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Bovine Spongiform Encephalopathy (BSE) and Other Animal Related Transmissible Spongiform EncephalopathiesMarch 2001 (Revised January 2004)AWIC Series #2001-01Updates Bovine Spongiform Encephalopathy, 1990
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BSE, also called bovine spongiform encephalopathy or "mad cow disease" is a progressive neurological disorder of cattle that results from infection by an unconventional and extraordinary transmissible agent. BSE is one of several known animal transmissible spongiform encephalopathies including transmissible mink encephalopathy, scrapie, chronic wasting disease of mule deer, and elk, and feline spongiform encephalopathy. The disease name refers to the fact that at the end of the disease, the brain is full of holes like a sponge. The disease may develop in a relatively short time or, as is more usual, will take decades to develop. Scrapie may be the most well known of the spongiform encephalopathies. It occurs in sheep and goats. In general, as in cattle, diseased animals lose coordination of their legs and body movements and eventually cannot stand. The name "scrapie" refers to the fact that the animals can become irritable and develop an intense itch. The unrelenting itch leads them to "scrape" off their wool/fur. Although the majority of the information in this resource is on BSE, the publication covers the recent information on all these diseases as they may affect human health, farm animals and wildlife species.
There are also human conditions that are similar to the animal diseases. In most cases the human diseases are not due to transmissible agents. They can be genetic diseases that run in families, a mutation that happens sporadically in individuals and probably animals as well, or they may be transmitted by ingestion of the infectious agent (e.g. kuru of the Fore people was caused by ritualized cannibalism).
There is still some controversy regarding the nature of the transmissible agent that causes these fatal conditions, but the most accepted theory is that the agent is a modified form of a normal cell surface component known as a prion (proteinaceous infectious articles and (pronounced preeon) protein) (PrP). This modified version of PrP is disease causing, and is both less soluble and more resistant to enzyme degradation then the normal protein. "Currently there is no known treatment for prion diseases, and the fear that prions passed from cattle to humans may be justified." 1
Dr. Prusiner also states that "prions appear to multiply in an incredible way: they convert normal protein molecules into dangerous ones (PrPsc) simply by inducing the benign molecules to change their shape." "There are hints that the prions causing the diseases " such as BSE and scrapie "may not be the only ones. Prions made of different proteins may contribute to other neurogenerative diseases that are quite prevalent in humans."
It is the transmissible possibilities of the infectious agent moving between animal species and between animals and humans via an oral route that is currently of greatest concern. This concern is due to an outbreak of the BSE disease in United Kingdom (UK) cattle, and the increase of a human spongiform encephalopathy Creutzfeldt-Jakob Disease in the British population that was exposed to meat from cattle that had BSE.
BSE was first recognized in Great Britain in November 1986. The first cases probably occurred in early 1985. It is not definitive that the disease originated from scrapie infected meat and bone meal that was used as a protein supplement in cattle feeds, but there is strong evidence and general agreement that the outbreak was amplified by feeding rendered infected cattle meat-and-bone meal to young calves. "Some other captive ungulates, captive exotic cats and domesticated cats in the UK contracted the disease probably by eating the same feed material. During the peak of the disease (1992), about 1% of the adult cattle in the UK had the disease. Lower incidences have occurred in indigenous cattle in Ireland, France, Switzerland, the Netherlands, and Portugal. A few cases have been recorded in Canada, Germany, Denmark, Italy, the Falkland Islands, and the Sultanate of Oman in animals exported from Great Britain." 2
As of November 2000, in more than 35,000 herds, about 177,500 cases of BSE were confirmed in the UK alone. For current information, see the website of the Office of International Des Epizooties at http://www.oie.int/eng/info/en_esb.htm. According to the Animal and Plant Health Inspection Service of the U.S. Department of Agriculture, the first case of BSE in the United States was confirmed on December 23, 2003. The USDA's web site provides current news and surveillance information on BSE in the United States.
Concurrent with the cattle epidemic in the UK has been a rise of a new variant of CJD (NvCJD) in humans. This form of CJD "predominately affects younger individuals (median age at death 27.5 years as of October 2000), has atypical clinical features, coordination problems within weeks or months, dementia and myoclonus late in the illness, a duration of illness of at least 6 months, and an abnormal brain scan. There is beginning to be strong epidemiologic and laboratory evidence for a causal relationship between the NvCJD and BSE. The absence of confirmed cases of NvCJD in other geographic areas free of BSE supports a causal relationship." 3
Because of the BSE and NvCJD incidence, the Animal Welfare Information Center decided to provide a science based information resource about these diseases and all other potentially important TSEs. This resource includes a bibliographic listing of articles and website resources about the disease, the emergence of the disease in the UK and the political and social events surrounding the BSE crisis. It is a dynamic resource and additional materials on BSE and other TSEs will be added as they are identified.
Note: Also see Special Reference Brief, Bovine Spongiform Encephalopathy by Janice C. Swanson, December 1990, Animal Welfare Information Center.References:
1. Prusiner, S.B. Prion biology and diseases fatal conformations of proteins during a journey from heresy to orthodoxy. In Prions and Brain Diseases in Animals and Humans. Edited by D.R.O. Morrison. Plenum Press, NY 1998, p. 135-139. 30 refs. ISBN 0-306-45825-X. Part of the NATO ASI series. Series A, Life Sciences: v. 295. It is the proceeding of a NATO Advanced Research workshop on Prions and Brain Diseases in Animals and Humans, held August 19-23, 1996, in Erice, Italy.
2. The Merck Veterinary Manual 8th Edition. eds. S.E. Aiello and A. Mays. Published by Merck & Co., Inc. of Whitehouse Station, NJ. and in cooperation with Merial Limited. Printed by National Publishing Inc. of Philadelphia, PA 1998, p. 897. ISBN: 0-911910-29-8
3. Center for Disease Control, National Center for Infectious Diseases. Questions and Answers Regarding Bovine Spongiform Encephalopathy (BSE) and Creutzfeldt-Jakob Disease. Bovine Spongiform Encephalopathy and Creutzfeldt-Jakob Disease. April, 2001 http://www.cdc.gov/ncidod/dvrd/vcjd/qa.htm
Garcia, Rebeca; Jukes, David. The
Spanish system of food controls: Its administration and enforcement.
Food Control. January 2004; 15(1): 51-59. ISSN: 0956-7135
NAL call no.: TP372.7.F66
Descriptors: food safety, BSE, dioxin,
European Food Safety Authority (EFSA), EU, Spanish Agency of Food Safety,
general structure, Spanish ministries, Spain.
Liechti, R. The international conference on
bovine spongiform encephalopathy and food safety, April 17-18, 2002.
Food Control. January 2004; 15(1): 71-77. ISSN: 0956-7135
NAL
call no.: TP372.7.F66
Descriptors: current scientific knowledge,
BSE, TSEs, food safety risks, a forum for discussion, prion diseases, social
science, consumer groups.
Moya, K.L.; Hassig, R.; Creminon, C.; Laffont, Di Giamberardino, L.
Enhance and retrograde axonal transport of Prpc in peripheral nerve.
Journal of Neurochemistry. 2004; 88(1): 155-160. ISSN:
0022-3042.
NAL
call no.: QP351.J6
Descriptors: PrPC axonal transport, abundance of
PrPC in peripheral nerves, prion protein resistant to detergent extraction,
prion neuroinvastion, nerve extraction conditions, prion disease application,
TSE entry pathway, prion neuroinvasion, scrapie, CNS access.
Adjou, Karim Tarik;
Simoneau, Steve; Sales, Nicole; Lamoury, Francois; Dormont, Dominique;
Papy-Garcia, Dulce; Barritault, Denis; Deslys, Jean Philippe; Lasmezas,
Corinne Ida. A novel generation of
heparan sulfate mimetics for the treatment of prion diseases.
Journal of General Virology. September 2003; 84(9):
2595-2603. ISSN: 0022-1317
NAL call no.: QR360.A1J6
Descriptors: transmission of
spongiform encephalopathies, PrPres, protease resistant abnormal form,
cellular prion protein, heparan sulfate mimetics, HM 2602, effect is to
abolish prion propagation in scrapie-infected GT1 cells, in vivo testing, 263K
scrapie-infected hamsters, toxicity, dextran sulfate
500, mode of action.
Alexandru, N. Detectia PrPSC in trunchiul cerebral la
doua ovine in
NAL call no.: SF604.R48
Descriptors: ewes, sheep, natural
scrapie diagnosed, prion diseases, brain stem samples by foramen magnum rapid
method, immunohistochemistry, Romania.
Belay, Ermias D.;
Maddox, Ryan A.; Gambetti, Pierluigi; Schonberger, Lawrence B. Monitoring the occurrence of emerging
forms of Creutzfeldt-Jakob disease in the
Descriptors: BSE, 19 European
countries, Israel, Japan, vCJD in four European countries, U.S. Centers for
Disease Control, National Prion Disease Pathology Surveillance Center, human
cases.
Bhakdi, S.; Bohl, J. Prions and mad cow disease. Kraftfutter. 2003, 86(3): 56-65.
ISSN: 0023-4427. In English and
German.
NAL call no.: 389.78 K85
Descriptors: BSE, cattle, cows,
bovine spongiform encephalopathy, CJD, epidemiology, prion disease, foodborne
meat diseases, new infections declining in
Bozzetta, E.;
Caramelli, M.; Casalone, C.; Acutis, P.L.; Ru, G. BSE surveillance in
NAL call no.: 41.8 Z4
Descriptors: cattle, BSE, the
272/98/EC Decision, 52 animals with clinical signs, CNS, histopathology,
immunohistochemistry (IHC) or Western blot (WB) for PrPSc, no BSE detected,
improvement in passive surveillance needed.
Bosques, Carlos J.;
Imperiali, Barbara. The interplay of
glycosylation and disulfide formation influences fibrillization in a prion
protein fragment. Proceedings of the
NAL call no.: 500 N21P
Descriptors: prion proteins, PrPC,
preteinase K-resistant prion protein scrapie, PrPSc, role of glycosylation,
disulfide stability, retarding rate of fibril formation, intermolecular
disulfide formation via Cys-179, structure transition.
Brodmann, Peter D.;
Moor, Dominik. Sensitive and semi-quantitative TaqManTM
real-time polymerase chain reaction systems for the detection of beef (Bos taurus)
and the detection of the family Mammalia in food and feed. Meat Science. September 2003;
65(1): 599-607. ISSN: 0309-1740
NAL call no.: TX373.M4
Descriptors: beef, BSE
contamination bovine-based products,
vCJD, variant Creutzfeld Jacob Disease, consumer confidence, PCR
analysis, mammal DNA, beef DNA, meat and bone meal products, two methods.
Brown, David R. Prion protein expression modulates
neuronal copper content. Journal of Neurochemistry.
October 2003; 87(2): 377-385. ISSN: 0022-3042
NAL call no.: QP351.J6
Descriptors: prion protein, copper
binding capacity, prion disease, transmissible spongiform encephalopathies,
copper content of the brain, transgenic mice animal model, copper levels of
the synapse, age effects.
Brown, D.A.; Bruce,
M.E.; Fraser, J.R. Comparison of the
neuropathological characteristics of bovine spongiform encephalopathy (BSE)
and variant Creutzfeldt-Jakob disease (vCJD) in mice. Neuropathology and Applied
Neurobiology. June 2003; 29(3): 262-272. ISSN: 0305-1846
Descriptors: neuropathology,
inbred mouse strains, RIII, C57BL, VM, C57BL x VM, PrPres deposition,
astrocytosis, vacuolation, vCJD linked to BSE,
comparison study.
Bruce, Moira E. TSE strain
variation. British Medical Bulletin. 2003; 66: 99-108. ISSN: 0007-1420
Descriptors: scrapie, cattle,
goats, humans, mice, prion disease, strain differences, transmissible
spongiform encephalopathy.
Concepcion, G. P.;
Padlan, E.A. Are humans getting 'mad-cow disease' from
eating beef, or something else? Medical Hypotheses. May 2003; 60(5): 699-701. ISSN: 0306-9877
Descriptors: hypothesis, gastric
digestion of human and various animal prion proteins, ingestion of infected
rodent parts, possibly droppings, possible transmission mode of scrapie or BSE
to humans.
Carp, Richard I.;
Kascsak, Richard J. Taking aim at the
diagnosis of TSE infectious agents. Abstracts of Papers American Chemical
Society. 2003; 226(1-2): ANYL 9. ISSN: 0065-7727. Note: The 226th American Chemical Society
National Meeting,
NAL call
no.: 381 Am33Pa
Descriptors: BSE, bovine
spongiform encephalopathy, diagnosis, prion-disease, transmissible spongiform
encephalopathy, variant Creutzfeldt-Jakob disease, vCJD.
Castilla, J.;
Gutierrez, Adan A.; Brun, A.; Pintado, B.; Ramirez, M.A.; Parra, B.; Doyle,
D.; Rogers, M.; Salguero, F.J.; Sanchez, C.; Sanchez-Vizcaino, J.M.; Torres,
J.M. Early detection
of PrPres in BSE-infected bovine PrP transgenic mice. Archives of Virology. April 2003; 148(4): 677-691.
ISSN:
0304-8608
NAL call no.: 448.3 AR23
Descriptors: BSE, scrapie,
transgenic mouse lines, bovine protein gene expression at different levels,
lines exhibited characteristics of bovine disease, PrPres detected, Western
blot, immunohistochemistry assays, prions levels of inoculum, pathognomonic
markers of disease, incubation period, prion changes from original
infection.
Chaala, A.; Roy, C. Recycling of meat and bone meal animal
feed by vacuum pyrolysis. Environmental Science and
Technology.
NAL call no.: TD420 A1E5
Descriptors: BSE, European beef,
alternative disposal of waste animal products and bone meal, vacuum pyrolysis,
laboratory reactor, animal flour, combustible gas, high calorific value oil,
mineral residue, aqueous phase of organic, pollution
control/reduction.
Caughey, Byron. Prion protein conversions: Insight into
mechanisms, TSE transmission barriers and strains. British Medical Bulletin. 2003; 66: 109-120. ISSN: 0007-1420
Descriptors: prions, transmissible
spongiform encephalopathies, disease transmission factors, prion protein
isoforms, biochemistry, scrapie.
Chesebro, Bruce. Introduction to the
transmissible spongiform encephalopathies or prion diseases. British Medical
Bulletin. 2003; 66: 1-20. ISSN: 0007-1420
Descriptors: TSE, BSE, CJD, prion
diseases, etiology, prion protein, disease transmission,
theories.
Clauss, M. Do cows fed BSE-infected meat and bone
meal in the colostrum-producing stage pass on infectious BSE agent to their
calves? Medical Hypotheses. October
2003; 61(4): 439-443. ISSN:
0306-9877
Descriptors: BSE, cows, calves,
disease transmission, digestion of infectious agent in meat and bone meal,
colostrum infectivity, hypothesis.
Cranmer, Morris;
McChesney, Thomas. Chronic wasting disease: Risks to hunters
and consumers of deer and elk meat. Neurotoxicology. March 2003; 24(2): 313-314. ISSN: 0161-813X. Note: Twentieth International Neurotoxicology
Conference: Emerging Issues in
Neurotoxicology,
NAL call no.: RC321.N437
Descriptors: elk, deer, chronic
wasting disease, human health risks, prion disease, transmissible spongiform
encephalopathy, meat product, abstract.
Dahlanuddin; Van, Tien
Dam; Liang, J.B.;
NAL call no.: SF781.R4
Descriptors: world risk of BSE,
cattle, ruminant production systems, presence of infective agent, transmission
and amplification of disease, lack of cattle-based meat and bone meal reduces
risks,
Dahms, S. Epidemiologische Modellbildung am
Beispiel BSE -- Betrachtungen aus statistischer Sicht. [Epidemiological modelling taking BSE as an example -- reflections
from a statistical viewpoint. Berliner und Munchener Tierarztliche
Wochenschrift. 2003, 116(1-2): 22-30. ISSN: 0005-9366. In German.
NAL call no.: 41.8 B45
Descriptors: BSE, epidemiology
modeling, analytical methods, epidemiological surveys, epidemiology,
mathematical models, nervous system diseases.
Daude, Nathalie;
Marella, Mathieu; Chabry, Joelle. Specific inhibition of pathological prion
protein accumulation by small interfering RNAs. Journal of Cell Science.
NAL call no.: QH301.J6
Descriptors: transmissible
spongiform encephalopathies (TSEs) pathogenesis, PrP, prion protein,
proteinase-K resistant isoform, PrPres, small interfering RNA (siRNA)
duplexestrigger specific Prnp gene silencing, scrapie-infected neuroblastoma
cells, possible therapeutic approach for treatment of prion disease.
De Vlieger, J.J.;
Puister-Jansen, L.F.; Sengers, H.H.W.J.M.; Ouweltjes, W. Ontwikkelingen in de export van
Nederlands fokvee. [Developments in the export of Dutch
breeding cattle.] Rapport, Landbouw Economisch Instituut
LEI. 2003; No. 2.03.07, 60 pp. ISBN: 90-5242-803-4. In Dutch.
Descriptors: dairy cattle,
Holstein-Friesian, effects of BSE and FMD on markets, animal welfare, European
Union, exports, international trade, laws, legislation, market competition,
prion diseases, transport of animals, viral diseases, Algeria, Denmark,
France, Germany, Lebanon, Netherlands, Poland, Spain.
Dedet, V. En tysk ante mortem BSE blodprove
vurderes: Forelobige resultater praesenteret pa World Buiatric 2002. [A German ante-mortem BSE blood test
is evaluated. Provisional results presented at the World Buiatric conference,
2002.] Dansk Veterinaertidsskrift. 2003;
86(2): 24. ISSN: 0106-6854. In Danish.
NAL call no.: 41.9 D23
Descriptors: cattle, BSE, bovine
spongiform encephalopathy, ante-mortem blood test, diagnostic technique,
short-strand RNA coated with phospholipids, possible specificity to BSE.
Den Hartog, Johan. Feed for food: HACCP in the animal feed
industry. Food Control.
March 2003; 14(2): 95-99. ISSN:
0956-7135
NAL call no.: TP372.7.F66
Descriptors: Dutch animal feed
industry, food and feed safety, GMP standard Animal Feed, BSE and dioxin,
integration of HACCP, quality system, proactive approach, the
Netherlands.
Dimcheff, Derek E.;
Portis, John L.; Caughey, Byron. Prion proteins meet protein quality
control. Trends in Cell Biology. July
2003; 13(7): 337-340. ISSN:
0962-8924
NAL call no.: QH573.T73
Descriptors: protein quality
control mechanisms, prion protein aggregation, pathogenesis, proteasome
inhibition, neurogeneration.
Ducrot, Christian;
Roy, Pascal; Morignat, Eric; Baron, Thierry; Calavas,
Didier. How the surveillance system may bias the
results of analytical epidemiological studies on BSE: Prevalence among dairy
versus beef suckler cattle breeds in
NAL call no.: SF602.A5
Descriptors: dairy cattle, beef
cattle, BSE, disease levels, reliability of surveillance programs, data
analysis, Mandatory Reporting Systems of clinically suspect
bovines.
Ersdal, Cecilie;
Simmons, Marion M.; Goodsir, Caroline; Martin, Stuart; Jeffrey,
Martin. Sub-cellular pathology of scrapie: Coated
pits are increased in PrP codon 136 alanine homozygous scrapie-affected sheep.
Acta Neuropathologica. July
2003; 106(1): 17-28. ISSN: 0001-6322
Descriptors: scrapie, sheep,
sub-cellular studies, transmissible spongiform encephalopathies, heads of
scrapie-affected sheep and controls were perfusion fixed with mixed aldehydes,
obexes immunohistochemically labeled, PrP antibodies, electron microscopy of
vagal dorsal motor nucleus, coated pits in infected animals, dystrophic
neuritis, variable gliosis, plasmalemma invagination, intemalisation.
Ersdal, C.; Ulvund,
M.J.; Benestad, S.L.; Tranulis, M.A. Accumulation of pathogenic prion protein
(PrPSc) in nervous and lymphoid tissues of sheep with subclinical
scrapie. Veterinary
Pathology. 2003; 40(2):
164-174.
NAL call no.: 41.8 P27
Descriptors: Rygia breed sheep,
pathogenic prion protein, PrPSc, immunohistochemistry, obex, cerebellum,
medial retropharyngeal lymph nodes, off spring of PrPSc examined, ileal
Peyer’s patch, distal jejunal lymph node, spleen, pathogenesis, prion
diseases, BSE.
NAL call no.: 501 L84B
Descriptors: back-calculation
model to analyse data, reported clinical cases of bovine spongiform
encephalopathy, BSE, analysis of demographic data, levels of human exposure
estimated, discussion of possibilities of deaths from variant
Cruetzfeldt-Jakob disease, vCJD.
Fries, R.; Eggers, T.;
Hildebrandt, G.; Rauscher, K.; Buda, S.; Budras, K.D. Autonomous nervous system with respect to
dressing of cattle carcasses and its probable role in transfer of PrPres
molecules. Journal of Food
Protection. 2003; 66(5), 890-895.
NAL call no.: 44.8 J824
Descriptors: cattle, carcasses,
autonomic nervous system, cranial, cervical, and stellage ganglia, the chain
of paravertebral ganglia, bovine spongiform encephalopathy, BSE, esophagus,
vagus nerve, risk assessment, removal of possible infective material from the
food chain.
Galbraith, D.N. Transmissible spongiform encephalopathies
and tissue cell culture. Cytotechnology 2003; 39(2): 117-124.
ISSN: 0920-9069
NAL call no.: QH585.C97
Descriptors: TSE, prion proteins,
transmission, risks of using living cells and materials for therapeutic
compounds, prion biology and pathobiology, discussion of issues.
Geldermann, H.;
Preuss, S.; Eckert, J.; Han, Y.; Ollesch, K. Analysis of polymorphic microsatellites
within the bovine and ovine prion protein (PRNP) genes. Animal Genetics. August 2003;
34(4): 283-289. ISSN: 0268-9146
NAL call no.: QP98.A1A5
Descriptors: bovine prion protein
gene, microsatellite sites, sheep prion protein genes, distances between
microsatellites, pylogenetic origin of alleles, BSE, scrapie, molecular
genetics.
Gerweck, G. Ein blick auf status der tieraerzte in
der lebensmittelueberwachung und tierseuchenbekaempfung. [The status of veterinarians in food surveillance and zoonosis
control.] Tieraerztliche Umschau.
NAL call no.: 41.8 T445
Descriptors: zoonotic disease,
food safety, role of veterinarians, prion disease surveillance.
Ghani, Azra C.;
NAL call no.: 501 L84B
Descriptors: variant of
Creutzfeldt-Jakob disease, vCJD, epidemiology, human mortality prediction for
2 and 5 years, exposure to BSE, age dependent susceptibility, incubation
period distribution.
Gonzalez, Lorenzo;
Martin, Stuart; Jeffrey, Martin. Distinct profiles of PrPd
immunoreactivity in the brain of scrapie- and BSE-infected sheep: Implications
for differential cell targeting and PrP processing. Journal of General Virology.
May 2003; 84(5): 1339-1350. ISSN: 0022-1317
NAL call no.: QR360.A1J6
Descriptors: scrapie infected
sheep, bovine spongiform encephalopathy infected sheep, PrP antibodies, on the
disease causing prion protein, immunohistochemical examination of brains, 20
sheep, 4 different PrP antibodies (P4, 521.7, 505.2, R486), strain source
differences, source differentiation, cell tropism, PrP processing, variations
in PrPd conformation seem influenced by the cell type supporting infection,
modulated by the interaction between the infectious agent and the
host.
Gravenor, M.B.; Ryder,
S.J.; Gubbins, S.; Hunter, N.; Baylis, M.; Kao, R.R. Searching for BSE in sheep: interpreting
the results so far. Veterinary Record. 2003;
152(10) 298-299.
NAL call no.: 41.8 V641
Descriptors: sheep, screening for
BSE, scrapie, confidence limit for BSE is no more that 2%, disease prevalence,
Grigoletto, G.;
Bagordo, F.; Pongolini, S.; Cantoni, A.; Cabassi, E.; Corradi, A. TSE e test diagnostici: valutazione
critica e risvolti pratici nel controllo dell'encefalopatia spongiforme
bovina. [TSE and diagnostic
tests: critical evaluation and practical implications for the control of
bovine spongiform encephalopathy.] Obiettivi e Documenti
Veterinari. 2003; 24(3) 7-16.
In Italian.
Descriptors: rapid diagnostic
tests, BSE, Western blotting, Elisa, comparison study, use and application in
Gubbins, Simon;
Simmons, Marion M.; Sivam, Kumar; Webb, Cerian R.; Hoinville, Linda J. Prevalence of scrapie infection in
NAL call no.: 501 L84B
Descriptors: prevalence of
scrapie, sheep, human health risks, sheep transmissible spongiform
encephalopathies, TSEs, slaughter plant survey, prevalence of scrapie
infection, GB sheep flock of 0.22% (95% confidence interval: 0.01-0.97%).
Haywood, S.; Brown,
D.R. Transmissible spongiform
encephalopathies. Veterinary Times. 2003; 33(2) 8-9, 10.
ISSN: 1352-9374
Descriptors: cattle, man, sheep,
TSE, CJD, scrapie, binding proteins, copper, manganese, disease transmission,
environmental factors manganese.
Heim, D.; Kihm, U. Risk management of transsmissible
spongiform encephalopathies in
NAL call no.: SF 781.R4
Descriptors: BSE, scrapie, sheep,
goats, cattle, risk management decisions were inaccurate, active and passive
surveillance system, ban on feeding meat-and-bone meal (MBM) to ruminants,
brain and spinal column as high risk material, European measures.
Hein, Wayne R.;
Griebel, Philip J. A road less travelled: Large animal
models in immunological research. Nature Reviews Immunology.
January 2003; 3(1): 79-84. ISSN:
1474-1733
Descriptors: many diseases,
discussion of large animals as experimental models, viruses, bacteria, TSE’s.
Herrmann, Lynn M.;
Cheevers, William P.; Davis, William C.; Knowles, Donald P.; O' Rourke,
Katherine I. CD21-positive follicular
dendritic cells: A possible source of PrPSc in lymph node macrophages of
scrapie-infected sheep. American Journal of
Pathology. April 2003; 162(4): 1075-1081. ISSN: 0002-9440
NAL call no.: 448.8 AM39
Descriptors: natural sheep
scrapie, lymph node analysis, presence PrPSc and macrophage or FDC markers
using dual immunohistochemistry, follicular macrophages contain proteases that
process full-length PrPSc to N-terminally truncated PrPSc.
Hetz, Claudio;
Maundrell, Kinsey; Soto, Claudio. Is loss of function of the prion protein
the cause of prion disorders? Trends in Molecular
Medicine. June 2003;
9(6): 237-243. ISSN:
1471-4914
Descriptors: prion diseases, TSE, transmissible spongiform encephalopathies,
mechanism of neurogeneration in spongiform encephalopathies is unknown.
Hetz, C.; Soto, C. Protein misfolding and disease: The case
of prion disorders. CMLS Cellular and Molecular
Life Sciences. January
2003; 60(1): 133-143. ISSN: 1420-682X
NAL call no: QH301.C45
Descriptors: TSE, review article,
recent data, link between prion protein misfolding, pathogenesis of prion
diseases.
Hlasny, J. Nektere poznatky z Britanie o historii
vyzkumu deficitu horciku u prezvykavcu a BSE. [Some information from
Descriptors: cattle, ruminants,
BSE, prion diseases, magnesium, mineral deficiencies,
Houston, E.F.;
Gravenor, M.B. Clinical signs in sheep
experimentally infected with scrapie and BSE. Veterinary Record. 2003;
152(11): 333-334.
NAL call no.: 41.8 V641
Descriptors: sheep, clinical
signs, subcutaneous injection, 2g SSBP/1 (scrapie group), intracerebral
inoculation with 0.05 BSE brain homogenate, intravenous 0.2g BSE brain
homogenate, or 550ml scrapie infected sheep blood, clinical signs compared.
Hunter, Nora. Scrapie and experimental
BSE in sheep. British Medical Bulletin. 2003; 66: 171-183. ISSN: 0007-1420
Descriptors: sheep, BSE, scrapie,
experimental infection, Creutzfeldt-Jacob disease, prion
disease.
Ironside, James W. The spectrum of safety: Variant
Creutzfeldt-Jakob disease in the
NAL call no.: RC633.A1S44
Descriptors: vCJD, sheep, cattle,
prion diseases, BSE, scrapie, transmission, beef,
animal feed, meat products, blood supply safety, bone meal products, immune
response,
Jeffrey, Martin;
Martin, S.; Gonzalez, L. Cell-associated variants of
disease-specific prion protein immunolabelling are found in different sources
of sheep transmissible spongiform encephalopathy. Journal of General Virology.
April 2003; 84(4): 1033-1045. ISSN: 0022-1317
NAL call no: QR360.A1J6
Descriptors: scrapie, BSE, prion
disease, prion proteins, BSE and scrapie, intracellular accumulation patterns
disease specific prions, (PrPd) lymphoreticular system (LRS) in sheep
brains clinically affected with scrapie or BSE. BSE-infected PrPARQ/ARQ sheep
of different breeds compared with scrapie-infected sheep of different PrP
genotypes.
Kaneider, Nicole C.;
Kaser, Arthur; Dunzendorfer, Stefan; Tilg, Herbert; Wiedermann, Christian
J. Sphingosine kinase-dependent migration of
immature dendritic cells in response to neurotoxic prion protein
fragment. Journal of
Virology. May 2003; 77(9): 5535-5539. ISSN: 0022-538X
NAL call no.: QR360.J6
Descriptors: TSE, circulating
dendritic cells mediate neuroinvasion, prion protein expressed in myeloid
dendritic cells, prion protein fragment 106-126, chemo-attractant for
monocyte-derived immature dendritic cells, signaling events enzymes downstream
of Gq protein, inhibition by sphingosine kinase,
suggest trans-activation of sphingosine-1-phosphate-dependent cell motility by
priori protein.
Kang, Shin Chung; Li,
Ruliang; Wang, Chuanping; Pan, Tao; Liu, Tong; Rubenstein, Richard; Barnard,
Geoff; Wong, Boon Seng; Sy, Man Sun. Guanidine hydrochloride extraction and
detection of prion proteins in mouse and hamster prion diseases by ELISA.
Journal of Pathology. April
2003; 199(4): 534-541. ISSN:
0022-3417
NAL call no.: 448.8 J82
Descriptors: testing methods,
invitro test for TSE, differential extraction, brain homogenates using
guanidine hydrochloride followed by DELFIA (Dissociation Enhanced Lanthanide
FluoroImmunoAssay), differentiate disease associated PrP isoforms without
proteinase K digestion.
Kellar, J.A.; Lees,
V.W. Risk management of the
transmissible spongiform encephalopathies in
NAL call no.: SF781.R4
Descriptors: North American Free
Trade Agreement partners, Canada, the United States of America (USA), Mexico,
harmonized transmissible spongiform encephalopathy (TSE) risk management
strategies, quarantine and internal surveillance, BSE, feed bans, scrapie,
chronic wasting disease, transmissible mink encephalopathy, national and
sub-national veterinary infrastructures, laboratory networks.
Kim, Jae Il; Kuizon, Salomon; Rubenstein, Richard. Comparison of PrP
transcription and translation in two murine myeloma cell lines. Journal of Neuroimmunology.
July 2003; 140(1-2): 137-142. ISSN:
0165-5728
Descriptors: knockout mice myeloma
cell lines, hybridomas, prion protein, MAbs.
Descriptors: prion protein,
cattle, CJD, scrapie, TSE, scrapie, prion diseases, pathogenesis.
Kimura, Nobuhiro.
BSE outbreak and
feed security. Japanese Poultry
Science. May 2003; 40(J2): J98-J104. ISSN: 0029-0254. In Japanese.
NAL call no.: 47.8 N57
Descriptors: food safety and
security, public health risks, bovine spongiform encephalopathy, BSE,
epidemiology, prion disease, transmission.
Klass, Michael R.;
Hodges, Steven; Sayers, Riona; Clarke, John; Lyons,
Vanessa. Testing for TSE: Mad cows, scrapie sheep
and wasted deer and elk. Abstracts of Papers American Chemical
Society. 2003; 226(1-2): ANYL 10. ISSN: 0065-7727. Note: 226th American Chemical Society
National Meeting,
NAL call no.: 381 AM33Pa
Descriptors: cattle, deer, elk,
sheep, scrapie, BSE, chronic wasting disease, testing, prion protein
detection, ELISA, immunologic techniques, laboratory techniques,
Enfer-TSE-test,
Kocisko, David A.;
Baron, Gerald S.; Rubenstein, Richard; Chen, Jiancao; Kuizon, Salomon;
Caughey, Byron. New
inhibitors of scrapie-associated prion protein formation in a library of 2,000
drugs and natural products.
Journal of
Virology. October
2003; 77(19): 10288-10294. ISSN:
0022-538X
NAL call no.: QR360.J6
Descriptors: prion protein,
scrapie-infected mice neurobalstoma cells, scrapie strain RML, high-throughput
screening assay for PrPSc, 96 well format, polyphenols (e.g., tannic acid and
tea extracts), phenothiazines, antihistamines, statins, antimalarial
compounds.
Larski, Zdzislaw. Niektore nowe dane dotyczace wirusologii i zakaznych gabczastych
encefalopatii. [Some new data concerning virology and
transmissible spongiform encephalopathies.] Medycyna Weterynaryjna. 2003; 59(2):
95-99. ISSN: 0025-8628. In Polish.
NAL call no.: 41.8 M463
Descriptors: review article, lipid
rafts, virons, various diseases, imbalance of trace elements and changes in
antioxidant function of prion protein, BSE in sheep vs scrapie, cannibalism as
a cause of BSE.
Lasmezas, C.I. The transmissible
spongiform encephalopathies. Revue Scientifique et Technique Office International des Epizooties. April
2003; 22(1): 23-36. ISSN: 0253-1933
NAL call no.: SF781.R4
Descriptors: TSE’s, Creutzfeldt
Jakob disease, CJD, etiology, prion diseases, transmission, prevention and
control, scrapie, risk
management, general features of the diseases, mode of replication,
pathogenesis, molecular basis of PrP accumulation.
Ledoux, J.M. Features of the comparative
pharmacokinetics of lithium; a potential application of its use in livestock
farming. Medical Hypotheses. August
2003; 61(2): 278-281. ISSN:
0306-9877
Descriptors: cattle, mink,
lithium’s neuroprotective and neurotropic properties, treatment for sub-acute
transmissible spongiform encephalopathies, proposed pharmacokinetic
tests.
Leucht, Christoph;
Simoneau, Steve; Rey, Clemence; Vana, Karen; Rieger, Roman; Lasmezas, Corinne
Ida; Weiss, Stefan. The 37 kDa/67 kDa
laminin receptor is required for PrPSc propagation in scrapie-infected
neuronal cells. EMBO Reports. March 2003; 4(3):
290-295. ISSN: 1469-221X
NAL call no.: QH506.E46
Descriptors: prions, scrapie
infected, neuronal cells, infection prevention, PrPSc, laminin receptor
(LRP/LR) is necessary for PrPSc propagation in vitro, LRP/LR-specific
antibodies as possible therapeutic tools for transmissible spongiform
encephalopathies.
Lewicki, Hanna;
Tishon, Antoinette; Homann, Dirk; Mazarguil, Honore; Laval, Francoise;
Asensio, Valerie C.; Campbell, Iain L.; DeArmond, Stephen; Coon, Bryan; Teng,
Chao; Gairin, Jean Edouard; Oldstone, Michael B.A. T cells infiltrate the brain in murine
and human transmissible spongiform encephalopathies. Journal of Virology. March 2003; 77(6): 3799-3808.
ISSN:
0022-538X
NAL call no.: QR360.J6
Descriptors: CD4 and CD8 T
lymphocytes infiltrate parenchyma, mouse brains, intracerebral,
intraperitoneal, or oral inoculation, Chandler strain of mouse scrapie,
pattern compared to prion protein knockout (PrP-/-) mice, MHC class I and II
molecules, elevated levels of T-cell chemokines, macrophage inflammatory
protein 1beta, IFN-gamma-inducible protein 10, and RANTES, PrPSc in CNS
associated with chemokines.
Liu, Wing Gee; Brown,
Debbie A.; Fraser, Janet R. Immunohistochemical comparison of
anti-prion protein (PrP) antibodies in the CNS of mice infected with scrapie.
Journal of Histochemistry and
Cytochemistry. August
2003; 51(8): 1065-1071. ISSN: 0022-1554
NAL call no.: 381 J822
Descriptors: transmissible
spongiform encephalopathies, TSEs, tissue fixative affects, formol saline,
periodate lysine paraformaldehyde,
PLP, MAbs, 6H4, 7A12 and 8H4 revealed targeted PrPsc labeling, scrapie
mouse models.
Lloyd, T.; McCorriston, S.; Morgan, W.; Chern, W.S. (ed.);
Rickertsen, K. How do markets respond
to food scares? Health, Nutrition and Food
Demand. 2003; 247-270. ISBN: 0-85199-647-7
NAL call no.: 381 J8222
Descriptors: food scares, beef,
bovine spongiform encephalopathy, impact on consumer attitudes, consumer
behavior, food safety and consumer protection, economics, food consumption,
food contamination, food hygiene and safety, food-intake, market economics,
humans, UK.
Lucassen, Ralf;
Nishina, Koren; Supattapone, Surachai. In vitro
amplification of protease-resistant prion protein requires free sulfhydryl
groups. Biochemistry
NAL call no.: 381 B523
Descriptors: PrPSc, prion
misfolding, molecular mechanism of misfolding, in-vitro PrPSc amplification
techniques, scrapie infected brain homogenate, in vitro amplification with
Syrian hamster Sc237PrPSc, pH7 and CD-1 mouse RML PrPSc pH6, thiolate-specific
alkylating agent N-ethylmaleimide (NEM), reversible thiol-specific blockers
p-hydroxymercuribenzoic acid (PHMB) and mersalyl acid inhibited PrPSc
amplification.
Mabbott, Neil A.;
Young, Janice; McConnell, Irene; Bruce, Moira E. Follicular dendritic cell
dedifferentiation by treatment with an inhibitor of the lymphotoxin pathway
dramatically reduces scrapie susceptibility. Journal of Virology. June 2003
2003; 77(12): 6845-6854. ISSN:
0022-538X
NAL call no.: QR360.J6
Descriptors: transmissible
spongiform encephalopathies, TSEs, mouse scrapie animal model of disease,
dendritic cells, prion protein for replication in lymphoid tissue and
subsequest neuroinvasion, lymphotoxin beta receptor-immunoglobulin fusion
protein (LTbetaR-Ig), temporary dedifferentiation, intraperitoneal scrapie
inoculation blocked early accumulation of PrPSc in spleen, reduced disease
susceptibility, 28 and 49 days, routes of exposure, possible early
intervention.
Mainsant, P. Meat consumption before and after BSE in
France and the European Union. Sciences des Aliments. 2003; 23(1):
37-39. ISSN: 0240-8813
NAL call no.: TX341.S34
Descriptors: consumer responses, meat and meat
product consumption, bovine spongiform encephalopathies, beef cattle,
comparison study, EU.
Manuelidis, Laura. Transmissible encephalopathies:
Speculations and realities. Viral Immunology. Summer 2003;
16(2): 123-139. ISSN:
0882-8245
Descriptors: scrapie, CJD, BSE,
prion theory, review article, PrP, transmission factors, pathology, response
to infectious agent, possible viral caused disease.
Matthews, D.; Cooke,
B.C. The
potential for transmissible spongiform encephalopathies in non-ruminant
livestock and fish. Revue Scientifique et Technique Office International des Epizooties. April
2003; 22(1): 283-296. ISSN: 0253-1933
NAL call no.: SF781.R4
Descriptors: pigs, poultry,
susceptibility to BSE agent, parenteral challenge causes infection in pigs,
oral exposure to BSE-infected cattle brain, oral challenge with sheep scrapie,
chickens show resistant to oral challenge with sheep scrapie.
Matthews, D. BSE: A global update. Society for Applied Microbiology Symposium
Series. 2003; (32): 120S-125S. ISSN: 1467-4734
NAL call no.: QR1.S64
Descriptors: BSE, active
surveillance in
McCrea, D. Risk communication of the transmissible
spongiform encephalopathies. Revue Scientifique et Technique Office International des Epizooties. April
2003; 22(1): 251-257. ISSN:
0253-1933
NAL call no.: SF781.R4
Descriptors: risk communication,
public, prion disease, epidemiology, disease prevention and control,
transmission, transmissible spongiform encephalopathy, food products, food
safety, risk communication, definitions, goals.
McKintosh, Edward;
Tabrizi, Sarah J.; Collinge, John. Prion diseases. Journal of Neurovirology. April
2003; 9(2): 183-193. ISSN:
1355-0284
Descriptors: BSE, vCJD, history,
epidemiology, prion diseases, TSE, current research human prion disorders.
Miele, G.; Blanco,
A.R. Alejo; Baybutt, H.; Horvat, S.; Manson, J.; Clinton, M. Embryonic activation and developmental
expression of the murine prion protein gene. Gene Expression. 2003; 11(1):
1-12. ISSN: 1052-2166
NAL call no.: QH450.G46S
Descriptors: prion protein, PrP
mRNA expression, murine embryos and various adult tissues, expression PrP RNA
not in adult kidney and liver, investigated effected
superoxide radicalin cultured neuroblastoma and astrocyte cells, suggest that
PrPC is part of cellular antioxidant defense mechanism.
Morley, R.S.; Chen,
S.; Rheault, N. Assessment of the risk
factors related to bovine spongiform encephalopathy. Revue Scientifique et Technique Office International des Epizooties. April
2003; 22(1): 157-178. ISSN: 0253-1933
NAL call no.: SF781.R4
Descriptors: status of BSE, cattle
populations, risk assessment, surveillance criteria, International Animal
Health Code, consumption of meat-and–bone-meal (MBM) by cattle, importation of
cattle, possible contamination of MBM, livestock population structure,
rendering processes, animal feeding practices. Application
of the OIE, BSE guidelines, costs and losses with introduction and
establishment of BSE in other countries,
Nishida, Yuzo. Elucidation of endemic neurodegenerative
diseases: A commentary. Zeitschrift fuer Naturforschung Section C, Journal
of Biosciences. September-October
2003; 58 (9-10): 752-758. ISSN: 0939-5075
NAL call no.: QH301.Z4
Descriptors: scrapie, CJD, chronic
wasting disease, soil metal ion levels, copper, manganese, iron, aluminum,
cellular accumulation of metallic ions, acid rain effects on solubility,
iron-overload syndrome, hydrogen peroxide, prion isoforms, PrPc and PrPSc,
Iceland, Slovakia, Colorado.
