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Last Updated: Nov 12th, 2006 - 20:38:00 |
June 22 (fodoconsumer.org) - The Netherlands reported a second case of the human variant of mad cow disease after a woman died of the disease in 2005, Rueters cited Dutch health authorities as saying Thursday.
The second person might have died since a diagnosis of the brain wasting disease is only possible after death because to be diagnosed a biopsy of the brain is needed. But here is no reporting that the person has died.
No details about the victim were disclosed for protection of the person's privacy, according to Reuters.
The Dutch authorities say in a statement that the person might have contracted the human variant of mad cow disease by eating tainted meat products.
By definition, the human variant of Creutzfeldt-Jakob disease (vCJD) or the human form of bovine spongiform encephalopathy (BSE) can only be acquired by eating meat from cattle with BSE, the brain waiting disease in bovines.
Another form of human mad cow disease called Creutzfeldt-Jakob disease (CJD) is believed to occur naturally in humans at about one in a million of populations or less.
The US government says some 150 people are diagnosed CJD each year in the US, but the number might be underestimated, according to experts.
vCJD strikes young people and have shorter dormant period while CJD has longer dormant period and affect mostly the elderly.
More than 150 cases of vCJD have been reported with most cases in the UK, and France. In the U.S, two cases have been reported.
There is no cure for the human mad cow disease or vCJD. It can kill the victim in a matter of a few months.
The risk of vCJD might be far more widespread than thought. Experts believe that at least more than 3000 people in the UK have vCJD. It's just that those who have the disease have not had clicnical symptoms yet.
In many cases, the symptoms of vCJD may manifest after a few decades. S urgery tools are known to transmit vCJD because the first person who undergoes brain s urgery may transmit the disease to the next person. Even though the equipment is normally sterilized, the contagious agent can not be destroyed by the normal sterilization process.
Questions and Answers About Mad Cow Disease
What is bovine spongiform encephalopathy?
Bovine spongiform encephalopathy (BSE) is a progressive neurological disorder of cattle that results from infection by an unconventional transmissible agent.
Through the end of April 2005, more than 184,000 cases of BSE had been confirmed in the United Kingdom alone in more than 35,000 herds. Regularly updated numbers of reported BSE cases, by country, are available on the website of the Office International Des Epizooties at: http://www.oie.int/eng/info/en_esb.htm.
The BSE epidemic in the United Kingdom peaked in January 1993 at almost 1,000 new cases per week. The outbreak may have resulted from the feeding of scrapie-containing sheep meat-and-bone meal to cattle. There is strong evidence and general agreement that the outbreak was amplified by feeding rendered bovine meat-and-bone meal to young calves.
The nature of the transmissible agent is unknown. Currently, the most accepted theory is that the agent is a modified form of a normal cell surface component known as prion protein. The pathogenic form of the protein is both less soluble and more resistant to enzyme degradation than the normal form.
Is BSE occurring in the United States?
On June 24, 2005, the U.S. Department of Agriculture (USDA) announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming bovine spongiform encephalopathy (BSE, or "mad cow" disease) in a cow for which conflicting test results had been reported in 2004. No parts of the animal entered the human and animal food supply. As a result of the findings for this BSE-positive animal, the USDA plans to develop a new laboratory testing protocol to evaluate future inconclusive BSE screening test results.
On December 23, 2003, the USDA announced a presumptive diagnosis of BSE in an adult Holstein cow from Washington State. Samples were taken from the cow on December 9 as part of USDA's BSE surveillance program. The BSE diagnosis was made on December 22 and 23 by histopathology and immunohistochemical testing at the National Veterinary Services Laboratory, Ames, Iowa. The diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Preliminary trace-back based on an ear-tag identification number suggests that the BSE-infected cow was imported into the United States from Canada in August 2001.
Is BSE a foodborne hazard in the United States?
Strong evidence indicates that BSE has been transmitted to humans primarily in the United Kingdom, causing a variant form of Creutzfeldt-Jakob disease (vCJD). In the United Kingdom, where over 1 million cattle may have been infected with BSE, a substantial species barrier appears to protect humans from widespread illness. As of June 2005, a total of 177 cases of vCJD had been reported worldwide; of these, 156 had occurred in the United Kingdom. The risk to human health from BSE in the United States is extremely low.
Is there any monitoring of the incidence of Creutzfeldt-Jakob disease in the United States?
