Mad Cow Update - Enough
To Make One Mad
New Case Of Mad Cow Found In Poland

From Patricia Doyle, PhD

Hello, Jeff - There were 18 animals on the farm. Eight had been exposed to the risk of mad cow and were culled. Hmm...What about the other 10? They remain on the farm? The other articles below will also provoke some anger and amazement.
New Case Of Mad Cow Disease In Poland
WARSAW (AFX) - A new case of bovine spongiform encephalopathy (BSE), or mad cow disease, has been detected in Poland, the country's veterinary service said.
The head of the national veterinary service, Krzysztof Jazdzewski, said that the infected animal was found on a farm in the northwest of the country and had been put down.
'The disease was detected on a farm with a total of 18 animals. Eight of them have been identified as exposed to risk (of contamination) and have been killed,' he said.
There have been more than 22 cases of mad cow disease in Poland since it began testing for BSE in 2001.
Japan Lab May Have Succeeded In Inducing Mad Cow Infection l
Japanese scientists believe they may have successfully infected cattle with mad cow disease as part of an experiment aimed at an early detection for the fatal bovine illness, a laboratory official said Thursday.
The Hokkaido Animal Research Center in northern Japan injected prions from infected cows into the brains of 14 Holstein calves in 2004 -- six in February, three in July and five in September -- and some in the first group have developed what seems to be early symptoms of the mad cow disease, said Tsutomu Ogi, director of the institute's livestock engineering section. Prions are proteins thought to cause the disease.
Several of the calves became groggy when walking -- changes considered typical early symptoms of bovine spongeform encephalopathy, or BSE, Ogi said.
"They've become jerky when they walk and we noticed the change since last month," he said. "But we're not absolutely certain yet and we want to make sure before making a conclusion."
Ogi said the six Holsteins, all still alive, have been sent to the National Institute of Animal Health near Tokyo, where they will be dissected and analyzed in detailed tests later this month to confirm the infection.
If confirmed, they will be the first successful cases of artificially induced mad cow disease in Japan, Ogi said. British scientists have succeeded in similar experiments.
Researchers hope the findings will eventually lead to developing a method of early detection while the animal is alive and further study of how the affected prions spread inside the animal. All 21 past cases of mad cow in Japan were detected only after the cattle were killed for blanket testing before shipment for sale.
Ogi said regular sampling of urine and blood of the controlled cows could also show how prions spread in an infected cow before they develop a full-blown case and help scientists to find a possible marker to detect early signs of infection.
Injecting mashed-up brain parts taken from sickened cows is the fastest way to induce BSE in a healthy cow and is believed to take about two years, he said.
Eating beef from cattle infected with mad cow disease can cause the fatal brain disorder Creutzfeldt-Jakob disease in humans.
Japan has reported 21 cases of mad cow disease since 2001, and one human victim who died of Creutzfeldt-Jakob disease in December 2004. (AP)
US Safeguards Against Mad Cow Disease Said Inadequate
Strict Regulations On Cattle Feed Are Needed, Critics Say
By Libby Quaid
Associated Press
WASHINGTON -- Researchers and the nation's number one burger seller say the government is not fully protecting animals or people from mad cow disease.
Stronger steps are needed to keep infection from entering the food chain for cattle, the critics wrote in comments to the Food and Drug Administration.
The group includes McDonald's Corp., seven scientists and specialists, and a pharmaceutical supplier, Serologicals Corp.
The government proposed new safeguards two months ago, but researchers said that effort ''falls woefully short" and could fail to keep cattle from eating infected feed, the primary way mad cow disease is spread.
''We do not feel that we can overstate the dangers . . . from these diseases and the need to control and arrest them to prevent any possibility of spread," the researchers wrote.
McDonald's said the risk of exposure to the disease should be reduced to zero, or as close as possible. ''It is our opinion that the government can take further action to reduce this risk," wrote Dick Crawford, company vice president.
In people, eating meat or cattle products contaminated with mad cow disease is linked to a rare but fatal nerve disorder, variant Creutzfeldt-Jakob disease.
No one is known to have contracted the disease in the United States. The disease has turned up in two people who lived in the United States, but it's believed that they were infected in the United Kingdom during an outbreak there in the 1980s and 1990s.