Nishida, Noriyuki;
Sakaguchi, Suehiro; Katamine, Shigeru. Prion disease and antiprion
substance. Journal of Pharmacological
Sciences. 2003; 91(Supplement I): 48P. ISSN: 1347-8613. Note: 76th Annual Meeting of the Japanese
Pharmacological Society,
Descriptors: anti-prion substance,
Congo Red, prion disease, drug screening system, cell
culture model, histology and cytology techniques.
Nunziante, Max; Gilch,
Sabine; Schaetzl, Hermann M. Essential
role of the prion protein N terminus in subcellular trafficking and half-life
of cellular prion protein. Journal of Biological
Chemistry.
NAL call no.: 381 J824
Descriptors: prion protein life
history, biochemistry, glycosylphosphatidylinositol anchor, prion-protein
N-terminus, cellular half-life, transmissible spongiform
encephalopathies.
O'Rourke, Katherine
I.; Knowles, Donald P.; Baszler, Timothy V.; Parish, Steven
M. Methods for detection of prion protein as
an indication of transmissible spongiform encephalophathies. Official Gazette of the
NAL call no.: T223.A21
Descriptors: PrPSc, prion protein,
detection methods, diagnostic techniques. infected
live animals, postmortem detection methods, third eyelid-associated lymphoid
tissue, monoclonal antibodies, conserved epitope of PrPSc protein, fixed or
frozen tissue.
Ochel, H. J.;
Gademann, G.; Trepel, J.; Neckers, L. Modulation of prion protein structural
integrity by geldanamycin. Glycobiology. September 2003; 13(9): 655-660. ISSN: 0959-6658
NAL call no.: QP552.G59G593
Descriptors: prion protein,
transmissible spongiform encephalopathies, HSP90 inhibitors, geldanamycin or
radicicol effects, eukaryotic cells, tunicamycin, bands of western blot
analysis.
Office International
des Epizooties. Risk analysis of prion diseases in animals. Revue Scientifique et Technique Office International des
Epizooties. 2003; 22(1), 344 pp. ISSN: 0253-1933. In English, French,
and Spanish.
NAL call no.: SF781.R4
Descriptors: BSE, TSE, scrapie,
prion diseases, current and established knowledge, risk assessment, management
in different countries, diagnosis and disease prevention.
Ozawa, T.;
Lopez-Villalobos, N.; Blair, H.T. Beef
traceability systems in
NAL call no.: 49.9 N483
Descriptors: BSE, tracing systems,
farm to consumer systems, not affective in
Ozawa,Y. Risk management
of transmissible spongiform encephalopathies in
NAL call no.: SF781.R4
Descriptors: questionnaire-based
survey, distributed to the Office International des Epizooties Member
Countries in
Peelman, L.J.; van
Poucke, M. Een eerste bepaling van de
PRNP-genotypenfrequenties bij de voornaamste schapenrassen in
Belgie. [The first
determination of PRNP genotype frequency in the most important sheep breeds in
NAL call no.: 41.8 V84
Descriptors: scrapie, sheep,
selection of scrapie resistant sheep, ARR allele, sampled most breeds use in
Pennington, H. Science, governments and microbes: Food
safety in the 21st century. FEMS Congress of
European Microbiologists Abstract Book. 2003; (1): 1. Note: 1st Federation of European
Microbiological Societies (FEMS) Congress of European Microbiologists,
Descriptors: research,
governmental policies, infectious organisms, food borne pathogens, bacteria,
E. coli O157, production animals, prions, viruses, BSE.
Periago, P.M.;
Fernandez, A.; Collado, J.;
NAL call no.: TP368.F66S
Descriptors: BSE, bovine
spongiform encephalopathy, prion-disease, Weibull models, two parameter
empirical model, mathematical and computer techniques for statistical
analysis, canned food industry, kinetics, prion inactivation curves, different
temperatures under different conditions, Europe.
Polak, M.P.;
Zmudzinski, J.F.; Larska, M.; Rozek,W.; Kozaczynski,
W.; Reichert, M. Skutecznosc systemu monitorowania BSE w
Polsce na przykladzie pierwszych wykrytych przypadkow
choroby. [Efficacy of the BSE monitoring system in
NAL call no.: SF604.Z9
Descriptors: cattle, BSE, bovine
spongiform encephalopathy, case reports, disease monitoring, immunological
techniques, public health concerns,
Prendergast, D.M.;
Sheridan, J. J.; Daly, D. J.; McDowell, D.A.; Blair, I.S. Dissemination of central nervous system
tissue from the brain and spinal cord of cattle after captive bolt stunning
and carcass splitting. Meat Science.
December 2003; 65(4): 1201-1209. ISSN:
0309-1740
NAL call no.: TX373.M4
Descriptors: BSE, cattle, measures
to exclude specified risk materials from human food chain, CNS tissue
dissemination, slaughter practices, captive bolt stunning, carcass splitting,
CNS material contamination of meat.
Polak, Miroslaw P.;
Larska,
NAL call no.: 41.8 M463
Descriptors: cattle, BSE, rapid
diagnostic test comparison, screening methods and techniques, sensitivity,
specificity, limiting detectable levels, PrPSc, prions, Scientific Steering
Committee of the European Commission, post-mortem testing.
Purdey, Mark. Does an infrasonic acoustic shock wave
resonance of the manganese 3+ loaded/copper depleted prion protein initiate
the pathogenesis of TSE? Medical Hypotheses. June 2003; 60(6): 797-820. ISSN: 0306-9877
Descriptors: copper, Cu, Mn3+,
hyper-polarization, paramagnetic-status, piezoelectric atomic structure,
cupro-protein expression, transmissible spongiform encephalopathy, prion
diseases, UV radiation, acoustic radiation, circadian auditory pathway,
electromagnetic superexchange, electron phonon coupling, endogenous
electromagnetic energy, geomagnetic radiation, infrasound rich environment,
tetonic disturbances, supersonic airplanes, ratios of high MN/low copper and
low zinc of mammals brains, 2 stage TSE pathogenesis initiated when MN
substitutes for vacant Cu domain on PrPC (sleeping) when infrasonic shock the
atomic structure of Mn3+ starts the distortion of the protein, Cu prions
replaced by hyperpolarized Mn 3+ prions, self perpetuating 'cluster bombs' of
free radical mediated neurodegeneration.
Rachidi, Walid; Mange,
Alain; Senator, Abderrahmene; Guiraud, Pascale; Riondel, Jacqueline;
Benboubetra, Mustapha; Favier, Alain; Lehmann, Sylvain. Prion infection impairs copper binding
of cultured cells. Journal of Biological
Chemistry.
NAL call no.: 381.J824
Descriptors: TSE, molecular
mechanism of neurogeneration, 64CU, radioactive copper, prion infected cells,
reduction in copper binding, prion infection modulates copper content at a
cellular level, modification of copper homeostasis has determinant role in
neuropathology.
Richard, Marlene;
Biacabe, Anne Gaelle; Streichenberger, Nathalie; Ironside, James West; Mohr,
Michel; Kopp, Nicolas; Perret, Liaudet Armand. Immunohistochemical localization of
14.3.3 zeta protein in amyloid plaques in human spongiform
encephalopathies.
Acta
Neuropathologica. March 2003; 105(3): 296-302. ISSN: 0001-6322
Descriptors: MV2 CJD, kuru,
VV2cjd, vCJD, Gerstmann-Straussler-Scheinker, Alzheimer, paraffin-embedded
brain section, different subtypes of brain amyloid plaques, comparison of
PrPSc and 14.3.3 zeta deposits presence, data suggests, 14.3.3 zeta protein
could interact with PrP, other components of PrPSc deposites in CJD,
immunostaining.
Rico, Andre. Prion: Toxic or infectious agent?
Medical Hypotheses. February 2003; 60(2): 209-214. ISSN: 0306-9877
Descriptors: TSE, caused by
deficiency of chemo-defense system (CDS), unable to destroy or eliminate
PrPsc, immune defense system (IDS) accommodates PrPsc as an inert particle
that is moved through lymphoreticular system, PrPSc acts as cellular toxic
disruptor of post-translational phase of PrP biosynthesis.
Ridley, Rosalind M. What would T. H. Huxley have made of
prion diseases? Molecular Biotechnology. July
2003; 24(3): 243-256. ISSN:
1073-6085
NAL call no.: TP248.13.M65
Descriptors: speculating on T.H.
Huxle’s thoughts regarding transmissible spongiform encephalopathies,
scientific debate over prion hypotheses.
Roels, Stefan L.M. F.;
De Meyer, Gaelle; Tedik, Kamile; Foubert, Raphael; Vanopdenbosch,
Emmanuel. Variation of mass (volume) taken with the
calibrated syringe and of the results provided by the Bio-Rad PlateliaTM BSE
test upon storage of brainstem samples at -20degrees C. Animal Research. November-December 2002(2003); 51(6):
493-499. ISSN: 1627-3583
Descriptors: suspected BSE
brainstem material, sampling with a kit calibrated syringe, quick PlateliaTM
test from Bio-Rad, decrease in optical density after 1 week cold storage,
density change did not affect diagnosis of BSE.
Rudyk, Helene; Knaggs,
Michael H.; Vasiljevic, Snezana; Hope, James; Birkett, Chris; Gilbert, Ian H.
Synthesis and evaluation of analogues
of congo red as potential compounds against transmissible spongiform
encephalopathies. European Journal of Medicinal
Chemistry. June 2003;
38(6): 567-579. ISSN: 0223-5234
Descriptors: anti-TSE compounds,
analogues, Congo red 4, 6, 8, diazonium salts, symmetrical bis azoic dyes 14-19,
21-22, 24 and 26-29 as their sodium salts, molecular modeling, potential
structure activity relationships.
NAL call no.: SF604.J342
Descriptors: deer, elk, chronic
wasting disease, CWD, disease history, pathogenesis, susceptibility of
animals, transmission, potential origins, diagnostic methods, control
strategies, economic impact, food and food safety, public health risks,
infectivity to humans, North America.
Schreuder, B.E.C.;
Somerville, R.A. Bovine spongiform
encephalopathy in sheep?
Revue Scientifique et Technique Office
International des Epizooties. April 2003; 22(1): 103-120. ISSN: 0253-1933 ISSN: 0253-1933
NAL call no.: SF781.R4
Descriptors: BSE infected sheep
hypothetical, risk management and pre-emptive measures, experimental BSE in
sheep, differentiating BSE and scrapie in same host, classical strain typing
in a mouse model.
Sellier, P. Protein nutrition for ruminants in
European countries, in the light of animal feeding regulations linked to
bovine spongiform encephalopathy. Revue Scientifique et Technique Office International des Epizooties. April
2003; 22(1): 259-269. ISSN: 0253-1933
NAL call no.: SF781.R4
Descriptors: BSE, protein in
production animal diets, new sources of protein, minerals and lipids in animal
diets, manufactured concentrates, vegetals as feed source alternatives, feed
regulations, implementation and management, Europe, World.
Simoneau, Steve; Haik,
Stephane; Leucht, Christoph; Dormont, Dominique; Deslys, Jean Philippe; Weiss,
Stefan; Lasmezas, Corinne. Different
isoforms of the non-integrin laminin receptor are present in mouse brain and
bind PrP. Biological
Chemistry. February
2003; 384(2): 243-246. ISSN:
1431-6730
NAL call no.: QP501.B56
Descriptors: prion protein, mouse
brain fractions, laminin receptor, isoforms interaction with prion protein,
physiological role, laminin receptor/PrP interaction in the brain, relevance
for transmissible spongiform encephalopathies.
Smith, Peter G.;
Bradley, Ray. Bovine spongiform encephalopathy (BSE)
and its epidemiology. British Medical Bulletin. 2003; 66: 185-198. ISSN: 0007-1420
Descriptors: BSE, cattle, food
safety, sheep, humans, processed animal waste, prion diseases, epidemiology,
Smith, Peter G. The epidemics of bovine spongiform
encephalopathy and variant Creutzfeldt-Jakob disease: Current status and
future prospects. Bulletin of the World
Health Organization. 2003; 81(2): 123-130. ISSN: 0042-9686
NAL call no.: 449.9 W892B
Descriptors: BSE, epidemic,
Europe, UK, control measures, EU, Switzerland, testing post mortem, tests for
live animals needed, risks small and diminishing in Europe, 150 diagnosed with
vCJD, control of iatrogenic transmission via blood transfusion or contaminated
surgical instruments, new tests, decontamination methods needed.
Speare, Jonathan O.;
Rush, Thomas S. III; Bloom, Marshall E.; Caughey, Byron. The
role of helix 1 aspartates and salt bridges in the stability and conversion of
prion protein. Journal of Biological
Chemistry.
NAL call no.: 381.J824
Descriptors: pathogenesis, transmissible spongiform
encephalopathies, conversion of PrPsen to PrPres, constructed mutants of
hamster prion protein, replacing aspartic acids, salt bridges, cell-free
conversion data, Asp-144 and Asp-147 and the respective salt bridges stabilize
PrPsen from converting to PrPres.
Stoltze, L.; Rezaei,
H.; Jung, G.; Grosclaude, J.; Debey, P.; Schild, H.; Rammensee, H.G. CD4+ T cell-mediated immunity against
prion proteins. CMLS—Cellular and Molecular
Life Sciences. March 2003; 60(3): 629-638. ISSN: 1420-682X
NAL call no.: QH301.C45
Descriptors: prion protein, amino
sequences of PrP, differences in amino acid sequence, presentation of distinct
peptides on major histo-compatibility complex class II molecules, activation
of specific CD4+ T cells, effective immune response against foreign PrP,
antibody production, distinguish self and foreign.
Tahiri, Alaoui
Abdessamad; Bouchard, Mario; Zurdo, Jesus; James, William. Competing intrachain interactions
regulate the formation of beta-sheet fibrils in bovine PrP peptides. Protein Science. March 2003;
12(3): 600-608. ISSN:
0961-8368
NAL call no.: QD431.A1P78
Descriptors: bovine prion protein
biochemistry, pathogenesis of TSE, PrPC helix converted to aberrant
beta-sheet-dominated form (PrPSc), peptide analysis. Native PrPC helix 1 might inhibit the
strong intrinsic beta-sheet-forming propensity of sequences immediately
N-terminal to the globular core of PrPC, by keeping in place intrachain
interactions that would prevent these amyloidogenic regions from triggering
aggregation.
NAL call no.: SF781.R4
Descriptors: BSE, scrapie, meat
and bone meal, rendering of infected animal tissues, safety of tallow and
tallow by-products, relationship between BSE and variant Creutzfeldt-Jakob
disease, vCJD, UK.
Terry,
NAL call no.: 41.8 V641
Descriptors: BSE, cattle, distal
ileum, PrPSc, mesemteric lymph nodes, experimental orally dosed animals,
naturally occurring clinical cases, Peyer’s patches, differences,
immunohistochemistry, macrophages.
Thackray, Alana M.;
Madec, Jean Yves; Wong,
NAL call no.: QP 501.B64
Descriptors: BSE, scrapie, prion
proteins, monoclonal antibodies for copper-refolded PrP, diagnosis of normal
and abnormal forms of protein, disease-susceptible allelic form V136R154Q171
('VRQ'; where single-letter amino-acid notation has been used) and
disease-resistant allelic form A136R154R171 ('ARR') of recombinant ovine PrPc,
reaction unglycosylated and monoglycosylated forms of PrPSc from
prion-infected tissue samples, different species tested by Western blot,
distinquished between bovine
spongiform encephalopathy & scrapie PrPSc from experimentally infected
sheep due to different electrophoretic mobilities.
Thomzig, Achim;
Kratzel, Christine; Lenz, Gudrun; Krueger, Dominique; Beekes,
Michael. Widespread PrPSc accumulation in muscles
of hamsters orally infected with scrapie. EMBO Reports. May 2003; 4 (5):
530-533. ISSN: 1469-221X
NAL call no.: QH506.E46
Descriptors: hamsters, animal
model of disease, scrapie, BSE, chronic wasting disease, TSE, spongiform
encephalopathies, prion proteins, PrPSc, western blotting, skeletal muscle
levels, forelimb, hindlimb, head, back, shoulder, tongue, peripheral routing
of infection, question whether muscles contain the infectious agent.
Travis, Dominic;
Miller, Michele. A short review of transmissible
spongiform encephalopathies, and guidelines for managing risks associated with
chronic wasting disease in captive cervids in zoos. Journal of Zoo and Wildlife
Medicine. June 2003; 34 (2): 125-133. ISSN: 1042-7260
NAL call no.: SF601.J6
Descriptors: prion diseases,
transmissible spongiform encephalopathies, TSE, scrapie, kuru, variant
Creutzfeld-Jakob disease, review article, zoo and wildlife veterinarians,
wildlife biologists, chronic wasting disease, cervids, risk management
strategies, disease prevention.
Trevitt, Clare R.;
Singh, Pramil N. Variant
Creutzfeldt-Jakob disease: Pathology, epidemiology, and public health
implications. American Journal of
Clinical Nutrition. September 2003; 78(3 Supplement): 651S-656S.
ISSN: 0002-9165
NAL call no.: 389.8 J824
Descriptors: BSE, vCJD,
transmissible spongiform encephalopathies, cattle, sheep, scrapie, prion
diseases, review, outline public health implications, data, emphasizing
preventative measures, areas of research for screening and
diagnosis.
Van Gelderen, C.;
Gimeno, E.J.; Schudel, A.A. Bovine
spongiform encegphalopathy in
NAL call no.: SF781.R4
Descriptors: bovine spongiform
encephalopathy, BSE, cattle, prion diseases, disease prevention, safeguarding
animal health, preventative action adopted in 1989, region is free of BSE, South American programs, harmonizing
BSE prevention programs, maintenance of disease free status.
Watt, Nicole T.;
Hooper, Nigel M. The
prion protein and neuronal zinc homeostasis. Trends in Biochemical
Sciences. August 2003; 28(8): 406-410. ISSN: 0968-0004
NAL call no.: QH345.T73
Descriptors: prion protein, PrP,
transmissible spongiform encephalopathies, TSE, binding of metal ions, protein
role may be in zinc concentration management, effects of conformation change.
Weiss, D. Beef is back? Rindfleischmarkt auf niedrigerem Niveau stabilisiert. [Beef is back? Stabilization of the beef market at a lower level.] May. 2003; 31(1): 25-27. ISSN: 0341-5155. In German.
Descriptors: cattle, beef bulls,
level of veal and beef consumption, BSE crisis, producer prices, European
Countries,
Wells, Gerald A.H.;
Hawkins, Stephen A. C.; Austin, Anthony R.; Ryder, Stephen J.; Done, Stanley
H.; Green, Robert B.; Dexter, Ian; Dawson, Midchael; Kimberlin, Richard H. Studies of the transmissibility of the
agent of bovine spongiform encephalopathy to pigs. Journal of General
Virology. April 2003;
84(4): 1021-1031. ISSN: 0022-1317
NAL call no.: QR360.A1J6
Descriptors: BSE, transmissibility
to pigs, parenteral inoculation via intracranial, intravenous, and
intraperitoneal routes, incubation period of 69-150 weeks, infectivity
testing, bioassay in inbred mice, infectivity found in pig’s stomach, jejunum,
distal ileum, pancreas, CNS, orally exposed animals not infected.
Wichert von Holten,
S. Psychosoziale Belastungen der
Menschen bei Massentoetungen von Nutztieren. [Psycho-social
stress in humans at mass slaughter of farm animals.] DTW Deutsche Tieraerztliche
Wochenschrift. May
2003; 110(5): 196-199. ISSN:
0341-6593. In German.
NAL call no.: 41.8 D482
Descriptors: veterinarians,
concerned people, slaughter teams, mass slaughter, contaminated animals, BSE,
MKS epidemics, emotional consequences, pastoral care task force service,
crisis and stress, Lower Saxony.
Williams, E.S.;
Miller, M. W. Transmissible spongiform
[encepiharopathies] (encephalopathies) in
non-domestic animals: Origin, transmission and risk factors. Revue Scientifique et Technique Office International des Epizooties. April
2003; 22(1): 145-156. ISSN: 0253-1933
NAL call no.: SF781.R4
Descriptors: transmissible
spongiform encephalopathies, TSE, scrapie, bovine spongiform encephalopathy,
BSE, transmissible mink encephalopathy, chronic wasting disease, deer, elk,
oral transmission, impact on free ranging cervids, captive animal feed stuffs
as sources, recommended surveillance of domestic and wild, infectious
agent.
Descriptors: TSE theory, prion
proteins, nerve regeneration and repair, prions modulate tryosine kinase
activation, abnormal prion isoforms, damaged and release fragments of prion
PrP106-126, stimulate release of nerve growth factor, which activates tyrosine
kinase once more, setting up the vicious spiral of slow neurodegeneration
found in transmissible spongiform encephalopathies.
Ye, X; Carp, R.I.;
Meeker, H.C.; Scallet, A.C.
Identification and detection of transmissible spongiform encephalopathies.
Current Medicinal Chemistry, Immunology,
Endocrine, and Metabolic Agents. June 2003; 3(2): 95-111. ISSN: 1568-0134
Descriptors: TSE, sheep, goats,
scrapie, prion disease, ELISA, Western blot, brain biopsy.
Abiola, Oduola O.; Iyegbe, Conrad; Lantos, Peter; Plomin, Robert; Anderton,
Brian H.; Whatley, Stephen A. Profound
sex-specific effects on incubation times for transmission of bovine spongiform
encephalopathy to mice. Intervirology. 2002; 45(1): 56-8 ISSN:
0300-5526.
Abstract: Four strains of mice were inoculated
intracerebrally with a primary isolate of bovine spongiform encephalopathy
(BSE) and the cloned mouse-adapted scrapie strain ME7. Clinical prion disease
diagnosis was made at the appearance of three or more neurological symptoms
and their persistence for 3 consecutive weeks and confirmed by
neuropathological criteria. For BSE, incubation periods were profoundly
different between the sexes in all four mouse strains, being longer in the
females. In contrast, ME7 scrapie incubation times were similar between the
sexes. Our results indicate that sex-specific processes are involved in the
course of primary BSE transmission. Research into this phenomenon may provide
clues to the prophylaxis of BSE and have possible implications for new variant
Creutzfeldt-Jakob disease in humans.
NAL call no.
QR355.I5
Descriptors: BSE, scrapie strain ME7, 4 strains of mouse
models, inbred C57BL, inbred DBA; experimental infections, brain inoculation,
sex differences, NvCreutzfeldt-Jakob Disease, prion physiology.
Agerholm, J. S.; Tegtmeier, C. L.; Nielsen, T. K. Survey of laboratory findings in suspected cases of
bovine spongiform encephalopathy in Denmark from 1990 to 2000.
APMIS, Acta Pathologica, Microbiologica, et Immunologica
Scandinavica 2002 Jan; 110(1): 54-60 ISSN: 0903-4641.
Abstract:
A survey of the laboratory findings in suspected cases of bovine spongiform
encephalopathy (BSE) in Denmark from 1 June 1990 to 31 December 2000 is
presented. During this period BSE was a notifiable disease, and the heads of
suspected cases were submitted according to the legislation on BSE. A total of
176 submissions were made, mostly from bovines with neurological disorders and
mainly during the last 3 years of this period. Lesions or other laboratory
findings consistent with severe neurological disorders were found in 115
cases. The most frequent diagnosis was encephalic listeriosis (35.8% of
submissions) followed by other forms of inflammatory lesions. A wide range of
lesions were diagnosed less prevalent. BSE was diagnosed twice. The first case
occurred in an imported cow in 1992, while the second confirmed case was
diagnosed in a native cow in February 2000. A marked increase in the number of
submissions occurred following the detection of BSE in February 2000.
NAL
call no. QR1.A6
Descriptors: cattle, BSE, checking bovines
exhibiting neurological disorders, Denmark.
Aguzzi, Adriano. Die Prion-Hypothese und
Prionen-Krankheiten des Menschen. [The prion hypothesis and the human
prion diseases]. Berliner und Munchener Tierarztliche Wochenschrift
2002 Mar-Apr; 115(3-4): 91-8 ISSN: 0005-9366. In German.
Abstract:
Our understanding of the pathogenesis of the transmissible spongiform
encephalopathies (TSE) has made terrific headway over the past 40 years and
some scientists are even of the opinion that this group of diseases belongs to
the neurodegenerative syndromes best understood. On the other hand, the
investigation of TSE has led to a multitude of unexpected and surprising
results and consequently has initiated impassioned discussions among
scientists. Although the human forms of TSE are very rare, the wildfire-like
spread of the bovine spongiform encephalopathy (BSE) raises the pressing
question as to whether BSE is communicable to humans. This overview summarizes
some current hypotheses about the nature of the infectious agent and about the
pathogenesis of the damage of the central nervous system.
NAL call no. 41.8
B45
Descriptors: pathogenesis, transmissible spongiform
encephalopathies, BSE, infectous agent, prion diseases, cattle, humans.
Alperovitch, Annick; Will, Robert G. Predicting the size of the vCJD epidemic in France.
Comptes Rendus Biologies. Janvier, 2002; 325 (1):
33-36.
DOI: 10.1016/S1631-0691(02)01410-5
NAL
call no. Q2 C6
Descriptors: NvCJD, Creutzfeldt-Jakob disease, BSE,
France, France/UK ratios of disease, exposure to high risk foods,
epidemiology.
Anand, P. Public health. Decision-making
when science is ambiguous. Science. 2002 Mar 8; 295(5561): 1839.
ISSN: 1095-9203.
NAL call no. 470 SCI2
Descriptors: BSE, bovine
spongiform encephalopathy, prevention and control, public health, disease
transmission, policy making, probability.
Anonymous. Embryo transfer and BSE.
Veterinary Record. London : The British Veterinary Association.
Mar 23, 2002. v. 150 (12) p. 357. ISSN: 0042-4900.
NAL call no. 41.8
V641
Descriptors: cattle, embryo transfer, BSE, bovine spongiform
encephalopathy, disease transmission, UK.
Anonymous. Harvard study finds BSE poses
little threat to U.S. consumers, agriculture. Journal of the
American Veterinary Medical Association. 2002 Feb 1; 220(3): 279-80. ISSN:
0003-1488.
NAL call no. 41.8 AM3
Descriptors: animal feed
standards, BSE, bovine spongiform encephalopathy, prevention and control, US
laws.
Aucouturier, Pierre. Dendritic cells and
prion propagation. The Scientific World Journal [online] Feb,
2002; 1 (Cited April 4, 2002): 38-40.
Descriptors: prion protein,
movement of protein from the intestinal system, dendretic cells, lymph system.
Aupperle, H.; Lucker, E.; Overhoff, M.; Schoon, H. A. Verfahren zum Nachweis von im Hinblick auf die BSE
unerwunschten Zutaten in Fleischerzeugnissen: 6. Immunhistologischer Nachweis
von zentralem und peripherem Nervengewebe in Fleischerzeugnissen.
[Procedures for the unwanted ingredients in meat products with regard
to BSE: immunohistochemical procedures for the detection of central and
periphere nervous tissue in meat products.] Fleischwirtschaft. 2002.,
82: 3, 100-104; 27 Ref. In German with an English summary.
NAL call no.
280.38 F62
Descriptors: BSE, bovine spongiform encephalopathy,
diagnostic techniques, CNS tissue in muscle tissue, food safety, prevention,
quality control.
Balen, Adam. Is there a risk of prion
disease after the administration of urinary-derived gonadotrophins?
Human Reproduction. Oxford. July, 2002; 17 (7): 1676-1680.
DOI: 10.1093/humrep/17.7.1676-a/
NAL
call no. QP251 H85
Descriptors: prion protein, scrapie, bovine
spongiform encephalopathy, BSE, Creutzfeldt Jakob disease, CJD, contaminated
urine in pharmaceuticals, bovine serum.
Balter, Michael BSE in sheep? Humiliated
lab fights to save face. Science. 2002 Feb 1; 295(5556): 792-3
ISSN: 1095-9203
NAL call no. 470 SCI2
Descriptors: brains, sheep,
bovine spongiform encephalopathy, cattle, specimen handling, Scotland.
Barclay, G. Robin; Houston, E. Fiona; Halliday, Sue I.; Farquhar, Christine
F.; Turner, Marc L. Comparative analysis of
normal prion protein expression on human, rodent, and ruminant blood cells by
using a panel of prion antibodies. Transfusion. 2002 May; 42(5):
517-26. ISSN: 0041-1132.
Abstract: BACKGROUND: It is not known
whether variant CJD can be transmitted within the human population by blood
transfusion. The expression of normal cellular prion protein (PrPC) by
different blood cell types may permit selective uptake and dissemination of
infectivity. STUDY DESIGN AND METHODS: The normal distribution of PrPC on the
major blood cell types of species known to be susceptible to natural or
experimental transmissible spongiform encephalopathies was studied. Blood from
healthy humans, mice, hamsters, cattle, and sheep was examined by flow
cytometry by using a large panel of antibodies with different prion protein
(PrP) epitope specificities to maximize the detection of PrP variants across
species and cell type. RESULTS: PrP was detected on all major human blood
cells types except eosinophils, but was not detected as ubiquitously or
uniformly on major blood cell types of different animal species. CONCLUSION:
Different animal species have unique patterns of expression of PrPC on blood
cell types, with none equivalent to the human pattern. This needs to be
considered when extrapolating from animal models of blood-borne transmissible
spongiform encephalopathy infectivity, particularly in regard to the risk
assessment of potential variant CJD spread within the human population. The
relationship between PrP distribution and infectivity distribution in blood
needs further investigation.
Descriptors: NvCreuzfeldt-Jakob
Disease, prion protein, major blood cells types, humans, C57BL mice hamsters,
cattle, sheep, detection of PrP variants, comparison of human results to
animals models.
Barnicle, D.A. Analysis by Western
immunoblotting of differential enzymatic digestion of PrPSc to determine
strain of agent. Research in Veterinary Science. April, 2002; 72
(Supplement A): 47. 56th Annual Conference of the Association of Veterinary
Teachers and Research Workers on Current Topics in Veterinary Science,
Scarborough, England, UK, March 25-27, 2002.
NAL call no. 41.8
R312
Descriptors: prion protein, PrPSc, strain typing, Western blot
analysis.
Baron, Thierry. Identification of
inter-species transmission of prion strains. Journal of
Neuropathology and Experimental Neurology. 2002 May; 61(5): 377-83 ISSN:
0022-3069
Journal URL: http://www.jneuropath.com/pt/re/jnen/home.htm/
Abstract:
The concern of the potential transmission of animal spongiform
encephalopathies to humans, which arose as soon as the interspecies
transmission of these diseases was recognized, has been reinforced with the
emergence of bovine spongiform encephalopathy (BSE) in cattle. Recent
experimental findings suggest that the infectious agent causing BSE in cattle
can lead to the occurrence of a new form of Creutzfeldt-Jakob disease in
humans. These findings help us understand how the transmission to humans of an
animal disease may be recognized. This can involve an indirect approach
through the analysis of neurodegeneration, either in the disease host, or more
specifically, in genetically well-defined experimental hosts to which the
disease can be transmitted. Recent experimental studies have also shown that
the different molecular features of the abnormal form of the prion protein,
which accumulates in the infected tissues, can provide important clues to the
relationships between different spongiform encephalopathies. However, a better
understanding of the molecular features associated with the specific
pathogenic behavior of different strains is required. Complex relationships
between the infectious agents involved in spongiform encephalopathies and the
disease host can make the recognition of a link between animal prion strains
and the human disease difficult to establish.
Descriptors: cattle,
bovine spongiform encephalopathy, prion proteins, molecular features, specific
pathogenic behavior of different strains.
Beekes, M.; Kurth, R. BSE und
Creutzfeldt-Jakob-Krankheit - Gesundheitspolitische Bedeutung fur die
Bundesrepublik Deutschland und Europa. [BSE and Creutzfeldt-Jakob
disease. Implication on health politics in Germany and Europe]. Deutsche
Medizinische Wochenschrift 2002 Feb 15; 127(7): 335-40. ISSN: 0012-0472.
In German
NAL call no. 448.8 D48
Descriptors: bovine spongiform
encephalopathy, prevention, control, epidemiology, transmission, cats, cattle,
sheep, Belgium, Germany, France, Europe, meat contamination.
Behrens, Axel; Aguzzi, Adriano. Small is
not beautiful: Antagonizing functions for the prion protein PrPC and its
homologue Dpl. Trends in Neurosciences. March, 2002; 25 (3):
150-154.
DOI: 10.1016/S0166-2236(00)02089-0
NAL
call no. RC321 T74
Descriptors: prion conformation variant, doppel
protein, homology with PrPC, Dpl is dispensable for prion disease progression,
prion biology.
Biedermann, Wolfgang; Lucker, Ernst; Hensel, Andreas. Detection of tissues of the central nervous system
(CNS) as specified risk material (SRM) in meat products by means of gas
chromatography-mass spectrometry (GC-MS). Berliner und Munchener
Tierarztliche Wochenschrift 2002 Mar-Apr; 115(3-4): 131-3 ISSN: 0005-9366
Abstract: Determination of specified risk material (SRM) in
processed meat products was performed by quantification of brain specific
fatty acids using gas chromatography-mass spectrometry (GC-MS). Results from
SMP (internal standardised meat products) based analyses showed that absolute
concentrations of CNS are correlated (r2 = > 0.97) with the contents of the
CNS typical fatty acids docosahexaenoic acid (C 22:6), nervonic acid (C 24:1),
lignoceric acid (C 24) and cerebronic acid (C 24oh). GC-MS detection limits
were measured at 0.01% CNS. The cut off value was calculated at 0.39% (w/w)
CNS in SMP. In a controlled blindfold experiment we were able to identify
correctly all positive and negative SMP samples, respectively. Our results
indicate that GC-MS based SRM detection may serve as a reference method for
immunochemical and immunohistochemical determination of SRM in processed meat
products.
NAL call no. 41.8 B45
Descriptors: neural tissue
contamination, meat products analysis, immunochemical and immunohistochemical
determination.
Biffiger, Karin; Zwald, Daniel; Kaufmann, Lukas; Briner, Alexandra; Nayki,
Inci; Purro, Mario; Bottcher, Sigrid; Struckmeyer, Thomas; Schaller, Olivier;
Meyer, Rudolf; Fatzer, Rosemarie; Zurbriggen, Andres; Stack, Mick; Moser,
Markus; Oesch, Bruno; Kubler, Eric. Validation
of a luminescence immunoassay for the detection of PrP(Sc) in brain
homogenate. Journal of Virological Methods. 2002 Mar;
101(1-2): 79-84. ISSN: 0166-0934.
Abstract: A luminescence
immunoassay (LIA) was developed for the diagnosis of bovine spongiform
encephalopathy (BSE) in brain tissue using two different monoclonal antibodies
for capture and detection of the protease-resistant fragment of the
pathological prion protein (PrP27-30). PrP27-30 currently represents the most
reliable marker for the infectious particle (denominated prion) causing
transmissible spongiform encephalopathies (TSEs). Internal and official
validation studies of this assay are described using brain homogenates from
ascertained BSE positive and negative cows. Using more than 300 positive and
1400 negative bovine or ovine samples, an excellent sensitivity and
specificity of 100% were demonstrated. More than 1000-fold dilutions of a BSE
positive homogenate still resulted in a clear positive signal. In combination
with a simple homogenisation procedure for the preparation of the samples,
this assay lends itself for large scale screening of cattle and sheep for TSEs
using complete automation of the process.
NAL call no.
QR355.J6
Descriptors: BSE, brain tissue analysis, cattle, diagnostic
test, luminescense immunoassay, brain homogenates, screening of cattle and
sheep for transmissible spongiform encephalopathies.
Bingham, Brian. New variant CJD-BSE (mad
cow disease). The need for disposable ENT instruments.
International Journal of Pediatric Otorhinolaryngology. 2002 Feb 25;
62(3): 203-6. ISSN: 0165-5876.
Abstract: This paper outlines the
development of Bovine Spongiform Encephalopathy (BSE) in the United Kingdom.
The relationship between BSE and new variant Creutzfeldt-Jakob disease (vCJD)
is considered and the risks of iatrogenic spread reviewed. The rationale for
disposable surgical instruments in adenotonsillectomy to prevent iatrogenic
spread is discussed.
Descriptors: BSE, bovine spongiform
encephalopathy, iatrogenic spread, surgical instruments, risks of
transmission, UK.
Blattler, Thomas. Transmission of prion
disease. APMIS. Acta Pathologica, Microbiologica, et Immunologica
Scandinavica. 2002 Jan; 110(1): 71-8. ISSN: 0903-4641
Abstract:
The transmission of bovine spongiform encephalopathy to humans as variant
Creutzfeldt-Jakob disease (vCJD) has focused public attention on how prion
diseases are transmitted and how prions reach the brain after exposure. Prion
diseases are characterised by transmissibility and neuropathological features
of gliosis, neuronal loss and microscopic vacuoles, termed spongiosis. The
principal component of prions is the glycoprotein PrP(Sc), which is a
conformational modified isoform of the normal membrane protein PrP(C). How are
prions transmitted and how do prions find their way once they have been
ingested? Prion models in mouse and hamster point to lymphoreticular cells
which support an early replication phase of prions before reaching the central
nervous system via peripheral nerves. Whilst some key players seem to have
been identified so far, the mechanisms of prion propagation to the brain are
still not fully understood. Seemingly contradictory results have led to some
confusion and have provoked discussion.
NAL call no.
QR1.A6
Descriptors: BSE, spongiform encephalopathies, transmission,
Nv Creutzfeldt-Jakob Disease, path to brain after exposure, mouse and hamster
animal models, pmyphoreticular cells, peripheral nerve pathway, discussion of
mechanism of prion propagation.
Bons, Noelle; Lehmann, Sylvain; Mestre, Frances-Nadine; Dormont, Dominique;
Brown, Paul Brain and buffy coat transmission
of bovine spongiform encephalopathy to the primate Microcebus murinus.
Transfusion. May, 2002; 42 (5): 513-516.
Descriptors: BSE,
NvCreutzfeldt-Jacob Disease, secondary transmission, blood and blood products,
macaque monkeys, Microcebus murinus, challenged with brain homogenate and
buffy coat, transmission of infection.
Bons, Noelle; Lehmann, Sylvain; Nishida, Noriyuki; Mestre, Frances Nadine;
Dormont, Dominique; Belli, Patrick; Delacourte, Andre; Grassi, Jacques; Brown,
Paul. BSE infection of the small short-lived
primate Microcebus murinus. Comptes Rendus Biologies. Janvier,
2002; 325 (1): 67-74.
DOI: 10.1016/S1631-0691(02)01390-2
NAL
call no: Q2 C6
Descriptors: Microcebus murinus (lemur) primates,
disease susceptibility, intracerebrally/orally infected prion proteins, BSE
/macaque-adapted BSE brain inoculates, hyperaggregated and paired-helical
filaments-immunoreactive Tan proteins, beta42-amyloid plaques and
astrogliosis, PrPres.
Boratynski, J.; Gorski, A. BSE: A
consequence of cattle feeding with glycated molecules host-unknown?
Medical Hypotheses. April, 2002; 58 (4):
276-278.
Descriptors: pathogenesis, BSE, transmissible spongiform
encephalopathies, scrapie, sheep, goats, cattle, disease origins, glycated
proteins in feeds, high temperature glycation process.
Borchers, Kerstin. Transmissible
Spongiforme Enzephalopathien (TSE): Alte Krankheiten mit neuer Brisanz.
[Transmissible spongiform encephalopathies (TSE): old diseases with new
explosive force]. Berliner und Munchener Tierarztliche Wochenschrift
2002 Mar-Apr; 115(3-4): 81-90 ISSN: 0005-9366. In German.
Abstract:
In view of the first 64 BSE cases (date: 11.5.01) in German cattle herds an
overview on TSE and their similarities and differences regarding clinic,
pathogenesis and pathology is given. The mechanism of the unconventional
agent, an infectious protein (prion), is explained based on the prion model of
Stanley Prusiner. The knowledge on transmission, incubation time, host
specificity as well as resistance and immunity drawn from experimentally
infected animals is discussed. Thus, after oral infection prions are
transported by lymphocytes from the stomach-intestinal tract to the spleen.
The way to the CNS is still unknown. The presumption for crossing the species
barrier is twofold: first the prions of different species have to be
biochemically homologous and a genetical disposition has to exist. This is the
case for BSE and the new variant of Creutzfeldt-Jakob-Disease (vCJD). There is
evidence that in Great Britain so far 97 (date: 30.3.01) young people acquired
vCJD due to consumption of food that contained bovine risk material. Regarding
the infectious prion dosis brain, spinal cord and lymphoid tissues are
regarded to be most dangerous. The principle of the BSE-test, its evidence as
well as steps for prevention and control of BSE are presented.
NAL call no.
41.8 B45
Descriptors: cattle, transmissible spongiform
encephalopathies, comparisons, pathogenesis, pathology, prion proteins,
incubation time, immunity, vCreutzfeldt-Jakob Disease, Germany.
Bosque, Patrick J.; Ryou, Chongsuk; Telling, Glenn; Peretz, David; Legname,
Giuseppe; DeArmond, Stephen J.; Prusiner, Stanley B. Prions in skeletal muscle. Proceedings of
the National Academy of Sciences of the United States of America. 2002 Mar
19; 99(6): 3812-7. ISSN: 0027-8424.
Abstract: Considerable evidence
argues that consumption of beef products from cattle infected with bovine
spongiform encephalopathy (BSE) prions causes new variant Creutzfeldt-Jakob
disease. In an effort to prevent new variant Creutzfeldt-Jakob disease,
certain "specified offals," including neural and lymphatic tissues, thought to
contain high titers of prions have been excluded from foods destined for human
consumption [Phillips, N. A., Bridgeman, J. & Ferguson-Smith, M. (2000) in
The BSE Inquiry (Stationery Office, London), Vol. 6, pp. 413-451]. Here we
report that mouse skeletal muscle can propagate prions and accumulate
substantial titers of these pathogens. We found both high prion titers and the
disease-causing isoform of the prion protein (PrP(Sc)) in the skeletal muscle
of wild-type mice inoculated with either the Me7 or Rocky Mountain Laboratory
strain of murine prions. Particular muscles accumulated distinct levels of
PrP(Sc), with the highest levels observed in muscle from the hind limb. To
determine whether prions are produced or merely accumulate intramuscularly, we
established transgenic mice expressing either mouse or Syrian hamster PrP
exclusively in muscle. Inoculating these mice intramuscularly with prions
resulted in the formation of high titers of nascent prions in muscle. In
contrast, inoculating mice in which PrP expression was targeted to hepatocytes
resulted in low prion titers. Our data demonstrate that factors in addition to
the amount of PrP expressed determine the tropism of prions for certain
tissues. That some muscles are intrinsically capable of accumulating
substantial titers of prions is of particular concern. Because significant
dietary exposure to prions might occur through the consumption of meat, even
if it is largely free of neural and lymphatic tissue, a comprehensive effort
to map the distribution of prions in the muscle of infected livestock is
needed. Furthermore, muscle may provide a readily biopsied tissue from which
to diagnose prion disease in asymptomatic animals and even humans.
NAL call
no. 500 N21P
Descriptors: BSE, infected beef products,
NvCreutzfeldt-Jacob disease, mouse model, skeletal muscle accumulations,
PrPSc, Me7, Rocky Mountain Laboratory strain murine prions, possible
diagnostic tissue for testing.
Bousset, Luc; Melki, Ronald. Similar and
divergent features in mammalian and yeast prions. Microbes and
Infection. Institut Pasteur 2002 Apr; 4(4): 461-9. ISSN:
1286-4579.
Abstract: Mammalian transmissible spongiform
encephalopathies are likely due to the propagation of an abnormal form of a
constitutive protein instead of traditional genetic material (nucleic acids).
Such infectious proteins, which are termed prions, exist in yeast. They are at
the origin of a number of phenotypes that are inherited in a non-Mendelian
manner. These prions are very useful to dissect the molecular events at the
origin of this structure-based inheritance. The properties of mammalian and
yeast prions are presented and compared. This review highlights a number of
similarities and differences.
NAL call no. QR180 M53
Descriptors:
TSEs, transmissible spongiform encephalopathies, infectious proteins, prions,
yeast and mammalian prions compared, a review.
Boyce, Nell. The madness of the elk.
US News and World Report. 2002 Mar 25; 132(9): 56. ISSN:
0041-5537.
NAL call no. 280.8 Un33A
Descriptors: animal diseases,
etiology, wild deer, epidemiology, transmissible spongiform encephalopathy,
BSE, USA.
Bradley, Ray. Bovine spongiform
encephalopathy update. Polish Journal of Pathology Official Journal
of the Polish Society of Pathologists 2002; 53(1): 7-16. ISSN:
1233-9687.
Abstract: Bovine spongiform encephalopathy (BSE) is a
zoonosis being the origin of variant Creutzfeldt-Jakob disease and an
important cattle disease in its own right. Countries have been slow to learn
the importance of protecting, not only their cattle populations, but also
their human populations. Since 2000, several additional European countries
have reported BSE in native-born stock and this has led to a concern about the
BSE status of countries that have imported cattle and cattle products from
infected countries. Extensive feed and offal bans and application of
newly-developed, "Rapid" tests for prion protein in central nervous tissue of
targeted, high-risk animals and slaughter cattle over 30 months old now
provides the tools whereby the public are fully protected and BSE can be
eradicated.
Descriptors: BSE, NvCreutzfeldt-Jakob Disease, cattle,
human health risks, prion protein testing in slaughtered animals, control,
eradication.
Bren, Linda. FDA continues work to help
prevent mad cow disease. FDA Consumer. 2002 May-Jun; 36(3):
31-2. ISSN: 0362-1332
NAL call no. HD9000.9 U5A1
Descriptors:
BSE, bovine spongiform encephalopathy, transmission prevention and control,
U.S. Food and Drug Administration, sentinel and surveillance, cattle, animal
feeds, U.S.
Brenig, Bertram; Schutz, Ekkehard; Urnovitz, Howard. Zellulare Nucleinsauren im Serum und Plasma als neue
diagnostische Werkzeuge. [Cellular nucleic acids in serum and plasma as
new diagnostic tools]. Berliner und Munchener tierarztliche Wochenschrift
2002 Mar-Apr; 115(3-4): 122-4 ISSN: 0005-9366. In
German.
Abstract: Currently, the diagnosis of bovine spongiform
encephalopathy is only possible in the brain stem of dead animals. Protease
resistant prions are detected in the obex region of the brain stem. However,
from a veterinary medical and agricultural point of view the development of an
in vivo detection assay is of utmost importance. Because infectious prions are
detectable relatively late in the central nervous system during an infection,
efforts are made searching for surrogate markers. Besides neuronal proteins
that are released into the liquor and blood during neurodegenerative processes
or other neuronal diseases, cellular nucleic acids circulating in the plasma
or serum are an absolutely new approach for the detection of infectious
diseases.
NAL call no. 41.8 B45
Descriptors: BSE, bovine
spongiform encephalopathy, vivo detection assay, new approach, cellular
nucleic acids in plasma or serum.
Breslin, P. D.; Bassett, H. F.; McElroy, M.C.; Markey, B. K.; Weavers,
E. Brainstem cell populations in BSE-affected
and clinically normal cattle. Research in Veterinary Science.
April 2002; 72 (Supplement A): 46. 56th Annual Conference of the Association
of Veterinary Teachers and Research Workers on Current Topics in Veterinary
Science, Scarborough, England, UK, March 25-27, 2002
NAL call no. 41.8
R312
Descriptors: cattle, bovine spongiform encephalopathy,
brainstem cells, comparison study, diseased and normal animals.
Brown, David R Mayhem of the multiple
mechanisms: modelling neurodegeneration in prion disease. Journal of
Neurochemistry. 2002 Jul; 82(2): 209-15 ISSN:
0022-3042.
Abstract: This review examines recent attempts to advance
the understanding of the mechanism by which neurones die in prion disease.
Prion diseases or transmissible spongiform encephalopathies are characterized
by the conversion of a normal glycoprotein, the prion protein, to a
protease-resistant form that is suggested to be both the infectious agent and
the cause of the rapid neurodegeneration in the disease. Death of the patient
results from this widespread neuronal loss. Thus understanding the mechanism
by which the abnormal form of the prion protein causes neuronal death might
lead to treatments that would prevent the life-threatening nature of these
diseases.
NAL call no. QP351.J6
Descriptors: prion diseases,
neuronal death patterns, animal models, physiopathology, transmissible
spongiform encephalopathies.
Brown, David R. Molecular advances in
understanding inherited prion diseases. Molecular Neurobiology.
June, 2002; 25 (3): 287-302.
NAL call no. QP365.2
M64
Descriptors: BSE, bovine spongiform encephalopathy, variant
Creutzfeldt Jakob disease, CJD.
Brown, Paul. Drug therapy in human and
experimental transmissible spongiform encephalopathy. Neurology.
2002 Jun 25; 58(12): 1720-5. ISSN: 0028-3878.
Abstract: During the
past 30 years, over 60 different chemical compounds have been used to treat
experimental animals infected with transmissible spongiform encephalopathies
(TSE), including a wide variety of anti-infectious agents, immunomodulating
drugs, and chemicals interacting with the lympho-reticular system. Some
compounds achieved a prolongation of the incubation period, but this effect
decreased or disappeared when they were administered at or near the onset of
symptomatic disease. Recent in vitro and tissue culture studies support
earlier speculation about the importance of a chemical structure containing
both water-soluble and lipid-soluble components, evidently as a means of
interaction with the misfolded membrane-bound 'prion' protein. A number of
compounds shown to eliminate the protein (or infectivity) in TSE-infected
tissue cultures are the subject of ongoing studies in animals, and are under
consideration for human drug trials. As with other recalcitrant infections,
combinations of drugs with different modes of action are likely to be
necessary for any effective therapy. Also, very recent work in developing
antibodies that can neutralize in vitro infection (and, in conjunction with
genetic engineering, in vivo infection) has renewed interest in the strategies
of both active and passive immunization.
Descriptors: drugs,
treatments, TSEs, anti-infectious agents, immunomodulation drugs, chemicals,
experimental animals, prion diseases, prion proteins.
Bruce, Moira E.; Boyle, Aileen; Cousens, Simon; McConnell, Irene; Foster,
James; Goldmann, Wilfred; Fraser, Hugh Strain
characterization of natural sheep scrapie and comparison with BSE.
Journal of General Virology. 2002 Mar; 83(Pt 3): 695-704 ISSN:
0022-1317.
Abstract: Scrapie was transmitted to mice from ten sheep,
collected in the UK between 1985 and 1994. As in previous natural scrapie
transmissions, the results varied between scrapie sources in terms of the
incidence of disease, incubation periods and neuropathology in challenged
mice. This contrasted with the uniformity seen in transmissions of BSE to
mice. The scrapie and BSE isolates were characterized further by serial
passage in mice. Different TSE strains were isolated from each source
according to the Sinc or PrP genotype of the mouse used for passage. The same
two mouse-passaged strains, 301C and 301V, were isolated from each of three
BSE sources. Despite the variation seen in the primary transmissions of
scrapie, relatively few mouse-passaged scrapie strains were isolated and these
were distinct from the BSE-derived strains. The ME7 scrapie strain, which has
often been isolated from independent sheep sources in the past, was identified
in isolates from four of the sheep. However, a new distinct strain, 221C, was
derived from a further four scrapie sheep. These results suggest that there is
agent strain variation in natural scrapie in sheep and that the spectrum of
strains present may have changed over the last 20 years. The tested sample is
too small to come to any conclusions about whether the BSE strain is present
in sheep, but the study provides a framework for further more extensive
studies.
NAL call no. QR360.A1J6
Descriptors: scrapie,
transmitted to mice, BSE isolates, serial passage in mice, ME7 strain, 221C
strain, strain evolution.
Brufau, J.; McCartney, E. 'Feed scares':
where is Europe leading? Feed International. 2002, 23: 2,
6-8.
Descriptors: animal feeds, transmissible spongiform
encephalopathies, livestock animals, epidemiology, control, Europe.
Bucciantini, Monica; Giannoni, Elisa; Chiti, Fabrizio; Baroni, Fabiana;
Formigli, Lucia; Zurdo, Jesus; Taddei, Niccolo; Ramponi, Giampietro; Dobson,
Christopher M.; Stefani, Massimo. Inherent
toxicity of aggregates implies a common mechanism for protein misfolding
diseases. Nature. April 4, 2002; 416 (6880): 507-11. ISSN:
0028-0836
DOI: 10.1038/416507a
Abstract:
A range of human degenerative conditions, including Alzheimer's disease,
light-chain amyloidosis and the spongiform encephalopathies, is associated
with the deposition in tissue of proteinaceous aggregates known as amyloid
fibrils or plaques. It has been shown previously that fibrillar aggregates
that are closely similar to those associated with clinical amyloidoses can be
formed in vitro from proteins not connected with these diseases, including the
SH3 domain from bovine phosphatidyl-inositol-3'-kinase and the amino-terminal
domain of the Escherichia coli HypF protein. Here we show that species formed
early in the aggregation of these non-disease-associated proteins can be
inherently highly cytotoxic. This finding provides added evidence that
avoidance of protein aggregation is crucial for the preservation of biological
function and suggests common features in the origins of this family of protein
deposition diseases.
NAL call no. 472 N21
Descriptors: spongiform
encephalopathies, proteinaceous aggregates, fibrillar aggregates, bovine
phosphatidylinositol-3-kinase chemistry. PC12 cells, rats.
Budka, Herbert; Dormont, Dominique; Kretzschmar, Hans; Pocchiari, Maurizio;
van-Duijn, Cornelia.. BSE and variant
Creutzfeldt-Jakob disease: never say never. Acta
Neuropathologica 2002 Jun; 103(6): 627-8 ISSN:
0001-6322
Descriptors: bovine spongiform encephalopathy, NvCJD,
prion pathogenicity, epidemiology, animal models, transmission and
control.
Busk, N.; Vaughan, K.; Watkins, R.; Hawkins-S.A.C. Review and refinement of clinical monitoring methods
for TSE mouse bioassay/strain typing studies. Research in Veterinary
Science. April, 2002; 72 (Supplement A): 46-47. 56th Annual Conference of
the Association of Veterinary Teachers and Research Workers on Current Topics
in Veterinary Science, Scarborough, England, UK, March 25-27, 2002.
NAL
call no. 41.8 R312
Descriptors: transmissible spongiform
encephalopathies, mouse model bioassay, strain typing, prions.
Cai, Kang; Miller, Jeanette L.C.; Stenland, Christopher J.; Gilligan, Kevin
J.; Hartwell, Randal C.; Terry, Jarrett C.; Evans-Storms, Rosemary B.;
Rubenstein, Richard; Petteway, Stephen R. Jr; Lee, Douglas C. Solvent-dependent precipitation of prion protein.
Biochimica et Biophysica Acta - Protein Structure and Molecular Enzymology. 20 May, 2002; 1597 (1): 28-35.
ISSN: 0006-3002.
NAL
call no. 381 B522
Descriptors: misfolded isoform, prion protein,
PrPSc, solvents, physiological buffer, pH effects, salt, ethanol
concentration.
Carlson, George A. Postexposure prophylaxis
against transmissible spongiform encephalopathies: CpG oligodeoxynucleotides
in mice. Lancet. 2002 Jul 20; 360(9328): 184. ISSN:
0140-6736.
NAL call no. 449.8 L22
Descriptors: cattle, adjuvants,
immunologic therapeutic use, BSE, control, mouse models,
oligodeoxyribonucleotides.
Carruthers, Jean; Carruthers, Alastair, Mad
cows, prions, and wrinkles. Archives of Dermatology. 2002 May;
138(5): 667-70 ISSN: 0003-987X.
NAL call no. 448.8
AR242
Descriptors: BSE transmission risks, collagen, prion
physiology, prion disease prevention and control, cosmetic formulations,
injections, intradermal.
Chamberland, Mary E. Emerging infectious
agents: do they pose a risk to the safety of transfused blood and blood
products? Clinical Infectious Diseases, Official Publication of the
Infectious Diseases Society of America. 2002 Mar 15; 34(6): 797-805. ISSN:
1537-6591.
Abstract: The blood supply is safer than it has been at
any other time in recent history, and, in the context of other health
care-related adverse events, the risks associated with blood transfusion are
extremely small. The current high level of safety is the result of successive
refinements and improvements in how blood is collected, tested, processed, and
transfused; nonetheless, blood and plasma products remain vulnerable to newly
identified or reemerging infections. In recent years, numerous infectious
agents-including several newly discovered hepatitis viruses, the agents of
transmissible spongiform encephalopathies, and tickborne pathogens-have been
identified as potential threats to the safety of blood and plasma. Continued
vigilance is critical to protect the blood supply from known pathogens and to
monitor for the emergence of new infectious agents. Recent terrorist
activities in the United States add new considerations to maintaining the
safety and supply of blood. Education of clinicians and patients regarding the
benefits and risks associated with the judicious use of blood and blood
products can assist in informed decision making.
NAL call no. RC111
R4
Descriptors: blood supply, safety risks, transmissible spongiform
encephalopathies, recommendations for decision making.
Chaplin, M.J.; Barlow, N.; Ryder, S.; Simmons, M.M.; Spencer, Y.; Hughes,
R.; Stack, M. J. Evaluation of the effects of
controlled autolysis on the immunodetection of PrPSc by immunoblotting and
immunohistochemistry from natural cases of scrapie and BSE. Research
in Veterinary Science. February, 2002; 72 (1): 37-43.
NAL call no. 41.8
R312
Descriptors: sheep, cattle, scrapie, BSE, histopathological
examination, medulla brain exam, Western immunoblotting for detection of
PrPSc, Prionics diagnostic test, routine immunohistochemical technique.
Cochrane, N. Pressures for change in
Eastern Europe's livestock sectors. Agricultural Outlook. 2002,
No.288, 17-20.
NAL call no. aHD1751.A42
Descriptors: Central
Europe, disease control, transmissible spongiform encephalopathy, livestock
testing, trade, disease prevention and control.
Cooper, J.E. Diagnostic pathology of
selected diseases in wildlife. Revue Scientifique et Technique
Office International des Epizooties. April, 2002; 21 (1):
77-89.
URL: www.oie.int/eng/publicat/rt/2101/A_R2115.htm
NAL
call no. SF781 R4
Descriptors: wildlife, detection, management,
infectious disease, field diagnosis, sampling, principles, diagnostic
pathology, mycobacteriosis, Rift Valley fever, rabies, spongiform
encephalopathies, morbillivirus and poxvirus infections, viral encephalitides,
West Nile virus infection and chytridiomycosis.
Croes, E.A.; van Gool, W.A.; Jansen, G. H.; van Duijn, C. M. Ziekte van Creutzfeldt-Jakob: diagnostiek,
incidentie, preventie en behandeling. [Creutzfeldt-Jakob disease:
diagnosis, incidence, prevention and treatment]. Nederlands Tijdschrift
voor Geneeskunde 2002 Apr 20; 146(16): 750-4. ISSN: 0028-2162. In
Dutch.
Abstract: Creutzfeldt-Jakob disease (CJD) is a rare,
neurodegenerative disorder belonging to the spongiform encephalopathies. A
variant form (vCJD) is most likely the result of infection with the agent that
causes bovine spongiform encephalopathy (BSE). Diagnostic information can be
obtained by EEG, testing cerebrospinal fluid for the presence of the 14-3-3
protein, MRI, brain biopsy, tonsil biopsy, and postmortem brain examination.
Some tests, such as MRI and postmortem brain examination, can be used to
distinguish between CJD and vCJD. Pathological prions in a tonsil biopsy are
only found with vCJD. In the Netherlands, there are four known cases of
iatrogenic CJD. On the basis of certain exposure to BSE via the food chain,
cases of vCJD are also to be expected. Chloropromazine and mepacrine are known
to inhibit the formation of pathological prion conformations, but clinical
trials have not yet been carried out.
Descriptors: NvCJD, bovine
spongiform encephalopathy, BSE, diagnosis of CJD and NvCJD, humans, iatrogenic
disease, MRI, brain biopsy, tonsil biopsy, postmortem brain examination,
chloropromazine, mepacrine, treatment.
Dalsgaard, Niels Jorn. Prion diseases. An
overview. APMIS Acta Pathologica, Microbiologica, et Immunologica
Scandinavica. 2002 Jan; 110(1): 3-13. ISSN: 0903-4641.
Abstract:
Prion disease is the new designation of a group of spongiform
encephalopathies, all invariably fatal, which show similar clinical and
neuropathological changes. They comprise a range of distinct diseases in both
animals and man, and spontaneous, hereditary and transmissible forms are
recognized. Until the sudden occurrence in the mid-1980s of an epizootic of a
formerly unknown disease, popularly named 'mad cow disease', in cattle in the
UK, very little attention had been paid to these rather obscure diseases.
Concurrently it was asserted that the disease-causing agent appeared to be a
ubiquitous mammalian brain constituent, and the disease mechanism a
conformational change of its structure. These events have not only led to a
new understanding of these extraordinary diseases, but have also provided
insight into both neurodegeneration and disease mechanisms at the molecular
level. Moreover, in 1997 the prion concept earned its originator the second
Nobel price for medicine within this scientific field. In this introduction
and overview of prion diseases, historical and philosophical perspectives are
presented along with descriptions of the diseases in both animals and man.
Epidemiology, genetics and transmissibility are also covered.
NAL call no.
QR1.A6
Descriptors: spongiform encephalopathies, BSE, bovine
spongiform encephalopathies, neurodegeneration, disease mechanisms, prions,
overview, history, descriptions of diseases, epidemiology, genetics,
transmissibility, US, UK.
Daly, D. J.; Prendergast, D. M.; Sheridan, J. J.; Blair, I.S.; McDowell,
D.A. Use of a marker organism to model the
spread of central nervous system tissue in cattle and the abattoir environment
during commercial stunning and carcass dressing. Applied and
Environmental Microbiology. 2002 Feb; 68(2): 791-8. ISSN:
0099-2240.
Abstract: Due to concerns about a link between variant
Creutzfeldt-Jakob disease in humans and similar prion protein-induced disease
in cattle, i.e., bovine spongiform encephalopathy (BSE), strict controls are
in place to exclude BSE-positive animals and/or specified risk materials
including bovine central nervous system (CNS) tissue from the human food
chain. However, current slaughter practice, using captive bolt guns, may
induce disruption of brain tissues and mobilize CNS tissues into the bovine
circulatory system, leading to the dispersion of CNS tissues (including prion
proteins) throughout the derived carcass. This project used a marker
(antibiotic-resistant) strain of Pseudomonas fluorescens to model the effects
of commercial captive bolt stunning procedures on the movement of mobilized
CNS material within slaughtered animals and the abattoir environment. The
marker organism, introduced by injection through the bolt entry aperture or
directly using a cartridge-fired captive bolt, was detected in the slaughter
environment immediately after stunning and in the abattoir environment at each
subsequent stage of the slaughter-dressing process. The marker organism was
also detected on the hands of operatives; on slaughter equipment; and in
samples of blood, organs, and musculature of inoculated animals. There were no
significant differences between the results obtained by the two inoculation
methods (P < 0.05). This study demonstrates that material present in, or
introduced into, the CNS of cattle during commercial captive bolt stunning may
become widely dispersed across the many animate and inanimate elements of the
slaughter-dressing environment and within derived carcasses including meat
entering the human food chain.
NAL call 448.3 AP5
Descriptors:
NvCreutzfeldt-Jakob Disease, BSE, bovine spongiform encephalopathy, cattle,
control and prevention of prion disease, slaughter, Pseutomonas fluorescens to
model captive bolt stunning, facility monitoring, carcass contamination.
Dealler, Steve. vCJD: the epidemic that
never was. Possibility of BSE being cause of variant CJD is indeed
biologically plausible. BMJ Clinical Research Ed 2002 Jul 13;
325(7355): 102. ISSN: 1468-5833.
Descriptors: cattle, bovine
spongiform encephalopathy, NvCreutzfeldt-Jakob Syndrome transmission,
contaminated meat, public health risks.
Debeer, Sabine O. S.; Baron, Thierry G.M.; Bencsik, Anna A. Transmissible spongiform encephalopathy diagnosis
using PrPsc immunohistochemistry on fixed but previously frozen brain samples.
Journal of Histochemistry and Cytochemistry. The official journal of
the Histochemistry Society 2002 May; 50(5): 611-6. ISSN:
0022-1554.
URL: www.jhc.org/cgi/content/abstract/50/5/611
Abstract: The
histological diagnosis of transmissible spongiform encephalopathies (TSEs),
such as scrapie and bovine spongiform encephalopathy (BSE), relies on
identification in the brain of spongiosis, gliosis, and neuron loss without
inflammatory lesions. Because of its sensitivity, immunohistochemistry of
abnormal prion protein (PrPsc) is of great help in this diagnosis and can be
used on its own or complementary to the biochemical detection of PrPsc.
However, in some cases no formalin-fixed material is available, rendering its
use as a complementary method impossible. For that purpose, we studied the
possibility of detecting PrPsc immunohistochemically in fixed brain samples
that had been previously frozen and used for Western blotting analysis. We
compared freshly and fixed-frozen brain samples originating from the same
sheep, either affected or unaffected with scrapie. We also studied
fixed-frozen brain samples from scrapie-affected goats and from cows showing
BSE. We showed that in all the species tested, despite damage to the
histological structures, PrPsc was still detectable in the fixed-frozen brain
sections without unspecific background staining. Notwithstanding the limited
number of cases thus far analyzed, we have already demonstrated the
possibility of using PrPsc immunohistochemistry on fixed-frozen brain samples
with very good efficacy, thus rendering possible its use for diagnostic
purposes in TSEs.
NAL call no. 381 J8222
Descriptors: scrapie,
BSE, immunohistochemistry of abnormal prion protein, PrPsc, diagnosis,
compared fresh and frozen brain tissue, diagnostic method.
Dedet,V. BSE screeningsprover pa levende
dyr: tre vaesentlige eksempler pa videnskabelige undersogelser. [BSE
screening for live animals. Three good examples of scientific experiments.]
Dansk Veterinaertidsskrift. 2002, 85: 1, 18-19. In Danish.
NAL call
no. 41.9 D23
Descriptors: cattle, sheep, bovine spongiform
encephalopathy, diagnostic methods.
Delgado-Hachmeister, J.E.; Rangel-Frausto, M.S.; Ponce de Leon, S; de Leon,
S. Ponce. Encefalopatias espongiformes
transmisibles. [Transmissible spongiform encephalopathies.] Salud
Publica de Mexico. 2002, 44: 1, 69-75; 22 ref. In Spanish with an English
summary.
Descriptors: TSE, public health concerns, Mexico.
Dickmeiss, Ebbe; Gerstoft, Jan. Blood
infectivity in transmissible spongiform encephalopathies. APMIS.
Acta Pathologica, Microbiologica, et Immunologica Scandinavica 2002 Jan;
110(1): 99-103 ISSN: 0903-4641.
Abstract: Blood infectivity in
transmissible spongiform encephalopathies (TSE) is reviewed with special
emphasis on transmission by blood transfusion in human beings. It is concluded
that transmission by transfusion seems biologically plausible as regards
variant Creutzfeld-Jakob Disease (vCJD), albeit present knowledge suggests
that it is extremely uncommon. Precautionary measures against the putative
risk of vCJD transmission by blood transfusion are discussed.
NAL call no.
QR1.A6
Descriptors: blood products, transmissibility concerns,
transmissible spongiform encephalopathies, emphais on humans,
NvCreutzfeldt-Jakob Disease, risks.
Docampo, Roberto. New and re-emerging
infectious diseases. Trends in Parasitology. August, 2002; 18
(8): 334-336. The 5th Annual Conference on New and Re-emerging Infectious
Diseases, Urbana-Champaign, IL, USA, April 18-19, 2002.
DOI: 10.1016/S1471-4922(02)02351-6
NAL
call no. QL757 P374
Descriptors: transmissible spongiform
encephalopathies, various diseases are addressed, zoonotic and animal
diseases.
Dodd, Roger Y.; Busch, Michael P. Animal
models of bovine spongiform encephalopathy and vCJD infectivity in blood: two
swallows do not a summer make. Transfusion. 2002 May; 42(5):
509-12. ISSN: 0041-1132.
Descriptors: Creutzfeldt Jakob Syndrome,
transmission, BSE, CJD, bovine spongiform spongiform encephalopathy, animals
models, blood transfusion research, lemur, Macaca fascicularis,
phosphoprotein-phasphatase analysis, sheep, species specificity.
Doherr, M.G. Aetiologie, Uebertragung und
epidemiologische Situation von BSE in Europa. [Etiology, transmission
and epidemiological situation of BSE in Europe.] Praktische Tierarzt
2002 vol. 83, no. 2, pp. 156-161. In German.
NAL call no. 41.8
P882
Descriptors: BSE, European status, epidemiology, etiology,
public health concerns, transmissible spongiform encephalopathies.
Doherr, M.G.; Hett, A.R.; Cohen, C.H.; Fatzer, R.; Rufenacht, J.;
Zurbriggen, A.; Heim, D. Trends in prevalence
of BSE in Switzerland based on fallen stock and slaughter surveillance.
Veterinary Record. London : The British Veterinary Association.
Mar 16, 2002. v. 150 (11) p. 347-348. ISSN: 0042-4900
NAL call no. 41.8
V641
Descriptors: cattle, BSE, bovine spongiform encephalopathy,
disease prevalence, trends, disease surveys, Switzerland.
Domingo, Jose L. Lack of experimental
studies on human transmission of BSE in relation with the consumption of
specified risk materials (SRM): The case of the milk. Preventive
Medicine. June, 2002; 34 (6): 655-656.
DOI: 10.1006/pmed.2002.1027
NAL
call no. RA421 P684
Descriptors: BSE, bovine spongiform
encephalopathy, transmissible spongiform encephalopathy, public health risks,
animal derived foods, milk, research recommendations.
Eaton, S.L.; Foster, J. D.; Hunter, N. Follicular dendritic cell involvement in ovine
scrapie. Research in Veterinary Science. April, 2002; 72
(Supplement A): 44. 56th Annual Conference of the Association of Veterinary
Teachers and Research Workers on Current Topics in Veterinary Science,
Scarborough, England, UK, March 25-27, 2002.
NAL call no. 41.88
R312
Descriptors: sheep, scrapie, prion disease, effects on
follicular dendritic cells.
Eberl, Heike; Glockshuber, Rudi. Folding
and intrinsic stability of deletion variants of PrP(121-231), the folded
C-terminal domain of the prion protein. Biophysical Chemistry. 2
May, 2002; 96 (2-3): 293-303.
DOI: 10.1016/S0301-4622(02)00015-7
NAL
call no. QP1.B5
Descriptors: transmissible spongiform
encephalopathies, prions, PrPSc, PrPC structure, deletion variants of C
terminal PrPC domain, tertiary structure context, conformation of the segment
comprising alpha-helix 2 and 3 in the solution structure of recombinant
PrP.
Farrugia, Albert. Laboratory practice and studies of bovine spongiform
encephalopathy. Lancet. 2002 Mar 23; 359(9311): 1067-8. ISSN:
0140-6736.
NAL call no. 448.4 L22
Descriptors: bovine spongiform
encephalopathy transmission, laboratory standards, cattle, sheep.
Fatzer, R.; Vandevelde, M.; Gottstein, B. Cerebral taeniid oncospheral lesions in two BSE
suspects. Veterinary Record. London : The British Veterinary
Association. Jan 12, 2002. v. 150 (2) p. 46-47. ISSN: 0042-4900.
NAL call
no. 41.8 V641
Descriptors: cattle, brain lesions, oncospheres,
symptoms, BSE, bovine spongiform encephalopathy, histopathology, Taenia
saginata, case report, Switzerland.
Ferguson, N.M.; Ghani, A.C.; Donnelly, C.A.; Hagenaars, T.J.; Anderson,
R.M. Estimating the human health risk from
possible BSE infection of the British sheep flock. Nature.
London : Macmillan Magazines Ltd. Jan 24, 2002. v. 415 (6870) p. 420-424.
ISSN: 0028-0836
DOI: 10.1038/nature709
Abstract:
Following the controversial failure of a recent study and the small numbers of
animals yet screened for infection, it remains uncertain whether bovine
spongiform encephalopathy (BSE) was transmitted to sheep in the past via feed
supplements and whether it is still present. Well grounded mathematical and
statistical models are therefore essential to integrate the limited and
disparate data, to explore uncertainty, and to define data-collection
priorities. We analysed the implications of different scenarios of BSE spread
in sheep for relative human exposure levels and variant Creutzfeldt-Jakob
disease (vCJD) incidence. Here we show that, if BSE entered the sheep
population and a degree of transmission occurred, then ongoing public health
risks from ovine BSE are likely to be greater than those from cattle, but that
any such risk could be reduced by up to 90% through additional restrictions on
sheep products entering the food supply. Extending the analysis to consider
absolute risk, we estimate the 95% confidence interval for future vCJD
mortality to be 50 to 50,000 human deaths considering exposure to bovine BSE
alone, with the upper bound increasing to 150,000 once we include exposure
from the worst-case ovine BSE scenario examined.
NAL call no. 472
N21
Descriptors: cattle, BSE, bovine spongiform encephalopathy,
infections, sheep, disease transmission. human diseases, zoonosis, public
health, NvCreutzfeldt Jakob Disease, ovine BSE, statistical models, UK.
Ferguson-Smith, Malcolm A. Reaction to the
emergence of BSE in the UK: What was done and what perhaps might have been
done better. Comptes Rendus Biologies. Janvier, 2002; 325 (1):
25-26.
DOI: 10.1016/S1631-0691(02)01395-1
NAL
call no. Q2 C6
Descriptors: BSE, bovine spongiform encephalopathy,
the UK epidemic, governmental actions, historical perspectives.
Fernie, K. Heat/hydroxide combinations as
novel decontamination methods for surgical instruments. Research in
Veterinary Science. April, 2002; 72 (Supplement A): 43-44. 56th Annual
Conference of the Association of Veterinary Teachers and Research Workers on
Current Topics in Veterinary Science, Scarborough, England, UK, March 25-27,
2002
NAL call no. 41.8 R312
Descriptors: transmissible spongiform
encephalopies, prions, potential contamination of surgical instruments,
decontamination methods.
Foster, J.D.; Parnham, D.W.; Hunter, N.; Bruce, M. Distribution of the prion protein in sheep
terminally affected with BSE following experimental oral transmission.
Research in Veterinary Science. April, 2002; 72 (Supplement A):
45. 56th Annual Conference of the Association of Veterinary Teachers and
Research Workers on Current Topics in Veterinary Science, Scarborough,
England, UK, March 25-27, 2002
NAL call no. 41.8
R312
Descriptors: sheep, BSE, bovine spongiform encephalopathy,
prion proteins, experimental infection via oral route, distribution in the
body.
Fraser, J.R. What is the basis of
transmissible spongiform encephalopathy induced neurodegeneration and can it
be repaired? Neuropathology and Applied Neurobiology 2002 Feb;
28(1): 1-11. ISSN: 0305-1846.
Abstract:
Once an animal becomes infected with a prion disease, or transmissible
spongiform encephalopathy (TSE), the progression of infection is relentless
and inevitably fatal, although often with such prolonged incubation periods
that an alternative cause of death can intervene. Infection has been compared
to 'setting a clock' which then runs inexorably as the disease spreads,
usually through the lymphoreticular system and then via peripheral nerves to
the central nervous system (CNS), although the mechanism controlling the
protracted progression is not known. Clinical disease develops as
characteristic degenerative changes in the CNS progress, but the molecular
basis for this pathology is not clear, particularly the relationship between
the deposition of abnormal PrP and neuronal dysfunction. Recent research has
identified several means of slowing (if not stopping) the clock when infection
has not yet reached the CNS; although the potential for later stage therapies
seems limited, neuroprotective strategies which have been shown to be
effective in other neurodegenerative conditions may also ameliorate TSE
induced CNS pathology. This review focuses on our current knowledge of the key
events following infection of the CNS and the opportunities for intervention
once the CNS has become infected.
Descriptors: prion disease, TSE,
review of current knowledge of infection, possible opportunities for
intervention of disease process.
Frey, Jacques. Bovine spongiform
encephalopathy: Are the cows mad or full of carbohydrates? Clinical
Chemistry and Laboratory Medicine. February, 2002; 40 (2):
101-103.
Descriptors: dairy cows, diet, dysregulation of
carbohydrate metabolism, neurodegenerative disorders, BSE, origin, prion
proteins.
Gargani, G. Le encefalopatie spongiformi
trasmissibili. Storia, epidemiologia, ipotesi eziologiche.
[Transmissible spongiform encephalopathies. History, epidemiology,
etiological, hyphotheses]. Minerva Medica 2002 Feb; 93(1): 59-73.
ISSN:0026-4806. In Italian.
Abstract: The history of transmissible
spongiform encephalopathies is shortly reviewed beginning with the Westminster
parliament act in the year 1755 up to the description in 1996 of the variant
of the Creutzfeldt-Jakob disease, transmitted from cattle to man by alimentary
route. The epidemiological patterns of encephalopathies of the various animal
species and of the four encephalopathies up to date reported in man are
shortly described: Creutzfeldt-Jakob disease, Kuru,
Gerstmann-Straussler-Scheinker disease, Fatal Familial Insomnia. Etiological
hypotheses are discussed until the identification of Prions: PrPcell, on the
surface of normal cells, PrPscr in the brain of humans and animals dead for
these diseases. The strains of the PrPscr are described on the basis of some
characters observed through the passages in rodents and of molecular pattern.
The possible future epidemiological evolution of the vCJD is also
discussed.
Descriptors: TSEs, historical review, 1755-1996,
NvCreutzfeldt-Jakob Disease, cattle, man, epidemiology, Creutzfeldt-Jakob
disease, Kuru, Gerstmann-Straussler-Scheinker disease, Fatal Familial
Insomnia, PrPscr strains.
Ghani, Azra C. The epidemiology of variant
Creutzfeldt-Jakob disease in Europe. Microbes and Infection.
2002 Mar; 4(3): 385-93.ISSN: 1286-4579.
Abstract: Variant
Creutzfeldt-Jakob disease is one of a family of neurodegenerative diseases,
first diagnosed in 1996. Scientific evidence strongly supports the hypothesis
that it is acquired through consumption of bovine spongiform
encephalopathy-infected meat. The majority of cases have been diagnosed in the
UK in young individuals, with an excess of cases in the north and a
significant cluster of cases in Leicestershire. Many uncertainties in its
biology and epidemiology, in particular the length of the incubation period,
make predictions of any future epidemic difficult. Studies are currently under
way to obtain more precise estimates of the prevalence of asymptomatic
infection through testing tonsil and appendix tissues for the abnormal prion
protein.
NAL call no. QR180 M53
Descriptors: NvCreutzfeldt-Jakob
Disease, bovine spongiform infected meat consumption, human cases, young,
biology, epidemiology, incubation period, estimates of asymptomatic
infection.
Ghani, Azra C.; Donnelly, Christl A.; Ferguson, Neil M..; Anderson, Roy
M. The transmission dynamics of BSE and
vCJD. Comptes Rendus Biologies. Janvier, 2002; 325 (1): 37-47.
DOI: 10.1016/S1631-0691(02)01389-6
NAL
call no. Q2 C6
Descriptors: BSE, cattle, NvCreutzfeldt-Jakob
disease, epidemiological models, transmission dynamics, case projections,
Great Britian, Northern Ireland, Portugal, France.
Gray, George; Kreindel, Silvia; Ropeik, David. Mad cow disease risk in the United States. Does
perceived threat overshadow true likelihood of occurrence?
Postgraduate Medicine. 2002 Feb; 111(2): 13-4,16. ISSN:
0032-5481.
Descriptors: BSE, bovine spongiform encephalopathy,
animal feeds, epidemiology, transmission, NvCreutzfeldt-Jakob Disease, public
health risk factors.
Groschup, Martin H.; Stolze, Anne. BSE- und
Scrapie-Diagnostik in Deutschland. [BSE and scrapie diagnosis in
Germany]. Berliner und Munchener Tierarztliche Wochenschrift 2002
Mar-Apr; 115(3-4): 106-10 ISSN: 0005-9366. In German.
Abstract: The
detection of pathological prion protein is considered as pathognomonic for the
diagnosis of transmissible spongiform encephalopathies. According to the EU
regulations cattle older than 30 months of age (Germany 24 months) and
slaughtered for human consumption must be tested by using BSE rapid tests.
Likewise must be fallen stock and clinically affected animals. This article
gives an overview over the diagnostic hierarchy and organization of the
diagnostic system for BSE and scrapie in Germany. All suspect cases found by
rapid testing are reinvestigated and clarified by the National reference
laboratory for these diseases which is part of the recently founded Institute
of Novel and Emerging Infectious Diseases at the Federal Research Centre for
Virus Diseases of Animals located on the isle of Riems. Until the end of 2001
130 BSE cases were confirmed out of 230 submissions.
NAL call no. 41.8
B45
Descriptors: cattle, slaughtered animals, BSE and scrapie rapid
tests, diagnostic hierarchy, Germany.
Gunn, H. M.; Lynch, D.; Sheridan, H.; Costelloe, A.; Weavers, E.; McElroy,
M.; Cooney, J.; Sammin, D.; Good, M.; O' Sullivan, M.; Caulfield, L.; Kennedy,
S.; Smyth, K.; Carr, M.; Sheridan, J.; Casey, V.; Curley, L.; Lynch, M.;
Gleeson, B. Alteration in age profile of BSE
cases in Ireland. Irish Veterinary Journal. 2002, 55: 2,
84-85.
NAL call no. 41.8 IR4
Descriptors: bovine spongiform
encephalopathy, age comparison, disease incidence, Irish Republic, UK.
Harrison, M. The dairy industry looks to the future. Food Science and Technology. 2002, 16: 1, 24-30.
Heppner, F. L.; Aguzzi, A. Immunitat gegen Prionen? [Immunity
against prions?] Deutsche Medizinische Wochenschrift 2002 Feb 15;
127(7): 328-30. ISSN: 0012-0472. In German.
NAL call no. 448.8
D48
Descriptors: bovine spongiform encephalopathy, prions,
immunology, scrapie, B and T lymphocytes, cattle, cell cultures, disease
prevention and control, mice.
Hernandez-Sanchez, Jules; Waddington, Dave; Wiener, Pamela; Haley, Chris S;
Williams, John L. Genome-wide search for
markers associated with bovine spongiform encephalopathy. Mammalian
Genome. 2002 Mar; 13(3): 164-8 ISSN: 0938-8990.
Abstract: A
genome-wide search for markers associated with BSE incidence was performed by
using Transmission-Disequilibrium Tests (TDTs). Significant segregation
distortion, i.e., unequal transmission probabilities of alleles within a
locus, was found for three marker loci on Chromosomes (Chrs) 5, 10, and 20.
Although TDTs are robust to false associations owing to hidden population
substructures, it cannot distinguish segregation distortion caused by a true
association between a marker and bovine spongiform encephalopathy (BSE) from a
population-wide distortion. An interaction test and a segregation distortion
analysis in half-sib controls were used to disentangle these two alternative
hypotheses. None of the markers showed any significant interaction between
allele transmission rates and disease status, and only the marker on Chr 10
showed a significant segregation distortion in control individuals.
Nevertheless, the control group may have been a mixture of resistant and
susceptible but unchallenged individuals. When new genotypes were generated in
the vicinity of these three markers, evidence for an association with BSE was
confirmed for the locus on Chr 5.
NAL call no.
QL738.5.M359
Descriptors: BSE, cattle, Transmission-Disequilibrium
Tests, Chromosomes 5, 10, 20, genome-wide markers
Herrmann, Lynn M.; Baszler, Timothy V.; Knowles, Donald P.; Cheevers,
William P. PrPSc is not detected in peripheral
blood leukocytes of scrapie-infected sheep: Determining the limit of
sensitivity by immunohistochemistry. Clinical and Diagnostic
Laboratory Immunology. March, 2002; 9 (2): 499-502.
Descriptors:
Peripheral blood leukocytes, scrapie-infected sheep, presence of PrPSc,
dissociated retropharyngeal lymph node (DRLN) cells, immunohistochemistry,
detection methods.
Hildebrandt, G.; Luy, J.; Simon, O. Kannibalismus und Rinderwahn: Ein Argument gegen
jegliche Tiermehlfuetterung? [Cannibalism and mad cows: An argument
against feeding of mammalian meat and bone meal (MBM)?] Tieraerztliche
Umschau. 1 Februar, 2002; 57 (2): 77-89. In German.
NAL call no. 41.8
T445
Descriptors: bovine spongiform encephalopathy, cattle, feed
formulations, mammalian meat and bone meal, cannibalism, offal recycling,
rendering.
Hill, Andrew E.; Collinge, John Species-barrier-independent prion replication in
apparently resistant species. Acta Pathologica, Microbiologica, et
Immunologica Scandinavica. 2002 Jan; 110(1): 44-53. ISSN:
0903-4641.
Abstract: Prion diseases of humans and animals are
associated with the accumulation of an abnormal isoform (PrP(Sc)) of the
host-encoded prion protein (PrP(C)). Transmission of these diseases between
mammalian species is usually limited by a 'species barrier', which can be
mediated by differences in primary sequence of the prion protein between donor
and host species. Studies on species barriers usually rely on the development
of clinical disease in inoculated animals as an assessment of susceptibility
in a particular host. Recent studies by a number of groups have demonstrated
that the absence of clinical symptoms does not necessarily exclude
transmission of prion disease across a species barrier. Such results indicate
that subclinical or carrier states exist in these diseases, which has public
health implications regarding human exposure to BSE prions and iatrogenic
transmission from apparently healthy humans. Here the issue of subclinical
prion diseases is reviewed and implications are discussed.
NAL call no.
QR1.A6
Descriptors: prion diseases, hamsters, mice, laboratory
animal models, subclinical and carrier state implications for human disease,
BSE, iatrogenic transmission, review.
