Pigs

New Chimp Status and Strategic Swine

milhayser — Wed, 15 Jul 2015 12:56:55 +0000

New Chimp Status and Strategic Swine

As researchers continue to document the intelligence and emotional acuity of animals, beasts begin to look more like brethren, and food more like friend. On Pharyngula, PZ Myers shares a decision by the U.S. Fish and Wildlife Service that gives chimpanzees used in research the same endangered status as their wild cousins. According to Science, "organizations that want to continue working with chimpanzees will have to document that the work enhances the survival of the species and benefits chimps in the wild." PZ writes, "I want to see more studies done on our closest relatives — but it has to be done in a way that respects their right to live." Meanwhile, Greg Laden considers commonalities humans share with one of our preferred sources of animal protein—pigs. A new review of past swine research emphasizes that pigs have excellent long-term memories, comprehend simple symbols, demonstrate empathy, and are very social: they play with, help, and even deceive each other. Greg stresses that pig-human similarity is qualitatively different from chimp-human similarity, resulting not from close ancestry, but from parallel evolutionary histories—including an affinity for eating roots.

milhayser Wed, 07/15/2015 - 08:56

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Are we sure Ebola isn't airborne?

tsmith — Sun, 03 Aug 2014 14:36:47 +0000

Are we *sure* Ebola isn't airborne?

Since yesterday's post, several people have asked me on various social media outlets about the airborne nature of Ebola. Didn't I know about this paper ("Transmission of Ebola virus from pigs to non-human primates"), which clearly showed that Ebola could go airborne?

Indeed I do--I wrote about that paper two years ago, and it in no way changes my assertion that Ebola doesn't spread between people in an airborne manner.

Let me back up. The paper in question was an experimental study done in the wake of the 2008 finding of the Reston Ebola virus in pigs and a previous study looking at the Zaire virus in pigs. In the air transmission study, they inoculated pigs with Ebola and examined transmission to macaques (who were not in direct contact with the infected pigs). They did find aerosolized Ebola in air samples, and some of the macaques did come down with symptoms of Ebola. So, it looked like pigs could spread Ebola through the air, which is something that had already been suggested by the epidemiology of the 2008 pig Ebola outbreak. It's always nice when experimental data matches up with that observed during a real-life occurrence of the virus.

*However*, the kicker was not that Ebola is transmitted by air in human outbreaks, but rather that there may be something unique about pig physiology that allows them to generate more infectious aerosols as a general rule--so though aerosols aren't a transmission route between primates (including humans, as well as non-human primates used experimentally), pigs may be a bigger threat as far as aerosols. Thus, this may be important for transmission of swine influenza and other viruses as well as Ebola.

So unless you're sitting next to an Ebola-infected pig, seriously, airborne transmission of Ebola viruses isn't a big concern. (Perhaps this corollary should be added to this handy diagram examining your risk of Ebola).

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tsmith Sun, 08/03/2014 - 10:36

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Pigs don't wear pants.

Read it as sufficient number of pigs, humans or other potential hosts infected and living in close quarters for the above comment. Such mutation events are more likely in industrial farms

I would like to see some molecular epidemiology study of ebola virus

Considering the symptoms for a late-stage Ebola victim are heavy sweating, vomiting and diarrhea, I am not so sure that humans arent effective at creating aerosols at the height of infection.

Do we actually have data on the aersolization potential of humans at the height of infection, or are you assuming?

We have 40 years of epidemiological studies in humans and many experimental manipulations of various non-human primates.

If this ebola variant isn't airborne, how did more than 100 health workers outfitted with Biohazard suits contract the disease? It is pretty obvious, I think, that this ebola outbreak is spreading through the air.

HCWs are special cases. One, they're in very close contact with a variety of body fluids. Two, they don't always have access to the protective suits you mention. This outbreak has dispersed so widely that especially when it hits a new area, most workers will not have such gear, and that's typically when it's most lethal for doctors/nurses/etc. If it were indeed spreading efficiently through the air, you would expect other close contacts who live in proximity to cases to become infected at high rates. We just have not seen this epidemiologically, and if it were efficiently airborne, honestly the number of cases would be much higher than it is right now.

Ebola is a very bad disease but why that doctor that treat this disease must cover there body mostly there face when this disease isn't airborne? Moreover can this disease be transmitted by hand shake or by sharp object like needle,blade etc.....|

This is an excerpt from an update on the CDCs website. Correct me if I'm wrong but this sounds like the definition of a airborne virus (or bacterium) and the same words are used when describing airborne TB, influenza and others.

"Provide the sick person with a surgical mask (if the sick person can tolerate wearing one) to reduce the number of droplets expelled into the air by talking, sneezing, or coughing"

http://www.cdc.gov/quarantine/air/managing-sick-travelers/ebola-guidanc…

TJ Harvey @#7 - I think it'll be most telling to ultimately hear from Dr. Kent Brantly as to how he thinks he was infected. Since Ebola hadn't been seen in west Africa since 1994, facilities were underprepared administratively for such an outbreak. Patient intake was reported as chaotic and not well-controlled. All you need is one infected person running in from outside and you getting vomited on (often at your nose and mouth) for you to be infected when the suit is off.

Until the new virus is tested in human / primate scenarios, we will not know if this version of Ebola is spread via air. Any volunteers?

Drew, that is basic protocol for a lot of illnesses. Ebola also doesn't seem to be spread efficiently by fomites (inanimate objects such as doorknobs, countertops etc.) but using a mask like that will also minimize any fomite contamination and therefore exposure to others in numerous ways. Of course when transporting or caring for someone who is infected, they will always recommend an abundance of caution--understandably so.

"So unless you’re sitting next to an Ebola-infected pig"

So how does that not apply to half of africa? I have seen no mention of domestic animals being considered as disease vectors in current outbreak, even tho its known that most domestic animals can get infected with ebola and thus spread it.

Is it "not airborne" in the same way that norovirus is not airborne? (i.e. - can be ingested in the aerosolized droplets of vomit/feces if you're standing near the person when they get sick?)

Because norovirus is not technically "airborne" like influenza, but you can still become infected by breathing in the airborne vomit/diarrhea droplets of an infected person. If that's the case for Ebola, this article is not wholly truthful.

Following article from July 2014 in the same journal as the original article from 2012 relatives to pigs and NHP

http://www.nature.com/srep/2014/140725/srep05824/full/srep05824.html

#15 r2K, animals are usually considered as a possible source of an outbreak (eg an animal becomes infected by the bat reservoir, humans hunt/eat it, and become sick). It is theoretically possible domestic animals may also become infected by their ill owners but that doesn't really seem to be a factor once the outbreak is already underway.

Until someone in the know can make statements that do not contain "may be" (appears 3 times in the above 316 word blog) - I suggest assuming the worst and taking maximum precautions against infectious spread of ebola via all routes, including airborne..

Reality chick, again, theoretically that is possible, but you have to consider the difference in infectious doses between the two viruses and their route of entry into the body. It only takes ~18 viral particles for Noro to cause an infection, and typically the issue with aerosolized vomit and other materials is that they can land all over and then be ingested (landing directly on food, landing on fomites where food will touch, contaminating hands, etc.) Very different picture with Ebola, where it needs to be directly inhaled.

Lawrence, absolutely--and they are. Dr. Brantly arrived and has been transported in a suit and so were others working with him (http://www.nbcnews.com/storyline/ebola-virus-outbreak/ebola-patient-dr-…). An abundance of caution is always used. However, my point is that for the average Joe, even if Dr. Brantly were ill and next to you on a bus/train etc. (as happened with Patrick Sawyer, the American who died in Nigeria), you're at extremely low risk of contracting the virus. Thus, all the panic about bringing Ebola victims into the U.S. as if that were going to set off an epidemic are extremely overblown, and particularly those who are using the research article cited above to do so.

I am shocked, LITERALLY shocked, that no one--not a single person on here including the author(op)--has read "The Hot Zone". It was proven back in 1983 and 1986 by nancy jaax and eugence johnson thst ebola zaire was airborne. These two people both worked in level 4 biolevel labs at USAMRID in maryland. In the book both commented and proclaimed how monkeys came down with ebola without direct contact (no, pigs weren't even mentioned in the book at this point. It would take a minute to text their work, but feel free to read it yourself. Theh have known for years of its airbornw capability.

I've read the Hot Zone more than once. Please don't get your science from the Hot Zone. It's a great book and very entertaining but...dramatized. Please note the lack of any citations or references in that book as well. Or, frustratingly, an index. Do you have a page # for that so I can comment?

I understand that. My concern is how they word it exactly the same way for TB, influenza and others. They keep mentioning "air" in new updates which is what bothers me. Also the NIH has a document about how it can be aerosolized.

Set aside I want to thank you and all other health professionals for what you do. It's truly an honor the battle you all fight. It's the unknown and the extremely rare possibility of a mutation that scares me.

I also fear that the disease is airbone, if not, then how come its spreading so fast? 700 cases is a huge & a very serious number

So is evolution of the primate viral strain out of the question?

Pumia, it's actually more than 700 cases, but remember that is spread over (now 4) countries. There are more malaria cases than that every hour.

Drew, well, the news often gets things wrong. And sure, it *can* be aerosolized mechanically. That's a concern for bioterrorism--that someone would make Ebola in large quantities and somehow spread it via aerosols. Pretty much any pathogen can be aerosolized, but what I'm talking here is what actually happens during an outbreak, not theoretical manipulations of the virus. And multiple studies have shown that aerosol transmission just is not a factor in spreading this virus in human outbreaks.

Eric, I'm not sure what you mean by "primate viral strain."

I don't think this is correct. There are papers discussing human cases of Ebola and Marburg in which no direct contact with an infected person or animal can be shown. I will look for them as I've lost track of which ones they are.

Also, these are viruses we're talking about, which evolve faster than any known organisms. To some degree it doesn't matter whether or not there have been definite transmissions apart from direct contact, what matters is whether that potential exists, such as where different strains recombine in a carrier or host. That's exactly the concern with H5N1 flu and humans.

I´m no doctor like most of you but isnt the zaire strain (among others) quite likely to fail in its reproductions process? In other words, likely to mutate.

Isnt it just math. Eventually it will mutate and become airborne right? The most efficient strain at infecting new hosts will eventually be the prominent one.

So. If we dont already have more then one strain going its pretty likely that we will eventually, right?

We have never had such a large outbreak before, so the risk of getting a serious mutation is now larger then ever before and it will become theoretically larger for each new victim infected.

Then again, Im no doctor and I dont really know this stuff. But that was my theory anyhow. Please prove me wrong.

Best regards. Tobias

Jim, you are correct, there are. But that doesn't necessarily mean they are airborne--it just means there is a gap there and we can't definitively identify the source.

I'm well aware of the rapidity of viral evolution, but will point out again that this strain has been very stable over the 40 years that we've been observing it, despite it being an RNA virus. And again I'll ask if you think, then, that the same precautions should be taken with HIV? Also an RNA virus, also evolves rapidly, also transmitted by close contact with blood and body fluids. Do you expect it to become efficiently airborne any minute? If not, why not, and why the focus on Ebola in this manner?

Tobias, yes, it mutates. However, there is no inevitable path that the virus will take to become readily transmissible by air. Evolution is always a tradeoff between advantages to the virus and disadvantages experienced by the host, and whatever combination of factors that enables more efficient transmission to a new host will win over the long term. However, keep in mind that humans aren't really Ebola's host--bats are. We're incidental.

I am reading that the medical personnel in Africa wore BL3 suits and became infected. The returning Ebola-infected missionaries are now being handled with BL4 suits which have O2. Another interesting read:

"Why Aren’t Previously Successful Methods Used to Stop Ebola Working Against This New Strain?" (Pacific Standard) by Rebecca Buckwalter-Poza

Tara - It is true that some of the HCWs may not have taken the appropriate precautions. But we're talking about more than a handful of HCWs. Some of the top ebola doctors have become infected and died, and we can only presume they were aware of the dangers and were taking every possible precaution. Moreover, if you read journal entries of some of the HCWs you will notice that extreme precautions were being taken (rubber boots, gloves, biohazrd suits, masks, etc.) and yet in those entries HCWs were still reported as contracting the disease.

If you graph the progression of ebola cases (and deaths), you will see that the disease has been spreading at an exponential rate, with a noticeable upturn in the "hockey stick" in early June. The non-linear nature of the incidence rate suggests we are dealing with a virus that is more akin to an airborne flu than a "fluids exchange" virus.

Looking at the numbers you will also see that the fatality rate is presently around 50%, which is historically a low rate for ebola. However, you will also see that despite a lower fatality rate, the virus is infecting and killing far more people than any other ebola outbreak in history. In my opinion, this seems to suggest that this variant has mutated and is achieving increased transmission combined with reduced host fatality, which is a hallmark of evolving pathogens.

So in short, I'm very concerned at this point, and think it very unwise to assume that airborne transmission is off the table.

The elephant in the room is the possibility of weaponization - by US biowarfare or any number of other countries. Apparently, the US and other players were dead center of the outbreak in Sierra Leone...where they were conducting advance studies on ebola like fevers....

http://www.globalresearch.ca/what-are-us-biological-warfare-researchers…

I looked at the set up they have to transporting the two infected persons to the US.

It's basically a gutted Gulfstream III with plastic tent in it. The pilots do not wear Racal suits.

The pilots are either craziest or bravest people in the world.

TJ, that chart does look concerning, but if you look at the doubling intervals going back to March 25th, I don't think it's necessarily showing exponential growth that would be evidence of easy airborne transmission.

Starting with 86 cases on 3/25, the doubling period to 170 cases was only about 16 days. If the infection were spreading at an exponential rate, then you'd expect to see subsequent doubling periods of roughly the same duration.

But the next doubling took about 50 days. The next two doubling periods after that have each taken about 30 days - with 1200 total infections being reported on July 23rd.

My read on that is that the infection started out spreading rapidly in one location (Guinea), but once it was recognized and a response was organized, the rate of new infections began to slow... until it spread into new areas, Sierra Leone and Liberia, where the process of organizing a response and educating the population had to start all over again.

So that's a plausible alternate explanation for why you might see a "knee" in a curve that isn't necessarily demonstrating exponential growth - we may be seeing an uptick in infection rates when the virus appears in a new area.

With more data, which unfortunately is a certainty at this point, the picture should become more clear.

I am no scientist and I am no virologist, but I feel that the virus has either become airborne or has become MUCH easier to transmit. I am also horribly angry that the risk, no matter how small, has been taken to bring these people back into our country for treatment. I'm literally petrified to touch anything outside my home. I am going to go tomorrow and buy masks and gloves and hand sanitizer and bleach. My home is now a 'no one in' zone. All foods will be thoroughly cooked until nothing could have survived and water will be boiled and all items coming into my house will be cleaned with a bleach solution. Call me crazy, I don't give a damned, but I am protecting myself and everyone else should be too. Regardless if this woman says it mostly is not airborne. To me that means she doesn't have any more of a clue than I do.

"Eric, I’m not sure what you mean by “primate viral strain.”"

I mean the strain of the virus that has evolved to infect primates more specifically. I am assuming that there is not a single strain that infects all living hosts. The virus must evolve to different hosts at different rates depending on the virus life cycle, and this would lead to genetic differences that increase the infection rates of the virus within certain hosts. I am ignorant of the Eboli virus. My question is, more explicitly, why is the pig strain more easily transmitted? Is it due to a viral phenotype? Could the stain of the virus that infects primates more readily evolve to increase host-to-host infectivity?

Hi Tara,

Been reading your some of your papers on Staph aureus ST398, interesting reading…I'm a materials scientist not an epidemiologist thou. Been following the Ebola outbreak since March… With the numbers that we are seeing what do you think the possibilities of droplet transmission are?

I'm sorry Tara i just read your post of earlier today! Oops!

I know comparably nothing on the subject of VHF's and other viral pathogens compared to you but I agree with you about the possibility of increased transmission efficacy!

No, that was not by you but TJ Harvey…Coffee and wake up required…I'm not usually this dappy with my reading, honest!

Tara re. Nancy Jaax and transmission of Ebola zaire between monkeys with no direct contact, there was an article in the Lancet the abstract of which can be found here http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(95)92841…
And another regarding the aerosolized transmission of ebola zaire in rhesus monkeys can be found here http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1997182/pdf/ijexpath00004-0… (this is a full pdf version)

Rachel, if you live there you've already been an hour and a half away from Ebola, as it's been at the CDC since the 1970s. Nothing has changed so no need to panic. You may want to check out this post by Maryn McKenna, a reporter who covers infectious diseases and lives 2 miles away from Emory/CDC in Atlanta. http://www.wired.com/2014/08/ebola-1/

Chris, thanks--I've seen those before. Nice studies but still not what one would be exposed to during an outbreak situation unless, again, you're either a HCW or a family member of a victim--in which case odds are you'd have other exposures anyway.

TJ, to add to what Paul said, the epidemic curve alone doesn't show the route by which Ebola is transmitted. You can have the exact same curve for an infectious agent transmitted by air versus, say, oral-fecal. The curve will just tell you whether the outbreak is growing and if person-to-person transmission appears to be the reason why. We already know Ebola is transmitted person-to-person so the use of the curve is not as helpful in these situations (other than to monitor how bad it's getting in various areas in order to allocate resources).

Also, no one is taking airborne transmission "off the table." In every outbreak, a full work-up is done to figure out what can be done better, examine transmission, etc. That will surely be done in this case since it was so large and has so many complicating factors. If airborne transmission is shown to be a route of infection, that will be published and noted. But until that happens, inciting panic about airborne Ebola when years of studies and dozens of outbreaks have shown that type of transmission just isn't occurring in human outbreaks is irresponsible.

Eric, none have evolved "to affect primates more specifically." All are bat viruses which occasionally spill over into other animal populations (including primates).

Here's what I don't get. The argument is that the HCW who were infected just didn't take the right precautions or didn't have the right equipment available. However, some of these docs were leading Ebola experts. Not only did they know how to protect themselves, but they had (presumably) encountered the virus before, treated patients and never been infected. I'm assuming this of course, because I don't know how you become known as an Ebola expert without having treated Ebola patients. So what changed? Why did they become infected now? Something must be different in the virus to increase the infection rate and make the typical precautions ineffective in limiting exposure.

In response to Paul Anderson:

"Starting with 86 cases on 3/25, the doubling period to 170 cases was only about 16 days. If the infection were spreading at an exponential rate, then you’d expect to see subsequent doubling periods of roughly the same duration."

Except that there are reports speculating that family members are secretly burying their dead and failing to report some cases. As news of the outbreak spreads, there may actually be increasing numbers of unreported cases (due to fear, superstition, ignorance, political pressure, etc). Just because the rate of reported cases is not following a more aggressive track doesn't mean the reality matches the spin.

Tara, my heart goes out to you, having to deal with questions from all us laypeople, some of whom are pretty far out on the limb.

That said...;-)

What are the current best conclusions about:

1) Transmission via direct contact with a patient's sweat?
2) Transmission via contact with sweat recently deposited on fomites?
3) Transmission via any other bodily fluids recently deposited on fomites?

From those three points, we should be able to arrive at reasonable opinions about the risk of transmission under the conditions that people are worrying about in the US, such as if an Al Qaeda suicide terrorist got himself infected over there, came over here, and sought to spread it.

Re. HCW cases:

"In the field" precautions such as are being used in Africa, are less effective than the kinds of precautions we have at these special hospital facilities and in labs where dangerous bacteria and viruses are handled.

Per an interview on Public Radio, with a volunteer who had returned from Africa: Temperatures inside the field suits get up to 134 degrees, you're sweating rivers and it's getting in your eyes and causing serious discomfort, meanwhile you're trying to handle patients' IV lines and so on. The heat and dehydration alone make for compromised cognitive performance, increasing the chances of a fatal mistake.

OTOH, the systems in use at these hospitals include positive air pressure to the HCWs' suits, presumably air conditioned, and various measures to prevent dehydration and the like. If someone would publish a complete writeup about the safety precautions in use there, it would do much to reduce the anxiety and overt paranoia about this.

What I'm most baffled by is the fact that we even brought the cases here in the first place. My biggest question I'm left with is why didn't the doctors go to them? Is it because there were too many and that would be more difficult and dangerous? Because that seems rather preposterous.. They could've set up an isolation unit IN AFRICA but hey let's bring them here because there's "little odds of it spreading."

So Tara, you're absolutely positive that there is no possibility at all Eboila will not mutate to an airborne disease among humans?

I read this morning that four health care workers in Nigeria who attended to Patrick Sawyer have now contracted ebola. So are we to assume that there was an exchange of body fluids between Sawyer and four separate individuals? I really think it stretches credulity at this point to continue with the standard refrain that ebola cannot be transmitted through the air. At the very least, our health care experts should be warning the public that we simply not sure at this point.

Common sense tells me that if an animal can spread Ebola thru the air to another animal, then humans can possibly become infected from that animal with ebola from the air, which can possibly mutate at that point to an airborne disease. Am I right or wrong?

Too many uncertainties to just assume it is safe. I don't know why we would risk spreading an outbreak here...just doesn't seem logical to me. Why couldn't they treat the patients there? Fly all the equipment there and treat them in the plane on the tarmac, but to bring it back to Atlanta?! If you have to bring them back they why not Alaska? Why Georgia where the climate is more comprable to what you would find in Africa?

Ebola is not something anyone wants to expierience, and I wouldn't take anyones word on this not being airbourne. The real answer current signs point to it not being so, but noone knows for sure.

And for anyone to have much faith in the CDC is a bit ludacris considering the recent smallpox viles found "lost" in some storage closet. I don't feel too cozy...

Tara - If you extrapolate the current epidemic curve, you find that by June 2015 every person in the world will have caught this disease. Now we all know that this is impossible, but my point is that we are looking at very significant rate of exponential increase. I'm not a microbiologist, but I have a hard time believing that a virus that can only be spread by an exchange of bodily fluids would move at such a rapid rate.

It is true that no one is taking airborne transmission "off the table." So I apologize for my loose choice of words. But there can be no doubt that at present the overwhelming message coming from the media and its "popular scientists" is that ebola is not an airborne disease, that this is a typical ebola virus, and that for most of the world there is not yet a real concern. I think these are very dangerous assumptions to make.

You state that "If airborne transmission is shown to be a route of infection, that will be published and noted." So let me ask you a few questions on that point:

> What is the objective standard for making the formal, worldwide determination that this ebola is airborne?

> Who gets to make that determination? The medical establishment? The CDC? The UN?

> How is that determination made? Unanimity between a certain group of bureaucrats? A proclamation from the President? A majority vote from a panel of international scientists?

> What is the time table for making that determination? Do we give a week for debate? A month?

My hunch is that neither you, nor any other person in government, academia, or medicine, has any idea how to answer these questions. And that is a big problem because when dealing with non-linear, complex systems that enter positive feedback loops, you don't have the time to figure these things out on the fly. You don't have the time to engage in a debate about the evidence. You don't have the time to engage the bureaucratic process. You don't have the time to weigh your options. By the time you recognize that a positive feedback loop is in place and is becoming a threat it is too late to do anything about it. This is especially the case with a disease like ebola, where there is a significant lag in the time that it takes for the disease to produce visible symptoms in its victims.

So in closing, what I am saying is this: You and other experts will be proven correct about ebola until you aren't. And when you aren't we could very well witness the greatest loss of life in the last 10,000 years of recorded human history. When dealing with non-liner systems, nothing is gained (in the long run) by trusting that standard assumptions (all based on a very short historical period) will hold true. Nothing is gained by assuming a best case scenario. Nothing is gained by allaying people's concerns for the sake of preventing a panic. To the contrary, when dealing with a virus that could potentially kill the majority of human beings on earth, we should be assuming the worst, and should be taking every precaution available ensure that the world is protected should standard assumptions fail.

