Scientists Warn Of Mad
Cow/CJD Spread In Dental
And Surgical Procedures
By Kate Kelland
Note - I have been warning of this for the last couple years. It is impossible to kill prions with all routine, standard dental/medical sterilization procedures. Period. Every invasive dental intrument used on the teeth and gums CAN carry prions into the mouth and bloodstream of the patient. The same is true of scalpals and all invasive, re-usable medical devices which undergo 'sterilization.' It is time scientists begin to speak out on this issue. How many people have already been infected through contaminated re-usable instruments? Remember, CJD/Mad Cow can have a 10 year incubation period. Most never know they are infected as there is no simple CJD test available. -Jeff
LONDON (Reuters) - British government scientists said on Tuesday there was a theoretical risk that variant Creutzfeldt -Jakob Disease (vCJD), the human form of mad cow disease, could be transmitted from person to person via dental instruments.
The Spongiform Encephalopathy Advisory Committee (SEAC), set up by the government to monitor the brain-wasting disease, told a news conference it had asked the Department of Health to urge dentists to be vigilant in their sterilization practices.
"There is a theoretical risk of person to person transmission of the disease (from dentistry),'' said Peter Smith, acting chairman of SEAC.
He stressed ``the need for thorough cleaning and sterilization practices be observed'' and did not think there was any reason at the moment to recommend changes in dental procedures.
But he also warned: ``Sterilization does not completely inactivate the agent that causes the disease'', and called for a full theoretical risk assessment and further analysis of oral tissue from vCJD patients to improve knowledge of the risk.
SEAC said last month that incidence of the deadly human form of BSE in Britain was increasing by a "statistically significant'' 20 to 30 percent a year.
Smith said on Tuesday that latest figures show a total of 77 ``definite'' and ``probable'' cases of the disease had been identified in Britain. Eight of those patients are still alive.
Last month the government launched an urgent inquiry into a cluster of CJD deaths around the small village of Queniborough in Leicestershire.
Three of the four victims died within weeks of each other and all lived within a close radius.
Dr Robert Will, head of the government's CJD surveillance unit, said at the time that baby food and school meals may have been a major source for the Queniborough outbreak.
The Health Department has ordered tests of more than 10,000 tonsils and appendices removed since 1985 to find out how many people in Leicestershire have contracted the disease.
Smith said the investigation, which is unlikely to report its findings until the end of the year, might give scientists more clues about the disease.
But he warned that investigations into cluster groups of other diseases did not always prove that useful.
"But that is not to prejudge what is going to happen with the Leicestershire cluster. The hope is of course that this will tell us something.''
Many scientists believe humans contract the disease by eating meat from cattle infected with bovine spongiform encephalopathy (BSE), or mad cow disease.
Outbreaks of BSE all but crippled Britain's beef industry in the late 1990s and provoked a bitter political row within Europe over whose beef was safe to eat.
European Union scientists said on Tuesday that mad cow disease is probably present in cattle in Germany, Spain and Italy even though these countries say they are free of it.
The EU executive said scientists believed that in these states the risk of mad cow infection in cattle was "likely to be present at levels below the detection limits of their surveillance systems.''
CJD And Mad Cow/BSE Shown To
Be The SAME Infectious Protein
From UC San Francisco
"Researchers are reporting what they say is the most compelling evidence, to date, that the infectious proteins called prions that cause bovine spongiform encephalopathy (BSE), or "mad cow" disease, have infected humans, causing fatal brain degeneration.
Recent studies have suggested that the outbreak of mad cow disease in the late 1980s in Great Britain was responsible for the emergence of a new variant of Creutzfeldt-Jakob disease, a fatal brain-degenerative disease in humans also caused by prions. However, the link has been inconclusive. The current study establishes that the particular strain of prions, responsible for mad cow disease, is, in fact, the same strain that causes new variant Creutzfeldt-Jakob disease.
The finding, reported in the December 20 issue of Proceedings of National Academy of Sciences, is particularly unsettling because it undermines the comforting presumption that a "species barrier" dramatically lessened the likelihood that people exposed to "mad cow" disease through meats, cosmetics, and medicinal supplies would be infected. The species barrier refers to the relative lack of susceptibility of one species to prions derived from another species.
While Great Britain took the necessary measures in the late 1980s to limit spread of the disease, the disease is believed to incubate for at least 10 years, making it impossible to predict, the researchers said, how many people have been infected.
