An Historic Timeline of Important Events Related to the

Discovery, Development and Understanding of TSEs.

Year Finding Investigator(s)
1730 description of ovine TSE, Scrapie, in British and European sheep l
1920 description of human TSE, Creutzfeldt-Jakob (CJD) disease, in humans; Germany Creutzfeldt/Jakob
1946

vaccination of sheep with formalin-treated ovine brain causes Scrapie outbreak

Gordon
1
first accidental cause of such a TSE outbreak and initial proof of the stability of the disease causing agent
l
1947 Scrapie found in the US in sheep imported from the UK  
1947 TSE described in mink; Transmissible mink encephalopathy, US  
1950s description of Kuru (shaking disease) in humans; Papua, New Guinea Gajdusek
1954-9

similiarity between CJD & Kuru and between Kuru & Scrapie recognized

Klatzo or Hadlow
11 TSEs believed to be the effect of a "slow virus"; one that acted slowly with a long latency period; proposed in 1954 and 1959 but now known not to be the case Sigurdsson or
Hadlow
1966 Kuru brain shown to experimentally infect chimpanzee brain Gajdusek
1 finding eventually lead to the end of canabalism and control of Kuru in New Guinea l
1963
National Pituitary Agency initiation of the US government and later European programs to distribute glands for the extraction of hormones to treat endocrine disorders, esp. treatment dwarfism in children with pituitary-derived growth hormone
 
1967 TSE found in wild ungulates, i.e. Chronic Wasting Disease of deer and elk described, US  
1976 Nobel prize awarded for TSE work Gajdusek
1982 purified fragment of the prion protein (PrP 27-30) was shown to have Scrapie infectivity laying the ground work to prove that a protein (not a bacterium or virus) was the infectious agent Prusiner or Bolton
1983 PrP (prion) accumulation in neuronal tissue of CJD and other prion diseases proven McKinley
1985 Pitsham Farm syndrome of "mad cows" discovered on British farm, BSE appears l
1985 US last imported beef from UK l
1985 children injected with 'contaminated' hormones eventually develop CJD in their 20's; first four cases identified l
1985 after ~27,000 children are injected worldwide since 1963 a link between CJD and contaminated growth hormone is realized; genetically engineered growth hormone now used to treat dwarfism  
1986 first verified case of BSE l

1988

mandated destruction of BSE stricken cows in Britain l
1988 BSE cases must be reported; i.e. BSE is a notifiable disease

l

1988 ruminant to ruminant feed ban introduced to prohibit feeding cattle the rendered remains of other animals including other cattle and Scrapie infected sheep l
1989 US bans import of ruminants and ruminant products from BSE infected countries, all cattle imported from UK between 1981 to 1989 into the US being watched (only 4 alive at end or 2000)  
1989 hereditary linkage of human prion diseases with PrP mutations described Hsiao
1990 surveillance setup in Britain to ascetain possible links between BSE and CJD l
1990 TSE found in cats, caused by feeding feeds with meat and bone meal containing BSE or prion-contaminated bovine tissues  
1992 BSE epidemic begins to decline in UK l
1992 TSE found in a zoo monkey (marmoset) caused by feeding BSE containing foods  
1994 first case of vCJD discovered l
1995 several cases of CJD described in unusually young patients; extensive amyloid plaques found; vCJD established as a unique form of CJD ll
1996 cause-effect link between BSE and vCJD proposed Will
1997 Second Nobel prize awarded for TSE work Prusiner
1997 US banned all import of rendered products from Europe: all species l
1997 ruminant to ruminant feed ban introduced in US to prevent chance of an epidemic of BSE in US cattle  
2000 a total of 87 cases of vCJD described in Britain, 3 other cases outside the UK (France & Ireland) l
2001 as of April 2001 all cattle slaughtered in US must be certified that they have not been fed ruminant MBM l
2001 almost 200,000 diseased cattle dead and 4,500,000 asymptomatic cattle destroyed in UK
no cases identified in US
l