If we are so sure the virus isn't airborne, then how are so many ppl that were in contact with Patrick Sawyer now infected with the disease. We know once he collapsed they whisked him away to quarantine, they knew where he originated from. I doubt very seriously people in the airport where rushing over and getting in contact with his bodily fluids. They are terrified over there.

Don't get me wrong I'm not panicking nor do I believe this will turn into a worldwide pandemic. Anything of course is possible, but I choose not to freak out just yet. I am very curious though, we all know the government will not tell us right away if it is airborne or any real threat to the US. We are on a need to know basis as far as the government is concern. I understand in part, not wanting to panic an entire country.

TJ, instead of looking at the infection growth as a single curve, I think it makes more sense to look at the curves for each country where there has been an outbreak.

Each country has its own public health system and its own challenges in term of educating the population in how to avoid becoming infected, and each one started dealing with the problem at different times.

When you look at the data that way, the growth in Guinea looks linear, and the later outbreaks in Liberia and Sierra Leone, which are still in the early rapid growth phase are expanding more rapidly than the original Guinea outbreak, but also in a linear fashion.

I think it's the combination of those numbers into a single chart that creates the impression of an exponential curve.

Take a look at the charts at this link to see what I mean:
http://s697.photobucket.com/user/paulanderson27/media/Public/ScreenShot…

Scott, I haven't seen a good report on the level of experience some of these docs have. They're characterized as "leading doctors" etc. but they were in & from Sierra Leone & LIberia, countries which had never seen Ebola before. I don't know (and haven't seen) info on whether they worked in outbreaks previously in DRC or Uganda etc., but it's possible they were "leading experts" just because of this epidemic and had no experience previously treating Ebola. Just take some of those characterizations with a grain of salt for now.

G, yes, exactly re: suits etc. Re these:

"What are the current best conclusions about:

1) Transmission via direct contact with a patient’s sweat?
2) Transmission via contact with sweat recently deposited on fomites?
3) Transmission via any other bodily fluids recently deposited on fomites?"

1) risky. 2 & 3) uncertain. Fomites probably do play a role (bed linens, virus on protective gear/suits etc.) but it's tough to quantitate how much during an outbreak like this.

Re Nigeria, I've seen only 2 cases confirmed. http://www.lsmoh.com/news/lagos-confirms-another-case-of-ebola#.U-DYeYC… from 4 hours ago. Excerpt: "Idris noted that the occurrences of secondary cases disease was expected giving the nature of contacts these persons had with the patient from Liberia adding that this was because they were unaware of his status until the management of the hospital reported their suspicions to the State government."

Realist--"So Tara, you’re absolutely positive that there is no possibility at all Eboila will not mutate to an airborne disease among humans?"

I've never said that. I've pointed out the analogy to HIV. Why aren't people worked up about that "mutating to an airborne disease among humans"? Because it's biologically implausible. Not impossible, but unlikely. Same for Ebola. Some small amount of aerosolized transmission (usually mechanically) is not the same as saying Ebola is an airborne disease.

TJ, science works by reporting, evaluating, and re-evaluating facts and observations. There are already a number of publications on the West African outbreak. In 1999 there was an entire issue of the Journal of Infectious Diseases devoted to Ebola. It has nothing to do with a presidential proclamation and everything to do with weight of scientific evidence.

Scott, I agree that the reported numbers very likely understate the actual size of each outbreak.

But it's not the magnitude of the numbers that's of as much concern as the rate of change. In other words, let's say for the sake of discussion that 80% of infections are not reported.

If those infections were reported, that would change the scale of these curves, but it wouldn't necessarily change their slope.

If there's some reason to believe that the rate of reporting is dropping as time goes by and more effort is put in to tracking cases and educating the public, then that would be a reason to question the rate of change in the infection curves, but thus far I haven't heard of any reason why the reporting rate would trend in that direction.

The pig study is meaningless . The evidence to look at are the more than 100 medical staff and doctors who have contracted ebola while treating patients.
I could even ponder that the staff were at fault for mishandling urine and other bodily fluids. But not the doctors . They would not touch any of them without gloves.
This indicates that the ebola virus has mutated and now is airborne.

I am not a physician or scientist, but I think that most people here are making some serious errors in deduction. If the virus had become truly "airborne", meaning that it could spread in a similar fashion to influenza or the common cold, we would be seeing a dramatically higher rate of infection. For example, of all the people who came into contact with Patrick Sawyer while he was symptomatic, the first person to contract the disease was his doctor. None of the passengers who share the flights with him have been diagnosed positive.
You can argue semantics, but I think Tara has acknowledged the possibility that the HCWs could have been subjected to aerosolized (not airborne) infected fluids from their patients. This is much more likely than a true airborne mutation.
And yet another point which which I agree, is that we seem too ready to believe that this disease has become airborne, when so many other blood-borne viruses, like HIV, have not.
Is it scary? Hell yes! But I think the panic is going to hurt more people in this country than the Ebola outbreak ever will.

Re the comments in "Hot Zone" and airborne transmission-
It's been years since I read it, but I reread the section where Nancy Jaax relates that she believes EBOV spread via air from monkeys injected with the Reston strain to uninjected ones. In her quoted statement, she notes that monkeys "throw poop", literally, in such settings.

She showed, that when forced to inhale EBOV directly, that primates can be infected (Johnson, E., Jaax, N., White, J. & Jahrling, P. Lethal experimental infections of
rhesus monkeys by aerosolized Ebola virus. Int. J. Exp. Pathol. 76, 227–236 (1995).)

A more precise way to summarize the evidence is that while experimental airborne transmission to primates via an airborne route is possible only under very constrained conditions, the human epidemiology shows that practically, it isn't transmitted between humans by air. Absence of proof isn't proof of abscence, but well designed, controlled experiments in primates show "that airborne transmission of EBOV between NHPs does not occur readily, and ... suggests that the route of exposure may impact shedding and the subsequent opportunity for transmission"

Evaluation of transmission risks
associated with in vivo replication of
several high containment pathogens in a
biosafety level 4 laboratory
Judie Alimonti1*, Anders Leung1*, Shane Jones1, Jason Gren2, Xiangguo Qiu1, Lisa Fernando1,
Brittany Balcewich3, Gary Wong1,4, Ute Stro¨her1{, Allen Grolla1, James Strong1,4,6 & Gary Kobinger1,4,5,7

http://www.nature.com/srep/2014/140725/srep05824/pdf/srep05824.pdf

I totally get why people are concerned about airborne transmission, but it seems like it really isn't a thing.

I've yet to see any study that shows person to person airborne transmission. In lab settings, we've got pig to monkey, and monkey to monkey. This suggests that Ebola is reproducing at higher rates in different tissues in different species, and/or there is something about they way those non human animals are producing aerosols that is different.

There are, at the same time, a couple of studies that looked for airborne transmission in humans and ruled it out, along with the general observations of people in the field.

http://jid.oxfordjournals.org/content/179/Supplement_1/S87.short

Abstract: The surviving members of 27 households in which someone had been infected with Ebola virus were interviewed in order to define the modes of transmission of Ebola hemorrhagic fever (EHF). Of 173 household contacts of the primary cases, 28 (16%) developed EHF. All secondary cases had direct physical contact with the ill person (rate ratio [RR], undefined; P < .001), and among those with direct contact, exposure to body fluids conferred additional risk (RR, 3.6; 95% confidence interval [CI], 1.9–6.8). After adjusting for direct contact and exposure to body fluids, adult family members, those who touched the cadaver, and those who were exposed during the late hospital phase were at additional risk. None of the 78 household members who had no physical contact with the case during the clinical illness were infected (upper 95% CI, 4%). EHF is transmitted principally by direct physical contact with an ill person or their body fluids during the later stages of illness.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2536233/
Abstract:
Between 31 July and 6 October 1979, 34 cases of Ebola virus disease (22 of which were fatal) occurred among five families in a rural district of southern Sudan; the disease was introduced into four of the families from a local hospital. Chains of secondary spread within the family units, accounting for 29 cases resulted from direct physical contact with an infected person. Among all persons with such contact in the family setting, those who provided nursing care had a 5.1-fold increased risk of infection, emphasizing the importance of intimate contact in the spread of this disease. The absence of illness among persons who were exposed to cases in confined spaces, but without physical contact, confirmed previous impressions that there is no risk of airborne transmission. While the ecology of Ebola virus is unknown, the presence of anti-Ebola antibodies in the sera of 18% of persons who were unassociated with the outbreak suggests that the region is an endemic focus of Ebola virus activity.

Airbonre transmission in Ebola does not seem to happen at this time. There is no reason to think it would emerge as a characteristic of this disease, but there is also no reason to rule it out for the future. But there is also no way to assess the probability of that happening other than to say that it seems very unlikely with this kind of pathogen.

Now, put on your tin hats for a moment. Various military research units around the world have, it seems, looked a Ebola very closely. On one hand one might want to make a nice airborne version of it but, officially and (hopefully) more likely, one might want to assess the efficacy or possibility of that, in order to respond if the bad guys (whoever they may be) do so. As far as I am aware this led to nothing for Ebola. If Ebola could be made to be airborne, one might expect that there would be a USAMRIID response to that.

Also worth mentioning since the comparison is made here and there.. Influenza reproduces in such a way that the chance of a major genetic change in the virus is potentially very high. Ebola does not, I'm pretty sure.

Ok so the consensus I'm getting all over everything about Ebola is they are mistaking droplets being expelled by coughing and sneezing as being defined as airborne. From what I can tell that is not the scientific definition or a airborne classification. That's also where I got confused. I think people need to understand the difference between the two because it confused me along with almost everyone I seen about it. Education and not fear mongering should be our goal. Another ignorant response I see from people is why do they suit up in full gear when "it's transmitted the same as hiv". Being ex military who responded to CBRNe incidents we always dressed up to respond at the highest level until we can prove and justify lowering ppe. My conclusion is I think the lack of factual education is the number one problem in the US while the main problem in Africa is the lack of human resources and medical supplies/facilities. Since my first post I have changed my perspective about Ebola. Dangerous yes but awareness and proper ppe and proper decon procedures must be strictly followed as one mistake could lead to infection. Also I want to add that most people seem to think that the 2-21 incubation period means that people can be contagious without knowing it. According to cdc and WHO you must be experiencing symptoms to be contagious. Correct me if I'm wrong but that's where I'm sitting on the situation now compared to the earlier "i don't understand definitions but it sounds like they are saying it's airborne". Also reading that 2012 study the hot zone is seemed very flawed as a experiment.

I think I know where this problem is coming from:

People are confusing "aerosol" with "airborne." Aero as in aeroplane, and since aeroplanes are airborne, QED (mistake).

Therefore the following descriptions (I'm doing this from memory):

Aerosol: Sprayed into the air but NOT carried by air currents. Droplets, usually macroscopic, that can be sprayed into the air but rapidly fall out of the air onto surfaces. Think of someone spitting by going "pppppptooie!" and large and small droplets of spit landing on whatever is nearby. You don't generally inhale aerosols, but if the droplets land on your skin and get into an unprotected cut or scrape, or if you get them on your hand and touch your face, the infectious material can get to you that way.

Airborne: Sprayed into the air AND carried by air currents. Very tiny droplets, usually microscopic, that remain floating in the air and can be carried by air currents. Think of a cough or sneeze: you usually don't see the droplets spewing into the air but there they are, and there they remain, floating around to be picked up by anyone who is breathing nearby. Airborne particles aren't usually picked up through cuts and the like, but are usually picked up by breathing the air in which the particles are floating.

Is this useful?

Hi, thank you for your time. What about the following comments that this version of Ebola is not actually the Zaire strain?

"This particular strain of Ebola is not Ebola Zaire. This is a new strain, and it may in fact be more dangerous than the Zaire variety. Not because of any difference in the symptoms (the symptoms are identical), but because this new virus seems to be harder to contain. Whether this is due to some characteristic of the virus itself or merely dumb luck is uncertain at this time, but the rate at which this outbreak has extended its range is unprecedented.

According to the CDC this virus is genetically 97% similar to the Zaire strain. However if you are interested in this virus’ phylogenetic relationship (genetic lineage) to the Zaire strain you should look read “Phylogenetic Analysis of Guinea 2014 EBOV Ebolavirus Outbreak” on plos.org.

Another study by the New England Journal of medicine (this was the one referenced by the CDC) specifically names the parts of the genetic code which differ:

The three sequences, each 18,959 nucleotides in length, were identical with the exception of a few polymorphisms at positions 2124 (G→A, synonymous), 2185 (A→G, NP552 glycine→glutamic acid), 2931 (A→G, synonymous), 4340 (C→T, synonymous), 6909 (A→T, sGP291 arginine→tryptophan), and 9923 (T→C, synonymous).

Note that there doesn’t yet seem to be a consensus as to what this new strain is called. One study referred to it as “Guinean EBOV”, another as “Guinea 2014 EBOV Ebolavirus” and others are still referring to it as Zaire. Given that we can specifically name the points where the virus has mutated, using the old name is misleading. "

Source, which has further links to other sources: http://consciousmedianews.com/ebola-what-youre-not-being-told/

Unfortunately, some comments are being censored by the moderator.

However, regarding the aerosol issue - here are the definitions from the CDC:

Definitions
The following definitions are used in
the list of diseases and guidelines
developed pursuant to Section 2695[42
U.S.C. 300ff–131]:
Aerosol means tiny particles or
droplets suspended in air. These range
in diameter from about 0.001 to 100 μm
(Baron P, accessed 2010) (Baron PA and
Willeke K, 2001; 1065).
Aerosolized transmission means
person-to-person transmission of an
infectious agent through the air by an
aerosol. See ‘‘aerosolized airborne
transmission’’ and ‘‘aerosolized droplet
transmission.’’
Aerosolized airborne transmission
means person-to-person transmission of
an infectious agent by an aerosol of
small particles able to remain airborne
for long periods of time. These are able
to transmit diseases on air currents over
long distances, to cause prolonged
airspace contamination, and to be
inhaled into the trachea and lung (Baron
P, accessed 2010) (Seigel et al., 2007;
18).
Aerosolized droplet transmission
means person-to-person transmission of
an infectious agent by large particles
only able to remain airborne for short
periods of time. These generally
transmit diseases through the air over
short distances (approximately 6 feet),
do not cause prolonged airspace
contamination, and are too large to be
inhaled into the trachea and lung (Baron
P, accessed 2010) (Seigel et al., 2007;
17).
Contact or body fluid transmission
means person-to-person transmission of
an infectious agent through direct or
indirect contact with an infected
person’s blood or other body fluids
(Seigel et al., 2007; 15).
Exposed means to be in circumstances
in which there is recognized risk for
transmission of an infectious agent from
a human source to an ERE (Seigel et al.,
2007; 14).
Potentially life-threatening infectious
disease means an infectious disease to
which EREs may be exposed and that
has reasonable potential to cause death
or fetal mortality in either healthy EREs
or EREs who are able to work but take
medications or are living with
conditions that might impair host
defense mechanisms.

www.gpo.gov/fdsys/pkg/FR-2010-12-13/pdf/2010-31149.pdf

what I would like to see more of is how we CAN catch the disease?..for example..yes by direct contact with bodily fluids..ie..even sweat on a persons hand?..is that during the incubation stage..(is that 3 weeks from initial contact?)..or does the contact have to be in the later stages?..I am planning to go to Kenya soon to meet someone flying there ALSO from LIBERIA...He has had a medical and blood examination to clear him for leaving the country... but that was a week before he plans to leave!!!...when I meet this person should I avoid physical contact with him of any kind??

Denise - From what we know historically, a person is not contagious until the symptoms are present. At that point, all bodily fluids, including sweat, can carry the virus.
A lot has been said about this strain being harder to contain, which has led to speculation that something has fundamentally changed with the virus. People are claiming that it has to have become airborne, or may now be contagious during the incubation period. In reality, it is the same cultural and sociological factors that are contributing to the ongoing outbreak, compounded by the fact that it appeared in a region that was not used to handling Ebola outbreaks.
As long as the person you are meeting is not sick, you should be OK.

Wasn't there also a case in the 80s with monkeys? The monkeys spread it to each other through the air ventilation system. So it can happen with 2 different types of animals but never humans?

I think you're being too dismissive of the *possibility* of airborne transmission. There are some paper in the literature suggesting that it's possible. For instance, a study back in the 90s that found transmission among monkeys without direct contact.

The best way to state this is that airborne transmission is not likely. Not that it doesn't happen.

I think you're being too dismissive of the *possibility* of airborne transmission. There are some papers in the scientific literature suggesting that it's possible. For instance, a study back in the 90s found transmission among monkeys without direct contact.

The best way to state this is that airborne transmission is not likely. Not that it doesn't happen.

Andrew, 97% still makes it Zaire per naming conventions. That's pretty damn closely related.

Questions and concerns:
So, because Ebola symptoms appear to be just like influenza in the begining but Ebola has high fatality rates, and requires the medical staff who treat your symptoms to test something that presents the same way as the flu...more than likely, the medical staff will send you home with scripts for nothing and wont take it seriously, nevermind how dangerous it is or easily communicable to others who are lax about sanitation and protection..Just walk into any ER these days....unless you are bleeding profusely from an known accident, they dont wear masks, the dont wear gowns, it is all "business as usual".. Why would they test vomiting and diarrhea and dehydration symptoms as anything other than common ailments, with a special Ebola test that they are unfamiliar with? They WONT until it is TOO late and many others are exposed.

i still struggle to understand how intelligent american health workers who know EXACTLY how to avoid contamination, know EXACTLY how to use safe hygiene, wearing max security hazmat suits or whatever, still caught the virus if it's not airborne. i refuse to believe either of them directly touched an ebola patient without protection.

if the ebola patient coughs on his hand and then turns a door knob, can i catch it by touching the same door later? that's just as bad as airborne to me. elevator buttons, bathroom door handles, stair rails, hand shakes... we are an unsanitary society. this virus will spread like wildfire if it gets out and can be transmitted this way.

not just cough on hand. i meant anything.. wipe sweat from forehead, suck their thumbs, etc.

My two cents on the "how can the HCW get infected if they were wearing PPE" issue - We dont know just how closely they are following their protocols, and they are putting themselves at risk every time they come in to contact with these patients. Ebola is so infectious that it only takes a tiny glove tear, improperly sterlized equipment, or other small mistake, to become infected. In a high stress environment such as that, human error is highly probable and even the "experts" are at risk.

Amber, the 80's case with the monkeys was the Reston strain, which does not cause disease in humans. Very different virus.

Paul, I'm addressing human to human transmission in the context of this outbreak. Note I said right in the opening story that it's "not a concern." Not that it never can happen, but that it's rare enough that it's never been documented in humans to date, that experimentally it's rare even in animal models--hence, not a concern.

Andrew, they are doing this already. There have been reports from all over the country of possible patients being tested, including one in my neck of the woods in Ohio. It's more likely they're going overkill on this than missing cases with obvious symptoms.

"me" #82, except that they're *not* using "max security hazmat suits" or anything of the like in most of the hospitals/clinics. They're using suits but they're really just to keep off most of the fluids. Sometimes these are even washed/reused. It's very basic protection and sometimes it's not enough. Plus I noted earlier the issues with how hot the suits are, they can be claustrophobic, doctors and nurses are tired/overworked, etc. It doesn't take much of a lapse to expose one's self, unfortunately.

I appreciate your cogent explanations, but wish you'd stop using HIV as a counter-example. HIV when first identified was the subject of the same hysterical fear-mongering that we're now getting about Ebola from certain quarters - the American obsessions with doorknobs, toilet seats, and skin color were on full display. But HIV is actually far harder to spread. A news story has claimed that after the index case for one local outbreak took a long bus ride to the city where she was hospitalized, four or five of her fellow passengers came down with Ebola. That suggests not airborne transmission (otherwise there'd be a million cases, just like in flu epidemics), but pretty darn effective aerosol transmission. If you're in a vehicle with a guy with AIDS and he happens to have a stomach bug and vomits near you, you simply aren't going to catch HIV. I agree that the precautions they're taking at Emory are quite adequate, but the cheery statement one physician offered a while back that you'd be safe sitting on the bus next to a sick person doesn't seem to be true, at least in this outbreak.

Tara, thank you for your efforts and patience here. You are a hero for dealing with general scientific illiteracy and a freakin martyr for attempting to deal with conspiracy theorists. This has been a very informative article and Q&A. Thanks again!

Jane, yes, and in Africa Ebola is carrying the same or worse stigma because of all the misinformation. I've not seen that news story but I'd caution against some of those--there is, again, a lot of inaccurate information that is out there in the early days, and after actual scientific study, ends up getting rescinded. I'm also talking about the *evolution* of HIV--it's currently a blood-borne pathogen like Ebola, so why aren't people freaking out about its potential to become airborne? It is a more mutable RNA virus than Ebola is, which is my point on that comparison.

Tara

It takes 18 particles to infect with the norovirus.... How many particles does it take to infect with Ebola?

Tara

Sorry left some details out let me rephrase the questions.

1) It takes only 18 particles to infect with a Norovirus GII.4. Genotype so how many particles does it take to infect with the Zaire strain of Ebola or do we know?

2) what are the particulates exactly?

3) and thank you for shedding some much needed light as to the mechanical heavy aerosols humans make but more talk is needed. There are only a few studies I have found on human sneeze on aresolization but the best one suggested that some of the particulates (saliva droplet) could be airborn for hours. Explain the relationship to the up to 40,000 droplets especially the smaller ones that come rushing out nearly 100 MPH and how these particles suspended potentially for hours are not infectious?

Thanks again for your commitment to the science, the truth.

Jerry L

Tara, never mind HIV; why aren't we freaking out about airborne rabies or airborne HPV (hardly deadly, but an American peur du jour just the same)? Because there's been no indication that these viruses can ever be dispersed into the air, enter an intact human body, and cause infection. Same for HIV. I, not a virologist, would have assumed that just like some plants wouldn't survive in the desert no matter how much selective pressure to do so they might experience, some viruses just won't ever go airborne. But even if you assume there's no such thing as a virus that couldn't somehow become transmissible by respiration and tough enough to survive on surfaces, if a given virus isn't even aerosol-spread, it's a long, long way from being airborne.

I don't know that "scientific study" is either needed or possible in the case I asked about, unless by that you mean "waiting to hear results of final diagnostic tests, should those ever be publicized". It's either true or false that five bus passengers near this woman fell sick. If it's true, that's reason enough for people in the region to be uncomfortable sitting for long next to someone who looks acutely ill. The stigmatization of people who have had Ebola and recovered is a real shame, but where avoidance of sick people is concerned, you can't expect people to be comfortable possibly exposing themselves to a disease with a 55% to 60% mortality rate just because official experts have not yet definitively confirmed that they'd be in danger.

I just read that there are now eight health care workers in Nigeria who came into contact with Patrick Sawyer and died from ebola. This seems to suggest that this variant of ebola is highly transmissible, whether it be by air or even very slight contact with a victim's fluids.

Honestly, at this point the difference between airborne transmission and highly contagious droplet transmission is largely semantic. If this ebola virus is so contagious that it can be contracted by very slight contact with a droplet (e.g., touching a contaminated door handle, pen, or credit card) - which seems to be the case - then we are dealing with a very serious worldwide threat, and serious countermeasures need to be taken now.

TJ - I read that Patrick Sawyer urinated on his nurses when they told him he had tested positive for Ebola. If true, it seems the most likely reason they got infected, not from exposure to single droplets of fluids. Sensational stuff, but no more so than all of the uncertainties and half-truths that are being reported out of Africa.
Whether the urination story is true or not, it seems likely that Mr. Sawyer was in denial about the cause of his symptoms, and had dangerous contact with others while symptomatic.

