"Mad Cow" Disease


Adv. Bio-2


Bovine spongiform encephalopathy (BSE) is a relatively new disease found primarily in cattle. This disease of the bovine breed was first seen in the United Kingdom in November 1986 by histopathological examination of affected brains (Kimberlin, 1993) . From the first discovery in 1986 to 1990 this disease developed into a large-scale epidemic in most of the United Kingdom, with very serious economic consequences (Moore, 1996).


BSE primarily occurs in adult cattle of both male and female genders. The most common age at which cows may be affected is between the ages of four and five (Blowey, 1991). Due to the fact that BSE is a neurological disease, it is characterized by many distinct symptoms: changes in mental state \'mad-cow\', abnormalities of posture, movement, and sensation (Hunter, 1993). The duration of the clinical disease varies with each case, but most commonly lasts for several weeks. BSE continues to progress and is usually considered fatal (Blowey, 1991).


Transmission of BSE is rather common throughout the cattle industry. After the incubation period of one to two years, experimental transmission was found possible by the injection of brain homogenates from clinical cases (Swanson, 1990). This only confirmed that BSE is caused by a scrapie-like infectious agent.


To help control the outbreak, the British government in 1988 introduced a ban on the feeding of ruminant protein to other ruminant animals (Lacey, 1995). Such knowledge for the pathogenesis of the BSE disease shows precisely the actions that must be taken in order to control and minimize the risk of infection in healthy cattle around the world (Darnton, 1996).


The appearance of BSE has made a sizable impact throughout much of the world even though few countries, other than the United Kingdom, have experienced positive cases (Burton, 1996). The scare of an outbreak in other countries has led to a great disruption in the trade economy, as well as other factors concerning each of the country\'s general welfare. However, a rapid increase in the understanding of the disease over the last four years leaves few unanswered questions of major importance (Masood, 1996). BSE has been prevented, controlled and eradicated.


BSE is clearly not a disease of genetic origin. It has occurred in the majority of United Kingdom dairy breeds and their crosses, in the proportion expected from their representation in the national herd (Kimberlin, 1993). Analysis of available pedigrees excludes a simple Mendelian pattern of inheritance as the sole cause of the disease. Studies further showed that the occurrence of BSE was not associated with the importation of cattle, the use of semen, or the movement of breeding animals between herds (Hunter, 1993).


By examining the epidemic curve, one can deduce that the disease is characteristic to that of an extended-source epidemic. By a simple process of elimination, the only common factor to be identified was the feeding of proprietary feedstuffs (Darnton, 1996).


These three most common clinical signs are consistent with a diffuse central nervous system disorder (Stadthalle, 1993). Other common signs were loss of body condition (78 percent), live weight loss (73 percent), and a reduced milk yield (70 percent). At some stage in the clinical course, about 79 percent of all cases showed one of the above general signs along with signs in each of the three neurological categories previously listed (Swanson, 1990).


Unfortunately, the slaughter of the great majority of affected animals becomes necessary at an early stage because of unmanageable behavior and injury from repeated falling and uncontrollable behavior (Cowell, 1996). The duration of the clinical disease, from the earliest signs to death or slaughter, can range from under two weeks to as long as a year. The average period is about one to two months (Lyall, 1996).


At times, only one of the above will occur in an infected animal, while more often a combination of the three will occur (Swanson, 1990).


There are two scenarios for the future course of BSE. The first is that BSE, like TME and kuru, is a dead-end disease. If this is true and meat and bone meal was the sole source of the infection, then removing this source would be sufficient for the eventual eradification of BSE from the United Kingdom (Hager, 1996). The alternative scenario is that there are natural routes of transmission of BSE and