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Bovine Spongiform Encephalopathy: Hypothetical Risk of Emergence As a Zoonotic Foodborne Epidemic

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Bovine Spongiform Encephalopathy: Hypothetical Risk of Emergence As a Zoonotic Foodborne Epidemic 1106 Journal of Food Protection, Vol. 59, No. 10, 1996, Pages 1106-1111 Copyright©, International Association of Milk, Food and Environmental Sanitarians Bovine Spongiform Encephalopathy: Hypothetical Risk of Emergence as a Zoonotic Foodborne Epidemic HARLEY w. MOON* Plum Island Animal Disease Center, Agricultural Research Service, U.S. Department of Agriculture, P.O. Box 848, Greenport, New York 11944, USA (MS# 95-505: Received 20 December 1995/Accepted 29 March 1996) ABSTRACT much lower incidence in other countries. Cases outside Great Britain have been attributed to cattle or meat and bone Bovine spongiform encephalopathy (BSE) is a fatal neurologi- meal imported from Great Britain. Imports of British cattle cal disease of cattle, recognized in Great Britain in 1986. Cases in and meat and bone meal into the U.S. are prohibited. The other countries have been attributed to imports from Great Britain. USDA has been conducting active surveillance for BSE The disease has not occurred in the U.S. BSE is one of a group of among U.S. cattle. The disease has not been detected and diseases (other examples are scrapie of sheep and Creutzfeld-Jacob apparently has not occurred in the U.S. (25). disease of humans) referred to as prion diseases or transmissible spongiform encephalopathies. Under some circumstances prion BSE is the most recently emerged disease in a group of diseases can be transmitted by injection or by feeding infected diseases of animals and people that are referred to as (abnormal prion protein-containing) tissue to susceptible hosts. transmissible spongiform encephalopathies (TSE) or more BSE was disseminated by feeding meat and bone meal containing frequently in recent years as prion diseases. Among animals, BSE agent which was not completely inactivated by rendering. these diseases include BSE in cattle, scrapie in sheep and BSE is hypothesized to have emerged from scrapie via recycling of goats, chronic wasting disease in deer and elk, and transmis- rendered by-products in cattle. There is also evidence of spontane- sible mink encephalopathy; the human diseases are kuru, ous feed-borne transmission of BSE to wild ruminants in zoologi- Creutzfeldt Jakob disease, and Gerstmann-Straussler- cal parks and to domestic cats. It has been hypothesized that Scheinker syndrome. Sheep scrapie has been used as a foodborne transmission of BSE to humans has occurred or could model to determine how spongiform encephalopathies are occur, This hypothesis can neither be definitively refuted nor transmitted and to define mechanisms of disease. supported. However, it seems unlikely. In spite of hundreds of years of human exposure to scrapie, there is no evidence of transmission of scrapie to humans. Even if BSE is ultimately found CHARACTERISTICS OF TSE DISEASES to be somehow transmissible to humans, the risk of foodborne transmission appears to be low for several reasons: (i) The oral route is several orders of magnitude less sensitive than the The major characteristics of the prion diseases are, first parenteral route for transmission of prion diseases; (ii) the BSE and foremost, that they are slow diseases. They have an agent is only detectable in brain, spinal cord, and intestine of incubation period of years. The diseases are characterized by infected cattle, tissues infrequently used for human food; and (iii) progressive neurologic degeneration and histologically by a Great Britain (where the disease occurs) destroys and bans the use spongelike degeneration of the brain, which gives the group of all tissues from BSE-infected cattle as well as the brains, spinal one of its names (spongiform encephalopathies). The accu- cords, and intestinal tracts from clinically normal cattle. mulation of an abnormal form of prion protein in the brain is Key words: BSE, foodborne risk, zoonosis, epidemic a characteristic that gives the group another of its names (prion diseases). Although prion diseases can arise in a number of ways, Bovine spongiform encephalopathy (BSE) is a fatal including by genetic mutation and inheritance, they have all neurological disease of cattle (22, 32, 36). BSE has been been shown to be infectious and transmissible (1, 10, 26, recognized in Great Britain since 1986, where it has affected 32). By and large, however, in the ordinary context they are more than 150,000 head of cattle. It has also occurred at a not contagious. Discrete and substantial species barriers exist for transmission across species lines. The agents tend to be more readily transmissible in their original host species than in other species. They tend to adapt to a new (suscep- * Author for correspondence. Current address: Iowa State University, Veterinary Medical Research Institute, 1802 Elwood Drive, Ames, IA tible) species during serial passage in that new species. 