I'll note for TJ and Jane that the WHO still, as of today, doesn't list any confirmed cases in Nigeria--so most of those which are being reported are still awaiting laboratory confirmation. Again, with cases like these, the news gets ahead of the science which is where a lot of misinformation comes from. http://www.who.int/csr/don/2014_08_06_ebola/en/

Jane - There are two or three rabies deaths per year in the United States. If we suddenly experienced 20 or 30 rabies deaths in a three month period would you be concerned? Would you be even more concerned if some of the victims hadn't been bitten by rabid animals, and had simply been in the same vicinity of other victims? Would you register alarm if there seemed no end in sight to the rapid increase in rabies deaths and we were on track for 10,000 deaths per year?

What we are witnessing in Western Africa is unprecedented in the history of the disease (by many multiples). To not recognize the reality that something has changed seems more motivated by wishful thinking than actual logic or reason.

The media, medical establishment, and governments, are uniformly repeating the refrain that this is typical ebola and that there is nothing to fear if you live outside Western Africa. But the message is so consistent, so (dare I say) nonchalant, and so seemingly contrary to the facts on the ground that many people are doubting the veracity of the message and are left suspecting the worst. A more balanced message - one that recognizes that something is very different with this particular outbreak - would do a much better job allaying people's fears and helping the world properly prepare for what might be coming our way.

I'm with TJ. The facts don't add up. This virus is spreading too quickly and infecting too many medical professionals. Last time I checked a person with HIV or rabies didn't infect their doctor and everyone that saw them when they went to the doctors office. Aerosolized transmission is likely IMO. Only a matter of time before it evolves to full airborne. The world needs to quarantine west Africa immediately, though it might be too late.

TJ, what you are minimizing is the behavioral aspects. Yes, unprecedented--but we simply cannot jump to the conclusion that it's because somehow, the virus has changed. Much more likely (& based on historical precedent) that large outbreak is due to fact that it's multi-national, in places that have never seen Ebola before (and thus are untrained & inexperienced), in countries with weak governments & infrastructures because of years of civil wars and instability.

Scared, actually, people with HIV have and do infect medical workers. The difference is that now we have protocols in place if workers get exposed (eg needlesticks) and we have drugs to treat/control HIV infection. We don't have that for Ebola.

I'm still not buying it. The comparison to HIV infecting workers isn't comparable - you're telling me a person with HIV can get off an airplane and infect 8 people they came into contact with that cared for them? Not happening. The story about him urinating on the nurses and that's how they got infected is ludicrous.

As far as poor facilities/training being to blame, the previous high for outbreak in Uganda (I think) was 430 cases or something....is Uganda a shining beacon of healthcare and safety protocols and that's why the otubreak was limited? I don't think so.

Hi Tara,

Thanks for this post. You've done a great job addressing the issue and answering questions and comments. The more one looks at the popular media frenzy now occurring, the more one appreciates a sane response like this.

Regarding comments 32 and 34, I do agree that, AFAIK, there are no confirmed cases of aerosolized transmission. And even if there were a few such, this transmission mode would pale by comparison to direct contact with the symptomatic and/or their body fluids. This is very fortunate and it's definitely very important that people realize this, so as to avoid elevating the panic level even more than it already is. My point is simply that we cannot fully rule out this mode of transmission (which I think you agree with), even in the present, and definitely in the future.

I need to read that Science Reports article you reference, which I'd not seen before, to see what it says about the difference between pigs and humans w.r.t. clinical pathology and transmission mode, because that's a big concern, obviously, w.r.t. the possibility of genetic recombination of strains of potentially different transmission modes. Regardless, I think it's important to remember that the Filoviridae are still negative sense RNA viruses, and hence require RNA-dependent DNA polymerases, which have high copy error rates compared to DNA-dependent polymerases. This does not promote stability.

Here are a few references that discuss the possibility of airborne transmission. None are definitive, they just discuss the possibility. There are more, including some for Marburg, but I ran out of time tracking them down.

1. Gatherer, 2014, (in press). The 2014 Ebola virus disease outbreak in west Africa, lines 185-198
http://vir.sgmjournals.org/content/early/2014/05/01/vir.0.067199-0.short

2. WHO RISK ASSESSMENT, Human infections with Zaïre Ebolavirus in West Africa, 24 June 2014.
pg 4, "Evidence of human-to-human transmission"
http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&…

3. Roels etal 1999. Ebola hemorrhagic fever, Kikwit, Democratic Republic of the Congo, 1995: risk factors for patients without a reported exposure
http://jid.oxfordjournals.org/content/179/Supplement_1/S92.full

4. Bausch etal 2007. Assessment of the Risk of Ebola Virus Transmission from Bodily Fluids and Fomites
First paragraph of discussion section regarding live virus in saliva.

5. Dowell etal 1999. Transmission of Ebola Hemorrhagic Fever, A Study of Risk Factors in Family Members, Kikwit, Democratic Republic of the Congo, 1995
http://jid.oxfordjournals.org/content/179/Supplement_1/S87.long
Table 2: "Exposures during late illness: Conversation"

Scared - The reason I brought up the urination story (and I agree, it is pretty ludicrous) was to highlight the fact that simply reading the stories published about this outbreak is not enough to really develop an informed and rational opinion. Added to this is the fact that Ebola is a virus that triggers a primal fear response in many people.
I think Tara has done a great job commenting on the specific, historical data that help explain how this outbreak grew to where it is now. Your reference to the previous high death total for an outbreak is actually relevant. The very first outbreak in Zaire (DR Congo) in 1976 killed 280 people. That was the first time it had ever been experienced in that country. Now it is in three countries (maybe four) where it has ALSO appeared for the very first time. That alone is enough to magnify all of the things that make an Ebola outbreak dangerous. There are no space suits, healthcare workers are overheated and overworked, and the locals are scared to death and threatening violence against the doctors trying to control the epidemic. It is already a perfect storm of awfulness, without the additional panic that somehow the virus has mutated and now we are all at risk.

Tara, let me thank you for your dedication to enlighten us and assuage our fears. I also want to thank the CDC for bringing our citizens back home to be treated. I too have read the Hot Zone ages ago, which is why I know it was the right coarse of action and the safest place to treat them as effectively as possible. Like others though, I am concerned about this outbreak. I do not believe that this particular strain of the virus has gone airborne. If it had gone airborne, then the infection rate would be exponentially higher than what it is now. I do not however, rule out short travel through the air by means you have already covered.
Notice how so many keep saying, something about it has changed for it to infect so many. They are correct. Ebola Zaire had a high (90% or so) mortality rate and a very short incubation period (24-48hrs if remember correctly) which is why it basically "burned itself out" once the world's health organizations stepped in. This slightly mutated version has a significantly lower mortality rate and a much longer incubation period which helps a pathogen spread more easily. One of the first symptoms people tend to miss when they become infected with almost anything, is a low grade fever. They tend to write it off to being hotter out or they're working harder than normal and think nothing more of it until other symptoms hit and they have a noticeable fever. But if this pathogen is like most, then even with a low grade fever with no other symptoms yet, they could be contagious if someone were exposed to their bodily fluids. So I think it is quite possible, it is being spread in the earlier stages before people realize what they are dealing with and seek medical treatment. Close family members are more likely to become infected. After putting their very ill relative in the hospital, they probably went to stay with extended family members or close friends that lived nearby not realizing that by this time, they themselves were infected, thereby giving the pathogen new hosts to infect and spread from.
From my understanding of infectious diseases, the lower the mortality rate and given a decent incubation period, the more likely it is to become widespread (not as widespread if it were airborne) before it became noticed. So, to me, it's not surprising that this slightly mutated version has infected so many. I'm just thankful that it's spread has been so slow as maybe this will give the CDC, NIH, and/or WHO the time to come up with something to effectively combat it before it takes too many more lives.

there may be something unique about pig physiology that allows them to generate more infectious aerosols as a general rule

I've worked with pigs as lab and farm animals. Pigs snuffle, snort and produce amazing quantities of snot (nasal mucus) even when they are healthy ... it's an adaptation to keep their nostrils clear of dirt when they are rooting for food. One big snort blows the dirt out, stuck in a glob of mucus.

Thanks for this. It's nice reading a professional opinion on the matter with some clarity about the pig/monkey report. I know many people who are freaking out about this. We hear the weird outbreak and think the world is ending. It is a very serious outbreak, but there are many factors that have made this outbreak worse, including lack of proper supplies, lack of doctors, and many people afraid of taking loved ones to the hospital (they don't trust them from past experiences, and they believe ebola to be fatal anyway, so they don't see the point in going).

As said before by others, I take my hat off in admiration for the health workers who selflessly and relentless strive to care for those currently affected by ebola… After seeing the WHO press conference regarding their declaration of International Emergency and the unavailability of experimental agents due to them being untested and in extremely short supply, I find this explanation a little weak. As if health care professionals didn't have a hard enough time over streched and battling 40 C heat in protective suits, they have no drugs to offer both to the citizens or to each other.

I just read a paper on an incredibly simple molecule which would be both cheap, easy to produce (in a reactor not a monkey) and has also been through phase I, II and III trials for Influenza viruses, H5N1 and others, which has shown at least some efficacy in small animal models. The drug, Favipiravir, showed suppression of replication of Zaire EBV (Mayinga 1976 strain) in cell cultures by 4 log Units and in type 1 interferon receptor lacking mice when administered 6 days post infection (2-4 days before death in control animals) prevented lethal outcome in 100% of mice. With the safety assessed in phase I trials already established and it's simplicity and low cost to make I wonder why this is not on the table to establish its efficacy in health workers and patients at this current juncture in the proceedings?

It is nice to see that someone actually conducted a follow-up study to the 2012 Canadian Pig-to-Monkey study. Seems that everything we are speculating about pigs being more likely to spread droplets may be correct. https://www.sciencenews.org/article/airborne-transmission-ebola-unlikel…

yes. I have a post on that ready to go but was waiting on a comment from the senior author. I'm guessing that probably won't be forthcoming though...

Tara, I think it's awesome you posted this AND also follow up, patiently answering concerns. Thank you for doing this and for the education.

Question(s): Can the virus (or any virus) be spread by both bodily fluids AND be airborne or aesolized? Can they have multiple modes of transmissions? Can mosquitoes be spreading this current form of Ebola?

I have read every single comment and your answers Tara. Thank you so much for giving straight answers to difficult questions in such a way that I now have more insight into this disease than any news article, WHO or the CDC have given us up to now. And thanks to others who have posted on here who actually KNOW what they are talking about.
THANK YOU TARA!!

Dr, Smith, thank you so much for the great information!

And PEOPLE, PEOPLE...calm down. Like I told my dad twenty years ago, if AIDS was as easy to get as the common cold, it would spread just as quickly as the common cold.

I'd still love to know why ZMapp and TMK Ebola, both I think yet to complete Phase I trials, and therefore without any proven safety, when Favipiravir has phase 2 completed and showed such promising results with EVD. It's cheap and simple to make, I mean damn, its got a molecular weight of 157.1, Ibuprofen's is 206. Any comment Tara?

There was some question about the number of confirmed cases in Nigeria. The CDC is reporting on August 9th that Nigeria has 13 suspected cases and 2 deaths. http://www.cdc.gov/vhf/ebola/outbreaks/guinea/ . The the health minister for Nigeria 2 days ago said there were 10 confirmed cases and two deaths. . http://www.theglobeandmail.com/news/world/nigerian-officials-announce-1…

So at the time of the story, Patrick Sawyer arrived in Lagos July 20th, so the maximum time that they had to be infected by him and show symptoms is 3 weeks. Frankly 10 confirmed cases from one guy is pretty astounding given that the transmission is bodily fluids. The article states that they were all close to Patrick Sawyer.

Dr. Smith,
I just finished reading hot zone. Let me clarify a couple of things. It is non-fiction. It is not dramatized. It is not a study by any means, therefore citations were not made. However he does quote many phd and md type people. In particular, Peter Jahrling Ph.D, who is the co-discoverer of Ebola Reston which was brought to the US by infected monkeys in Reston, Virginia, and is currently Chief scientist NIAID, emerging viral pathogens section, and who became, after the 1990 Reston outbreak, principal scientidt at USAMRIID. All four monkey caretakers tested positive for Ebola, only one of whom cut himself. They all recovered and were asymptomatic during their infection. Although USAMRIID did not do experiments to verify airborne transmission, it was clear that the monkeys transmitted the virus to each other through the air and hundreds of monkeys were euthanized in the Reston Virginia facility called Hazelton. The caretakers' viral load lessened and eventually disappeared.
Genetically, Ebola Reston and Ebola Zaire are almost identical, and appear identical under the electron microscope. This is what Dr. Jahrling said: ”Why is the Zaire stuff hot for humans? why isn't Reston hot for humans, when the strains are so close to each other? The Ebola Reston virus is almost certainly transmitted by some airborne route. Those Hazelton workers who had the virus- I'm pretty sure they got it through the air.” Reread the last section of the hot zone about the Reston outbreak and see what you think. For everybody else- if you want a vivid description of what ebola can do to a human being, without hyperbole, read the hot zone. It is a hell of a book. I challenge Dr. Smith to find a factual error in the book.

Harry,
I just read the study, and I agree with you. The sad truth is that Favipiravir is too simple, too cheap to manufacture, not profitable enough. Besides, Zmapp us being developed by a private company through some kind of development contract with the US army.

Rick, just because the Hot Zone may not contain few "factual errors" doesn't mean it's not dramatized. I love the book, but Preston chooses what facts to include and which to leave out, which overall leave the impression that things are much worse than they really are regarding the virus. Ask any Ebola researcher and you'll get the same answer--they cringe when anyone mentions "The Hot Zone" because it's NOT a textbook.

Thanks for your response Rick. Tara... What do you think about my previous post? Am I missing some vital facts perhaps?

WHO is now saying the virus counts may be substantially underestimated. http://abcnews.go.com/Health/wireStory/liberia-ebola-drug-ponders-24976…

SARS infected 8,000 people I think, Ebola has now infected potentially well over 2,000. Everyone that had close contact with Patrick Sawyer in Nigeria has become infected with Ebola. Still think it is not airborne?

Yes, I still think it's not airborne. As you note, close contact with Sawyer...not minimal contact (as in the airplane, airport, etc.) If that was the case you'd expect way more cases. Not surprising that the case count is also currently understimated--I've been talking about this on Twitter for days.

harry, sorry, day job calls. I'm not as familiar with the drugs so beyond the basics I don't have anything to add.

Nah, I don't think it's airborne either. Thanks for the reply Tara!

Ok, so we should be concerned of airborn Ebola if we are around pigs that have Ebola right? Well what happens if the West Africa outbreak gets worse as it appears to be doing so, not because of the deadliness of the decease but more so because of human fear and lack of education. As the disease spreads and more people get infected couldn't the chances of pigs get infected thus creating a spiral of new strains of the virus potentially an airborne version of the disease? I guess that brings me to one question, do West Africans eat pig? Apparently not but that doesn't mean there is some other animal out there that has to potential to do the same...

Ok here's a question Tara--why has our US Ebola gentleman been released into the general public if as the Canadian government asserts that Ebola can be transmitted via semen for up to seven weeks. This obviously puts his wife at risk--what if he had a mistress. The CDC who oversees these things should not take these blatant risks. Also has anybody else noticed from CDC reports that this disease is now doubling in number of cases in less than 30 days and accelerating. By that logic we could have 10,000,000 cases by this time next August. Something to consider.

Dr Tara, I read your article and ALL the comments and have to commend you on your handling of questions and queries thus far. Unfortunately there is breaking news of an unrelated outbreak in the Democratic Republic of Congo (DRC) where up to 70 people are reported to have died in the last 10 days of hemorrhagic fever. Out of 8 patients' samples tested for Ebola, 2 are said to have been positive for EVD. Although this appears to have no connection with the West African outbreak, this now makes 5 countries that are dealing with Ebola concurrently. Should we start worrying now?

http://www.dw.de/drc-confirms-first-ebola-cases-making-it-fifth-african…

Jason, that is a possibility, but remote. Dave, even if he is positive per seminal fluid, that's not exactly putting "the public" at risk. I already wrote about that here if you want to read my overview: http://mic.com/articles/96990/now-that-the-american-ebola-patients-have… TL;DR: not even a very big risk to his wife. Bob, keep in mind that as of now, it is only 2 confirmed cases, and we're not sure if they're linked to the West Africa outbreak or if these are separate. Obviously DRC has a long history with Ebola.

Dear friends, am glad about the excellent info on ebola. Here are my opinions
1. Ebola is an RNA virus, not a retrovirus, it multiplies rapidly but doesn't mutate to other forms, like being airborne, I would still think it can be spread through air if the air is moist and people in closed room and sweating, since all that is required is just a slight mucosal entry, I would think that the Nigerian doctor who died of ebola could have got it this way. So the word airborne is quite tricky.

2 . The second point is about shaking hands, I wouldn't think for a moment that shaking hands is a risk, how in the world could a virus breach the innate protection we all have...never...in which way?? so we shouldn't panic over such a thing, yes offcourse see the odds..one has to come in contact with an ebola infected person.... again that person has to sweat, and then you shake hands...it's safe...and then unless you rub your nose or eyes..perhaps that's when it's pathogenic...We don't know the role of our innate defences at the mucosa like the dendritic cells, neutrophils and macrophages...perhaps they could play a role in preventing the virus from binding on to cells. So hand shakes to me is ok.

3 . Had it been airborne the entire plane carrying the American sawyer could have been infected..If we are to fight the virus..we should fight the panic that is being caused, and in the media they paint a frightening picture that blood comes out from eye balls etc.... that's not true, only ten percent percent of victims experience this...the British nurse who survived ebola said he didn't even vomit..

For a virus to mutate from its current transmission into being airborne is only theoretically possible.. for a pathogen to change course is not usual.

Thanks, samuel kumar

CDC now estimating there could be 1.4M cases by end of year -
http://www.usatoday.com/story/news/nation/2014/09/22/ebola-last-forever…

Still think it sounds like it could be airborne to me with that kind of exponential growth.

University of Minnesota CIDRAP seems to think differently from you.
http://www.cidrap.umn.edu/news-perspective/2014/09/commentary-health-wo…

from USAMRIID 1995,
"Lethal experimental infections of rhesus monkeys by aerosolized Ebola virus"
http://www.ncbi.nlm.nih.gov/pmc/arti...00004-0007.pdf

We also demonstrated aerosol transmission of
Ebola virus at lower temperature and humidity than that
normally present in sub-Saharan Africa. Ebola virus
sensitivity to the high temperatures and humidity in
the thatched, mud, and wattel huts shared by infected
family members in southern Sudan and northern Zaire
may have been a factor limiting aerosol transmission of
Ebola virus in the African epidemics. Both elevated
temperature and relative humidity (RH) have been
shown to reduce the aerosol stability of viruses
(Songer 1967). Our experiments were conducted at
24ºC and < 40% RH, conditions which are known to
favour the aerosol stability of at least two other African
haemorrhagic fever viruses, Rift Valley fever and Lassa
(Stephenson et a/. 1984; Anderson et a/. 1991). If the
same holds true for filoviruses, aerosol transmission is
a greater threat in modern hospital or laboratory
settings than it is in the natural climatic ranges of
viruses.

So, aerosolized transmission on humane primates of filoviruses is pretty much established.
Maybe, the environmental conditions on equatorial and tropical Africa are not ideal for this route, but it could well be the case, that in colder climates, given the high infectivity shown in this study (400 FPU vs the usual 1×10^4, 1×10^6, or 1×10^8 for Influenza viruses) it could become a very viable route for infection on settings similar to the ones where Influenza viruses thrives, that is, confined, cold and dry spaces common on developed countries.

Marcos, I have no idea of your background--do you understand the difference between experimental studies between lab monkeys within the setting they describe, and what actually happens in an outbreak? Hint: they are quite different, as is even noted in the part you quote. It's the pig paper all over again--just because it can be artificially created doesn't mean it actually happens. Just about any pathogen can be artificially put into an aerosol form using physics and chemistry alone, but clearly they all are not spread in that manner.

Thanks for your response Tara.
Yes, you are right and by no means I am trying to create panic or be a scare monger, I am just curious if given the fact that we only have data on outbreaks that occurred in vastly different environmental conditions than the ones that are common in western countries, how EBOV could behave in said different conditions.
So, forgive me for being so insistent, but those are my questions:
As mentioned in that article aren't those experimental settings closer to the environmental conditions on a modern western hospital setting in terms of temperature and Relative Humidity? Could this be relevant in your point of view?

And then, given the high infectivity and the possibility of EBOV infecting epithelial cells on the respiratory tract, couldn't be possible for a patient in such a setting to generate aerosolized particles enough to be infective, should said particles remain viable on open air for a certain amount of time?

"As mentioned in that article aren’t those experimental settings closer to the environmental conditions on a modern western hospital setting in terms of temperature and Relative Humidity?"

Possibly

"Could this be relevant in your point of view?"

No. Here's the thing and why I asked about labs. Creating an artificial aerosol really has no bearing on what's out there in nature, so the first part of your question regarding humidity really doesn't matter, because we have no reason to think that those conditions would ever exist in a real life setting. Our bodies don't work the same way an artificial device does in creating these Ebola aerosols, period, so how they behave at various temperatures and humidities etc. is an interesting theoretical question, but one that has little real-life application. Everything else follows from your first assumption, which is fatally flawed. Vincent's article here may be of interest to you on airborne Ebola: http://www.virology.ws/2014/09/18/what-we-are-not-afraid-to-say-about-e…

I also missed your CIDRAP comment earlier, but they're like a hammer who sees everything as a nail. I'll just say there has been a lot of controversy over that article and a lot of people who were not fond of it and leave it at that.

Fair points Tara,
I see now things from another point of view. I've searched if other institutions went ahead with this position from CIDRAP, and it looks like they have taken an isolated stand.
Liked a lot the article you've linked, but also for a very different reason. As a layman, I always thought that the outcry against Fouchier and Kawaoka with making H5N1 airborne in mammals obscurantist fear-mongering, but couldn't quite explain why I thought so in practical terms. Now I see the relevance of their research and can explain as a layman for other layman why this kind of research is important.
Thanks for your patience Tara.

Happy to assist, Marcos.

Hiya Marcos Eliziario Santos!
Glad to hear you understand Tara's points about Ebola and aerosolization. However, it's really important to not conflate the Ebola models with what Kawaoka and Fouchier are doing. They're very different scenarios; no one is suggesting that Ebola research is gain-of-function or dual-use research of concern, whereas the flu-related studies are.

I don't want to derail Tara's excellent Ebola-explanation thread on the differences and details, but suggest that you read up on GOF and DURC concerns, especially as put forth by Marc Lipsitch and the Cambridge Working Group.

Cheers!

The article published by CIDRAP may draw a slightly alarmist, and certainly costly, conclusion, but it offers literature citations showing that the virus could survive in droplets long enough to be inhaled and that a few people in past outbreaks have been infected through casual, or occasionally no physical contact with a symptomatic person. The reported case where one woman in a taxicab infected four or five other people is a recent example. The news didn't say whether she might have gotten sick in the cab, but surely she didn't vomit directly on everyone around her.

You said we should wait to draw any conclusions from that case until the disease suffered by all the secondary cases was definitively identified, but it doesn't appear that that information will ever be publicized - the health authorities have bigger fish to fry by now - and as far as I know the original diagnoses have not been debunked. Surely the passengers' exposure was less than that which a nurse or nurse's aide would experience. Given that this virus is often fatal, though surely the death rate in a place with good supportive care would be under 60%, and that it seems to spread that readily at least sometimes, I'd sure want to use some kind of protective gear if I were taking care of actively sick people.

Also, reading that kind of article always makes me think I should find someplace other than the shelf above the toilet to keep my toothbrush. Blech.

A newspaper story that "has not been debunked" is a pretty low bar for scientific investigation.

Tara,
First let me premiss my comment with I am by no means educated in virology nor am I much for the sciences. So with that 1 could a virus be tricked or manipulated to become asymptomatic in a human host? Also can you tell me have there been any studies on the effects on the virus on dogs?
Sincerely
Michael

I would think that when Tara says it's not airborne that she would mean though breath not inhalation on vomit etc...Isn't that obvious?

"Michael T. Osterholm, director of the Center for Infectious Disease Research and Policy at the University of Minnesota, acknowledged in a recent New York Times op-ed that virologists are 'loath to discuss openly but are definitely considering in private' the possibility that Ebola has gone airborne. Some have questioned why hundreds of health workers have become sick and died from Ebola given that they take extreme precautions to avoid bodily contact with victims."

"there may be something unique about pig physiology that allows them to generate more infectious aerosols as a general rule"

There MAY be? That's comforting.

Scared, you sound like one of those people that will panic no matter what anyone more knowledgeable than you tells you. You worried about something before this outbreak and you'll find something to worry about after this outbreak - whether it's another disease or lizardmen or whatever else conspiracy you fear that gives you some (non)purpose in life.

Just wondered if you had commented on the NIH.GOV article PMC3100998 which under the Heading "TIM-1 Expressed on Human Airway..." includes the following statement: "One established route of infection for Ebola virus is the inhalation of aerosolized particles"?

Robert, that refers to a lab setting. Just about any pathogen can be mechanically made into an aerosol. Doesn't mean they are actually transmitted via that route.

Also, Martha, Osterholm has backed off that (after being told by virologists how unlikely it is). Se for example http://thelead.blogs.cnn.com/2014/10/06/the-bigger-risk-of-ebola/

"Ebola going airborne would be devastating, says Dr. Michael Osterholm, with the Center for Infectious Disease Research and Policy. But he said such a mutation of the disease is not a big risk.

"A much bigger risk is this virus moving out of West Africa and getting into the slum areas like Lagos and Nairobi and making the cases in West Africa only a small part of the outbreak," Osterholm said in an interview with CNN's "The Lead with Jake Tapper.""

I imagine that pig physiology is radically different than human in the sense that a pig snout has larger orifices, and is predominantly a wet configuration. The content of expelled air would contain larger quantities of non-dry air than humans, even if exhaling via the mouth. To reproduce a similar amount of moist exhaled air, we would need to cough, or sneeze. It is at this point that infectious particles would be distributed, up to 10 feet from an infected person. With a 16 hour life on fomite surfaces, this provides a bit of a window for risk. The NBC cameraman that became infected says he thinks it was a result of assisting in the decontamination of a transfer vehicle used to transport an infected patient. That would mean he came into contact with the fomite variance, but then what? Wipe his face? Inhale air droplets?

What about:
http://www.ncbi.nlm.nih.gov/pubmed/23155478 and http://www.ncbi.nlm.nih.gov/pubmed/21651988 ???

Clearly, aerosolized Ebola can infect the lungs. The only issue is the aerosolized viral load put out by someone who is sick. I would tend to think that someone with the Flu could generate a similar or worse aerosolized viral load compared to the pigs in the aforementioned study. This will be a significant problem.

If the virus proteins mutate will a vaccine be useless?

Are we sure it's not airborne? Well... Just as a population may contain a statistical outlier, such as how the human population contains a few people who can multiply faster than a computer - so to, then, there are people whose systems will be statistically different enough from normal that they could aerosolize anything. But I feel that is localized and rare. If you are really curious about ebola being airborne, cia has a paper by james petro called "mitigating threats from bioterrorism". In this paper in the second bulleted list, Mr. Petro discusses how scientists at the university of pennsylvania created a special virus that would help treat leukemia patients. It uses the surface proteins of ebola combined with parts of HIV plus some cool genetic engineering. This way they were able to spray it into the lungs of leukemia patients (aerosolization) and the little viruses were able to repair a certain type of genetic damage. You see, Ebola and Hiv both share the exact same budding technique, about as rare as lightning striking the rose bush you don't have in your front yard 50 times. Anywho, oh! where are my manners? Here is the link.
https://www.cia.gov/library/center-for-the-study-of-intelligence/csi-pu…
Finally-er, many moons ago, there was this man that was very bad. His name was shoko asahara. He led a cult and they were the ones behind the sarin subway attacks in tokyo. Well, this wasn't enough for our little friend, so he starts a multi-million dollar research lab and breeds weaponized anthrax, and still wasn't happy, so he actually sent a team to south africa to find live samples of eeee-bola. Unfortunately for them they used digital communications systems running across eshy's backbone, and apparently as soon as they stepped into the jungle they met a very untimely demise.

Bad science about GMOs: It reminds me of the antivaccine movement (revisited)

oracknows — Mon, 17 Jun 2013 01:18:05 +0000

Bad science about GMOs: It reminds me of the antivaccine movement (revisited)

I never used to write much about genetically modified organisms (GMOs) before. I still don't do it that often. For whatever reason, it just hasn't been on my radar very much. That seems to be changing, however. It's not because I went seeking this issue out (although I must admit that I first became interested in genetic engineering when I was in junior high and read a TIME Magazine cover article about it back in the 1970s), but rather because in my reading I keep seeing it more and more in the context of anti-GMO activists using bad science and bad reasoning to justify a campaign to demonize GMOs. Now, I don't have a dog in this hunt (Forgive me, I have no idea why I like that expression, given that I don't hunt.) I really don't. I was, not too long ago, fairly agnostic on the issue of GMOs and their safety, although, truth be told, because I have PhD in a biomedical science and because my lab work has involved molecular biology and genetics since I was a graduate student in the early 1990s. I found the claims of horrific harm attributable to GMOs not particularly convincing, but hadn't bothered to take that deep a look into them. It was not unlike my attitudes towards the the claims that cell phones cause cancer a few years ago, before I started finding dubious studies and looking into them and noted despite the utter lack of a remotely plausible mechanism and uniformly negative studies except for a group in Sweden with a definite ax to grind on the issue. None of this stops activists from likening cell phone companies to tobacco companies, the way antivaccine loons liken vaccine manufacturers to tobacco companies. Back then, I realized that there wasn't really a plausible mechanism by which radio waves from cell phones could cause cancer in that the classic mechanisms by which ionizing radiation can break DNA molecular bonds and cause mutations don't apply, but I didn't rule out a tiny possibility that there might be an as yet unappreciated mechanism by which long term exposure to radio waves might contribute to cancer.

As was the case for the nonexistent cell phone-cancer link, there has now been a steady drip-drip-drip of bad studies touted by anti-GMO activists as "evidence" that GMOs are the work of Satan that will corrupt or kill us all (and make us fat, to boot). Not too long ago, I came across one such study, a truly execrable excuse for science by Gilles-Eric Séralini at the University of Caen purporting to claim that Roundup-resistant genetically modified maize can cause horrific tumors in rats. I looked at the methods and conclusions and what I found was some of the worst science I had ever seen, every bit as bad as the quack "science" used by the antivaccine movement, as anti-GMO activists worry about GMOs sapping and impurifying their precious bodily fluids. Then, not too long ago, I discovered a truly quacktastic bit of fear mongering by Jack Heinemann about GMOs in which, or so it is claimed, GMOs produce silencing RNAs that not only survive transit through the gut, get into the bloodstream and thence into cells to inhibit the expression of specific genes, and even get passed down to the next generation to kill your children.

The GMO fear mongering can even reach ridiculous extremes, such as this little bit dug up by GMO Pundit:

In the comments, the stupid truly burns:

So it wasn't for nothing that I made the comparison between the antivaccine movement and the anti-GMO, because the anti-GMO movement is very much like the antivaccine movement and the cranks who claim that cell phone radiation causes cancer. Indeed, there's a lot of—shall we say?—cross pollination between the groups. As if to demonstrate that very point, last week I came across an article by the all-purpose crank to rule all cranks, Mike Adams, at NaturalNews.com entitled GMO feed turns pig stomachs to mush! Shocking photos reveal severe damage caused by GM soy and corn:

If you have stomach problems or gastrointestinal problems, a new study led by Dr. Judy Carman may help explain why: pigs fed a diet of genetically engineered soy and corn showed a 267% increase in severe stomach inflammation compared to those fed non-GMO diets. In males, the difference was even more pronounced: a 400% increase. (For the record, most autistic children are males, and nearly all of them have severe intestinal inflammation.)
The study was conducted on 168 young pigs on an authentic farm environment and was carried out over a 23-week period by eight researchers across Australia and the USA. The lead researcher, Dr. Judy Carman, is from the Institute of Health and Environmental Research in Kensington Park, Australia. The study has now been published in the Journal of Organic Systems, a peer-reviewed science journal.

Judy Carman? that name certainly sounds familiar. Oh, I remember. She was quoted extensively supporting Jack Heinemann's claims about GMOs. Here's just one example:

We have not yet seen the worst damage that genetic engineering may do. Australia's governmental agency, Commonwealth Scientific and Industrial Research Organisation (CSIRO), is developing a wheat species that is engineered to turn off genes permanently.

Professor Jack Heinemann at the University of Canterbury's Centre for Integrated Research in Biosafety has studied the wheat's potential. Digital Journal reports that he says1:

What we found is that the molecules created in this wheat, intended to silence wheat genes, can match human genes, and through ingestion, these molecules can enter human beings and potentially silence our genes. The findings are absolutely assured. There is no doubt that these matches exist.

The implications are clarified by Professor Judy Carman of Flinders University:

If this silences the same gene in us that it silences in the wheat—well, children who are born with this enzyme not working tend to die by the age of about five.

Silencing the equivalent gene in humans that is silenced in this genetically modified wheat holds the potential of killing people. But it gets worse. Silenced genes are permanently silenced and can be passed down the generations.

That's right. To Judy Carman, siRNA from GMOs has the potential to kill your future children before they turn five!

But back to Carman's most recent study. As described by Mike Adams, it sounds pretty damning, doesn't it? It sounds truly horrific, just as the Séralini study did. Adams is useful in that he takes the messages of anti-GMO activists (well, actually, he takes the messages of just about all cranks and quacks) and, as they said in This Is Spinal Tap, turns them up to 11. On the surface, it does, anyway. But what about the actual study. There was really only one thing for me to do, and that's the same thing I did with the Séralini study: Go and see for myself. So I did.

Judy Carman's study was, fortunately, published in an open access journal, and there was a direct link to the study itself. The first thing I did was to look at the journal. I had never heard of it before. The journal seems to cater to the organic crowd, being sponsored by groups like the Organic Federation of Australia and CSAFE, while the guidelines for authors state that "topics are to be consistent with current principles of organic farming and its associated industries, especially those in Australia, New Zealand, Asia, and the Pacific Islands." The journal itself appears not to be indexed on PubMed, which tends to indicate either that it's a new journal or not a very good journal. On the other hand, to be fair, there are plenty of CAM journals indexed in PubMed, and many of them are pure pseudoscience; so I can no longer conclude that lack of indexing in PubMed automatically means a journal is dodgy. It is, however, often an indications that it is. Moreover, if you wander over to Judy Carman's website, gmojudycarman.org, you'll see that it's chock full of anti-GMO activism.

After having seen this study, I think that the editors of this open access journal have made a massive mistake and have, either wittingly or unwittingly, allowed their journal to become a tool of anti-GMO activist groups, a couple fo which which gleefully announced the results of the study with press releases (for example here and here) calling the study "groundbreaking," asserting that it was evidence of "adverse effects" due to GMO feed, and claiming that the results "clear evidence that regulators need to safety assess GM crops containing mixtures of GM genes, regardless of whether those genes occur in the one GM plant or in a mixture of GM plants eaten in the same meal, even if regulators have already assessed GM plants containing single GM genes in the mixture."

Here's a hint: It's none of the above.

As I read the study itself, the first thing that became apparent to me is that it's a massive fishing expedition. What do I mean by that? I mean that there's no clear hypothesis. Basically, the only seeming hypothesis was "GMOs bad," and the study was designed to find bad things associated with GMOs. At first glance, the design seems simple enough. The investigators used 168 just-weaned pigs at a commercial piggery in the US. The pigs were fed a standard diet, but half the pigs were fed widely used varieties of GM soy and GM corn, while the control group fed an equivalent non-GM diet. Basically, one protein made the plant resistant to a herbicide and two proteins were insecticides. The specific GM varieties used were as follows:

The corn used in this study contained 90% DK 42-88 RR YG PL (a triple stack of NK603, MON863 and MON810 genes) with the remainder being equal quantities of Pannar 5E-900RR (containing NK603), Pannar 4E-705RR/Bt (a double stack of NK603 and MON810) and Producers 5152 RR (containing NK603). Therefore, the GM corn that was used was genetically modified to produce three new proteins. Two were Bt proteins that protected the plant against insect attack, while the third protein provided the plant with tolerance to the herbicide glyphosate (Testbiotech, 2012; Monsanto, 2012). Because Roundup ReadyTM (RR) soy is predominant in the GM soy market, this was used. This crop contains a gene that provides tolerance to the herbicide glyphosate. GM DNA analysis (Genetic ID, Fairfield, Iowa, US) confirmed that the GM corn contained a combination of NK603, MON863 and MON810 genes (expressing the CP4 EPSPS, Cry 3Bb1 and Cry 1Ab proteins respectively), that the RR soy was 100% RR soy (expressing the CP4 EPSPS protein), that the non-GM feed contained a median of 0.4% GM corn and that the non-GM soy contained a median of 1.6% GM soy. Such GM contamination of apparent non-GM material is common in the US.

So the investigators fed piglets a diet of GMO grain versus non-GMO grain, let the pigs mature according to the normal methodology, and then after slaughter looked at a variety of outcomes. Worse, the authors measured these variables without any sort of control for multiple comparisons. Of course they found differences! Actually, what surprised me is how few differences they found between the groups, not how many. I'm going to hone in on the main finding of the paper first. It's the finding that seemed the most dramatic and was the most highly publicized, the one mentioned by Mike Adams in his breathless description of he results, as though they were slam-dunk evidence that GMOs are evil. I'm referring, of course, to the claim that more stomach inflammation was observed in the pigs fed a GMO diet, specifically a 267% increase in severe stomach inflammation in the GMO group, with a whopping 400% increase in male pigs. It's the result that produced pictures like this one in the paper (and, not surprisingly the same picture posted to many an anti-GMO website):

These images certainly look striking, but what do they mean? Well, not much. First of all, as many have pointed out, the photos chosen are deceptive in that not enough of the groups are shown, nor can we be sure that these are representative. Also, as Mark Hoofnagle points out, the assay for inflammation in the gastric mucosa of the piglets was only based on gross pathology. Basically, there was no histological study and pathological examination of the tissue to detect and quantify actual inflammation. Basically, the assay was based just on a gross visual inspection of the the tissue by a veterinarian (not even a veterinary pathologist, even, as far as I can tell). Unfortunately, such inspections can be highly misleading, particularly after animals have been slaughtered in an abattoir, as described by Professor Robert Friendship, University of Guelph:

Dr. Robert Friendship, a professor in the Department of Population Medicine at the Ontario Veterinary College, University of Guelph and a swine health management specialist, reviewed the paper [see reference below]. He concluded that “it was incorrect for the researchers to conclude that one group had more stomach inflammation than the other group because the researchers did not examine stomach inflammation. They did a visual scoring of the colour of the lining of the stomach of pigs at the abattoir and misinterpreted redness to indicate evidence of inflammation. It does not. They would have had to take a tissue sample and prepare histological slides and examine these samples for evidence of inflammatory response such as white blood cell infiltration and other changes to determine if there was inflammation. There is no relationship between the colour of the stomach in the dead, bled-out pig at a slaughter plant and inflammation. The researchers should have included a veterinary pathologist on their team and this mistake would not have happened. They found no difference between the two experimental groups in pathology that can be determined by gross inspection.”

What I found particularly suspicious was Table 3. Notice how the level of inflammation is divided into no inflammation, mild inflammation, moderate inflammation, severe inflammation, erosions, pin-point ulcers, frank ulcers, and bleeding ulcers. This is not really a standard way of scoring inflammation. I don't know about pigs, but in humans there are a variety of scoring systems for the endoscopic assessment of inflammation (for example, this one), particularly chronic gastritis (which is what we're talking about, although such redness as described would, if associated with gastritis, be more associated with acute gastritis). Worse, gross visual assessment of gastric mucosa is subject to high inter-observer variability, and, although the personnel caring for the pigs and doing the autopsies were blinded to the experimental group (which is good), I don't see any attempt to control for inter-observer variability, and, again, no control for multiple comparisons.

I also note that the difference between pin-point ulcers, frank ulcers, and bleeding ulcers is rather arbitrarily defined and not entirely clear. Also notice how twice as many pigs had no inflammation in the non-GMO group and that there was actually a lower risk of mild and moderate inflammation, as well as erosions and pin-point ulcers. Of course, the p-values are all non-significant, except for one: that for severe inflammation. In fact, on the entire table, the only "statistically significant" result is for "severe inflammation." In fact, as Mark Lynas points out, many more pigs fed non-GMO feed had stomach inflammation than those with GMO feed.

Lynas also points out that the data are all over the place with respect to reported levels of inflammation, asking the very apt question, "If GMO feed is causing the severe inflammation, why is the non-GMO feed causing far more mild to moderate inflammation?" One also can't help but notice that for "moderate" inflammation, there was a difference favoring the non-GMO feed, and I echo the question, "Do Carman et al perform a test for statistical significance to see if GMO feed has a protective effect on pigs stomachs? Of course not – that’s not the result they are after." Exactly. Even worse, they used the wrong statistical analysis to analyze categorical data. When the data are analyzed more appropriately, there appears to be no statistically significant difference between the groups, just as there was no real statistically significant difference in the tumor burden of the rats in the Séralini study. Come to think of it, Carman's study resembles the Seralini study in that it basically looks at a whole lot of outcomes in a fairly arbitrary fashion and cherry picks the inevitable "positive" result. In fact, if you take all the groups together, there actually appears to be a non-statistically significant trend towards less stomach inflammation in the GMO group. Yes, less. As Karl Haro von Mogel put it, the authors appeared to be "trying to shoe-horn individual categories that aren’t binary data into a statistical test designed for binary data is the wrong approach." Basically, however you look at it, there's just no "there" there. Analyzed correctly, there is no statistically significant (or, no doubt, biologically significant) difference in stomach inflammation in this study. As for the reported increase in uterus weights, as Professor David Spiegelhalter, Winton Professor of the Public Understanding of Risk at the University of Cambridge points out, "There are also 19 other reported statistical tests, which means we would expect one significant association just by chance: and so the apparent difference in uterus weight is likely to be a false positive."

There's another aspect of this paper that's very troubling, and that these animals were all very sick. Indeed, I have to wonder how they were being cared for. Over half the animals are reported in Table 3 to have pneumonia, defined as "consolidating bronchopneumonia of the cranial ventral lung lobe(s) and/or caudal lobes." That is just not normal, and it doesn't sound like a minor pneumonia. True, this pneumonia wasn't histologically verified, either, as far as I can tell, although pneumonia can be viewed grossly if it's bad enough. It is, after all, basically puss mixed with mucous in the alveolae and bronchial passages. As has been pointed out in multiple discussions of this study, such a high percentage of animals with pneumonia is an indicator of very bad animal husbandry, indeed. The bottom line is that there are many, many problems with this study, the totality of which are more than enough to render its results meaningless. There is no dose-dependent mechanism for the effects reported, no rhyme or reason consistent with a mechanism that would explain why GMOs would affect just the stomach (and then only to cause severe inflammation) and and uterus size. The study was a fishing expedition and not hypothesis-driven. It's not surprising that it found something. I'd be shocked if it hadn't. In the end, this study abused a fairly large number of innocent pigs to produce no useful data. She might try to defend it against criticism, but she basically fails. In particular, one notes that she can't seem to defend against the charge of a lack of hypothesis and that she didn't even try to defend the criticism that she didn't bother to look at stomach histology to verify that there really was inflammation in the gastric mucosa, despite Carman's touting that the "authors have over 60 years of combined experience and expertise in medicine, animal husbandry, animal nutrition, animal health, veterinary science, biochemistry, toxicology, medical research, histology, risk assessment, epidemiology and statistics." Sad that they didn't use all that experience to produce a paper whose results are believable and useful.

Scientific failures are seldom so spectacular.

oracknows Sun, 06/16/2013 - 21:18

Tags

biology

medicine

Skepticism/Critical Thinking

genetically modified organisms

When one of my friends posted a link to the pig study on Facebook, this was my response:

"[friend], there's some serious bias here. This was an attempt to reproduce the rat study, but remove the feeding problem, and thus prove the point. Unfortunately, the results really don't prove out.

http://www.organic-systems.org/journal/81/8106.pdf

The introduction spends FAR too much time trying to correlate pigs directly to humans and to convince the reader that a 22.7 week study is "long term" because that time equals the time for pigs to go to slaughter. 22.7 weeks is not a long term study, and shouldn't be considered one. (Pigs can live for years.)

The problems don't end there. The abstract tries to point a finger claiming only damages caused by GMOs, but it ignores the full results of the study.

Pg. 47 Is where you need to look to see the errors.

First, take a look at the "dramatic" differences in weight of the ovaries.
0.0040 - 0.019 for non-GMO vs.
0.0047 - 0.014 for GMO

The mean reported was
0.0085 for non-GMO vs.
0.0086 for GMO

The only reason that there's such a difference in weight is that they opted to comment on the tiniest of the organs tested. Had they volunteered information about the Standard Deviation, you would have seen that the overall mean weight for the ovaries of the tested groups was equal!

Then we can talk about the "bloated stomachs". What these researchers failed to note is that for the hearts, livers, and spleens - abnormalities were seen in MORE non-GMO than GMO pigs. (This result was not acknowledged in their abstract - even though other results were stated.) Even in the stomachs, more erosion and more moderate inflammation was noted in non-GMO.

This was NOT a successful study."

Here's the "Occupy Monsanto" link that provided his original source. I followed it to find the study results, and it provided the source link I used.
http://occupymonsanto360.org/blog/new-study-proves-gmos-cause-severe-in…

The reason I kept my discussion so short (believe me, I saw other problems) was that I was responding in a Facebook comment thread! Fortunately, the post was received well, and all information about the study - including the flaws - was left available on my friend's page.

It gets worse than the statistical fishing trip and lack of correct pathology data collection. The various authors of the study are failing to agree on what was done.

Here is Howard Vlieger being interviewed about the study:

http://www.foodsafetynews.com/2013/06/study-says-gmo-feed-may-harm-pigs/

Vlieger told Food Safety News that while the study could not include any anecdotal behavioral observations of the pigs, the researchers did notice a marked difference in temperament between the two groups. When recording the pigs’ weights each week, researchers say that the non-GM pigs were easy-going and generally cooperative, while the GM pigs were noticeably more irritable.

“For whatever reason, as soon as you brought them into confined quarters, they were fighting and biting each other,” Vlieger said. “Every time we did a weighing, the same scenario presented itself.”

However, the study itself stated:

Individual weights were recorded weekly and animals were monitored daily by observers who were blinded to a pig's dietary group.

FSM only knows what was going on.

As Orac notes, it is very poor science to look at redness in an autopsy stomach and conclude that it must relate to inflammation (there are other causes of erythema, including nonspecific postmortem changes, vascular dilatation for a variety of reasons etc.). You need to look at microscopic levels of inflammation AND correlate them to significant health outcomes (the authors of this crappy study admit that such outcomes did not differ significantly between the GM-fed and non-GM-fed pigs).

