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Chapter 28 : Bovine Spongiform Encephalopathy: Consequences for Human Health
Authors:
Paul Brown1,
Linda A. Detwiler2
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Affiliations:
1: National Institutes of Health, Bethesda, MD 20814;
2: Center for Public and Corporate Veterinary Medicine, Virginia-Maryland Regional College of Veterinary Medicine, 8075 Greenmead Dr., College Park, MD 20742
Content Type: Reference
Publication Year:
2007
Category: Applied and Industrial Microbiology; Food Microbiology
Book DOI:
10.1128/9781555815912
Chapter DOI:
10.1128/9781555815912.ch28
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Abstract:
Human transmissible spongiform encephalopathies (TSEs) include the prototypic disease kuru, which is limited to Papua New Guinea and is now virtually extinct. In the event that infectivity is definitively found to be present in muscle from cattle infected with Bovine Spongiform Encephalopathy (BSE), available scientific and epidemiological evidence to date suggests that it does not appear to exist in amounts sufficient to increase the risk to human health in countries with adequate prevention and control measures. The continuance of BSE cases due to cross contamination and cross feeding of ruminant meat and bone meal (MBM) has resulted in extended feed bans which have prohibited feeding of all mammalian or animal meat and bone meal (MBM) to any animals used for human food. Humans most likely became infected with the agent that causes BSE through the consumption of beef products contaminated by central nervous systems (CNS) tissue, such as mechanically recovered meat that was pressure extracted from carcasses and often contained spinal cord tissue and paraspinal ganglia in addition to residual muscle shards. The combination of psychiatric and sensory symptoms in an adolescent or young adult is sufficient to raise a suspicion of Creutzfeldt-Jakob disease (CJD) together with its variant form (vCJD) in patients who reside or have resided in countries in which BSE has occurred.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
Figures
Bovine Spongiform Encephalopathy: Consequences for Human Health
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Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28fig01
Figure 28.1
The family of transmissible spongiform encephalopathies. TME, transmissible mink encephalopathy; GSS, Gerstmann-Straüssler-Scheinker disease; FFI, fatal familial insomnia.
10.1128/9781555815912/f0612-01_thmb.gif
10.1128/9781555815912/f0612-01.gif
Figure 28.1
The family of transmissible spongiform encephalopathies. TME, transmissible mink encephalopathy; GSS, Gerstmann-Straüssler-Scheinker disease; FFI, fatal familial insomnia.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28fig02
Figure 28.2
Western blots of misfolded prion protein (PrPTSE) extracted from the brains in two cases of sporadic CJD(s) (types 1 and 2A) and a case of vCJD (v) (type 2B). The combination of the lower molecular mass and the comparatively higher density of the topmost protein band (asterisk) distinguishes vCJD from all other TSEs. M, methionine; V, valine. Courtesy of Mark Head, CJD Surveillance Unit, Western General Hospital, Edinburgh, Scotland.
10.1128/9781555815912/f0612-02_thmb.gif
10.1128/9781555815912/f0612-02.gif
Figure 28.2
Western blots of misfolded prion protein (PrPTSE) extracted from the brains in two cases of sporadic CJD(s) (types 1 and 2A) and a case of vCJD (v) (type 2B). The combination of the lower molecular mass and the comparatively higher density of the topmost protein band (asterisk) distinguishes vCJD from all other TSEs. M, methionine; V, valine. Courtesy of Mark Head, CJD Surveillance Unit, Western General Hospital, Edinburgh, Scotland.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28fig03
Figure 28.3
The chronology of BSE (black) in the United Kingdom compared to those of vCJD in the United Kingdom (gray) and non-United Kingdom countries (white). The BSE scale is at the left, and the vCJD scale is at the right. SBO, specified bovine offals; MRM, mechanically recovered meat.
10.1128/9781555815912/f0617-01_thmb.gif
10.1128/9781555815912/f0617-01.gif
Figure 28.3
The chronology of BSE (black) in the United Kingdom compared to those of vCJD in the United Kingdom (gray) and non-United Kingdom countries (white). The BSE scale is at the left, and the vCJD scale is at the right. SBO, specified bovine offals; MRM, mechanically recovered meat.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28fig04
Figure 28.4
Age at onset in United Kingdom cases of vCJD and sporadic CJD, 1994 to 2005. Courtesy of Robert Will, CJD Surveillance Unit, Western General Hospital, Edinburgh, Scotland.
