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. 2001 Jun 23;322(7301):1544.

BSE and variant CJD

Assumption that BSE originated from scrapie in sheep led to misjudgment

M A Ferguson-Smith 1
PMCID: PMC1120584  PMID: 11439995

Editor—In espousing the scrapie origin of bovine spongiform encephalopathy Brown fails to explain adequately why scrapie outside Britain has not led to bovine spongiform encephalopathy.1

Does Brown believe that scrapie “has mysteriously chosen the United Kingdom as its only geographical site and the early 1980s as its only historical occurrence” to appear in cattle? He explains that the comparatively high incidence of scrapie in sheep in the United Kingdom and the changes in rendering were responsible. This seems implausible, for reasons set out in the report of the BSE [bovine spongiform encephalopathy] inquiry.2

I am not aware of comparative data on the incidence of scrapie in the United Kingdom and abroad. Similar changes in rendering were occurring elsewhere, and no rendering process either before or since the emergence of bovine spongiform encephalopathy has been capable of completely inactivating scrapie.

The BSE inquiry was impressed by the more plausible alternative view that the agent giving rise to bovine spongiform encephalopathy was a novel strain of unknown origin that was pathogenic to humans. This view held that the strain arose in southern England in the 1970s and that the infection spread in waves through recycled infected cattle waste in meat and bonemeal. We will probably never know the origin of the agent—whether it arose in cattle or sheep or, indeed, any other species whose waste was incorporated into meat and bonemeal.

It was the assumption that bovine spongiform encephalopathy originated from an infection in sheep that led to the judgment that the risk of transmission to humans was remote. Brown's own research has indicated that scrapie was not linked to Creutzfeldt-Jakob disease, although humans have been exposed to scrapie for over 200 years.3

The uncertainties about the origin of bovine spongiform encephalopathy were not appreciated by many of those involved at the time. This is not a matter of criticism. As a result, however, the public was reassured unjustifiably.

References

  • 1.Brown P. Regular review: Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease. BMJ. 2001;322:841–844. doi: 10.1136/bmj.322.7290.841. . (7 April.) [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.BSE Inquiry. Report, evidence and supporting papers of the inquiry into the emergence and identification of bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease (vCJD) and the action taken in response to it up to 20 March 1996. London: Stationery Office; 2000. [Google Scholar]
  • 3.Brown P, Cathal F, Raubertas RF, Gajdusek DC, Castaigne P. The epidemiology of Creutzfeldt-Jacob disease: conclusion of a 15-year investigation in France and review of the world literature. Neurology. 1987;37:895–904. doi: 10.1212/wnl.37.6.895. [DOI] [PubMed] [Google Scholar]
BMJ. 2001 Jun 23;322(7301):1544.

Humans can live with BSE as long as they do not eat brains

Helen Grant 1

Editor—Brown not only understands bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease but gives a coherent account of them in plain English not embellished by jargon.1-1 Even he, however, falls into the trap of writing that “epidemiological evidence indicates that scrapie does not affect humans.”

Epidemiological evidence indicates that we do not know whether scrapie affects humans—a very different matter. If Brown had interrogated abattoir workers in 1989 (as I did) about their routine in dealing with sheep and cattle brains he would have been told that, whereas cattle brains were always removed to be added to “meat products,” sheep's brains were routinely left inside the skulls (it wasn't worth the bother to remove them) to be cooked up with the rest of the carcase and fed to cattle in the form of “meat and bonemeal.”

The reason that humans have had little trouble with scrapie over the centuries (but not none—how else could sporadic Creutzfeldt-Jakob disease have arisen?) is that we were never forced to swallow sheep's brains, some of them infected with scrapie. But we were forced to swallow cattle brains, which after 1981 contained the proliferating scrapie agent.

The rendering process changed in 1981: fat solvents, previously added to collect fat for tallow, were withdrawn, and from then on the (lipid) sheep's brains, complete with the organisms, went into cattle feed instead of into candles. It was not “inactivation,” or the lack of it, that enabled scrapie to get into cattle rations after 1981 but stopping its diversion into tallow. These vital facts about fat solvents, given in the Southwood report in 1989, were overlooked by the BSE inquiry, which is why the chairman of the inquiry, Lord Phillips, postulated that bovine spongiform encephalopathy must have some other origin.1-2

The apparent preference of variant Creutzfeldt-Jakob disease for young people, which Brown finds puzzling, is surely because the victims were children between 1981 and 1989 (cattle brains were finally banned from human foods in November 1989) and therefore shedding teeth. The resultant raw areas in their gums provided the organism with direct access to the bloodstream, thus shortening the incubation period. Nobody knows how many humans are incubating variant Creutzfeldt-Jakob disease, but we can live with bovine spongiform encephalopathy, just as we have lived with scrapie for three centuries, as long as we are not forced to eat the brains.

References

  • 1-1.Brown P. Regular review: Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease. BMJ. 2001;322:841–844. doi: 10.1136/bmj.322.7290.841. . (7 April.) [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 1-2.BSE Inquiry. Report, evidence and supporting papers of the inquiry into the emergence and identification of bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease (vCJD) and the action taken in response to it up to 20 March 1996. London: Stationery Office; 2000. [Google Scholar]

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