It is noteworthy that a co-author of the study, Howard Vlieger has a glaring conflict of interest that doesn't get mentioned in the publication:

"Vlieger is president and co-founder of Verity Farms, a US ‘natural foods’ outfit which markets non-GMO grain. Despite this, the paper declares that the authors have no conflicts of interest, although it seems to me that he would have a very clear commercial interest in scaring people about GMOs in order to drum up business of his GMO-free offerings."

http://www.marklynas.org/2013/06/gmo-pigs-study-more-junk-science/#stha…

Typically the Mike Adamses and anti-GM shouters of the world trumpet conflicts of interest in science, real and imaginary (at least when they disagree with what's found), but they are curiously silent about the huge conflict of interest inherent in the pig inflammation study.

Followup note: despite my username, I declare that I have no commercial swine investments that would constitute a conflict of interest, though I love a good pulled pork sandwich.

I am a pathologist. It is true that, in the best of hands, gross examination will be wrong about 30% of the time. You all can figure out what happens when gross examination is not in the best of hands. That's why we spend so much time looking at slides.

Looking at the gross images from that paper raises a number of issues for me. First of all, I think that I can produce similar appearances by manipulating fixation artifact. From what I can tell of the material and methods presented in the paper, the examination by the veterinarians was done fresh, but were the pictures taken fresh? There seems to be fresh blood on the examination table in the photos, which by itself is an indication of sloppiness (it's not that difficult to spend an extra 10 seconds cleaning up the table so your pictures are presentable), but the paper doesn't really say what was done. Formalin will take much of the color out of the tissue, leaving an appearance much like that in the top left (nil) image. I find it hard to draw any conclusions here without seeing the full resolution images, but I am suspicious that we are being manipulated.

The images in the PDF are low resolution, so it is really hard to tell what the stomachs really look like. I think I should be able to tell a fixed stomach from a fresh stomach, but it's really hard to do so here.

Judging from the way the images are lighted (note the reflection from the light around the edges of the specimens), there should be significant specular reflections on the stomachs themselves if the specimens are fresh and much less so if they are fixed. I do not see the reflections that I would expect from a fresh specimen, but perhaps that has more to do with the poor quality of the reproductions.

Taking the images at face value, the image marked moderate (lower left) looks much worse to me than the image labelled severe (lower right). I have to ask what is really going on here.

One other thing is that autopsies are a messy business, and I expect that veterinary autopsies performed in a slaughterhouse would be much messier than the autopsies that I perform in a hospital setting. So how is it that the blood on the examining table in all four images is identical even though one of the stomachs is touching the blood, and there are no smears of blood immediately adjacent to the stomachs? Is it reasonable to think that they cleaned up the blood right around the specimens but not in the rest of the field? Also note that the labels are immaculate even though two of the stomachs appear to be touching them. It is very difficult to clean up all of the blood around this sort of fresh specimen.

The more I look, the more questions I have.

In my (limited) experience, telling people who are against GMOs that the studies they cite are faulty is every bit as effective as telling alties that the studies they cite are faulty. They assume bias because they assume a war -- a battle between different ways of thinking and being.

On one side you've got the Good Guys who care about living with Nature, harmony, and love. On the other side you have the Bad Guys who care about acquiring Power, money, and control.

You don't have to know any science to realize it's just common sense that the second group can't be trusted. Science on one side cancels out the science on the other and puts everyone on even footing. So forget the actual details of the issue: choose your side. Make a decision for the kind of person you want to be.

I probably don't need to add that in my (limited) experience the anti-GMOs and the alternative medicine proponents happen to be the same group. And they are very, very emotionally attached to the spiritual implications of the Naturalistic Fallacy. They think I am going along with the Bad Guys because I'm the sort of person who decided to be an atheist and thus it's ultimately my core values which are screwed up. They honestly can't tell the difference between good science and bad ... so they go with what they're comfortable with.

Obviously, alt med/ natural health advocates have a conflict of interest and usually mis-represent research because:
their creed indulges reverence for natural plant products as therapeutic and necessary for maintaining life and health.
Phyto-nutrients are superior to pharmaceuticals and tampering with Nature may destroy their pristine essences- which, of course, could heal all of our ills ( especially if given in supplement form).

GMOs often are involved with pesticide use- which is already taboo to organic food producers/ users. These manipulations and torture of 'natural medicines' ( i.e. vegetables and fruits) resemble the horrors that vaccines have wrought upon innocent children - and the research cited in support is just as awful.

Natural News and PRN have gone whole hog as anti-GMO advocates, writing articles, encouraging political action and creating films:
( @ Gary Null's You Tube channel) you may view his entire documentaries, " Seeds of Death"** and "GMOs: Ticking TIme Bombs" which incorporate the wisdom of Mike Adams, Jeffery Smith, RIma, Laibow, Dr Mercola and many other well-known rabble rousers whose careers rely upon the myth that "natural is better".

No COIs here we're told.

** I've actually viewed the entire claptrap fiesta- what I do for scepticism.

I'm sympathetic to the view that Monsanto is a Giant Evil Corporation--I'd include them on my list of Top Ten Evil Corporations myself. But that's more because of how Monsanto tries to control the supply chain: making farmers buy seeds from them, rather than planting seeds from previous crops as has been done since humans invented agriculture. In at least one case, Monsanto successfully sued a farmer for growing one of their products from seeds that had blown onto his property.

The GMO strain(s) we have heard the most about are the Roundup Ready products, in which the inserted gene(s) allow the crop to survive spraying with the weed killer Roundup (conveniently, a Monsanto product). This is basically a biological arms race, in that the weeds will eventually (either by natural selection or cross-species genetic transfer) develop resistance to Roundup. But there isn't any evidence that the crop itself (as opposed to pesticide residues) is harmful to people. And I don't think Monsanto is intentionally trying to harm consumers' health (at least directly), because that would be bad for business.

Sixty cumulative years of experience over 8 people averages out to a little over 7 years. Is that considered a lot in a scientific research context? Or am I right in thinking she used the cumulative figure so it would look better?

In at least one case, Monsanto successfully sued a farmer for growing one of their products from seeds that had blown onto his property.

This is inaccurate. The farmer was sued for replanting seeds that he knew (because there is record of him getting them tested) came from Monsanto. If he had simply harvested the grain that grew from the seed that allegedly blew onto his property and sold it on the market, he would have faced no penalty. It's the fact that he knowingly replanted GMO seed that brought the lawsuit.

What I'd like to see Monsanto do is have a replanting option in their licensing scheme. This would work as follows: for the standard price, you get to buy seed, but can't replant it after harvest. For a higher price, you get to replant seed, but the license covers the acreage per year you can replant. This could even be split into a multi-year license and an indefinite license.

This is the same arguments from vaccines just with the words GMO instead. In the words of another man who explained it very well "for centuries people kept going 'My crops keep being destroyed by bugs, Help us Science!' and 'my crops struggle to survive drought, help us science' and science did and suddenly they all turned around and went 'YOU MONSTERS. You altered life and put chemicals on our crops!'" The whole reason there is GMO is because people wanted and it is beneficial in the first place. If they didn't no one would have invested in it and we would not be here today.

@Jericho -- no kidding!

I have said this before, but if anyone really wants to see the difference between "pure" corn and modern hybrids, go to the 19th century farm at Greenfield Village near Detroit and look at their cornfield. There's no consistency in stalk height, ear size, or row yield (I'm not a farmer so this is possibly not the correct agricultural description).

Kevin,
Monsanto don't make anyone buy their seeds. It seems reasonable to me that they require people who buy their products to sign an agreement that they will not sow seeds for a next crop, since they need a return on their considerable investment in this biotechnology. There is nothing to stop farmers from buying traditional non-GM seeds if they don't want to sign such a contract. They were initially going to introduce terminator seeds that would only produce crops with sterile seeds, but were dissuaded from this, but the widespread pirating of their technologies, in India for example, is making them reconsider this.

As W. Kevin Vicklund pointed out, it isn't true that any farmers who have accidentally grown their GM seeds have been prosecuted - it's a myth spread by anti-GMOers. all the cases I have seen have been where farmers have quite deliberately and knowingly grown their seeds.

As for Roundup Ready crops, I don't see how these make it more likely that weeds will develop resistance and more than they do to regular, and very much more toxic, weedkillers. Glyphosate has remarkably low toxicity - the detergent they add to it is more toxic, which I think is pretty good, when you compare it to earlier weedkillers.

^ "any more", not "and more"

About the "pneumonia" that the pigs had. I would bet money that all they were seeing was blood pooling the lungs from the slaughter process. Not everyone may want to hear about this, so quit reading if you are squeamish. When pigs are slaughtered, first they are stunned, usually with a mechanical stunner applied to the head, carbon dioxide, or an electrical stunner. Then they are shackled by the rear legs and raised off the floor, and their carotid arteries and jugular veins are severed. So, at slaughter, blood in their lungs would be cranial. Unless they actually saw pus in the lungs, they can't diagnose pneumonia. Oh, and BTW, slaughter weight for most pigs is 220 pounds, about 4-6 months of age. And, as a vet with a PhD in pathology, no, you can't diagnose inflammation on gross exam. In fact, the first stomach from the non-GMO feed looks more anemic than non-inflamed to me. Iron deficient anemia is pretty common in young pigs, so much so that most piglets get an iron injection right after birth. And the alleged differences in how the two groups of pigs behaved--most likely handling differences, from the blinded (HAH!) animal workers.

@Krebiozen

I don’t see how these make it more likely that weeds will develop resistance and more than they do to regular, and very much more toxic, weedkillers.

A number of years ago, I recall (from memory, so grain o' salt) reading about this problem occurring in Canada. A resistant variety of flax was developed, but it cross-polinated with some wild plants that were closely related, resulting in resistant weeds. I forget the details, but that's the gist of it.

Todd W.,
That makes sense, though weeds seem quite capable of developing resistance without any assistance from cross-pollination.

@Krebiozen

True. The more they dominate a niche, the more opportunities they have to develop resistance.

A lot like cancer, really.

Monsanto don’t make anyone buy their seeds. It seems reasonable to me that they require people who buy their products to sign an agreement that they will not sow seeds for a next crop, since they need a return on their considerable investment in this biotechnology. There is nothing to stop farmers from buying traditional non-GM seeds if they don’t want to sign such a contract. They were initially going to introduce terminator seeds that would only produce crops with sterile seeds, but were dissuaded from this, but the widespread pirating of their technologies, in India for example, is making them reconsider this.

Oh, I understand why their licensing is the way it is, and agree there's nothing illegal about it. I was merely expressing a preference.

Monsanto don’t make anyone buy their seeds.

Oh, but then they can't experience the wonders of RoundUp ready. The non-GMO people bitch and moan about Monsanto, while at the same time wanting the technology to increase their yields while not using harsh herbicides. They just don't want to pay for it. *boggle*

Sorry Kevin, that was supposed to be directed to Eric Lund, not you. Mea culpa.

@ Michael Finfer, MD (#5)

Excellent comment overall, but a couple of points of possible correction. First, the legend to Fig. 1 says the stomachs are arranged in clockwise order from upper left: nil, mild, moderate, and severe. So the lower left is indeed severe.

Second, the reddish area in the lower right, that I assume you're calling blood, looks more like an upside down logo to me. In particular, the upper left image appears to show some lettering, including the word "INC". It also looks to me like they have covered the table, and probably also the labels and scales, with plastic wrap prior to placing & photographing each stomach. So I think your concerns about those particular issues can probably be discounted.

That is NOT meant to suggest that I think this study is sound - I don't.

From the piggy tummy study:

There were no statistically significant differences in food intake, feed conversion ratios,
number or nature of illnesses, number or nature of veterinary interventions, veterinary
costs or mortality between the non-GM-fed and GM-fed groups of pigs. Mortalities were
13% and 14% for the non-GM-fed and GM-fed groups respectively, which are within
expected rates for US commercial piggeries. All dead pigs were autopsied by blinded
veterinarians and deaths were assessed as due to usual commercial piggery-related
matters and not to their diets. There was also no difference in body weights between the
two dietary groups, initially, during, or at the end of the experiment. Initial weights in kg
were : non-GM-fed group: 6.71 + 1.05 (mean + standard deviation); GM-fed group: 6.87 +
0.97. Final weights were: non-GM-fed group: 100.42 + 22.84; GM-fed group: 101.75 +
21.92.

Sounds like both groups were equally healthy to me, which makes the claims of "inflammation" on the gross examination rather suspect.

If red = inflammation, then I guess my arteries are just full o' that stuff....

Frankly, if they blinded the veterinarians for the purposes of this one study, that is cruel and certainly detrimental to the veterinarians' continued livelihood.

If the veterinarians were previously blinded for some unrelated reason, then that would be different.

Yes, given that GMOs are no problem, you wonder why Monsanto spends millions of dollars fighting any labeling law rather than using the same money to educated people.

Since the introduction of the first genetically modified food crop - a tomato - in the early 1990s, genetically modified foods have been in the middle of controversy.

Consumers are confused about GMOs due to conflicting reports about their benefits and risks; many don't know who to trust.

We hear reports of GMOs leading to pesticide-resistant insects and weeds, yet some say gene technology may be a solution to world hunger via drought resistant plants. In the news we see things about the demise of the honey bees and we hear that Monsanto's chemicals are responsible. We, ourselves or our families or friends have increased food allergies and poor health.

U.S. agribusiness see substantial economic benefits, and yet the farmers are suffering from the single grow seed cycle and the dependence on single source fertilizer and pesticides.

Few issues touch every human being on the planet as much as food. And, as technology has opened new doors in producing enough food for our ever-growing world population, it has raised troubling new questions.

The U.S. government has established a rigorous approval process for biotech products that includes the Food and Drug Administration, the Environmental Protection Agency and the U.S. Department of Agriculture. Moreover, since the first biotech crop hit the market in 1996, about 1 billion acres of U.S. farmland have been planted to biotech crops and trillions of pounds of U.S. soybeans and corn have been consumed worldwide, all with no credible reports of harm to human health. However, the EU won't grow GM foods and there is suspicious secrecy around the food industry that makes consumers mistrust this process. Furthermore, it is difficult to know who to trust when many, many of the former employees of agribusiness are now in our U.S. government and agribusiness are major contributors to our governments political processes.

There are many problems with GMOs and it isn't just the scientific research. We really need some transparency in reporting, we need some honesty from our government, and we need some accountability from agribusiness.

Now the research!
In the research to date, I don't see replication and I don't see peer review. Replication involves the process of repeating a study using the same methods, different subjects, and different experimenters. It can also involve applying the theory to new situations in an attempt to determine the generalizability to different situations. Replication, therefore, is important for a number of reasons, including (1) assurance that results are valid and reliable; (2) determination of generalizability or the role of extraneous variables; (3) application of results to real world situations; and (4) inspiration of new research combining previous findings from related studies.

It seems that we are just at the beginning of understanding the full implications of GMOs and all the spin that has been happening in order to confuse and confound. I don't think we need to fight with each other, I think we need to work alongside each other to figure out what is safe and what is not so we can protect our planet and the abundance of human life.

I do find it odd that opponents of GMOs seem to be so determined to lay health risks to consumers at the door of GMO products. I suppose it's because this plays better with the twitchy anti-science section of the population.

I do have some concerns about GMOs cross-fertilising with wild species and spreading their genes with the eventual effect that the selective advantage given to crops by the process of genetic modification is lost- see also antibiotics. I think this is a rational reason for some concern about use of GMOs but the anti-GMO campaigners do their cause no good at all with me my pushing bad science down my throat.

The farmer was sued for replanting seeds that he knew (because there is record of him getting them tested) came from Monsanto.

We're talking about Bowman? What he did was buy silo seed, spray the plants with Roundup, and harvest the seed from the survivors.

Sailor,

Yes, given that GMOs are no problem, you wonder why Monsanto spends millions of dollars fighting any labeling law rather than using the same money to educated people.

Not to defend the folks at Monsanto (who I'm sure are motivated by self interest like many of us) but why would someone willing accept labeling requirements that a) you know will drive off some of your customers, b) will cost you a substantial amount of money to implement; and c) will be the source of unending lawsuits when someone detects (real or imagined) that what is labelled one thing contains something else? Particularly when that product is sold in bulk and mixed and re-portioned at various times before getting to the consumer? Particularly if some stock person at the local store can mess it up?

you wonder why Monsanto spends millions of dollars fighting any labeling law

It's not really that odd...mandated labeling would hurt Monsanto financially, as many uninformed consumers would be turned off simply by the sight of a GMO label. That's why I disagree with the pro-labeling side of things...why should Monsanto have to incur financial penalties because of the public's unfounded fears?

Imagine there's a new movement out there that claims that only plants grown from seeds sown between 1 and 3PM are suitable for consumption, and all other plants are unsafe. Should corporations be required to label products with the time of day they were grown? What if this movement included millions of people?

The point is that for mandated labeling laws, you need to have evidence that the labeling is appropriate and useful. There's no evidence that a GMO label would do anything but continue to sow fear in an already undereducated public.

I don't want to ban GMO at this time―just Label it on food. Sure there'll be some that avoid it, so what, if it's safe, the stigma will fade, and scaremongers will soon be laughed at. If it's not harmful, as some $cientists claim, it'll all work out in the end.

Narad, I think the reference was to percy Schmeiser who claimed the 1000 acres of Roundup Ready canola blew on to his farm. He elsewhere claimed it fell off a truck going past his farm.

His worker, in his evidence in the court case, states that Percy Schmeiser had him spary "a good 3 acres of canola" with Roundup, harvest it separately and store it separately. This seed was then used to plant the next year.

Since the introduction of the first genetically modified food crop – a tomato – in the early 1990s, genetically modified foods have been in the middle of controversy.

Consumers are confused about GMOs due to conflicting reports about their benefits and risks; many don’t know who to trust.

Tina, plagiarism is generally frowned upon.

Narad, I think the reference was to percy Schmeiser who claimed the 1000 acres of Roundup Ready canola blew on to his farm.

Oh, right, he initially found it growing on the perimeter, right?

Yes. He sprayed 3 acres of canola on the side of one field and found most of the plants survived.

It is perfectly normal that, farmers spraying acres of their crops with herbicides that will kill them, just on the off chance there will be a survivor.

I'm kind of p!ssed about anti-GMO propaganda, as I swallowed a lot of it without much thought, and was only disabused of my misconceptions by some comments here, as I recall. Though my sympathies have always tended towards environmentalism, I don't like being lied to by anyone, and I'm always annoyed (mostly with myself) when I am fooled by misinformation.

The knee-jerk anti-technology tendencies I often see among those concerned about the environment both worry and scare me. I'm a technophile, and I like to think that technology will be the answer to a lot of the problems humans face, as insurmountable as they may seem right now.

Organic farms, companion plants, natural pest predators and hand-weeding, as laudable as they may be, are not going to feed 10 billion people.

He elsewhere claimed it fell off a truck going past his farm.

Funny thing, that's how I got my new wide-screen TV.

if it’s safe, the stigma will fade

Why is this necessarily true? In fact, I think it's likely the opposite. Just look at what happened to MSG.

Regarding the Monsanto farmers- wasn' t the problem that the judge in one case agreed the farmer took the seeds deliberately but seemed to rule that even if the seeds blew onto the farm accidentally, Monsanto could sue the farmer?

@sailor

Yes, given that GMOs are no problem, you wonder why Monsanto spends millions of dollars fighting any labeling law rather than using the same money to educated people.

What, exactly, is implied by this question?

1) If the foods were labeled, then third parties would be able to do experiments on GMO food safety. (Except that third parties are already doing such experiments)

2) If the foods were labeled, then people who avoided eating GMO food would not only be healthier than those who ate GMO food, but would healthier to such a large degree that it would be obvious that GMO food is unhealthy.

3) Something else.

[Off-topic: no comment preview? blah!]

There are more problems with the experimental design. the experimental unit in this experiment is not the pig, it is the pen of pigs. The treatment was not given to individual pigs, it was provided to each pen. At the end of the study, there were 4 pens total, 2 for each treatment. yet, the authors were claiming N values of almost 40. That is wrong and is horribly overstating their statistical power. The individual pig can only be the experimental unit if the individual pig is directly fed the diet. If the diet or treatment is given to the pen, then pen is the experimental unit. This is the standard methodology for research in animals sciences.

So Orac is saying that evolution is bad science since anti-GMO folks point out that GM crops produce bt resistant weeds and pests?

Orac's post is just another example of the horrible arguments in favor of GMOs. Anti-vaxxers are kooks, therefore let's lump the anti-GMOs in with them and take a couple examples of bad science (ignoring the bad science from the GMO crowd), and voila, anti-gmo folks are debunked.

Rather lame. But when you don't have the science on your side I guess folks like Orac have to resort to emotional appeals, like the people he criticizes.

Michael, the Judge ruled in the Canadian case that the farmer involved knew, or should have known, these were Roundup Ready canola and planted them deliberately without a license. How they got on the farm was deemed not relevant, because it was what happened next that mattered. Had the farmer just left the plants, not harvested the seed off them and not planted his whole farm to that seed, the judgement would not have gone against him.

The recent US Supreme Court ruling in the case brought by the organic industry has clarified the level below which Monsanto cannot make a claim. That is about 1%.

Doug, do you have anything other than strawmen to present?

This post was very specifically about some bad science that was published and pointed out why it was bad. Orac didn't state or imply that evolution was bad or that all statements made by anti-GMO people are wrong.

What is your scientific field Doug? Are you trained to read studies? Please provide us some citations to high-quality studies and we'll all have a look. But I imagine you're a drive-by, your high-dudgeon pearl-clutching is revealing . . .

Really, Doug?

Horrible arguments?

You mean, expecting people who wish to perform science to do it properly, and without an axe to grind, like the anti-gmo, anti-vax folks do?

I mean, learning how to control your experiment is junior high science. Why is it so difficult for folks performing studies like this one, or Tomlijenovic and Shaw, Goldman and Miller, etc to pay attention to one of the basic tenets of scientific experimentation?

#13 "They were initially going to introduce terminator seeds that would only produce crops with sterile seeds..."

OMG teh corn is trying to kill us!1!!!! GMOs are lik so bad!

#12 Shay - if you want to see natural 'corn' you need to look at teosinte grass. Any form of corn or maize is an unnatural mutant created by and dependent upon farmers - ears have been selected to the point where they cannot release their seeds naturally and self sow.

I love the irony of anti-GMO activists getting bent out of shape about corn. An unnatural food that only exists because it was was genetically modified thousands of years ago. I think it qualifies as a long term experiment, as do orange carrots, zucchinis, tomatoes, potatoes, cauliflower, and all the rest of them.

Qetzal,

I did misread the caption, sorry.

I looked at the image again, upside down this time, and I still don't see anything that I recognize as a logo. Logos on autopsy tables are usually on the sides, not on the working surface, where they would make the table hard to clean if they introduced any relief at all. I don't think that's a logo even in retrospect, but I would be willing to admit I was wrong if enough people agreed with you.

@ Natural News, yesterday:

Mike Adams, as a follow-up to the 'successful' global protest he rankled about recently ( "March on Monsanto"), now is helping to publicise the "Monsanto Video Revolt" which will commence in a few weeks: people are to make videos with those three words in the title and put them on video sites on the 'net thus causing HAVOC and CONFUSION and getting media attention.

( Isn't that what woo-meisters have been doing for the past several years- creating videos that lead to confusion?)

I'm sure the entire world will stand up and take notice and the powers-that-be will quake in their boots**.

** Do you wear still boots, Vladimir? David? Barry?

Haven't plants evolved to resist various pests and/or create symbiotic relationships with other plants to provide mutual benefits? Not to say that plants would have evolved to incorporate the Bt gene Monsanto put in to make them RoundUp Ready by themselves, but I suppose it.could be possible if someone were to work on developing a hybrid. (I am not a biologist, although I have lots of farming relatives, and DeKalb Ag used to hire high school students to do corn tasseling during summer vacation.)

Doug:

So Orac is saying that evolution is bad science since anti-GMO folks point out that GM crops produce bt resistant weeds and pests?