Yes. The possibility that BSE can spread to humans has focused increased attention on the desirability of enhancing national surveillance for Creutzfeldt-Jakob disease (CJD) in the United States.
The Centers for Disease Control and Prevention (CDC) monitors the trends and current incidence of CJD in the United States by analyzing death certificate information from U.S. multiple cause-of-death data, compiled by the National Center for Health Statistics, CDC. A summary of these data was published in the Journal of the American Medical Association on November 8, 2000 (Volume 284, No. 18, pp. 2322-3). and in Clinics of Laboratory Medicine in December 2002 (Volume 22, pp. 849-62).
The average annual CJD death rate in the United States has remained relatively stable at about one case per million population per year. In addition, CJD deaths in persons aged <30 years in the united states remain extremely rare<1 case per 100 million per yearWhat is the variant form of CJD that the experts in the United Kingdom believe might be related to the BSE outbreak in cattle?
In contrast to the classic form of CJD, the variant form in the United Kingdom predominantly affects younger persons (median age at death around 29 years) and has atypical clinical features. These atypical features include prominent psychiatric or sensory symptoms at the time of clinical presentation or early in the course of the illness, delayed onset of neurologic abnormalities, duration of illness of at least 6 months, and a diffusely abnormal non-diagnostic electroencephalogram.
The characteristic neuropathologic profile of variant CJD includes, in both the cerebellum and cerebrum, numerous kuru-type amyloid plaques surrounded by vacuoles and prion protein (PrP) accumulation at high concentration indicated by immunohistochemical analysis.
Recently published data indicate that the epidemic of variant CJD in the United Kingdom may have already reached a peak. A listing of monthly updated numbers of variant CJD cases in the United Kingdom is available at: http://www.dh.gov.uk/PolicyAndGuidance/
HealthAndSocialCareTopics/CJD/CJDGeneralInformation/
CJDGeneralArticle/fs/en?CONTENT_ID=4032396&chk=5shT1Z.
Is there evidence directly linking this newly recognized variant of CJD to BSE exposure?
There is strong epidemiologic and laboratory evidence for a causal association between variant CJD and BSE. The absence of confirmed cases of variant CJD in other geographic areas free of BSE supports a causal association.
In addition, the interval between the most likely period for the initial extended exposure of the population to potentially BSE-contaminated food (1984-1986) and onset of initial variant CJD cases (1994-1996) is consistent with known incubation periods for CJD.
An experimental study reported in June 1996 showed that three cynomologus macaque monkeys inoculated with brain tissue obtained from cattle with BSE had clinical and neuropathological features strikingly similar to those of variant CJD (Nature 1996;381:743-4).
A study published in 1996 indicated that a Western blot analysis of infecting prions obtained from 10 variant CJD patients and BSE-infected animals had similar molecular characteristics that were distinct from prions obtained from patients with other types of CJD (Nature 1996;383:685-90).
An experimental study involving inoculation of a panel of inbred mice with the agents causing BSE and variant CJD substantially increased the strength of the scientific evidence for a causal association between variant CJD and BSE (Nature 1997;389:498-501). In this study, groups of inbred mice and a group of cross-bred mice inoculated with brain homogenates from variant CJD cases were reported to have had latency periods and lesion profiles consistent with the BSE pattern.
The latency period, neuropathology, and disease-causing PrP isoforms in transgenic mice expressing bovine PrP that were inoculated with variant CJD, BSE, and scrapie brain extracts provided additional evidence supporting the link between BSE and variant CJD (Proc Natl Acad Sci 1999;96:15137-42).
Has CDC initiated increased surveillance efforts to determine whether the newly recognized variant of CJD occurs in the United States?
Yes. In addition to the ongoing review of national CJD mortality data, CDC has conducted active CJD surveillance in its four established Emerging Infections Program areas (Minnesota, Oregon, Connecticut, and the San Francisco Bay area, California) and in a metropolitan Atlanta site.
Additionally, with the support of the Council of State and Territorial Epidemiologists, CDC conducts follow-up review of clinical and neuropathology records of CJD decedents aged <55 years who are identified through the national mortality data analysisIs BSE a foodborne hazard for travelers to Europe?
The current risk for infection with the BSE agent among travelers to Europe is extremely small, if it exists at all. Information describing this risk is available in the document titled "Risk for Travelers" available on this site.
Date: June 29, 2005
Content source: National Center for Infectious Diseases
© 2004-2005 by foodconsumer.org unless otherwise specified
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