Cruitsfield Jakobs? (sp?) Mad Cow

Discussion in 'Fibromyalgia Main Forum' started by JaciBart, Oct 19, 2002.

  1. JaciBart

    JaciBart Member

    Anyone out there with Cruksfield Jacobs or knowledge of it and connection?

    Just up to my usual research (if you want to call it that).


    Jaci

    [This Message was Edited on 10/19/2002]
  2. JaciBart

    JaciBart Member

    Anyone out there with Cruksfield Jacobs or knowledge of it and connection?

    Just up to my usual research (if you want to call it that).


    Jaci

    [This Message was Edited on 10/19/2002]
  3. dlizard

    dlizard New Member

    I read just the other day that there is a case in florida involving a woman from britian. But watch out now cause its here!!!! I have no personal ezxperience but I can tell you that I've seen some cows with funny looking eyes LOL>(( JOKE)) LOL>>>> Good luck.... this could be a bad bad thing for us......
  4. JaciBart

    JaciBart Member

    I have seen in the paper where it is now in deer & elk, I think it is also called "chronic wasting disease"


    Jaci
  5. sickandtired

    sickandtired New Member

    The disease is now known formally as "bovine spongiform encephalopathy" or BSE for short. BSE is one of a small family of diseases called transmissible spongiform encephalopathies, or TSEs. TSEs destroy neurons, the main nerve cells in the brain, creating holes that leave the brain resembling a sponge (thus "spongiform"). BSE, like the other TSEs, is an infectious disease, meaning that it can be transmitted from one cow to another.

    In 1985, cows in Britain began to die of a mysterious ailment that no one had ever seen before. The symptoms were strange. At first the cows staggered and drooled, their ears twitching. Then they began to show signs of fear, grinding their teeth, acting aggressively toward other animals. Soon they died. Farmers named the condition "mad cow disease" and the name stuck.

    During the 13 years since it first appeared, mad cow disease has killed more than 167,000 cows in Britain[1] and many more became infected but were slaughtered for food before symptoms appeared. Symptoms take an average of 5 years to show up after a cow is infected. Until the late 1990s, there was no test that could detect whether a cow was infected -- only the appearance of symptoms and microscopic examination of the brain could provide a definitive diagnosis. (Even today, tests require brain tissue, so they cannot be conducted on live animals.) British-type BSE has now been observed in cows in Switzerland, the Netherlands, Ireland, Portugal, France, Oman and the Falkland Islands. To date, the disease has not been observed in cows in the U.S.

    When the disease first struck in Britain in 1985, health authorities insisted that British beef was safe to eat. For 10 years they defended that position aggressively, despite mounting evidence to the contrary. Then in 1996, the official story changed suddenly and the public was stunned. A panel of government scientists told Parliament in 1996 that the "most likely explanation" for 10 cases of a new TSE disease in humans was that BSE had moved from cows into people. That explanation is now widely accepted by most scientists, though airtight evidence remains elusive.

    By the time of the stunning announcement in 1996, some British experts calculated that more than a million infected cows had already been consumed in Britain.[2]

    In humans, the BSE-like disease is called "new variant Creutzfeld-Jacob disease," or nvCJD for short. Creutzfeld-Jacob disease (CJD) is a member of the TSE family, a brain-destroyer. CJD has been recognized for a long time as a rare disease of the elderly - very similar to Alzheimer's disease - but nvCJD is different. It has somewhat different symptoms, a different pattern of disintegration in the brain, and it strikes young people, even teenagers. Between 1995 and early 1998, at least 23 people died of nvCJD in Britain and at least one in France,[3] the oldest of them age 42 and the youngest 15.

    In January 1997, British epidemiologists tried to estimate how large the outbreak of nvCJD might become. They concluded that the data were not sufficient to allow a precise estimate: somewhere between 75 people and 80,000 people would eventually die of the new disease, they estimated.[4] Only time will tell. More precise estimates of the size of the problem are not possible because no one knows for sure how long nvCJD "incubates," how much time elapses between infection and the appearance of symptoms.




    New Variant CJD (nvCJD)
    Discovery

    New variant Creutzfeldt-Jakob Disease (nvCJD) was first documented in March of 1996 after 10 Britons under the age of 45 displayed symptoms similar to those associated with a TSE. CJD was initially suspected as the specific disease, but further scientific analysis showed symptomatic and pathological differences of affected brain tissues compared with CJD victims. It was certain, however, that the 10 victims suffered from a strain of a Transmissible Spongiform Encephalopathy, and researchers termed this condition new variant CJD (nvCJD).
    Incidence

    The number of definite and probable new variant CJD cases is 138 people (128 in the U.K., six in France, one in Ireland, one in Italy, one in the United States, and one in Canada. Scientists have concluded that the patients in the United States and Canada contracted nvCJD in the U.K.).*22 To date, the disease has occurred almost exclusively in people under the age of 55, a number of whom were teenagers.

    Scientists do not believe it is possible to predict the number of anticipated nvCJD cases with any accuracy given the unknowns about the disease, including method and amount of exposure, route of transmission and incubation period. Steps taken to remove the disease agent should help minimize potential future exposure to the agent and thereby limit the occurrence of nvCJD cases.
    Transmission

    Recent research from the U.K. supports an association between BSE and nvCJD, in that nvCJD likely developed as a result of people consuming products contaminated with central nervous system tissue of BSE-infected cattle. Documented studies report that the BSE agent, to date, only has been found in brain, spinal cord and retina (eye) tissue of naturally infected cattle. **

    Additional research indicates that all nvCJD patients tested to-date have been homozygous for the amino acid methionine at codon 129, which is one of the amino acids on the gene that comprises PrP. Research continues to see if this commonality would indicate a genetic predisposition to infection by the BSE agent. 15-19
    Symptoms

    New variant CJD differs markedly from CJD. Symptoms of nvCJD last up to 14 months, compared with 4 months for CJD patients. Patients afflicted with nvCJD experienced early psychiatric symptoms such as depression, earlier loss of coordination and later onset of dementia. In addition, nvCJD has, to date, occurred almost exclusively in people under the age of 55, a number of whom were teenagers, whereas CJD typically strikes people over 55. 2, 8, 15, 18
    Diagnosis

    Diagnostic procedures for nvCJD are similar to those of CJD, keeping in mind that patients with nvCJD lack periodic sharp-wave complexes typically found on EEG results of CJD patients. Perhaps the most striking and consistent neuropathological difference between CJD and nvCJD is found in the amyloid plaques. Plaques in nvCJD cases are extensively distributed throughout the cerebrum and cerebellum, compared with the absence of plaques in CJD cases. Plaques in nvCJD victims also typically have a dense center and are surrounded by a zone of spongiform change which give the plaques a daisy-like floral pattern. This pattern is not found in CJD patients. 4, 6, 7, 9, 15, 20

    Recently, researchers developed a new test that may allow for an earlier diagnosis of nvCJD. Patients with nvCJD, but not CJD, appear to have detectable disease associated prion protein in their tonsils. By removing a small piece of tonsil tissue and analyzing it for the protein, researchers may now be able to provide a definite diagnosis of nvCJD at an earlier stage. No indigenous cases of nvCJD have been discovered in the U.S. A probable nvCJD case was reported in Spring 2002 in a British woman residing in Florida.

    * As of October 4, 2002

    ** Evaluation of experimentally inoculated cattle has found BSE infectivity in additional nervous and other tissues, specifically the dorsal root ganglia (nervous tissues connected to the spinal cord) and trigeminal ganglia (nervous tissue connected to the brain), as well as distal ileum (tissues in the intestines) and bone marrow. This research involved a series of experiments in which calves were either intracranially injected with or fed relatively large amounts of heavily infected brain from clinical BSE cases. Examination of the animals fed BSE-infected brain showed infectivity in the distal ileum six to eight months after exposure and in other central nervous tissues 30 months or more after exposures. Reports on the research state that muscle meat and other tissues were tested for infectivity at every stage of these experiments, and no infectivity was found.
    Differing Characteristics of Sporadic CJD and nvCJD


    CJD
    _____________________________________
    Discovery

    * Identified by German psychiatrists Hans Gerhard Creutzfeldt and Alphons Maria Jakob in the 1920s

    Incidence

    * Affects approximately one person per million worldwide each year, representing an average over time that increases with age
    * Usually strikes people over the age of 55 (median age of death is 68 in the U.S.11)

    Transmission

    * Sporadic form is of an unknown origin and accounts for about 85% of all CJD cases

    Symptoms

    * Includes poor concentration, lethargy and unsteadiness followed by agitation, dementia and chronic muscle spasms
    * Duration of the typical form of illness averages four months

    Diagnosis

    * Sharp-wave complexes present in EEG results
    * Neuropathological features include spongiform change, neuronal loss, and astrocytosis.


    nvCJD
    _____________________________________
    Discovery

    * First documented in March 1996 in Great Britain

    Incidence

    * There are 138 definite and probable cases (128 in the U.K., six in France, one in Ireland, one in Italy, one in the United States, and one in Canada. Scientists have concluded that the patients in the United States and Canada contracted nvCJD in the U.K) as of October 4, 2002 22
    * Disease has stricken almost exclusively people under the age of 55, a number of whom were teenagers
    * There have been no indigenous cases reported in the United States. A probable nvCJD case was reported in Spring 2002 in a British woman residing in Florida.

    Transmission

    * Research from the U.K. supports an association between BSE and nvCJD in that nvCJD likely developed as a result of people consuming products contaminated with nervous system tissue from BSE-infected cattle

    Symptoms

    * Patients experience early psychiatric symptoms, earlier loss of coordination and later onset of dementia
    * Duration of illness averages about 14 months

    Diagnosis

    * Lack sharp-wave complexes in EEG results
    * Amyloid plaques are extensively distributed throughout the cerebrum and cerebellum
    * Plaques typically have a dense center surrounded by spongiform change that give the plaque a daisy-like floral pattern

    Last Updated - October 2002[This Message was Edited on 10/20/2002]
  6. sean

    sean New Member

    The human form of bovine spongiform encephalopathy, claimed the lives of 2 people a few years ago, from the village next to mine, and a further person who visited the village on a regular basis. Much has already been covered here by a previous post, so I won't go on. Just to say that the early symptoms of the disease, are as follows: depressive type symptoms, lack of coordination, and unspecified pains. These go on to develop into more serious symptoms, eventually resulting in fatality. It was feared that the disease would go on to infect 1 in every 10 people in the U.K, as yet there is no evidence that this will be the case. BSE is suspected to have been caused by feeding cattle the remains of other dead animals, believe it of not. Cows as you will no doubt know are herbivores, and not carnivores, so why feed them dead meat? Don't mess with nature unless you are propared for the consequences, that's all I can say.
  7. karen2002

    karen2002 New Member

    Sean--it's all a matter of Bucks, money is at the root. Cattle in feedlots are fed high protein feeds to get them to the feedlot quicker, and with a higher weight gain. Feeds are made higher in protein by the addition of animal by-products, and urea. Although feeding bovine to bovine (cow to cow) is not allowed here in the US, other animal species may be feed to cattle. Cross species contamination has been observed in the lab. I don't know about anyone else, but I would prefer the steak I am ingesting, not to have been feed neurological tissues from sheep, pigs, and horses, either. Nor do I want them to consume, excretement, as well. There is a wonderful book, written by an ex-cattle rancher, ex-meat eater, who is very much intune with the Cattle Growers Associations, and Beef Industry greed, instead of concern, as he was part of the problem, for years. It covers so many of the questionable practices in the meat industry, and is an inexpensive book.....You will be horrified after reading it. It is titled "Mad Cowboy", by Howard F. Lyman. It is filled with scientific data, on Mad Cow Disease.
    This is the guy who created quite a stir on the Oprah Show, when he revealed the deadly impact of the livestock industry on our well-being. It will really make you question your decision to eat commercially raise beef, chicken, turkey, etc.
    Karen
    [This Message was Edited on 10/20/2002]