Holada, Karel; Vostal, Jaroslav G.; Theisen, Patrick W.; MacAuley, Claudia;
Gregori, Luisa; Rohwer, Robert G. Scrapie
infectivity in hamster blood is not associated with platelets.
Journal of Virology. May, 2002; 76 (9): 4649-4650. ISSN:
0022-538X.
DOI: 10.1128/JVI.76.9.4649-4650.2002
Abstract: The
infectivity of hamster scrapie strain 263K was measured in platelets isolated
from blood pooled from six hamsters with clinical scrapie. The total number of
infectious doses present in the blood pool was 220, out of which only 3.5
infectious doses were associated with platelets. A larger proportion of the
total infectivity was recovered from the mononuclear leukocyte fraction. This
result indicates that platelets are not the source of blood-borne infectivity
in transmissible spongiform encephalopathy-infected hamsters.
NAL call no.
QR360.J6
Descriptors: scrapie strain 263K, infected hamster blood,
platelet fraction analysed, mononuclear leukocytes, infective source, scrapie
transmission.
Hooper, Nigel M. Prion disease: Close
encounters of the cellular kind. Current Biology. April 2, 2002;
12 (7): R248-R249.
DOI: 10.1016/S0960-9822(02)00783-2
NAL
call no. QH301.C85
Descriptors: prion diseases, BSE, CJD.
Horby, Peter. Rendering beef safe. Clinical Infectious Diseases. 1
January, 2002; 34 (1): 129. ISSN: 1058-4838.
NAL call no. RC111
R4
Descriptors: food products, beef, human health risks, BSE.
Hsich, Gary; Kenney, Kimbra; Gibbs, Clarence J.Jr; Harrington, Michael, G.
Method of detecting transmissible spongiform
encephalopathies. Official Gazette of the United States Patent and
Trademark Office Patents. [e-file] June 18, 2002; 1259 (3): No
Pagination.
Journal URL: www.uspto.gov/web/menu/patdata.html
NAL
call no. T223 A22
Descriptors: detection method, 14-3-3 proteins,
cerebrospinal fluid, elevated levels indicate transmissible spongiform
encephalopathies, CJD in humans, BSE in cattle.
Huang, Fang Ping; Farquhar, Christine F.; Mabbott, Neil A.; Bruce, Moira
E.; MacPherson, G. Gordon. Migrating
intestinal dendritic cells transport PrP(Sc) from the gut. Journal
of General Virology. 2002 Jan; 83(Pt 1): 267-71. ISSN:
0022-1317.
Abstract: Bovine spongiform encephalopathy, variant
Creutzfeldt-Jakob disease (vCJD) and possibly also sheep scrapie are orally
acquired transmissible spongiform encephalopathies (TSEs). TSE agents usually
replicate in lymphoid tissues before they spread into the central nervous
system. In mouse TSE models PrP(c)-expressing follicular dendritic cells
(FDCs) resident in lymphoid germinal centres are essential for replication,
and in their absence neuroinvasion is impaired. Disease-associated forms of
PrP (PrP(Sc)), a biochemical marker for TSE infection, also accumulate on FDCs
in the lymphoid tissues of patients with vCJD and sheep with natural scrapie.
TSE transport mechanisms between gut lumen and germinal centres are unknown.
Migratory bone marrow-derived dendritic cells (DCs), entering the intestinal
wall from blood, sample antigens from the gut lumen and carry them to
mesenteric lymph nodes. Here we show that DCs acquire PrP(Sc) in vitro, and
transport intestinally administered PrP(Sc) directly into lymphoid tissues in
vivo. These studies suggest that DCs are a cellular bridge between the gut
lumen and the lymphoid TSE replicative machinery.
NAL call no.
QR360.A1J6
Descriptors: bovine spongiform encephalopathy,
NvCreutzfeldt-Jakob disease, vCJD, sheep scrapie, orally acquired
transmissible spongiform encephalopathies, TSEs, mouse models, transport of
dendritic cells directlyinto lymphoid tissues in vivo, replicatation.
Ingrosso, Loredana; Vetrugno, Vito; Cardone, Franco; Pocchiari, Maurizio
Molecular diagnostics of transmissible
spongiform encephalopathies. Trends in Molecular Medicine. June,
2002; 8 (6): 273-280.
Descriptors: post mortem diagnosis,
immunochemical based kits, PrPSc, preclinical screening tests, blood, blood
derived products, meat safety, Europe.
Ironside, James W. Neuropathology of
variant Creutzfeldt-Jakob disease. [Neuropathologie de la maladie
variant de Creutzfeldt Jakob]. Comptes Rendus Biologies. Janvier, 2002;
325 (1): 27-31.
DOI: 10.1016/S1631-0691(02)01381-1
NAL
call no. Q2 C6
Descriptors: human prion diseases,
NvCreutzfeldt-Jakob Disease, BSE, florid cluster plaques, cerebrum,
cerebellum, PrPRES, morphology, histology, biochemistry, codon 129, compared
to CJD.
Ironside, J.W.; McCardle, L.; Horsburgh, A.; Lim, Z.; Head, M.W.
Pathological diagnosis of variant Creutzfeldt-Jakob disease. APMIS.
Acta Pathologica, Microbiologica, et Immunologica Scandinavica 2002 Jan;
110(1): 79-87 ISSN: 0903-4641.
Abstract: The neuropathological and
biochemical features of the 89 histologically confirmed cases of variant
Creutzfeldt-Jakob disease (vCJD) diagnosed up to the end of October 2001 in
the UK are reviewed. Histology of the central nervous system, lymphoid tissues
and other organs was accompanied by immunocytochemistry and Western blot
analysis of the disease-associated form of the prion protein (PrP(RES)). All
patients with vCJD were methionine homozygotes at codon 129 of the PrP gene.
The pathology of vCJD showed relatively uniform morphological and
immunocytochemical characteristics, which were distinct from other forms of
CJD. PrP(RES) accumulation was widespread in lymphoid tissues in vCJD, but was
not identified in other non-neural tissues. PrP(RES) in vCJD brain tissue
showed a uniform glycotype pattern distinct from sporadic CJD. Given the
increasingly widespread occurrence of bovine spongiform encephalopathy in
Europe and Asia, there is a major need for widespread CJD surveillance. This
should be accompanied by a multidisciplinary laboratory approach to the
investigation and diagnosis of all forms of CJD, with the need to investigate
autopsy tissues from suspected cases by the histological and biochemical
techniques described herein.
NAL call no. QR1.A6
Descriptors:
NvCreutzfeldt-Jakob Disease, histology, histology, immunocytochemistry,
Western blot analysis, CNS, lymphoid tissue, other organs.
Kaaden, O.R.; Eichhorn, W.; Essbauer, S. Recent developments in the epidemiology of virus
diseases. J Vet Med, Ser B. Berlin : Blackwell
Wissenschafts-Verlag. Feb 2002. v. 49 (1) p. 3-6. ISSN:
0931-1793.
Abstract: There is continual variation in viral epidemics
regarding clinical symptoms, duration and disappearance, and the emergence of
new diseases. This can be observed in both human and animal diseases. This
evolution of virus diseases is mainly related to three factors: aetiological
agent, host and environment. As far as genetic alterations of the virus are
concerned, two major mechanisms are involved: mutations such as recombination
and reassortment; and selection for resistance or susceptibility. This review
focuses on the epidemiology of newly emerged virus diseases in man and
animals, such as acquired immunodeficiency syndrome, haemorraghic fevers,
bovine spongiform encephalopathy, canine haemorraghic disease and respiratory
syndrome in horses.
NAL call no. 41.8 Z52
Descriptors: human,
livestock, viral diseases, epidemiology, epidemics, symptoms, duration,
evolution, etiology, genetic variation, mutations, recombination, natural
selection, hemorrhagic fevers, bovinespongiform encephalopathy, literature
reviews, acquired immune deficiency syndrome, canine hemorrhagic disease,
respiratory syndrome in horses.
Kahler, Susan C. The rationale for ridding
U.S. of scrapie. Journal of the American Veterinary Medical
Association. 2002 May 1; 220(9): 1280-1. ISSN: 0003-1488
NAL call no.
41.8 AM3
Descriptors: BSE, bovine spongiform encephalopathy,
prevention and control, scrapie, cattle, sheep, animal feed formations and
processing, contaminated feeds, prion diseases, US.
Kao, R. R.; Gravenor M.B.; Baylis, M.; Bostock, C.J.; Chihota, C. M.;
Evans, J.C.; Goldmann, W.; Smith, A. J. A.; McLean, A.R. The potential size and duration of an epidemic of
bovine spongiform encephalopathy in British sheep. Science.
Washington, DC. 11 January, 2002; 295 (5553): 332-335. ISSN:
0036-8075
Abstract: Because there is a theoretical possibility that
the British national sheep flock is infected with bovine spongiform
encephalopathy (BSE), we examined the extent of a putative epidemic. An age
cohort analysis based on numbers of infected cattle, dose responses of cattle
and sheep to BSE, levels of exposure to infected feed, and number of
BSE-susceptible sheep in the United Kingdom showed that at the putative
epidemic peak in 1990, the number of cases of BSE-infected sheep would have
ranged from fewer than 10 to about 1500. The model predicts that fewer than 20
clinical cases of BSE in sheep would be expected in 2001 if maternal
transmission occurred at a rate of 10%. Although there are large uncertainties
in the parameter estimates, all indications are that current prevalence is
low; however, a simple model of flock-to-flock BSE transmission shows that
horizontal transmission, if it has occurred, could eventually cause a large
epidemic.
NAL call no. 470 Sci2
Descriptors: BSE, bovine
spongiform encephalopathy, cattle, sheep diseases, horizontal disease
transmission, cohort studies, genetic predisposition to Disease,
Great-Britain, epidemiology, logistic models, prevalence, prions chemistry and
genetics, probability, scrapie epidemiology and transmission, sheep
genetics.
Kaup F. J.; Schwibbe, M. Primaten als
Versuchstiere. [Nonhuman primates as laboratory animals.] DTW
Deutsche-Tieraerztliche-Wochenschrift. Marz, 2002; 109 (3): 104-108. In
German.
NAL call no. 41.8 D482
Descriptors: non-human primates,
biomedical models, disease models, viral infections, transmissible spongiform
encephalopathies.
Kersseboom, R.; Koekoek, S. C.; Richardus, J. H. Het risico van de variant van de ziekte van
Creutzfeldt-Jakob in Nederland en het effect van preventieve
maatregelen. [The risk of variant Creutzfeldt-Jakob disease in the
Netherlands and the effect of preventive measures]. Nederlands Tijdschrift
voor Geneeskunde. 2002 Apr 20; 146(16): 754-9 ISSN: 0028-2162. In
Dutch.
Abstract: Variant Creutzfeldt-Jakob disease (vCJD) is a fatal
and untreatable neurological disease, in which pathogenic prions (PrPSc) are
involved. There is convincing epidemiological and experimental evidence that
vCJD is a human expression of bovine spongiform encephalopathy (BSE). The risk
of transmission of pathogenic prions which cause vCJD to humans is influenced
by the species barrier, genetic susceptibility of the host, dose of infection
and route of exposure. Transmission of pathogenic prions from bovines to
humans is possible through meat products containing nerve and lymphatic
tissue, and through medical products derived from bovine material. Human to
human transmission is, in principle, also possible via blood and blood-derived
products, human organs and tissues for transplantation, and through surgical
instruments. Preventive measures to reduce transmission from bovines to humans
have been introduced step by step in the Netherlands since 1989. With proper
implementation, the current risk of becoming infected by Dutch meat products
is small. It is very likely, however, that in the past decade BSE-infected
bovines have entered the food chain. The Dutch population has also been
exposed to foreign infected meat products. Measures to prevent human to human
transmission are currently being improved in the Netherlands. It is expected
that cases of vCJD will occur in the Netherlands in the future, but the number
cannot be estimated accurately. The presence of PrPSc in both the livestock
and in the human population in the Netherlands constitutes a permanent public
health threat and is a reason for continued vigilance and active
prevention.
Descriptors: NvCJD, transmission of pathogenic prions,
control measures, public health concerns, Netherlands, risk assessment, level
of PrPSc in livestock and people.
Kirk, Sara F. L.; Greenwood, Darren; Cade, Janet E.; Pearman, Alan D. Public perception of a range of potential food
risks in the United Kingdom. Appetite. June, 2002; 38 (3):
189-197. ISSN: 0195-6663
DOI: 10.1006/appe.2001.0478
NAL
call no. QP141.A1A64
Descriptors: public/consumer survey, potential
food risks, BSE, bovine spongiform encephalopathy, Salmonella, 1998, 1999,
UK.
Kneipp, Janina; Beekes, Michael; Lasch, Peter; Naumann, Dieter. Molecular changes of preclinical scrapie can be
detected by infrared spectroscopy. Journal of Neuroscience.
April 15, 2002; 22 (8): 2989-2997.
URL: http://www.jneurosci.org/cgi/content/abstract/22/8/2989
Descriptors:
infrared microspectroscopy, molecular changes, cryosections, scrapie-infected
brain tissue, 263K scrapie infected hamster nervous tissue, medulla
oblongata.
Krebs, John R.; May, Robert M.; Stumpf, Michael P.H. Theoretical models of sheep BSE reveal
possibilities. Nature. 2002 Jan 10; 415(6868): 115 ISSN:
0028-0836.
DOI: 10.1038/415115a
NAL call
no. 472 N21
Descriptors: bovine spongiform encephalopathy, etiology,
sheep diseases, animal feed formulations, cattle, disease prevention and
control, public policy, risk assessment.
Kohnlein, C.; Poser, S. Schwerpunktheft
Creutzfeldt-Jakob-Krankheit/BSE. [Creutzfeldt-Jakob disease/BSE special
issue]. Deutsche Medizinische Wochenschrift. 2002 Jun 14; 127(24):
1344. ISSN: 0012-0472. In German.
NAL call no. 448.8
D48
Descriptors: BSE, humans, cattle, epidemiology, historical
notes, risk factors, transmission, UK, Scotland.
Larski, Zdzislaw Niektore nowe dane
dotyczace wirusologii i zakaznych gabczastych encefalopatii. [Some new
data concerning virology and transmittable spongiform encephalopathies.]
Medycyna-Weterynaryjna. 2002; 58 (1): 13-17. In Polish.
NAL call no.
41.8 M463
Descriptors: review, preclinical diagnosis, transmissible
spongiform encephalopathies, TSE.
Lawlor, D.; Hockley, J.; Hawkins, S.A.C.; Simmons, M.M.; Matthews, D. The TSE Archive at VLA Weybridge. Research
in Veterinary Science. April, 2002; 72 (Supplement A): 46. 56th Annual
Conference of the Association of Veterinary Teachers and Research Workers on
Current Topics in Veterinary Science, Scarborough, England, UK, March 25-27,
2002
NAL call no. 41.8 R312
Descriptors: transmissible
spongiform encephalopathies, prions.
Lehmann, Sylvain. Metal ions and prion
diseases. Current Opinion in Chemical Biology. April, 2002; 6
(2): 187-192.
Descriptors: prion, metal ions, BSE, other prion
diseases.
Lehmann, Sylvain; Beranger, Florence; Solassol, Jerome; Ceschia, Audrey;
Perrier, Veronique; De Gassart, Aude; Vilette, Didier; Laude, Hubert;
Kellermann, Odile; Mange, Alain. Modeles en
culture cellulaire des encephalopathies spongiformes transmissibles.
[Cell culture models of transmissible spongiform encephalopathies.] Comptes
Rendus Biologies. Janvier, 2002; 325 (1): 59-65.
DOI: 10.1016/S1631-0691(02)01391-4
NAL
call no. Q2 C6
Descriptors: invitro cell cultures, experimental
models, prion infected lines, wild-type, mutated or chimeric prion proteins,
useful for investigating the biology of pathogenicity.
Levieux, A.; Rivera, V.; Levieux, D.
Immunochemical control of the species origin of porcine crude heparin and
detection of ovine and caprine materials. Journal of Pharmaceutical
and Biomedical Analysis. 2002 Jan 1. 27(1-2): 305-313 ISSN:
0731-7085
Abstract: As a consequence of the outbreak of bovine
spongiform encephalopathy (BSE), ruminants materials have been generally
banned from the production of heparin. Immunochemical methods have been
recently developed for the control of the raw materials used by manufacturers
of materials such as porcine mucosa and for the detection of bovine crude
heparins. To certify the porcine origin of crude porcine heparins and to
exclude ovine or caprine materials, new ELISAs were developed. Rabbit antisera
were produced against species-specific antigenic contaminants present in crude
heparins or in eluted materials (EM) from the chromatographic step of the
purification process. When analysed by line immunoelectrophoresis, these
antisera revealed five to eleven antigenic contaminants in the EMs, the major
one being the most anodic and predominant antigen in crude heparins. Using the
best antisera, competitive indirect ELISAs were optimised. They allowed the
detection of porcine, ovine and caprine crude heparins down to a dilution of
0.6 to 1.5 parts per 1000, with CVs ranging from 3 to 12%. These ELISAs
complete the set of immunological techniques which can be routinely used by
heparin manufacturers to secure their supply chain.
Descriptors:
BSE, bovine based pharmaceuticals, health risks, ELISA test, antibodies.
Lucker, Ernst; Hardt, Michael; Groschup, Martin H. Detection of CNS and PrPSc in meat products.
Berliner und Munchener Tierarztliche Wochenschrift 2002 Mar-Apr;
115(3-4): 111-7. ISSN: 0005-9366.
Abstract: Several methods for the
detection of tissues of the central nervous system (CNS) in meat products have
been developed and partly validated for use in official food control as
pertaining to human BSE-exposure risk. So far, however, methods for the
detection of abnormal prion protein (PrPSc) were not evaluated for their
potential applicability to the matrix of heat treated meat products. We
developed a micro technological procedure for the preparation of meat products
suitable for high security laboratories as masses were 6 to 8 orders of
magnitude lower than in conventional meat technology. Thus it was possible to
produce standard micro sausages containing defined amounts of bovine
BSE-positive brain. This material showed all characteristics of normal meat
products and a homogeneous distribution of brain as indicated by NSE and GFAP
western immunoblotting and GFAP immunometric analyses. Using a commercially
available and certified immunometric assay for detection of PrPSc in untreated
brain it was possible to detect BSE-positive CNS down to a content of 0.25% in
heat treated meat products. We found a high correlation between PrPSc
OD-values and CNS content and linearity up to 10% CNS. In 30 samples of retail
meat products no sample transgressed the official cut off value for untreated
bovine brain. Further studies are needed to show whether an increase of
sensitivity in PrPSc detection from the meat product matrix is possible, in
particular by optimisation of the extraction procedure.
NAL call no. 41.8
B45
Descriptors: CNS, PrPSc, detection of central nervous tissue in
meat, immunometric assay, detection of PrPSc in untreated brain.
Lucker, Ernst; Schlottermuller, Beate; Martin, Antje Studies on contamination of beef with tissues of the
central nervous system (CNS) as pertaining to slaughtering technology and
human BSE-exposure risk. Berliner und Munchener Tierarztliche
Wochenschrift. 2002 Mar-Apr; 115(3-4): 118-21 ISSN:
0005-9366
Abstract: Contamination of beef by tissues of the central
nervous system (CNS) due to slaughter technology causes some concern
considering the potential health hazard by food borne exposure to the
infectious agent of BSE. The present study was designed to quantify the extent
of CNS contamination as pertaining to stunning and splitting technology. Of
the 726 animals 48 contained a total of 58 emboli-like particles in lungs
and/or right ventricles. The incidence of emboli-like particles was found to
be slightly higher in animals slaughtered without pithing (5.9%) than in the
animals slaughtered with pithing (4.1%). Of the 58 emboli-like particles only
two were positive in the anti-NSE western immunoblotting (0.3% of the 726
animals). The immuno reaction of these NSE-positive particles was several
orders of magnitude lower as obtained by pure brain material. The
microscopical analysis of the two NSE-positive emboli-like particles for
presence of CNS-like tissues was negative. Following splitting of carcasses by
sawing with and without prior removing the spinal cord we found NSE-positive
reactions in 32% and 17% of the samples, respectively. The immuno reaction,
however, was predominantly comparable to standard material containing less
than 0.5% CNS. Overall the results show that CNS contamination of bovine
carcasses cannot be excluded by current slaughter technology. However, the
additional human BSE-exposure risk can be judged to be at least minor when
considering extent of contamination, dilution effects and BSE-testing.
NAL
call no. 41.8 B45
Descriptors: cattle, slaughter processes, level of
beef meat contamination, central nervous system tissue, emboli-like
particles.
Lunney, Joan K.; Fossum, Caroline; Alm, Gunnar V.; Steinbach, Falko;
Wattrang, Eva. Veterinary immunology:
Opportunities and challenges. Trends in Immunology. January,
2002; 23 (1): 4-6. 6th International Veterinary Immunology Symposium, Uppsala,
Sweden, July 15-20, 2001. ISSN: 1471-4906
NAL call no. QR180
I56
Descriptors: Veterinary medicine, animal immunology.
Lupi, Omar. Prions in dermatology.
Journal of the American Academy of Dermatology. 2002 May; 46(5):
790-3 ISSN: 0190-9622
Abstract: Prion diseases are uncommon fatal
neurodegenerative disorders that have gained scientific importance as a result
of the emergence of new forms of these diseases in both animals and humans.
Prions appear to be composed principally or entirely of abnormal isoforms of a
host-encoded glycoprotein. There is substantial scientific evidence to support
the notion that bovine spongiform encephalopathy ("mad cow disease") has
affected humans. Recent studies have demonstrated that prions can adhere
easily to metal surfaces, and normal sterilization procedures are not likely
to completely inactivate them. Iatrogenic transmission of prion diseases, such
as Creutzfeldt-Jakob disease, was recognized after corneal transplantations,
dura mater grafts, neurosurgical procedures, and the use of human hormones
(growth hormone and gonadotropin). Although bovine collagen has long been
recognized as a safe and biocompatible material, dermatologists should be
aware of the theoretical potential for prion transmission when materials from
bovine origin and products obtained from cultured cells fed with fetal or
newborn calf serum are used.
Descriptors: spongiform
encephalopathies, prions, iatrogenic transmission, bovine based products,
fetal or newborn calf serum, risks.
Mabbott, Neil A; McGovern, Gillian; Jeffrey, Martin; Bruce, Moira E. Temporary blockade of the tumor necrosis factor
receptor signaling pathway impedes the spread of scrapie to the brain.
Journal of Virology 2002 May; 76(10): 5131-9. ISSN:
0022-538X
DOI: 10.1128/JVI.76.10.5131-5139.2002
Abstract:
Although the transmissible spongiform encephalopathies (TSEs) are
neurodegenerative diseases, their agents usually replicate and accumulate in
lymphoid tissues long before infection spreads to the central nervous system
(CNS). Studies of a mouse scrapie model have shown that mature follicular
dendritic cells (FDCs), which express the host prion protein (PrP(c)), are
critical for replication of infection in lymphoid tissues. In the absence of
mature FDCs, the spread of infection to the CNS is significantly impaired.
Tumor necrosis factor alpha (TNF-alpha) secretion by lymphocytes is important
for maintaining FDC networks, and signaling is mediated through TNF receptor 1
(TNFR-1) expressed on FDCs and/or their precursors. A treatment that blocks
TNFR signaling leads to the temporary dedifferentiation of mature FDCs,
raising the hypothesis that a similar treatment would significantly delay the
peripheral pathogenesis of scrapie. Here, specific neutralization of the TNFR
signaling pathway was achieved through treatment with a fusion protein
consisting of two soluble human TNFR (huTNFR) (p80) domains linked to the Fc
portion of human immunoglobulin G1 (huTNFR:Fc). A single treatment of mice
with huTNFR:Fc before or shortly after intraperitoneal injection with the ME7
scrapie strain significantly delayed the onset of disease in the CNS and
reduced the early accumulation of disease-specific PrP in the spleen. These
effects coincided with a temporary dedifferentiation of mature FDCs within 5
days of huTNFR:Fc treatment. We conclude that treatments that specifically
inhibit the TNFR signaling pathway may present an opportunity for early
intervention in peripherally transmitted TSEs.
NAL call no.
QR360.J6
Descriptors: scrapie, TSE's mouse scrapie model, follicular
dendritic cells, replication of i nfection in lymphoid tissues, blocking tumor
necrosis factor alpha, pathogenesis delays.
MacDiarmid, S.C. Bovine spongiform
encephalopathy (BSE) in sheep? Australian Veterinary Journal
2002 Mar; 80(3): 148-9 ISSN: 0005-0423
NAL call no. 41.8
Au72
Descriptors: BSE, epidemiology, disease transmission, cattle,
goats, sheep, population surveillance methods, risk assessment, etiology,
Australia, New Zealand.
Marella, Mathieu; Lehmann, Sylvain; Grassi, Jacques; Chabry, Joelle. Filipin prevents pathological prion protein
accumulation by reducing endocytosis and inducing cellular PrP release.
Journal of Biological Chemistry, 2002 Jul 12; 277(28):
25457-64. ISSN: 0021-9258
Abstract: Conversion of the normal
membrane-bound prion protein (PrP-sen) to its pathological isoform (PrP-res)
is a key event in the pathogenesis of transmissible spongiform
encephalopathies. Although the subcellular sites of conversion are poorly
characterized, several lines of evidence have suggested the involvement of
membrane lipid rafts in the conversion process. Here we report that copper
stimulates the endocytosis of PrP-sen via a caveolin-dependent pathway in both
microglia and neuroblastoma cells. We show that the polyene antibiotic filipin
both limits endocytosis of PrP-sen and dramatically reduces the amount of
membrane-bound PrP-sen. This reduction results from a rapid and massive
release of full matured PrP-sen into the culture medium. Finally, we
demonstrate that filipin is a potent inhibitor of PrP-res formation into
chronically infected neuroblastoma cells. Our results reinforce the role of
rafts in PrP trafficking and raise the possibility that the release of PrP-sen
from the plasma membrane decreases the amount of available substrate PrP-sen
at the conversion sites.
NAL call no. 381 J824
Descriptors: cell
culture, microglia, neuroblastoma cells, copper, endocytosis, Prp-sen, effects
of filipin antibiotic, inhibition of PrP-res formation, nystatin
pharmacology.
Martin, S.; Gonzalez, L.; Jeffrey, M.; Bellworthy, S.J. Differential diagnosis of BSE agent and scrapie
infection of sheep. Research in Veterinary Science. April, 2002;
72 (Supplement A): 44. 56th Annual Conference of the Association of Veterinary
Teachers and Research Workers on Current Topics in Veterinary Science,
Scarborough, England, UK, March 25-27, 2002
NAL call no. 41.8
R312
Descriptors: bovine spongiform encephalopathy, scrapie,
diagnostic techniques.
Martinsen, T.C.; Taylor, D.M.; Johnsen, R.; Waldum, H.L. Gastric acidity protects mice against prion
infection? Scandinavian Journal of Gastroenterology. May, 2002;
37 (5): 497-500.
URL: http://www.ingentaconnect.com/content/apl/sgas/2002/00000037/00000005/art00001
NAL call no.
RC799 S33
Descriptors: transmissible degenerative encephalopathies,
sheep scrapie, bovine spongiform encephalopathy, Creutzfeldt-Jakob Disease,
gastric acidity and susceptibility to infection, mouse model,
experimentalinfection, implications for eating contaminated meats.
Matorras, Roberto; Rodriguez Escudero, Francisco, J. The use of urinary gonadotrophins should be
discouraged. Human Reproduction. Oxford. July, 2002; 17 (7):
1675.
NAL call no. QP251 H85
Descriptors: prion proteins,
infectivity concerns, transmissible spongiform encephalopathies, FSH, LH.
McCormack, James E.; Baybutt, Herbert N.; Everington, Dawn; Will, Robert
G.; Ironside, James W.; Manson, Jean C. PRNP
contains both intronic and upstream regulatory regions that may influence
susceptibility to Creutzfeldt-Jakob Disease. Gene. 2002 Apr 17;
288(1-2): 139-46 ISSN: 0378-1119
Abstract: The Prion protein (PrP)
plays a central role in Creutzfeldt-Jakob Disease (CJD) and other
transmissible spongiform encephalopathies (TSEs). Mutations in the protein
coding region of the human PrP gene (PRNP), which have been proposed to alter
the stability of the PrP protein, have been linked to a number of forms of
TSE. However, the majority of CJD cases are not associated with mutations in
the PRNP coding region and alternative mechanisms must therefore underlie
susceptibility to these forms of CJD. Transgenic mice, that over- or
under-express PrP genes, have shown a correlation between the level of PrP
gene expression and the incubation time of disease. Polymorphisms that lead to
alterations in human PRNP gene expression, could therefore be candidates for
influencing susceptibility of an individual to CJD. In order to investigate
this hypothesis, we have defined an upstream and intronic regulatory region of
the PRNP gene. Sequencing of these regions in controls, sporadic CJD (sCJD)
and variant CJD (vCJD) patients has identified three polymorphisms, all of
which are more common in sCJD patients than controls. Our data suggests that
polymorphisms in the regulatory region of the PRNP gene may be a risk factor
for CJD.
NAL call no. QH442.A1G4
Descriptors: risk factors for
disease, humans, polymorphisms, regulatory regions.
Milhavet, Ollivier; Lehmann, Sylvain. Oxidative stress and the prion protein in
transmissible spongiform encephalopathies. Brain Research. Brain
Research Reviews. 2002 Feb; 38(3): 328-39 ISSN: 0165-0173
Abstract:
Transmissible spongiform encephalopathies form a group of fatal
neurodegenerative disorders that have the unique property of being infectious,
sporadic or genetic in origin. These diseases are believed to be the
consequence of the conformational conversion of the prion protein into an
abnormal isoform. Their exact pathogenic mechanism remains uncertain, but it
is believed that oxidative stress plays a central role. In this article, we
will first review in detail the data supporting the latter hypothesis.
Subsequently, we will discuss the relationship between the prion protein and
the cellular response to oxidative stress, attempting ultimately to link PrP
function and neurodegeneration in these disorders.
Descriptors: TSE,
prion protein conformation, oxidative stress, pathogenic mechanism.
Morgenthaler, Jean Jacques; Maring, Jacques Andre; Rentsch,Markus. Method for the removal of causative agent(s) of
transmissible spongiform encephalopathies from protein solutions.
Official Gazette of the United States Patent and Trademark Office
Patents. [e-file] June 18, 2002; 1259 (3): No Pagination
Journal URL:
www.uspto.gov/web/menu/patdata.html
NAL
call no. T223 A22
Descriptors: non-conventional transmissible
agents, causative agents, transmissible spongiform encephalopathies,
contaminated protein solution, absorbent, kieselguhr, diatomaceous earth,
silicic acid, clay minerals, metal hydroxide, metal oxihydrate, cellulose,
perlite, bentonite, and water-insoluble synthetic polymers.
Newgard, Jason R.; Rouse, Glenda C.; McVicker, Jerry K. Novel method for detecting bovine immunoglobulin G
in dried porcine plasma as an indicator of bovine plasma contamination.
Journal of Agricultural and Food Chemistry 2002 May 22; 50(11):
3094-7. ISSN: 0021-8561
Abstract: Current U.S. Food and Drug
Administration regulationsprohibit feeding of protein derived from mammalian
tissue, excluding blood and blood products and any product that consists
entirely of porcine or equine protein. A novel lateral flow immunoassay device
has been developed that can quickly and qualitatively determine the presence
of bovine immunoglobulin G (IgG), a major component in blood products, at very
low levels (0.01% v/v). The device can be used to test for bovine IgG
commingling in spray-dried porcine plasma used in the feed industry. Producers
and consumers alike could use this device to verify product content at
threshold levels.
NAL call no. 381 J8223
Descriptors: US FDA,
animal feeds, and swine or horse protein comtaminants, immunoassay for bovine
IgG contaminants, BSE control and prevention.
Nair, Bindu; Elmore, Amy R. Final report on
the safety assessment of Human Placental Protein, Hydrolyzed Human Placental
Protein, Human Placental Enzymes, Human Placental Lipids, Human Umbilical
Extract, Placental Protein, Hydrolyzed Placental Protein, Placental Enzymes,
Placental Lipids, and Umbilical Extract. International Journal of
Toxicology. 2002; 21 (Supplement 1): 81-91.
NAL call no. RA1190
J61
Descriptors: cosmetic ingredients, human and animal pracental
proteins, transmissible spongiform encephalopathies risks, EU prohibited use,
FDA, toxicology recommendations.
Narang, Harash. A critical review of the nature of the spongiform
encephalopathy agent: protein theory versus virus theory. Experimental
Biology and Medicine. 2002 Jan; 227(1): 4-19. ISSN:
1535-3702.
Abstract: All spongiform encephalopathies (SEs) result in
brain disorders brought about by a slow virus. Since the origin of bovine SE
(BSE), the infectious nature of the disease has been firmly established.
Tubulofilamentous particles/scrapie termed nemavirus (NVP) and
scrapie-associated fibrils (SAF) are ultrastructural markers, whereas
protease-resistant protein (PrP(sc)) is a protein marker. The PrP molecules
aggregate to form SAF. Each NVP consists of three layers: an outer protein
coat, an intermediate ssDNA layer, and inner PrP/SAF. Therefore, ssDNA and
PrP/SAF are physically associated with each other. The existence of at least
20 stable strains of SEs implies that a nucleic acid molecule serves as the
information molecule. Animals inoculated with PrP(sc) do not develop the
clinical disease, however, ssDNA purified from scrapie-hamster brains by
alkaline gel electrophoresis mixed with binding proteins before inoculation
developed the clinical disease. It appears that an "accessory protein" coded
by the ssDNA of the NVP interacts with normal PrP(c) molecules, resulting in
their conversion to PrP(sc)/SAF. The pathogenesis process in the infected
animal, with increasing incubation periods, reveals that larger amounts of
normal PrP molecules are modified to form SAF. This interferes with the normal
supply of PrP to cell membranes, which become disrupted and eventually
fragment, resulting in the vacuoles typical of those found in the SEs.
Critical review of scientific literature has demonstrated that the agent
contains a DNA genome.
NAL call no. QH301 E9
Descriptors: bovine
spongiform encephalopathy, brain disorders, scrapie, PrPSc, interaction
between nemavirus and scrapie associated fibrils cause the disease,
pathogenesis.
Nunnally, Brian K. It's a mad, mad, mad,
mad cow: A review of analytical methodology for detecting BSE/TSE.
Trends in Analytical Chemistry. February, 2002; 21 (2):
82-89.
DOI: 10.1016/S0165-9936(01)00134-0
NAL
call no. QD71T7
Descriptors: review, analytical detection, bovine
spongioform encephalopathy, BSE, transmissible spongioform encephalopathy,
TSE, golden Syrian hamster bioassay, immunoassays and capillary
electrophoresis methods, blood, bio-fluids.
Ockerman, H. W.; Basu, L. Update on Bovine
Spongiform Encephalopathy (BSE, mad cow disease). Special Circular
Ohio Agricultural-Research and Development Center. 2002, No.183, 61-65; 5
ref.
NAL call no. 100 Oh3S
Descriptors: BSE, state of the U.S.
cattle industry.
Oldstone, Michael B.A.; Race, Richard; Thomas, Diane; Lewicki,Hanna;
Homann, Dirk; Smelt, Sara; Holz, Andreas; Koni, Pandelakis; Lo, David;
Chesebro, Bruce; Flavell, Richard. Lymphotoxin-alpha- and lymphotoxin-beta-deficient
mice differ in susceptibility to scrapie: evidence against dendritic cell
involvement in neuroinvasion. Journal of Virology 2002 May; 76(9): 4357-63. ISSN:
0022-538X.
Abstract: Transmissible spongiform encephalopathy or prion
diseases are fatal neurodegenerative disorders of humans and animals often
initiated by oral intake of an infectious agent. Current evidence suggests
that infection occurs initially in the lymphoid tissues and subsequently in
the central nervous system (CNS). The identity of infected lymphoid cells
remains controversial, but recent studies point to the involvement of both
follicular dendritic cells (centers is dependent on lymphotoxin alpha
(LT-alpha) and LT-beta signaling components. We report here that by the oral
route, LT-alpha -/- mice developed scrapie while LT-beta -/- mice did not.
Furthermore, LT-alpha -/- mice had a higher incidence and shorter incubation
period for developing disease following inoculation than did LT-beta -/- mice.
Transplantation of lymphoid tissues from LT-beta -/- mice, which have cervical
and mesenteric lymph nodes, into LT-alpha -/- mice, which do not, did not
alter the incidence of CNS scrapie. In other studies, a virus that is tropic
for and alters functions of CD11c(+) cells did not alter the kinetics of
neuroinvasion of scrapie. Our results suggest that neither FDC nor CD11c(+)
cells are essential for neuroinvasion after high doses of RML scrapie.
Further, it is possible that an as yet unidentified cell found more abundantly
in LT-alpha -/- than in LT-beta -/- mice may assist in the amplification of
scrapie infection in the periphery and favor susceptibility to CNS disease
following peripheral routes of infection. FDC) and CD11c(+) lymphoid dendritic
cells. FDC generation and maintenance in general.
NAL call no. QR360
J6
Descriptors: scrapie, oral intake, infectious material, lymphoid
tissue, NCS, LT alpha mice, LT beta mice, incubation periods.
Paisley, Larry G. Monitoring and analysis
of bovine spongiform encephalopathy (BSE) testing in Denmark using statistical
models. APMIS. January, 2002; 110 (1): 61-70.
Abstract:
The evolution of monitoring and surveillance for bovine spongiform
encephalopathy (BSE) from the phase of passive surveillance that began in the
United Kingdom in 1988 until the present is described. Currently, surveillance
for BSE in Europe consists of mass testing of cattle slaughtered for human
consumption and cattle from certain groups considered to be at higher risk of
having clinical or detectable BSE. The results of the ongoing BSE testing in
Denmark have been analyzed using two statistical approaches: the "classical"
frequentist and the Bayesian that is widely used in quantitative risk
analysis. The analyses were intended to provide information for
decision-markers, the media and the public as well as to provide inputs for
future BSE surveillance models. The results to date suggest that the total
number of BSE cases that will be found in Denmark in 2001 will not exceed
16.
NAL call no. QR1.A6
Descriptors: cattle, prions, bovine
spongiform encephalopathy, disease surveillance, statistical methods,
epidemiology, Denmark.
Parnham, D.W.; Foster, J. D.; Hunter, N.
Immunocytochemical tales of the unexpected and the power of the PET
Blot. Research in Veterinary-Science. April, 2002; 72
(Supplement A): 47-48. 56th Annual Conference of the Association of Veterinary
Teachers and Research Workers on Current Topics in Veterinary Science,
Scarborough, England, UK, March 25-27, 2002
NAL call no. 41.8
R312
Descriptors: prion diseases, diagnostic measures.
Pedersen, Nils Strandberg; Smith, Else. Prion diseases: epidemiology in man. APMIS
Acta Pathologica, Microbiologica, et Immunologica Scandinavica 2002 Jan;
110(1): 14-22 ISSN: 0903-4641.
Abstract: Prion disease in man was
first described as Creutzfeldt-Jacob disease (CJD) in the 1920s. CJD may have
three different origins: sporadic, familial, due to mutations in the prion
gene, or infectious, due to iatrogenic exposure to infectious brain material.
As an example of the latter, kuru, in Papua New Guinea, was a variant of CJD
transmitted by cannibalism. Between 1957 and 1982 more than 2500 died of kuru.
Sporadic CJD is the most common form of CJD and occurs with an incidence of
around one per million in most parts of the world. Familial CJD accounts for
approximately 10% of all European cases of CJD, and is associated with
inherited mutations of the prion protein gene, caused by one of the 24 single
amino acid substitutions or insertions of octapeptide repeats. CJD caused by
infections involves either iatrogenic cases of CJD, resulting from exposure to
infectious brain, pituitary or ocular tissue, or from ingestion of infected
food items. As of today, a few hundred iatrogenic cases of CJD have been
diagnosed worldwide, the majority due to transmission by cadaveric pituitary
HCG. So far, 111 cases of vCJD have been diagnosed caused by BSE-contaminated
food. The size of the epidemic is still unclear and worst-case scenarios
indicate that we may expect many thousands of cases in the future.
NAL call
no. QR1.A6
Descriptors: Creutzfeldt-Jacob disease, CJD, sporadic,
familial, kuru, NvCJD, BSE, contaminate meat products, epidemiology,
cannabilism, cornal transplants, iatrogenic disease epidemiology, prion
diseases, prion genetics and biochemistry, zoonotic disease.
Polak, Miroslaw P.; Rozek, Wojciech; Zmudzinski, Jan F. Monitoring BSE. [BSE monitoring.] Medycyna
Weterynaryjna. 2002; 58 (4): 265-266. In Polish.
NAL call no. 41.8
M463
Descriptors: review paper, active surveillance principles,
bovine spongiform encephalopathy, Switzerland, EU, Poland, diagnostic
tests.
Polak, M.P.; Rozek, W.; Zmudzinski, J.F.
Monitoring BSE w Polsce. [BSE monitoring in Poland.] Medycyna
Weterynaryjna. 2002; 58 (5): 344-347. In Polish.
NAL call no. 41.8
M463
Descriptors: diagnostic tests, Prionics-Check(R), monitoring of
BSE, EU, cattle, randon sampling.
Poser, Charles M. Notes on the history of
the prion diseases. Part I. Clinical Neurology and
Neurosurgery. 2002 Jan; 104(1): 1-9 ISSN: 0303-8467.
Abstract:
The astute observation by William Hadlow, an American veterinary
neuropathologist of the similarity between the histopathology of kuru, an
obscure disease of the primitive tribe in New Guinea, and scrapie of sheep,
was the first clue to the etiology of the transmissible spongiform
encephalopathies (TSE). The knowledge that scrapie was transmissible but only
after an unusually long incubation period, that the causative agent was highly
resistant to heat and formalin, and that it seemed to be able to replicate in
the absence of nucleic acid, eventually led to the discovery of the prion by
Stanley Pruisner and the still controversial protein-only hypothesis of
etiology of the TSE.
Descriptors: kuru, scrapie, transmissible
spongiform encephalopathies, prion disease theory.
Poser, Charles M. Notes on the history of
the prion diseases. Part II.
Clinical Neurology and Neurosurgery. 2002 May; 104(2): 77-86
ISSN: 0303-8467
Abstract: The protein-only theory of transmission of
the prion diseases remains controversial. Other mechanisms such as the virus,
virino, and viroid hypotheses are still under consideration. All these fit in
the concept of 'slow' infections that had been proposed in 1954 by Bjorn
Sigurdsson, an Icelandic pathologist. Regardless of the exact mode of
infection, the presence of prions in the brain has served to unite
Creutzfeldt-Jakob disease (CJD), the Gerstmann-Straussler-Scheinker syndrome
and fatal familial insomnia, as well as scrapie and a number of other animal
diseases, into a single pathological entity, the transmissible spongiform
encephalopathies. The appearance of bovine spongiform encephalopathy in the
United Kingdom and its putative relationship to new variant CJD, have put a
new and unpredictable light on these unusual and uncommon
diseases.
