Mad Cow Disease
Mad Cow Disease is the layperson's name for Bovine Spongiform Encephalopathy (BSE), a transmissible, slowly progressive, degenerative, fatal disease affecting the central nervous system of adult cattle.
BSE is a disease that affects cattle. However, there is a disease similar to BSE called variant Creutzfeldt-Jakob Disease (CJD), or vCJD, which is found in humans. There have been a small number of cases of vCJD reported, primarily in the United Kingdom, occurring in people who consumed beef that may have been contaminated. (As of May 2003, there have been a total of approximately 139 cases of vCJD worldwide.) There is strong scientific evidence (epidemiological and laboratory) that the agent that causes BSE in cattle is the agent that causes vCJD in people. The one reported case of vCJD in the United States was from a young women that contracted the disease while residing in the UK. The symptoms appeared years later after the young woman moved to the U.S.
The disease, vCJD, which primarily affects younger persons, is very hard to diagnose until the disease has nearly run its course. In its early stages, the disease may manifest itself through neurologic symptoms, but it is not until the latter stages of the disease that brain abnormalities detectable by x-ray or MRI can be seen.
Milk and milk products are not believed to pose any risk for transmitting BSE to humans. Experiments have shown that milk from BSE-infected cows has not caused infections in the same species or in other test animals
BSE has been of great concern since 1985, when it was first reported among cattle in the United Kingdom. At its peak, in January 1993, almost 1,000 new cases per week were identified. The outbreak in the United Kingdom may have started from the feeding of scrapie-contaminated sheep meat-and-bone meal to cattle. Scrapie is a disease of sheep that is related to BSE in cattle. There is strong evidence that the outbreak in cattle was amplified in the United Kingdom by feeding rendered bovine meat-and-bone meal to young milk producing cttles. The nature of the transmissible agent in BSE is not known. Currently, the most accepted theory is that the agent is a modified form of a normal cell surface component known as a prion protein. Why or how this substance changes to become disease-producing is still unknown. Prions are resistant to common treatments such as heat, to reduce or eliminate its infectivity or presence.
The fatal illness, called variant Creutzfeldt-Jakob disease, occurs when normal proteins found in the brain, known as prions, change shape and prompt healthy prions to do the same. When enough prions have done so, they deposit a plaque on the brain and surround the mark with spongy holes killing the victim.
The disease concentrates in the brain, but has also been found in the tonsils, spleen, lymph nodes, spinal cord, the retina of the eye and the rectum. It has not been detected in blood.
Many different "Transmissible Spongiform Encephalopathies" (TSE) exist in different animals (including people). FDA is working closely with other government agencies and the public health community to address the disease in wild and domesticated herds. Wildlife and public health officials advise people not to harvest, handle, or consume any wild deer or elk that appear to be sick, regardless of the cause, especially in those states where CWD has been detected
Sread of the disease: In cattle , usually herbiverous in nature , to improve milk production in them people used to feed themby mixing the original feed with meat ,meatproducts and bonepowders of sheep and goat etc.
Cattle feed sellers mixing the meat of dead sheep(scapy disease) in cattle feeds leading to contamination.
BSE has a prolonged incubation period in cattle, ranging from three to eight years; for vCJD in humans, the incubation period is unknown, but is at least five years and could extend up to 20 years or longer
Incubation period
It is believed that BSE is spread when cattle eat animal feed that contains the mammalian protein from other infected rendered animals. FDA, with its feed ban, has restricted the use of rendered mammals in ruminant fe
PREVENTION AND THERAPEUTICS
Preventive Measures
Therapy
There is no known effective therapy for treating or preventing
CJD. With one possible exception, there are no well-documented cases of patients with CJD showing recovery either spontaneously or after therapy.Several compounds have been demonstrated to eliminate prions from prion-infected cultured cells. A class of compounds known as "dendrimers" seems particularly efficacious in this regard. Several drugs delay the onset of disease in animals inoculated with prions if the drugs are given around the time of the inoculation. The most common scenarios in which one would want to treat humans are either patients showing signs of disease or presymptomatic patients carrying mutations predisposing them to develop prion disease. No treatment has shown any efficacy in animal models of these two scenarios.
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