10.1128/9781555815912/f0618-01_thmb.gif
10.1128/9781555815912/f0618-01.gif
Figure 28.4
Age at onset in United Kingdom cases of vCJD and sporadic CJD, 1994 to 2005. Courtesy of Robert Will, CJD Surveillance Unit, Western General Hospital, Edinburgh, Scotland.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28fig05
Figure 28.5
Duration of illness in United Kingdom cases of vCJD and sporadic CJD (sCJD), 1994 to 2005. Courtesy of Robert Will, CJD Surveillance Unit, Western General Hospital, Edinburgh, Scotland.
10.1128/9781555815912/f0619-01_thmb.gif
10.1128/9781555815912/f0619-01.gif
Figure 28.5
Duration of illness in United Kingdom cases of vCJD and sporadic CJD (sCJD), 1994 to 2005. Courtesy of Robert Will, CJD Surveillance Unit, Western General Hospital, Edinburgh, Scotland.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28fig06
Figure 28.6
The pathognomonic vCJD daisy plaque consisting of a core of amyloid protein surrounded by vacuolar petals. Courtesy of James Ironside, CJD Surveillance Unit, Edinburgh, Scotland.
10.1128/9781555815912/f0619-02_thmb.gif
10.1128/9781555815912/f0619-02.gif
Figure 28.6
The pathognomonic vCJD daisy plaque consisting of a core of amyloid protein surrounded by vacuolar petals. Courtesy of James Ironside, CJD Surveillance Unit, Edinburgh, Scotland.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28fig07
Figure 28.7
Red “RM” identification labels are used to differentiate between slaughterhouse tools used to handle specified risk materials (SRMs) and those for edible product. Courtesy of Ana Carolina Alonso Simplicio de Oliveira, Frigoalta, Brazil.
10.1128/9781555815912/f0621-01_thmb.gif
10.1128/9781555815912/f0621-01.gif
Figure 28.7
Red “RM” identification labels are used to differentiate between slaughterhouse tools used to handle specified risk materials (SRMs) and those for edible product. Courtesy of Ana Carolina Alonso Simplicio de Oliveira, Frigoalta, Brazil.
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
References
/content/book/10.1128/9781555815912.ch28
1.
Alper, T.,, W. A. Cramp,, D. A. Haig, and, M. C. Clarke. 1967. Does the agent of scrapie replicate without nucleic acid? Nature 214: 764– 766.
2.
Andreoletti, O,, S. Simon,, C. Lacroux,, N. Morel,, G. Tabouret,, A. Chabert,, S. Lugan,, F. Corbiere,, P. Ferre,, G. Foucras,, H. Laude,, F. Eychenne,, J. Grassi, and, F. Schelcher. 2004. PrP Sc accumulation in myocytes from sheep incubating natural scrapie. Nat. Med. 10: 591– 593.
3.
Angers, R. C.,, S. R. Browning,, T. S. Seward,, C. J. Sigurdson,, M. W. Miller,, E. A. Hoover, and, G. C. Telling. 2006. Prions in skeletal muscles of deer with chronic wasting disease. Science 311: 1117.
4.
Bishop, M. T.,, P. Hart,, L. Aitchison,, H. N. Baybutt,, C. Plinston,, V. Thomson,, N. L Tuzi,, M. W. Head,., J. W. Ironside,, R. G. Will, and, J. C. Manson. 2006. Predicting susceptibility and incubation time of human-to-human transmission of vCJD. Lancet Neurol. 5: 393– 398.
5.
Bolton, D. C.,, M. P. McKinley, and, S. P. Prusiner. 1982. Identification of a protein that purifies with the scrapie prion. Science 218: 1309– 1311.
6.
Brown, P. 2005. Blood infectivity, processing and screening tests in transmissible spongiform encephalopathies. Vox Sanguinis 89: 63– 70.
7.
Brown, P.,, C. J. Gibbs Jr.,, P. Rodgers-Johnson,, D. M. Asher,, M. P. Sulima,, A. Bacote,, L. G. Goldfarb, and, D. C. Gajdusek. 1994. Human spongiform encephalopathy: the National Institutes of Health series of 300 cases of experimentally transmitted disease. Ann. Neurol. 35: 513– 529.
8.