Descriptors: disease transmission theories, BSE,
Creutzfeldt-Jakob disease, CJD, the Gerstmann-Straussler-Scheinker syndrome,
fatal familial insomnia, scrapie, NvCJD, pathological agent.
Poser, S.. BSE - Eine Ursache fur die
Creutzfeldt-Jakob-Krankheit? [BSE - A cause for Creutzfeldt-Jakob
disease?] Deutsche Medizinische Wochenschrift 2002 Feb 15; 127(7): 311
ISSN: 0012-0472. In German.
NAL call no. 448.8 D48
Descriptors:
BSE, bovine spongiform encephalopathy, transmission, diagnosis, epidemiology,
biological markers, cattle, iatrogenic disease, risk factors, France, Germany,
Great Britain, Ireland.
Poser, S.; Zerr, I.; Felgenhauer, K. Die
neue Variante der Creutzfeldt-Jakob-Krankheit. [New variant
Creutzfeldt-Jakob disease]. Deutsche Medizinische Wochenschrift. 2002
Feb 15; 127(7): 331-4 ISSN: 0012-0472. In German.
NAL call no. 448.8
D48
Descriptors: NvCreutzfeldt-Jakob Disease, epidemiology, BSE,
bovine spongiform encephalopathy, diagnosis, transmission, contaminated meat,
human risk factors, incidence of disease.
Ramsay, A. R145: Evolution of a TSE
diagnostic antibody. Research in Veterinary Science. April,
2002; 72 (Supplement A): 48. 56th Annual Conference of the Association of
Veterinary Teachers and Research Workers on Current Topics in Veterinary
Science, Scarborough, England, UK, March 25-27, 2002.
NAL call no. 41.8
R312
Descriptors: transmissible spongiform encephalopathies,
diagnostic test, R145 antibody, development.
Redman, C.A.; Coen, P.G.; Matthews, L.; Lewis, R. M.; Dingwall, W.S.;
Foster, J.D.; Chase-Topping, M. E.; Hunter, N.; Woolhouse, M. E. J. Comparative epidemiology of scrapie outbreaks in
individual sheep flocks. Epidemiology and Infection 2002 Jun;
128(3): 513-21.
Abstract: Data recording the course of scrapie
outbreaks in 4 sheep flocks (2 in Cheviot sheep and 2 in Suffolks) are
compared. For each outbreak the data on scrapie incidence and sheep demography
and pedigrees cover periods of years or decades. A key finding is that the
incidence of clinical cases peaks in sheep 2-3 years old, despite very
different forces-of-infection. This is consistent with age-specific
susceptibility of sheep to scrapie, as has been reported for cattle to bovine
spongiform encephalopathy and for humans to variant Creutzfeldt-Jakob disease.
Scrapie incidence was higher in ewes than rams and at certain times of years,
though these effects were not consistent between flocks. There was no evidence
for high levels of vertical transmission.
NAL call no.
RA651.A1E74
Descriptors: scrapie, sheep, disease outbreaks, vertical
transmission, male and female comparisons.
Resende, C.; Parham, S.N.; Tinsley, C.; Ferreira, P.; Duarte, J.A.B.;
Tuite, M.F. The Candida albicans Sup35p
protein (CaSup35p): function, prion-like behaviour and an associated
polyglutamine length polymorphism. Microbiology. 2002, 148: 4.
ISSN: 1049-1060.
NAL call no. QR1 J64
Descriptors: prions, yeast
protein, comparison, biochemistry, Sup35pprotein.
Riley, Maria Louise; Leucht, Christoph; Gauczynski, Sabine; Hundt,
Christoph; Brecelj, Martina; Dodson, Guy; Weiss, Stefan High-level expression and characterization of a
glycosylated covalently linked dimer of the prion protein. Protein
Engineering. June, 2002; 15 (6): 529-537.
NAL call no. TP248
P77P763
Descriptors: prion protein dimers, scrapie prion protein
PrPSc, PrPc, human dimeric form, digestibility by proteinase, life cycle of
proteins.
Rosted, Palle; Jorgensen, Viggo Kragh. Prion strain causing bovine spongiform
encephalopathy (BSE) in cattle. Annals of Surgery. 2002 Feb;
235(2): 311. ISSN:
0003-4932.
Descriptors: cats diseases, prion diseases, BSE,
cattle.
Sabate, Raimon; Estelrich, Joan.
Aggregation characteristics of ovalbumin in beta-sheet conformation determined
by spectroscopy. Biopolymers. 2002; 67(2): 113-20 ISSN:
0006-3525.
Abstract: Protein misfolding and aggregation are involved
in a number of the so-called "conformational" diseases (e.g., transmissible
spongiform encephalopathies and Alzheimer disease). The development of
rational strategies to interfere with aggregation is a potential therapeutic
approach that requires complete knowledge of the aggregation process. We
studied the aggregation of ovalbumin in beta-sheet conformation using mainly
the spectral changes in the spectra of two dyes (Congo Red and pinacyanol)
caused by the aggregates. We assumed a linear model of polymerization that fit
to the experimental data. The critical aggregation constant, concentration of
half-aggregation, nucleation parameter, growth parameter, and number of
aggregation and free energy changes (total and per residue) were determined as
aggregation-related parameters. Beta-Ovalbumin aggregates in a cooperative
way. Moreover, the differences between such parameters obtained with Congo Red
and pinacyanol suggest that each dye interacts with the protein in its own
way.
NAL call no. 381 B524
Descriptors: protein structure,
misfolding, prions, transmissible spongiform encephalopathies.
Sasaki, Kensuke; Dohura, Katsumi; Ironside, James W; Iwaki, Toru. Increased clusterin (apolipoprotein J) expression in
human and mouse brains infected with transmissible spongiform
encephalopathies. Acta Neuropathologica (Berl). 2002 Mar;
103(3): 199-208. ISSN: 0001-6322.
Abstract: Clusterin
(apolipoprotein J), a multifunctional protein involved in amyloidogenesis in
Alzheimer's disease, was studied immunohistochemically in both human
transmissible spongiform encephalopathies (TSEs) and a mouse model of human
TSE. Clusterin immunoreactivity was co-localized with plaque-type deposits but
not with punctate-type prion protein (PrP) deposits in human TSEs. On the
other hand, clusterin-positive astrocytes were readily demonstrated in the
regions of punctate PrP deposits, but not around plaque PrP deposits despite
the presence of surrounding astrocytes. Clusterin expression in astrocytes was
not disease specific, but the punctate immunoreactivity for clusterin was more
prominently demonstrated in TSEs with punctate PrP deposits. Serial analysis
in the mouse model of human TSE revealed that clusterin expression in
astrocytes was enhanced in the lesions with punctate-type PrP deposits during
the disease progression. Thus, the induction of clusterin expression in
astrocytes could be more enhanced by punctate-type PrP deposits than by
plaque-type deposits. The clusterin molecules co-localized in plaque PrP
deposits might be derived not from surrounding astrocytes but from other
resources such as cerebrospinal fluid and blood plasma, both of which contain
clusterin in significant amounts. Taken together with previously reported
findings of the anti-amyloidogenic property in clusterin, our findings suggest
that clusterin may be induced as one of the important molecules participating
in the neurodegeneration caused by abnormally deposited
PrP.
Descriptors: protein analysis, immunohistochemical assay, TSE's
mouse model, plaque PrP deposites, neurodegeneration process.
Scholz, Roland. 25 Thesen gegen die
Behauptung, BSE und vCJK seien oral ubertragbare Infektionskrankheiten und BSE
gefahrde die menschliche Gesundheit. [25 theses against the assertion
that BSE and vCJD are orally transmissible infectious diseases and endanger
human health]. Deutsche Medizinische Wochenschrift. 2002 Feb 15;
127(7): 341-3. ISSN: 0012-0472. In German.
NAL call no. 448.8
D48
Descriptors: Nv Creutzfeldt-Jakob Disease, bovine spongiform
spongiform encephalopathy, transmission theories, cattle, epidemiology, meat
products, human health food risks, risk factors.
Schreuder, B.E.C.; Wever, C.J.G. Waar komt
BSE in Nederland vandaan? [The possible origin of BSE in the
Netherlands.] Tijdschrift voor Diergeneeskunde. 2002, 127: 2, 40-50; 29
ref. ISSN: 0040-7453. In Dutch with an English summary.
Abstract: It
is only in the last 5 years that the Netherlands has been confronted with
cases of bovine spongiform encephalopathy (BSE). The cases diagnosed to date
have not been clearly linked to imports from the United Kingdom. This article
describes the various possible explanations for the Dutch cases. The risk
factors involved, have either a connection with imported BSE, local origin of
BSE, or both. These factors can also be divided into introductory risk and
propagation risk, terms that were also used in an EU risk assessment study.
Research at ID-Lelystad since the early 1990s and at IKC-Ede has tried to
assess the relative importance of the various risk factors, the results of
which are discussed in this paper. The paper does not deal with the specifics
of the cases diagnosed to date, because of the absence of an in-depth
epidemiological investigation, but provides a general assessment of the risk
factors that might have played a role. Important factors have been, in
addition to the initial imports of cattle and meat and bone-meal from the UK,
the continuing imports from other countries with covert BSE and the
cross-contamination within the animal feed production lines. Emphasis is on
the period of the early and mid-1990s, the period in which most calves with
diagnosed BSE were born.
NAL call no. 41.8 T431
Descriptors:
bovine spongiform encephalopathy, BSE, history of disease introduction, animal
feeds, Netherlands, importance of risk factors leading to disease
introduction, importation of infected animals, animal feed formulations.
Schulz-Schaeffer, Walter J. BSE und
variante CJK. Von den Schwierigkeiten, ein neues Krankheitsprinzip zu
etablieren. [BSE and variant CJD: about the difficulties to establish a
new pathogenetic principle.] Deutsche Medizinische Wochenschrift 2002
Feb 15; 127(7): 344-6. ISSN: 0012-0472. In German.
NAL call no. 448.8
D48
Descriptors: bovine spongiform encephalopathy, cattle, consumer
food safety, Europe, epidemiology, NvCreutzfeldt-Jakob Disease, cattle,
hamsters, mice, primates, prions, risk factors, scrapie, time factors.
Schutt-Abraham, Ingrid. BSE-Praventivmassnahmen bei der Schlachtung von
Rindern. [Measures preventing BSE-contamination during the slaughter of
cattle.] Berliner und Munchener Tierarztliche Wochenschrift. 2002
Mar-Apr; 115(3-4): 125-30. ISSN: 0005-9366. In German.
Abstract:
SRM-regulations and the prohibition of pithing have removed major risks of
spreading BSE-infection. Traditional slaughter technology, especially captive
bolt stunning, head handling and carcass splitting nevertheless still provide
non-negligible risks for contamination with the BSE-agent if present in
cattle, and should therefore be replaced by safer techniques. However,
alternative methods like electrical stunning or removal of the spinal cord
prior to splitting the carcass cannot yet be considered a reliable and
practical option. Surface contamination could be prevented altogether by
abandoning the practice of carcass splitting and by removing the vertebral
column while still connected to the head, although this would result in
disadvantages for post mortem inspection.
NAL call no. 41.8
B45
Descriptors: cattle, slaughter, captive bolt, head handling,
carsass splitting, contamination with CNS tissue, alternative methods, spinal
cord removal.
Sethi, Shneh; Lipford, Grayson; Wagner, Hermann; Kretzschmar, Hans. Postexposure prophylaxis against prion disease with
a stimulator of innate immunity. Lancet. 2002 Jul 20; 360(9328):
229-30 ISSN: 0140-6736.
Abstract: The absence of an immune response
to prions--the infectious agents of scrapie, bovine spongiform encephalopathy
(BSE), and Creutzfeldt-Jakob disease--might be related to the fact that these
agents do not contain nucleic acids. We aimed to use CpG
oligodeoxynucleotides, which have been shown to stimulate innate immunity, as
a form of postexposure prophylaxis in mice. We inoculated healthy mice with
brain homogenates from mice infected with the RML scrapie prion, and then
injected CpG oligodeoxynucleotides. This postexposure prophylaxis with CpG
oligodeoxynucleotides resulted in 38% longer survival times than treatment
with saline (p<0.0001), or even longer after repeated application. The
explanation for this finding remains to be elucidated, but the most likely is
stimulation of TLR9-expressing cells of the innate immune system such as
macrophages, monocytes, and dendritic cells. CpG oligodeoxynucleotides have
not been shown to have adverse effects to human health and could therefore be
considered as a therapeutic choice in postexposure prophylaxis.
NAL call
no. 448.8 L22
Descriptors: infectious agents, scrapie, bovine
spongiform encephalopathy (BSE), and Creutzfeldt-Jakob disease, mouse model,
CpG oligodeoxynucleotides, stimulation of immunity.
Shaked, Yuval; Engelstein, Roni; Gabizon, Ruth. The binding of prion proteins to serum components
is affected by detergent extraction conditions. : Journal of
Neurochemistry. 2002 Jul; 82(1): 1-5 ISSN: 0022-3042.
Abstract:
As many GPI anchored proteins, PrP(C) and its abnormal conformer PrP(Sc),
are inserted into membrane microdomains known as rafts. Upon raft disruption,
PrP(C) becomes soluble, while PrP(Sc) aggregates into insoluble structures. It
was recently published that, as opposed to PrP(C), PrP(Sc), as well as its
protease resistant core PrP27-30, can bind specifically to plasminogen and
other serum components. These findings were suggested to have important
physiological implications in transmissible spongiform encephalopathies (TSE)
diagnosis and pathogenesis. In this work, we show that the binding of PrP(Sc)
or PrP 27-30 to serum proteins occurs only at specific detergent combinations,
in which disease associated PrPs are present in aggregated structures. At
detergent conditions in which rafts are intact, it is actually PrP(C.) that
binds to blood proteins, albeit not directly, but through neighboring rafts
components. Our results therefore indicate that the binding of PrP(Sc) to
blood components has no physiological relevance.
NAL call no. QP351
J6
Descriptors: raft disruption, PrPSc, factors affecting
transmissibility, diagnosis, and pathogenesis, serum protein binding, affects
of detergent combinations, physiological relevance.
Simak, Jan; Holada, Karel; D'Agnillo, Felice; Janota, Jan; Vostal, Jaroslav
G. Cellular prion protein is expressed on
endothelial cells and is released during apoptosis on membrane microparticles
found in human plasma. Transfusion. 2002 Mar; 42(3): 334-42
ISSN: 0041-1132.
Abstract: BACKGROUND: Blood and plasma of animals
experimentally infected with transmissible spongiform encephalopathies (TSEs)
can transmit TSE infection by transfusion. A conformational isoform of prion
protein (PrPsc) is believed to be the TSE-infectious agent that propagates by
converting the cellular prion protein (PrPc) to additional molecules of PrPsc.
In orally infected animals, PrPsc accumulates in intestinal endothelial cells.
In blood, two thirds of PrPc resides in plasma, but its source is not known.
STUDY DESIGN AND METHODS: The expression of PrPc in cultured human umbilical
vein endothelial cells (HUVECs) was studied using flow cytometry,
immunoblotting, and RT-PCR. Flow cytometry was used to characterize
endothelial membrane microparticles (MPs) in cell culture supernatants and in
normal human plasma. RESULTS: HUVECs and bovine aorta endothelial cells
express PrPc. The number of surface PrPc molecules per cell in HUVECs was
58,000 +/- 2,800. The induction of apoptosis in HUVECs led to a marked release
of membrane MPs (60,000-80,000 MPs/10(3) cells) that expressed PrPc and other
endothelial antigens. The presence of endothelial cell-derived MPs expressing
PrPc was demonstrated in platelet-free human plasma. CONCLUSION: Endothelial
cell apoptosis is associated with the release of PrPc-positive MPs. These MPs
contribute to the PrPc pool in plasma and may have a role in disseminating TSE
infectivity in blood.
Descriptors: experimental infections, TSEs,
transmissible spongiform encephalopathies, PrPsc, cultured human umbilical
vein endothelial cells, membrance microparticles carriers.
Singh, Neena; Gu, Yaping; Bose, Sharmila; Kalepu, Sudheera; Mishra, Ravi
Shankar; Verghese, Susamma. Prion peptide
106-126 as a model for prion replication and neurotoxicity.
Frontiers of Bioscience Computer File: a Journal and Virtual
Library. 2002 Apr 1; 7: a60-71. ISSN: 1093-4715.
Abstract: Prion
diseases or transmissible spongiform encephalopathies are neurodegenerative
disorders that are genetic, sporadic, or infectious. The pathogenetic event
common to all prion disorders is a change in conformation of the cellular
prion protein (PrPC) to the scrapie isoform (PrPSc), which, unlike PrPC,
aggregates easily and is partially resistant to protease digestion. Although
PrPSc is believed to be essential for the pathogenesis and transmission of
prion disorders, the mechanism by which PrPSc deposits cause neurodegeneration
is unclear. It has been proposed that in some cases of prion disorders, a
transmembrane form of PrP, termed CtmPrP may be the mediator of
neurodegenerative changes rather than PrPSc per se. In order to understand the
underlying cellular processes by which PrPSc mediates neurodegeneration, we
have investigated the mechanism of neurotoxicity by a beta-sheet rich peptide
of PrP in a cell model. We show that exposure of human neuronal cell lines
NT-2 and M17 to the prion peptide 106-126 (PrP106-126) catalyzes the
aggregation of endogenous cellular prion protein (PrPC) to an amyloidogenic
form that shares several characteristics with PrPSc. Intracellular
accumulation of these PrPSc-like forms upregulates the synthesis of CtmPrP,
which is proteolytically cleaved in the endoplasmic reticulum and the
truncated C-terminal fragment is transported to the cell surface. In addition,
we have isolated mutant NT-2 and neuroblastoma cells that are resistant to
toxicity by PrP106-126 to facilitate further characterization of the
biochemical pathways of PrP106-126 neurotoxicity. The PrP106-126-resistant
phenotype of these cells could result from aberrant binding or internalization
of the peptide, or due to an abnormality in the downstream pathway(s) of
neuronal toxicity. Thus, our data suggest that PrPSc aggregation occurs by a
process of 'nucleation' on a pre-existing 'seed' of PrP. Furthermore, the
PrP106-126-resistant cells reported here will provide a unique opportunity for
identifying the cellular and biochemical pathways that mediate neurotoxicity
by PrPSc.
Descriptors: Prion diseases, transmissible spongiform
encephalopathies, PrPSc, human neuronal call lines Nt-2, M17, PrP 106-126,
process is nucleation on a pre-existing seed.
Somerville, R.A.; Oberthur, R.C.; Havekost, U.; Macdonald, F.; Taylor,
D.M.; Dickinson, A.G. Characterization of thermodynamic diversity between
transmissible spongiform encephalopathy agent strains and its theoretical
implications. J Biol Chem. Mar 29, 2002. v. 277 (13) p.
11084-11089. ISSN: 0021-9258
DOI: 10.1074/jbc.M111766200
Abstract: Some
transmissible spongiform encephalopathy (TSE) (or "prion") strains, notably
those derived from bovine spongiform encephalopathy, are highly resistant to
total inactivation by heat. When three TSE strains derived from sheep with
scrapie were heated, little inactivation took place at low temperatures, but
at higher temperatures, considerable inactivation occurred. The temperature at
which substantial inactivation first occurred varied according to TSE strain,
and it was calculated to be 70 degrees C for the 22C strain, 84 degrees C for
ME7, and 97 degrees C for 22A by fitting the data to a model based on
competition between a destructive and a protective reaction. However, PrP(Sc)
from mice infected with a range of TSE strains retained similar resistance to
proteinase K digestion after heating to below or above these temperatures,
showing that the properties of PrP(Sc) responsible for proteinase resistance
do not correlate with those conferring thermostability on the TSE agent. The
simplest explanation of these data is that the causal agent contains a
macromolecular component that is structurally independent of the host, that it
varies covalently between TSE strains, and that it is protected by other
macromolecular components. The model is in accord with the virino hypothesis,
which proposes a host-independent informational molecule protected by the host
protein PrP.
NAL call no. 381 J824
Descriptors: TSE, scrapie
agents, strains, isolation, sheep, strain differences, heat inactivation,
temperature effects, infectivity, mouse model, glycoproteins, proteolysis,
animal prion proteins.
Soto, Claudio; Saborio, Gabriela P.; Anderes, Laurence. Cyclic amplification of protein misfolding:
Application to prion-related disorders and beyond. Trends in
Neurosciences. August, 2002; 25 (8): 390-394.
DOI: 10.1016/S0166-2236(02)02195-1
NAL
call no. RC321 T74
Descriptors: methods, amplify cyclically
misfolded proteins in vitro, PMCA, potential diagnostic technique,
transmissible spongiform encephalopathies, new technology, applications.
Spraker, T.R.; Zink, R.R.; Cummings, B.A.; Wild, M.A.; Miller, M.W.;
O'Rourke, K.I. Comparison of histological
lesions and immunohistochemical staining of proteinase-resistant prion protein
in a naturally occurring spongiform encephalopathy of free-ranging mule deer
(Odocoileus hemionus) with those of chronic wasting disease of captive mule
deer. Veterinary Pathology. 2002 January; 39(1): 110-119 ISSN:
0300-9858.
NAL call no. 41.8 P27
Descriptors: mule deer,
comparison between captive and free ranging, PrPRES, chronic wasting disease,
TSE, histological lesions and immunohistochemical staining.
Spraker, T.R.; O' Rourke, K. I.; Balachandran, A.; Zink, R.R.; Cummings,
B.A.; Miller, M.W.; Powers, B.E. Validation of
monoclonal antibody F99/97.6.1 for immunohistochemical staining of brain and
tonsil in mule deer (Odocoileus hemionus) with chronic wasting disease.
Journal of Veterinary Diagnostic Investigation. 2002, 14: 1, 3-7; 18
ref.
NAL call no. SF774.J68
Descriptors: deer, transmissible
spongiform encephalopathies, brain and tonsil tissue staining, diagnosis,
chronic wasting disease, immunohistochemical staining method,
wildlife,Colorado, Montana.
Staufenbiel, Rudolf; Hamalainen, Mira. Zur
klinischen Diagnostik der BSE. [The clinical diagnosis of BSE.]
Berliner und Munchener Tierarztliche Wochenschrift. 2002 Mar-Apr;
115(3-4): 99-105 ISSN: 0005-9366. In German.
Abstract: Diagnosis of
Bovine spongiform encephalopathy (BSE) is confirmed by specified laboratory
methods on brain material. On the other hand clinical signs of manifest BSE
are quite obvious. The first part of this paper describes case histories,
clinical signs, laboratory findings and the most common differential
diagnoses. On the basis of the data of actual prevalence in Germany, the role
of clinical examination in eradication of BSE is dealt in the second part.
Clinical diagnosis is a very sensitive and specific method when there is a
high prevalence. According to the data from December 2000 to November 2001
prevalence in Germany was beyond 1 BSE case per 100,000 cattle or 3 cases per
100,000 cows. This very low prevalence decreases rapidly sensitivity and
specificity of the diagnosis made by clinical examination. Therefore the main
focus of field-diagnostics has to be laid on specified laboratory diagnostic
methods. On the other hand prevalence of BSE-positive cattle is distinctly
higher in the group of animals slaughtered in cases of illness or emergency
than in cattle slaughtered on the regulatory bases. Nevertheless every
veterinary practitioner should be aware of the clinical picture of BSE,
clinical examination-routine and differential diagnosis, because occurrence of
BSE is still possible in any dairy herd. At the moment it is not possible to
make any statement if eradication of BSE can be reached in future.
NAL call
no. 41.8 B45
Descriptors: cattle, bovine spongiform encephalopathy,
case histories, clinical signs, lab findings, differential diagnoses, control
and eradication.
Stewart, Gordon T.More on BSE/vCJD.
Journal of the Royal Society of Medicine 2002 Feb; 95(2): 112. ISSN:
0141-0768.
NAL call no. 448.9 R814
Descriptors: NvCreutzfeldt
Jakob syndrome, epidemiology, bovine spongiform encephalopathy, cattle, humans
transmission.
Sugaya, Makoto; Nakamura, Koichiro; Watanabe, Takahiro; Asahina, Akihiko;
Yasaka, Nami; Koyama, Yoh Ichi; Kusubata, Masashi; Ushiki, Yuko; Kimura,
Kumiko; Morooka, Akira; Irie, Shinkichi; Yokoyama, Takashi; Inoue, Keiichi;
Itohara, Shigeyosi; Tamaki, Kunihiko. Expression of cellular prion-related protein by
murine Langerhans cells and keratinocytes. Journal of Dermatological
Science. February, 2002; 28 (2): 126-134. ISSN: 0923-1811.
DOI:
10.1016/S0923-1811(01)00160-8
Abstract:
Transmissible spongiform encephalopathies are characterized by the
accumulation of a proteinase-resistant isoform of the cellular prion-related
protein (PrPc) within the central nervous system (CNS). The accumulation of
scrapie-associated PrP (PrPSc) within cells of the lymphoreticular system
prior to its accumulation in the CNS is regarded as important for the
development of neurological diseases after peripheral inoculation. Little,
however, is known as to which cells are the targets for peripheral
inoculation. Here, the presence of PrPc on murine Langerhans cells (LC),
dendritic cells in the skin and mucosa, and keratinocytes (KC) is demonstrated
by immunohistochemical staining, Western-blotting and FACS analysis. The
expression of PrPc mRNA in freshly purified LC and KC was also detected by
reverse transcriptase-polymerase chain reaction. The expression of PrPc on LC
was slightly increased during culture. These data suggest that LC and KC may
be the targets for peripheral infection with prions.
Descriptors:
Keratinocytes metabolism, Langerhans cells metabolism, phosphoprotein
phosphatase metabolism, base sequence, gene expression, immunohistochemistry,
mouse model inbred-BALB-C, inbred-C57B, knockout mice,
phosphoprotein-phosphatase genetics, prion disease genetics, prion diseases
metabolism, transmissible spongiform encephalopathies.
Supattapone, Surachai; Nishina, Koren; Rees, Judy R. Pharmacological approaches to prion
research. Biochemical Pharmacology. 2002 Apr 15; 63(8): 1383-8
ISSN: 0006-2952
Abstract: The "protein-only" mechanism by which
infectious agents of prion diseases such as Creutzfeldt-Jakob disease and
bovine spongiform encephalopathy replicate remains undetermined. The
identification of several distinct classes of prion inhibitors has created an
opportunity to investigate the mechanism of prion formation using
pharmacological tools. These new inhibitors include substituted tricyclic
derivatives, tetrapyrrole compounds, cysteine protease inhibitors, branched
polyamines, and specific antibodies. Each inhibitor class contains at least
one active compound that inhibits prion propagation in cell culture at
sub-micromolar concentrations and several structurally related, inactive
compounds. Work with branched polyamines and specific antibodies has already
provided insight into the kinetics and cell biology of endogenous prion
clearance mechanisms. Other anti-prion compounds do not appear to bind
directly to the prion protein. Detailed investigation of the mechanism of drug
action of these compounds may lead to the identification of novel prion
propagation factors.
NAL call no. 396.8 B52
Descriptors: prion
diseases, infectious agents, CJD, BSE, bovine spongiform encephalopathy,
tricyclic derivatives, tetrapyrroles, cysteine protease inhibitors, branched
polyamines, specific antibodies, drug actions.
Sy, Man Sun; Gambetti, Pierluigi; Wong, Boon Seng. Human prion diseases. Medical Clinics of
North America. May, 2002; 86 (3): 551-571.
NAL call no. RC660 S95
F&N B-4343
Descriptors: BSE, Creutzfeldt Jakob Disease,
NvCreutzfeldt Jakob Disease, kuru, other transmissible or genetic spongiform
encephalopathies.
Takekida, Kaori; Kikuchi,Yutaka; Yamazaki, Takeshi; Horiuchi, Motohiro;
Kakeya, Tomoshi; Shinagawa, Morikazu; Takatori, Kosuke; Tanimura, Akio;
Tanamoto, Ken-Ichi; Sawada, Jun ichi. Quantitative analysis of prion protein by
immunoblotting. Journal of Health Science. June, 2002; 48 (3):
288-291.
URL: http://jhs.pharm.or.jp/data/48(3)/48_288.htm
Descriptors:
TSE, transmissible spongiform encephalopathy, PrPSc, quantitiative analysis
technique, immunoblotting, densitometry data, bovine PrPC, deglycosylated
forms.
Taylor, David. Inactivation of the BSE
agent. Comptes Rendus Biologies. Janvier, 2002; 325 (1):
75-76.
DOI: 10.1016/S1631-0691(02)01386-0
NAL
call no. Q2 C6
Descriptors: BSE, resistant to inactivation
procedures, sodium hypochlorite solutions and autoclaving combined, mouse
passaged agent, acid treated bone.
Tibayrenc, Michel; Mas, Coma Santiago; Piffaretti, Jean Claude; Struelens,
Marc. The European Centre for Infectious
Diseases: An adequate response to the challenges of bioterrorism and major
natural infectious threats. Infection Genetics and Evolution.
May, 2002; 1 (3): 179-181.
DOI: 10.1016/S1567-1348(02)00035-7
Descriptors:
government center, Europe, organization to address invasive diseases such as
bovine spongiform encephalopathy, other zoonotic diseases.
Tompa, Peter; Tusnady, Gabor E; Friedrich, Peter; Simon, Istvan The role of dimerization in prion
replication. Biophysical Journal. April, 2002; 82 (4):
1711-1718.
URL: http://www.biophysj.org/cgi/content/abstract/82/4/1711
Descriptors:
prion disease, conformational transition, dimerization role in prion
replication, intramolecular disulfide bridge, theory to explain prion
conformational changes.
Tuzi, Nadia L.; Gall, Elaine; Melton, David; Manson, Jean C. Expression of doppel in the CNS of mice does not
modulate transmissible spongiform encephalopathy disease. Journal of
General Virology. 2002 Mar; 83(Pt 3): 705-11. ISSN:
0022-1317.
Abstract: Late onset ataxia reported in three
independently derived PrP null lines of mice has been attributed to the
overexpression of the doppel protein in the CNS of these mice rather than to
the loss of PrP. The central role of PrP in the transmissible spongiform
encephalopathies (TSEs), the proximity of the gene which encodes doppel (Prnd)
to the PrP gene (Prnp) and the structural similarity shared by PrP and doppel
have led to the proposition that ataxia which develops during TSE disease
could, in part, be due to doppel. In order to address this hypothesis, we have
crossed our two inbred lines of PrP null mice, which either express (RCM) or
do not express (NPU) the Prnd gene in the CNS, with mice expressing two
Prnp(a[108F189V]) alleles of the PrP gene. We have found that the TSE
infection does not influence the level of expression of Prnd in the CNS at the
terminal stages of disease. Moreover, we have demonstrated that the level of
expression of Prnd in the CNS has no influence on the incubation period,
vacuolar pathology nor amount or distribution of deposition in the brains of
the TSE-infected mice. Doppel has therefore no apparent influence on the
outcome of TSE disease in transgenic mice, suggesting it is unlikely to be
involved in the naturally occurring TSE diseases in other species.
NAL call
no. QR360.A1J6
Descriptors: PrP, doppel protein, mouse models,
TSE.
VandeVondele, Joost; Colombo, Maria Carola; Laio, Alessandro; Guidoni,
Leonardo; Rothlisberger, Ursula. QM/MM study
of the copper binding site of prion protein. Biophysical Journal.
January, 2002; 82 (1 Part 2): 487a. 46th Annual Meeting of the Biophysical
Society, San Francisco, California, USA, February 23-27, 2002
NAL call no.
442.8 B5238
Descriptors: prion proteins, molecular binding
structure, copper, QM/MM study.
Van't Hooft, A. J.G. BSE en de
soortspecifieke barriere. [BSE and species specificity.] Tijdschrift
voor Diergeneeskunde. 2002 Mar 1; 127(5): 175 ISSN: 0040-7453. In
Dutch.
NAL call no. 41.8 T431
Descriptors: Creutzfeldt Jakob
syndrome, etiology, bovine spongiform encephalopathy, transmission, species
specificity.
Wahlstrom, Helene; Elvander, Marianne; Engvall, Anders; Vagsholm, Ivar
Risk of introduction of BSE into Sweden by
import of cattle from the United Kingdom. Preventive Veterinary
Medicine. 25 June, 2002; 54 (2): 131-139.
DOI: 10.1016/S0167-5877(02)00019-3
NAL
call no. SF601.P7
Descriptors: cattle, BSE risks, transported cattle
from UK to Sweden, 1980, surveillance system.
Wiemer, Udo. Veterinarrechtliche
Schutzmassnahmen im Hinblick auf BSE. [Protective measures taken with
regard to BSE under veterinary law]. Berliner und Munchener Tierarztliche
Wochenschrift. 2002 Mar-Apr; 115(3-4): 134-9 ISSN: 0005-9366. In
German.
Abstract: BSE was established for the first time in 1986 as
a separate disease complex. Since 1989 measures to protect human and animal
health have been adopted at Community level and under German law. The article
describes the most important provisions governing the prevention, control and
eradication of TSE. It addresses in detail the ban on feeding, active
monitoring of BSE, active monitoring of small ruminants, measures taken after
the detection of BSE, the removal and destruction of specified risk material
and briefly addresses trade bans and restrictions.
NAL call no. 41.8
B45
Descriptors: BSE, transmissible spongiform encephalopathies,
prevention, control, eradication, animal feeds, small ruminants, trade base
and restructions.
Will, R.G. Variant Creutzfeldt-Jakob
disease - How new is new?. Journal of Neurology Neurosurgery and Psychiatry.
March, 2002; 72 (3): 285-286.
URL: http://jnnp.bmj.com/cgi/content/extract/72/3/285
Descriptors:
BSE, bovine spongiform encechalopathy, NvCJD, pathogenesis.
Wrathall, A.E.; Brown, K.F.D.; Sayers, A.R.; Wells, G.A.H.; Simmons, M.M.;
Farrelly, S.S.J.; Bellerby, P.; Squirrell, J.; Spencer, Y.I.; Wells, M.;
Stack, M.J. Studies of embryo transfer from
cattle clinically affected by bovine spongiform encephalopathy (BSE).
Veterinary Record. Mar 23, 2002. v. 150 (12) p. 365-378. ISSN:
0042-4900
NAL call no. 41.8 V641
Descriptors: cattle embryo
transfer, bovine spongiform encephalopathy, disease transmission, washing,
semen, fertilizing ability, gametogenesis, prion proteins, genotypes,
infectivity, UK.
Wuthrich, Kurt; Calzolai, Luigi; Guntert, Peter; Luhrs, Thorsten; Lysek,
Dominik; Schorn, Christian; Von Schroetter, Christine; Zahn, Ralph. Species variation of the three-dimensional prion
protein structure in the cellular form. Biophysical Journal.
January, 2002; 82 (1 Part 2): 169a. 46th Annual Meeting of the Biophysical
Society, San Francisco, California, USA, February 23-27, 2002
NAL call no.
442.8 B5238
Descriptors: prion proteins, protein structions and
conformation, species variation.
Zaaijer, H. L. Interpretatie van de toename
van boviene spongiforme encefalopathie buiten Groot-Brittannie.
[Interpretation of the increase in bovine spongiform encephalopathy outside
Great Britain.] Nederlands Tijdschrift voor Geneeskunde 2002 Apr 20;
146(16): 748-50. ISSN: 0028-2162. In Dutch.
Abstract: Outside Great
Britain, the number of clinical cases of bovine spongiform encephalopathy
(BSE) seems to be rising. It is unclear whether this increase is real, or
whether it is caused by improved recognition and improved registration of BSE.
A strict and independent control of the implementation of measures intended to
keep human food free of the BSE agent is imperative.
Descriptors:
bovine spongiform encephalopathy, cattle, consumer food safety, Europe,
epidemiology, Great Britian, control measures.
Zentek, J.; Oberthur, R.C.; Kamphues, J.; Kreienbrock, L.; Flachowsky, G.;
Coenen, M.. Futtermittel tierischer Herkunft
als mogliche Verbreitungsursache fur die bovine spongiforme Enzephalopathie
(BSE) in Deutschland. 2. Mitteilung: Einschatzung des Verbreitungsrisikos uber
Mischfutter. [Animal-derived feedstuffs as possible vectors for bovine
encephalopathy (BSE) in Germany. Part 2: Assessment of vector risk for
compounded feed.] . DTW. Deutsche Tierarztliche Wochenschrift. 2002
Feb: 109 (2): 43-51 ISSN: 0341-6593. In German.
Abstract: Specific
conditions and practices of cattle feeding in Germany have to be taken into
account for assessing the risk of feed born transmission of bovine spongiform
encephalopathy, especially regarding the situation before the year 2000 when
specific directives were introduced for feed production. The present
retrospective epidemiological study includes data on feed production and the
estimated amount of animal derived feedstuffs for the production of compounded
feed for cattle. Risk assessment was performed based on the 'reproduction
rate' (R0), that is defined as the estimated number of infections resulting
from the processing of brain and spinal cord of BSE affected cattle that is
recycled to bovines via feed. Under the conditions as given in Germany until
the year 2000 the reproduction rate of BSE via the inclusion of animal derived
feedstuffs in compounded feed production for cattle was estimated to be 1.1.
Thus, it can be expected that BSE could be reproduced in the system, but with
comparatively low efficiency. The expected incidence of BSE should be
considerably lower compared to the situation during the 90th in the UK, due to
the markedly lower recycling rate of animal protein in cattle feeding. Animal
fat could have been a significant factor for BSE transmission due to
contamination by proteinaceous brain and spinal cord material during the
production process. The relative significance of fat containing feedstuffs for
BSE transmission could have been higher in Germany compared to the situation
in the UK where meat and bone meal was produced under different conditions and
frequently used in higher proportions as an ingredient for compounded feed for
ruminants.
NAL call no. 41.8 D482
Descriptors: cattle, feeding
and feeds, BSE, disease transmission risks, animal derived feed additives,
Germany.
United States. General Accounting Office. Mad cow disease:
improvements in the animal feed ban and other regulatory areas would
strengthen U.S. prevention efforts. Report to Congressional
Requestors, Washington, D.C.: GAO, January 2002. 59 p.
URL: www.gao.gov/new.items/d02183.pdf
Descriptors:
Bovine spongiform encephalopathy, animal feed, prevention strategies, public
and animal health risks, animal feed ban compliance, probablistic simulation
model, detection in imported animal products, economic impacts of the disease,
recommendations to USDA and FDA, GAO report.
Abbott, A. BSE fallout sends shock waves
through Germany. Nature. 2001 Jan 18. 409(6818): 275 ISSN:
0028-0836
NAL call no. 472 N21
Descriptors: Bovine spongiform
encephalopathy, meat, cattle, consumer product safety, Germany, legislation,
food, meat products.
Abbott, A. Mad-cow outbreak spurs German
drive to combat prion diseases. Nature. 2001 Aug 9. 412(6847):
571-572 ISSN: 0028-0836
NAL call no. 472 N21
Descriptors: BSE,
Germany, strategies to combat the disease, prion diseases, protective
measures.
Adam, D. Fears rise over BSE infection in
UK abattoirs. Nature. 2001 Jun 14. 411(6839): 728 ISSN:
0028-0836
NAL call no. 472 N21
Descriptors: Bovine spongiform
encephalopathy, slaughter plants, transmission of contaminated material,
UK.
Adam, D. Catgut sutures--possible BSE risk.
Australian Veterinary Journal. 2001 Apr. 79(4): 245-246 ISSN:
0005-0423
NAL call no. 41.8 Au72
Descriptors: Bovine spongiform
encephalopathy, catgut, transmission, adverse effects, standards, cattle, risk
factors.
Adam, D. Review blames BSE outbreak on calf
feed. Nature. 2001 Aug 2. 412(6846): 467. ISSN: 0028-0836
NAL
call no. 472 N21
Descriptors: BSE, calf feeding
Aguzzi A. Bovins, humains: quelles
connexions? [Cattle and people: what are the connections?]
Biofutur. 2001, No. Hors Serie, 26-29; 11 ref. ISSN: 0294-3506. In
French.
NAL call no. TP248.13 B565
Descriptors: asymptomatic
infections, bovine spongiform encephalopathy, brain, carrier state, cattle
diseases, NvCreutzfeldt-Jakob disease, digestive tract, routes of disease
transmission, lymphocytes, prion diseases.
Aguzzi, A.; Montrasio, F.; Kaeser, P.S.
Prions: Health scare and biological challenge. Nature Reviews:
Molecular Cell Biology, 2001 vol. 2, no. 2, pp. 118-126 ISSN:
1471-0072
Descriptors: yeasts, central nervous system, prion
proteins, NvCreutzfeldt-Jakob-disease, BSE, bovine spongiform encephalopathy,
cattle, immune system lymphocytes and follicular dendritic cells, transport of
prions.
Andersson I.; Svendsen L.S.; Gustafsson B. Vad hander med lantbrukets husdjur i
katastrofsituationer? [What happens to farm animals in emergency
situations?] Svensk Veterinartidning. 2001, 53: 6, 333-339; 11 ref.
ISSN: 0346-2250. In Swedish.
NAL call no. 41.9 SV23
Descriptors:
animal welfare, bovine spongiform encephalopathy, emergencies, foot and mouth
disease, livestock.
Anil, M.H.; Love, S.; Helps, C.R.; McKinstry, J,L.; Brown, S.N.; Philips,
A.; Williams, S.; Shand, A.; Bakirel, T.; Harbour, D. Jugular venous emboli of brain tissue induced in
sheep by the use of captive bolt guns. Veterinary Record. 2001,
148: 20, 619-620; 10 ref. ISSN: 0042-4900
NAL call no. 41.8
V641
Descriptors: sheep, experimental procedure, jugular sampling,
pre- and post-stunning, stunning, electrical stunning, emboli of CNS tissue
compared to stunning methods.
Axelsson, S. The basic reality of mind and
spongiform diseases. Medical Hypotheses. November, 2001;
57 (5): 549-554. ISSN: 0306-9877
Descriptors: prions,
Creutzfeldt-Jakob Disease, bovine spongiform encephalopathy, Alzheimer's
disease, chirality, cholinergic system, pathophysiology, beef products.
Bachmann, M.F. Complements for mad-cow
disease. Trends in Immunology 2001 Jun. 22(6): 297 ISSN:
1471-4906
NAL call no. QR180 I56
Descriptors: Bovine spongiform
encephalopathy, immunology, complement immunology, cattle.
Balter, M. Infectious diseases. Is BSE in
sheep a no-brainer? Science. 2001 Oct 26. 294(5543): 771
NAL
call no. 470 Sci2
Descriptors: BSE, scrapie, cattle, sheep,
transmissible spongiform encephalopathies, prion typing.
Balter, M. Infectious diseases.