The United States has found two cases of mad cow disease in cows. Since the first case, confirmed in December 2003 in a Canadian-born cow in Washington state, the government has tested more than half a million of the nation's 95 million cows. The second case was confirmed in June in a Texas-born cow.
''While this surveillance has not uncovered an epidemic, it does not clear the US cattle herd from infection," the researchers said.
The primary firewall against mad cow disease is a ban on using cattle remains in cattle feed, which the United States put in place in 1997. The feed ban, however, has loopholes that create potential pathways for mad cow disease. For example, restaurant plate waste is allowed in cattle feed.
The Food and Drug Administration proposed in October to tighten the rules, but critics said glaring loopholes would remain.
The FDA, which regulates animal feed, accepted public comments on the proposal through last month. An agency spokeswoman said yesterday that it would be inappropriate to respond to those comments.
The critics said their biggest concern is that tissue from dead animals would be allowed in the feed chain if brains and spinal cords have been removed. Brains and spinal cords are tissues that can carry mad cow disease, but in dead cattle that had the disease, the infection had spread beyond the brains and spinal cords.
Leaving tissue from dead cattle in the feed chain would negate the FDA's attempt to strengthen its safeguards, the critics said.
© Copyright 2006 Globe Newspaper Company.
History Of Human Cannibalism Eats Away At Researchers
New Study Challenges Previous Reports Of Cannibalism As A Worldwide Selective Force
Cold Spring Harbor Laboratory
New study challenges previous reports of cannibalism as a worldwide selective force
In a new study published by the journal Genome Research, a team of scientists reports that 'mad cow'-like diseases have not been a major force in human history, nor have been cannibalistic rituals that are known to be associated with disease transmission. Prof. Jaume Bertranpetit, a scientist at the Universitat Pompeu Fabra, and his colleagues used a fresh set of genetic data to show that balancing selection associated with cannibalism has not been a major selective driving force on the prion protein gene, as has recently been proposed. Their work also has important scientific implications for researchers using a specific class of DNA markers called SNPs (single nucleotide polymorphisms) to examine genetic associations with diseases or to evaluate historical patterns of human migration.
The prion protein gene (PRNP) encodes a protein that can abnormally fold and amass in brain tissues to cause fatal neurodegenerative diseases such as mad cow disease. These diseases are cumulatively known as transmissible spongiform encephalopathies (TSEs) and in humans, include CJD (Creutzfeldt-Jakob disease) and kuru. Kuru is confined to a human population in Papua-New Guinea and is transmitted by cannibalism at ritualistic mortuary feasts.
A high-profile study published nearly three years ago suggested that individuals who were heterozygous for a common polymorphism in the PRNP gene were relatively resistant to the disease. Over time, homozygotes who participated in the cannibalistic rituals purportedly diminished in numbers due to their increased susceptibility to kuru. This indicated that cannibalism conferred an effect of balancing selection on the PRNP gene throughout human history.
Bertranpetit and his colleagues sequenced 2,378 base pairs of the PRNP gene in 174 individuals; in addition, they genotyped two SNPs (or single nucleotide polymorphisms) from the PRNP gene in 1000 individuals from populations worldwide. They identified 28 different haplotypes or combinations of DNA variants in the PRNP gene and used this data to assess the ages of the mutations, to identify geographic patterns of variation, and to evaluate selective forces that have potentially influenced these patterns.
"In contrast to the previous study, which concluded that variation in the PRNP gene was strongly skewed toward intermediate frequency variants, our results showed that there was, in fact, a deficit of intermediate frequency variants," says Bertranpetit. "Our results are consistent with a complex history of episodic or fluctuating selection, including positive selection, purifying selection, and possibly even short periods of balancing selection."
On a more technical note, the study cautions researchers involved in SNP-based population genetics studies. The work is one of the first to empirically demonstrate how SNP ascertainment can introduce a strong bias in population genetics studies and severely affect the conclusions. Bertranpetit and his colleagues point out that at a time when a flood of ascertained SNP data is being generated, it is essential that SNP ascertainment be taken into consideration in data analyses.
The first author on the study is Dr. Marta Soldevila, who completed her Ph.D. at the Universitat Pompeu Fabra and performed a substantial part of the sequencing work at DeCODE Genetics (Reykjavik, Iceland).

Patricia A. Doyle, DVM, PhD- Bus Admin, Tropical Agricultural Economics
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