virtualeyes2001
  HOME BOOKSTORE SUPPORT CONTACT US  
Rocky Mtn. Compost News
The New Spiritual Wonders
Onyx for President
FirstStart, L.L.C.

External Links
Science &Technology

About Virtualpath.com
21st Century
SCIENCE & TECHNOLOGY

- Feature Story -

 

The WorldWide Threat: TSE Disease

January 19, 2001
January 23, 2001
January 31, 2001
March 5, 2001

What is "Mad Cow" Disease?

BSE (Bovine Spongiform Encephalopathy - mad cow disease) is a specific term which refers to the bovine form of a mind-wasting prion disease, or a generic term for prion-induced disease passed between sheep, cattle, humans and other mammals, now more appropriately referred to as TSE (Transmissible Spongiform Encephalopathy). Some of TSE's threat was identified by the year 1988, at which time the United States began measures to keep infected cattle from being brought into the country, specifically from the U.K. and other isolated parts of Europe. TSE incubation in humans results in the symptomatic Creutzfeldt-Jakob Disease (CJD; pronounced Kruts-felt Yok-ob Disease) of the same TSE prion, with a 100% fatality rate. Once symptomatic, all TSE manifestations in all animals are fatal following extended and horrid effects of neural degeneration.

As of January 2001, the epidemic of the prion's spread through Europe is being realized as Germany, and Belgium, formerly free of BSE, have been cut off from beef exportation to most of the European Union since November, 2000, joining 30 other countries with known BSE infection. It was not realized early on that scrapie or mad sheep disease, afflicting sheep even during the 18th century, and in many parts of the world including North America, is also a TSE disease, nor did anyone imagine the extent that this disease would spread throughout the world during the late 20th century, nor its implications for our world as it spreads.

In North America, mad sheep disease (scrapie), mad deer disease (wasting disease) and mad elk disease have been endemic throughout regions of Canada, the U.S. states of Wyoming, Colorado and Montana, and sheep production facilities in the eastern U.S. During January, 2001, it was announced that the first deer death from wasting disease had been discovered in the U.S. beef producing heartland of Nebraska, USA.


All these diseases are variant manifestations of the same TSE prion. TSE prions attack nervous tissue, eventually causing death by brain damage as neuronal brain cytoplasm transforms into spongy, diseased tissue full of fluid-filled holes, like swiss cheese. TSE has killed 80 people in Europe to date, while 15+ million cattle have been slaughtered and burned in attempts to prevent its spread. (See Updates at the bottom of this page.)

As of New Year's, 2001, the United States, Australia and Argentina, of the major beef producing countries, have not reported BSE within their cattle industry nor CJD in humans *(See update, Jan 23). Unfortunately, that does not guarantee that TSE is excluded from these countries.

 
Where did it come from?
(Contempt for Nature)

Cattle were designed by Nature to convert nearly pure cellulose into sugars, amino acids and proteins to support the production of muscle and fat, bone, milk, and baby cattle, of course, who would carry on the original design specifications for each model into new generations.

Cattle are true herbivores. These "primary grazers" are plant-matter cellulose conversion machines at the lower end of a planetary food chain which includes predators, like humans, "higher" on the chain. Humans are not capable of ingesting clumps of grass or other pure plant cellulose into nutrients to sustain life. True herbivores include rabbits, sheep, deer, elk, cattle, horses, and other primary grazers.

During the 1950s, dairy farmers began to pump massive amounts of proteins into cattle feed. Cattle, that can mow grass effectively without killing it, aren't as ruthlessly efficient as sheep that rip grass and roots from soil and metabolize the whole plant. The 20th Century solution was to put sheep on leased grazing land until the land had been denuded of edible vegetation, then slaughter the sheep, grind them into high-protein feed and shovel it into cattle to make cattle bodies to do things that Nature had not intended.

A conservative dairy farm allows cattle to graze, with dairy cows returning (happily) during early mornings and late afternoons to be milked. Under these conditions, dairy cows produce milk for about ten years.


Many of today's large, commercial, high-production dairy operations do not allow dairy cows to walk around or graze. Dairy cattle remain penned during their productive life, which is as short as two years. They are crammed full of protein-enriched feed and milked four times each day. After two years, the animals simply burn-out and are discarded for harvesting as meat.

Bovine gastrointestinal systems use symbiotic bacterial digesters to break down cellulose into sugars that can produce energy and tissues for growth. The breakdown is a slow process, requiring all the stomachs cattle have to do this gradual but effective conversion properly. Cattle do not have the same acids and enzymes that exist within predator intestines to process food. Consequently, a bovine gut cannot effectively render animal proteins into constituent building blocks for absorption and reuse like a carnivore gut can, since cattle were not engineered for that sort of lifestyle.

Ground sheep contains ground-up sheep cell structure which includes sheep DNA. The DNA, inside a bovine gastrointestinal system, ineffectually decays into billions of variously-sized protein fragments. In at least one out of a million humans, sheep and cattle, a naturally-occurring genetic defect produces "beta sheet" folding structures with production of infectious, deadly protein fragments. At least one of those fragments has now found a new environmental niche in which to propagate itself as a significant, new type of organic entity on our planet, called a TSE prion, which propagated through the 20th Century farming practice of feeding animals the tissues of other animals. The infectious prion's nearly insignificant appearance in past history is now a major source of concern and alarm in Europe and the world.

Mammalian DNA contains specific protein groups coded as "prion," as part of the normal DNA sequence. Forty two prion sites along human DNA have been postulated as potential sites for spontaneous mutation of normal prion between bonding sites in DNA structure. One of these, human PrP(C)117, has been the subject of most tests and speculation regarding lethal CJD in humans. In the presence of infectious proteins under low pH conditions (~4.5 or lower within the cell solutions surrounding the prion area), PrP(C)117 can mutate to PrP(Sc) - a small but deadly substitution of hydrogen-bonded lysene to glutamate. Once the substitution occurs, a helix'es prion site whips into unstable coils and loops which can apparently break and rebond repeatedly, popping off more copies of the infectious prion. The mutation is not compatible with continued integrity of affected tissue. Cell membranes, the membrane itself being coded by the altered DNA site, cannot be maintained by the faulty genetic program. Affected tissue turns to fluids, without membranes to differentiate cell tissue boundaries. "Prion," in relation to TSE, means infectious, altered prion PrP(Sc). It is believed that TSE prion was created by feeding high-protein food to cattle that contained sheep DNA. Sheep protein fragments provided the necessary source of proteins for replication of the infectious, mutated prion from within small populations of normally-benign but mutated, bovine cells. The World Health Organization now reports that studies of feed shipment records show that ground-sheep feed has been distributed worldwide since the 1950s. This high-protein feed not only contained the constituent proteins to encourage random, mutated cells to begin pumping out infectious prions instead of just disappearing within a healthy body, it also carried infectious prion from diseased sheep. If this mechanism of mad cow disease spread is correctly understood, the current world BSE crisis was inevitable as cattle were fed with sheep protein. This feed was shipped worldwide until only a few months ago.


 
Now what?
(What can we do?)

BSE has spread to over thirty countries, effectively destroying dairy production of each country as many millions of cattle have been slaughtered and burned in attempts to control the spread of BSE. Britain, Ireland and France are among these countries. Germany joined them in November, 2000. Italy discovered positive BSE cases in January, 2001. The US and most other "BSE-free" countries ban beef product imports from much of Europe including all of the 30+ countries with known BSE, however the disease appears to be unstoppable and mad sheep, mad deer and mad elk are evidence that the prion is firmly entrenched in the United States and Canada, even though the public has not been notified of any incidence of BSE in domestic herds of cattle.

In the U.K. and Germany, known government cover-ups of BSE allowed BSE infected foods to reach the food shelves in other countries. This is causing massive political turmoil as politicians are sued and expelled from office over their cover-ups and inaction. But after tracking as many details of the BSE issue as possible for the past two years, it now seems unlikely that much of the human population has not been exposed to at least some prion infection.

This tiny monster has a tremendous incubation period, possibly up to ten and even fifty years, making sources of the infection difficult to identify. Also, it's possible that the prion is spreading through many sources of food in human populations that have not identified vCJD yet.

In one of the early lab tests of the prion, viable prion was discovered by one scientist in his flower planter outside a laboratory window. After autoclaving surgical instruments, the scientist would pour autoclave ash into his flower planter. His discovery resulted in further testing to learn that autoclaving was not adequate to destroy the prion.

Nothing compatible with any other life-form has been found to destroy this prion. It has no natural enemies, inoculations or barriers, and mammalian immune systems cannot recognize it or fight it. BSE is terrorizing the world except for the U.S., where it's politically incorrect for news media to upset Americans with bad news.

Higher risks of prion infection to humans may occur from "mechanically-separated meat by-products;" sausage, bratwurst, lunchmeat, and other by-products produced by machines that remove meat, including nervous tissue, from bones. Prions can apparently be absorbed by plant life and passed to grazing mammals. Huge Canadian elk herds, condemmed due to infection during December, 2000, were probably contaminated by scrapie-infected sheep tissue sent to a wastewater plant for disposal, with the sludge later spread on forest grasslands.

Scientists believe that people are infected by their food, although there is one case in the U.K. being analyzed right now where a man may have been infected by casual contact with another man who later developed vCJD. The contact was non-sexual and the mechanism of infection is currently a mystery. One of the men was an avowed vegetarian while the other rarely ate red meat of any kind. Food is primarily considered to be the vector of infection, although experiments where fly larvae consumed infected brain tissue successfully transferred TSE to hamsters through oral consumption. Establishing an insect as a possible vector of disease spread was important, but hardly surprising. In any case where DNA proteins can be communicated as prion fragments, some infectious prion will remain viable.


In January, 2001, some scientists suggested that space debris brought the prion to earth. Although the suggestion may have been honestly proposed, it seems rather absurd. Such suggestions are not likely to allow an escape for British politicians who are being pursued via litigation, as they are accused of criminal incompetence for allowing BSE-contaminated meat to reach store shelves in France. The idea is mentioned here in an attempt to be condescendingly supportive of even the stupidest contributions of science. More realistically, the massive (and insipid) agricultural use of slaughtered animal tissues and blood, fed to cattle, is a known to have contributed heavily to the current BSE crisis.

Prions may now be in our food, our pet food, our pets, our lawns and ourselves.

The first symptom of vCJD in humans has included overnight personality changes. "She woke up as a different person." Initial symptoms seem to resemble stroke as the disease disconnects portions of the brain that accomplish the unique traits of Self. Memory is quickly destroyed. -Confusion, regression of developmental thought, defensive behavior, rage. -Staggering, loss of feeling and loss of control. Speech is impared. The ability to think clearly is rapidly destroyed. Human death after symptoms first appear normally requires 1 - 2 years while the quickest documented case (a fourteen year-old girl) resulted in death five months after symptoms first appeared. Victims often spend their final year as screaming vegetables.

To date, a test to detect infectious prion in a living creatures does not exist *(See Jan 23 Update), with the exception of costly DNA sequencing tests. Human and bovine brains are examined for spongiform vacuolization after death. For humans, diagnosis is only confirmed after autopsy. Only cattle younger than 30 months old are not inspected, but that's because the EFFECT of the prion has never been observed in a young brain. It may take up to ten years for the prion to incubate into symptomatic stages, although it may be reasonable to suggest that prions may already be present in many more of earth's mammalian populations than we would like to know about. Original studies by Dr. Creutzfeldt and Dr. Jakob, independantly, were centered on manifestations of senility, including premature dementia and Alzheimer's disease. During their studies, both doctors reported vacuolization on brain tissue after death of patients as well as disorientation, mental regression and loss of coordination. Very obviously, both doctors worked with TSE prion victims and the human variant was later named after these two scientists. It may be staggering to determine how much senseless violence and how many diagnosis of Alzheimer's disease are actually CJD.

John Stauber and Sheldon Rampton, authors of Mad Cow USA: Could the Nightmare Happen Here? are highly critical of efforts in the U.S. to limit the spread of prions. "They [people] should be very angry that the U.S. government is covering up the risks of mad deer and mad elk disease to hunters and to those who eat venison products," Stauber said. "And also that our regulations in the U.S., with regard to feeding slaughterhouse waste to animals, are inadequate."

It is our nature to push the extreme edge of productivity, constantly. But trying to circumvent natural contraints may be our undoing. We play with powers we cannot fathom and if we haven't already created the monster of our own destruction, we will probably do so through other genetic manipulation of plants and animals, or genetic creation of other diseases which we cannot control; forms of life we artificially create which were not selected into coexistence within our carefully-balanced environment of planetary ecosystems through millions of years of tweaking to environmental stresses. In this matter, we agree with Michael Crichton: "Genetic engineering is the most powerful force on the planet. You play with it like a kid who has just found his dad's gun."

No one seems willing to face the responsibility for thinking through the implications of incredible corruptions of natural effrontery before releasing the latest toys for maximum, commercial exploitation. -That's assuming that we have anything near the wisdom required to evaluate such implications in the first place. While some groups protest G.M. (Genetically Modified) crops, our ignorance of the possible effects of this science may have already created other monsters that have just begun to breathe their first, stinking breaths of terror into the future of world agriculture. Ecological justice is absolute and inescapable. Our planet's balance of the ecosystem is not only required, but it will be enforced by our world at the cost of our own extermination, if necessary.


It's important to note the differences between selective breeding of plants and animals, including hybrid pollenation, to that of genetic modification of crops which produces traits previously unknown. As an example, the former has exemplified desirable traits in crops and animals that were already inherent, but not new. The latter science has produced creatures and crops with completely new genetic traits that did not evolve within our ecosystem, such as traits that are genetically resistant to certain chemicals so that the chemicals can be produced as pesticides to destroy target insects and blight. Farmers not planting the GM crops often cannot compete with the genetically-enhanced crops that can produce massive, short-term advantages. To create new wonders is seductive science; to be an individual farmer against the trend is economic suicide. But often, other plagues appear within a few years to wipe out not only the GM crops but many others besides. Such plagues include previously benign insects that become agricultural terrors when the original pests are wiped out and no longer compete to control populations of the new parasitic threat. The potential to create monumental horrors between genetically modified lifeforms and indigenous life is staggering to contemplate. Individual agriculturists do not have the option to refuse GM products. That is up to us - world opinion can direct the future.

Greed is a good thing. Greed fuels economies in the quest for technology, development and wealth, without which progress would stagnate and return human life to the era of sticks and stones, But ignorance, untempered greed and highly-advanced science without ethical constraints are a dangerous combination that may threaten all of our futures, if it continues to run amok.

* UPDATE: January 23, 2001

Not only has more information about CJD deaths in the United States and Australia shown that numerous cases have occurred, but the numbers are shocking.

Remember that the effects of this prion has many different names, but misdiagnosis is very, very common. It's nearly impossible to positively identify except through genetic tests or autopsy after death, and the horror of dealing with victims of CJD leaves others in shock, having themselves suffered through the tragedy of this cruel disease. So incorrect diagnosis are usually not followed up with corrections. Regions are also not anxious to advertise that someone has died of prion disease which requires super-extraordinary measures to control contagion, striking terror in medical professionals and hospitals who use incredible biological containment rooms to handle anyone suspected of CJD. Meanwhile, governments irresponsibly babble about no evidence of contagion while TSE sweeps through our planet. (See new informational links at the end of this article.) After Britian, France, Germany, Italy, and some thirty EU countries have already played the idiotic game of TSE denial while prion spreads outward to the world, why are politicians in other countries still unwilling to support justified measures to identify and control this contagion before entire populations are exposed and well on their way to a future of horror as the insidious prion inclubates into CJD? The prion defies all political denials of its existence, and is firmly establishing itself worldwide. Ignorance is this monster's friend.

There is evidence that TSE has not only claimed 80 lives in recent history, (recent history is the period of time from now back to the last, major elections,) but has killed thousands of people since the 1950s. In the jungles of New Guinea, TSE is called kuru. Rituals of death, abominable agricultural practices, organ transplants (including corneal transplants), fertility hormone injections, innoculations made from bovine products, reuse of surgical instruments, blind ignorance of the disease and its incredibly, contagious nature, plus the long incubation period (two to fifty years) and irresponsible politics have all ensured widespread prion contamination throughout the world.

Regarding the political aspect, enormous pressure applied by agricultural interests to suppress evidence of contamination merely defeats any hope of containment, while politicians can usually expect their terms to expire before TSE's long incubation period ignites the truth of how far the disease has spread. Meanwhile, TSE scientists and researchers have been snubbed for the evidence they've obtained before their results are published, and politicians buckle to special interests, even though ignorance promoted by the special interest coverups may kill the politicians and "us" and "them" (who knows how many?) in the future.