Uncertainties plague projections of vCJD toll. Science. 2001 Oct
26. 294(5543): 770-771 ISSN: 0036-8075
NAL call no. 470
Sci2
Descriptors: BSE, variant Creutzfeldt-Jakob Disease, potential
incidence.
Balter, M. Origins of BSE: Intriguing clues
to a scrapie-mad cow link Science (US) 2001 vol. 292, no. 5518,
pp. 827-829 ISSN: 0036-8075
NAL call no. 470 Sci2
Descriptors:
BSE, feeds formulation, transmissibility, cattle, sheep, scrapie, prion
protein, NvCreutzfeldt-Jakob disease, Uk, France, connection between BSE and
NvCJD
Baron Thierry, G M; Biacabe, Anne-Gaelle. Molecular analysis of the
abnormal prion protein during coinfection of mice by bovine spongiform
encephalopathy and a scrapie agent. Journal of Virology. Jan. 2001.
v. 75 (1) p. 107-114.
Abstract: Molecular features of the proteinase
K-resistant prion protein (PrP res) may discriminate among prion strains, and
a specific signature could be found during infection by the infectious agent
causing bovine spongiform encephalopathy (BSE). To investigate the molecular
basis of BSE adaptation and selection, we established a model of coinfection
of mice by both BSE and a sheep scrapie strain (C506M3). We now show that the
PrP res features in these mice, characterized by glycoform ratios and
electrophoretic mobilities, may be undistinguishable from those found in mice
infected with scrapie only, including when mice were inoculated by both
strains at the same time and by the same intracerebral inoculation route.
Western blot analysis using different antibodies against sequences near the
putative N-terminal end of PrP res also demonstrated differences in the main
proteinase K cleavage sites between mice showing either the BSE or scrapie PrP
res profile. These results, which may be linked to higher levels of PrP res
associated with infection by scrapie, were similar following a challenge by a
higher dose of the BSE agent during coinfection by both strains
intracerebrally. Whereas PrP res extraction methods used allowed us to
distinguish type 1 and type 2 PrP res, differing, like BSE and scrapie, by
their electrophoretic mobilities, in the same brain region of some patients
with Creutzfeldt-Jakob disease, analysis of in vitro mixtures of BSE and
scrapie brain homogenates did not allow us to distinguish BSE and scrapie PrP
res. These results suggest that the BSE agent, the origin of which remains
unknown so far but which may have arisen from a sheep scrapie agent, may be
hidden by a scrapie strain during attempts to identify it by molecular studies
and following transmission of the disease in mice.
NAL call no. QR360
J6
Descriptors: mouse model, scrapie, bovine spongiform
encephalopathy, laboratory inoculation, variant differences, identification of
strains. proteinase K-resistant prion protein.
Bartels, Dennis. Mad cows and market
forces. Journal of Human Ecology. May, 2001; 12 (3): 163-170.
ISSN: 0970-9274
Descriptors: bovine spongiform encephalopathy, safe
of food, consumer attitudes, British government claims.
Beale, A. J. BSE and vCJD: what is the
future? Journal of the Royal Society of Medicine 2001 May.
94(5): 207-209 ISSN: 0141-0768
NAL call no. 448.9
R814
Descriptors: bovine spongiform encephalopathy,
Cruetzfeldt-Jakob Disease, epidemiology, bovine based products.
The beef CMO and BSE -- making a bad
problem worse. Agra Europe (Brit. edition.) 2001, No.
1937, A-1-A-2. ISSN: 0002-1024
NAL call no. 286.8
AG3AE
Descriptors: BSE, agricultural crises, EU beef industry,
bovine spongiform encephalopathy, consumption, costs, impacts on international
trade, subsidies, surpluses, consumer concerns and declining consumption
trends.
Beiglbock, C. Die Chronic Wasting Disease
(CWD) der Cerviden in Nordamerika -- eine Literaturubersicht. [Chronic
Wasting Disease (CWD) in cervids in North America -- a review.] Wiener
Tierarztliche Monatsschrift. 2001, 88: 6, 147-152; 30 ref. ISSN:
0043-535X. In German with an English summary.
NAL call no. 41.8
T345
Descriptors: etiology, diagnosis, disease control, prevention
strategies, epidemiology, pathology, reviews, transmissible spongiform
encephalopathy; wasting disease, deer, elk, North America.
Belay, E. D.; Gambetti, P.; Schonberger, L. B.; Parchi, P.; Lyon, D.R.;
Capellari, S.; McQuiston, J.H.; Bradley, K.; Dowdle, G.; Crutcher, J.M.;
Nichols, C. R. Creutzfeldt-Jakob disease in
unusually young patients who consumed venison. Archives of
Neurology. 2001 Oct. 58(10): 1673-1678 ISSN: 0003-9942
Abstract:
BACKGROUND: Creutzfeldt-Jakob disease (CJD) in humans and chronic wasting
disease (CWD) in deer and elk occur in the United States. Recent reports of 3
unusually young patients with CJD who regularly consumed deer or elk meat
created concern about the possible zoonotic transmission of CWD. OBJECTIVE: To
examine the possible transmission of CWD to humans. PATIENTS: Three unusually
young patients (aged 28, 28, and 30 years) with CJD in the United States
during 1997-2000. METHODS: We reviewed medical records and interviewed family
members and state wildlife and agriculture officials. Brain tissue samples
were tested using histopathologic, immunohistochemical, immunoblot, or prion
protein gene analyses. MAIN OUTCOME MEASURES: Presence or absence of
established CJD risk factors, deer and elk hunting in CWD-endemic areas, and
comparison of the evidence for the 3 patients with that of a zoonotic link
between new variant CJD and bovine spongiform encephalopathy. RESULTS: None of
the patients had established CJD risk factors or a history of travel to
Europe. Two patients hunted game animals and 1 was a daughter of a hunter.
Unlike patients with new variant CJD, the 3 patients did not have a unique
neuropathologic manifestation, clinicopathologic homogeneity, uniformity in
the codon 129 of the prion protein gene, or prion characteristics different
from those of classic variants. CONCLUSIONS: Although the occurrence of 3
unusually young patients with CJD who consumed venison suggested a possible
relationship with CWD, our follow-up investigation found no strong evidence
for a causal link. Ongoing CJD surveillance remains important for continuing
to assess the risk, if any, of CWD transmission to
humans.
Descriptors: chronic wasting disease, zoonotic transmission
concerns, case study, NvCreutzfeldt-Jakob disease infection, deer and elk
meat, 3 young patients, codon 129.
Bergmann, W.; Beringer, H. Kupfermangel,
ein moglicher BSE-auslosender Faktor? [Copper deficiency -- a potential
factor in BSE?] Journal of Plant Nutrition and Soil Science. 2001, 164:
2, 233-235; 13 ref. ISSN: 1436-8730. In German with an English summary.
NAL
call no. QK867 J68
Descriptors: BSE, normal and pathogenic prions
chemistry, bovine spongiform encephalopathy, copper, trace minerals, mineral
deficiencies, reviews.
Berthelin, Baker C.; Konold, T.; Clifford, D.; Ryder, S.; Bellworthy, S.;
Dexter, G.; Brittin, D.; Wood, D.; Simmonds, M.; Bone, G.; Jeffrey, M. Interim observations on the clinical features of
Bovine Spongiform Encephalopathy in sheep of the Romney and Suffolk breeds.
Research in Veterinary Science. April, 2001; 70 (Supplement A):
28. ISSN: 0034-5288. 55th Annual Conference on Current Topics in Veterinary
Science, Scarborough, England, UK, April 09-12, 2001
NAL call no. 41.8
R312
Descriptors: BSE, sheep breed susceptibility differences,
transmissible spongiform encephalopathies.
Bin Kingombe, C.I.; Luthi, E; Schlosser, H; Howald, D; Kuhn, M; Jemmi, T.
A PCR-based test for species-specific determination of heat treatment
conditions of animal meals as an effective prophylactic method for bovine
spongiform encephalopathy. Meat science. Oxford: Elsevier
Science Limited. Jan. 2001. v. 57 (1) p. 35-41. Includes references.
NAL
call no. TX373.M4
Descriptors: polymerase chain reaction, fish
meal, pork, ELISA, monitoring, screening, mitochondrial DNA, cytochrome B,
genes, cattle, prevention, bovine spongiform encephalopathy.
Bindon, B.M.; Jones, N.M. I. Cattle supply,
production systems and markets for Australian beef. Australian
Journal of Experimental Agriculture. 2001; 41 (7): 861-877. ISSN:
0816-1089
NAL call no. 23 Au792
Descriptors: beef cattle, market
impacts, BSE, foot and mouth disease, history of industry, 20th
century, brucellosis, tuberculosis, Dick Austen, trade, standards, food safety
concerns, new market forces, Australia.
Birkett, C.R.; Hennion, R.M.; Bembridge, D.A.; Clarke, M.C.; Chree, A.;
Bruce, M.E.; Bostock, C. J. Scrapie strains
maintain biological phenotypes on propagation in a cell line in culture.
EMBO Journal 2001 Jul 2. 20(13): 3351-3358. ISSN:
0261-4189
Abstract: Bovine spongiform encephalopathy (BSE) and its
human equivalent, variant Creutzfeldt-Jakob disease (vCJD), are caused by the
same strain of infectious agent, which is similar to, but distinct from,
>20 strains of their sheep scrapie homologue. A better understanding of the
molecular strain determinants could be obtained from cells in monoculture than
from whole animal studies where different cell targeting is commonly a
strain-related feature. Although a few cell types can be infected with
different strains, the phenotypes of the emergent strains have not been
studied. We have cured the scrapie-infected, clonal SMB cell line with
pentosan sulfate, stably re-infected it with a different strain of scrapie and
shown that biological properties and prion protein profiles characteristic of
each original strain are propagated faithfully in this single non-neuronal
cell type. These findings attest to the fact that scrapie strain determinants
are stable and host-independent in isolated cells.
NAL call no. QH506
E46
Descriptors: BSE, NvCreutzfeldt-Jakob Disease, molecular
differences, strains, sheep scrapie, clonal, SMB.
Bittante, G. Mercato e tecnica di
alimentazione: cosa cambia dopo la BSE. [The market and animal feeding
techniques: changes since the BSE crisis.] Informatore Agrario. 2001,
57: 11, 81-85. ISSN: 0020-0689. In Italian.
NAL call no. 281.8
IN32
Descriptors: animal feeding, beef, bovine spongiform
encephalopathy, disease control, economic impact; feeds, producer prices.
Blood-based prion test.
Analytical Chemistry. 2001 May 1. 73(9): 252A ISSN:
0003-2700
NAL call no. 381 J825A
Descriptors: diagnostic test,
screening live mammals, fluorescently labeled peptide from PrP and peptide
antibodies, economical preclinical method, CE or size exclusion HPLC.
Bol, P. BSE en andere prionziekten.
[BSE and other prion diseases] Nederlands Tijdschrift voor Tandheelkunde
2001 Feb. 108(2): 72-73 ISSN: 0028-2200 In Dutch.
Descriptors:
transmissible spongiform encephalopathies.
Bonnardiere, C la; la Bonnardiere, C. BSE:
le depistage s'organise. [Early detection of bovine spongiform
encephalopathy is progressing.] Biofutur. 2001, No. Hors Serie, 52-56;
8 ref. ISSN: 0294-3506. In French.
NAL call no. TP248.13
B565
Descriptors: bovine spongiform encephalopathy, diagnostic
techniques, Western blot assay, Prionics, brain stem testing. Biorad enzyme
assay.
Bosch, X. BSE panic spreads to Spain.
Nature Medicine. 2001 Feb. 7(2): 138 ISSN:
1078-8956
Descriptors: bovine spongiform encephalopathy, incidence,
disease risks, Spain.
Bosch, X. European concern over BSE
transmission. JAMA. 2001 Jan 24-31. 285(4): 397-398. ISSN:
0098-7484
NAL call no. 448.9 AM37
Descriptors: bovine spongiform
encephalopathy, transmissibility, human and animal health risks.
Bradley, R.; Rabenau, H.F. (ed.); Cinatl, J. (ed.); Doerr, H.W. Bovine spongiform encephalopathy and its
relationship to the new variant form of Creutzfeldt-Jakob disease.
Prions: a challenge for science, medicine and public
health-system. 2001, 105-144; 48 ref. Published by: S. Karger AG; Basel;
Switzerland. ISBN: 3-8055-7124-0
NAL call no. QR1 C66 v.
7
Descriptors: BSE, bovine spongiform encephalopathy, NvCreutzfeldt
Jakob disease, prion diseases, pathogenesis
Bradley, R. A brief overview of bovine
spongiform encephalopathy and related diseases including a TSE risk analysis
of bovine starting materials used during the manufacture of vaccines for use
in humans. Przegl Epidemiol. 2001. 55(3): 387-405 ISSN:
0033-2100
Descriptors: BSE, transmissible spongiform
encephalopathies, bovine based pharmaceutical products, vaccines, public
health risks
Bradley, R. Obecna sytuacja badan nad
pasozowalnymi encefalopatiami gabczastymi. [The current situation of
investigation of bovine spongiform encephalopathy] Przeglad Epidemiologiczny.
2001. 55(1 Suppl 2): 37-59 ISSN: 0033-2100. In Polish.
Descriptors:
BSE, Polish situation, epidemiology.
Bratberg B.; Benestad S.L.; Schonheit J. "Ny type" scrapie. ["New type" scrapie.]
Norsk Veterinaertidsskrift. 2001. 113: 2, 79-80; 4 ref. ISSN:
0332-5741. In Norwegian.
NAL call no. 41.8 N81
Descriptors: BSE,
bovine spongiform encephalopathy; pathology; scrapie, experimental
animals.
Brazil, Instituto Brasileiro de Economia. Vaca louca. [Mad cow.] Agroanalysis.
2001, 21: 2, 39-46. ISSN: 0100-4298. In Portuguese.
Descriptors:
BSE, cattle prion diseases, bovine spongiform encephalopathy, pastures grazing
systems, cattle feeding, low risk.
Bren, L. Trying to keep "Mad Cow Disease"
out of U.S. herds. FDA Consumer Rockville, Md. : Food and Drug
Administration, Department of Health & Human Services. Mar/Apr 2001. v. 35
(2) p. 12-14. ISSN: 0362-1332
NAL call no.
HD9000.9.U5A1
Descriptors: bovine spongiform encephalopathy, disease
prevention, Creutzfeldt-Jakob Disease. USDA, federal government, disease
transmission, surveillance, meat inspection, Federal regulations, meat and
livestock industry, ruminant feeding, consumer protection, USA.
Brewer, M.S. Bovine spongiform
encephalopathy--food safety implications. Adv Food Nutr Res. San
Diego : Academic Press, c1989-. 2001. v. 43 p. 265-317. ISSN: 1043-4526
NAL
call no. TX537.A38
Descriptors: bovine spongiform encephalopathy,
food safety, food contamination, rendering, disease transmission, prions,
strains, prion diseases, genetic factors, species differences, human health
risks, Creutzfeldt-Jakob-Disease, infectivity, bovine-based products, tallow,
gelatin, diagnostic techniques, surveillance, disease control, disease
prevention, literature reviews, UK, USA.
Bromley, D.W. Mad cows, drugged cows, and
juggled genes: purpose and necessity in science policy and public
opinion. Choices. The Magazine of Food, Farm, and Resources Issues.
2001, No. 2, 6-9. ISSN: 0886-5558
NAL call no.
HD1751.C45
Descriptors: beef, biosafety, BSE, bovine spongiform
encephalopathy, food contamination, food safety, milk, food related public
health scares, public, BST.
Brown, D.R. BSE: a post-industrial disease?
Chemistry and Industry. 2001, No. 3, 73-76; 13 ref. ISSN:
0009-3068
Descriptors: BSE, etiology, bovine spongiform
encephalopathy, NvCreutzfeldt-Jakob disease, prion diseases, cattle, human
health risks.
Brown, D.R. BSE did not cause variant CJD:
An alternative cause related to post-industrial environmental contamination.
Medical Hypotheses. November, 2001; 57 (5): 555-560. ISSN:
0306-9877
Descriptors: prion diseases, Bovine spongiform
encephalopathies, NvCreutzfeldt-Jakob Disease, etiology, theories,
manganese-rich pollutants.
Brown, Paul. Afterthoughts about bovine
spongiform encephalopathy and variant Creutzfeldt-Jakob disease.
Emerging Infectious Diseases. 2001; 7 (3 Supplement):
598-600. ISSN: 1080-6040.
NAL call no. RA648.5 E46
Descriptors:
BSE, NvCreutzfeldt-Jakob Disease, issues, new diseases, prion diseases
Brown, P. Bovine spongiform encephalopathy
and variant Creutzfeldt-Jakob disease. BMJ Clinical Research ed.
2001 Apr 7. 322(7290): 841-844 ISSN: 0959-8138
Descriptors:
Creutzfeldt-Jakob Syndrome, etiology, epidemiology, age distribution,
cattle.
Brown, P.; Will, R.G.; Bradley, R.; Asher, D.M.; Detwiler, L. Bovine spongiform encephalopathy and variant
Creutzfeldt-Jakob disease: background, evolution, and current concerns.
Emerging Infectious Diseases 2001 Jan-Feb. 7(1): 6-16 ISSN:
1080-6040
Abstract: The epidemic of bovine spongiform encephalopathy
(BSE) in the United Kingdom, which began in 1986 and has affected nearly
200,000 cattle, is waning to a conclusion, but leaves in its wake an outbreak
of human Creutzfeldt-Jakob disease, most probably resulting from the
consumption of beef products contaminated by central nervous system tissue.
Although averaging only 10-15 cases a year since its first appearance in 1994,
its future magnitude and geographic distribution (in countries that have
imported infected British cattle or cattle products, or have endogenous BSE)
cannot yet be predicted. The possibility that large numbers of apparently
healthy persons might be incubating the disease raises concerns about
iatrogenic transmissions through instrumentation (surgery and medical
diagnostic procedures) and blood and organ donations. Government agencies in
many countries continue to implement new measures to minimize this
risk.
NAL call no. RA648.5 E46
Descriptors: BSE,
NvCreutzfeldt-Jakob Disease, UK, human disease risks, tranmissibility
concerns, incidence, iatrogenic transmission risks, governmental measures,
risk control, epidemiology.
Brown, P. The pathogenesis of transmissible
spongiform encephalopathy: routes to the brain and the erection of therapeutic
barricades. Cellular and Molecular Life Sciences. 2001, 58: 2,
259-265; 51 ref. ISSN: 1420-682X
NAL call no. QH301
C45
Descriptors: BSE, bovine spongiform encephalopathy,
pathogenesis, NvCreutzfeldt-Jakob disease, treatments, prion diseases,
scrapie, spongiform encephalopathy.
Brugere-Picoux, J.; Brugere, H.
Encephalopathie spongiforme bovine: un tournant dans l'evolution de
l'epidemie? [Bovine spongiform encephalopathy: a change in the etiology
of the epidemic?] Revue de Medecine Interne, 2001 Aug. 22(8): 693-698
ISSN: 0248-8663. In French.
Descriptors: BSE, etiology, disease
incidence.
BSE bij gezelschapsdieren. [BSE in
companion animals] Tijdschrift voor Diergeneeskunde 2001 Feb 15.
126(4): 120-121 ISSN: 0040-7453. In Dutch.
NAL call no. 41.8
T431
Descriptors: BSE, issues of transmissible spongiform
encephalopathies, cats, dogs.
Butler, D. Spotlight on scrapie in hunt for
sheep BSE. Nature. 2001 Nov 1. 414(6859): 7 ISSN:
0028-0836
NAL call no. 472 N21
Descriptors: Bovine spongiform
encephalopathy, diagnosis, scrapie, sheep, cattle, Great Britain.
Buzby, J.C.; Detwiler, L.R. BSE: anatomy of
a crisis. Choices. The Magazine of Food, Farm, and Resources
Issues. 2001, No.2, 41-45. ISSN: 0886-5558
NAL call no.
HD1751.C45
Descriptors: agricultural crises, BSE, bovine spongiform
encephalopathy, Creutzfeldt NvJakob disease, economic impact, epidemics,
impacts on exports and international trade, meat and livestock industry, US
policies, cattle protection.
Calavas, D.; Ducrot, C.; Baron, T.; Morignat, E.; Vinard, J.L.; Biacabe,
A.G.; Madec, J.Y.; Bencsik, A.; Debeer, S.; Eliazsewicz, M. Prevalence of BSE in western France by screening
cattle at risk: preliminary results of a pilot study. Vet Rec.
London : The British Veterinary Association. July 14, 2001. v. 149 (2) p.
55-56. ISSN: 0042-4900
NAL call no. 41.8 V641
Descriptors:
cattle, bovine spongiform encephalopathy, disease prevalence, age risk, France
Calza, L.; Manfredi, R.; Chiodo, F.
Epidemia di encefalopatia spongiforme bovina e nuova variante della malattia
di Creutzfeldt-Jakob nell'uomo. Ultime acquisizioni sulle malattie da prioni.
[Epidemics of bovine spongiform encephalopathy and new variant of
Creutzfeldt-Jakob disease in humans. Most recent findings on prion disease.]
Recenti Progressi in Medicina. 2001 Feb. 92(2): 140-149 ISSN:
0034-1193. In Italian.
Abstract: Prion diseases have been
popularized by extensive media coverage of bovine spongiform encephalopathy
(BSE) or "mad cow disease" epidemic, observed in Great Britain since 1986, and
new variant Creutzfeldt-Jakob disease (nvCJD), reported for the first time in
1996. In contrast to the classical form of the disease, nvCJD affects younger
patients, presents a relatively longer duration of illness and is caused by
the same agent as BSE. Evidence from laboratory studies now strongly supports
the hypothesis that new variant represents human form of animal disease,
linked to exposure, probably through food, to bovine prions. Number of BSE
reports in the United Kingdom began to decline in 1993, and has continuously
decreased year by year since then, but a great worry spread in European
countries in association with new BSE reported cases outside of the Great
Britain, and increasing incidence of nvCJD. New epidemiological, clinical,
histopathological and experimental data on prion diseases are reviewed,
focusing our attention on the possible transmission of prion proteins from
animals to humans.
Descriptors: NvCreutzfeldt-Jakob Disease, BSE,
epidemiology, clinical data, UK, European incidence, transmission, human
health risks.
Caramelli, M; Ru, G; Casalone, C; Bozzetta, E; Acutis, PL; Calella, A;
Forloni, G. Evidence for the transmission of
scrapie to sheep and goats from a vaccine against Mycoplasma
agalactiae. Veterinary Record. 2001, 148: 17, 531-536; 21 ref.
ISSN: 0042-4900
NAL call no. 41.8 V641
Descriptors: BSE, bovine
spongiform encephalopathy, brain, codon 171, cross infection, epidemiology,
genotypes, mortality, polymorphism, scrapie, transmission, Mycoplasma
agalactiae vaccine as infective source, sheep, goats, brain lesions.
Cardone, F.; Pocchiari, M. A role for
complement in transmissible spongiform encephalopathies. Nature
Medicine 2001 Apr. 7(4): 410-411 ISSN: 1078-8956
Descriptors:
BSE, CJD, blood factors, role in disease formation.
Carlier, F. Vers une economie du principe
de precaution. [Economy of the precautionary principle.]
Biofutur. 2001, No. Hors Serie, 16-20; 7 ref. ISSN: 0294-3506. In
French.
NAL call no. TP248.13 B565
Descriptors: BSE, traceability
measures, bovine spongiform encephalopathy, consumer protection, disease
prevention, labeling, meat and meat products, prion diseases, Europe.
Carson, C.; McKay, J.S.; Brooks, H.W.; Kelly, D.F.; Stidworthy, M.F.;
Wibbelt, G.; Morgan, K.L. Establishment and
maintenance of a longitudinal study of bovine spongiform encephalopathy (the
ULiSES scheme). Preventive Veterinary Medicine. 2001 Oct 11.
51(3-4): 245-257 ISSN: 0167-5877
Abstract: This paper addresses the
issues of tracing and compliance encountered in setting up and maintaining a
UK-wide 5-year observational study of beef cattle. The 5-year prospective
study was initiated in 1997 to investigate the occurrence of bovine spongiform
encephalopathy (BSE) in a single herd of pedigree Aberdeen Angus cattle, in
which BSE had been detected at low prevalence. The study was given the acronym
ULiSES (University of Liverpool Spongiform Encephalopathy Scheme). All cattle
present on the farm at the start of the scheme were registered as members of
the study population (n=320), as were all calves standard histopathological
techniques) for the presence of spongiform change. Remaining samples were
stored at -70 degrees C for future investigation by alternative tests. At the
halfway point of the scheme in October 1999, 75.2% (506/673) of the study
population was still alive; 42% (284) of the population was still alive on the
study farm and 33% (222) was distributed on other farms throughout the UK.
Complete sets of specimens had been recovered from 77% (129/167) of dead
animals. All brainstem sections were negative by histopathological
examination. No suspect cases of BSE were reported in ULiSES animals. Failure
to recover specimens occurred principally in animals which had left the study
farm. The main cause of specimen loss was a failure of compliance in a small
number of individuals who had purchased large numbers of ULiSES animals, and
subsequently slaughtered them without contacting the University. Despite this,
farmer compliance was generally high. The ULiSES scheme shows the feasibility
of a country-wide longitudinal observational study spanning a period of
several years and indicates the large impact of small numbers of non-compliant
individuals.
NAL call no. SF601.P7
Descriptors: University of
Liverpool Spongiform Encephalopathy Scheme, Aberdeen Angus beef cattle, 5 year
observational study, post mortem sampling, BSE surveillance.
Cashman, N.R. Transmissible spongiform
encephalopathies: Vaccine issues. In Developments in Biologicals.
Evolving scientific and regulatory perspectives on cell substrates for vaccine
development. 2001; (106): 455-461. Fred Brown; Andrew Lewis Jr.; Keith
Peden; and Philip Krause Eds S. Karger Publishers Inc., 79 Fifth Avenue, New
York, NY, 10003, USA; S. Karger AG, CH 4009, Basel, Switzerland. ISBN
1424-6074
NAL call no. QR180.3 D4 v. 106
Descriptors: BSE,
transmissible spongiform encephalopathies, vaccine development, techniques,
approaches.
Caughey, B.; Dobson, C. M. (ed.); Ellis, R. J. (ed.); Fersht, A. R. Prion protein inter-conversions. Protein
misfolding and disease. Papers of a Discussion Meeting held at the Royal
Society, London, UK, on 23 and 24 February 2000. Philosophical Transactions of
the Royal Society of London. Series B, Biological Sciences. 2001, 356:
1406, 197-202; Many ref. ISSN: 0962-8436.
NAL call no. 501
L84Pb
Descriptors: BSE, bovine spongiform encephalopathy,
NvCreutzfeldt Jakob disease, in vitro models, prion diseases, conversion
inhibitors, prion proteins, scrapie
Cervenakova, L. The safety of human blood:
experimental TSE/prion infectivity studies. Transfusion Clinique et
Biologique Journal de la Societe Francaise de Transfusion Sanguine. 2001
Jun. 8(3): 260. ISSN: 1246-7820
Descriptors: Cattle, blood
transfusion, adverse effects, diseases, Creutzfeldt-Jakob Syndrome,
transmission, prevention and control, bovine spongiform encephalopathy, Great
Britain, human, prion diseases, safety.
Cesar, Isigidi K.; Luthi, E.; Schlosser, H.; Howald, D.; Kuhn, M.; Jemmi,
T. A PCR-based test for species-specific
determination of heat treatment conditions of animal meals as an effective
prophylactic method for bovine spongiform encephalopathy. Meat
Science. 2001, 57: 1, 35-41; 17 ref. ISSN: 0309-1740
NAL call no. TX373
M4
Descriptors: PCR- based assay, screening method, animal meals,
bovine spongiform encephalopathy, disease prevention, heat treated meat meal,
meat products, pork, polymerase chain reaction.
Cesbron, JY; Lemaire, C; Gagnon, J. Comment
se propage l'infection. [How the infection is propagated.]
Biofutur. 2001, No. Hors Serie, 37-40; 8 ref. ISSN: 0294-3506. In
French.
NAL call no. TP248.13 B565
Descriptors: BSE, bovine
spongiform encephalopathy, mouse scrapie, disease course and models, ileum,
immune system, laboratory animals, peripheral nerves, scrapie, comparison.
Clarke, A.R.; Jackson, G.S.; Collinge, J.; Dobson, C.M. (ed.); Ellis, R.J.
(ed.); Fersht, A.R. The molecular biology of
prion propagation. Protein misfolding and disease. Papers of a
Discussion Meeting held at the Royal Society, London, UK, on 23 and 24
February 2000. Philosophical Transactions of the Royal Society of London.
Series B,-Biological Sciences. 2001, 356: 1406, 185-195; Many ref. ISSN:
0962-8436
NAL call no. 501 L84Pb
Descriptors: BSE, bovine
spongiform encephalopathy; NvCreutzfeldt Jakob disease; prion protein
molecular biology, scrapie, PrPSc, prion propagation.
Coe, John E.; Race, Richard E.; Ross, Mary J. Serological evidence for an inflammatory response in
murine scrapie. Journal of Infectious Diseases. 15 January,
2001; 183 (2): 185-191. ISSN: 0022-1899.
NAL call no. 448.8
J821
Descriptors: transmissible spongiform encephalopathies, murine
scrapie experimental model, C57BL10 and IRW mice, serum amyloid P component
levels, possible diagnostic test.
Collinge, J. Prion diseases of humans and
animals: their causes and molecular basis. Annual Review of
Neuroscience. 2001. 24: 519-550 ISSN: 0147-006X
Abstract: Prion
diseases are transmissible neurodegenerative conditions that include
Creutzfeldt-Jakob disease (CJD) in humans and bovine spongiform encephalopathy
(BSE) and scrapie in animals. Prions appear to be composed principally or
entirely of abnormal isoforms of a host-encoded glycoprotein, prion protein.
Prion propagation involves recruitment of host cellular prion protein,
composed primarily of alpha-helical structure, into a disease specific isoform
rich in beta-sheet structure. The existence of multiple prion strains has been
difficult to explain in terms of a protein-only infections agent, but recent
studies suggest that strain specific phenotypes can be encoded by different
prion protein conformations and glycosylation patterns. The ability of a
protein to encode phenotypic information has important biological
implications. The appearance of a novel human prion disease, variant CJD, and
the clear experimental evidence that it is caused by exposure to BSE has
highlighted the need to understand the molecular basis of prion propagation,
pathogenesis, and the barriers limiting intermammalian transmission. It is
unclear if a large epidemic of variant CJD will occur in the years
ahead.
NAL call no. QP351.A68
Descriptors: NvCreutzfeldt-Jakob
disease, bovine spongiform encephalopathy, scrapie, abnormal isoforms, prion
protein isoforms, prion propagation, pathogenesis, barriers to transmission.
Comincini, S.; Foti, M.G.; Tranulis, M.A.; Hills, D.; Di Guardo, G.;
Vaccari, G.; Williams, J.L.; Harbitz, I.; Ferretti, L. Genomic organization, comparative analysis, and
genetic polymorphisms of the bovine and ovine prion Doppel genes
(PRND). Mammalian Genome. 2001 Sep. 12(9): 729-733 ISSN:
0938-8990
Abstract: The doppel protein (Dpl) is a prion-like protein
encoded by the gene PRND, which has been found downstream of the prion gene,
PRNP, in human and mouse. This paper describes the isolation and structural
organization of the bovine and ovine PRND genes, which are composed of two
exons compared with the three of human and mouse. Intergenic distances between
PRNP and PRND were covered by means of long-range PCR and found to be 16.8 and
20 kb, in cattle and sheep respectively. The 5' and 3' untranslated regions
(UTR) were analyzed to identify transcription regulatory sequences and
compared with those from the PRND and PRNP sequences published for other
species. Three polymorphisms (R50H, N110H, and R132Q) were revealed in the
cattle coding region; two synonymous substitutions (I12I, A26A) were found in
sheep. None of the polymorphisms was significantly associated with either
Bovine Spongiform Encephalopathy (BSE) in cattle or scrapie in sheep.
NAL
call no. QL738.5.M359
Descriptors: doppel protein, bovine, ovine
PRND genes, structure, isolation, PCR polymorphisms, association with BSE and
scrapie.
Comincini, S.; Castiglioni, B. M.; Foti, G. M.; Del Vecchio, I.; Ferretti,
L. Isolation and molecular characterization of
rasfadin, a novel gene in the vicinity of the bovine prion gene.
Mammalian Genome. 2001 Feb. 12(2): 150-156 ISSN:
0938-8990
Abstract: A novel gene, rasfadin (RASSF2) was identified
close to the bovine prion gene, and its genomic structure was derived with a
combination of exon trapping and RACE. The gene covers at least 28 kb and maps
to the same chromosomal region as the prion gene in cattle, sheep, and human.
The RASSF2 ORF is composed of 987 base pairs divided into nine exons and shows
a high nucleotide (88%) and amino acid similarity (95%) with a previously
described human cDNA, KIAA0168. The bovine 3'UTR region is significantly
shorter than the human counterpart, but shares with it two highly conserved
nucleotide blocks. The expression of the gene was investigated in brain,
liver, and spleen. Alternative splicing yields a shorter product in the liver
composed of only four exons. Computer analysis showed a highly significant
similarity of the rasfadin protein with the Ras association (Ral-GDS/AF-6)
domain family 2 and with the afadin family, respectively, for the longer
brain/spleen and the shorter liver variants.
NAL call no.
QL738.5.M359
Descriptors: rasfadin gene, bovine prion gene, exon
trapping, RACE, cattle, sheep, humans
Cooley, W.A.; Clark, J.K.; Ryder, S.J.; Davis, L.A.; Farrelly, S.S.J.;
Stack, M.J. Evaluation of a rapid western
immunoblotting procedure for the diagnosis of bovine spongiform encephalopathy
(BSE) in the UK. J Comp Pathol. London : W.B. Saunders Company
Ltd. July 2001. v. 125 (1) p. 64-70.
Abstract: Bovine brain tissue
samples from 625 UK cattle, clinically suspected as bovine spongiform
encephalopathy (BSE) cases, were used in a blind analysis to assess a rapid
Western immunoblotting technique (Prionics Check; Prionics AG, Zurich), which
detects bovine disease-specific protease-resistant prion protein (PrP(Sc)). By
means of statutory histopathological examination, 599 of the 625 cattle were
confirmed as BSE cases by the demonstration of spongiform encephalopathy, the
remaining 26 being classified as negative. Duplicate samples from the same
animals were also examined by electron microscopy for the presence of abnormal
brain fibrils (scrapie-associated fibrils; SAFs). The Prionics technique
showed a high sensitivity, particularly when compared with the fibril
detection test; the detection rates were 99.3% and 92.0% respectively, with
histopathology being used as the "gold standard". The false negative results
by the Prionics test were possibly related to the sampling procedure. Analysis
of 50 BSE-positive samples revealed similar glycoprofiles, the majority of
PrP(Sc)isoforms being di-glycosylated protein. The Prionics test also detected
PrP(Sc)in the four brain samples from the 26 histopathologically negative
animals, apparently reducing the specificity of the test to 84.6%; however,
confirmatory positive results in these samples were obtained by demonstrating
SAF or by immunohistochemical examination, or both. It was concluded that the
Prionics test detected PrP(Sc)in a small percentage (0.64%) of clinically
suspected BSE cases showing no spongiform change. Since January 2000, the
Prionics Western blot test has been introduced as one of the statutory tests
for the diagnosis of clinically suspected BSE and scrapie cases in the
UK.
NAL call no. 41.8 J82
Descriptors: cattle, bovine spongiform
encephalopathy, immunoblotting, brain, diagnostic techniques and value,
histopathology, electron microscopy, prion proteins, UK.
Corn, Joseph L.; Nettles, Victor F. Health
protocol for translocation of free-ranging elk. Journal of Wildlife
Diseases 37(3), July, 2001: 413-426.
NAL call no. 41.9
W64B
Descriptors: elk, Cervus elaphus, health protocol for
restoration programs, health scoring, ectoparasites, some diseases, internal
parasites, quarantines, diagnostic testing, prophylactic treatment.
Coulthart, M.B.; Cashman, N.R. Variant
Creutzfeldt-Jakob disease: a summary of current scientific knowledge in
relation to public health. CMAJ-Canadian Medical Association
Journal 2001 Jul 10; 165(1): 51-58. ISSN: 0820-3946
Abstract:
The prion diseases pose unique scientific, medical, veterinary and regulatory
challenges. Here, we summarize current information bearing on the natural
history, pathobiology and epidemiology of these disorders and public policy
responses to the potential threats to public health posed, particularly, by
bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease (vCJD).
Six years after the first case reports of vCJD, there is still no clear
indication of the magnitude of the primary epidemic, or of the likelihood of
lateral transmission of this untreatable disease by iatrogenic means,
particularly by blood and blood products. However, the unsettling nature of
the available evidence warrants prudence regarding public health policy and
regulation, as well as a forward-looking approach to research.
NAL call no.
R11 C3
Descriptors: NvCJD, natural history, pathobiology,
epidemiology, public health risks, UK, transmission issues, iatrogenic
transfer.
Cousens, S.; Smith, P.G.; Ward, H.; Everington, D.; Knight, R.S.; Zeidler,
M.; Stewart, G.; Smith-Bathgate, E.A.; Macleod, M. A.; Mackenzie, J.; Will,
R.G. Geographical distribution of variant
Creutzfeldt-Jakob disease in Great Britain, 1994-2000. Lancet.
2001 Mar 31. 357(9261): 1002-1007 ISSN: 0140-6736
Abstract:
BACKGROUND: Geographical variation in the distribution of variant
Creutzfeldt-Jakob disease (vCJD) might indicate the transmission route of the
infectious agent to man. We investigated whether regional incidences of vCJD
were correlated with regional dietary data. METHODS: The National CJD
Surveillance Unit prospectively identified 84 people with vCJD up to Nov 10,
2000, in Great Britain. Their lifetime residential histories were obtained by
interviews with a close relative. Cumulative incidences of vCJD by standard
region were calculated. Grid references for places of residence in 1991 were
identified and evidence of geographical clusters were sought. Data on diet in
the 1980s were analysed for regional correlations with vCJD incidence. The
socioeconomic status of the places of residence of people with vCJD was
compared with that of the general population. FINDINGS: vCJD incidence was
higher in the north of Great Britain than the south. The rate ratio (north vs
south) was 1.94 (95% CI 1.27-2.98). The mean Carstairs' deprivation score for
areas of residence of people with vCJD was -0.09 (-0.73 to 0.55), which is
close to the national average of zero. Regional rates of vCJD were correlated
with consumption of other meat or meat products as classified and recorded by
the Household Food Consumption and Expenditure Survey (r=0.72), but not with
data from the Dietary and Nutritional Survey of British Adults. Five people
with vCJD in Leicestershire formed a cluster (p=0.004). INTERPRETATION:
Regional differences in vCJD incidence are unlikely to be due to ascertainment
bias. We had difficulty determining whether regional variations in diet might
cause these differences, since the results of dietary analyses were
inconsistent.
NAL call no. 448.8 L22
Descriptors: disease
incidence, NvCreutzfeldt-Jakob Disease, diet analysis, socioeconomic levels,
regional differences, Carstairs’ deprivation score, results.
Crise de l'ESB: le secteur bovin toujours
dans l'incertitude. [The BSE crisis: still uncertainty for the cattle
sector.] Chambres-d'Agriculture. 2001, No. 896, 3-9. ISSN: 0396-7883.
In French.
NAL call no. 14 T69
Descriptors: BSE, effects on beef
consumption and international trade, bovine spongiform encephalopathy, cattle
diseases, 2 scenarios, cattle prices, prion diseases, GATT trade agreements
Cutlip, R.C.; Miller, J.M.; Hamir, A.N.; Peters, J.; Robinson, M.M.; Jenny,
A.L.; Lehmkuhl, H.D.; Taylor, W.D.; Bisplinghoff, F.D. Resistance of cattle to scrapie by the oral route.
Canadian Journal of Veterinary Research; Revue Canadienne de
Recherche Veterinaire. 2001 Apr. 65(2): 131-132 ISSN:
0830-9000
Abstract: Early epidemiological information indicated that
bovine spongiform encephalopathy (BSE) originated from scrapie in sheep. The
question arose if scrapie in North America would induce a BSE-like disease in
cattle. Six years ago, we reported that brain tissue from sheep with scrapie
caused a neurologic disease when injected directly into the brains of cattle,
but the disease induced was different from BSE as it occurs in the United
Kingdom and Europe. Here, we report that cattle fed raw brain or meat and bone
meal and tallow prepared from sheep with scrapie remained normal for 8 years
after exposure. This work indicates that cattle are highly resistant to North
American scrapie by the oral route.
NAL call no.
SF601.C24
Descriptors: BSE, scrapie, cattle, sheep, North American
scrapie, oral feeding of raw brain and meat, resistance to infection.
Cyranoski, D. Japan's first BSE case fuels
fears elsewhere. Nature. 2001 Sep 27. 413(6854): 337 ISSN:
0028-0836
NAL call no. 472 N21
Descriptors: BSE, Japan, cattle,
introduced zoonosis.
de Vries, H. Het afvoeren van alle dieren
van een bedrijf naar de destructie bij het aantonen van BSE van een dier op
dat bedrijf. Een goede strategie? [Destruction of all animals on the
farm after diagnosis of BSE in one animal. Is that a good strategy?]
Tijdschrift voor Diergeneeskunde 2001 Feb 15. 126(4): 113-115 ISSN:
0040-7453. In Dutch.
NAL call no. 41.8 T431
Descriptors: BSE,
bovine spongiform encephalopathies, cattle, livestock, disease control,
veterinary care issues, The Netherlands.
Dealler, S. Should young UK cattle be
considered free of BSE or is it endemic? British Food Journal.
2001, 103: 4, 264-280; 30 ref. ISSN: 0007-070X
NAL call no. 389.8
B77
Descriptors: BSE, bovine spongiform encephalopathy; calves;
disease transmission; epidemiology; law; pathogenesis; reviews
Debeer, S.O.; Baron, T.G. Bensik, A.A.
Immunohistochemistry of PrPsc within bovine spongiform encephalopathy brain
samples with graded autolysis. Journal of Histochemistry and
Cytochemistry 2001 Dec. 49(12): 1519-1524 ISSN:
0022-1554
Abstract: Bovine spongiform encephalopathy (BSE) is a
transmissible neurodegenerative disease of cattle. Clinical diagnosis can be
confirmed by investigation of both spongiform changes and abnormal prion
protein (PrPsc), a marker considered specific for the disease. Tissue
autolysis, often unavoidable in routine field cases, is not compatible with
histological examination of the brain even though PrPsc is still detectable by
immunoblotting. To determine how autolysis might affect accurate diagnosis
using PrPsc immunohistochemistry, we studied 50 field samples of BSE brainstem
(obex) with various degrees of autolysis. We demonstrated that the
antigen-unmasking pretreatments necessary for PrPsc immunohistochemistry were
compatible with the preservation of autolyzed brain sections and that PrPsc
detection was unaffected by autolysis, even though anatomic markers were
sometimes lost. In tissue samples in which anatomic sites were still
recognizable, PrPsc accumulation was detected in specific gray matter nuclei.
