|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From Bethesda, MD (P.B.); CJD Surveillance Unit, Hôpital de la Salpêtrière, Paris, France (J.-P.B.); Institute of Child Health, London, England (M.P.); and Department of Neurology, Higashiyamato Hospital, Japan (T.S.).
Address correspondence and reprint requests to Dr. Paul Brown, 7815 Exeter Road,Bethesda, MD 20814; e-mail: paulwbrown{at}comcast.net
The outbreaks of iatrogenic CreutzfeldtJakob disease (CJD) from cadaveric human growth hormone and dura mater are winding down and, like the only other environmentally acquired form of CJD (variant CJD due to infection with the agent of bovine spongiform encephalopathy), iatrogenic disease seems to have reached its high water mark during the 1990s. The total number of cases has reached 405, and the diminishing number of new cases is due to extremely long incubation periods from infections acquired before 1985 (up to 23 years for dura mater and 36 years for growth hormone). Although no cases associated with surgical or other invasive procedures have been identified during the past several decades, the recent discovery of three transfusion-associated variant CJD infections has provoked new concerns about the possibility of further secondary transmissions from operative procedures as well as blood and tissue donations. Therefore, at least in those countries in which variant CJD has occurred, precautionary measures must continue for the indefinite future.
This article was previously published in electronic format as an Expedited E-Pub at www.neurology.org
Disclosure: The authors report no conflicts of interest.
Received February 6, 2006. Accepted in final form May 10, 2006.
This article has been cited by other articles:
![]() |
J. D. F. Wadsworth, S. Joiner, J. M. Linehan, M. Desbruslais, K. Fox, S. Cooper, S. Cronier, E. A. Asante, S. Mead, S. Brandner, et al. Kuru prions and sporadic Creutzfeldt-Jakob disease prions have equivalent transmission properties in transgenic and wild-type mice PNAS, March 11, 2008; 105(10): 3885 - 3890. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Brown Transmissible spongiform encephalopathy in the 21st century: Neuroscience for the clinical neurologist Neurology, February 26, 2008; 70(9): 713 - 722. [Full Text] [PDF] |
||||
![]() |
A. Kobayashi, M. Asano, S. Mohri, and T. Kitamoto Cross-sequence Transmission of Sporadic Creutzfeldt-Jakob Disease Creates a New Prion Strain J. Biol. Chem., October 12, 2007; 282(41): 30022 - 30028. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Noguchi-Shinohara, T. Hamaguchi, T. Kitamoto, T. Sato, Y. Nakamura, H. Mizusawa, and M. Yamada Clinical features and diagnosis of dura mater graft-associated Creutzfeldt-Jakob disease Neurology, July 24, 2007; 69(4): 360 - 367. [Abstract] [Full Text] [PDF] |
||||
![]() |
U. Heinemann, A. Krasnianski, B. Meissner, D. Varges, K. Kallenberg, W. J. Schulz-Schaeffer, B. J. Steinhoff, E. M. Grasbon-Frodl, H. A. Kretzschmar, and I. Zerr Creutzfeldt-Jakob disease in Germany: a prospective 12-year surveillance Brain, May 1, 2007; 130(5): 1350 - 1359. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. H. Peden, D. L. Ritchie, H. P. Uddin, A. F. Dean, K. A. F. Schiller, M. W. Head, and J. W. Ironside Abnormal prion protein in the pituitary in sporadic and variant Creutzfeldt-Jakob disease J. Gen. Virol., March 1, 2007; 88(3): 1068 - 1072. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |