p=0.005). The absolute number of cases in the UK is still low, but such an increase should be a matter of concern.


    6. Science DOI: 10.1126/science.1064748; October 25, 2001
    Predictability of the UK Variant Creutzfeldt-Jakob Disease Epidemic
    Jerome N. Huillard d'Aignaux, Simon N. Cousens , Peter G. Smith
    Back calculation analysis of the variant Creutzfeldt-Jakob disease epidemic in the UK is used to estimate the number of infected individuals and future disease incidence. The model assumes a hazard of infection proportional to the incidence of BSE in the United Kingdom, accounts for precautionary control measures and very wide ranges of incubation periods. The model indicates that current case data are compatible with numbers of infections ranging from a few hundred to several millions. In the latter case, the model suggests that the mean incubation period must be well beyond the human life-span, resulting in disease epidemics of at most several thousand cases.

    7. Science. 2001 Nov 23;294(5547):1729-31. Epub 2001 Oct 25.
    Predictability of the UK variant Creutzfeldt-Jakob disease epidemic.
    d'Aignaux JN, Cousens SN, Smith RG.
    Back-calculation analysis of the variant Creutzfeldt-Jakob disease epidemic in the United Kingdom is used to estimate the number of infected individuals and future disease incidence. The model assumes a hazard of infection proportional to the incidence of bovine spongiform encephalopathy in the United Kingdom and accounts for precautionary control measures and very wide ranges of incubation periods. The model indicates that current case data are compatible with numbers of infections ranging from a few hundred to several millions. In the latter case, the model suggests that the mean incubation period must be well beyond the human life-span, resulting in

    8. Lancet. 2003 Mar 1;361(9359):751-2.
    Deaths from variant Creutzfeldt-Jakob disease in the UK.
    NJ Andrews , CP Farrington , HJT Ward , SN Cousens , PG Smith , AM Molesworth , RSG Knight , JW Ironside , RG Will

    In 2002, 17 people died from variant CJD (vCJD) in the UK, compared with 20 in 2001 and 28 in 2000. We analysed data for deaths from vCJD since 1995 and estimated the underlying trend in mortality. The trend had a quadratic component (p=0.005), suggesting that the increase was not exponential, and that the previously increasing trend is slowing down. The death rate peaked in 2000. These findings are encouraging, but mortality might increase again in the future.

    9. Stat Methods Med Res. 2003 Jun;12(3):203-20.
    The predictability of the epidemic of variant Creutzfeldt-Jakob disease by back-calculation methods.
    Huillard d'Aignaux JN, Cousens SN, Smith R,G.
    We present a back-calculation analysis of the variant Creutzfeldt-Jakob (vCJD) epidemic in the UK to estimate the number of infected individuals and to explore the likely future incidence of the disease. The main features of the model are that the hazard of infection was assumed proportional to the incidence of BSE in the UK with allowance for precautionary control measures taken in 1988 and in 1996, and that the incubation period distribution of vCJD follows an offset generalized F distribution. Our results indicate that current the numbers of cases with onset up to 31 December 2000 data are broadly compatible with numbers of primary infections ranging from a few hundred to several million. However, if a very large number of persons were infected, the model suggests that the mean incubation period is likely to be well beyond the human lifespan, resulting in a disease epidemic of much smaller size (maximum several thousand). A sensitivity analysis indicates that our results are sensitive to the underreporting of vCJD cases before 1996. Finally, we show that, in the absence of a reliable test for asymptomatic infection, uncertainty in estimates of the total number of infections is likely to remain for at least several years, even if the number of clinical cases remains low.

    10. Curr Top Microbiol Immunol.2004;284:161-91.
    The epidemiology of variant Creutzfeldt-Jakob disease.
    SMITH, P.G.; COUSENS, S.N.; HUILLARD D'AIGNAUX, J.N.; Ward, H.J.; Will, R.G.;
    Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. p.smith@lshtm.ac.uk
    Variant Creutzfeldt-Jakob disease (vCJD) was identified as a new disease in 1996. It was linked to infection with the bovine spongiform encephalopathy (BSE) agent although the epidemiological evidence for this was not strong, but later strain typing studies confirmed the association. The disease has affected predominantly young adults whose dietary and other characteristics are unexceptional compared to control groups, other than that all patients to date have been methoinine homozygous at codon 129 of the prion protein gene and the incidence has been about two times higher in the North of the UK. The number of cases in the 7 years after first identification of the disease has been considerably lower than initially feared, given the likely widespread exposure of the UK population to the BSE agent through contaminated beef products. Predictions of the possible future course of the epidemic have many associated uncertainties, but current mathematical models suggest that more than a few thousand cases is unlikely. Such modelling is limited by the absence of a test for infection with the vCJD agent. The development of a test that could be used on easily accessible tissue to detect infection early in the incubation period would not only advance understanding of the epidemiology of infection with the agent but would also aid the implementation of control measures to prevent potential iatrogenic spread.