No, he said nothing even close to that. I don’t think he even mentioned evolution of bt resistance.

Rather lame. But when you don’t have the science on your side I guess folks like Orac have to resort to emotional appeals, like the people he criticizes.

You’re not really big in self awareness are you Doug?

I love the irony of anti-GMO activists getting bent out of shape about corn. An unnatural food that only exists because it was was genetically modified thousands of years ago. I think it qualifies as a long term experiment, as do orange carrots, zucchinis, tomatoes, potatoes, cauliflower, and all the rest of them.

Exactly. My GMO alarmist acquaintances get very huffy when I point this out to them and start sputtering things like "but now we're changing the actual MOLECULES!! BLAERGGH!"

Yet these same people laugh uproariously at things like Ray Comfort's display of total ignorance about selective breeding in the "bananas are evidence for creationism" video. It never occurs to them that their own viewpoint is just as biased.

#50+55: The argument that conventional breeding and selection also gets you new genes in the population is fine, but don't twist the conventional meaning of genetically modified when you do it. Cause having a phrase for that is useful.

@Dew, #33

$cientists

Just what is that supposed to mean?

Ass.

drksky - I assumed Dew wanted to avoid confusion with 5cientsts, so put a line through the S. But I cannot be sure.

#50+55: The argument that conventional breeding and selection also gets you new genes in the population is fine, but don’t twist the conventional meaning of genetically modified when you do it. Cause having a phrase for that is useful.

The problem I have is the vagueness about so many anti-GMO complaints. They tend not to be specific about what's so much worse about doing it deliberately versus the old fashioned approach taking advantage of new traits that form from random mutation (natural or deliberately induced by irradiation). To me, it's just a matter of increased control, not something fundamentally different.

Personally, I like the idea behind GM technology because we can use it to know what's in our food, rather than blindly trust in the benevolence and subservience of Mother Nature like many anti-GMO people seem to advocate.

@Bronze Dog
To avoid vagueness and be specific:-
Modern methods of genetic modification, unlike conventional breeding, involve the splicing of distantly related or completely unrelated genes into a gene sequence of a given species.
This involves a 'breaking' of the species barrier, something that does not normally occur naturally except occasionally when a pathogen attacks a host. Indeed, it is this ability of pathogenic microbes that insures their use as 'gene canons' in the splicing process, a process which is crude and unpredictable to say the least.
For every desired outcome achieved there are many unexpected traits that are expressed in the resulted progeny including toxic principles in many of the genetically modified plants produced to date and horrific mutations in the work on cloned sheep and salmon to name just a couple of examples in the animal work.
The pathogenic gene material has been shown to recombine with microbes in the human gut in the work of Pro. Terje Traavik at the University of Oslo creating super bugs, and the antibiotic marker genes widely used in splicing have contributed greatly to the spread of antibiotic resistance
Unleashing such a shoddily imprecise and unpredictable technology on the general population is what I call 'bad science'
Good science on the other hand will always have a 'duty of care' with the precautionary principle at it's very core.
I guess most of the comments here prove that modern science has sold it's soul to the highest bidder.To avoid vagueness and be specific:-
Modern methods of genetic modification, unlike conventional breeding, involve the splicing of distantly related or completely unrelated genes into a gene sequence of a given species.
This involves a 'breaking' of the species barrier, something that does not normally occur naturally except occasionally when a pathogen attacks a host. Indeed, it is this ability of pathogenic microbes that insures their use as 'gene canons' in the splicing process, a process which is crude and unpredictable to say the least.
For every desired outcome achieved there are many unexpected traits that are expressed in the resulted progeny including toxic principles in many of the genetically modified plants produced to date and horrific mutations in the work on cloned sheep and salmon to name just a couple of examples in the animal work.
The pathogenic gene material has been shown to recombine with microbes in the human gut in the work of Pro. Terje Traavik at the University of Oslo creating super bugs, and the antibiotic marker genes widely used in splicing have contributed greatly to the spread of antibiotic resistance
Unleashing such a shoddily imprecise and unpredictable technology on the general population is what I call 'bad science'
Good science on the other hand will always have a 'duty of care' with the precautionary principle at it's very core.
I guess most of the comments here prove that modern science has sold it's soul to the highest bidder.

Modern methods of genetic modification, unlike conventional breeding, involve the splicing of distantly related or completely unrelated genes into a gene sequence of a given species.
This involves a ‘breaking’ of the species barrier, something that does not normally occur naturally except occasionally when a pathogen attacks a host. Indeed, it is this ability of pathogenic microbes that insures their use as ‘gene canons’ in the splicing process, a process which is crude and unpredictable to say the least.

To me, this mention of a species barrier sounds like Platonism or a declaration of sacred ground via the naturalistic fallacy. Genes are genes. How a new gene gets into the genome doesn't really matter all that much in how it behaves. Inserting a gene and having the same gene mutate from a spare copy or a "junk" sequence doesn't affect the result.

For every desired outcome achieved there are many unexpected traits that are expressed in the resulted progeny including toxic principles in many of the genetically modified plants produced to date and horrific mutations in the work on cloned sheep and salmon to name just a couple of examples in the animal work.

1. You'll have to get more specific about how the insertion of individual genes relates to cloning animals.

2. Nature and breeders are constantly doing the same thing on a random or semi-random basis and no one complains.

The pathogenic gene material has been shown to recombine with microbes in the human gut in the work of Pro. Terje Traavik at the University of Oslo creating super bugs, and the antibiotic marker genes widely used in splicing have contributed greatly to the spread of antibiotic resistance

A link would be nice. Why wouldn't this also be a risk with conventionally bred plants? What's so fundamentally different about GM genes once they're inside the crop's genome?

Unleashing such a shoddily imprecise and unpredictable technology on the general population is what I call ‘bad science’
Good science on the other hand will always have a ‘duty of care’ with the precautionary principle at it’s very core.

From what I see so far, the same argument applies for conventionally bred plants as well. The double standard I see is that conventional breeding allowed us to get similar results while being blissfully ignorant of the details. It gets grandfathered in because it's easier to not think about it. If there's a problem with a GM crop, I'd think it'd be easier to track down and shut down the dangerous strain.

I guess most of the comments here prove that modern science has sold it’s soul to the highest bidder.

You're rather casual with that sort of accusation, which doesn't speak well of your critical thinking abilities or your desire to approach the topic seriously. Myself, I'm just a skeptic/atheist blogger who tries to pay attention to science and pseudoscience. My degree is in spatial science, so if anyone puts a lot of money in my pocket, it'll be because I drew an informative map.

"I guess most of the comments here prove that modern science has sold it’s soul to the highest bidder."

So where's my check?

This involves a ‘breaking’ of the species barrier

Breaking? "Species barrier"? Human-made abstractions. Nature doesn't care about our rules.

My opinion on GMO has generally been that the genetic modification itself is in all likelihood harmless. Although a plant that self produces pesticide could be worrisome, if it occurred on the edible parts.

What one does because they have genetically modified plants seems more likely to create problems. Spraying extra herbicide because your crop is resistant to it does not seem good. A tendency to even less genetic diversity in critical food crops could be very bad if a disease or pest decided it liked the GMO crop. Cross pollination of herbicide resistance to pest species. The actions taken by GMO patent holders against farmers (in some cases), And, other side effects.

On the other hand drought resistance or better yields with less fertilizer and less water could have huge positive impacts in the areas of water and energy conservation. So, I guess I am not a GMO bad or GMO good person, but more of a GMO "it depends" person.

sailor
June 17, 2013
"Yes, given that GMOs are no problem, you wonder
why Monsanto spends millions of dollars fighting
any labeling law rather than using the same money
to educated people."

I don't like the court ruling which prevents a competing dairy from stating a fact on their label ("no artificial growth hormones" or something like that). It seems politically wrong.

However, from a practical point of view, I am not surprised that Monsanto would focus on lawsuits rather than education. Generic staple crops need to be sold to the entire population, and people are don't respond well to education. Besides, a few million bucks pays for a lot of lawyers and long-term court rulings, but it doesn't pay for much temporary TV time. Right or wrong, their approach makes sense for them.

herr doktor bimler
June 19, 2013
"'This involves a ‘breaking’ of the species barrier'
Breaking? “Species barrier”? Human-made
abstractions. Nature doesn’t care about our rules"

I think Texas has a law about "breaking the species barrier" on a farm, but it doesn't have anything to do with farming.

Narad
June 17, 2013
"We’re talking about Bowman? What he did
was buy silo seed, spray the plants with
Roundup, and harvest the seed from the survivors."

No, we are talking about Percy Schmeiser. He is the origin of a lot of the "sued because Monsanto seeds blew onto your property" claims.

It is true that some seeds blew onto the edge of his property and some grew. He took seeds from the plants which appeared to be herbicide resistant, planted them on a section of his farm as a test to confirm that they were indeed Roundup seeds. Upon the positive results, he then took seeds from the test batch and planted them.

In both cases, it seems obvious that the people being sued knew what they were doing, and did so because they wanted to use Monsanto's product without paying for it. They consciously challenged the licensing system and lost. They were not victims of circumstance.

I have a lot of sympathy for their legal arguments, and I am not sure if the courts are correct in rejecting patent exhaustion (essentially ruling that 2nd-generation seeds are not inherently part of the intended use for which the 1st-generation planting was licensed). It seems to me that Monsanto would have to engineer seeds which don't produce a 2nd generation with so little help.

Charles Clearwater

Modern methods of genetic modification, unlike conventional breeding, involve the splicing of distantly related or completely unrelated genes into a gene sequence of a given species.
This involves a ‘breaking’ of the species barrier, something that does not normally occur naturally except occasionally when a pathogen attacks a host. Indeed, it is this ability of pathogenic microbes that insures their use as ‘gene canons’ in the splicing process, a process which is crude and unpredictable to say the least.

“Breaking the species barrier” occurs all the time. In fact a good percentage of your genome is nucleic acid acquired from viruses. Most of the wheat grown in the world has genes recently moved across from wild grasses, deliberately so to provide things like rust resistance.

For every desired outcome achieved there are many unexpected traits that are expressed in the resulted progeny including toxic principles in many of the genetically modified plants produced to date and horrific mutations in the work on cloned sheep and salmon to name just a couple of examples in the animal work.

Cloning and genetic modification are two different things. Many of the genetically modified plants don’t have “toxic principles” at least not more so than the parental plant. This is tested for.

The pathogenic gene material has been shown to recombine with microbes in the human gut in the work of Pro. Terje Traavik at the University of Oslo creating super bugs, and the antibiotic marker genes widely used in splicing have contributed greatly to the spread of antibiotic resistance

Traavik has shown no such thing. He has speculated about it, but without evidence. In the same way that he once claimed Bt corn in the Philippines caused allergies. Nine years later, no evidence of this happening has been presented.

Good science on the other hand will always have a ‘duty of care’ with the precautionary principle at it’s very core.

The precautionary principle is a political construct. It has no place in science.

I guess most of the comments here prove that modern science has sold it’s soul to the highest bidder.

The ‘when you can’t win on evidence accuse others of being shills’ gambit.

Let's see now. The standard plasmid cloning vectors typically contain an ampicillin resistance gene, and some are also designed to carry a neomycin resistance gene. The amp resistance marker allows us to select for plasmid uptake into the bacteria, and the neomycin resistance marker allows us to select for mammalian cells that have received a dose of the plasmid DNA. There are also a few plasmids engineered to have kanamycin resistance.

In other words, the cloning vectors used in the laboratory do not contain scary killer multiple antibiotic resistance genes, but rather some commonplace and limited selection markers.

None of this has anything to do with the evolution of multiple antibiotic resistance in pathogenic bacteria. The control over the use of antibiotic resistance markers in the lab goes back to the Asilomar meeting in the mid 1970s. The discovery of multiple antibiotic resistance in human pathogens came long before then, and long before genetic engineering -- in fact, it was a clue that plasmids are passed back and forth routinely among bacteria, and this led to discoveries that ultimately led to the introduction of genetic engineering and cloning.

As for all the rest of the discussion about "breaking the species barrier" and so forth, perhaps we ought to remind ourselves that DNA is DNA, and it exists in everything from ancient microbes to modern microbes to all the modern plants and animals. Only a few viruses use RNA as a genetic carrier, and they can only do this because they take advantage of the cells they infect to make DNA as the intermediate. There is no species barrier in terms of the makeup of the genetic material, and we know that our own DNA is the product of lots of mixing and churning. Within this context of DNA getting moved around within our own genomes over the course of evolution, it is also true that the sequences that code for the workhorse proteins that run the cells are themselves very similar from one species to another. One journal not too long ago pointed out that we humans share the genetic information in a banana at about the fifty percent level. That suggests pretty strongly that the organisms that predated the split between plants and animals already carried the modern complement of biochemical pathways to a great extent.

What should this mean to the consumer, who is, most of the time, not a practicing molecular biologist? Mostly, we should remind people that the DNA within our cells is derived from our younger cells, going back to the fertilized egg, and that protection of our genomes is something that our cells do aggressively and fairly efficiently. Replication of our DNA occurs via synthetic processes in the cells, and has to happen via the very long chromosomal DNA strands, each one being hundreds of millions of nucleotides long. It's true that we eat lots of DNA because it's a component of food. Our digestive systems are built to break down DNA in food into nutritional components which we recycle as biological building blocks. It doesn't much matter whether that DNA came from a chicken or a tomato, it's all food to our system.

In brief, adding a few nucleotides to part of the plant genome so that it carries out one single solitary extra enzymatic reaction, namely the one that cuts Roundup into 2 ordinary biological molecules, and does so using an enzyme that is made in plenty of other species, does not seem that scary to me. As we discussed on this board long ago, you already get that same enzyme and the DNA that codes for it in the normally occurring bacteria that come along with the produce you buy at the grocery store.

Conspicuous Carl,

I don’t like the court ruling which prevents a competing dairy from stating a fact on their label (“no artificial growth hormones” or something like that). It seems politically wrong.

I tend to agree with you, but we have to bear in mind that are very similar hormone levels (BST and IGF1) in milk from untreated and rBST-treated cows, and no significant nutritional differences. The labeling isn't really very useful unless you want to boycott milk from rBST cows because of the animal welfare issues, which are what concern me. It might be worth mentioning that rBST use reduces the amount of greenhouse gases produced.

Personally I refuse to buy milk from dairies that use homeopathy to treat their cows (Yeo Valley in the UK, I'm looking at you).

Conspicuous Carl,

It seems to me that Monsanto would have to engineer seeds which don’t produce a 2nd generation with so little help.

They already have, but were persuaded not to develop them commercially.

That suggests pretty strongly that the organisms that predated the split between plants and animals already carried the modern complement of biochemical pathways to a great extent.
The way that we can *eat* most other life-forms suggests the same thing.

@Charles Clearwater, June 19, 2013 (#60)

“Modern methods of genetic modification, unlike conventional breeding, involve the splicing of distantly related or completely unrelated genes into a gene sequence of a given species.”

They could do. They could also involve genes in the same genus or even use more copies of a gene already present in the original plant. In some case the GE isn’t in the final product at all, just used for testing aspects. Like all techniques/tools, GE can be used a wide range of ways.

“This involves a ‘breaking’ of the species barrier,”

Genes don’t really have a ‘species barrier’ in that way.

“something that does not normally occur naturally except occasionally when a pathogen attacks a host.”

Actually it also occurs in symbiotic relationships too, where two different species both benefit from eachother. There’s some evidence that it occurs as part of normal development, too.

“Indeed, it is this ability of pathogenic microbes that insures their use as ‘gene canons’ in the splicing process, a process which is crude and unpredictable to say the least.”

This is hand-waving.

“For every desired outcome achieved there are many unexpected traits that are expressed in the resulted progeny including toxic principles in many of the genetically modified plants produced to date”

Evidence wanted.

“and horrific mutations in the work on cloned sheep and salmon to name just a couple of examples in the animal work.”

Cloning animals hasn't much to do with GMOs per se, let alone plant GMOs.

And so on.

“I guess most of the comments here prove that modern science has sold it’s soul to the highest bidder.”

Straw-man. You’d find most academic research scientists aren’t paid that way—in fact, aren't paid especially well at all—and mostly care for accuracy. (There will always be a few exceptions, as is the case for any type of career.)

The "species barrier" nonsense is still gnawing at me. It stinks of the idea of genetic purity. There is no such thing.

Krebiozen
June 20, 2013

Conspicuous Carl,

I tend to agree with you, but we have to bear in
mind that are very similar hormone levels (BST and
IGF1) in milk from untreated and rBST-treated cows,
and no significant nutritional differences.

I know, and I actually avoided the "no rbst" brands because I thought it was empty marketing. But if its a fact, they should be able to say it. The same goes for "organic". They should be free to declare adherence to rules which don't matter.

Normal preamble… I am a Monsanto employee, the thoughts and various whimsies contained in the following are entirely my own and not those of my employer. (this, by the way is the best way to tell a real Monsanto employee… we’re straight up told to tell folk who we work for when discussing things, which gets rather old, hence use of terms such as whimsies)

Modern methods of genetic modification, unlike conventional breeding, involve the splicing of distantly related or completely unrelated genes into a gene sequence of a given species.

Actually, they involve the insertion (splicing is a nice word, scary souding and all, but has a somewhat different technical meaning, which rather illustrates where you’re coming from I think), of exactly homologous genes all the way through spectacularly distantly related genes (it is however false that the genes are unrelated… the relationship just happens in many cases to be utterly ancient)) plus attendant sequences to assist in expression and translation (which again, may be sourced from the species itself, although far more commonly from a viral or viral/synthetic source) into the genome (“gene sequence” again is something with a technical meaning (probably many, depending on which flavor of biology you prefer) of a given species.

blah blah species barrier

This appears to have been dealt with well upthread, and thus I shall merely mock you here with a blah or two.

For every desired outcome achieved there are many unexpected traits that are expressed in the resulted progeny including toxic principles in many of the genetically modified plants produced to date and horrific mutations in the work on cloned sheep and salmon to name just a couple of examples in the animal work.

Partially true, but largely meaningless. Randomly blasting fragments of DNA into a genome is a terribly good way to produce monsterous phenotypes – you simply hope to knock out vital genes and thus characterize what they are for, although many plants are a pain in the ass to do this with due to genome duplications…. However… this isn’t really of great import when talking about commercial transgenics, because, you see, we actually check for that – any transgenic event (as single transformation of a given sequence into the target species) that lands in a gene (or even particularly near one) will never make it past early testing – either it’ll be so disruptive that it causes negative effects, or, should it disrupt something non-vital it’ll be picked up by molecular analysis (those pesky regulators are sticklers for knowing where your event lies). So these horrible mutations which can be produced by genetic modification (and have been so to greatly increase the sum of human knowledge I might add) will never see the light of day as an agricultural product.

The pathogenic gene material has been shown to recombine with microbes in the human gut in the work of Pro. Terje Traavik at the University of Oslo creating super bugs, and the antibiotic marker genes widely used in splicing have contributed greatly to the spread of antibiotic resistance
Pathogenic, again, means something, and you’re misusing it here. I assume for effect. Although I shan’t rule out good ole Dunning-Kruger. Citation needed… I do have one for Terje Traavik, but it would appear that you simply aren’t up to date with Prof. Traavik’s work:-
http://www.biomedcentral.com/1756-0500/5/170/
concludes – “Natural transformation occurring among members of the bacterial community in the lower GIT remains to be demonstrated.”.
One must also be mindful that the antibiotics and selection techniques utilized in plants are different (from what I recall the most used marker genes are to stuff which is commonly, and was commonly prior to GMOs being mainstream, stuff that many species of bacteria were already resistant to (because the E.coli and Agrobacterium strains used in transformation are kept weak as weak can be to facilitate selection – you don’t need to use the newest and greatest antibiotics to knock them on their ass, you can, at times, just look at them funny) – also the main selection markers used to check you have transformed plants are rather predictably herbicide tolerance genes – and nobody, I should hope, is overly concerned about roundup resistant bugs (weeds is another issue obviously, but if you have weeds growing in your guy I suggest perhaps you have bigger issues)

Unleashing such a shoddily imprecise and unpredictable technology on the general population is what I call ‘bad science’

Whereas unleashing such a shoddily imprecise and unpredictable rant about a topic you haven’t the first clue about is simply bad form.

I guess most of the comments here prove that modern science has sold it’s soul to the highest bidder.

This would certainly explain the wholesale acceptance of AGW by the scientific community at large given that opposition to such *only* plays into the hands of an industry which utterly dwarfs all of Agriculture, nevermind simply the small piece of agriculture which Monsanto represents (Net revenue of $10-$20Bn p/a isn’t small change to be sure, but other companies in the food chain make much more (ADM net revenue is ~$80Bn) and oil companies, who one might expect have the capacity to actually buy scientists… well… BP has net revenues closer to $300Bn…. No doubt however your explanation is correct. The companies with the least money can buy scientific opinion, those with the most money… well, they’re too busy or something, that probably explains it.

It is unfortunate that virtually all safety testing of genetically modified food products focus on acute reactions when intuitively it is the potential for chronic effects that is most concerning. We have millions of years of adaptation and symbiosis with the biosphere, and somehow we think we can create whole new species that could not occur in nature by splicing together segments of completely different species (such as GM salmon or BT corn) and as long as it is cosmetically acceptable and doesn't kill someone the moment they touch it assume it is safe. In my opinion any particular transgenic requires consistent and regular consumption by a study group for at least three generations before it should be allowed to market.

However the health concerns aside, genetic modification of food crops and animals is an attempt at masking the inherent problems of our unsustainable agricultural practices, namely synthetic chemical and petroleum energy intensive monoculture. We're placing plants in a completely alien environment and then wondering why nature is fighting back. We create monocultures, so pests have a feeding frenzy. We plant in rows leaving deserts between them, so nature tries to fill it. We engineer the crops to produce their own pesticides and tolerate being drenched in herbicides, so nature denies us the pollinators we need to grow the crops and produces super weeds to defeat our herbicides. In turn, we start using stronger and stronger herbicides... when will we discover the MRSA of weeds? Perpetual escalation always ends in mutually assured destruction.

I personally do my best to avoid genetically modified "foods" however that is relatively easy given I consider the major modified crops - wheat, corn, and soy - to be unsuitable for regular human consumption anyway. In addition, the notion that GMOs will "feed the starving people of the world," is an obfuscation of the real problem - there are too many people.

1. What is the basis for your concern about chronic exposure? How are inserted genes significantly different from those that form from natural mutations and modifications brought about by conventional breeding? These plants we call "crops" were already quite unnatural before we started tinkering with genes in a more direct manner. They would have never developed in nature without human effort and couldn't survive or reproduce on their own. What about chronic health concerns about new cultivars brought about by conventional breeding and natural mutation?

2. What's all this holier-than-thou talk about natural species versus artificial species? Genes are genes. They are what they are, regardless of their origin. It's also kind of creepy, since it's sounds like you believe in a concept of genetic purity. No. Such. Thing.

3. Genetic modification and monocultures are two entirely different concepts. We know monocultures are a problem.

In addition, the notion that GMOs will “feed the starving people of the world,” is an obfuscation of the real problem – there are too many people.

So - let 'em starve?

Not a surprise to see Orac again unable to refer to any true science, ignoring the problems with basic safety in corporate products & again denying the avoidable injuries caused to a small, but growing, percentage of our kids who are susceptible to being permanently damaged or killed by inadvertant vaccination.

One of Orac's problems is that he is fully aware of the truth & the science, but knowingly spouts lies & deceptions anyway. He has violated every tenet that should guide scientific inquiry & commentary.

He disingenuously associates extreme examples of ignorance (chemtrails, bigfoot, 911 theories) with honest people trying to get to the truth about unregulated & toxic consequences in genetic engineering of our food and the bloated & unsafely administered vaccination schedule.