Brown, P.,, E. H. Rau,, P. Lemieux,, B. K. Johnson,, A. Bacote, and, D. C. Gajdusek. 2004. Infectivity studies of both ash and air emissions from simulated incineration of scrapie-contaminated tissues. Environ. Sci. Technol. 38: 6155– 6160.
9.
Brown, P.,, R. G. Rohwer, and, D. C. Gajdusek. 1986. Newer data on the inactivation of scrapie virus or Creutzfeldt-Jakob disease virus in brain tissue. J. Infect. Dis. 153: 1145– 1148.
10.
Brown, P.,, R. G. Rohwer,, E. M. Green, and, D. C. Gajdusek. 1982. Effect of chemicals, heat, and histopathologic processing on high infectivity hamster-adapted scrapie virus. J. Infect. Dis. 145: 683– 687.
11.
Brown, P.,, R. G. Will,, R. Bradley,, D. M. Asher, and, L. Detwiler. 2001. Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease: background, evolution, and current concerns. Emerg. Infect. Dis. 7: 6– 16.
12.
Brown, P.,, R. Meyer,, F. Cardone, and, M. Pocchiari. 2003. Ultra-high-pressure inactivation of prion infectivity in processed meat: a practical method to prevent human infection. Proc. Natl. Acad. Sci. USA 100: 6093– 6097.
13.
Bruce, M. E.,, R. G. Will,, J. W. Ironside,, I. McConnell,, D. Dummond,, A. Suttie,, L. McCardle,, A. Chree,, J. Hope,, C. Birkett,, S. Cousens,, H. Fraser, and, C. J. Bostock. 1997. Transmissions to mice indicate that “new variant” CJD is caused by the BSE agent. Nature 389: 498– 501.
14.
Buschmann, A., and, M. Groschup. 2005. Highly bovine spongiform encephalopathy-sensitive transgenic mice confirm the essential restriction of infectivity to the nervous system in clinically diseased cattle. J. Infect. Dis. 192: 934– 942.
15.
Cardone, F.,, P. Brown,, R. Meyer, and, M. Pocchiari. 2006. Inactivation of transmissible spongiform encephalopathy agents by ultra high pressure-temperature treatment. Biochim. Biophys. Acta 1764: 558– 562.
16.
Colchester, A. C. F., and, N. T. H. Colchester. 2005. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 366: 856– 861.
17.
Cuillé, J., and, P. I. Chelle. 1936. La maladie dite “tremblante” de mouton; est-elle inoculable? Compte Rendu Acad. Sci. 203: 1552.
18.
Cutlip, R. C.,, J. M. Miller,, R. E. Race,, A. L. Jenny,, J. B. Katz,, H. D. Lehmkuhl,, B. M. DeBey, and, M. M. Robinson. 1994. Intracerebral transmission of scrapie to cattle. J. Infect. Dis. 169: 814– 820.
19.
Cutlip, R. C.,, J. M. Miller,, A. N. Hamir,, J. Peters,, M. M. Robinson,, A. L. Jenny,, H. D. Lehmkuhl,, W. D. Taylor, and, F. D. Bisplinghoff. 2001. Resistance of cattle to scrapie by the oral route. Can. J. Vet. Res. 65: 131– 132.
20.
Department for Environment, Food and Rural Affairs. 4 May 2006, revision date. BSE: statistics—youngest and oldest cases by year of onset (for passive surveillance cases) and on year of slaughter (for active surveillance cases). [Online.] Department for Environment, Food and Rural Affairs, London, United Kingdom. http://www.defra.gov.uk/animalh/bse/statistics/bse/yng-old.html.
21.
Department for Environment, Food and Rural Affairs. 25 Oct. 2005, rivision date. Distribution of Infectivity. [Online.] Department for Environment, Food and Rural Affairs, London, United Kingdom. http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#distribute.
22.
Department for Environment, Food and Rural Affairs. 25 Oct. 2005, revision date. Infectious Dose Experiment. [Online.] Department for Environment, Food and Rural Affairs, London, United Kingdom. http://www.defra.gov.uk/animalh/bse/science-research/pathog.html#dose.
23.
Doherr, M. G.,, A. R. Hett,, J. Rufenacht,, A. Zurbriggen, and, D. Heim. 2002. Geographical clustering of cases of bovine spongiform encephalopathy (BSE) born in Switzerland after the feed ban. Vet. Rec. 151: 467– 472.
24.
