.
Incidence is much higher in dairy herds, probably because cows are fed more
protein and remain on feed a longer period of time. There is no evidence to
date of genetic susceptibility (breed differences). BSE is so named because brain tissue sections of infected cattle appear spongy and infiltrated with amyloid (starch like) plaques when examined under a microscope
Cattle affected by BSE experience a progressive degeneration of the nervous
system.
Affected animals may display:
BSE elicits no immune or inflammatory reaction. BSE is an afebrile (without a fever) neurological disease affecting primarily mature cattle.
Clinical signs include:
The common name, "Mad Cow Disease", is related to abnormal motor nerve control coupled with aggressiveness. Most cases have been reported in the Holstein-Fresian breed, although all cattle are susceptible to the disease. Onset of clinical symptoms has been observed in cattle as young as 1 year 10 months, and may be precipitated by stress, estrous or calving. The disease course varies from less than 2 weeks to 14 months usually resulting in death or humane destruction within 4 months. Clinical signs worsen with time. Confirmation of disease is only possible following post-mortem examination of brain tissue.
Epidemiological evidence indicates that the primary cause of BSE in British cattle was probably the use of commercial cattle feed concentrates which contained meat and bone meal derived from sheep (and possibly cattle) presumed to have been infected with scrapie. Current data are consistent with 90% of cases occurring from infected feed. The feeding of animal protein specifically derived from ruminants ceased in the Britain in July 1988.
BSE was first observed in Great Britain in April, 1985, and was specifically diagnosed in 1986. By June, 1990, there were some 14,000 confirmed cases out of an estimated population of 10 million cattle in Great Britain. Since 1986, almost 200,000 cases of BSE in cattle have been identified in Britain. The epidemic peaked in 1992-93 at almost 1,000 cases per week. Currently, less than 100 cases are occurring per week. In the United Kingdom, 54% of the dairy herds and 15% of the beef herds have had at least one case of BSE.
When BSE was first observed in 1985, 200-300 infections had probably occurred
already. Based on British epidemiology, age at infection is 1.3 ± 1.8
years and the mean incubation period (time between infection and clinical symptoms)
is 5 years. The United Kingdom Spongiform Encephalopathy Advisory Committee
(July 20, 1996) stated that cows can transmit BSE to their calves, but the rate
of transmission is so low that it is not expected to perpetuate the disease.
In a preliminary study, the rate of maternal transmission was approximately
10%, however the committee estimated that under UK field conditions the maternal
transmission rate would be approximately 1%. A statistically significant correlation
existed between BSE infected dams and BSE occurrence in calves, however, no
causal relationship was established .
Incidence is much higher in dairy herds, probably because cows are fed more
protein and remain on feed a longer period of time. There is no evidence to
date of genetic susceptibility (breed differences).
Experienced cattle practitioners claim to have seen BSE cases prior to the epidemic; these were (and in many countries, still are) often categorized as unresponsive "downer cows" or cows with "staggers". This led to the theory that BSE existed in the British cattle herd at some low level prior to the epidemic. The alterations in rendering practices (primarily loss of solvent extraction) may have led to recycling (and concentrating) of BSE infective agent through the cattle population via ruminant to ruminant feeding of offal until the titre was sufficient to result in an outbreak of sufficient magnitude that it was readily identified (Wood, 1996).
As of 2001, the disease has been reported in domestic cattle of several European countries including: