COMMENTARY

vCJD and the gut

vCJD and the gut: implications for endoscopy

M W Head, J W Ironside

National Creutzfeldt–Jakob Disease Surveillance Unit, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh, UK

Correspondence to:
Correspondence to:
Professor J W Ironside
National Creutzfeldt–Jakob Disease Surveillance Unit, School of Molecular and Clinical Medicine, University of Edinburgh, Western General Hospital, Edinburgh EH4 2XU, UK; james.ironside@ed.ac.uk

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Surveillance for infection by endoscopy for variant CJD and other human prion diseases

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The first 150 words of the full text of this article appear below.

The agents responsible for transmissible spongiform encephalopathies or prion diseases target the central nervous system, but their unique nature and pathophysiology has meant that prion diseases have made an impact in disciplines as diverse as dentistry and transfusion medicine, in large measure because of their resistance to decontamination by conventional means.¹

In 1996, a new variant form of Creutzfeldt–Jakob disease (CJD) was described in the UK that preferentially affects young adults, resulting in a disease that often presents with psychiatric symptoms progressing to ataxia, dementia and terminating in akinetic mutism.² The cause of this disease was proposed to be oral exposure to the bovine encephalopathy (BSE) agent, and subsequent studies have only served to strengthen this link, with no credible alternative explanation having been proposed.^3–6 All human prion diseases are progressive and uniformly fatal neurodegenerative conditions, and, in the case of the acquired forms (iatrogenic CJD . . . [Full text of this article]

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Prion infectivity in variant Creutzfeldt–Jakob disease rectum

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This article has been cited by other articles:

• Glover, D G, Pollard, B J, Gonzalez, L, Siso, S, Kennedy, D, Jeffrey, M (2007). A non-invasive screen for infectivity in transmissible spongiform encephalopathies. Gut 56: 1329-1331 [Full Text]