Donnelly, C. A. 1998. Maternal transmission of BSE: interpretation of the data on the offspring of BSE-affected pedigree suckler cows. Vet. Rec. 142: 579– 580.
25.
Donnelly, C. A.,, N. M. Ferguson,, A. C. Ghani, and, R. M. Anderson. 2002. Implications of bovine spongiform encephalopathy (BSE) screening data for the scale of the British BSE epidemic and current European infection levels. Proc. R. Soc. Lond. Ser. B 269: 2179– 2190.
26.
Flan, B., and, J.-T. Aubin. 2005. Evaluation de l’effiacité des procédés de purification des protéines plasmatiques à éliminer les agents transmissibles non conventionnels. Virologie 9: S45– S56.
27.
Hadlow, W. J.,, R. C. Kennedy, and, R. E. Race. 1982. Natural infection of Suffolk sheep with scrapie virus. J. Infect. Dis. 146: 657– 664.
28.
Hill, A. F.,, M. Desbruslais,, S. Joiner,, K. C. L. Sidle,, I. Gowland,, J. Collinge,, L. J. Doey, and, P. Lantos. 1997. The same prion strain causes vCJD and BSE. Nature 389: 448– 450.
29.
Hoinville, L. J. 1994. Decline in the incidence of BSE in cattle born after the introduction of the “feed ban.” Vet. Rec. 134: 274– 275.
30.
Hoinville, L. J.,, J. W. Wilesmith, and, M. S. Richards. 1995. An investigation of risk factors for cases of bovine spongiform encephalopathy born after the introduction of the “feed ban.” Vet. Rec. 136: 312– 318.
31.
Horn, G.,, M. Bobrow,, M. E. Bruce,, M. Goedert,, A. McLean, and, J. Webster. 2001. Review of the Origin of BSE. Stationery Office, London, United Kingdom.
32.
Ironside, J. W.,, M. T. Bishop,, K. Connelly,, D. Hegazy,, S. Lowrie,, M. LeGrice,, D. L. Ritchie,, L. M. McCardle, and, D. A. Hilton. 2006. Variant Creutzfeldt-Jakob disease: prion protein genotype analysis of positive appendix tissue samples from a retrospective prevalence study. BMJ 332: 1186– 1188.
33.
Llewelyn, C. A.,, P. E. Hewitt,, R. S. G. Knight,, K. Amar,, S. Cousens,, J. Mackenzie, and, R. G. Will. 2004. Possible transmission of variant Creutzfeldt-Jakob disease by blood transfusion. Lancet 363: 417– 421.
34.
Middleton, D. J., and, R. M. Barlow. 1993. Failure to transmit bovine spongiform encephalopathy to mice by feeding them with extraneural tissues of affected cattle. Vet. Rec. 132: 545– 547.
35.
Oesch, B.,, D. Westaway,, M. Walchli,, M. P. McKinley,, S. B. H. Kent,, R. Aebersold,, R. A. Barry,, P. Tempst,, D. B. Teplow,, L. E. Hood,, S. B. Prusiner, and, C. Weismann. 1985. A cellular gene encodes scrapie PrP 27–30 protein. Cell 40: 735– 746.
36.
Peden, A.,, M. W. Head,, D. L. Ritchie,, J. E. Bell, and, J. W. Ironside. 2004. Preclinical vCJD after blood transfusion in a PRNP codon 129 heterozygous patient. Lancet 364: 527– 529.
37.
Philips, Lord of Worth Matravers,, J. Bridgeman, and, M. Ferguson-Smith. 2000. The BSE Inquiry. [Online.] Stationery Office, London, United Kingdom. http://www.bseinquiry.gov.uk/pdf/index.htm.
38.
Schreuder, B. E. C.,, R. E. Geertsma,, L. J. M. van Keulen,, J. A. A. M. van Asten,, P. Enthoven,, R. C. Oberthür,, A. A. de Koeijer, and, A. D. M. E. Osterhaus. 1998. Studies on the efficacy of hyperbaric rendering procedures in inactivating bovine spongiform encephalopathy (BSE) and scrapie agents. Vet. Rec. 142: 474– 480.
39.
Stevenson, M. A.,, J. W. Wilesmith,, J. B. M. Ryan,, R. S. Morris,, A. B. Lawson,, D. U. Pfeiffer, and, D. Lin. 2000. Descriptive spatial analysis of the epidemic of bovine spongiform encephalopathy in Great Britain to June 1997. Vet. Rec. 147: 379– 384.
