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Mad cow and the history, cause and spread of prion diseases

Mad cow disease, also known as bovine spongiform encephalopathy (BSE) was first discovered in cattle in the UK in 1986. In 1996, BSE made its way into humans for the first time, setting off panic and fascination with the fatal disease that causes rapid onset dementia. In this episode, Sam and Deboki cover the cause, spread and concern surrounding mad cow and other prion diseases.

Transcript of this Episode

Sam: As a young kid I became pretty fascinated by the things that could kill me, particularly infectious diseases. Don’t ask me why, I just was. And the first one I remember becoming obsessed with was mad cow. The formal name for mad cow disease is bovine spongiform encephalopathy or BSE. The name makes sense — the brain of a cow with BSE looks spongy under a microscope, because of holes left by the disease. Although it can take years from the time a cow is infected to the time it first shows symptoms, like issues with coordination, once it does show symptoms things escalate quickly and the cow is usually dead within a couple weeks to six months.

Deboki: Mad cow disease was first discovered in 1986 in the UK, where it wreaked havoc for over a decade, killing nearly 200,000 cows and devastating many farming communities. In 1996, BSE made its way into humans for the first time, causing a decline in coordination, issues with vision, and the rapid onset of dementia. Over 200 cases of BSE have been reported — mostly in the UK — and everyone who was infected has died.

And in December 2003, mad cow made its first appearance in the US when an infected cow was discovered on a farm in Washington State. Today cases of BSE and of BSE making its way into people are pretty much nonexistent, thanks in large part to practices designed to keep us safe.

For example, mad cow kicked off because the feed being given to cows was infected. But since August 1997, the US FDA has banned the use of most cow parts and other animals to be used to make cow feed, limiting the risk of infected meat making it into their food.

Sam: I think we’re all used to hearing about infectious diseases caused by bacteria, viruses and a bunch of different parasites. But BSE is quite unusual: it’s not caused by any of those things. It’s caused by a protein, a fundamental building block of all living things.

Welcome to Tiny Matters. I’m Sam Jones and I’m joined by my co-host Deboki Chakravarti.

Deboki: Today on the show, we’re going to be focusing on prion diseases — rare, fatal brain diseases like mad cow that are caused by a protein malfunctioning and folding in a way it shouldn’t. I know the concept might sound a little weird and confusing, but Sam and I, and the scientists we chatted with, are going to break it down for you and talk about what’s being done to detect these diseases before something like mad cow happens again.

So what is a prion? It’s a protein that can take on two forms. The first one is what we consider the normal form, which doesn’t cause disease. Normal prions are found in the brain, although researchers don’t know much about what they do. But when people say “prion,” they’re usually not talking about the normal form. They’re usually talking about the other form…the bad, misfolded form that causes disease.

Mark Zabel: You can think of the normal form as sort of a really nice three-dimensional structure. Sort of balloon looking. When it misfolds into the prion, that balloon, three-dimensional structure becomes basically almost a two-dimensional structure. Think of it as like a bathroom tile. Very small, thin, flat.

Sam: That’s Mark Zabel, who’s the associate director of the Prion Research Center in the College of Veterinary Medicine and Biomedical Sciences at Colorado State University. He told us that when the misfolded prion — the bathroom tile as he described it — comes into contact with a normal prion, it causes it to also misfold. I think of it like a domino effect.

Deboki: And once you get a bunch of misfolded prions, those tiles stack up together and form fibers that tangle around each other, which then kills your neurons. As your neurons die off, it leaves holes in your brain—like the spongy brains seen in mad cow. And when you have holes in your brain it causes dementia, difficulty walking and speaking, sometimes even hallucinations, and ultimately death.

So how many misfolded prions is enough to cause disease?

Brian Appleby: I would say we don’t know that for sure except that prions aren’t desired to have. But is one misfolded prion protein enough to cause disease? Probably not. But the problem with prion disease is they aggregate, you know, they're kind of like the bad kids in the schoolyard. The bad kids recruit the good kids, and you have more bad kids, and that keeps amplifying and amplifying until you get disease. So that's kind of what happens — you get enough bad prions in the brain that it causes a variety of diseases in animals and humans.

Deboki: That’s Brian Appleby, a professor of neurology, psychiatry, and pathology at Case Western Reserve University.

Sam with Brian Appleby: What are some of the ways that someone could develop this disease? What would allow for these proteins to misfold?

Brian Appleby: So in humans, there's three main causes of prion disease. The most common cause by far is what we call sporadic. And there's a lot of similarity to that with Alzheimer's disease and Parkinson's disease, which are also sporadic illnesses for the most part. And what that means is that for reasons that we don't really understand, that normal protein becomes misfolded and misshapen spontaneously within the body after it's already been made. I equate it a lot to cancer. We all make cancer cells as we get older, but our body's generally able to detect them and get rid of them. The same is true with our proteins — we make bad proteins every day, but the likelihood of making bad proteins increases as we age, as well as our ability to detect them and clear them. And then you get these protein misfolding diseases like prion disease and Alzheimer's. Deboki: Brian told us around 85% of prion diseases are sporadic. But there are also prion diseases caused by a mutation in the gene that codes for the prion protein PRNP. This genetic mutation makes it more likely for the prion protein to misfold over a person’s lifetime.

And in addition to sporadic and genetic causes of prion disease, there are also acquired prion diseases. This is by far the most rare version and typically happens because of a medical procedure — say brain surgery, if there’s prion contamination on surgical equipment. It can also be caused by eating meat that contains infected nervous tissue. I think this is the version most people know about, because that’s what happened with mad cow.

People came down with the human version of BSE by eating beef that had been contaminated with nervous tissue of infected cows. But the cows developed BSE in the first place because they were fed sheep products infected with a prion disease called scrapie that’s been documented in sheep for over 300 years.

Sam: Another somewhat well-known acquired prion disease is kuru, which is caused by eating contaminated human brain tissue. In the 1950s and 60s, the Fore people in the highlands of Papua New Guinea experienced high levels of the disease, which turned out to be the result of ritualistic cannibalism where relatives prepared and consumed the bodies of deceased family members, including their brains.

So overall, there are 3 main categories of prion diseases — sporadic, genetic, and acquired — and within those categories you have more specific diseases like kuru which is of course acquired, fatal familial insomnia which is passed on genetically, and Creutzfeldt-Jakob disease, or CJD, the most common prion disease that affects humans. CJD falls under all 3 categories — it can develop sporadically, genetically or be acquired. This is a form of prion disease that people exposed to BSE — mad cow — developed. 

Deboki: And because the symptoms are pretty much identical throughout all of these diseases, the only way to really tell them apart is by looking at brain tissue under a microscope to see the size and distribution of the holes or prion protein deposits.

Brian Appleby’s work focuses on all three categories of human prion disease.

Sam with Brian Appleby: So what is it about prion diseases that you find so interesting?

Brian Appleby: A lot actually. So I am a trained neuropsychiatrist, geriatric psychiatrist by training. And I really got interested in the field primarily from the caregiver side because this is a very rapidly progressive neurodegenerative illness. It's horrible for families to go through and there's not a whole lot of clinical expertise to help them out. So that's how I originally got interested in it. And then of course at that time I was also kind of a dementia doctor, so there's a good overlap between the two. And then I got really interested in the science, which of course is extremely interesting. I think from the clinical side, seeing the patients, they're very difficult to diagnose sometimes. And then of course the biology and trying to understand that and how it affects public health.

Deboki: Brian is the director of the National Prion Disease Pathology Surveillance Center.

Brian Appleby: the National Prion Disease Pathology Surveillance Center was founded in 1997, mainly in response to the mad cow epidemic. Most countries wanted to develop surveillance programs to know whether or not people were being affected by mad cow disease. It's funded by the CDC and we're funded to do neuropathologic surveillance. So we collect brain tissue on patients who had CJD or another form of prion disease and examine it underneath the microscope to see whether or not it is in fact prion disease, because that's the only way to definitively diagnose it.

Deboki: They’re also working on developing tests to be able to more specifically diagnose people who appear to have a prion disease.

Brian Appleby: We also do a lot of outreach and education to clinicians, but also to funeral home providers because there's a lot of fear of potentially contracting this disease and people that deal with that.

Sam with Brian Appleby: I actually have a follow up based on what you just said, which was this sort of fear for people who are handling bodies of people who have passed away from prion diseases. There is some anxiety that you could actually get prion disease. How likely is that?

Brian Appleby: My predecessor used to say that the fear of prion disease was way more infectious than prion disease itself. And that's certainly true, right? It’s difficult to transmit prion disease and you really can only do it in certain scenarios. So you need to have infectious tissue which is almost always gonna be brain tissue. And then that either needs to be injected into a person, consumed orally by a person, or placed in another person's brain for transmission to occur. Now most of those scenarios don't happen in everyday life, right? So there are specific scenarios where it could happen though — neurosurgery, brain surgery, autopsies where we were removing the brain, and then in the past we used to reuse brain tissue and pieces that surrounded the brain in healthy individuals.

And in fact, that's how some prion disease got transmitted. One example is we used to get human growth hormone from cadavers through their pituitary gland, which is part of the brain. They would grind it up and inject it into children of short stature to treat their short stature and it would transmit prion disease. But we don't do that anymore. Now we make what we call recombinant human growth hormone or made in a laboratory human growth hormone. So we don't have to do those things. So it is hard to transmit. There are certain scenarios where you have to take precautions, but they are few.

Deboki: One place where precautions are of course necessary is if someone is doing laboratory research involving prions. In 2019, a researcher in France named Émilie Jaumain died of acquired CJD — at age 33, 10 years after pricking her thumb during an experiment with prion-infected mice. In 2021, a second lab worker in France was diagnosed with CJD, leading to a months-long moratorium on prion research at a number of public research institutions in the country.

Sam: Again, prion diseases in humans are incredibly rare and the scenarios where you’d be at risk for acquiring one are quite specific. But in other species, a prion disease called chronic wasting disease spreads easily and is on the rise.

Mark Zabel: Chronic wasting disease is a prion disease that affects cervids. Cervids include elk, deer, moose, caribou, reindeer, red deer. It’s a highly infectious disease. It's one of the most infectious prion diseases we've ever studied. It’s very similar to the sheep prion disease known as scrapie.

Sam: That’s Mark Zabel again, from Colorado State University. You heard him briefly at the top of the episode. Mark’s research focus is chronic wasting disease or CWD.

Mark Zabel: Until recently, within the past five to 10 years, it was thought that it jumped species and was caused from sheep scrapie and thought that maybe some deer came in contact with some contaminated environments, or came into contact with infected sheep. And that has been turned on its head just a little bit, based on some studies that my lab has done and others, but also the fact that CWD has most recently been found in Northern Europe, in Nordic countries, first in Norway, but since then, Sweden and Finland, and it's interesting because there's no known connection of CWD in those Nordic countries to North America.

There is sheep scrapie in Scandinavian countries, so there's a chance that it could have been a trans species event from sheep scrapie. We can't rule that out. But there's a really interesting story emerging in the Nordic countries, and that is they're finding a lot of moose with CWD. And the reason that's interesting is moose, unlike other cervid species, they're solitary animals. And we think that CWD is passed from deer to deer, elk to elk, by direct and indirect contact. But moose don’t behave that way, so how do they get it? That indicates that it's potentially a spontaneous disease.

Deboki: Remember a spontaneous disease is just that — it’s spontaneous. It’s like a form of cancer where, for no rhyme or reason, you just have cells that go rogue and start dividing like crazy. In the case of prion disease, it’s the prion proteins going rogue and misfolding like crazy.

Unlike human prion diseases, prions that cause CWD can be excreted in saliva. Deer are super social, they have nose to nose contact. Which is very cute, unless one of them has CWD. They can also excrete prions in urine and feces. And those prions can stick around in the environment for a long time, even decades.

Mark Zabel: We think they can accumulate to a point where now a deer sniffing around in the ground eating plants that have been contaminated with urine or feces can now be ingested in that way as well. So that's another indirect transmission. Also decaying carcasses in the environment from deer that passed away from CWD and other deer, elk or moose will come and kind of sniff around that carcass as well.

Deboki: The good and very important news to share is that at this point, there is no documented transmission of CWD to humans. But that doesn’t mean we should assume it will stay that way. Remember, BSE did cross the species barrier, from sheep to cows and then cows to humans.