He helps to obscure the genuine questions about the science, application & administration of these technologies & the lack of meaningful safety studies (as well as changes in technological methods, regulations & legislation).

Rules are crafted to favor profit potential rather than safety through science. Studies pretend to be science-based, having credentialed authors (like Orac) willing to sacrifice their integrity & reputations for bribes or job security, no matter the consequences to the general public.

His original article, like everything Orac blogs about, lacks independent science references and relies on industry-sponsored "science" or industry-dependent minions (such as Orac) who pander to drug companies or govt regulators to gain materially.

I may expose all the problems with this "article" in the future, as I have done with other "articles" Orac has posted.

For right now, I'm just noting his fact-less & fact-twisted antics

I'm researching & communicating with regulators & industry. I have suspended detailed time-consuming blog posting... for the moment...

I may expose all the problems with this “article” in the future, as I have done with other “articles” Orac has posted.

What like in this comment of yours? http://scienceblogs.com/insolence/2010/07/26/cancer-treatment-centers-o…

Michael, you have an odd idea of what constitutes a fact.

It is unfortunate that virtually all safety testing of genetically modified food products focus on acute reactions when intuitively it is the potential for chronic effects that is most concerning.

Ignoring of course the long term multigenerational studies which are performed and show no chronic effects. Or, y'know, the abject lack of any plausible mechanism by which chronic effects would occur.

and somehow we think we can create whole new species

Perhaps this is semantics, although I feel not (meaningful terminology appears to be something the anti-GM movement cares not one fig about), but these aren't new species. They are at best (and at a push) new varieties of already extant species.

In my opinion any particular transgenic requires consistent and regular consumption by a study group for at least three generations before it should be allowed to market.

One assumes if 3 generations were used you'd demand 5, or 10, or whatever made it economically non-viable to do GMOs... however given that multigenerational studies have been done, and a recent review of the literature suggests they are not worthwhile and that 90 day studies are sufficient... http://www.sciencedirect.com/science/article/pii/S0278691511006399 one wonders exactly what foundation other than fantasy your demand for multigenerational studies rests on?

genetic modification of food crops and animals is an attempt at masking the inherent problems of our unsustainable agricultural practices, namely synthetic chemical and petroleum energy intensive monoculture.

It really isn't. Bt for instance doesn't mask the use of synthetic chemicals, it replaces it. RR merely switches to an easier to use chemical input, other efforts target other areas (my own current are of research has bugger all to do with altering the chemicals used and simply looks to increase the intrinsic yield of crop plants under stress conditions)

We plant in rows leaving deserts between them, so nature tries to fill it.

Deserts? You must live by some really odd farmers, because row cropping rather relies on canopy closure and no-gaps in order to maximize the capture of sunlight (both Soy and Corn are moving to smaller spacing)

. We engineer the crops to produce their own pesticides and tolerate being drenched in herbicides, so nature denies us the pollinators we need to grow the crops and produces super weeds to defeat our herbicides.

"Drenched" in herbicides? I suppose if you consider a 0.5ml (ish) application of herbicide drenching... (back of the envelope calculation taking into account the planting density of corn (about 28,000 to 36,000 plants per acre) and the application rates of glyphosate mixes suggested)...

Denied pollinators? What on earth are you on about? One assumes you're perfectly aware that links between GM production and CCD (I assume that is what you're talkign about in terms of pollinators anyway...) is utterly spurious.

In addition, the notion that GMOs will “feed the starving people of the world,” is an obfuscation of the real problem – there are too many people.

I guess you'll be signing up then to watch your friends and family starve to death - it's for the good of the planet after all.

I’m researching & communicating with regulators & industry. I have suspended detailed time-consuming blog posting… for the moment…

Oooooh, we so scared.
Good that you're taking a break. Posting drivel is so tiring.

Michael Polidori is gullible and/or ignorant enough to take vet and naturopath Joel Wallach's 'Dead Doctors Don't Lie' seriously. This is crankery of a high degree indeed.

People in China who live for 250 years? Cystic fibrosis (not a genetic disorder, he claims) cured with selenium supplements? Diabetes is the result of a chromium and vanadium deficiency? Cardiomyopathy is also due to selenium deficiency? Wallach promotes all these idiotic beliefs and more.

There's also the unfortunate incident of a patient under his care dying while being chelated.

Ewan R

Normal preamble… I am a Monsanto employee

So, you you should be able answer something I have always wondered about - what does roast puppy taste like?

I have suspended detailed time-consuming blog posting…

One can only hope that you'll continue revolutionizing physics in YouTube comments.

So, you you should be able answer something I have always wondered about – what does roast puppy taste like?

Broccoli.
At least our version does, for some reason we have been told it is uncommercializable though. Which is odd because I didn't see anything come up in the allergen hit database.

I'm reminded of an urban legend behind Kentucky Fried Chicken's name change to KFC. One explanation I heard from a KFC spokesperson on TV was that people like initialisms and acronyms. Another, more likely, one I've heard is that they wanted to take people's mind off of "Fried" and the fatty connotation that comes with it. There are a lot of stupid marketing departments out there, as well as marketing departments that assume customers are largely stupid. Of course, the latter tend to be right a lot of the time.

The crazy urban legend one was that KFC had genetically engineered monstrous mutant chickens for mass production pen farming who no longer legally qualified as chickens, so government regulations required them to change the name of the franchise, but apparently not the names on the menus.

Bronze Dog: what really cracks me up about that urban legend was that some versions claimed the chickens were genetically engineered to be boneless, and conveniently tube-shaped for easier processing. Which, of course, means that anybody who forwards that to you has never actually seen a KFC or watched one of their commercials, as apart from their new experimental boneless wing product, they have always sold bone-in chicken.

In fact, so clearly are they *not* massively engineered that you can do what I like to do whenever I have KFC: pick apart the wings to see the fingerprints of evolution. Chickens still have claws on their thumbs, like the good little dinosaurs they really are. ;-)

Oh, minor addendum: they do use boneless chicken in their sandwiches, for obvious reasons. ;-)

The crazy urban legend one was that KFC had genetically engineered monstrous mutant chickens for mass production pen farming who no longer legally qualified as chickens, so government regulations required them to change the name of the franchise, but apparently not the names on the menus.

There is a similar legend about McDonald's, claiming that they buy their meat from a company called "100% Beef" so they can say their burgers are 100% beef.

Both of these legends are debunked on Snopes.com if people are interested in the details.

"Bronze Dog
June 22, 2013

1. What is the basis for your concern about chronic exposure? How are inserted genes significantly different from those that form from natural mutations and modifications brought about by conventional breeding? These plants we call “crops” were already quite unnatural before we started tinkering with genes in a more direct manner. They would have never developed in nature without human effort and couldn’t survive or reproduce on their own."

Ah, but they can. Terminator seeds are currently off the market. GM wheat, corn, and soy, are self replicating. For comparison, mules are typically sterile. Show me a corn crop that has naturally bred with a bacterium. Show me a fish that has naturally bred with a fish of an entirely different species. Is it possible after a million years of evolution? Sure. After nature has repeatedly bred out the lines that proved unfavorable to the biosphere. Instead we strictly replicate the lines that are favorable to profits with total disregard to the biosphere.

A species that lives a hundred years tampering with processes that span millions. Kinda defines arrogance.

"3. Genetic modification and monocultures are two entirely different concepts. We know monocultures are a problem."
Oh do you now? So, tell me, what role does genetic modification have in polyculture? In permaculture? Genetic modification is an affront to systems engineering.

"TBruce
June 23, 2013

In addition, the notion that GMOs will “feed the starving people of the world,” is an obfuscation of the real problem – there are too many people.

So – let ‘em starve?
"
No. But stop supplying them with the excess calories they need to breed.

"Ignoring of course the long term multigenerational studies which are performed and show no chronic effects."
On rodents. Because mice always translate to humans.

"but these aren’t new species. "
That depends on how you define a species, which is obviously subjective. Somehow I think a species of corn that does not inherently produce a pesticide might just be a different species than one that does.

"One assumes if 3 generations were used you’d demand 5, or 10, or whatever made it economically non-viable to do GMOs… however given that multigenerational studies have been done, and a recent review of the literature suggests they are not worthwhile and that 90 day studies are sufficient… http://www.sciencedirect.com/science/article/pii/S0278691511006399 one wonders exactly what foundation other than fantasy your demand for multigenerational studies rests on?"
Intuition. Even Einstein thought it was a good idea.

"It really isn’t. Bt for instance doesn’t mask the use of synthetic chemicals, it replaces it."
Precisely. It is a mask. Synthethic chemicals are entirely unnecessary. Bt is a natural bacterium with limited evidence of adverse effect in humans. But the use of Bt is a symptom of an unsustainable practice - monoculture. However Bt transgenics are granted GRAS (Generally Regarded As Safe) status, meaning no further safety testing is called for. Nevermind that Bt transgenics are commonly produced using microprojectile bombardment which is prone to random gene deletion and aberrant mutation. As long as it looks OK, it's safe, right?

"Deserts? You must live by some really odd farmers, because row cropping rather relies on canopy closure and no-gaps in order to maximize the capture of sunlight (both Soy and Corn are moving to smaller spacing)"

Where there are rows, there is bare soil.

"“Drenched” in herbicides? I suppose if you consider a 0.5ml (ish) application of herbicide drenching… (back of the envelope calculation taking into account the planting density of corn (about 28,000 to 36,000 plants per acre) and the application rates of glyphosate mixes suggested)…"
As a farmer who uses zero herbicides, I do. Glyphosate is an established environmental toxin and carcinogen with a soil half-life ranging from weeks to several months depending on soil microbial activity. Its agricultural use should be banned.

"One assumes you’re perfectly aware that links between GM production and CCD (I assume that is what you’re talkign about in terms of pollinators anyway…) is utterly spurious."
An opinion totally ignorant of evidence and risk.

"I guess you’ll be signing up then to watch your friends and family starve to death – it’s for the good of the planet after all."
Are you going to quote Revelations, as well?

APC,

These plants we call “crops” were already quite unnatural before we started tinkering with genes in a more direct manner. They would have never developed in nature without human effort and couldn’t survive or reproduce on their own.

Ah, but they can. Terminator seeds are currently off the market. GM wheat, corn, and soy, are self replicating. For comparison, mules are typically sterile.

You miss the point. Bronze Dog was referring to regular crops, not GM. Selective breeding, which humans have been doing for thousands of years, results in a number of plants that couldn't survive or reproduce on their own.What mules have to do with it, I don't know, unless you are suggesting that natural "abominations" cannot reproduce, while human abominations can, which is just silly.

Show me a corn crop that has naturally bred with a bacterium.

Haven't you heard of horizontal gene transfer?

Show me a fish that has naturally bred with a fish of an entirely different species. Is it possible after a million years of evolution? Sure.

Please tell me you don't think GM foods are the result of interbreeding different species.

After nature has repeatedly bred out the lines that proved unfavorable to the biosphere. Instead we strictly replicate the lines that are favorable to profits with total disregard to the biosphere.

Nature doesn't give a rat's posterior about the biosphere. A species will expand until something stops it. Humans are part of the biosphere too, you know.

A species that lives a hundred years tampering with processes that span millions. Kinda defines arrogance.

Worrying about a natural experiment that is destined to be utterly destroyed in a couple of billion years kinda defines futility. Plenty of species have made a mark on the planet that last millions of years.

there are too many people.
So – let ‘em starve?

No. But stop supplying them with the excess calories they need to breed.

What an obnoxious sentiment. Shall we start with your family? Thought not. Whose family shall we start with then?

“Ignoring of course the long term multigenerational studies which are performed and show no chronic effects.”

On rodents. Because mice always translate to humans.

Not just rodents, and don't forget the billions of human meals, without a trace of any adverse effects.

“but these aren’t new species. ”

That depends on how you define a species, which is obviously subjective.

It isn't subjective, there are some minor disagreements, but none of the GMOs we have seen thus far are different species by any definition I have seen. They are far too similar to the species they are based on.

Somehow I think a species of corn that does not inherently produce a pesticide might just be a different species than one that does.

Plenty of plants naturally produce toxins of one sort or another to protect themselves, this isn't unusual.

Intuition. Even Einstein thought it was a good idea.

I don't think Einstein meant that you can make stuff up and insist it's true without any evidence to support it.

It really isn’t. Bt for instance doesn’t mask the use of synthetic chemicals, it replaces it.

Precisely. It is a mask. Synthethic chemicals are entirely unnecessary.

You misunderstand. Bt isn't a mask, it allows you to increase yield without synthetic chemicals.

Bt is a natural bacterium with limited evidence of adverse effect in humans. But the use of Bt is a symptom of an unsustainable practice – monoculture. However Bt transgenics are granted GRAS (Generally Regarded As Safe) status, meaning no further safety testing is called for. Nevermind that Bt transgenics are commonly produced using microprojectile bombardment which is prone to random gene deletion and aberrant mutation. As long as it looks OK, it’s safe, right?

I don't really follow your point. You know what else is prone to random gene deletion and aberrant mutation? Organic plants, which are exposed to natural background radiation, and natural UV light.

Glyphosate is an established environmental toxin and carcinogen with a soil half-life ranging from weeks to several months depending on soil microbial activity. Its agricultural use should be banned.

An "established environmental toxin and carcinogen"? Citation?

One assumes you’re perfectly aware that links between GM production and CCD (I assume that is what you’re talkign about in terms of pollinators anyway…) is utterly spurious.

An opinion totally ignorant of evidence and risk.

Show us some evidence then. Making unsupported claims doesn't cut it here.

I guess you’ll be signing up then to watch your friends and family starve to death – it’s for the good of the planet after all.

Are you going to quote Revelations, as well?

You're the one suggesting we starve people just enough to make them infertile. Since it's your idea it's only fair that you should be first in the queue. However, I suspect you are thinking of people of a different color far away where you won't have to watch them suffer. Which I think is monstrous.

APC: If you think choosing to let the world starve (and yes, starving to the point of infertility *is* starving, and actually probably even crueler than killing them outright since you condemn them quite consciously to a lifetime of pain) is in any way sustainable . . . well. Enjoy the global war you will have created. BTW, people in starvation zones still breed, so I do not think you really understand what you are talking about.

Bt is a natural bacterium with limited evidence of adverse effect in humans. But the use of Bt is a symptom of an unsustainable practice – monoculture.

Bt-corn is beneficial whether you are practicing monoculture or not, and monoculture is widespread in GMO-free and even organic farms.

BTW, if you are concerned about creatures artificially created that cannot survive without human assistance and which are extremely vulnerable due to monoculture, why do you not focus your ire upon the Cavendish banana?

Point of fact: many Monsanto seed licenses require planting "refuges" as a percentage of acreage. The refuges are non-GMO crops designed to act as buffers to help prevent evolution of resistance, by giving a place for non-resistant pests to out-compete resistant pests.

Looks like I missed APC's nonsense while I was taking a break from RI. Thanks for doing your part, Kreb.

Of course, I'm disgusted with the starvation sentiment as well as the implicit racism and wingnuttery/trollish libertarianism I sense behind it.

It's counter-intuitive, but it seems to me that famine can provide incentives to have more children. Reproductive rates are high in areas of famine in part because the people are essentially trying to ensure there is a next generation by producing higher numbers so some can survive. They also tend to put children to work as farmhands and scroungers, thinking they can get a net increase in food for their family that way. If we can make GMO crops for them that produce higher or more reliable yields with less work, we'll remove those incentives that lead to population explosions.

Access to contraception also helps because it makes having a child a conscious decision to be approached sensibly, rather than an accident viewed as an inevitable consequence of having sexual instincts.

Overall, the general solution to overpopulation is to increase quality of life. Make it easier for children to survive into adulthood, and parents will feel safer about having fewer children while investing more resources per child. Provide education and there will be opportunity for their children to get more lucrative jobs to support the family while potentially providing economic power to the nation as a whole in the form of a better skilled labor force.

It's better than dehumanizing them so you can rationalize trampling on people who are already suffering.

@ChrisP -Comment # 83 - a personal attack without explanation or substance. I stand by every fact I posted. Chris doesn't take the time to cite a single factual error in my post.

@Tbruce - #85 - Another factless post abd personal attack. Where's your evidence?

@ Krebiozen - #86 - Wallach has never claimed people in China lived to be 250 years old. In one of his books he mentions a Chinese govt report of Chinese herbalist Li Ching-Yuen living to the age of 256, but it's anecdotal and not used by Wallach in the plural or as an example of something that can be achieved by any human being.

From the Cystic Fibrosis Foundation - "Antioxidants may have a role in the slowing or PREVENTION of CF lung disease". They go on to talk about selenium and zinc supplementation as necessary for everyone with Cystic Fibrosis.
In PMC2696206 it is stated "Se supplementation studies in individuals with CF suggest benefit"
There is no record of any patient dying while Dr Wallach was chelating them.
Both the 250 year old chinese people and the chelating story can be found on shill webistes like Skeptic's Dictionary... and no where else

.Obviously Kreb doesn't know what he is talking about... or he is deliberately knowingly lying

.Obviously Kreb doesn’t know what he is talking about… or he is deliberately knowingly lying

It took you nearly three weeks to come up with this?

Mr. Polidoro is very slow at responding to anything. I asked him a question on another blog NVIC cherry picking data and he never responded.

He also has a habit of commenting on year old comments on YouTube. He is not exactly the fastest or brightest match in the box.

Michael Polidori,
You are seriously defending Wallach? He has made so many ludicrous claims I'm surprised anyone takes him seriously.

Wallach has never claimed people in China lived to be 250 years old. In one of his books he mentions a Chinese govt report of Chinese herbalist Li Ching-Yuen living to the age of 256, but it’s anecdotal and not used by Wallach in the plural or as an example of something that can be achieved by any human being.

Here are Wallach's own words from 'Dead Doctors Don't Lie' (PDF):

The oldest living person that has some documentation (I'm sure there is a certain amount of exaggeration in there), was a fellow, a Dr. Li, along the Tibetan Border, and this fellow, when he was 150 years old received a big certificate from the Imperial Chinese Government. He was born in 1677, and 150 years later was given a certificate by the Imperial Chinese Government for being 150. And then when he got to be 200 years, they sent him another, and then 50 years later they sent him another certificate, and supposedly he died at age 256. It's people of that nature - he's written up in the New York Times in 1933 when he died, and The London Times, and so this is fairly well documented. But he may have only been 200 years old. I don't know if he was 256, but this is the person who led James Hilton to write that story.

I withdraw my statement that Wallach claimed that people in China live for 250 years; it was merely 200 years.

From the Cystic Fibrosis Foundation – “Antioxidants may have a role in the slowing or PREVENTION of CF lung disease”. They go on to talk about selenium and zinc supplementation as necessary for everyone with Cystic Fibrosis.

Wallach has claimed that CF is not a genetic disease (link is to his own website) and that it can be cured using selenium, which is nonsense. Also, here's the full quote from the CFF (from their website):

Antioxidants may have a role in the slowing or prevention of CF lung disease. A healthy diet, including fruit and vegetables supplemented by fat-soluble vitamins, can boost the CF patient’s antioxidant protection.

There is no mention of selenium and zinc supplementation being necessary for everyone with cystic fibrosis. Fat soluble vitamins may be important in CF patients because they suffer from pancreatic insufficiency which can reduce absorption of fats and fat-soluble vitamins. Antioxidants may (or may not) reduce the number of lung infections CF patients get, but it won't change their genome.

There is no record of any patient dying while Dr Wallach was chelating them.

The National Council Against Health Fraud reports that:

In 1995 NCAHF received a report from a consumer in California who stated that Wallach was dispensing chelation therapy for coronary artery disease at a clinic in San Francisco. The caller was concerned because her father-in-law had died following Wallach's care. He had become very weak, but Wallach had poisoned him against returning to his regular physician, so he did not seek medical help. His wife, who is also a disciple of Wallach's ideas and health care, had the body cremated.

This wouldn't be the first death associated with chelation, which isn't proven to be useful for anything other than documented heavy metal poisoning.

Both the 250 year old chinese people and the chelating story can be found on shill webistes like Skeptic’s Dictionary… and no where else

That's not true.

.Obviously Kreb doesn’t know what he is talking about… or he is deliberately knowingly lying

I demand an immediate apology for this outrageous besmirching of my character.

I'm still waiting for a clear, meaningful distinction between plants that had genes deliberately inserted and plants that were genetically modified by natural mutation and selective breeding. Why all the hubbub? (Aside from the obvious naturalistic fallacy in play.)

Whining about species barriers comes across as borderline evolution denialism, since evolution means any "species" we label is a moving target. The collective group of organisms that can produce fertile offspring through breeding are the reality. The "species" label is just a human symbol we invented to talk about those collections of organisms. I say slaughter the sacred eidolon cow of Platonism; it makes the best hamburger.

Talking about vague risks of new genes misses the whole point why we bring up selectively bred plants, since random mutations can also be dangerous for the same reasons. If you complain about a type of risk, you can't just demonize one source of it, whitewash another, and expect us to accept the double standard. I don't buy into Disneyfied views of nature.

Talking about monocultures completely misses the topic in question. I wouldn't be surprised if genetic modification could be used to reverse monoculture trends if harnessed the right way. The technology and how people can use or abuse it are two different things. We're talking about whether or not there are health risks from eating GM crops, which is a scientific question. How we deal with monocultures seems an unrelated and largely political question to me.

Talking about how these plants can't sustain themselves demonstrates the ignorance of what humankind has been doing to these plants over the millennia. We've bred numerous crops that are completely dependent on human care. We did this long before we knew genes existed. I don't recall hearing anyone complain about food crops growing in the wild as invasive species... You know, a food crop being unable to survive without human care would actually be a good thing if you're an environmentalist who hates invasive weeds.

I am not so sure there is bad science regarding the safety of GMOs. I think there are studies with limitations but I think that one must be careful to brand any peer reviewed study as bad science. In reality, no single study can do everything.

We must also be careful about what we brand as bad science. If a study shows a potential negative health issue regarding GMOs this begs the question whether the researchers were out to show that GMOs are bad? Does it then follow that every study showing potential negative effects of GMOs is bad science or conversely that if a study shows no adverse health effects of GMOs that the researchers were out to prove them safe – also making it bad science? Science is directed by hypothesis which defines the study. This simply means that the results from a study must be contextualized within the parameters of the study.

Since the lead article clearly complains about bad science in showing potential negative impacts of GMOs – let me give you an example of science with limitations but where the authors over extend their findings to determine that GMOs are the same as thir conventional counterpart.

In the study by Cromwell et al. 2002 (Soybean meal from Roundup Ready or conventional soybeans in diets for growing-finishing swine) the authors conclude “This study clearly demonstrates that genetic modification of soybeans to make them tolerant to glyphosate herbicide does not affect their nutritional composition or the performance of swine when fed the soybean meal derived from the soybeans.” And what did they do to substantiate such a very conclusive statement? They basically fed pigs GM and non-GM soy, respectively, then checked the amount of back fat and size of longissimus muscle (loin) from which chops were cut, cooked and eaten by “an experienced sensory panel”. Oh and they also determined the composition of the soybean meal and crude composition of the loin (water, protein, fat and ash) to be able to conclude that GM soybeans does not affect “the performance of swine”.
In this study, performance is based on a sensory test and crude analysis of the loin. Was this bad science or just a study with limitations?

Just as one study does not conclusively show safety, one study cannot show detriment. What is important is that research not be branded as good science or bad – especially if it is peer reviewed. The more research the better.

A recent study Thongprakaisang et al. 2013 (Glyphosate induces human breast cancer cells growth via estrogen receptors) concluded that “Furthermore, this study demonstrated the additive estrogenic effects of glyphosate and genistein which implied that the use of glyphosate-contaminated soybean products as dietary supplements may pose a risk of breast cancer because of their potential additive estrogenicity”. Does this mean that glyphosate residue in GM herbicide tolerant soybeans will cause breast cancer? No! But it does mean that more research is needed to understand the potential link between what we eat and how it affects our bodies.