40.
Taguchi, F.,, Y. Tamai,, K. Uchida,, R. Kitajima,, H. Kojima,, T. Kawaguchi,, Y. Ohtani, and, S. Miura. 1991. Proposal for a procedure for complete inactivation of the CreutzfeldtJakob disease agent. Arch. Virol. 119: 297– 301.
41.
Taylor, D. M. 2000. Inactivation of transmissible spongi-form encephalopathy agents: a review. Vet. J. 159: 10– 17.
42.
Taylor, D. M. 2004. Resistance of transmissible spongi-form encephalopathy agents to decontamination. Contrib. Microbiol. 11: 136– 145.
43.
Taylor, D. M.,, C. E. Ferguson,, C. J. Bostock, and, M. Dawson. 1995. Absence of disease in mice receiving milk from cows with bovine spongiform encephalopathy. Vet. Rec. 136: 592.
44.
Taylor, D. M.,, H. Fraser,, I. McConnell,, D. A. Brown,, K. L. Brown,, K. A. Lamza, and, G. R. A. Smith. 1999. Decontamination studies with the agents of bovine spongiform encephalopathy and scrapie. Arch. Virol. 139: 313– 326.
45.
Taylor, D. M.,, S. L. Woodgate, and, M. J. Atkinson. 1995. Inactivation of the bovine spongiform encephalopathy agent by rendering procedures. Vet. Rec. 137: 605– 610.
46.
Taylor, D. M.,, S. L. Woodgate,, A. J. Fleetwood, and, R. J. G. Cawthorne. 1997. Effect of rendering procedures on the scrapie agent. Vet. Rec. 141: 643– 649.
47.
Thomzig, A.,, F. Cardone,, D. Krugr,, M. Pocchiari,, P. Brown, and, M. Beekes. 2006. Pathological prion protein in muscles of hamsters and mice infected with rodent-adapted BSE or vCJD. J. Gen. Virol. 87: 251– 254.
48.
United Kingdom Health Protection Agency. 9 Feb. 2006, posting date. New Case of Variant CJD Associated with Blood Transfusion. [Online.] United Kingdom Health Protection Agency, London, United Kingdom. http://www.hpa.org.uk/hpa/news/articles/press_releases/2006/060209_cjd.htm.
49.
Wadsworth, J. D. F.,, S. Joiner,, A. F. Hill,, T. A. Campbell,, M. Desbruslais,, P. J. Luthert, and, J. Collinge. 2001. Tissue distribution of protease resistant prion protein in variant Creutzfeldt-Jakob disease using a highly sensitive immunoblotting assay. Lancet 358: 171– 180.
50.
Ward, H. J. T.,, D. Everington,, S. Cousens,, B. Smith-Bathgate,, M. Leitch,, S. Cooper,, C. Heath,, R. G. Knight,, P. Smith, and, R. G. Will. 2006. Risk factors for variant Creutzfeldt-Jakob disease: a case control study. Ann. Neurol. 59: 111– 120.
51.
Wells, G. A. H.,, A. C. Scott,, C. T. Johnson,, R. F. Gunning,, R. D. Hancock,, M. Jeffrey,, M. Dawson, and, R. Bradley. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121: 419– 420.
52.
Wells, G. A. H.,, J. Spiropoulos,, S. A. C. Hawkins, and, S. J. Ryder. 2005. Pathogenesis of experimental bovine spongiform encephalopathy: preclinical infectivity in tonsil and observations on the distribution of lingual tonsil in slaughtered cattle. Vet. Rec. 156: 401– 407.
53.
Wells, G. A. H.,, S. A. C. Hawkins,, A. R. Austin,, S. J. Ryder,, S. H. Done,, R. B. Green,, I. Dexter,, M. Dawson, and, R. H. Kimberlin. Studies of the transmissibility of the agent of bovine spongiform encephalopathy to pigs. J. Gen. Virol. 84: 1021– 1031.
54.
Wells, G. A. H.,, S. A. Hawkins,, R. B. Green,, A. R. Austin,, I. Dexter,, Y. I. Spencer,, M. J., Chaplin,, M. J. Stack, and, M. Dawson. 1998 Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet. Rec. 142: 103– 106.
55.