In samples with advanced autolysis, PrPsc deposits were still observed, at
least at the cellular level, as an intraneuronal pattern. We found that the
sensitivity of PrPsc immunohistochemistry as a diagnostic method for BSE was
undiminished even by severe tissue autolysis.
NAL call no. 381
J8222
Descriptors: BSE, diagnosis, brainstem tissue, field samples,
method sensitivity.
Deslys, J.P.; Lasmezas, C.I.; Comoy, E.; Domont, D. Diagnosis of bovine spongiform encephalopathy.
Vet J. London : Balliere Tindall, c1997-. Jan 2001. v. 161 (1)
p. 1-3. ISSN: 1090-0233
NAL call no. SF601.V484
Descriptors:
bovine spongiform encephalopathy, diagnosis, diagnostic techniques.
Deslys, Jean Philippe.; Picot, Andre. La vache folle: les risques pour
l'homme. [Mad cow disease: the risks for humans.] Dominos (Paris, France);
229. Paris : Flammarion, c2001. 127 p., ill., map. In French. ISBN:
2080300261
NAL call no. SF967.B63D47 2001
Descriptors: bovine
spongiform encephalopathy, public health risk assessment.
Deslys, J. P.; Comoy, E.; Hawkins, S.; Simon, S.; Schimmel, H.; Wells, G.;
Grassi, J.; Moynagh, J. Screening slaughtered
cattle for BSE. Nature. 2001 Jan 25. 409(6819): 476-478 ISSN:
0028-0836
NAL call no. 472 N21
Descriptors: brain, International
organizations, slaughter survey, abattoirs, prion protein, bovine spongiform
encephalopathy; European Union, cattle.
Doherr, M.G.; Heim, D.; Fatzer, R.; Cohen, C.H.; Vandevelde, M.;
Zurbriggen, A. Targeted screening of high-risk cattle populations for BSE
to augment mandatory reporting of clinical suspects. Prev. Vet. Med.
Amsterdam, The Netherlands : Elsevier Science B.V. Sept 20, 2001. v. 51
(1/2) p. 3-16. ISSN: 0167-5877. In the special issue: Structure mirrors
function / edited by M. Thrusfield and E. Goodall. Paper presented at a
meeting held March 29-31, 2000, Edinburgh, Scotland, UK.
Abstract:
In Switzerland, the first case of bovine spongiform encephalopathy (BSE) was
diagnosed in November 1990. Case numbers peaked in 1995, with a total of 352
BSE cases identified by 30 April 2000. Reporting of clinically suspect cattle
is currently the most commonly used method world-wide to detect BSE cases. The
effectiveness of mandatory reporting depends on a variety of factors; for
other diseases passive surveillance underestimates the incidence of clinical
cases. The efficiency of passive surveillance systems for BSE will remain
unknown until screening tests able to identify clinically affected cattle have
been applied in several countries. This paper provides the first detailed
description of a targeted screening programme for BSE. Two populations of cows
>24 months of age were included in the targeted screening: (i) cows found
dead or culled on site where the carcass was submitted to rendering (fallen
stock) and (ii) cows with health-related problems unfit for routine slaughter
that were slaughtered under emergency procedures (emergency slaughter).
Between 1992 and 1999, on average 81 clinical BSE suspects per year were
reported to the veterinary authorities (passive surveillance), of which 43%
were confirmed with BSE. A total of 30 clinical cases were captured by passive
surveillance and an additional 20 BSE cases detected by targeted screening
between May 1999 and April 2000. The odds of finding a BSE case was 49 times
higher in the fallen stock and 58 times higher in emergency-slaughtered cattle
when compared to passive surveillance. The targeted screening of fallen stock
and emergency-slaughtered cattle considerably increased the number of detected
cases in this 12-month period. Targeted-screening cases were on average 4
months younger than the clinical suspect cases. In conclusion, post-mortem
testing of fallen stock and emergency-slaughtered cows >24 months for BSE
is an important active surveillance element within a total surveillance system
that principally is based on mandatory reporting of clinical suspect cases.
Without ante-mortem screening tests to detect BSE-infected cattle during the
incubation period, a combination of effectively functioning passive and active
BSE surveillance strategies might be the only approach to assess the BSE
situation reliably in a given country or region - and it is necessary to
substantiate claims of freedom from the disease.
NAL call no.
SF601.P7
Descriptors: cattle, bovine spongiform encephalopathy,
screening, monitoring, diagnosis, identification, outbreaks, incidence,
detection, efficacy, postmortem examinations, mortality, epidemiology,
Switzerland.
Dominguez-Carmona, M. Epidemiologia de las
enfermedades prionicas animales. [Epidemiology of the animal prion
diseases] Anales de la Real Academia Nacional de Medicina (Madr.).
2001. 118(1): 233-245; discussion 245-258. ISSN: 0034-0634 In
Spanish.
Abstract: The authors review the epidemiology of spongiform
encephalitis, discussing the possible mechanism of appearance of the epidemic
bovine spongiform encephalitis epidemic, leaving aside to another publication
the epidemiology of the human spongiform encephalitis and its
pathogeny.
Descriptors: review, epidemiology, BSE, spongiform
encephalopathies.
Dormont, D. Les mecanismes de la mort
neuronale. [Mechanisms of neuron death.] Biofutur. 2001, No.
Hors Serie, 22-25; 7 ref. ISSN: 0294-3506. In French.
NAL call no. TP248.13
B565
Descriptors: BSE, apoptosis, bovine spongiform encephalopathy,
central nervous system lesions, cytokines, free radicals, human diseases,
neurons, pathogenesis, pathology, prion peptide 106-126, prion diseases.
Dove, A. US throws money at TSE research.
Nature Medicine. 2001 Oct. 7(10): 1075 ISSN:
1078-8956
Descriptors: US, transmissible spongiform
encephalopathies, prion diseases, research funding initiatives.
Dumas, E., Cabre, O., Bornert, G. Mesures
prises en France pour la prevention de la transmission de l'Encephalopathie
Spongiforme Bovine. [French mandatory regulations to prevent
transmission of Bovine Spongiform Encephalopathy.] Medecine et Armees.
Juillet, 2001; 29 (4): 363-368. In French. ISSN:
0300-4937
Descriptors: Bovine Spongiform Encephalopathy, BSE, food
safety concern, mandatory regulations, prevention strategies, surveillance,
use of animal proteins in animal feeds, screening tests.
Enders, M.; Frohlich, E.; Hassler, D.; Kretzschmar, H. BSE und die neue Variante der
Creutzfeldt-Jakob-Krankheit. [BSE (bovine spongiform encephalopathy)
and the new variant of Creutzfeldt-Jakob disease] Deutsche medizinische
Wochenschrift 2001 Jan 26. 126(4): A55-A56 ISSN: 0012-0472
NAL call no.
448.8 D48
Descriptors: NvCreutzfeldt-Jakob Disease, BSE,
relationship, human health risks.
Engvall, A.; Elvander, M. Riskvardering av
lander avseende BSE. [Risk assessment of countries with regard to
BSE.] Svensk Veterinartidning. 2001, 53: 8-9, 451-454; 4 ref. ISSN:
0346-2250 In Swedish.
NAL call no. 41.9 SV23
Descriptors: BSE,
bovine spongiform encephalopathy, European Union, geographical distribution,
human health risk assessment.
Enserink, M. Infectious diseases. Is the
U.S. doing enough to prevent mad cow disease? Science. 2001 Jun
1. 292(5522): 1639-1641 ISSN: 0036-8075
NAL call no. 470
Sci2
Descriptors: BSE, scrapie, destruction of Vermont heard of
sheep, prevention safeguards, border controls, prion diseases, chronic wasting
disease in deer and elk, transmissible mink encephalopathy, testing measures,
feed contamination, risk of bovine-based pharmaceuticals.
Enserink, M. Prion diseases. U.S. gets
tough against chronic wasting disease. Science. 2001 Nov 2.
294(5544): 978-979 ISSN: 0036-8075
NAL call no. 470
Sci2
Descriptors: Deer, disease outbreaks, prion disease, wasting
syndrome, animal husbandry, chronic disease, prevention and control.
Eskens, U. Bovine spongiform encephalopathy
(BSE)/transmissible spongiform encephalopathy/mad cow disease.
Environmental Science and Pollution Research International 2001.
8(2): 79-83 ISSN: 0944-1344
Descriptors: BSE, issues, public health
concerns, pollution concerns.
Estades, J.; Barbier, M.; Remy, E.; Aubert, F. (ed.); Sylvestre, J.P. TI:
Le comite d'experts comme dispositif de
production de confiance dans la gestion publique des risques: le cas de
l'ESB. [The committee of experts as the mechanism for the production of
confidence in the management of public risks: the case of BSE.] Confiance
et rationalite, Dijon,-France, 5-6-mai 1999. 2001, 113-129; 31 ref. ISBN:
2-7380-0963-8. Publisher: Institut National de la Recherche Agronomique;
Paris; France. In French.
Descriptors: bovine spongiform
encephalopathy, cattle diseases, food marketing, food safety, health, meat
products, prion diseases, public opinion, public relations
FDA finds more evidence of BSE compliance
problems. Journal of the American Veterinary Medical Assoc. 2001
Aug 15. 219(4): 427. ISSN: 0003-1488
NAL call no. 41.8
Am3
Descriptors: BSE, US feed industry, compliance in using animal
based products, ruminant feeds.
Federici, C. La reazione del mercato alla
vacca pazza. [Reaction of the Italian meat market to mad cow disease.]
Rivista di Avicoltura. 2001, 70: 2, 8-10. ISSN: 0005-2213. In
Italian.
NAL call no. 47.8 R523
Descriptors: beef consumption
decline, BSE, bovine spongiform encephalopathy; pork and poultry meat
increases, trends.
Ferguson-Smith, M.A. BSE and variant CJD.
Assumption that BSE originated from scrapie in sheep led to
misjudgment. BMJ Clinical Research ed. 2001 Jun 23. 322(7301):
1544-1545. ISSN: 0959-8138
Descriptors: bovine spongiform
encephalopathy, NvCreutzfeldt-Jakob Disease, scrapie, etiology, theories.
Foster, J. D.; Parnham, D.; Chong, A.; Goldmann, W.; Hunter, N. Clinical signs, histopathology and genetics of
experimental transmission of BSE and natural scrapie to sheep and
goats. The Veterinary Record 2001 Feb 10. 148(6): 165-171 ISSN:
0042-4900.
Abstract: This paper compares the clinical signs,
histopathology, detection of PrPSc protein and PrP genetics of the
transmission of BSE to sheep and goats, with the effects of the transmission
of natural scrapie from a brain homogenate from a single sheep. After
intracerebral and oral inoculations there were similarities in the clinical
signs due to the two sources of infection, but there were differences in
pathology at the end stage of disease and in the genotypes of the sheep which
succumbed to the challenges. The incubation period of BSE was associated with
the sheep PrP codon 171 genotype, but the natural scrapie source, despite
inducing disease only in known susceptible genotypes, showed no clear
association with PrP genotype.
NAL call no. 41.8
V641
Descriptors: transmissibility, prion disease, scrapie, bovine
spongiform encephalopathy, sheep, goats, histopathology, comparison study, PrP
Sc, incubation period, behavior, genotype effects.
Foster, J. D.; Parnham, D.W.; Hunter, N.; Bruce, M. Distribution of the prion protein in sheep
terminally affected with BSE following experimental oral transmission.
Journal of General Virology. 2001 Oct. 82(Pt 10): 2319-2326 ISSN:
0022-1317
Abstract: This study has examined the distribution of
PrP(Sc) in sheep by immunocytochemistry of tissues recovered from terminally
affected animals following their experimental infection by the oral route with
BSE. Despite a wide range of incubation period lengths, affected sheep showed
a similar distribution of high levels of PrP(Sc) throughout the central
nervous system. PrP(Sc) was also found in the lymphoid system, including parts
of the digestive tract, and some components of the peripheral nervous system.
These abundant PrP(Sc) deposits in sheep in regions outside the central
nervous system are in direct contrast with cattle infected with BSE, which
show barely detectable levels of PrP(Sc) in peripheral tissues. A number of
genetically susceptible, challenged animals appear to have survived.
NAL
call no. QR360.A1J6
Descriptors: prion protein, PrP(Sc),
immunocytochemistry, oral experimental infections, levels in lymphoid and
nervous tissue.
Foster, J.; Goldmann, W.; Parnham, D.; Chong, A.; Hunter, N. Partial dissociation of PrPSc deposition and
vacuolation in the brains of scrapie and BSE experimentally affected goats.
J Gen Virol. Reading : Society for General Microbiology. Jan
2001. v. 82 (pt.1) p. 267-273. ISSN: 0022-1317
Abstract: The
diagnosis of transmissible spongiform encephalopathies (TSEs) depends on the
detection of vacuolation in brain sections taken from affected individuals
and/or the identification of the disease-associated isoform of the PrP (prion)
protein (PrP(Sc)). During the course of an investigation, goats clinically
affected following experimental infection with three different sources of TSE
(SSBP/1, CH1641 and BSE) developed widespread vacuolar degeneration in the
brain. With BSE, PrP(Sc) was clearly recognized in affected goat brain by
immunocytochemistry (icc) and Western blotting, but in contrast the
experimental scrapie sources SSBP/1 and CH1641 showed almost no or very little
PrP(Sc) by icc. Western blot analysis of PrP(Sc) from BSE-affected and
SSBP/1-affected goat brain showed that the protein was present in brain
affected by both TSE sources, but could not be used to determine how much
protein was present. It became clear that PrP(Sc) and vacuolation could be
partially dissociated following challenge with two of the three TSE sources.
Subtle differences in glycosylation patterns between BSE- and
SSBP/1-associated PrP protein isoforms could also be recognized, although
these experimentally generated results should not be regarded as a BSE/scrapie
differential test. However, our study warns that the reliance on PrP(Sc)
determination by icc alone as a means by which to diagnose TSE infection may
generate false negative results.
NAL call no.
QR360.A1J6
Descriptors: bovine spongiform encephalopathy, prion
proteins, PrPSc, scrapie, goats, brain changes, diagnostic testing,
reliability.
Fournier, J. G. Nonneuronal cellular prion
protein. International Review of Cytology 2001. 208: 121-160 ISSN:
0074-7696
Abstract: The normal cellular prion protein (PrP(c)) is a
membrane sialoglycoprotein of unknown function having the unique property of
adopting an abnormal tertiary conformation. The pathological conformer PrP(sc)
would be the agent of transmissible spongiform encephalopathies or prion
diseases. They include scrapie and bovine spongiform encephalopathy in animals
and Creutzfeldt-Jakob disease in humans. The conversion of PrP(c) into PrP(sc)
in the brain governs the clinical phenotype of the disease. However, the
three-dimensional structure change of PrP(c) can also take place outside the
central nervous system, in nonneuronal cells particularly of lymphoid tissue
where the agent replicates. In natural infection, PrP(c) in nonneuronal cells
of peripheral extracerebral organs may play a key role as the receptor
required to enable the entry of the infectious agent into the host. In the
present review we have undertaken a first evaluation of compelling data
concerning the PrP(c)-expressing cells of nonneuronal origin present in
cerebral and extracerebral tissues. The analysis of tissue, cellular, and
subcellular localization of PrP(c) may help us better understand the
biological function of PrP(c) and provide some information on
physiopathological processes underlying prion diseases.
NAL call no. 442.8
In82
Descriptors: prion protein, nonneuronal cerebral and
extracerebral organ receptors, physiopathological processes, prion
diseases.
Fricker, J. BSE crisis--transmission
through blood transfusions? Trends in Molecular Medicine.
2001 Jan. 7(1): 2-3 ISSN: 1471-4914
Descriptors: BSE, risk factors,
bovine-based pharmaceuticals, contamination of equipment.
Gabus, C.; Auxilien, S.; Pechoux, C.; Dormont, D.; Swietnicki, W.;
Morillas, M.; Surewicz, W.; Nandi, P.; Darlix, J. The Prion Protein has DNA Strand Transfer Properties
Similar to Retroviral Nucleocapsid Protein. Journal of Molecular
Biology 2001 vol. 307, no. 4, pp. 1011-1021 ISSN: 0022-2836
NAL call
no. 442.8 J8224
Descriptors: transmissible spongiform
encephalopathies, PrP, nucleic acids, experimental infection of mice, PrP
involvement in nucleic acid metabolism.
Gale, P. Developments on microbiological risk assessment for drinking
water. J Appl Microbiol. Oxford, U.K. : Blackwell Science Ltd. Aug
2001. v. 91 (2) p. 191-205. ISSN: 1364-5072
Abstract: This paper
considers the development of microbiological risk assessment models for
pathogenic agents in drinking water with particular reference to
Cryptosporidium parvum, rotavirus and bovine spongiform encephalopathy (BSE).
The available evidence suggests that there is potential for considerable
variation in exposures to C. parvum oocysts through drinking water, during
both outbreak and non-outbreak conditions. This spatial/temporal heterogeneity
arises both from variation in oocyst densities in the raw water and
fluctuations in the removal efficiencies of drinking water treatment. In terms
of risk prediction, modeling the variation in doses ingested by individual
drinking water consumers is not important if the dose-response curve is linear
and the oocysts act independently during infection. Indeed, the total pathogen
loading on the population as represented by the arithmetic mean exposure is
sufficient for risk prediction for C. parvum, BSE and other agents of low
infectivity, providing the infecting particles (i.e. oocysts or BSE prions)
are known to act independently. However, for more highly infectious agents,
such as rotavirus, ignoring the variation and just using the arithmetic mean
exposure may over-estimate the risk by a factor of about threefold. If it were
to be shown that pathogens co-operate with each other during initiation of
infection, such that the dose-response relationship is non-linear, then
modelling the variation in doses ingested by individual consumers would be
very important. Possible mechanisms for co-operation of pathogens during
infection are considered. Simulations show that acquired protective immunity
for C. parvum reduces the risk of infection during outbreak conditions by over
10-fold. Variation in virulence between strains of C. parvum is a further
source of uncertainty.
NAL call no. QR1.J687
Descriptors:
pathogens, water-microbiology, risks of BSE contamination.
Gale, P.; Stanfield, G. Towards a
quantitative risk assessment for BSE in sewage sludge. Journal of
Applied Microbiology. September, 2001; 91 (3): 563-569. ISSN:
1364-5072
NAL call no. QR1 J687
Descriptors:
Source-Pathway-Receptor approach, BSE, contaminated waste, arithmetic mean
concentration of BSE agent, slaughter house effluent, horizontal transmission
risk.
Garcia, B.M. Encefalopatia espongiforme
bovina. [Bovine spongiform encephalopathy.] Alimentaria. 2001,
No. Extr., 24-62; 32 ref. ISSN: 0300-5755. In Spanish.
Descriptors:
BSE, bovine spongiform encephalopathy, cattle diseases, Creutzfeldt-Jakob
disease, human diseases, nervous system diseases, prion diseases, reviews.
Gatnau R.; Polo J.; Robert, E.; Brufau J. Plasma protein antimicrobial substitution at
negligible risk. Feed manufacturing in
the Mediterranean region. Improving safety: from feed to food. Proceedings of
the III Conference of Feed Manufacturers of the Mediterranean, organized by
ASFAC, with the collaboration of IRTA, CESFAC, CIHEAM, Patronat Catala Pro
Europa and Fira de Reus, and sponsored by Port de Tarragona, Reus (Spain),
22-24 March 2000. Cahiers Options Mediterraneennes. 2001, 54:
141-150; 45 ref. ISSN: 1022-1379. In French with an English
summary.
Descriptors: blood derived proteins, feed ingredients,
disease risks, BSE, dioxin, biological safety, correlating blood derived
products and health benefits, risk assessment.
Gavier Widen, D.; Wells, G.A.; Simmons, M. M.; Wilesmith, J.W.; Ryan,
J. Histological observations on the brains of
symptomless 7-year-old cattle. Journal of Comparative Pathology.
2001 Jan. 124(1): 52-59 ISSN: 0021-9975
Abstract: The histological
changes in the brains of 506 clinically normal 7-year-old cattle, which were
part of a cohort study on maternal transmission of bovine spongiform
encephalopathy, are described. Vacuolation of the white matter, of unknown
aetiology, located particularly in the substantia nigra, was a frequent
finding. Vacuolated neurons were commonly observed in the red nucleus (64.3%
of the animals) and in the habenular nucleus (50.1%). Spheroids were found in
10.8% of the brains, most frequently in the vestibular nuclei. Cellular
inflammatory infiltrates in association with blood vessels occurred in 30% of
the animals at various locations in the brain; their aetiology remains
uncertain, but they may have reflected subclinical or latent infections.
Mineralization of the wall of blood vessels, with proliferation of the intima,
was observed frequently in vessels of the internal capsule and was probably
associated with ageing. The description of histological findings in the brain
of symptomless adult cattle in the present study provides a useful background
for diagnostic bovine neuropathology.
NAL call no. 41.8
J82
Descriptors: histological changes, normal 7 year old cattle,
maternal BSE transmission, vacuolated neurons, substantia nigra.
Gee, R.W. Communication of risk.
Australian Veterinary Journal. 2001 Feb. 79(2): 136. ISSN:
0005-0423
NAL call no. 41.8 Au72
Descriptors: zoonotic diseases,
TSE, media and governmental communications, BSE, UK, Australia.
Germany. Gesellschaft fuer Tierzuchtwissenschaft Position statement of the Gesellschaft fuer
Tierzuchtwissenschaft (GfT) (Society for Animal Husbandry Science) and the
Deutsche Gesellschaft fuer Zuechtungskunde (DGfZ) (German Society for Animal
husbandry) regarding the BSE crisis (Bovine Spongiform Encephalitis).
Zuechtungskunde. Marz-April, 2001; 73 (2): 81-84. ISSN:
0044-5401. In German.
NAL call no. 49 Z8
Descriptors: BSE,
Germany societies position paper.
Giles, J. Mad cow disease comes to Japan.
Nature. 2001 Sep 20. 413(6853): 240 ISSN: 0028-0836
NAL call
no. 472 N21
Descriptors: cattle, BSE, confirmed case, imported feed,
contaminated feed, UK, Japan.
Glatzel, Markus; Aguzzi, Adriano. The
shifting biology of prions. Brain Research Reviews. October,
2001; 36 (2-3): 241-248. ISSN: 0165-0173.
Descriptors: BSE,
transmissible spongiform encephalopathies, prion and prion diseases.
Goldwater, P.N. Bovine spongiform
encephalopathy and variant Creutzfeldt-Jakob disease: implications for
Australia. Medical Journal of Australia, 2001 Aug 6. 175(3):
154-158 ISSN: 0025-729X
Abstract: The bovine spongiform
encephalopathy (BSE) epizootic developed in the United Kingdom in the
mid-1980s. Feeding practices in the cattle industry amplified the causative
prion, and meat contaminated with BSE entered the market. Human consumption of
prion-contaminated meat led to the new zoonosis--variant Creutzfeldt-Jakob
disease (vCJD). The UK BSE Inquiry published its report in October 2000; while
praising policy decisions, it also documented failures in the execution of
these policies, specifically delays and lack of rigour. Australia is in an
excellent position to maintain its BSE- and scrapie-free status, but
widespread active surveillance of neural and non-neural tissue from all
species of farmed quadrupeds is needed.
Descriptors: disease free
status, BSE, scrapie, Australia.
Golsteyn, R. M. When being right is not
enough. Trends in Cell Biology 2001 Feb. 11(2): 59 ISSN:
0962-8924
NAL call no. QH573.T73
Descriptors: Bovine spongiform
encephalopathy, communication, transmission, politics, cattle.
Grant, H. BSE and variant CJD. Humans can
live with BSE so long as they do not eat brains. BMJ-Clinical
Research ed. 2001 Jun 23. 322(7301): 1545. ISSN:
0959-8138
Descriptors: bovine spongiform encephalopathy,
NvCreutzfeldt-Jakob Disease, scrapie, etiology, theories, diet, human health
risks.
Gravenor, M. B.; Cox, D. R.; Hoinville, L. J.; Hoek, A.; McLean, A.R. The flock-to-flock force of infection for scrapie in
Britain. Proceedings of the Royal Society of London. Series B.
Biological Sciences. 2001 Mar 22. 268(1467): 587-592 ISSN:
0962-8452
Abstract: A postal survey of British sheep farmers
provided information on the proportion of farms that experienced their first
case of scrapie in each year between 1962 and 1998. We found no evidence of a
large increase in the proportion of scrapie-affected farms prior to, during or
following the epidemic of BSE in British cattle. After correcting for
between-farm heterogeneity in the probability of acquiring scrapie, we
estimated the yearly between-flock force of infection since 1962. The current
force of infection is estimated at approximately 0.0045 per farm per year and
combined with a simple model of scrapie spread provides an estimate of the
average duration of a scrapie outbreak on an individual farm. Considering all
farms, the average outbreak lasts for five years, but if only those farms that
have cases in animals born on the farm are considered, it lasts 15 years. We
use these parameter estimates to compare the proportion of farms with scrapie
in time periods of different lengths. In the survey, 2.7% of farms had a case
in 1998. The 5.3% of farms reporting having a case between 1993 and 1997 is
consistent with the hypothesis that the scrapie force of infection remained
constant over this period.
NAL call no. 501 L84B
Descriptors;
Disease outbreaks, scrapie transmission, epidemiology, prevention and control,
sheep, diseases, cattle, bovine spongiform encephalopathy, Great Britain,
statistical models, questionnaires.
Griffiths, P.D. Variant CJD epidemiology:
joining up the dots. Reviews in Medical Virology 2001 vol. 11,
no. 4, pp. 203-204 ISSN: 1052-9276.
Descriptors: BSE, disease
transmission, NvCreutzfeldt-Jakob-disease, incidence of disease, mathematical
model of human exposure, disease projection.
Gross, John E.; Miller, Michael W. Chronic wasting disease in mule deer:
Disease dynamics and control. Journal of Wildlife Management.
Bethesda, MD: The Wildlife Society. April 2001 v. 65 (2) p. 205-215. ISSN:
0022-541X
Abstract: The authors developed a mechanistic model to
simulate the dynamics of CWD in mule deer populations. Estimated parameters
were projected for age-specific disease dynamics, changes in population size
and effects of control strategies. The parameters were estimated from
observations of infections and uninfected deer in Colorado. They found that
the culling rate (20% of infected populations) effectively eliminated the
disease at low disease levels. When disease rates were high, the likelihood of
disease control diminished rapidly. To eliminate CWD from wild populations may
take decades.
NAL call no. 41.9 W64B
Descriptors: chronic wasting
disease, (CWD) transmissible spongiform encephalopathies, Odocoileus hemionus,
mule deer, PrPres, prion protein, epidemiology, game-farmed wapiti, disease
control measure, wildlife populations, wildlife management, public health
threats, mathematical model, Monte Carlo techniques
Gunn, M. Observations on disposal of
BSE-infected carcasses. Irish Veterinary Journal. 2001,
54: 4, 192-193; 4 ref. ISSN: 0368-0762
NAL call no. 41.8
IR4
Descriptors: BSE, bovine spongiform encephalopathy, brain,
carcass disposal, sources of infection, human risk assessment.
Guo, Zhi Ru; Jin, NingYi; Guo, Z.R.; Jin, N.Y. Advances in research on bovine spongiform
encephalopathy. Chinese Journal of Veterinary Science. 2001, 21:
3, 307-311; 49 ref. ISSN: 1005-4545. In Chinese.
NAL call no.
SF604.J68
Descriptors: Bovine spongiform encephalopathy, research,
reviews.
Half a response. Vet Rec.
London : The British Veterinary Association. Feb 17, 2001. v. 148 (7) p. 189.
ISSN: 0042-4900
NAL call no. 41.8 V641
Descriptors: bovine
spongiform encephalopathy, guidelines, UK.
Hamir, A.N.; Cutlip, R.C.; Miller, J.M.; Williams, E.S.; Stack, M.J.;
Miller, M.W.; O'Rourke, K.I.; Chaplin, M.J. Preliminary findings on the experimental
transmission of chronic wasting disease agent of mule deer to
cattle. J Vet Diagn Invest. Lawrence, Kan. : AAVLD. Jan 2001. v.
13 (1) p. 91-96. ISSN: 1040-6387
NAL call no.
SF774.J68
Descriptors: cattle, mule deer, chronic wasting disease,
Odocoileus hemionus, spongiform encephalopathy, disease transmission,
experimental infections, disease course, brain lesions, diagnostic techniques,
prion proteins.
Hammer, G.F. Massnahmen-Bundel fur mehr
Sicherheit: die tierseuchen- und fleischhygienerechtliche Vorschriften zur
BSE-Bekampfung. [Combined measures for more security: the regulations
relating to animal epidemics and meat hygiene for BSE control.]
Fleischwirtschaft. 2001, 81: 4, 54-60; 25 ref. ISSN: 0015-363X. In
German.
NAL call no. 280.38 F62
Descriptors: animal health, BSE,
bovine spongiform encephalopathy, cattle, meat product safety measures, prion
diseases, regulations, Germany.
Haunhorst E. Lebensmitteluberwachung:
Umsetzung der BSE-Regelungen Massnahmen Massnahmen der Lander sollen Schutz
der Verbraucher gewahrleisten. [Implementation of BSE regulations to
protect consumers.] Fleischwirtschaft. 2001, 81: 6, 20-22. ISSN:
0015-363X. In German.
NAL call no. 280.38 F62
Descriptors: BSE,
bovine spongiform encephalopathy; legislation implementation, German
provinces.
Healy, B. vCJD: broad U.S. response
required. Science. 2001 Mar 9. 291(5510): 1859 ISSN:
0036-8075
NAL call no. 470 Sci2
Descriptors: Creutzfeldt-Jakob
Syndrome, diagnosis, prevention and control, cattle, lymphoid tissue,
population surveillance, United States.
Heeschen, W.H. Bovine Spongiforme
Enzephalopathie (BSE). "Milch ist als sicher anzusehen" -- derzeitiger Stand
wissenschaftlicher Erkenntnisse zu dieser Aussage. [Bovine spongiform
encephalopathy (BSE). "Milk is safe" -- current state of scientific results
regarding this quote.] DMZ, Lebensmittelindustrie und Milchwirtschaft.
2001, 122: 2, 60-67; 17 ref. ISSN: 0938-9369. In German.
NAL call no.
HD9275 G3D59
Descriptors: milk, food safety, food contamination,
human health risk assessment, BSE, bovine spongiform encephalopathy; cattle
prion diseases.
Heppner, Frank L.; Arrighi, Isabelle; Kalinke Ulrich; Aguzzi, Adriano.
Immunity against prions? Trends in
Molecular Medicine. November, 2001; 7 (11): 477-479. ISSN:
1471-4914
Descriptors: prion protein, antibodies, scrapie-infected
cells in vitro, feasibility of immunotherapeutical intervention, question
effectiveness of vaccines and post-exposure strategies based on antibodies
scrapie, BSE, Creutzfeldt-Jakob disease
Heppner, F. L.; Musahl, C.; Arrighi, I.; Klein, M. A.; Rulicke, T.; Oesch,
B.; Zinkernagel, R. M.; Kalinke, U.; Aguzzi, A. Prevention of scrapie pathogenesis by transgenic
expression of anti-prion protein antibodies. Science. 2001 Oct
5. 294(5540): 178-182 ISSN: 0036-8075
Abstract: Variant
Creutzfeldt-Jakob disease and bovine spongiform encephalopathy are initiated
by extracerebral exposure to prions. Although prion transmission from
extracerebral sites to the brain represents a potential target for
prophylaxis, attempts at vaccination have been limited by the poor
immunogenicity of prion proteins. To circumvent this, we expressed an
anti-prion protein (anti-PrP) mu chain in Prnp(o/o) mice. Transgenic mice
developed sustained anti-PrP titers, which were not suppressed by introduction
of Prnp+ alleles. Transgene expression prevented pathogenesis of prions
introduced by intraperitoneal injection in the spleen and brain. Expression of
endogenous PrP (PrP(C)) in the spleen and brain was unaffected, suggesting
that immunity was responsible for protection. This indicates the feasibility
of immunological inhibition of prion disease in vivo.
NAL call no. 470
Sci2
Descriptors: prion diseases, anti-prion protein, mouse model,
introperitoneal injection, spleen, brain, immunity response, possibilities for
effective vaccine.
Hill, A.F.; Collinge, J.; Rabenau, H.F. (ed.); Cinatl, J. (ed.); Doerr,
H.W. Strain variations and species barriers.
Prions: a challenge for science, medicine and public
health-system. 2001, 48-257; 48 ref. Published by: S. Karger AG; Basel;
Switzerland. ISBN: 3-8055-7124-0
NAL call no. QR1 C66 v.
7
Descriptors: BSE, bovine spongiform encephalopathy, Creutzfeldt
Jakob disease, prion diseases, scrapie, strain differences, species barriers.
Hof, G. Verwarring rond boviene spongiforme
encefalopathie (BSE) en het risico op de nieuwe variant van de ziekte van
Creutzfeldt-Jakob. [Confusion surrounding bovine spongiform
encephalopathy (BSE) and the risk of new variant Creutzfeldt-Jakob disease]
Nederlands Tijdschrift voor Geneeskunde 2001 Mar 10. 145(10): 501-502.
ISSN: 0028-2162. In Dutch.
Descriptors: BSE, transmissible
spongiform encephalopathies, NvCreutzfeldt-Jakob disease, human health risks,
exposure to contaminated bovine-based products.
Hossain, H.; Chakraborty, T.
Prion-Krankheiten. [Prion diseases] Anasthesiologie,
Intensivmedizin, Notfallmedizin, Schmerztherapie-AINS. 2001 Jan. 36(1):
15-24 ISSN: 0939-2661. In German.
Descriptors: prions, prion
diseases, BSE, CJD, human health risks.
Huillard-d'Aignaux, J. N.; Cousens, S.N.; Smith, P.G. Predictability of the UK variant Creutzfeldt-Jakob
disease epidemic. Science. 2001 Nov 23. 294(5547): 1729-1731
ISSN: 0036-8075
Abstract: 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 disease epidemics of at most several thousand
cases.
NAL call no. 470 Sci2
Descriptors: BSE, back-circulation
analysis model, epidemiology, human health risks, disease incidence projection
Investigation of vCJD cluster points to
butchering practices. Clinical Infectious Diseases 2001 Jun 15.
32(12): ii. ISSN: 1058-4838
NAL call no. RC111 R4
Descriptors:
cattle slaughter processes, BSE, NvCreutzfeldt-Jakob Disease, incidence,
disease transmission risks.
Jackson, G.S.; Collinge, J. The molecular
pathology of CJD: old and new variants. Mol Pathol. 2001 Dec.
54(6): 393-399 ISSN: 1366-8714
Abstract: The study of prion disease
has become an area of intense interest since experimental evidence emerged for
the transmission of phenotypic variation without the involvement of a nucleic
acid component. Additional impetus has come from the widespread concern that
exposure to bovine spongiform encephalopathy contaminated material poses a
distinct and, conceivably, a severe threat to public health in the UK and
other countries. The occurrence of new variant Creutzfeldt-Jakob disease has
dramatically highlighted the need for a precise understanding of the molecular
basis of prion propagation. The molecular basis of prion strain diversity,
previously a major challenge to the "protein only" model, can now be
reconciled with propagation of infectious protein topologies. The
conformational change known to be central to prion propagation, from a
predominantly alpha-helical fold to one predominantly comprising
beta-structure, can now be reproduced in vitro, and the ability of beta-PrP to
form fibrillar aggregates provides a plausible molecular mechanism for prion
propagation. Concomitantly, advances in the fundamental biology of prion
disease have done much to reinforce the protein only hypothesis of prion
replication.
Descriptors: BSE exposure, public health concerns,
NvCreutzfeldt-Jakob Disease, prion proteins, conversion to bets helical
structure, in vitro.
Jackson, G.S.; Beck, J.A.; Navarrete, C.; Brown, J.; Sutton, P.M.;
Contreras, M.; Collinge, J. Pathogenesis:
HLA-DQ7 antigen and resistance to variant CJD Nature 2001 vol.
414, no. 6861, pp. 269-270 ISSN: 0028-0836
NAL call no. 472
N21
Descriptors: NvCreutzfeldt-Jakob disease, bovine spongiform
encephalopathy (BSE)-like prion strain, human leukocyte antigen, differential
diagnosis, host susceptibility.
Japan's beef scandal. Nature.
2001 Sep 27. 413(6854): 333 ISSN: 0028-0836
NAL call no. 472
N21
Descriptors: BSE, bovine spongiform encephalopathy,
NvCreutzfeldt-Jakob Disease, biased government communications, Japan,
confirmed case, cattle, feed contamination concerns, UK, meat and bone meal
imports.
Jeffrey M.; Martin, S.; Gonzalez, L.; Ryder, S.J.; Bellworthy, S.J;
Jackman, R. Differential diagnosis of
infections with the bovine spongiform encephalopathy (BSE) and scrapie agents
in sheep. Journal Comparative Pathology. November, 2001; 125
(4): 271-284. ISSN: 0021-9975
NAL call no. 41.8 J82
Descriptors:
scrapie, bovine spongiform encephalopathy, BSE, NvCreutzfeldt-Jakob disease,
transmissible spongiform encephalopathies, prion diseases, sheep,
immunohistochemical methods, brain, lymphoreticular system, experimental and
natural infections, strain-dependent processing, strain identification.
Jeffrey, M.; Ryder, S.; Martin, S.; Hawkins, S.A.C.; Terry, L.;
Berthelin-Baker, C.; Bellworthy, S.J. Oral
inoculation of sheep with the agent of bovine spongiform encephalopathy (BSE).
1. Onset and distribution of disease-specific PrP accumulation in brain and
viscera. J Comp Pathol. London : W.B. Saunders Company
Ltd. May 2001. v. 124 (4) p. 280-289. ISSN: 0021-9975
Abstract:
Sixty-three Romney sheep aged 6 months, consisting of three groups
(PrP(ARQ/ARQ), PrP(ARQ/ARR), and PrP(ARR/ARR)genotypes) of 21 animals, were
infected orally with brain tissue from BSE-infected cattle. Sub-groups of the
21 PrP(ARQ/ARQ) animals were killed, together with uninfected controls 4, 10,
16, 22 or 24-28 (after the development of full clinical disease) months
post-inoculation (mpi). One sheep from each of the two groups of four killed
at 4 or 10 mpi were shown by immunohistochemical examination to possess
disease-specific PrP accumulations in single lymph nodes. At 16 mpi, such
accumulations were detected in two of four infected sheep in some viscera and
in the spinal cord and brain. At 22 mpi, three of five infected sheep had
widespread disease-specific PrP accumulations in all tissues examined, but the
remaining two animals gave positive results only in the central nervous
system. Clinical disease appeared at 20-28 mpi. Three sheep killed with
advanced clinical signs showed widespread PrP accumulation in brain, spinal
cord and peripheral tissues. These results confirmed that PrP(ARQ/ARQ) Romney
sheep are susceptible to experimental infection with the BSE agent. The
different sites at which initial PrP accumulations were detected suggested
that the point of entry of infection varied. Once established, however,
infection appeared to spread rapidly throughout the lymphoreticular system.
The results suggested that in some BSE-infected sheep neuroinvasion occurred
in the absence of detectable PrP accumulations in the viscera or peripheral
nervous system. In contrast to cattle with BSE, however, most sheep showed
disease-specific PrP accumulations in the lymphoreticular system. In this
respect, BSE-infected resembled scrapie-infected sheep; it is possible,
however, that future research will reveal differences in respect of targeting
of cell types within the lymphoreticular and peripheral nervous systems. The
PrP(ARQ/ARR)and PrP(ARR/ARR)sheep were also killed in sub-groups at intervals
after inoculation. Up to 24 mpi, however, none of these animals showed
disease-specific PrP accumulations. Further results will be reported
later.
NAL call no. 41.8 J82
Descriptors: sheep, bovine
spongiform encephalopathy, genotypes, prion proteins, brain experimental
infection, spinal cord, animal tissues, clinical aspects, pathogenesis,
peripheral nerves.
Kaaden, O.R.; Rabenau, H.F. (ed.); Cinatl, J. (ed.); Doerr, H.W. Animal transmissible spongiform encephalopathy:
clinical and diagnostic aspects. Prions: a challenge for science,
medicine and public health-system. 2001, 145-150; 48 ref. Published by: S.
Karger AG; Basel; Switzerland. ISBN: 3-8055-7124-0
NAL call no. QR1 C66 v.
7
Descriptors: BSE, bovine spongiform encephalopathy, clinical
aspects, diagnosis, pathogenesis, prion diseases, scrapie, animals.
Kahrs, R.F. Viral diseases of cattle. 2001, viii + 324 pp. Iowa
State University Press; Ames; USA ISBN: 0-8138-2591-1
NAL call no. SF961
K26 2001
Descriptors: Aujeszky's disease, bovine leukosis, BSE,
bovine spongiform encephalopathy, clinical aspects, disease diagnosis,
disinfectants, diagnostic-techniques, FMD, foot and mouth disease, rabies,
international trade, malignant catarrhal fever, rhinotracheitis, Rift Valley
fever, rinderpest, vaccines, vulvovaginitis, various viral diseases, herpes,
warts, poxvirus, etc.
Kamphues, J.; Zentek, J.; Oberthur, R.C.; Flachowsky, G.; Coenen, M. Futtermittel tierischer Herkunft als mogliche
Verbreitungsursache fur die bovine spongiforme Enzephalopathie (BSE) in
Deutschland: 1. Mitteilung: Vergleichende Risikobewertung der
Einzelfuttermittel tierischer Herkunft. [Animal-derived feeds as
possible vectors for bovine spongiform encephalopathy (BSE) in Germany. 1.
Comparative risk assessment for a single animal food of animal origin]
Deutsche Tierarztliche Wochenschrift 2001 Jul. 108(7): 283-290. ISSN:
0341-6593. In German.
Abstract: The occurrence of BSE cases in
Germany after the ban of meat and bone meal for ruminant feed in 1994 requires
a detailed investigation of animal derived feedstuffs regarding their specific
risks as vectors for the disease. Accepting the theory that BSE is a prion
transmitted disease, the theoretical infectious potential was calculated for
animal derived feedstuffs. This calculation was based on the assumption, that
risk material (brain, spinal cord) of one clinically diseased cattle was
rendered in the process as established in Germany (133 degrees C, 3 bar, 20
min) or, alternatively, that one diseased animal was slaughtered resulting in
normal processing of the by-products for human food production. From this risk
assessment it became obvious that meat and bone meal was one, but probably not
the most important source for the spreading of BSE. Taking into account the
high sensitivity of calves it can be speculated that certain products, e.g.
from bone processing (bone meal) and fat melting (mixed animal fats), commonly
used for the formulation of milk replacers, might have been more important as
pathways. As it can't be excluded retrospectively that infected meat and bone
meal was imported from the UK, this non-calculable influence may have been
related to the significance of the other products. The calculation model
underlines that efficient removal of specified risk material (brain, spinal
cord) and adequate processing (133 degrees C, 3 bar, 20 min) or alternatively
other equivalent treatments of fats are prerequisites for minimizing the risk
of feed borne transmission of BSE by animal derived feedstuffs. The
epidemiological consequences are part of a subsequent paper.