More confusion: "Sporadic CJD occurs at a rate of one per million..." Responsible reporting tends toward conservative calculations of issues like TSE, but more data has identified families in some areas with inherited E200K or A117V prion mutations found in 10 family members out of 10 subjects. Human E200K mutation is a result of inbreeding within a limited genetic population, and it causes physical weaknesses when the E200K mutation is present, with nearly 100% lethal CJD within 50 years of life. Entire closed populations can predominantly carry the mutation when close family intermarriages are common. The rate at which either A117V or E200K point mutations become clinical CJD can be predicted by laboratory results, where concentrations of prion (from food sources) under low cell pH conditions conspire to produce geometric translations from DNA normal helix cross-linked structure to a beta-sheet oligomer structure (this can occur in milliseconds of the occurrence of lysene>glutamate or alanine>valine mutations). With proteins to feed looping within DNA structure near the mutation site, mutant prion production becomes a runaway condition. While prion is associated with cell membrane formation, mutant (contagious) prion prevents mammal DNA coding for effective cell membranes, from mammal 90-231 inclusive of points 117 (within prion prior to a doppel gene) and 200 (also within prion-doppel) as well as attaching directly to existing membranes and causing those membranes to hemorrhage and dissolve where mutant prion attaches. It's not surprising that mutant prion is capable of the observed spongiform destruction. Other DNA prion-doppel sites exist. Research has concentrated on genetic effects of TSE alteration of 90-231 coding due to the obvious effects of spongiform in cellular tissue, but production of TSE prion may also involve DNA prion mutations at any prion protein structure.

As it attacks cells, contagious prion can break down healthy cell membranes, thereby eliminating the cell's protective barrier and exposing DNA for mutation by the contagious prion.

Several assay techniques have now been developed to detect marker proteins for communicable prion mutations. These range from poor (40%) to excellent with nearly 100% effictivity. The assays are being used for blood analysis. Blood donations by persons ever visiting, living or getting very close to Britian and other European areas are now refused by American hospitals. All other blood donations are tested with TSE marker assays now included with other batteries of tests.

Inherited prion mutation is simply a race between other attrition factors, or the prion's eventual contributions to alternate body wasting effects, or CJD itself. Animal prion availability feeds mutant prion production and contagious prion assures that both carriers of inherited mutant prion and, eventually, persons with normal prion, will develop CJD with faster incubation of clinical effects as prion concentration increases in the blood.

Known mammalian carriers of TSE now include mice, mink, cats, hamsters, sheep, pigs, cattle, deer, elk and humans. It may be vital for us to set aside short-term political objectives at this time and engage the maximum scientific resources at our disposal to offset potential epidemics of TSE, which evidence suggests may occur within the near future.

A number of additional links to world wide web TSE information have been added to this document.

Update, January 26, 2001

A British official has stated that Asia's TSE outbreaks are expected to begin appearing within two to three years. (Minimum incubation time.) China, Taiwan, Korea and other Asian countries have imported substantial amounts of suspect, infected feed. It's also common practice in these countries to grind up dead carcasses to recycle into feed for living animals.

Update, January 31, 2001

QUESTION: Scientists recognized "new variant" prion effects in U.K. CJD victims since 1997. Why do you say it is not a new variant?

ANSWER: As British CJD cases began to appear, medical experts were surprised that incubation times seemed to be faster (two years) than previous expectations of symptomatic CJD appearance after infectious exposure (five to ten years). An alternative explanation is that expected mean distribution of CJD will appear as a statistical curve peaking at the "normal" incubation times, and that the current 87 European deaths are simply the early responders at the very beginning of an epidemic. (We hope this is not the case.) Genetically, no "variant" of the infectious prion has been identified, although mutation sites within individuals (and probably individual cells) do vary.

It should be noted that inherited prion mutations, and how long it takes for symptoms to occur, depend on where mutations occur within DNA. Some inherited mutations have prion disease manifestations that appear up to fifty years later in life, with different names given to the different presentations of these mutations.

In the presence of infectious BSE prion, A117V mutation seems to be inevitable within humans. Chaperone proteins which protect other DNA struture from mutation don't seem to be able to control beta-sheet geometric mutation of normal prion when infective prion is present.

QUESTION: Does the amount of contaminated beef consumed matter?

ANSWER: In lab tests, the percentage of mutated prion present in cells, as well as cell pH, affected the rate of DNA damage. However, cell membrane barriers may introduce a time-rate control for attacking prion to gain access to DNA structure. That limitation may be responsible for TSE's long incubation periods.