    11. Journal of Royal Society Interface 22 March 2005 vol. 2 no. 2 19-31
    Projections of the future course of the primary vCJD epidemic in the UK: inclusion of subclinical infection and the possibility of wider genetic susceptibility
    Paul Clarke, Azra Ghani
    The incidence of variant Creutzfeldt–Jakob disease (vCJD) in the United Kingdom appears to be in decline, with only four deaths reported this year (to 6 September 2004). However, results of a survey of lymphoreticular tissues have suggested a substantially higher prevalence of vCJD than expected from the clinical data alone. There are two plausible explanations for this discrepancy: first, a proportion of those infected will not develop clinical disease (subclinical infection); and second, the genetic group in which no clinical cases of vCJD have yet occurred is susceptible. Using mathematical models for the primary transmission of bovine spongiform encephalopathy to humans, we explore the impact of these hypotheses on case predictions. Under the first hypothesis, the results suggest relatively few future cases will arise via primary transmission, but that these cases are a small proportion of those infected, with most having subclinical infection. Under the second hypothesis, results suggest a maximum fivefold increase in cases, but this hypothesis is unable to account for the discrepancy between clinical cases and the estimated prevalence. Predictions of future cases of vCJD therefore remain uncertain, particularly given the recent identification of additional cases infected via blood transfusion.

    12. Ann Neurol, 2006 Jan;59(1):111-20.
    Risk factors for variant Creutzfeldt-Jakob disease: a case-control study.
    Ward HJ, Everington D, Cousens SN, Smith-Bathgate B, Leitch M, Cooper S, Heath C, Knight RS, Smith PG, Will RG.
    OBJECTIVE: To investigate the potential risk factors for variant Creutzfeldt-Jakob disease (VCJD) in the United Kingdom. METHODS: Definite and probable vCJD cases (n = 136) were residing in Great Britain at disease onset, and were referred between May 1995 and November 2003. Control subjects (n = 922) were recruited between 2002 and 2003, from 100 randomly selected geographical clusters sampled to represent the geographical distribution of vCJD.
    RESULTS: Reported frequent consumption of beef and beef products thought likely to contain mechanically recovered or head meat, or both, including burgers and meat pies, was associated with increased risk for vCJD, as was reported frequent chicken consumption. Surgical operations were generally similarly reported for cases and control subjects, with the exception of a small group of minor operations, possibly attributable to underreporting in control subjects. Cases and control subjects had similar reported occupational histories and exposure to animals.
    INTERPRETATION: These findings are consistent with dietary exposure to contaminated beef products being the main route of infection of vCJD, but recall bias cannot be excluded. There was no convincing evidence of increased risk through medical, surgical, or ccupational exposure or exposure to animals.

    13. Lancet, 2006 Jun 24;367(9528):2068-74.
    Kuru in the 21st century--an acquired human prion disease with very long incubation periods.
    Collinge J, Whitfield J, McKintosh E, Beck J, Mead S, Thomas DJ, Alpers MP.
    BACKGROUND: Kuru provides the principal experience of epidemic human prion disease. Its incidence has steadily fallen after the abrupt cessation of its route of transmission (endocannibalism) in Papua New Guinea in the 1950s. The onset of variant Creutzfeldt-Jakob disease (vCJD), and the unknown prevalence of infection after the extensive dietary exposure to bovine spongiform encephalopathy (BSE) prions in the UK, has led to renewed interest in kuru. We investigated possible incubation periods, pathogenesis, and genetic susceptibility factors in kuru patients in Papua New Guinea.
    METHODS: We strengthened active kuru surveillance in 1996 with an expanded field team to investigate all suspected patients. Detailed histories of residence and exposure to mortuary feasts were obtained together with serial neurological examination, if possible.
    FINDINGS: We identified 11 patients with kuru from July, 1996, to June, 2004, all living in the South Fore. All patients were born before the cessation of cannibalism in the late 1950s. The minimum estimated incubation periods ranged from 34 to 41 years. However, likely incubation periods in men ranged from 39 to 56 years and could have been up to 7 years longer. PRNP analysis showed that most patients with kuru were heterozygous at polymorphic codon 129, a genotype associated with extended incubation periods and resistance to prion disease.
    INTERPRETATION: Incubation periods of infection with human prions can exceed 50 years. In human infection with BSE prions, species-barrier effects, which are characteristic of cross-species transmission, would be expected to further increase the mean and range of incubation periods, compared with recycling of prions within species. These data should inform attempts to model variant CJD epidemiology.

