Flaws in the conventional consensus on the origins of BSE

[Guest guest]

Flaws in the conventional consensus on the origins of BSE.

by Mark Purdey

http://www.markpurdey.com/science_the_origins_of_bse.htm

The conventional consensus on the origins of TSEs maintains that

these diseases are caused by " hyperinfectious " malformed PrP (prion)

that is capable of converting healthy PrPc into abnormal, protease

resistant prions in the mammalian brain (1). Advocates of this theory

propose that these so called `prions' can be transmitted horizontally

in the external environment via animal to animal contact or via

ingestion of TSE diseased/prion contaminated brain tissue. But no

evidence exists to substantiate this speculative, yet universally

held belief.

Environmental perspectives of TSEs have been entirely excluded by

research programmes to date.

Such a mindset dismissal has largely been based on the fact that TSEs

can be transmitted via injection of TSE affected brain homogenate

into TSE-free healthy laboratory animals (1).

But in the light of the fact that certain other neurodegenerative

diseases, (eg; familial Alzheimer's) can be transmitted in this way

(2), why don't we view these other conditions with the same degree

of `hyperinfectious' paranoia that has been misattributed to TSEs?

Furthermore, BSE fails to fulfil Koch's postulates(3) – the yardstick

for determining whether an `infectious' agent underpins the aetiology

of a given disease. Despite these major discrepancies, the notion

that Bovine Spongiform Encephalopathy (BSE) was caused by scrapie

infection became cemented as `gospel' into mainstream professional

and public mentality.

An impartial study of the epidemiology of BSE/vCJD suggests that the

conventional consensus on the origins of BSE/vCJD is severely flawed

(4)(5)(6) for the following reasons;

1. BSE has failed to surface in the cattle populations of the Middle

East, India, Africa, North America, Third World countries, etc,

despite these countries receiving substantial tonnages of the BSE

incriminated meat and bone meal (MBM) imported from the UK from the

1960s onwards (7). UK MBM was exported either in its straight feed

form or as an inclusion in cattle concentrate feeds (7).

2. 40,000 + cases of BSE have erupted in UK cows that were born after

the 1988 ban on MBM entering cattle feed, and more recently, 22 cases

of BSE have erupted in cows born after the 1996 ban on MBM going into

animal feeding stuffs designated for all types of domestic animal

(8). Furthermore, some BSE endemic countries have experienced a

greater total number of BSE cases in cattle born after their

respective MBM bans than in cows born before.

3. There have been no reported cases of BSE in TSE susceptible

species, such as sheep and goats (8), despite the customary inclusion

of an MBM protein source in their concentrated feeds.

4. Four of the original five Kudu antelopes which contracted BSE at

the London Zoo had no possible access to feeds containing MBM (9).

5. BSE erupted in four cattle that were raised on MAFF's former

Liscombe experimental farm on Exmoor – a beef suckler farm which was

designed to raise beef from an all grass/silage system without any

resort to purchased in concentrate feeds (personal communication; M.

Stanbury, formerly ADAS, Quantock House, Taunton, UK.)

6. Alterations in the rendering of MBM (cessation of solvent

extraction, lower temperatures) from the batch to the continuous flow

system had purportedly enabled the survival of scrapie agent in UK

MBM, thus initiating the outbreak of BSE (10). However several

scrapie endemic countries, such as the USA and Scandinavia, had also

adopted these same BSE-causing prerequisites into their rendering

systems (11), yet these countries remain BSE-free to date (8).

7. Several US trials failed to invoke BSE in cattle after feeding or

injecting massive doses of scrapie-contaminated brain homogenate (12)

(13).

8. The UK's mechanically recovered/processed beef products and baby

foods – blamed for causing vCJD in humans – were exported worldwide

to countries where the practise of " skull splitting " in small rural

vCJD has never erupted. Likewise, butchers were offered as an

explanation for the growing number of vCJD clusters in rural areas.

But this practise had been adopted universally by rural/urban

butchers across the UK.

Bee