United Kingdom epidemics

There are two basic kinds of epidemiological studies, descriptive and analytical. The goal of the first is to describe the occurrence of disease in populations. Analytical studies identify and explain the cause of the disease. For instance, descriptive epidemiology may identify a new disease such as AIDS. Interpretation of descriptive results leads to analytical studies that examine the disease in more detail. Since epidemiology is the study of disease in populations, the proportion of affected individuals in a population is of basic importance. However, the epidemic pattern has varied from country to country. In the United States and the United Kingdom, 65% and 85%, respectively, of AIDS cases have... 

The most serious association of antibiotics with salmonellosis was the 1965 outbreak in England of phage type 29 Salmonella typhimurium, resistant to tetracyclines. Six human deaths were attributed to this epidemic. It was traced to "shotgun" treatment of young calves with antibiotics followed by wide dispersal of the calves ( ). Although this epidemic did not involve the use of livestock feeds containing antibiotics, the seriousness of the outbreak led to an inquiry in the UK and a report by the Swann Committee, 1969, into this use. The report of the committee called for a stop to the use of certain common antibiotics in animal feeds in the United Kingdom. 

Bacteria in water are usually thought of in terms of human disease. Indeed, until quite late in the nineteenth century, disastrous outbreaks of waterborne diseases such as cholera, dysentery, and typhoid fever were common in the major cities of the world. The last outbreak of typhoid in the United Kingdom occurred in Croydon in 1937. Serious cholera epidemics still occur in some parts of the world one that began in Peru in 1991 spread to several countries in the Americas, causing 391,000 cases of illness and 4000 deaths that year. 

As animal fats are a potential feedstock for biodiesel production, Cummins et al. (142) assessed the danger of a human contracting CJD as a result of the use of tallow as a fuel in diesel engines. They concluded that the risk was several orders of magnitude less than the rate of spontaneous appearance of CJD. Thus, scientific analysis indicates that processed (i.e., rendered) animal fat is not an agent of transmission of BSE. Nonetheless, especially in the United Kingdom, the public remains skeptical. This has in some cases led to less use of animal fats in feed applications. Especially in the United Kingdom, the BSE epidemic has reduced the amount of domestically available tallow (because of condemnation) and increased the use of other lipids in place of animal fats. 

The impact of the epidemic was colossal. The overall economic costs in the food and farming sectors of the U.K. economy totaled an estimated 5 billion, roughly 10 billion [9]. This figure compares with an annual gross output of the entire U.K. agricultural sector of 25 billion [10]. The U.K. economy suffered other economic costs associated with the outbreak of FMD. Outside the agricultural sector costs, the United Kingdom endured additional losses to the leisure and tourism sector of the economy. The U.K. Department of Environmental Food and Rural Affairs estimated that the leisure and tourism sector of the economy lost 5-6 billion pounds as a result of the outbreak of FMD in 2001 [11]. 

Human TSEs are rare but include the Creutzfeldt-Jacob disease (CJD), Gertstmann-Straussler-Scheinker (GSS) disease, and famihal fatal insomnia. All three human diseases appear to have both familial and sporadic occurrence, and appear to be different manifestations of pathology of the same prion protein. Kuru is the human disease caused by ritual cannibalism of brain. Similarly, human vCJD appears to have originated in the mad cow BSE epidemic in the United Kingdom. The hypothesis... 

All evidence points to TSEs as a family of related diseases caused by the same homologous prion protein in all species (see reviews by Brown, 2005 Soto, 2006 Watts et al., 2006). Some comfort can be taken that the sporadic occurrences of TSEs are rare in all species and in human populations however, it is equally clear from recent events that a persistent threat of epidemics of TSEs exists. Such epidemics have potentially enormous consequences, such as the economically catastrophic epidemic of mad cow disease in the United Kingdom. Thus far, there is no early diagnosis during the long period of latency, although current research is demonstrating the possible presence of infectious prion protein in tissues at some time before clinical symptoms appear. 

The central issue in the progression of disease is how PrP = propagates itself from the source of exposure (food) to the brain. In the examples provided by kuru, the recent mad cow epidemic in the United Kingdom, and the resultant transmission of vCJD to humans, the common link is that infectious prions in contaminated food reached the brain by some mechanism, and once in the brain, seeded the conversion of native host PrP to an infective PrP conformation. 

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