NAL call no.
41.8 D482
Descriptors: contaminated feeds, meat and bone meal, feed
processing, cattle, risk assessment.
Kingombe, Cesar Isigidi Bin; Luthi, Elisabeth; Schlosser, Heidi; Howald,
Denise; Kuhn, Monika; Jemmi, Thomas. A
PCR-based test for species-specific determination of heat treatment conditions
of animal meals as an effective prophylactic method for bovine spongiform
encephalopathy. Meat Science. January, 2001; 57 (1): 35-41.
ISSN: 0309-1740
NAL call no. TX373 M4
Descriptors: animal waste
sterilization, animal based feeds, ELISA and PCR assays, pork tissue, bovine
tissue, screening method.
Kleinhanss W.; Haxsen G.; Uhlmann F.; Kamphues J. (ed.); Flachowsky G.
Okonomische Bewertung eines Verbots der
Tiermehlherstellung und verfutterung. [Economic assessment of a ban on
meat and bone meal production and feeding.] Animal nutrition - resources
and future developments. Workshop on Sustainable Animal Production, 15-16 June
2000, EXPO 2000, Hannover, Germany.
Landbauforschung-Volkenrode,-Sonderheft. 2001, No. 223, 159-166; 1 ref. ISSN:
0376-0723 ISBN: 3-933140-47-1. In German with an English
summary.
Descriptors: economic impact, alternative rendering system,
ban on meat and bone meals, waste disposal, carcass disposal, BSE.
Klimuszko, D. Priony -- czynnik
etiologiczny gabczastych encefalopatii. [Prions in the aetiology of
spongiform encephalopathies.] Zycie Weterynaryjne. 2001, 76: 3,
128-130; 14 ref. ISSN: 0137-6810. In Polish.
NAL call no.
SF604.Z9
Descriptors: BSE, etiology, bovine spongiform
encephalopathy, prion diseases, pathogenesis, public health risks, scrapie.
Kolb, E. Neuere Erkenntnisse uber die
Eigenschaften des Erregers der BSE und der Traberkrankheit sowie uber die
Infektionswege (Ubersichtsreferat). [Recent studies on the properties
of BSE and scrapie infectious agents and mechanisms of infection.]
Tierarztliche Umschau. 2001, 56: 4, 175-183; 37 ref. ISSN: 0049-3864.
In German with an English summary.
NAL call no. 41.8
T445
Descriptors: BSE, bovine spongiform encephalopathy, prion
disease, scrapie, sheep, cattle, disease process.
Koo, Hye Cheong; Park, Yong Ho; Lee, Byeong Chun; Chae, Chan Hee; O' Rourke
K.I.; Baszler, T.V.; Koo, H.C.; Park Y.H.; Lee, B.C.; Chae, C.H. Immunohistochemical detection of prion protein
(PrP-Sc) and epidemiological study of BSE in Korea. Journal of
Veterinary Science. 2001, 2: 1, 25-31; 43 ref. ISSN: 1229-845X
NAL call
no. SF604.J68
Descriptors: BSE, etiology, prion protein, cattle
survey, Korea, immunohistochemistry and western immunoblotting assays,
epidemiology.
Koppinen, J. The French reflect on BSE.
Australian Veterinary Journal 2001 Jul. 79(7): 452 ISSN:
0005-0423
NAL call no. 41.8 Au72
Descriptors: BSE, the French
situation.
Kramer, G. N.; Pauwels, J.; Le Guern, L.; Schimmel, H.; Trapmann, S. Recent production of candidate reference materials
at IRMM. Fresenius' Journal of Analytical Chemistry. 2001 Jun.
370(2-3): 142-146 ISSN: 0937-0633
Abstract: In the execution of its
mission to promote a common European measurement system in support of EU
policies, IRMM's Reference Materials Unit is currently involved in preparation
of proficiency-testing samples and candidate reference materials. Recent work
related to bovine spongiform encephalopathy in cows, genetically modified
organisms, and a variety of environmental materials is described.
NAL call
no. QD71.F7
Descriptors: EU policies, BSE, measurement systems,
reference materials.
Krammer, R. BSE crisis sinks German public
biotech programme. Nature. 2001 Feb 1. 409(6820): 549 ISSN:
0028-0836
NAL call no. 472 N21
Descriptors: bovine spongiform
encephalopathy, impacts on research, biotechnology research, Germany.
Krcmar, P.; Rencova, E. Identification of
bovine-specific DNA in feedstuffs. Journal of food protection
2001 Jan. 64(1): 117-119 ISSN: 0362-028X
Abstract: Considering
the menace of transmission of bovine spongiform encephalopathy, feed
components intended for cattle nutrition must be checked for the presence of
bovine-derived materials. We have been using a method based on polymerase
chain reaction for the identification of bovine-specific mitochondrial DNA
sequences for this purpose. The specificity of the primers for polymerase
chain reaction has been tested using samples of DNA of other vertebrate
species, which may also be present in rendering plant products. The method
allows the detection in concentrate mixtures of 0.125% of bovine-derived
material. Bovine DNA at concentrations corresponding to less than 0.5% of
bovine-derived material was detected in 3 of the 30 samples of concentrate
mixtures collected from distributors' stores all over the Czech Republic. All
44 samples of fish meal collected from the same sources were free of
bovine-derived material.
NAL call no. 44.8 J824
Descriptors:
BSE, bovine derived feed testing, feed contamination, mitochondrial DNA
testing, polymerase chain reaction method, detection method.
Kuzma, C.D. BSE: could it happen here?
Experts say probably not. Journal of the American Veterinary Medical
Association. 2001 Mar 1. 218(5): 646-647, 650 ISSN: 0003-1488
NAL call
no. 41.8 Am3
Descriptors: bovine spongiform encephalopathy, cattle,
US.
Laffling, A.J.; Baird, A.; Birkett, C.R.; John, H.A. A monoclonal antibody that enables specific
immunohistological detection of prion protein in bovine spongiform
encephalopathy cases. Neuroscience Letters. 2001 Mar 9. 300(2):
99-102 ISSN: 0304-3940
Abstract: The specificity of a monoclonal
antibody (mAB) raised against recombinant bovine prion protein (PrP) for the
immunohistological detection of PrP accumulation in the medulla oblongata of
bovine spongiform encephalopathy (BSE) and ovine scrapie cases was
investigated. mAB KG9 showed a diffuse low intensity reaction with the
cytoplasm of neurones in normal cattle and sheep sections. In BSE sections the
mAB detected widespread granular deposits of PrP associated with neurones and
the neuropil. Although scrapie sections showed similar levels of granular
deposits with another antibody to PrP these were not detected by KG9 which did
however detect diffuse staining in neuronal cytoplasm. Possible explanations
for the specificity of binding of KG9 are discussed.
NAL call no. QP351
N3
Descriptors: BSE, diagnosis, cattle, medulla oblongata, ovine
scrapie, mAB KG9 antibody, PrP, specificity of KG 9 binding.
Lahiff, S.; Glennon, M.; O' Brien, L.; Lyng, J.; Smith, T.; Maher, M.;
Shilton, N. Species-specific PCR for the
identification of ovine, porcine and chicken species in meat and bone meal
(MBM). Molecular and Cellular Probes. February, 2001; 15
(1): 27-35. ISSN: 0890-8508
NAL call no. RB43.7.M63
Descriptors:
silica-guanidiumthiocyanate DNA isolation procedure, commercial DNA
extraction kit, identification of source materials, animal feed formulations,
tissue identification, sheep, swine, poultry, transmissible spongiform
encephalopathies.
Langenfeld, T.W.; Menges, T.; Hempelmann, G. Bovine spongiforme Enzephalopathie (BSE).
[Bovine spongiform encephalopathy (BSE)] Anasthesiologie, Intensivmedizin,
Notfallmedizin, Schmerztherapie-AINS. 2001 Feb. 36(2): 77-78 ISSN:
0939-2661. In German
Descriptors: BSE, aspects of the disease,
cattle.
Lasky, Tamar; Etzel, Ruth; Angulo, Fred; Ward, Hester; Powell, Mark; Rubin,
Carol Food safety: Challenges to epidemiology.
American Journal of Epidemiology. June 1, 2001; 153 (11
Supplement): S13. ISSN: 0002-9262. Joint Meeting of the Society for
Epidemiologic Research, American College of Epidemiology, Epidemiology Section
of the American Public Health Association, and the Canadian Society for
Epidemiology and Biostatistics, Toronto, Canada, June 13-16, 2001
NAL call
no. 449.8 Am3
Descriptors: food safety, emerging diseases, public
health risks, BSE.
Lasmezas, C.I.; Fournier, J.G.; Nouvel, V.; Boe, H.; Marce, D.; Lamoury,
F.; Kopp, N.; Hauw, J.J.; Ironside, J.; Bruce, M. Adaptation of the bovine spongiform encephalopathy
agent to primates and comparison with Creutzfeldt-Jakob disease: implications
for human health. Proc Natl Acad Sci, USA. Washington, D.C. :
National Academy of Sciences, Mar 27, 2001. v. 98 (7) p. 4142-4147. ISSN:
0027-8424
Abstract: There is substantial scientific evidence to
support the notion that bovine spongiform encephalopathy (BSE) has
contaminated human beings, causing variant Creutzfeldt-Jakob disease (vCJD).
This disease has raised concerns about the possibility of an iatrogenic
secondary transmission to humans, because the biological properties of the
primate-adapted BSE agent are unknown. We show that (i) BSE can be transmitted
from primate to primate by intravenous route in 25 months, and (ii) an
iatrogenic transmission of vCJD to humans could be readily recognized
pathologically, whether it occurs by the central or peripheral route. Strain
typing in mice demonstrates that the BSE agent adapts to macaques in the same
way as it does to humans and confirms that the BSE agent is responsible for
vCJD not only in the United Kingdom but also in France. The agent responsible
for French iatrogenic growth hormone-linked CJD taken as a control is very
different from vCJD but is similar to that found in one case of sporadic CJD
and one sheep scrapie isolate. These data will be key in identifying the
origin of human cases of prion disease, including accidental vCJD
transmission, and could provide bases for vCJD risk assessment.
NAL call
no. 500 N21P
Descriptors: bovine spongiform encephalopathy, prions,
intravenous injection, disease transmission, Macaca fascicularis, symptoms,
mice, Creutzfeldt-Jakob Disease, cerebellum, cerebral cortex, histopathology,
immunohistochemistry, scrapie, strains.
Lawler, S. Farmer's research goes against
the grain. Trends in Cell Biology 2001 Mar. 11(3): 110. ISSN:
0962-8924
NAL call no. QH573.T73
Descriptors: Bovine spongiform
encephalopathy, chemically induced, insecticides, organothiophosphate
poisoning, cattle, copper and manganese chemistry, prions, intravenous, drug
effects.
Lledo, Pierre-Marie. Histoire de la vache folle. [‘The history of
mad cow.”]. Science, histoire et societe. Paris : Presses Universitaires de
France, c2001. xvi, 158, [1] p., ill. In French. ISBN: 2130515738
NAL call
no. SF967.S63 L58 2000
Descriptors: bovine spongiform
encephalopathy, prion diseases, animals prions disease history.
Lloyd, S.E.; Onwuazor, O.N.; Beck, J.A.; Mallinson, G.; Farrall, M.;
Targonski, P.; Collinge, J.; Fisher, E.M.C.
Identification of multiple quantitative trait loci linked to prion disease
incubation period in mice Proceedings of the National Academy of
Sciences, USA 2001 vol. 98, no. 11, pp. 6279-6283 ISSN: 0027-8424
NAL
call no. 500 P21P
Descriptors: prion proteins,
NvCreutzfeldt-Jakob-disease, scrapie, polymorphism, disease incubation times,
bovine spongiform encephalopathy quantitative trait loci, prion protein
gene.
Lloyd, T.; American Agricultural Economics Association. The impact of food scares on beef and inter-related
meat markets. [S.l. : s.n. 2001?]. "Selected paper, American
Agricultural Economics Association annual meeting, Chicago, IL, August
5-August 8, 2001."
NAL call no. HD9421.4.I47 2001
Descriptors:
meat industry and trade, meat inspection, BSE, Great Britain.
Lorenzen, S. BSE ist keine
Naturkatastrophe, sondern ein menschengemachtes Problem: Wie lasst es sich in
Wurde losen. BSE is not a natural disaster, but a man-made problem: how
can the BSE crisis be solved in dignity? Fleischwirtschaft. 2001, 81:
4, 127-133; Many ref. ISSN: 0015-363X. In German with an English
summary.
NAL call no. 280.38 F62
Descriptors: BSE, bovine
spongiform encephalopathy, disease control, public health concerns.
Lucker, E.; Horlacher, S.; Eigenbrodt, E. Brain in human nutrition and variant
Creutzfeldt-Jakob disease risk (vCJD): detection of brain in retail liver
sausages using cholesterol and neuron specific enolase (NSE) as markers.
British Journal of Nutrition 2001 Aug. 86 Suppl 1: S115-S119.
ISSN: 0007-1145
Abstract: No information is available about the
consumption of brain via meat products. With respect to the new variant of
Creutzfeldt-Jakob disease (vCJD) and the presumed food-borne transmission of
bovine spongiform encephalopathy (BSE) to humans, a preliminary survey for
brain and/or spinal cord (tissues of the central nervous system, CNS) was
conducted. We applied a previously developed integrated procedure using
cholesterol and neuron specific enolase (NSE) as markers. Quantification of
cholesterol had to be backed up by NSE immunochemistry in order to account for
low specificity and relatively high variances. Out of 126 high-quality finely
graded liver sausages, five samples (4 %) showed positive NSE immunoresponses.
In four of these samples a transgression of the normal maximum cholesterol
content was obtained. The identification of such a considerable number of
CNS-positive sausages indicates that brain consumption is not as rare as
previously assumed. Overall, the present integrated method could be
successfully applied for the detection of CNS in heat-treated meat products.
Its routine application in official food control would deter illegal practice
and thus help to control transmissible spongiform encephalopathies.
NAL
call no. 389.8 B773
Descriptors: detection method, brain material,
bovine-based meat products, food screening, contamination control, cholesterol
and neuron specific enolase.
Lundberg, P. O. Annu bara borjan av galna
ko-sjukan? Creutzfeldt-Jakobs sjukdom och andra prionsjukdomar: nulaget.
[Still a small problem with the mad cow disease? Creutzfeldt-Jakob
disease and other prion diseases: current status] Lakartidningen. 2001
Jan 10. 98(1-2): 19-24 ISSN: 0023-7205. In Swedish.
Abstract: This
review is based on recent published research on the BSE/CJD/vCJD problem
mainly from UK, Germany and France. The situation in Sweden seems to be
fortunate for several reasons. The use of meat and bonemeal as animal fodder
was forbidden in this country 13 years ago. Sweden has not had any sheep with
scrapie for many years. No animals with BSE have so far been found in our
country. The incidence of sporadic CJD in this country followed
retrospectively from 1985 to 1996 and prospectively from 1997 to 1999 has been
around 1.2 per million per year with no significant increase. Only few cases
of familial CJD are known. No patient with iatrogenic CJD has ever been found.
The use of growth hormone derived from human pituitary glands was abandoned in
1985 when recombinant human growth hormone became available. So far there is
no indication that any of the CJD cases diagnosed in Sweden has been of the
vCJD type, the one linked to BSE. However, as the incubation period for prion
diseases is very long and the Swedes are frequent travelers there is a risk
that people from our country could have contracted vCJD through consuming meat
products in countries with BSE. As a precaution the consumption of brain,
spinal cord, lymphatic tissue, lungs, and gastrointestinal tract should be
avoided. Human pituitary derived growth hormone is still available in some
countries and might be illegally imported into Sweden.
Descriptors:
Review article, BSE, NvCreutzfeldt-Jakob Disease, feed ingredients, incidence,
disease free, scrapie, battle, sheep, travel risks.
Lundberg, P.O. Far, kor--och slakt?
[Sheep, cattle--and slaughtering?] Lakartidningen. 2001 Feb 28.
98(9): 990-991 ISSN: 0023-7205. In Swedish.
Descriptors: sheep,
cattle, slaughtering issues, BSE, scrapie.
MacKnight, C. Clinical implications of
bovine spongiform encephalopathy. Clinical Infectious Diseases.
2001 Jun 15. 32(12): 1726-1731 ISSN: 1058-4838
Abstract: Bovine
spongiform encephalopathy (BSE) is a new prion disease that was first
identified in the United Kingdom in 1987. Its appearance was likely caused by
changes in the rendering process used to produce a meat and bone supplement
for cattle, changes that allowed this prion to enter the bovine food supply.
Despite measures that were made to reduce the risk to humans, a new variant of
Creutzfeldt-Jakob disease appeared in the mid-1990s and has been linked to
BSE. Although the extent of the disease's impact on humans is not yet known,
current estimates predict that there will be 136,000 cases of this fatal
disease by the year 2040. The risk to humans of medications produced with
bovine materials, gelatin, and blood transfusion is unknown.
NAL call no.
RC111 R4
Descriptors: BSE, risk to human health,
NvCreutzfeldt-Jakob-Disease, UK, disease incidence projections, transmission
risks of bovine-based pharmaceuticals and other materials, blood transfusions.
Magdzik,W. Encefalopatie gabczaste (choroby
prionowe) zwierzat. [Spongiform encephalopathy (prion diseases) in
animals] Przeglad Epidemiologiczny . 2001. 55(1 Suppl 2): 71-74. ISSN:
0033-2100. In Polish.
Descriptors: prion diseases, animal incidence,
BSE, scrapie.
Maissen, M.; Roeckl, C.; Glatzel, M.; Goldmann, W.; Aguzzi, A. Plasminogen binds to disease-associated prion
protein of multiple species. Lancet. 2001 Jun 23. 357(9273):
2026-2028 ISSN: 0140-6736
NAL call no. 448.8 L22
Descriptors:
prion protein, transmissible spongiform encephalopathies, biochemistry.
Mangen, M.J.J.; Burrell, A.M. Decomposing
preference shifts for meat and fish in the Netherlands. Journal of
Agricultural Economics. 2001, 52: 2, 16-28; 30 ref. ISSN:
0021-857X.
NAL call no. 281.9 AG8
Descriptors: beef, BSE, bovine
spongiform encephalopathy, consumer preferences, elasticities, fish, meat
products, pork, poultry meat, consumer preferences, demand changes,
Netherlands.
Manolakou, K.; Beaton, J.; McConnell, I.; Farquar, C.; Manson, J.; Hastie,
N.D.; Bruce, M.; Jackson, I.J. Genetic and
environmental factors modify bovine spongiform encephalopathy incubation
period in mice. Proc Natl Acad Sci USA. Washington, D.C.
: National Academy of Sciences, June 19, 2001. v. 98 (13) p. 7402-7407. ISSN:
0027-8424
Abstract: The incubation period (IP) and the
neuropathology of transmissible spongiform encephalopathies (TSEs) have been
extensively used to distinguish prion isolates (or strains) inoculated into
panels of inbred mouse strains. Such studies have shown that the bovine
spongiform encephalopathy (BSE) agent is indistinguishable from the agent
causing variant Creutzfeldt-Jakob disease (vCJD), but differs from isolates of
sporadic CJD, reinforcing the idea that the vCJD epidemic in Britain results
from consumption of contaminated beef products. We present a mouse model for
genetic and environmental factors that modify the incubation period of BSE
cross-species transmission. We have used two mouse strains that carry the same
prion protein (PrP) allele, but display a 100-day difference in their mean IP
following intracerebral inoculation with primary BSE isolate. We report
genetic effects on IP that map to four chromosomal regions, and in addition we
find significant factors of host environment, namely the age of the host's
mother, the age of the host at infection, and an X-cytoplasm interaction in
the host.
NAL call no. 500 N21P
Descriptors: mice, bovine
spongiform encephalopathy. isolation, cattle brain, prepatent period.
duration, alleles, animal proteins, application methods, animal models, man,
foodborne diseases, genetic effects, disease transmission, age, haplotypes,
major histocompatibility complex. quantitative traits. loci.
Marouby, H. La consommation de viandes dans
l'Union Europeenne: la situation avant la crise. [The consumption of
meat in the European Union: the situation before the crisis.] Techni
Porc. 2001, 24: 1, 3-4. ISSN: 0181-6764
NAL call no.
SF391.T4
Descriptors: meat, food consumption, pork, BSE, bovine
spongiform encephalopathy, cattle diseases, prion diseases.
Masters, C.L. The emerging European
epidemic of variant Creutzfeldt-Jakob disease and bovine spongiform
encephalopathy: lessons for Australia. Medical Journal of Australia,
2001 Feb 19. 174(4): 160-161 ISSN: 0025-729X
Descriptors: BSE,
NvCreutzfeldt-Jakob Disease, zoonotic diseases, health risks, trade concerns,
disease control.
Mastrangelo, P.; Westaway, D. The prion
gene complex encoding PrP(C) and Doppel: insights from mutational analysis.
Gene. 2001 Sep 5. 275(1): 1-18 ISSN: 0378-1119
Abstract:
The prion protein gene, Prnp, encodes PrP(Sc), the major structural
component of prions, infectious pathogens causing a number of disorders
including scrapie and bovine spongiform encephalopathy (or BSE). Missense
mutations in the human Prnp gene cause inherited prion diseases such as
familial Creutzfeldt-Jakob disease. In uninfected animals Prnp encodes a
glycophosphatidylinositol (GPI)-anchored protein denoted PrP(C) and in prion
infections PrP(C) is converted to PrP(Sc) by templated refolding. Though Prnp
is conserved in mammalian species, attempts to verify interactions of putative
PrP binding proteins by genetic means have proven frustrating and the ZrchI
and Npu lines of Prnp gene-ablated mice (Prnp(0/0) mice) lacking PrP(C) remain
healthy throughout development. This indicates that PrP(C) serves a function
that is not apparent in a laboratory setting or that other molecules have
overlapping functions. Current possibilities involve shuttling or
sequestration of synaptic Cu(II) via binding to N-terminal octapeptide
residues and/or signal transduction involving the fyn kinase. A new point of
entry into the issue of prion protein function has emerged from identification
of a paralogue, Prnd, with 24% coding sequence identity to Prnp. Prnd lies
downstream of Prnp and encodes the doppel (Dpl) protein. Like PrP(C), Dpl is
presented on the cell surface via a GPI anchor and has three alpha-helices:
however, it lacks the conformationally plastic and octapeptide repeat domains
present in its well-known relative. Interestingly, Dpl is overexpressed in the
Ngsk and Rcm0 lines of Prnp(0/0) mice via intergenic splicing events. These
lines of Prnp(0/0) mice exhibit ataxia and apoptosis of cerebellar cells,
indicating that ectopic synthesis of Dpl protein is toxic to central nervous
system neurons: this inference has now been confirmed by the construction of
transgenic mice expressing Dpl under the direct control of the PrP promoter.
Remarkably, Dpl-programmed ataxia is rescued by wild-type Prnp transgenes. The
interaction between the Prnp and Prnd genes in mouse cerebellar neurons may
have a physical correlate in competition between Dpl and PrP(C) within a
common biochemical pathway that when mis-regulated leads to apoptosis.
NAL
call no. QH442.A1G4
Descriptors: PrP, prion protein functions,
missence mutations, mouse models (ZrchI, Npu, Ngsk a Rcm0) transgenic mouse
model, doppel proteins.
Massara, F.; Scavone, M.; Ferraro, A.
Infezioni emergenti e sanita pubblica. [Emergent infections and public
health.] Obiettivi e Documenti Veterinari. 2001, 22: 1, 61-64. ISSN:
0392-1913. In Italian.
Descriptors: foodborne zoonotic diseases,
BSE, bovine spongiform encephalopathy, Escherichia coli, disease prevention,
public health concerns, salmonellosis, listeriosis, toxoplasmosis, disease
control and prrevention, disease-transmission, domestic animals, animal based
foods and products.
Mazzocchi, M.; Heckelei, T. (ed.); Witzke, H.P. (ed.); Henrichsmeyer,
W. Econometric methods for evaluating consumer
response to food scares: a structural approach. Agricultural sector
modelling and policy information systems. Proceedings of the 65th
European Seminar of the European Association of Agricultural Economists EAAE,
Bonn, Germany, 29-31-March, 2000. 2001, 111-120; 36 ref.
Wissenschaftsverlag Vauk Kiel KG; Kiel; Germany. ISBN:
3-8175-0329-6
Descriptors: BSE, bovine spongiform encephalopathy,
case studies, food demand models demand functions, food consumption, meat, EM
algorithm, Kalman filter.
Mazzoni, I.E.; Ledebur, H; Cashman, N. Signal transduction mechanisms linked to prion
protein. Society for Neuroscience Abstracts. 2001; 27 (1): 112.
ISSN: 0190-5295. 31st Annual Meeting of the Society for Neuroscience, San
Diego, California, USA, November 10-15, 2001
NAL call no.
QP351.S6
Descriptors: cortical postmitotic cultures, bse,
Creutzfeldt-Jakob disease, PrP knockout mice, concavalin A, calcium flux,
tyrosine phosphorylation, splenocytes.
McDonnell, K.; Desmond, J.; Leahy, J.J.; Howard, Hildige R.; Ward, S. Behavior of meat and bonemeal/peat pellets in a
bench scale fluidised bed combustor. Energy Oxford. 2001, 26: 1,
81-90; 11 ref. ISSN: 0360-5442
Descriptors: BSE, animal by-product
disposal, fluidised bed combustor, combustion tests, pellets with meat and
bone meal, alternative energy source.
McGill, I. Phillips report and the origin
of BSE. Veterinary Record. 2001 Jan 13. 148(2): 60 ISSN:
0042-4900
NAL call no. 41.8 V641
Descriptors: Bovine spongiform
encephalopathy, etiology, cattle, mutation, nerve tissue proteins, genetics,
prions.
Mead, Simon; Mahal, Sukhvir P.; Beck, John; Campbell, Tracy; Farrall,
Martin; Fisher, Elizabeth; Collinge, John. Sporadic: But not variant: Creutzfeldt-Jakob disease
is associated with polymorphisms upstream of PRNP exon 1. American
Journal of Human Genetics. December, 2001; 69 (6): 1225-1235. ISSN:
0002-9297.
NAL call no. QH431.A1A54
Descriptors: humans,
NvCruetzfeldt-Jakob Disease, etiologies, BSE, prions, PrP gene, codon 129,
mouse model, 56 polymorphic sites
Menges, T.; Langefeld, T.W.; Krumholz, W.; Hempelmann, G. Ubertragbare spongiforme
Enzephalopathien--Anaesthesiologisches und intensivmedizinisches
Management. [Transmissible spongiform encephalopathies--anesthetics and
intensive care management.] Anasthesiologie, Intensivmedizin,
Notfallmedizin, Schmerztherapie-AINS. 2001 Feb. 36(2): 79-89 ISSN:
0939-2661. In German.
Abstract: The transmissible spongiform
encephalopathies (TSE) are known to affect humans and various animals. The
bovine spongiform encephalopathy (BSE) and the human Creutzfeldt-Jacob disease
(CJD) are among the most notable degenerative disorders caused by prions.
Considering the BSE epidemic and the description of a new variant of
Creutzfeldt-Jacob disease (nvCJD), which is probably related to bovine
spongiform encephalopathy, TSE have recently gained a lot of public attention.
Although the causative factors (prions, viruses) are still under discussion,
none of the present concepts are explanatory for all aspects of the human CJD.
CJD may present as a sporadic, genetic, or infectious illness and there is now
considerable concern that bovine prions may have been passed to humans. To
exclude transmission of CJD via medical products and instruments, the
effectiveness of cleaning, disinfection and sterilization procedures must be
firmly established. This manuscript presents an overview to anaesthesiology
and intensive care medicine of recommended inactivation procedures and
assessed these procedures in the light of the inactivation of prions.
Descriptors: TSE’s, BSE, CJD, NvCreutzfeldt-Jacob Disease, prions,
disinfection/inactivations procedures, anesthetic and analgesic equipment.
Miele, G.; Manson, J.; Clinton, M. A novel
erythroid-specific marker of transmissible spongiform encephalopathies.
Nature Medicine. 2001 Mar. 7(3): 361-364 ISSN: 1078-8956
Abstract: Transmissible spongiform encephalopathies (TSE) are a
group of invariably fatal neurodegenerative diseases and include scrapie in
sheep, bovine spongiform encephalopathy (BSE) in cattle, chronic wasting
disease in deer and elk, and Kuru disease, Creutzfeldt-Jakob disease (CJD) and
variant CJD in humans. The pathological effects of disease occur predominantly
in the CNS (central nervous system), where common hallmarks include
vacuolation, gliosis, accumulation of a protease-resistant, abnormally folded
isoform of the prion protein (PrPSc) and neuronal cell death. Lack of
understanding of the molecular mechanisms underlying disease pathogenesis,
particularly in non-CNS tissues, means that there are currently no effective
strategies for early diagnosis or therapeutic intervention of TSEs. Here we
report the first identification of a molecular marker that is easily
detectable in readily accessible tissues. We demonstrate that a dramatic
decrease in expression of a transcript specific to erythroid lineage cells is
a common feature of TSEs. Our findings indicate a previously unrecognized role
for involvement of the erythroid lineage in the etiology of TSE pathogenesis
and should provide a new focus for research into diagnostic and therapeutic
strategies.
Descriptors: transmissible spongiform encephalopathies,
molecular marker, pathogenesis, research and diagnostic directions, non-CNS
tissues, early disgnosis, prion diseases.
Miles, S.; Frewer, L.J. Investigating
specific concerns about different food hazards. Food Quality and
Preference. 2001, 12: 1, 47-61; 35 ref. ISSN: 0950-3293
NAL call no.
TX367.F66
Descriptors: food safety, food hazards, consumer
attitudes, public health concerns, microbial and pesticide contamination of
food, genetic engineered; foods, BSE, bovine spongiform encephalopathy, risk
factors, laddering techniques.
Murphy, C.; Breen, C.; Rogers, M.; Giese, M. Interferon gamma and
prostaglandin in BSE-infected cattle. Cytokine. 2001 Feb 7. 13(3):
169-173 ISSN: 1043-4666
Abstract: Suspect field cases of BSE
infection (displaying clinical signs) were examined for possible alterations
of cytokine/autacoid plasma levels and were compared to control cases (not
displaying clinical signs of BSE infection). Interferon gamma (IFN-gamma)
plasma levels were demonstrated as being elevated in all suspected field cases
of BSE infection (irrespective of BSE status; determined via postmortem
histopathological examination). We demonstrated that plasma IFN-gamma levels
were significantly (P<0.005) higher in suspect cases of BSE infection than
in control cases. BSE-positive prostaglandin-E(2), (PGE(2)) plasma levels were
demonstrated as being elevated 1.25-fold above BSE-negative cases and
2.22-fold above control cases. No significant (P>0.5) increase in
PGE(2)plasma levels was recorded between BSE-positive and -negative. IFN-gamma
and PGE(2)plasma levels were examined using commercially available ELISA
assay. The results presented in this publication are the first demonstration
of alteration in immune state in animals with BSE.
NAL call no.
QR185.C95C986
Descriptors: bovine spongiform encephalopathy, cattle,
IFN-gamma levels, field cases, altered immune status.
Murray, G. Feed controls -- stopping BSE
(Mad Cow Disease). Agnote NSW Agriculture. 2001, No. DAI-227(1st
Ed.), 2 pp. NSW Agriculture; Orange; Australia. ISSN: 1034-6848
NAL call
no. SF55 A8 A36
Descriptors: BSE, bovine spongiform encephalopathy,
cows, feeds, labeling controls, meat and bone meal, prion diseases, control
measures.
Narang, H.K. A critical review of atypical
cerebellum-type Creutzfeldt-Jakob disease: its relationship to "new variant"
CJD and bovine spongiform encephalopathy. Experimental Biology and
Medicine (Maywood). 2001 Jul. 226(7): 629-639 ISSN:
1535-3702
Abstract: Shortly after the appearance of bovine
spongiform encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD) was
identified in young patients with nonclassical presentation such as difficulty
in balancing and ataxia. The classical CJD in older patients starts with
dementia. To distinguish between the two types, CJD in young persons has been
termed "new variant" (nvCJD). The distinguishing features of classical CJD
include initial presentation with dementia, confluent spongiform changes are
very unusual in the cerebellum, and PrP plaques are rarely observed. For
nvCJD, initially, difficulty with balancing and ataxia occurs, confluent
spongiform changes are seen in the cerebellum, and a large number of PrP
plaques are seen. The Icelandic observation of sheep scrapie revealed a
predominantly ataxic form of scrapie, termed Type II, rather than the itchy
form termed Type I. Both types have been known to exist in Europe. Since the
clinical signs of Type II scrapie in sheep with trembling and ataxia are
similar to those seen in BSE and nvCJD, this suggests that Type II is the
cause of BSE and nvCJD. Over 8 years, from 1989 to 1996, I examined the
clinical histories of 33 CJD cases aged between the ages of 18 and 84. Six
under the age of 40 and 15 over the age of 40 had leading clinical features
such as difficulty in balancing and ataxia similar to those seen in the young
cases classified as "nvCJD." Brains were examined from the six of 15 cases
over the age of 40, which revealed similar pathology to that seen in young
patients classified as "nvCJD." These findings suggest that all age groups are
susceptible to the strain of the agent derived from BSE cattle.
NAL call
no. QH301 E9
Descriptors: BSE, NvCreutzfeldt-Jakob Disease, young
humans, disease comparison, brain tissues, cerebellum.
Narang, H.K. Lingering doubts about
spongiform encephalopathy and Creutzfeldt-Jakob disease. Experimental
Biology and Medicine (Maywood). 2001 Jul. 226(7): 640-652 ISSN:
1535-3702
Abstract: Bovine spongiform encephalopathy (BSE) is an
infectious disease and has been transmitted orally to many other animals,
including humans. There is clear evidence of maternal transmission, although
disagreement on the source of the BSE agent remains. The current theories link
the origin of BSE to common scrapie in sheep. Twenty different strains of the
scrapie agent have been isolated from sheep. A search of the literature
indicates two distinct clinical syndromes in sheep, both of which have been
called scrapie. I have designated these Type I (the common type), which
exhibits itchiness and lose their wool, and Type II, which exhibits trembling
and ataxia. Sheep inoculated with BSE develop Type II scrapie and they exhibit
trembling. When cattle or mink are injected with the Type I strain, only a few
will develop a clinical disease. By contrast, no clinical disease has so far
been shown in cattle or mink by feeding them with Type I-infected sheep
brains. However, either by injecting or feeding with the BSE strain, 100% of
calves and mink develop the clinical disease. Evidence suggests that Type II
is the cause of BSE. Identical clinical signs of Type II trembling are found
in kuru and many of the recent cases of Creutzfeldt-Jakob disease. The BSE
agent has caused spongiform encephalopathies (SEs) in domestic cats, tigers,
and in some species of ruminants in zoos. The nature of the BSE agent remains
unchanged when passaged through a range of species, irrespective of their
genetic make up, demonstrating that variations in the host PrP gene are not a
major factor in the susceptibility to the BSE agent. Since more than 85 zoo
animals of many species have been diagnosed with SEs, from these studies it
seems reasonable to conclude that the BSE agent can infect almost all
mammalian species, including humans. For eradication of BSE and to reduce the
risk of infection to humans, the development of a vaccine against BSE is
suggested. Such a possibility should be fully explored.
NAL call no. QH301
E9
Descriptors: BSE, scrapie agents, Type I and Type II clinical
syndromes, sheep, mink, cattle, Type comparisons, etiology, zoo animals,
mammalian susceptibility.
Negro, A.; Ballarin, C.; Bertoli, A.; Massimino, M.L.; Sorgato, M.C. The metabolism and imaging in live cells of the
bovine prion protein in its native form or carrying single amino acid
substitutions. Molecular and Cellular Neurosciences 2001 Mar.
17(3): 521-538. ISSN: 1044-7431
Abstract: Prion diseases are
probably caused by an abnormal form of a cellular glycoprotein, the prion
protein. Recent evidence suggests that the prion strain causing BSE has been
transmitted to humans, thereby provoking a variant form of Creutzfeldt-Jacob
disease. In this work, we analyzed the behavior of normal and malformed
isoforms of the bovine PrP in transfected mammalian cell lines. Biochemical
and immunocytochemical assays were complimented with imaging of live cells
expressing fusion constructs between PrP and GFP. Bovine homologues of human
E200K and D178N (129M) mutations were used as models of pathogenic isoforms.
We show that the GFP does not impair the metabolism of native and mutant bPrPs
and is thus a valid marker of PrP cellular distribution. We also show that
each amino acid replacement provokes alterations in the cell sorting and
processing of bPrP. These are different from those ascribed to both murine
mutant homologues. However, human and bovine PrPs carrying the D178N genotype
had similar cellular behavior.
Descriptors: prion protein, behavior
of normal and isoforms, bovine PrP, transfected cell lines, GFP, E200K, D178N
(129M).
O'-Farrell, K.; Dillon, P.; Mee, J.; Crosse, S.; Nolan, M.; Byrne, N.;
Reidy, M.; Flynn, F.; Condon, T. Strategy for
restocking of Moorepark after depopulation following bovine spongiform
encephalopathy. Irish Veterinary Journal. 2001, 54: 2, 70-75; 5
ref. ISSN: 0368-0762.
NAL call no. 41.8 IR4
Descriptors: BSE,
bovine spongiform encephalopathy, cattle diseases, animal-health, dairy
cattle, disease control, Moorepark Centre Farm restocking strategy, herd
health status monitoring.
Office International des Epizooties. Foot
and mouth disease in Turkey, Peninsular Malaysia and Kazakhstan; Classical
swine fever in Spain and Slovakia; Bovine spongiform encephalopathy in Greece.
Disease Information Office International des Epizooties. 2001,
14: 27, 165-172. ISSN: 1012-5329
NAL call no. SF781
D57
Descriptors: BSE, bovine spongiform encephalopathy, disease
incidence statistics, epidemiology, foot and mouth disease, outbreaks, swine
fever
O'Mara F.; O' Doherty J. The effect of
removing fishmeal and meat-and-bone meal from animal diets. Irish
Veterinary Journal. 2001, 54: 5, 244-245. ISSN: 0368-0762
NAL call no.
41.8 IR4
Descriptors: BSE, animal protein in feeds, alternative
replacements, costs, nutritional values, Ireland.
Oomkes, C.; van Knapen, F. Cows, cats, and
FSE: death penalty justified? Veterinary Quarterly 2001 Jan. 23(1):
51-52 ISSN: 0165-2176
Abstract: Transmissible spongiform
encephalopathies affect a number of mammalian species. The most common
spongiform encephalopathies are scrapie in sheep and Bovine Spongiform
Encephalopathy (BSE) in cattle. Feline Spongiform Encephalopathy (FSE) is a
related disorder in domestic cats. Because of the link between BSE and FSE,
cats are put on a par with cattle, in terms of politics and regulations. In
the Netherlands, when a case of BSE is found on a farm, not only the
ruminants, but also the cats are taken away for post-mortem examination. So
far, the cats examined have always been negative for FSE. There are no
scientific reasons for destroying the cats on farms where BSE has been found.
NAL call no. SF601 V46
Descriptors: BSE, feline spongiform
encephalopathy, euthanizing cats, farms positive for BSE, incidence of
disease.
Operativi gli interventi per fronteggiare
la Bse. [Financial interventions to cope with BSE.] Informatore
Agrario. 2001, 57: 12, 13. ISSN: 0020-0689. In Italian.
NAL call no.
281.8 IN32
Descriptors: bovine spongiform encephalopathy, cattle
diseases, nervous system diseases, prevention, prion diseases, support
measures.
Overgaauw, P. A. BSE en petfood: is
diervoeding wel veilig? [BSE and pet food: is animal feed safe?]
Tijdschrift voor Diergeneeskunde. 2001 Apr 15. 126(8): 292 ISSN:
0040-7453. In Dutch.
NAL call no. 41.8 T431
Descriptors: BSE
contaminated pet foods, cats, transmissible spongiform encephalopathies.
Pallaroni, Lea; Bjorklund, Erland; von-Holst, Christoph; Unglaub, Wolfgang.
Determination of rendering plant sterilization
conditions using a commercially available ELISA test kit developed for
detection of cooked beef. Journal of AOAC-International.
November-December, 2001; 84 (6): 1884-1890. ISSN: 1060-3271.
NAL call no.
S583 A7
Descriptors: BSE, enzyme-linked immunosorbent assay (ELISA)
test kit, cooked beef/pork detection, rendering process, laboratory
conditions, temperature, time, particle size and meat composition.
Paukstadt, W. BSE-Rinder in Deutschland.
Mussen wir bald auch mit vCJK-Patienten rechnen? [BSE-cattle in
Germany. Must we soon also count on vCJK patients?]
MMW-Fortschritte-der-Medizin. 2001 Jan 25. 143(4): 12-13 ISSN:
1438-3276. In German.
Descriptors: Creutfeldt-Jakob Syndrome
transmission, brain pathology, cattle, diagnosis, Germany, risk factors.
Peretz, D.; Williamson, R.A.; Kaneko, K.; Vergara, J.; Leclerc, E.;
Schmitt-Ulms, G.; Mehlhorn, I. R.; Legname, G.; Wormald, M. R.; Rudd, P.M.;
Dwek, R.A.; Burton, D.R.; Prusiner, S.B. Antibodies inhibit prion propagation and clear cell
cultures of prion infectivity. Nature. 2001 Aug 16. 412(6848):
739-743 ISSN: 0028-0836
Abstract: Prions are the transmissible
pathogenic agents responsible for diseases such as scrapie and bovine
spongiform encephalopathy. In the favoured model of prion replication, direct
interaction between the pathogenic prion protein (PrPSc) template and
endogenous cellular prion protein (PrPC) is proposed to drive the formation of
nascent infectious prions. Reagents specifically binding either prion-protein
conformer may interrupt prion production by inhibiting this interaction. We
examined the ability of several recombinant antibody antigen-binding fragments
(Fabs) to inhibit prion propagation in cultured mouse neuroblastoma cells
(ScN2a) infected with PrPSc. Here we show that antibodies binding cell-surface
PrPC inhibit PrPSc formation in a dose-dependent manner. In cells treated with
the most potent antibody, Fab D18, prion replication is abolished and
pre-existing PrPSc is rapidly cleared, suggesting that this antibody may cure
established infection. The potent activity of Fab D18 is associated with its
ability to better recognize the total population of PrPC molecules on the cell
surface, and with the location of its epitope on PrPC. Our observations
support the use of antibodies in the prevention and treatment of prion