Mark told us that one of his biggest concerns is that hunters are being exposed to CWD in large quantities. When people were exposed to mad cow, they were usually eating a burger that had been made from different cows combined into one patty, and maybe just one of those cows had the disease, so it was watered down. But for hunters, things are different.

Mark Zabel: Consider a hunter who’s killed a CWD infected animal. They're gonna feed that animal to a very small number of people, family and friends, maybe a handful, maybe a half dozen. The prion titer, the load that they get from eating that one sick animal, it's not diluted into a bunch of other animals. The infectious dose they're receiving is orders of magnitude higher than the people who ate an infected hamburger. So that could really stress the species barrier to breaking. That's one of my big fears.

Deboki: By the species barrier breaking, Mark means that with enough of that infectious protein present there’s a greater chance of infection and CWD could go from a deer problem to a human problem.

Sam: And I feel like we should say this again, because Mark reiterated it many times throughout our conversation: no cases of CWD jumping to humans have been reported. And there are ongoing studies looking at hunters to see if they’re dying of prion disease at a higher rate than the general public. Mark says that so far there's no evidence suggesting that.

I also asked Mark if there was concern about dogs contracting CWD. I’m a dog owner, and if you’ve ever owned a dog, chances are you know they're prone to sniff around and seek out gross and dead stuff. So I wondered if they were at risk.

Mark Zabel: I do have some good news for you about your dog though, and my dog. It seems that there's some species, some mammals, that are particularly resistant to prion disease — dogs are one of them. If you're a cat owner, unfortunately there is feline spongiform encephalopathy, and that was produced during the BSE outbreak. So not only did humans get it, but they also made cat and dog food out of some of those infected cattle and some cats in Europe ended up getting this new FSE, this new prion disease of cats, but no dogs. There is no canine spongiform encephalopathy.

Deboki: Mark and his colleagues are working on a bunch of things. One is developing tests that can easily detect CWD in feces found in the environment to monitor its spread. Just like human prion diseases, there are no current treatments for CWD, so they’re also working on therapeutics that could interfere with production of the diseased prion protein.

And Mark told us something else that’s really important about prion research. It’s applicable to a huge range of diseases where proteins don’t fold correctly.

Mark Zabel: Prion diseases belong to a larger family of diseases that we refer to as protein misfolding diseases. These are diseases that also are caused by normal proteins that we all express that misfold and start causing these amyloid or these plaques in the brain. Many of these diseases are much more common than prion diseases. So Alzheimer's disease, for example, Parkinson's disease, Lou Gehrig's disease, ALS — amyotrophic lateral sclerosis — traumatic brain injuries, chronic encephalopathies, are associated with proteins that misfold. So prion diseases are just a member of these much larger family of protein misfolding diseases.

Sam with Mark Zabel: That's interesting. And it also is interesting because I would imagine that, to some degree, the work that's done to try and understand those other contexts in which you have protein misfolding like a traumatic brain injury or Alzheimer's, that what you gather from those studies could often be more broadly applied.

Mark Zabel: Absolutely. And, since obviously I'm a prion researcher, I would turn that converse, because one thing that's really interesting about prion diseases that helps researchers, is that these lab animals I'm talking about rodents, especially, that we can genetically manipulate, they actually get a prion disease, and it is a bonafide prion disease, unlike Alzheimer's, right? Where we do study that in the lab and we use these genetically altered animals from mice, but it's just a model because they don't really get Alzheimer’s. We can manipulate them so that they get a form of something that looks like Alzheimer's, but it's not exactly Alzheimer's. But prion diseases can be completely recapitulated in a mouse, and that disease is exactly the same disease that humans will get from a prion disorder as well.

It’s really changing the way we think about proteins and how they function and what they really do.

Sam: Prion diseases are no doubt scary but hopefully this episode made you feel a little better about them. Unless you didn’t know they existed before this episode and in that case oops sorry. I can say with certainty that this episode would have made kid me — the one obsessed with mad cow — feel better, knowing that prion diseases are incredibly rare and being monitored, and that there are researchers making big strides to catch these diseases early, develop treatments, and prevent them altogether.

I think we can hop into this Tiny Show and Tell.

Deboki: Yeah, I can go first.

Sam: Perfect.

Deboki: My Tiny Show and Tell, it's not relevant to this episode, but it's also very related, because it's about a condition that kind of comes on very quickly and is very, very hard to test for, but that people have been making really exciting progress on recently. And this is preeclampsia, which is a condition that comes up around the middle of pregnancy that basically causes a lot of issues with blood pressure and can be really, really dangerous for people. It usually happens in around one in 25 pregnancies and in the US it affects black women more than white women.

I remember from previous experiences of being pregnant that it's like a thing that they ask you about very early on and that you're kind of like, "Ah, I don't know. I don't know how to tell you what my risk factors are for this." Doctors and nurses, they're always just trying to make sure to mitigate the risk of preeclampsia.

And one of the things that's really exciting is that the FDA has approved a blood test for helping pregnant people figure out if they're at risk for preeclampsia. So it's not necessarily something that I think you can take from my understanding super early on. But the way that it works right now, at least in Europe where this test is used, is that if you're around those middle weeks of pregnancy and you're starting to show symptoms of preeclampsia or things that could maybe be preeclampsia-like, you could take this test to figure out just how likely you are to actually have preeclampsia develop. Like I said, this is something that comes on very quickly. So you might have the symptoms of it, but you might not actually know for sure that's going to happen. But then once it does happen, it just happens so quickly that you need to be able to address it really quickly.

So having a test to help people figure out are these symptoms potentially preeclampsia earlier on, is super helpful. And it looks specifically at two proteins in the placenta and their ratios of one versus the other because if these two proteins are really unbalanced, you're more likely to develop severe preeclampsia. There's about a 96% accuracy for predicting who won't develop preeclampsia. And meanwhile, two-thirds of the people who do get a positive test result will end up developing severe preeclampsia. There's still a lot that needs to be done in terms of monitoring how well this test works, but I think it's just super important because I didn't mention this earlier, but some of the things that can happen with preeclampsia is that you can have kidney and liver failure, you can have seizures. So having some kind of test that can help people who are pregnant figure out what's going on so they can get the right treatment is super important.

Sam: Yeah. That is really important. And I think preeclampsia is something that a lot of people don't really know about maybe until they're trying to get pregnant or are pregnant. And in graduate school, actually, the research group right next to the lab I was in worked on preeclampsia.