    14. Journal of Royal Society Interface 22 August 2007 vol. 4 no. 15 675-684
    Is there the potential for an epidemic of variant Creutzfeldt–Jakob disease via blood transfusion in the UK?
    Paul Clarke, Robert G Will, Azra C Ghani
    The discovery of three individuals suspected to have contracted variant Creutzfeldt–Jakob disease (vCJD) through blood transfusions has heightened concerns that a secondary epidemic via human-to-human transmission could occur in the UK. The Department of Health responded immediately to this threat by banning those who had received blood transfusions since 1980 from donating blood. In this paper, we conduct a sensitivity analysis to explore the potential size of a blood-borne vCJD epidemic and investigate the effectiveness of public health interventions. A mathematical model was developed together with an expression for the basic reproduction number (R0). The sensitivity of model predictions to unknown parameters determining the transmission of vCJD via infected blood was assessed under pessimistic modelling assumptions. We found that the size of the epidemic (up until 2080) was bounded above by 900 cases, with self-sustaining epidemics (R0>1) also possible; but the scenarios under which such epidemics could arise were found to be biologically implausible. Under optimistic assumptions, public health interventions reduced the upper bound to 250 and further still when only biologically plausible scenarios were considered. Our results support the belief that scenarios leading to large or self-sustaining epidemics are possible but unlikely, and that public health interventions were effective.

    15. Lancet Neurol 2009 Jan;8(1):57-66.
    Genetic risk factors for variant Creutzfeldt-Jakob disease: a genome-wide association study.
    Mead S, Poulter M, Uphill J, Beck J, Whitfield J, Webb TE, Campbell T, Adamson G, Deriziotis P, Tabrizi SJ, Hummerich H, Verzilli C, Alpers MP, Whittaker JC, Collinge J.
    BACKGROUND: Human and animal prion diseases are under genetic control, but apart from PRNP (the gene that encodes the prion protein), we understand little about human susceptibility to bovine spongiform encephalopathy (BSE) prions, the causal agent of variant Creutzfeldt-Jakob disease (vCJD).
    METHODS: We did a genome-wide association study of the risk of vCJD and tested for replication of our findings in samples from many categories of human prion disease (929 samples) and control samples from the UK and Papua New Guinea (4254 samples), including controls in the UK who were genotyped by the Wellcome Trust Case Control Consortium. We also did follow-up analyses of the genetic control of the clinical phenotype of prion disease and analysed candidate gene expression in a mouse cellular model of prion infection. FINDINGS: The PRNP locus was strongly associated with risk across several markers and all categories of prion disease (best single SNP [single nucleotide polymorphism] association in vCJD p=2.5 x 10(-17); best haplotypic association in vCJD p=1 x 10(-24)). Although the main contribution to disease risk was conferred by PRNP polymorphic codon 129, another nearby SNP conferred increased risk of vCJD. In addition to PRNP, one technically validated SNP association upstream of RARB (the gene that encodes retinoic acid receptor beta) had nominal genome-wide significance (p=1.9 x 10(-7)). A similar association was found in a small sample of patients with iatrogenic CJD (p=0.030) but not in patients with sporadic CJD (sCJD) or kuru. In cultured cells, retinoic acid regulates the expression of the prion protein. We found an association with acquired prion disease, including vCJD (p=5.6 x 10(-5)), kuru incubation time (p=0.017), and resistance to kuru (p=2.5 x 10(-4)), in a region upstream of STMN2 (the gene that encodes SCG10). The risk genotype was not associated with sCJD but conferred an earlier age of onset. Furthermore, expression of Stmn2 was reduced 30-fold post-infection in a mouse cellular model of prion disease.
    INTERPRETATION: The polymorphic codon 129 of PRNP was the main genetic risk factor for vCJD; however, additional candidate loci have been identified, which justifies functional analyses of these biological pathways in prion disease.

    So about professor Robert G.WILL - the "BSE saga mathematically" finished (2007);
    We found that the size of the epidemic (up until 2080) was bounded above by 900 cases, with self-sustaining epidemics (R0>1) also possible; but the scenarios under which such epidemics could arise were found to be biologically implausible. Under optimistic assumptions, public health interventions reduced the upper bound to 250 and further still when only biologically plausible scenarios were considered. Our results support the belief that scenarios leading to large or self-sustaining epidemics are possible but unlikely, and that public health interventions were effective.
    And about professor J. COLLINGE- the "BSE saga genetically" finished (2009); The polymorphic codon 129 of PRNP was the main genetic risk factor for vCJD; however, additional candidate loci have been identified, which justifies functional analyses of these biological pathways in prion disease.

    It is interesting; the "BSE saga" initiated in journal Lancet (1996) and there also finished (2009).

    Sincerely
    Josef Hlasny, DVM,PhD., veterinary surgeon, Czech Republic

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