More than 175,000 cattle, primarily dairy cows have died of BSE during the past decade. More than 50 teenagers and young adults have died of new-variant Creutzfeldt-Jakob disease (nvCJD) since 1995. Nine new deaths from CJD were reported in the last quarter of 1998.
While the origins of BSE remain obscure, one possibility is that the cattle developed the disease by being fed meat and bone meal contaminated with prions from the sheep with the disease, scrapie. ...
The researchers conducted their study by first creating a line of transgenic mice genetically engineered to contain genes for the bovine prion protein. (Prion proteins are not, in themselves, lethal. They exist in all mammals and birds that have been examined, including humans, and become destructive only when their shape is altered, a change that occurs either through infection by an already infectious protein or through a genetic mutation.) The line of mice was known as Tg(BOPrP).
The researchers then inoculated the mice with prions from diseased cows. And approximately 250 days after being inoculated, all of the transgenic mice developed the neurologic disease.
Next, another group of mice was inoculated with prions from the diseased mice, and this group became sick after a virtually identical period of time, confirming that the transgenic mice transmit mad cow disease prions with no detectable change of strain or species-specific properties attributable to the mice, themselves.
Finally, and most important, transgenic mice inoculated with prions from human cases of new variant Creutzfeldt-Jakob disease produced the same incubation period and pattern of brain damage as had inoculation with prions from diseased cows.
To test their findings, the researchers inoculated transgenic mice with prions from sheep with scrapie, another prion disease causing neurological damage, and determined that these prions have dramatically different biological properties.
"BSE and new variant CJD produce the identical disease pattern of disease in Tg(BOPrP) mice, and those characteristics were those different than that found with inocula from other CJD cases or scrapie from sheep. These findings argue unequivocally that BSE and new variant CJD are the same strain of prion," said senior author DeArmond.
"The fact that the human new-variant CJD prions so precisely duplicate the properties of native bovine BSE prions in their behavior on transmission to the transgenic mice creates a compelling argument for a persuasive link between BSE and nvCJD," said Michael R. Scott, PhD, UCSF associate adjunct professor in the Institute for Neurodegenerative Diseases and the lead author of the study.
Given the enormity of the affected cattle population in Great Britain, a means of assessing risk to the human population is paramount, and more sensitive methods for detection of prions are urgently needed, the researchers said. The newly developed mouse model, Tg (BoPrP), should provide a sensitive test for detecting BSE prions, they said."
Comment (webmaster): This work was presented at the International Virology Congress in Sydney, Australia in August 1999. The full text of the PNAS article became available mid-morning on Tuesday 21 Dec 99.
This is a solid paper and another nail in England's coffin. It is fairly well described by the UCSF press release. In conjunction with earlier work, this paper shows beyond any reasonable doubt that the nvCJD is the same strain of TSE as BSE. A signficant species barrier between cattle and humans is wishful thinking given this paper and earlier data.
The paper is a watershed in that influential scientists at both the Neuropathology Unit and UCSF, while not throwing caution to the winds, are now convinced that BSE is the causal agent of nvCJD and that little by way of species barrier can be expected. It is no coincidence of timing that ten new nvCJD cases were announced yesterday, the first time ante-mortem cases have been added into the total (62 in 3 countries).
The paper is already being criticized in a whisper campaign as 'alarmist and fear-mongering' -- the idea being floated (by those responsible for the epidemic) is that nothing should be revealed because the public might panic. The top scientists are saying with this paper that they no longer can support a cover-up. The hour is late: it is high time to get out of denial and instead really light a burner under the current half-baked research effort. There will not be money for research when the government can say 'Oh, it is only 62 victims so we mustn't alarm beef importing nations unduly.'
The bovine prion gene was inserted in knockout mice that were then challenged by US Suffolk scrapie, BSE, and nvCJD. The final genomic sequence is not described in the paper despite all the problems with doppel in different knockout backgrounds -- the reader is sent off on a wild goose chase in mouse strain nomenclature in older papers. The scrapie genotypes are not provided either, other than Q at 171. Was either really determined?
While it is all well and good to test nvCJD and scrapie in these mice, this is testing the species barrier from human to cow, not really the issue except possibly for animals grazing in cemetaries. Species barriers are not necessarily symmetric, as the UCSF lab well knows from studies of mouse-to-hamster compared to hamster-to-mouse.
To test cow-to-human, a met 129 human prion in transgenic mice is needed. No one will do this, though we have val 129 (these became ill from cow, suggesting valine will prove no protection at codon 129) and chimeric met 129 mouse-human data.