Photograph from Facebook Moustafa Jacob Page.

Variant CJD was first described in 1996, following intensive surveillance activities undertaken by the UK National CJD Surveillance Unit (NCJDSU) in Edinburgh.

CJD belongs to the family of what are called prion diseases, a unique group of neurodegenerative diseases that can be transmitted.

Wilhelm Carl Grimm (also Karl 24 February 1786 16 December 1859) was a German author, the younger of the Brothers Grimm.

Obviously, given the degree of suffering and public anxiety that variant CJD has caused, the possibility that it is receding is welcome news.

Indeed, secondary transmission by blood transfusion or surgical instruments might even result in variant CJD becoming endemic in the UK population.

In the UK, however, the epidemic of variant CJD seems to have peaked in 2000 and is now in decline, with 156 cases being identified so far. However, a retrospective study of abnormal prion protein accumulation in appendix and tonsil samples from over 12,600 people in the UK has yielded three more cases, which suggests that the level of BSE infection in the UK population is much higher than the actual number of confirmed variant CJD cases indicates.

They have only recently been recognized as the cause of several infectious diseases, including mad cow disease and Creutzfeldt Jakob Disease, which kill by crowding out healthy brain cells.

In the UK, however, the epidemic of variant CJD seems to have peaked in 2000 and is now in decline, with 156 cases being identified so far.

Optimists are proclaiming that variant Creutzfeldt Jakob disease (CJD), the human form always fatal of bovine spongiform encephalopathy (BSE), or Mad Cow Disease, is on the wane.

My colleagues and I in NCJDSU argued that this new form of human prion disease was likely to be linked to exposure to the BSE agent, probably by eating BSE infected meat products. Later investigations have shown that the transmitting agent in variant CJD shares identical biological properties with BSE s agent, supporting a causal relationship.

This pattern of trade has now been mirrored in the increasing geographical spread of BSE from the UK to other countries in Europe, and more recently to Japan and the United States. This unfortunately has been accompanied by increasing number of variant CJD cases in Canada, France, Ireland, Italy, Japan, Netherlands, Portugal, Saudi Arabia and the USA.

Later investigations have shown that the transmitting agent in variant CJD shares identical biological properties with BSE s agent, supporting a causal relationship.

This unfortunately has been accompanied by increasing number of variant CJD cases in Canada, France, Ireland, Italy, Japan, Netherlands, Portugal, Saudi Arabia and the USA.

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Further uncertainty regarding the future of variant CJD arises from the observation that the average age of the patients in the UK has not increased significantly over the past 10 years. If the epidemic were in decline, it might be anticipated that the average age of the patients would increase in the final stages (as occurred with cattle in the UK that were infected with BSE).

Further uncertainty regarding the future of variant CJD arises from the observation that the average age of the patients in the UK has not increased significantly over the past 10 years.

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Until we know the answers to these questions, it seems premature to decide that we are witnessing the beginning of the end of variant CJD.

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