Wilesmith, J. W., and, J. B. Ryan. 1992. Bovine spongiform encephalopathy: recent observations on the age-specific incidences. Vet. Rec. 130: 491– 492.
56.
Wilesmith, J. W., and, J. B. M. Ryan. 1997. Absence of BSE in the offspring of pedigree suckler cows affected by BSE in Great Britain. Vet. Rec. 141: 250– 251.
57.
Wilesmith, J. W.,, G. A. H. Wells,, J. B. M. Ryan,, D. Gavier-Widen, and, M. M. Simmons. 1997. A cohort study to examine maternally associated risk factors for bovine spongiform encephalopathy. Vet. Rec. 141: 239– 243.
58.
Wilesmith J. W.,, G. A. H. Wells,, M. P. Cranwell, and, J. B. M. Ryan. 1988. Bovine spongiform encephalopathy: epidemiological studies. Vet. Rec. 123: 638– 644.
59.
Wilesmith, J. W.,, J. B. Ryan, and, W. D. Hueston. 1992. Bovine spongiform encephalopathy: case-control studies of calf feeding practices and meat and bonemeal inclusion in proprietary concentrates. Res. Vet. Sci. 52: 325– 331.
60.
Will, R. G.,, J. W. Ironside,, M. Zeidler,, S. N. Cousens,, K. Estibeiro,, A. Alperovitch,, S. Poser,, M. Pocchiari,, A. Hofman, and, P. G. Smith. 1996. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 347: 921– 925.
61.
Will, R. G.,, M. Zeidler,, G. E. Stewart,, J. A. Macleod,, J. W. Ironside,, S. N. Cousens,, J. Mackenzie,, K. Estibeiro,, A. J. E. Green, and, R. S. G. Knight. 2000. Diagnosis of new variant Creutzfeldt-Jakob disease. Ann. Neurol. 47: 575– 582.
62.
World Health Organization. 1999. WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies. Report of a WHO Consultation. WHO/CDS/CSR/APH/2000.3 World Health Organization, Geneva, Switzerland.
63.
World Health Organization. 2003. WHO Guidelines on Transmissible Spongiform Encephalopathies in Relation to Biological and Pharmaceutical Products. World Health Organization, Geneva, Switzerland.
64.
World Organization for Animal Health. 22 May 2006, revision date. Bovine spongiform encephalopathy (BSE): geographical distribution of countries that reported BSE confirmed cases since 1989. [Online.]. OIE, Paris, France. http://www.oie.int/eng/info/en_esb.htm.
Tables
Bovine Spongiform Encephalopathy: Consequences for Human Health
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Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28tab01
Table 28.1
Categories of efficacy of various chemical and physical disinfection methods
Table 28.1
Categories of efficacy of various chemical and physical disinfection methods
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28tab02
Table 28.2
Proteinase-resistant protein (PrPTSE) and infectivity reductions under various pressure, temperature, and exposure time conditions
a
Table 28.2
Proteinase-resistant protein (PrPTSE) and infectivity reductions under various pressure, temperature, and exposure time conditions a
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28tab03
Table 28.3
Misfolded-protein (PrPTSE) reductions in various meat products spiked with 263K scrapie agent-infected hamster brain and then cooked for 5 min at 130°C under 690 MPa of pressure
Table 28.3
Misfolded-protein (PrPTSE) reductions in various meat products spiked with 263K scrapie agent-infected hamster brain and then cooked for 5 min at 130°C under 690 MPa of pressure
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28tab04
Table 28.4
Distribution of tissue infectivity and PrPTSE in naturally occurring human and animal TSE diseases
a
Table 28.4
Distribution of tissue infectivity and PrPTSE in naturally occurring human and animal TSE diseases a
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28tab05
Table 28.5
Consumable bovine materials used by humans
Table 28.5
Consumable bovine materials used by humans
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28
/content/10.1128/9781555815912.ch28.ch28tab06
Table 28.6
Principal governmental measures taken to protect human and animal health
Table 28.6
Principal governmental measures taken to protect human and animal health
Citation:
Brown P, Detwiler L.
2007.
Bovine Spongiform Encephalopathy: Consequences for Human Health,
p 611-626.
In
Doyle M, Beuchat L (ed),
Food Microbiology: Fundamentals and Frontiers, Third Edition.
ASM Press, Washington, DC.
doi: 10.1128/9781555815912.ch28