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Council Report |

Risk of Transmission of Bovine Spongiform Encephalopathy to Humans in the United States:  Report of the Council on Scientific Affairs

Litjen Tan, PhD; Michael A. Williams, MD; Mohamed Khaleem Khan, MD, PhD; Hunter C. Champion; Nancy H. Nielsen, MD, PhD; for the Council on Scientific Affairs, American Medical Association
JAMA. 1999;281(24):2330-2339. doi:10.1001/jama.281.24.2330.
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Context The risk of possible transmission of bovine spongiform encephalopathy (BSE) in the United States is a substantial public health concern.

Objective To systematically review the current scientific literature and discuss legislation and regulations that have been implemented to prevent the disease.

Methods Literature review using the MEDLINE, EMBASE, and Lexis/Nexis databases for 1975 through 1997 on the terms bovine spongiform encephalopathy, prion diseases, prions, and Creutzfeldt-Jakob syndrome. The Internet was used to identify regulatory actions and health surveillance.

Data Extraction MEDLINE, EMBASE, and Lexis/Nexis databases were searched from 1975 through 1997 for English-language articles that provided information on assessment of transmission risk.

Results Unique circumstances in the United Kingdom caused the emergence and propagation of BSE in cattle, including widespread use of meat and bonemeal cattle feed derived from scrapie-infected sheep and the adoption of a new type of processing that did not reduce the amount of infectious prions prior to feeding. Many of these circumstances do not exist in the United States. In the United Kingdom, new variant Creutzfeldt-Jakob disease probably resulted from the ingestion of BSE-contaminated processed beef. The United Kingdom and the European Union now have strong regulations in place to stop the spread of BSE. While BSE has not been observed in the United States, the US government has surveillance and response plans in effect.

Conclusions Current risk of transmission of BSE in the United States is minimal because (1) BSE has not been shown to exist in this country; (2) adequate regulations exist to prevent entry of foreign sources of BSE into the United States; (3) adequate regulations exist to prevent undetected cases of BSE from uncontrolled amplification within the US cattle population; and (4) adequate preventive guidelines exist to prevent high-risk bovine materials from contaminating products intended for human consumption.

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Figures

Figure 1. Schematic Representation of Conversion of Normal Prions to Abnormal Prions
Graphic Jump Location
Abnormal prion protein (PrPres) molecules (β-sheet isoform) become physically associated with normal prion protein (PrPsen) molecules (α-helix isoform) and induce a conformational change that converts PrPsen molecules to PrPres isoforms. The rate of conversion is influenced by the quality of the physical association between PrPsen and PrPres molecules. When accumulation of abnormal PrPres molecules is sufficient, clinical disease occurs. Abnormal PrPres molecules may originate from mutated human prion protein genes (inherited or sporadic), sporadic conformational abnormalities, or exogenous sources. If conformational differences between PrPsen and PrPres molecules prevent physical association of the isoforms, no conversion of PrPsen molecules occurs and clinical disease does not develop (lower panel).
Figure 2. Histopathology of Creutzfeldt-Jakob Disease and New Variant Creutzfeldt-Jakob Disease
Graphic Jump Location
Left, Typical spongiosis of the neuropil in the temporal cortex of a patient with Creutzfeldt-Jakob disease (hematoxylin-eosin, original magnification ×400). Photomicrograph courtesy of Carlos A. Pardo, MD, Johns Hopkins University School of Medicine, Baltimore, Md. Right, Cerebral cortex of a patient with new variant Creutzfeldt-Jakob disease containing 3 characteristic florid plaques with a dense core (arrowhead) surrounded by radiating fibrils and a halo of spongiform change (periodic acid–Schiff stain, original magnification ×120). Photomicrograph courtesy of James W. Ironside, National Creutzfeldt-Jakob Disease Surveillance Unit, Edinburgh, Scotland.

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