50011, USA. Tel: 515-294-9327; Fax: 515-294-1401. However, some species barriers have not been breached in BOVINE SPONGIFORM ENCEPHALOPATHY: FOODBORNE RISK? 1107 NUUBER 100001 9000 8000 7000 6000 ~ooo 4000 3000 2000 1000 o SOw J sow J sow J sow J sow J sow J S 0 ~ J S 0 V. J sow 1986 1987 1988 1989 1990 1991 1992 1993 19941995 DxMONITOR (Spring 1995) USDA-APHIS. Center for Epidemiology and Animal Health FIGURE 1. Number of new cases of BSE in Great Britain, September 1966 to March 1995 (36). Reproduced with permission. spite of experimental serial blind passage of the agent in that Prolonged exposures to moist heat or sodium hypochlorite new species. Susceptible host species are characterized by a are considered to be among the most effective practical striking intraspecies genetic predisposition. Some genetic means of inactivation. However, they cannot be considered lines of sheep are much more susceptible to scrapie than absolutely effective, because the agents have skewed inacti- others. Different genetic lines of laboratory mice are more or vation curves such that treatments which reduce their less susceptible to one or another strain of a TSE agent. infectivity by several orders of magnitude leave some residual infectivity. CHARACTERISTICS OF TSE AGENTS EPIDEMIOLOGY Prion disease agents exhibit strain behavior (1, 10, 26, 32, 34). For example, one strain of scrapie agent may have its greatest pathogenicity in one genetic line of mice, whiie The origin of BSE is not known. There is consensus another strain of scrapie agent has its greatest pathogenicity support for the hypothesis that BSE arose from scrapie, in another genetic line of mice. The incubation periods for which became adapted to cattle by the agent being recycled different strains of agent also vary with genetic line within a in rendered ruminant (sheep and cattle) meat and bone meal, susceptible host species. There is evidence that strain by-products used as cattle feed (5, 6, 22, 23, 30). An behavior and species barriers depend at least in part on the alternative hypothesis is that it arose de novo in cattle. degree of homology in prion genes between the hosts The mechanism of dissemination is much more clear. producing and receiving the agent. BSE has been disseminated in Great Britain and elsewhere There are several extraordinary characteristics of TSE through the feeding of rendered meat and bone meal (22, 30, agents. There is controversy as to their fundamental nature, 32). In 1988, the British authorities concluded that BSE whether they are viruses or whether prions are the ultimate probably was a strain of sheep scrapie that had adapted to infectious disease agent (32). Abundant evidence supports cattle, and a ban on feeding rendered ruminant by-products the infectious prion hypothesis (26, 34). This hypothesis back to cattle was put in place. Recognizing that it was a involves a posttranslational change in the prion protein to an TSE, the authorities predicted that there would be a lag abnormal conformation, which causes accumulation of period of years before the ruminant feed ban would have an additional abnormally conformed prion protein. The abnor- impact. Indeed, following the peak in the number of new mally conformed protein is, according to this hypothesis, the cases in 1992, there has been a falloff, and the epidemic self-replicating, transmissible, infectious agent. appears to be abating (Figure 1) (36). Whatever the nature of the causative agents, what is In addition to cattle, BSE has been transmitted spontane- important in managing them and understanding their epide- ously (in feed) to captive wild bovidae in zoos. Epidemio- miology is their extraordinary resistance to inactivation (9, logic evidence indicates that it has also been transmitted 19, 30). Resistance to inactivation during rendering allowed spontaneously to domestic cats and in zoos to captive wild dissemination of BSE in meat and bone meal and is thought felidae that have been fed either raw BSE-infected brain or to have allowed BSE to emerge (adapt) from scrapie. processed cat food (7, 32, 36). 1108 MOON TRANSMISSIBILITY cause human disease, it would perhaps manifest itself as CJD (3, 4, 22). The occurrence of CJD in 3 British farmers There have been a number of experimental trials, many with occupational exposure to BSE is of concern (28). of them still ongoing, on the transmissibility of BSE (10, 15, However, epidemiologic analysis does not show an in- 20, 21, 24, 27). BSE has been transmitted orally to several creased risk of CJD for any occupation (including farmers) species (mice, sheep, goats, and mink) by feeding raw in Great Britain, and the 1994 incidence of CJD there was BSE-infected brain and spinal cord. It has also been similar to that in other countries where the prevalence of transmitted parenterally to a larger number of species (mice, BSE is much lower or where BSE has not occurred (18, 28). sheep, goats, mink, cattle, pigs, and marmosets). The There is also concern about the possibility of scrapie sensitivity of the parenteral route is characteristically 105 to emerging in cattle in the United States from a U.S.
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