Read original article, http://wwwnc.cdc.gov/eid/article/7/1/70-0006_article.htm

Read author's reply, http://wwwnc.cdc.gov/eid/article/7/7/01-0744_article.htm

To the Editor: In regards to "Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease: Background, Evolution, and Current Concerns" (1), use of the name "variant Creutzfeldt-Jacob disease" (vCJD) for human cases of bovine spongiform encephalopathy (BSE) is regrettable. The disease that occurs in humans exposed to BSE is zoonotic and CJD is not; in addition, the human form of BSE has important clinical, pathologic, and epidemiologic differences from CJD. Continued use of this terminology perpetuates the error.

The fact that 12 years after the feed ban bovine cases continue to occur in the United Kingdom at a much higher rate than in any other country could have two possible causes: inefficient controls or additional routes of transmission. Data on alternative routes of transmission must be evaluated, and important gaps in our understanding of BSE in cattle must be addressed.

Extensive epidemiologic data on BSE in the United Kingdom seemed to clearly implicate the practice of feeding cattle bovine offal as the primary, if not the sole, cause of the spread of BSE. Alternative theories for the origin and spread of BSE, e.g., use of insecticides on bovines or the practice of artificial insemination, appear to have been ruled out quickly on the basis of early epidemiologic data. Confidence in the reliability of these data seems to have been so great as to unduly delay transmission experiments to assess the role of alternative pathways (e.g., artificial insemination) in the propagation of BSE. Is prion protein present in semen or is it not? What if it were present in semen? Would this route lead to shorter incubation than the alimentary route? There seems to be no experimental information on the effect of freezing mutated prion protein to -196°C and placing it, after thawing, directly on the stimulated uterine mucosa.

Although the United Kingdom has acknowledged that compliance with the feed ban improved after 1996, we should not be too eager to accept lack of compliance as the only possible reason for the persistence of BSE. Fifteen years after the BSE epidemic began, it cannot be disputed that the ban on offal feed has interrupted spread of the disease. However, if continued spread by the alimentary route can be excluded as the cause of more recent cases, each of these cases should be carefully evaluated to uncover heretofore unknown or underappreciated routes of transmission.

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