Deboki: Oh, interesting.

Sam: And that's how I learned about it. I had no idea what it was and I like the idea of a test that could help tune a lot of people in to the fact that they could have preeclampsia, that it's likely that and not something else, so that if things do escalate, they can say to the doctor right away, "Look, I'm high risk for preeclampsia. That could be what this is," and just save that time that would be spent trying to figure out what might be going on. That's I mean lifesaving, right? So-

Deboki: Totally. Yeah.

Sam: Yeah. Thanks for sharing Deboki.

Deboki: Mm-hmm.

Sam: That's good news. I like that.

Deboki: Yeah.

Sam: In my Tiny Show and Tell this week, I'm going to take us back 5,000 years. So this is not current day testing developments. This is very different. So in 2008, archeologists discovered a 5,000 year old grave in the town of Valentina in southwest Spain. And so in this super old grave, they found ivory tusks, amber, ostrich eggshells, and a crystal dagger. And so they thought, "Okay, this probably belonged to an elite leader." And so then they dubbed the individual, The Ivory Man. But now there's a team of researchers, and they use this new technique I had not heard about before. It actually looks at this enamel forming protein, amelogenin, which I guess sticks around much better than DNA does. And the other thing is, apparently male and female chromosomes have different versions of the gene that produces this amelogenin protein.

And so you can actually use it to determine sex. And so by analyzing these proteins on two of the teeth of this person found in the 5,000 year old grave, they confirmed that's not The Ivory Man. It's The Ivory Lady. So yeah, it was a woman.

They also found a bunch of chemical traces of cannabis, wine, even some mercury, because people loved mercury back in the day. They were using it as a pigment. They were ingesting it, thinking it was curing a bunch of things. Oops. But yes, they found a lot of other stuff near her body, which would suggest that maybe she was involved in some sort of religious rituals. And this was during the Copper Age. And it seems like in the Copper Age in the Mediterranean, that this was actually pretty much in line with a lot of what was happening.

A lot of prehistoric women actually had some prestige. They held authority. And so our modern assumption, which is very paternalistic and male dominated, we're kind of viewing the past through that lens. And actually, in some ways, a lot of these societies were more progressive than the ones we have today. And it also reminded me that last October, we did an episode about some of our travels last year, the travel that I shared was going to Greece. And so one of the islands that I went to when I was in Greece was Crete, where you had the Minoan Society. So the Minoans were around during the Bronze Age. There's some overlap with the Copper Age, but it's generally slightly after. So the Copper Age ends around 2000 BCE, whereas the Bronze Age ends around 1000 BCE. Again, with the Minoans, initially people thought, "Oh, it was all men that were in charge," the usual, and then more and more evidence kept coming forward really making a compelling argument that like, "No, the people in charge, the rulers, they were women."

Deboki: That's so cool. And it's so interesting how we've developed these techniques to be able to understand these questions in different ways and to look at these remains. And I got very excited just when I heard crystal dagger too. I was just like, "That sounds so amazing."

Sam: I know. I know. Right?

Deboki: Thanks for tuning in to this week’s episode of Tiny Matters, a production of the American Chemical Society. This week’s script was written by Sam, who is also our executive producer, and was edited by me and by Michael David. It was fact-checked by Michelle Boucher. The Tiny Matters theme and episode sound design are by Michael Simonelli and the Charts & Leisure team. Our artwork was created by Derek Bressler.

Sam: Thanks so much to Brian Appleby and Mark Zabel for joining us. If you’d like to support us, pick up a Tiny Matters coffee mug! Or through August 11th send us your questions and we’ll enter you into a raffle to win a Tiny Matters mug. These can be science questions, questions about a previous podcast episode, questions about how Deboki and I made our way to science communication. Truly the sky's the limit. Send your questions to tinymatters@acs.org . You can find me on social at samjscience.

Deboki: And you can find me at okidokiboki. See you next time.

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Emergence of a New Creutzfeldt-Jakob Disease: 26 Cases of the Human Version of Mad-Cow Disease, Days After a COVID-19 Injection

• Claire Moret-Chalmin Neurology; Luc Montagnier Foundation
• Luc Montagnier Virology; discoverer of the human immunodeficiency virus and Nobel Laureate 2008

Creutzfeldt-Jakob Disease, the formerly rare but universally fatal prion disease in humans, normally progresses over several decades before it leads to death. In the Appendix to this paper, we highlight the presence of a prion region in the spike protein of the original SARS-CoV-2, and in all the “vaccine” variants built from the Wuhan virus. The prion region in the spike of SARS-CoV-2 has a density of mutations eight times greater than that of the rest of the spike, and, yet, strangely that entire prion region disappears completely in the Omicron variant. In the main body of our text, we present 26 cases of Creuzfeldt-Jacob Disease, all diagnosed in 2021 with the first symptoms appearing within an average of 11.38 days after a Pfizer, Moderna, or AstraZeneca COVID-19 injection. Because the causal progression, the etiopathogenesis, of these atypical and new cases of human prion disease — cases of what is apparently a totally new form of rapidly developing Creuzfeldt-Jacob Disease — we focus on the chronology of the symptomatic development. We consider it from an anamnestic point of view — one in which we compare the typical development of pre-COVID cases of Creuzfeldt-Jacob Disease to the extremely accelerated development of similar symptoms in the 26 cases under examination. By such an approach, we hope to work out the etiopathogenesis critical to understanding this new and much more rapidly developing human prion disease. By recalling the sequential pathway of that the formerly subacute and slowly developing disease followed in the past, and by comparing it with this new, extremely acute, rapidly developing prion disease — one following closely after one or more of the COVID-19 injections — we believe it is correct to infer that the injections caused the disease in these 26 cases. If so, they have probably also caused a many other cases that have gone undiagnosed because of their rapid progression to death. By late 2021, 20 had died within 4.76 months of the offending injection. Of those, 8 died suddenly within 2.5 months confirming the rapid progression of this accelerated form of Creuzfeldt-Jacob Disease. By June 2022, 5 more patients had died, and at the time of this current writing, only 1 remains still alive.

