The articles that have appeared in recent scientific journals concerning BSE: December 1996-May 1997

There are always more articles than you can read about TSEs, and I can only make an apology that some may be missed. If you feel that your article is missing and should be here, please forward it

Articles will probably not be still present on this page for greater than 6 months

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If you want a monthly bulletin "BSE and CJD" send a cheque for 40 pounds payable to the 'PHLS Board' to the Library at the Public Health Laboratory, 61 Colindale Ave, Colindale, London NW9 UK.(phone 0181 200 4400 for further info)

The best direct free search is done via medline on http://www.ncbi.nlm.nih.gov/PubMed/

If you want to go to the articles

before September 1996

or

between September 1996 and December 1996

or

after May 1997

.

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Transmission of the BSE agent to mice in the absence of detectable abnormal prion protein.

Lasmezas CI, Deslys JP, Robain O et al

Science 1997;275:402-5

At attempt was made to detect prion protein in the inoculum, none was found and yet the disease was transmitted. The methods used for detection were highly sensitive but could be argued simply not to be adequately sensitive to find the small amounts present. The paper was argued at the time in the scientific community but further research is necessary.


Tonsil test hope for CJD

Jaqui Wise, news staff BMJ

BMJ 1997;314:170

The report from Collinge et al (Lancet) that the marker for CJD (prion) can be found in the tonsil of a 35 yr old woman that died of nv-CJD.


Blood tests urged for CJD

Judy Siegel-Itzkovich, news staff BMJ, Jerusalem

BMJ 1997;314:170

Four Israeli scientists have urged that all Jewish residents of Libya or Tunian origin should undergo a blood test to identify carriers of CJD before they donate blood or organs. Most of these jewish emigrants went to Israel and only 1 in 100 of those were affected. There are around 1000 Israeli carriers of CJD


BSE protein could help fight disease

Anonymus

New Scientist 11 Jan 1997 p15

This reports information from Moira Bruce of an experiment in which knock out mice' lymphphocytes that cannot produce any PrPc were stimulated with concavalin A. They did not increase activated T cells as much as normal mouse lymphocytes. They also found that PrPc on the surface of lymphocytes increased in response to con A stimulation. The article suggests that this may be the way in which the agent of TSE is spread to the brain (but this would not agree with Aguzzi's findings). The apparent necessessity of PrP in the genetics of animals when there does not seem to be any difference in the life expectancy of knock out mice vs normals might mean that lab conditions are artificially clean suggests Bruce. The work suggests 'that gene therapy is not an option in preventing prion disease' says Bruce.


Neuropathologyof scrapie: a study of the distribution patterns of brain lesion in 222 cases of natural scrapie in sheep, 1982-91

Wood JLN, McGill IS, Done SH, Bradley R. Central Vet Lab in Weybridge, London

Veterinary Record 15.2.97 140;140:167-74.

The most important factor of this paper is that it shows specific distribution petterns of disease in the brains of the sheep and that the distribution patterns cross breeds. Although certain breeds were most likely to develop specific pathology patterns they did not always. Only 7 patterns could be easily separated using microscopy. This surely should have led to much research into the specific strains of disease that would be indicated but no work seems to have been done looking into the validity of the apparent strains by inoculation into mice and no work has been done to associate the strains with BSE. The reason why the paper has taken around 6 years to become published is also unclear.


The emergence of infectious diseases: Societal causes and consequences

Neal Nathanson Univ Pennsyltania Med Center, Pa.

ASM news 1997;63:83-87

It explains how the change in society opens the possibility for the growth of specific diseases and how BSE is an example. The information given about BSE was taken directly from MAFF publications and hence consideres that BSE was derived from scrapie. It also assumes that the reason why BSE continued after the feed ban was because infectivity was still in stored MBM. It now seems that neither of these are true as there has been no association so far with scrapie and the MBM in the feed chain disappeared very quickly. A better explanation now given is that infected meat products continued to enter bovine feed from cattle slaughtered after the feed ban. The logic of the argument concerning societal changes remains reasonable, however: large number of genetically similar cattle receiving the same feed in an entire country and this opening the door to large outbreaks.


The beef crisis: free trade issues in European Law

Joan Upson, Senior Lecturer, School of Law, De Montford Univ, Leicester UK.
Brtitish Food Journal, 1997;99:62-8

This is the most complex discussion available of the law in Europe concerning the free trade laws and the ability of the EC to alter them at will. The problem was always that individual countries would continue with relatively selfish objectives and so the EC was arranged so that the EC as a whole could bypass the selfishness of this. As a result there has been a number of bruised politicians and high bills put to the EC. The beef crisis has been particularly bad in that incompitence by the UK Government has led to scientific mismanagement of BSE and that followed by a change in the eating habits of the population of the EC. i.e. many European countries see themselves as having paid, through a free market, for the action of one of their members.


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Steve Dealler at deal@airtime.co.uk


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