NR AJZI
AU Ridley,R.M.; Baker,H.F.
TI Creutzfeldt-Jakob disease and bovine spongiform encephalopathy. Aetiology of scrapie in certain circumstances is not evidence against another aetiology in different circumstances.
QU British Medical Journal 1996 Jan 20; 312(7024): 180
IA http://www.bmj.com/cgi/content/full/312/7024/180/a
KZ BMJ. 1995 Oct 21;311(7012):1071-5; discussion 1075-6. PMID: 7580668
PT comment; letter
VT
EDITOR, - We are pleased that, in the commentary on our article on the myth of maternal transmission of spongiform encephalopathy, R G Will agrees that maternal transmission does not occur in human or experimental forms of spongiform encephalopathy and that the only circumstance in which it requires serious consideration is natural scrapie.[i]
The genetics of natural scrapie and the genetics of susceptibility to experimental transmission of scrapie in sheep differ. The characteristics and quantity of the agent, the route of exposure, and the interaction between the host genotype and the strain of agent are known only for, or are relevant only to, experimental transmission; in some cases they apply only to the laboratory disease in rodents. Data on experimental transmission are therefore of only limited relevance to natural scrapie.
The occurrence of scrapie in two of 20 Suffolk sheep exported from New Zealand in the 1960s is interesting, but, obviously, if New Zealand were free of scrapie at that time then these two animals could not have acquired scrapie by maternal transmission or other perinatal events. Care should be taken, however, in interpreting these data, since the scrapie free status of New Zealand applies to the 70 million strong national sheep flock, which is based largely on English Romneys, Lincolns, Southdowns, and sub-breeds of Merinos.[ii] Natural scrapie has rarely if ever been recorded in these breeds.[iii] The number of Suffolks in New Zealand is extremely small, and all the cases of scrapie in New Zealand have occurred in Suffolks.[iv] Similarly, almost all the.outbreaks of scrapie in Canada, the United States, and Australia have been in Suffolks.[v]
The point of our article is that there is no evidence for maternal transmission of any form of spongiform encephalopathy and that the epidemiology of natural scrapie is adequately explained by the sheep genotype. Spongiform encephalopathy is undoubtedly transmissible, and knowledge of the circumstances in which transmission occurs is extremely important both for the control of the disease in animals and for the prevention of disease in humans, especially since, in the West, all known acquired cases in humans have been iatrogenic. But a better understanding of the disease process is achieved when it is recognised that cases are either idiopathic or acquired and that evidence for one aetiology in certain circumstances is not evidence against another aetiology in different circumstances.
R M RIDLEY Head, MRC comparative cognition team
H F BAKER Senior scientific officer
Department of Experimental Psychology Cambridge University Cambridge CB2 3LS
i. Ridley RM, BAKER HF The myth of maternal transmission of spongiform encephalopathy. BMJ 1995;311:1071-6. [With commentary by RG Will (21 October.)
ii. Bruere AN. Scrapie: a point of view. New Zealand Veterinary Journal 1977;25:259-60.
iii. Parry HB. Scrapie disease in sheep; historical, clinical, epidemiological and practical aspects of the natural disease. London: Academic Press, 1983.
iv. Brash AG. Scrapie in imported sheep in New Zealand. New Zealand Veterinary Journal 1952;l:27-30.
v. Hourrigan JL, Klingsporn A, Clark WW, de Camp M. Epidemiology of scrapie in the United States. In: Prusiner SB Hadlow WJ, eds. Slow transmissible diseases of the nervous system. Vol. 1. New York: Academic Press 1979:331-56.
ZR 5
MH Animal; Encephalopathy, Bovine Spongiform/transmission; Female; Human; Maternal Exposure; Scrapie/*etiology; Sheep
SP englisch
PO England
OR Prion-Krankheiten 7