Author Biography

Luc Montagnier, MD, and Nobel Laureate, esteemed colleague and friend, passed from this world on February 8, 2022 not long after the completion of the preliminary draft of this work which his co-authors have carried forward to this updated report with some additional cases and new information. Perhaps this may be the most important work of Luc’s lifetime expressing his incredible genius and spirit. While hospitalized, he continued to attach the greatest importance to the publication of this article. He is honored by the Luc Montagnier Foundation Quai Gustave-Ador 62 1207, Geneva, Switzerland.

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Santiago, D. (2022b). Playing Russian Roulette with every COVID-19 injection: The deadly global game. International Journal of Vaccine Theory, Practice, and Research, 2(2), 619–650. https://doi.org/10.56098/ijvtpr.v2i2.36

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Researchers link mad-cow culprit to stem cell health

What does mad cow disease have in common with stem cell research? MIT and Whitehead Institute scientists have found that the same protein that causes neurodegenerative conditions such as bovine spongiform encephalopathy (mad cow disease) is also important for helping certain adult stem cells maintain themselves.

"For years we've wondered why evolution has preserved this protein, what positive role it could possibly be playing," says MIT professor of biology and Whitehead member Susan Lindquist. "With these findings, we have our first answer."

Lindquist, Harvey Lodish (also an MIT biology professor and Whitehead member), and colleagues are co-authors on a paper to be published online in the Proceedings of the National Academy of Sciences during the week of Jan. 30.

For more than 10 years, researchers have known that a protein called PrP causes mad cow disease and its human equivalent, Creutzfeld-Jakob disease. PrP is a prion, a class of proteins that has the unusual ability to recruit other proteins to change their shape (PrP is shorthand for "prion protein."). This is significant, because a protein's form determines its function. When a prion changes shape, or "misfolds," it creates a cascade in which neighboring proteins all assume that particular conformation. In some organisms, such as yeast cells, this process can be harmless, even beneficial. But in mammals, it can lead to the fatal brain lesions that characterize diseases such as Creutzfeld-Jakob.

Curiously, however, PrP can be found throughout healthy human bodies, particularly in the brain where it's highly abundant. In fact, it's found in many mammalian species, and only on the rarest occasions does it result in disease. Clearly, scientists have reasoned, such a widely conserved protein also must play a positive role.

Chengcheng Zhang, a postdoctoral researcher in Lodish's lab, was studying hematopoietic (blood forming) stem cells in mouse fetal tissue when he discovered that PrP was expressed abundantly on the surfaces of these stem cells. "I found that while not all blood cells with PrP on their surface were stem cells, any cell that lacked PrP was definitely not a stem cell," says Zhang.

Zhang teamed up with the Lindquist lab's graduate student Andrew Steele, an expert in prions, to discover what role PrP might play in stem cell biology. Zhang and Steele took bone marrow from mice in which PrP had been knocked out, and transferred that marrow into normal mice whose blood and immune systems had been irradiated. The new bone marrow took hold, and these mice flourished, although all their blood cells lacked PrP. Zhang and Steele continued the experiment, this time taking bone marrow from the newly reconstituted mice, and transplanting it into another group of mice. They repeated this process again and again -- transplanting bone marrow from one group of mice to another like passing a baton.

Soon they noticed that with each subsequent transplant, the stem cells began to lose their ability to reconstitute. Eventually, the scientists ended up with mice whose hematopoietic stem cells completely lacked the ability to generate new cells. However, in the control group, where they mimicked the experiment with bone marrow abundant with PrP, each transplant was as good as the next, and at no point did stem cells lose their efficacy.

"Clearly, PrP is important for maintaining stem cells," says Lodish. "We're not sure yet how it does this, but the correlation is obvious."

"PrP is a real black box," Lindquist says. "This is the first clear indication we have of a beneficial role for it in a living animal. Now we need to discover its molecular mechanism."

This research was funded by the National Science Foundation, the National Institutes of Health, the Ellison Medical Research Foundation and the Leukemia and Lymphoma Society.

A version of this article appeared in MIT Tech Talk on February 1, 2006 (download PDF) .

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Peer-Reviewed Articles and Public Health : The Mad Cow Affair in Italian Newspapers

From the Centro di Riferimento AIDS e Servizio di Epidemiologia delle Malattie Infettive, Istituto di Ricovero e Cura a Carattere Scientifico "L. Spallanzani," Rome, Italy.

Context.—  It has been suggested that early announcements of research works to be published in peer-reviewed journals may diminish newsworthiness of scientific articles, but this issue has not been widely studied.

Objective.—  To analyze the impact on the news media, in terms of volume and prominence of coverage, of a scientific article published in peer-reviewed journals about issues with relevance to public health compared with the impact of preliminary release of information on the same issue.

Design.—  Analysis of press coverage of Creutzfeldt-Jakob disease (CJD) and bovine spongiform encephalopathy (mad cow disease) in the 7 newspapers with the widest circulation in Italy, between March 20, 1996, when the British secretary of state for health announced the identification of 10 cases of a new-variant CJD, described April 6, 1996, in The Lancet , and May 10, 1996. Related newspaper articles were identified by hand search.

Main Outcome Measures.—  Numbers of newspaper articles published before and after publication of the Lancet article.

Results.—  We collected 535 articles, of which 62 (11.6%) appeared on the front page. The number of articles published daily peaked on March 26 with 48 items and 1 article on the front page of all the newspapers. A total of 386 (72%) of the 535 articles and 56 (88.7%) of the 62 published on the front page were published in the first 2 weeks of the study period, before the Lancet publication.

Conclusions.—  Our analysis suggests that, in the case of issues of public health importance, when peer-reviewed research is published after a health risk is disclosed to the public, its impact in the media is small. Coordination between news release by public health authorities and publication by peer-reviewed journals may improve the quality of public information.

Conclusions.—  JAMA. 1998;280:292-294

JOURNALISTS consider peer-reviewed journals an important source of information on biomedical subjects 1 and there is evidence that articles published in peer-reviewed journals may have a significant impact on the lay press. 2 It has been suggested, however, that early announcements of research work to be published in peer-reviewed journals may greatly diminish newsworthiness of scientific articles. 3

The aim of the present study was to analyze the impact on the news media, in terms of volume and prominence of coverage, of a scientific article published in peer-reviewed journals about issues with great relevance to public health compared with impact of preliminary release of information on the same issue. To this end we analyzed how the "mad cow affair" was reported in Italian newspapers in the spring of 1996.

Mad cow disease is the popular name for bovine spongiform encephalopathy (BSE), identified in 1986 among British herds. 4 In 1989 concern was expressed on the possible risk of BSE transmission to humans, resulting in Creutzfeldt-Jakob disease (CJD). 5 On March 20, 1996, the British secretary of state for health made a statement in the House of Commons announcing the identification of a new-variant CJD (v-CJD) in 10 young people, and stating that the most likely cause of these cases was exposure to BSE, without mention of clinical and neuropathological findings that led to the identification of v-CJD. Immediately all over Europe concerns were raised on eating British beef. The scientific article describing these cases in detail was published in The Lancet on April 6, 1996. 6

We performed an analysis of press reports on CJD and BSE for the period March 20 to May 10, 1996, reviewing the 7 Italian newspapers with the highest nationwide circulations. 7 Relevant articles were identified by hand search, reading each headline, subheading, and half title, and were classified according to date of publication, page number, and proportion of page occupied. To identify articles that contained more specific scientific information, we collected information on whether newspaper articles mentioned the following characteristics of v-CJD reported in The Lancet : number of cases, age, mean duration of disease, short incubation period, mention of a new variant, and neuropathology findings. If the article contained an interview with biomedical scientists, this was recorded. For articles published after April 6, we also analyzed whether the Lancet article was mentioned.

For the 2 newspapers with the highest circulations, the 6-month period preceding March 20, 1996, was also analyzed.

Overall, 535 articles on the mad cow affair were published during the study period in the newspapers considered; 62 (11.6%) of them appeared on the front page. A total of 5 articles on this subject appeared in the 2 newspapers with the highest circulations during the 6 months preceding the study period.

On March 21, 1996, the day following the first statement on v-CJD, 2 newspapers each had 1 article on the mad cow affair. In the days that followed, the overall number of articles, and the number of those appearing on the front page, rapidly increased. The peak of press coverage was recorded on March 26, 1996, with a total of 48 items; at least 5 items, including 1 on the front page, appeared in each of the newspapers studied. The newspaper attention to the subject decreased after March 31, 1996, and no further peak of press coverage was recorded after the Lancet publication ( Figure 1 ). During the study period, 72% of all the articles and 89% of those appearing on the front page were published before the Lancet publication.

The median proportion of page occupied daily by the articles on the mad cow affair was 0.63 in the first week and 0.43 in the second week of our study. It dropped to 0.10 in the third week, and remained below this figure in the following 5 weeks.

Overall, 50 articles reporting at least 1 of the 6 characteristics of v-CJD were published in the 7 newspapers during the study period, and 46 (92%) of them appeared before April 6, 1996. After the Lancet publication, only 1 article reported 2 findings not reported before. Publication of the article on v-CJD in The Lancet was mentioned at least once by 3 of the 7 newspapers. Finally, 27 articles containing an interview with a scientist were identified; 21 (74%) of them were published before the Lancet article.

Our results show that the mad cow affair had a great impact on the press in Italy, and this finding is not surprising if its potential public health and economic importance is considered. 8

However, this impact was concentrated during the 2 weeks that followed the first announcement on the emergence of v-CJD. The attention of the Italian press had already decreased by the time the Lancet article was published and no further peak of press coverage followed its publication. Moreover, 4 of the 7 Italian newspapers studied did not mention the Lancet article.

Journalists apply 2 tests to any piece of information in the field of science and medicine: is it genuine, and is it news? 1 The information presented in the peer-reviewed article should be expected to have a higher scientific credibility for journalists than the official announcement that started the affair. However, the time period between the first news release and the scientific article publication (slightly more than 2 weeks) could have been a long enough time span to determine that the information on CJD had already partially lost its newsworthiness by the time the Lancet article was published.

These data suggest that when a peer-reviewed scientific article on a health risk is published after this risk is disclosed to the public by other means, its impact on the media is low. However, some limitations of this study must be considered. First, we did not analyze coverage patterns of other news media such as television, although there is evidence in Italy that in other cases of emerging health risk, television coverage follows the same pattern as newspapers (Carlo Fido, oral communication, 1998). Second, the case we analyzed was characterized by the potential of significant and immediate implications for public health; therefore, our results cannot be generalized to the routine publication of peer-reviewed research.

The lack of synchronicity between announcement to the media and full publication of scientific data may negatively affect the quality of information conveyed to the public.

In the case we analyzed, scientists were asked by the press to give an expert opinion, most often during the period of maximum mass media attention, when most of the scientific information on v-CJD was conveyed by newspapers to their readership. Moreover, physicians may have been asked by their patients to give out more detailed information about a possible new health hazard, as reported in similar situations. 9 However, the possibility for scientists and physicians to provide to the public a balanced view of this emerging problem could have been impaired by the fact that most of them did not have access to full scientific data eventually reported in the peer-reviewed article. 10

To improve the communication to the public and within the scientific community in the case of emerging public health risks, 3 points should be considered. First, research work with potential public health implication should be promptly submitted to peer-reviewed journals, without delays because of political or economic considerations. Such delay in submission apparently occurred in the v-CJD article. 11

Second, scientific journals should expedite the peer review and publication process as much as possible in these cases, for example, by providing a fast track for articles with relevant public health implications. 12 Improved coordination between news release by public health authorities and scientific publication by peer-reviewed journals should also be pursued.

Third, peer-reviewed journal editors should consider placing articles with potential public health implications in Web sites. In an era in which information on health matters is disseminated rapidly by the media, circulation of information within the scientific community should be at least as fast, while preserving the quality and reliability of scientific journals.

Girardi E , Petrosillo N , Aloisi MS , Ravà L , Ippolito G. Peer-Reviewed Articles and Public Health : The Mad Cow Affair in Italian Newspapers . JAMA. 1998;280(3):292–294. doi:10.1001/jama.280.3.292

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Chronic wasting disease linked to Fort Collins for 50 years

“Watch your step for rattlesnakes," Mike Miller cautions as he unlocks a squeaky gate that leads to a fenced field of dried, knee-high grass on the western outskirts of Fort Collins. “We usually don’t let anyone in here anymore."

Here, on Colorado State University's Foothills Campus sits a dilapidated animal pen that appears untouched since scientists discovered the mule deer they were studying were unexpectedly and mysteriously dying.

Researchers were baffled. Why were seemingly healthy deer taken from across Colorado's wilderness turning thin and wasting away toward premature death?

“The reaction to it, quite honestly at the time, was just frustration because it kept ruining good research experiments,’’ says Miller, Colorado Parks and Wildlife senior wildlife veterinarian, whose office is a short walk from the pens where the deer were dying. “The deer didn’t live long enough.’’

That was in 1967.

A half-century later, chronic wasting disease, a mysterious malady intricately tied to Fort Collins, is stirring renewed anxiety as federal officials study once again its potential to spread to humans.

This tale of a disease killing deer and elk across Colorado, Wyoming, Nebraska and pockets of other states is one few have heard. That could all change given recent research that suggests this disease has greater potential than originally thought to cross genetic barriers to harm humans .

Mad cow outbreak spreads first wave of fear 

As researchers remained perplexed for more than a decade following the 1967 discovery, the disease marched on mostly undetected, killing wild deer and elk while spreading to commercial game farms and in zoos across the United States and in Canada.

Then in February 1978, a breakthrough was made in the so-called wasting disease case. And it was unsettling.

The late Beth Williams, a veterinary pathology resident at Colorado State University, identified the disease as a transmissible spongiform encephalopathy (TSE). The always-fatal disease in deer, elk and to a lesser extent moose is caused when proteins go rogue, causing a deterioration of the central nervous system, slow emaciation and an ultimately ugly death.

Soon thereafter, researchers discovered chronic wasting disease in mule and black-tailed deer at the Wyoming Game and Fish Department’s Sybille wildlife research facility and soon thereafter in wild elk and deer in Colorado in 1981.

The genie was out of the bottle.

More: Fort Collins resident contracts West Nile virus

More: Colorado State-based researchers push closer to universal flu vaccine

“I was concerned, but we really didn’t know what to do, and initially no one really cared about it in Colorado because it was an odd disease in deer and not correlated to BSE (bovine spongiform encephalopothy, or mad cow disease),’’ said Terry Spraker, pathology professor at CSU. “Then it was found on the Western Slope and in commercial game farms, and that affected elk guides and commercial facilities and that got the governor wanting to test about all the animals (for the disease).’’

More: Why this deer disease could change the way Americans hunt forever

More: Beaver tests positive for tularemia at Rocky Mountain National Park

While the disease's initial identification meant little to people other than researchers, its relationship to a disease that a decade later would kill humans in Great Britain gained international attention.

Williams’ discovery of chronic wasting disease, as the disease became known, was related to scrapie in sheep and goats, mad cow disease in cattle and the fatal variant Creutzfeldt-Jakob disease in humans.

In the 1990s, variant CJD killed more than 200 people in Great Britain who ate tainted meat from cattle that were fed byproducts of animals infected with mad cow disease, which was discovered in cows in the 1980s. The disease is similar in some respects to Alzheimer's in that both are classified as prion protein diseases where dementia is followed by death. The feeding practice was banned and mad cow disease cases subsided.

Still, fear of an outbreak of variant CJD occurring in the United States from people eating deer, elk and moose infected with chronic wasting disease persisted.

While researchers in the U.S. couldn’t outright discount an outbreak in humans, it didn't seem plausible that eating meat from animals suffering chronic wasting disease would lead to an outbreak of a disease similar to variant CJD. Health experts found no uptick in the disease in the U.S., not even among hunters — the number of cases held steady, with about one in a million Americans infected.

The spread of chronic wasting disease in deer and elk prompted an increase in research, which to date is around $100 million, including $20 million in Colorado. That research has solved some of the mystery of the disease, but many unanswered questions remain.

And much of that research was spearheaded in Fort Collins by Miller; Spraker; Tom Hobbs, senior research scientist at CSU; as well as in Wyoming by Williams, who first heard of wasting disease in the 1970s as a CSU graduate student.

Did chronic wasting disease originate in Fort Collins?

While leaning against the pen at the CSU Foothills Campus, Miller is quick to point out that chronic wasting disease was first discovered in Fort Collins, but that doesn’t mean it started here.

“This is the place where the term was first coined, but the rest is urban legend of how it started here,’’ Miller said. “Using that same logic, then AIDS started in the U.S., which it didn’t. It was first diagnosed here but it started in Africa.’’

But Fort Collins remains linked to the disease.

Gene Schoonveld, a retired Colorado Division of Wildlife senior wildlife biologist who lives in Fort Collins, knows why.

More: 'Friendly' elk near Boulder worries Colorado Parks and Wildlife officials

Related: Colorado blessed with fabulous diversity of wildlife

When the disease was discovered, he was conducting experiments on mule deer in those pens to help them survive starvation during harsh winters. He said about a dozen mule deer were brought in from various areas of Colorado. He believes the deer might have already been infected.

Another hypothesis, he said, is the disease might have crossed species. CSU was conducting scrapie research on domestic sheep and the sheep and deer were together in pens at times.

“We can’t prove either one, and Mike, Terry and I will probably go to our graves never knowing what really happened,’’ Schoonveld said.

While they didn’t know how the disease got to Fort Collins, researchers began discovering by the turn of this century that the disease was spreading. In some hot spots, nearly half of wild adult male deer, or bucks, were infected.

Chronic wasting disease was also spreading among commercial game farms. Quarantines stopped the transfer of captive animals between facilities and zoos. Those restrictions, atop captive animals dying from the disease, crippled the commercial game industry.

Miller and Spraker concur there are likely several ways the disease has spread.

For certain, they said, the disease was spread through transportation of infected animals by commercial facilities and zoos. Some infected animals escaped, and some came into contact with wild animals entering their pens, thus spreading the disease.

Strict regulations on moving captive animals has greatly reduced that mode of contagion, Miller said. So has a ban on giving wild animals protein blocks containing rendered animal byproducts tainted with the disease.

There is also a theory of scrapie crossing over from sheep to wild deer, elk and moose.

“We don’t know all the ways it can be spread, and you could spend a lifetime pondering explanations and never come up with the answer,’’ Miller said.

Research can now explain that the disease is spread among wild and captive deer, elk and moose through saliva, blood and waste, and can persist in the soil — especially the clay soil largely found in Colorado — for long periods of time.