In general, such populations grow exponentially beginning with the initial population of pathogenic agents. With very small initial populations, integration of the early part of population curves will begin slowly with respect to time, yet inevitably toward symptomatic prion populations without intervention by some sort of controlling mechanism. No laboratory evidence out of many reams of research has provided any results which might suggest that a single, infectious prion cannot begin the destruction an entire animal or human being. But more exposure to BSE should cause CJD to become symptomatic sooner.

QUESTION: How many cattle have actually been positive for BSE in the U.K?

ANSWER: Testing for BSE has been based on inspection of cattle brain tissue until recently, meaning that only cattle in the symptomatic stages of mad cow disease were listed as "positive." Tests have improved during the past months through laboratory development to look for protein markers for infectious prion, vastly improving detection. To date, over 170,000 British cattle have been declared "positive" for BSE.


One of the best, dedicated sites for TSE information is http://www.mad-cow.org/, with comprehensive coverage of this subject matter. BSE, originally identified in the U.K. is also reported in frequent BBC stories. Wired News also reports occasional, but excellent, stories on this subject. Search for "BSE." Additional information may be found in the American Medical Association's Journal publications and from the World Health Organization's website.

MORE LINKS TO TSE INFORMATION (WorldWide)

Alzheimer's Society - CDJ Support Network
Australian Support Network
Blood Recall
BSE - CJD Home Page
CJD Foundation
CJD Support Network
CJD Voice
CJD U.K. Department of Health
CJD Harvard
CJD Foundation, Inc.
UK Creutzfeldt-Jakob Disease Surveillance Unit
Faces of CJD
Australian CJD HomePage [This page pops opens multiple browser windows for advertising. Since this violates our own policy, we've included this notice. The site is informal but does have some interesting information. Click here for the link.]

We've located about 2,700 web links to CJD to date. The obvious scope of this disease is becoming a staggering statistic of the 21st century.

Update, March 5, 2001

Within two weeks time, Hoof & Mouth Disease has appeared in Britian and spread to France, Wales, Belgium, Northern Ireland, Denmark and Scotland. The wild outbreak of Hoof & Mouth virus has already resulted in an additional 45,000 animals in the U.K. and 50,000 animals in France being destroyed to contain outbreaks.

The agricultural death toll from TSE in Europe has now reached 200,000 animals, with 94 human deaths from CJD.

The March 12th issue of Newsweek Magazine estimates that "millions" of human cases may be incubating at this time. See Newsweek's story, Cannibals to Cows: The Path of a Deadly Disease.

Q: Besides food, what kinds of products may be infected with TSE?
A: Innoculations, hormone supplements, any vitamins & supplements produced from animal tissues, herbs (or food) grown in organic fertilizer, food and extracts grown on soil occupied within two years by infected animals, all food sold for carnivorous pets including fish, soap made from animal fats (almost all soap), facial and skin creams, protein enricheners for hair, lip balm, shampoo, many cosmetics. Also, chicken, farm-raised fish and pets. It's reasonable to expect that short-lived animals like chickens and fish can carry prion disease from food enriched with animal proteins, even though they probably will not exhibit symptoms during their lifespans. Infectious prion has now been verified in cats.

Q: Is there something we should do?
A: As far as already-infected populations are concerned, fatal mutation occurs at the molecular-genetic level. There's no hope of specific antigens that could recognize such an insigificant difference in genetic structure between normal and damaged cells, much less the prion fragment itself. But various chaparrone proteins supervise and often correct genetic defects, although research has indicated that the beta-sheet defect is not reversible, so far. Continued research is important. Since the start of Y2001, a reliable (96%) lab test has improved TSE detection. Success against TSE demands heros, like Professor RIchard Lacey, who tried to warn the world of this danger years ago, and new heros to carry on against TSE.

We must completely halt the practice of feeding any agricultural livestock feedstocks containing other mammalian proteins. It's not adequate to maintain this practice with livestock that doesn't show symptoms and call that good enough. Any animal meant to graze should only feed on grass, grain, corn, and other non-animal feed, including domestic and wild herds of deer, elk and sheep. Animal residues must not be scattered on the earth where plants can absorb and propagate prion infection.  
 

 

return to virtualpath homepage return to science & technology index

Copyright 1998, 1999, 2000, 2001 Virtual Path Graphics