Efforts to find a vaccine to prevent the disease have proved unsuccessful. Management strategies to control infection rates have been met with resistance.

In Colorado, studies around Fort Collins have shown aggressive hunting pressure and/or culling of deer, especially bucks, has reduced the infection rate. But that strategy has been unpopular with some landowners, hunting guides and hunters who covet large bucks.

To date, the disease has not been found in cattle.

Miller said the best hope now is managing the disease so it doesn’t kill deer and elk in such large numbers that herds are reduced to sizes too low to allow hunting. That would be a problem for Colorado, as big game hunting, which recently started, annually draws hundreds of thousands of hunters who have an annual economic impact of around $1 billion, including $38 million in Larimer County, according to a 2014 Colorado Parks and Wildlife survey.

Opposing findings rekindle human infection fears

Years after chronic wasting disease research largely disarmed the public about a risk to human health, the disease continued its slow but steady in deer and elk.

Then, there came a bombshell.

Preliminary results from an unpublished Canadian study released last year found that three of five macaque monkeys contracted CWD when fed the equivalent of a 7-ounce steak of deer meat tainted with the disease once a month for three years.

A similar study conducted by National Institutes of Health in Montana found macaque monkeys did not contract the disease.

According to the NIH, macaques often are used to model human protein diseases because they are genetically similar and susceptible to several types of diseases known to infect people.

The results from the Canadian experiments caused health agencies enough concern that the U.S. Centers for Disease Control and Prevention posted this on its website:

“The reasons for the different experimental results are unknown. To date, there is no strong evidence for the occurrence of CWD in people, and it is not known if people can get infected with CWD prions. Nevertheless, these experimental studies raise the concern that CWD may pose a risk to people and suggest that it is important to prevent human exposures to CWD.’’

More: Bacteria spread through dog saliva linked to death of Wisconsin woman

More: Worried about hand, foot and mouth disease? Here's what you need to know

Health experts have long recommended people not eat tainted meat and for people to protect themselves from coming into contact with certain parts of deer, elk and moose when field dressing them.

As a scientist, Miller acknowledges you can never rule out a disease crossing species. And he agrees people should reduce the risk of exposure. He continues to research chronic wasting disease because he said reducing its occurrence in animals reduces humans' risk of exposure.

Still, he said he has cut his hand with a clever used to examine infected deer and has likely unwittingly eaten infected wildlife.

“I don’t want to be dismissive, but I don’t think about (becoming infected) a lot,’’ he said. “I don’t drive without a seat belt, some do. It’s a personal choice.’’

Schoonveld, 81, said he is pretty sure he unknowingly has eaten infected deer and likely fed it to his family. He would be much more careful now.

While he’s unsure if he will contract variant Creutzfeldt-Jakob disease, he knows one thing.

“Can you imagine what would happen if the monkey research simulated in the human population?’’ Schoonveld said. “I do. It would be hell on wheels.’’

5 important things to know about chronic wasting disease

What is chronic wasting disease?

CWD is a fatal neurological disease found in deer, elk and moose. It belongs to a family of diseases caused by prions (abnormally shaped proteins). This particular prion attacks the brains of infected animals, causing the animals to display abnormal behavior, become uncoordinated and emaciated, and eventually die.

Where is CWD found in Colorado?

CWD has been found in deer, elk and moose herds in various locations in Colorado. About half of Colorado’s deer herds and one-third of the state’s elk herds are known to be infected. Deer are about twice as likely to be infected as elk. In deer, bucks are twice as likely to become infected as does, but in elk, the infection rate is the same in males and females. Moose are infected at low rates.

Where else is it found?

It is found in 23 states and two Canadian provinces (Saskatchewan and Alberta) in the wild. Those states include Colorado, Wyoming, Nebraska, Utah, New Mexico, Montana, South Dakota, North Dakota, Kansas, Texas, Iowa, Missouri, Arkansas, Minnesota, Michigan, Wisconsin, Illinois, Pennsylvania, Maryland, Mississippi, New York, Virginia, West Virginia and the provinces of Alberta and Saskatchewan in Canada. The presence of CWD in captive locations includes several more states and provinces. It's found as far away as Norway, in reindeer, and in Korea.

Is there a risk to humans?

Disease in humans resulting from exposure has not been reported to date. However, there may be a small risk from eating meat from infected animals. Public health officials recommend that people avoid exposure to infected animals. The disease does not appear to be transmissible to cattle.

What CWD precautions and preventive measures should hunters take?

To minimize exposure, Colorado Parks and Wildlife and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When field-dressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord. Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat.

Why should people be concerned about CWD?

CWD poses a significant threat to the future health and vitality of captive and free-ranging mule deer, white-tailed deer, elk and moose populations throughout 26 states and provinces in North America. A growing body of evidence suggests that unchecked epidemics can impair the long-term population of affected herds.

Chronic wasting disease timeline

1967: Wasting syndrome is observed in captive mule deer at the Colorado State University wildlife research facility in west Fort Collins.

1975−81: Wasting syndrome is observed in Toronto Zoo mule deer transferred from the Denver Zoo.

1979: Recognized in captive mule deer at Wyoming wildlife research facility.

1981: Detected in wild elk in Colorado.

1985: Detected in wild mule deer in Colorado and Wyoming.

1996: Detected in a captive elk farm in Saskatchewan; 38 other linked farms eventually found positive.

1997: Detected in captive elk facilities in South Dakota.

1998: Detected in captive elk facilities in Montana and Oklahoma.

1999: World Health Organization indicates no evidence CWD is transmissible to humans, but advises that exposure should be avoided.

2000: Detected in wild mule deer in Nebraska and Saskatchewan.

2002: Colorado establishes guidelines to minimize transport of high-risk carcass materials. First International CWD Symposium is held in Denver.

2002: Detected in captive elk in Minnesota, wild and captive white-tailed deer in Wisconsin and Illinois, mule deer in New Mexico and elk in South Dakota.

2003: Detected in wild mule deer in Utah.

2004: Detected in wild elk in New Mexico.

2005: Detected in moose in Colorado.

2008: Research indicates CWD may be a plausible explanation for local deer population declines in Colorado.

2010:  Detected in captive white-tailed deer in Missouri and wild white-tailed deer in North Dakota and Virginia.

2016: Detected in wild elk and white-tailed deer in Arkansas and wild reindeer in Norway.

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