PS: What were the affiliations of the authors for the studies I referred to?
Cromwell et al. 2002: University of Kentucky and Monsanto Company - USA.
Thongprakaisang et al. 2013: Chulabhorn Graduate Institute and Chulabhorn Research Institute - Thailand

On the issue of herbicides and pecticides - like many of the household chemicals we use they are not healthy in the same way that detergent or brake fluid isn't healthy.
But we still use them because of the necessity or the choices we make. However, to think that these chemicals are "safe" is an error. The term safe refers to the correct and intented use in the context of specific paramenters.

Many studies have shown that glyphosate and formulations thereof are toxic – although little surprise there it is a herbicide – to mammals, Nile tilapia and sea urchin (Benachour et al., 2007; Clair et al., 2012; Daruich et al., 2001; Gasnier et al., 2009;Gui et al., 2012; Jiraungkoorskul et al., 2002; Koller et al., 2012; Malatesta et al., 2008b; Marc et al., 2002; Marc et al., 2004; Paganelli et al., 2010; Romano et al., 2012).

I have no problem with the use of pesticides and herbicides in a controlled and responsible manner – but it does amuse me to see how desperately the industry try to put a positive spin on something against all odds. A review sponsored by the industry not surprisingly concluded that “the available literature shows no solid evidence linking glyphosate exposure to adverse developmental or reproductive effects at environmentally realistic exposure concentrations” (Williams et al., 2012). They did concede that where glyphosate toxicity has been observed, it is the result of “surfactants present in the formulations and not the direct result of glyphosate exposure”. Why?” Because we say so!

Does this mean that we must stop using glyphosate? No! But it does mean we should start to think about sustainability, not from a fanatic "green" perspective but thinking about how much chemical pollution our ecosystem (including ourselves) can actually handle. One company rep admitted at a meeting a few years ago that in some areas farmers were spraying up to three times the concentration of glyphosate, than was recommended, because of the development of resistance in weeds.

In science we are taught that in an enclosed reactive system, one or more of the components will become limiting over time. In a sense the earth also represents an enclosed system and by the time one or more components becomes limiting it will be too late to do anything about it.

I am not so sure there is bad science regarding the safety of GMOs. I think there are studies with limitations but I think that one must be careful to brand any peer reviewed study as bad science.

So, that would be a long-winded failure right out of the gate?

In science we are taught that in an enclosed reactive system, one or more of the components will become limiting over time.

Ah, yes.

(Benachour et al., 2007; Clair et al., 2012; Daruich et al., 2001; Gasnier et al., 2009;Gui et al., 2012; Jiraungkoorskul et al., 2002; Koller et al., 2012; Malatesta et al., 2008b; Marc et al., 2002; Marc et al., 2004; Paganelli et al., 2010; Romano et al., 2012).

Is that copypasta I smell cooking?

Narad resorts to insults because he has no other defence. Yawn!

Dave, it's not the results that determines if it's bad science, it's bad methodology. You could have cited those studies without rehearsing your prejudices and throwing up straw men.

David Smith,

What is important is that research not be branded as good science or bad – especially if it is peer reviewed.

There are objective standards that can be used to assess the quality of studies, as used to decide which studies are included in systematic reviews and metaanalyses, for example here. I think you will find that Orac is quite justified in labeling the studies he refers to as bad science, and that he explains why in some detail.

@Chris AGAIN doesn't use any evidence & his post is a baseless and/or irrelevant personal attack

@kreb - kreb demanding an apology... when his entire post supported exactly what I said when I called him ignorant OR a knowing liar
The Cystic Fibrosis Foundation states – “Antioxidants may have a role in the slowing or PREVENTION of CF lung disease”.
How do anti-oxidants PREVENT what kreb & CFF claim is a genetic disease?
The benefit of selenium is admitted by CFF and in the study I quoted... but neither fully explain the degree of benefit
Then kreb again brings up the 256 year old ONE chinese person reported by the Chinese govt, kreb pretends Wallach has extrapolated that to more than one case when kreb's quote shows Wallach discounts the record as exagerated. Wallach NEVER states that 200 or 256 year old Chinese people are a regular occurrence nor does he cite ANY OTHER CHINESE PERSON LIVING TO ANY AGE APPROACHING WHAT WAS REPORTED IN CHINESE RECORDS
Stop twisting the truth & lyinglies about Dr Wallach, kreb... repetition doesn't make these things believable or fact-based... or are you a student of Nazi propaganda techmiques?
Then kreb quotes the NCAHF... really kreb? The Barrett/Baratz run organization associated with QuackWatch?
Barrett, the disgraced "doctor" & infamous king of the QuackPots?... please, kreb, stop embarrassing yourself.
Again, instead of using eidence against Dr Wallach you use an admitted THIRD-HAND description of a letter from an unamed source claiming to be a relative of someone who received chelation from Dr Wallach then subsequently died... really? this is the best you can do? This is the extent of your evidence against Dr Joel Wallach?
You besmirch yourself again, forcing me to pseudo-besmirch you... again!

Wow, just wow.

Mr. Polidoro would not know what real evidence is if fell into a pit of papers. Especially since I actually posted a bunch, and then asked him a question. Only he ran away instead.

The only pseudo-science involved in GMOs and their regulation is the phrase "substantially equivalent" which the FDA uses to avoid regulating GMO.
Through this industry-concocted phrase FDA claims GMO are essentially the same as conventional or organic food crops.
Of course this is nonsense as "pest-resistant" GMO corn (one example of MANY) has 2 insecticides in every part of the plant which will kill some insects that normally feed on corn, but chemical insecticides STILL have to be used to kill a wider range of corn pests..
"Round-up Ready" corn is regularly sprayed with herbicide, contaminating every part fo the crop, inside and out, with substances that have never been part of our diets, but are known to kill most plant life.
Changing the DNA of any plant or animal will cause inknown changes to the food. This cannot be avoided. When a crop is "instructed" by the random insertion of a multi-gene package to produce 2 types of insecticide it has to contruct those insecticides from existing nutrient bases in the soil. This will detract from the nutritional content as no changes were made to compensate for this added burden of poison-protein synthesis.
Additional changes occur in the nutritional levels (some are documented), but while companies may be aware of the changes they do not have to report them to the FDA or USDA as all gene altered crops are pre-approved for market based on the nonsensical phrase "substantially equivalent".
Biotech companies can engage the FDA in voluntary consultations... but they are VOLUNTARY.
Are the foods affecting us? It's hard enough to determine what foods may be making us ill... but if one of the potential causes is hidden so that no one knows if you are eating GMO because no labeling is required then it is IMPOSSIBLE to even guess that GMO may be involved in any trends, poisonings, nutritional deficiencies or immune problems
That pharase "substantially equivalent" is so blatant a lie I am surprised, to this day, that it is being used.
Conventional corn can be eaten by insects that normally feed on corn. GMO corn will kill some of those same insects... that is not substantially equivalent, from a bug's-eye view.
When we change the DNA of our food with a random insertion of a package of genes (viral bacterial animal and/or human) which causes the plant to divert resources to the creation of toxic proteins we diminish the corn's nutritional value, increase the growing time to mature harvest and cause changes to the corn that no one can predict & no one is looking for.
Arpad Pusztai's potatoes reveal 2 things.
1, causing potatoes to produce lectin resulted in some rats, being fed the potatoes, to sicken & die, This was alarming and unexpected... UNEXPECTED!!!
2, the reaction of British biotech companies and the British govt was to attack Pusztai's credibility and abilities as a researcher, even though he is a world renowned and respected geneticist.
This is typical corporate tactics & corporate-influenced govt tactics, to ignore safety and health issues in favor of corporate profits... in this case protecting the technology from bad press (the truth) so that ownership of our entire food supply by corporations can proceed... with farmers unable to save seed, paying more for GMO seed and consumers deprived of choice (this includes the destruction of the organic food industry by widespread contamination of the USA food crop. Organic corn and soy are the first 2 victims on USA and Canadian farms.
Anyone defending the current horrendous way in which we ignore safety, ignore concerns about nutrition, ignore widespread contamination of conventional & organic crops and ignore the overwhelming majority of informed Americans and Canadians who want GMO labeled... anyone who sides with this betrayal of trust and hijacking of our food supply is ignorant of the facts surrounding this misapplication of biotechnology and/or is working directly or indirectly for the industry.
There are unfortunately many individuals who will sell their soul for a narcissistic short term gain.
Slong with Pusztai's persecution we can also see industry and regulators cooperating to harass, injure and/or silence others...
Eric Topol of the Cleveland Clinic for his work exposing Merck killing people with Vioxx
FDA Associate Director of Drug Safety David Graham forced to seek whistleblower protection when he joined Topol & Nissen & 6 other researchers exposing Vioxx deaths & injuries
Dr Andrew Wakefield persecuted for suggesting in 1998 that MMR vaccine may need some safety studies, and blamed to this day for any instance of MMR uptake drops or flare ups of measles... even in vaccinated populations, Dr Wakefield is still somehow blamed.
GMO crops are not needed and will make food more expensive leading to more people starving while biotech corporations get wealthy in the short term.
Underutilizing much of our cropland in the world we still produce enough to feed 3 billion more people than we have. We must convert to sustainable farming practices because the alternative is, well how should I put this... unsustainable!

Dr Andrew Wakefield persecuted for suggesting in 1998 that MMR vaccine may need some safety studies, and blamed to this day for any instance of MMR uptake drops or flare ups of measles… even in vaccinated populations, Dr Wakefield is still somehow blamed.

Rest assured that the effort to tie it up with a bow is much appreciated, no matter how sloppy the execution.

Michael, you have no idea what substantial equivalence means.

Whenever you grow a crop, the make up of the product will differ slightly due to differences in the soil, the amount of rain, how much insect attack there was, the temperature, whether there had been a frost and if so when, what cultivar was grown and so on. Every lettuce you eat has a slightly different make up to every other lettuce.

The concept of substantial equvalence corrects for these variations in safety assessments. Something can be a bit different in make up, but not actually be harmful or less nutritious. The data has to establish that the GM product has the same same concentrations of nutrients that would normally be found within the range of conventional products.

It is really quite a sensible idea. Only if the product has something outside the range of what people already safely eat, should a concern be raised.

As for your other arguments: Arpad Pusztai showed that raw potatoes were harmful to rats. His data had more differences between raw and cooked potatoes than between cooked potatoes and GM potatoes.

And Merck, they have nothing to do with GM crops.

Wakefield was shown to have doctored his results and lied to his collaborators.

I could go on, but suggest it better if you were first to construct a coherent argument we could consider, rather than a rash of conspiracy theories.

Michael Polidori,

@kreb – kreb demanding an apology… when his entire post supported exactly what I said when I called him ignorant OR a knowing liar
The Cystic Fibrosis Foundation states – “Antioxidants may have a role in the slowing or PREVENTION of CF lung disease”.
How do anti-oxidants PREVENT what kreb & CFF claim is a genetic disease?

You are seriously claiming that this statement by the CFF supports Wallach's claims that selenium supplements cure cystic fibrosis? They wrote, following that statement:

A healthy diet, including fruit and vegetables supplemented by fat-soluble vitamins, can boost the CF patient’s antioxidant protection.

CF patients have trouble absorbing fat-soluble vitamins, not selenium. There is a big difference between cystic fibrosis and cystic fibrosis lung disease.

Cystic fibrosis is "an autosomal recessive genetic disorder that affects most critically the lungs, and also the pancreas, liver, and intestine. It is characterized by abnormal transport of chloride and sodium across an epithelium, leading to thick, viscous secretions." (From Wikipedia). I used to help diagnose CF by doing sweat tests, which show abnormally high sodium in sweat, which no amount of selenium will cure.

Cystic fibrosis lung disease is a consequence of cystic fibrosis, characterized by repeated infection and inflammation of the lungs. It is this progressive process that antioxidants may be able to slow or perhaps even prevent, not CF itself.

Selenium is not an antioxidant, though it is a component of some antioxidant enzymes.

Wallach clearly states that cystic fibrosis is not a genetic disease and that selenium can cure it. From his own website (I linked to it in one of my comments above):

Dr. Joel Wallach spent 41 years in nutritional and biomedical research as both a veterinarian and a human physician. He was the first person to recognize that cystic fibrosis is not genetic.

This is utter BS. There is no doubt at all that CF is a genetic disorder.

The benefit of selenium is admitted by CFF and in the study I quoted… but neither fully explain the degree of benefit

Even on the CFF's page on antioxidant therapies for CF there is no mention at all of selenium, nor on their page on vitamins and minerals, and on a page about a workshop on antioxidants and CF, which is the "study" you quoted, selenium is mentioned as possibly increasing glutathione levels which might help CF patients. That is a long, long way from curing CF as Wallach claims to be able to do.

Then kreb again brings up the 256 year old ONE chinese person reported by the Chinese govt, kreb pretends Wallach has extrapolated that to more than one case when kreb’s quote shows Wallach discounts the record as exagerated. Wallach NEVER states that 200 or 256 year old Chinese people are a regular occurrence nor does he cite ANY OTHER CHINESE PERSON LIVING TO ANY AGE APPROACHING WHAT WAS REPORTED IN CHINESE RECORDS

I never suggested he did. I wrote, "People in China who live for 250 years?" and later amended that to 200 years. Wallach claims there is a documented case of a person in China who lived to 200 years old. I quoted and linked to his own words doing just that. How can you possibly deny this?

Stop twisting the truth & lyinglies about Dr Wallach, kreb… repetition doesn’t make these things believable or fact-based… or are you a student of Nazi propaganda techmiques?

How is quoting a person's own words from their own publications and website, "twisting the truth and lying"? I'll ignore the Godwin, for now.

Then kreb quotes the NCAHF… really kreb? The Barrett/Baratz run organization associated with QuackWatch?
Barrett, the disgraced “doctor” & infamous king of the QuackPots?… please, kreb, stop embarrassing yourself.

I see you have swallowed the hateful lies and propaganda about Dr. Barrett. How is he disgraced exactly? Can you point to a single piece of inaccurate information on any of Barrett's websites?

Again, instead of using eidence against Dr Wallach you use an admitted THIRD-HAND description of a letter from an unamed source claiming to be a relative of someone who received chelation from Dr Wallach then subsequently died… really? this is the best you can do? This is the extent of your evidence against Dr Joel Wallach?

You wrote:

There is no record of any patient dying while Dr Wallach was chelating them.

I proved you wrong by linking to The National Council Against Health Fraud's record of a patient who died after being chelated by Dr. Wallach. It's not third hand, and The National Council Against Health Fraud are a reliable organization.

You besmirch yourself again, forcing me to pseudo-besmirch you… again!

People here can read what you wrote, what I wrote, and they can go to Wallach's words that I linked to. It is very clear that everything I wrote is accurate, and that it is you who is attempting, extremely ineptly, to twist the truth here.

Changing the DNA of any plant or animal will cause inknown changes to the food. This cannot be avoided. When a crop is “instructed” by the random insertion of a multi-gene package to produce 2 types of insecticide it has to contruct those insecticides from existing nutrient bases in the soil. This will detract from the nutritional content as no changes were made to compensate for this added burden of poison-protein synthesis.

Your rhetoric against artificial variation is equally applicable to natural variation and from what I can tell, would be pro-monoculture, if it were applied consistently.

But you aren't consistent. You demonize the risks of GM crops while deliberately ignoring the exact same risks when they're a product of natural variation. And natural variations happen all the time without human intervention. It doesn't help your case that the division between natural and artificial is pretty much arbitrary and stinks of outdated, ideological notions of genetic purity.

We, on the other hand, accept and expect some level of variation in our crops. We want humanity to be both aware of and responsible about all crop variation to the extent we can be.

Oh, and yes, everything is a trade-off. A gene that wards the crop against pests can provide a net increase in nutritional value if it prevents pests from eating the plant and lowering the nutritional value by a greater amount. It's all about finding better cost/benefit ratios, and those can vary depending on the local environment.

@michael polidori

Thank you for that astounding display of complete ignorance and stupidity as well as all your conspiracy-theory mongering. You are good for a few laughs at your utter ignorance and a prime example of D-K in action, especially since the regulars have posted evidence and you have not.

Please post more, we need a few more laughs at your ignorance. I certainly could use a few chuckles at your expense.

I don't have much to add to the conversation this evening, but I just HAD to comment. I am so glad to have found this blog and read through the comments.

Sigh. It's like "coming home."

Watch this:

www.youtube.com/watch?v=eUd9rRSLY4A

An hour and twenty freakin' minuets of Gary Null?

I'll pass.

Pig-to-monkey Ebola: is there something in the air?

tsmith — Mon, 19 Nov 2012 08:00:33 +0000

Pig-to-monkey Ebola: is there something in the air?

Ebola has long been known to be a zoonotic virus--one which jumps between species. Though it took several decades to find evidence of Ebola virus in bats, these animals had previously been associated with human index cases of Ebola disease have worked in bat-infested warehouses or traveled to caves where bats roost. Non-human primates have also become infected with the virus, sometimes transmitting the virus to humans when killed primates are butchered for food. Ebola has also been suggested to infect dogs and other wild animals. However, livestock are a newer angle to Ebola virus ecology.

Ebola was first found in pigs in 2008 in the Philippines. This was the Reston virus, named after its discovery in imported Filipino monkeys in a facility in Reston, Virginia, in 1989. Though this virus spread among the captive monkeys, no humans came down with symptoms. However, follow-up studies showed that some humans did develop an immune response to the Reston virus--suggesting they had been infected, even if they didn't realize it. At the time, there was suggestion that perhaps Reston might be spread via aerosol, as the virus appeared to spread amongst monkeys in two different rooms who did not come into physical contact with one another. However, this was not proven at the time and alternative explanations were possible.

When Reston resurfaced in swine and swine farmers in 2008, a similar phenomenon was observed. Though it was not known how the pigs initially became infected with the virus, they did appear to be able to spread it to humans working amongst them, even if those farmers didn't have contact with blood or other secretions (the most efficient way to transmit Ebola viruses). Suggestive of possible transmission from pigs to people via air, but far from conclusive. Since then, two experimental studies have examined airborne transmission of Ebola via pigs.

The first study examined transmission of the Zaire strain of Ebola--the nastiest one, which can kill up to 90% of those infected--within laboratory pigs. Pigs were inoculated with the Zaire virus and housed with uninfected pigs, who were later tested and found to have acquired the virus. Interestingly, when the pigs got sick with Ebola Zaire, the symptoms were mainly respiratory and the virus replicated in the lungs. This was quite unlike what Zaire does in humans and our other primate cousins, where it's a systemic disease and we can find virus in the blood. This suggests that pigs could be infected with even nasty types of Ebola, and we wouldn't realize it.

Last week, Ed Yong reported on a new paper examining transmission of Zaire virus from experimentally-infected pigs to co-housed macaques. Like the previous paper, they observed that Ebola in pigs was a respiratory disease, and that it could spread to other animals (in this case, non-human primates). The macaques they tested developed the symptoms of Ebola that were expected--a systemic disease, with virus isolated from the blood. In this study, they also added in an air sampling component, and were able to detect evidence of virus (via PCR) in the air. However, the authors do note that this could have been aerosolized in other manners than directly from the exhaling pigs (such as during the floor-cleaning process). Finally, even if it does become aerosolized and spread in this manner, as noted in Ed's article, Ebola is not "suddenly an airborne virus, like influenza." Certainly more efficient transmission takes place via close contact with infected secretions during hospital procedures and funeral rites.

Interestingly, the authors note that other experimental studies that have looked specifically at airborne, primate-to-primate transmission of Ebola have come up negative, and that swine are known to generate "infectious short range large aerosol droplets more efficiently then other species." Is there something specific about pig physiology that may make them better respiratory virus shedders? We know that pigs can be intermediate hosts for other viral pathogens as well, such as Nipah virus and of course influenza. Are pigs playing any role in Ebola ecology, either in Asia or Africa? Might Ebola have more airborne potential than we previously thought? According to Ed, the authors of the second study are currently working on field studies in Africa to examine the pig question outside of the laboratory. The timing may be good for them, as Uganda is currently experiencing another Ebola outbreak;--the country's third Filovirus outbreak in five months.

Reference

Weingartl, H., Embury-Hyatt, C., Nfon, C., Leung, A., Smith, G., & Kobinger, G. (2012). Transmission of Ebola virus from pigs to non-human primates Scientific Reports, 2 DOI: 10.1038/srep00811

tsmith Mon, 11/19/2012 - 03:00

Tags

[well off-topic...] Rather inappropriately the title line 'is there something in the air' made me think of the ABBA song.

Did the Ebola Reston strain replicate in the lungs like its cousin Zaire? If both of the strains are limited to replication in the lungs it makes for an interesting study to continue to look at possible factors that make it centralized instead of systemic.

The human origins of "pig" Staph ST398

tsmith — Tue, 21 Feb 2012 10:40:00 +0000

The human origins of "pig" Staph ST398

I recently gave a talk to a group here in Iowa City, emphasizing just how frequently we share microbes. It was a noontime talk over a nice lunch, and of course I discussed how basically we humans are hosts to all kinds of organisms, and analysis of our "extended microbiome" shows that we share not only with each other, but also with a large number of other species. We certainly do this with my particular organism of interest, Staphylococcus aureus. There are many reports in the literature showing where humans have apparently spread their strains of S. aureus to their pets (dogs, cats, hamsters)--and sometimes the pets have been nice enough to share it right back. My own research looks at S. aureus in pigs and the humans who care for them, and many studies have shown that a "pig" type of MRSA, dubbed sequence type 398 (ST398), can be transmitted from pig carriers to their human caretakers. The assumption has been that this is truly a "pig" strain, originating in swine, and has spread to humans (and other animals, including cattle, poultry, dogs and horses) from pig hosts, either directly or indirectly via contaminated meat products.

According to a new study (open access in mBio), it seems that there has been more sharing of ST398 than we'd realized. Led by Lance Price at TGEN (full disclosure--I'm a coauthor on the paper), his group analyzed 89 ST398 isolates from China, Europe, and North America, including isolates from humans and animals as well as both methicillin-susceptible and -resistant strains. Using whole genomic sequence typing, the evolutionary history of these isolates was reconstructed.

The findings throw the ST398 story a bit on its head. Instead of being a true pig strain, ST398 appears to have originated as a methicillin-susceptible human strain which was transferred into the pig population, picked up antibiotic resistance genes (including resistance to methicillin and tetracyclines), and then has been passed back to farmers as more resistant organisms. Some prophages were also gained or lost along the way, probably due to selection by host factors.

This also suggests that there is still likely a low level of "native human" ST398 circulating in people. There have been a few case reports of ST398 colonization and/or infection in people without any known livestock contact. Some of these have been resistant to methicillin and/or tetracycline, which are more frequently associated with livestock-adapted strains. Are these truly "human" strains which aren't involved in livestock at all, or are these ST398 findings in people lacking livestock contact still due to some livestock exposure along the chain of transmission (farmer neighbors? Transmission via food?) We still don't know, but carrying out more of this WGST will give us better targets in order to be able to differentiate true "human" ST398 strains from those that have been hanging out in animals, and then transmitted back to people.

Now, for long-time science blog readers, this story may sound a bit familiar. Indeed, it looks like ST398 has taken a very similar path to that of another animal-associated S. aureus strain, ST5. As Ed Yong described back in 2009, humans are also the ultimate origin of a "chicken" type of S. aureus ST5, which spread around the world in broiler chicken flocks. In Ed's article, the first author of the chicken ST5 paper, Bethan Lowder, notes that the change in chicken farming from small farms to multinational corporations likely aided the spread of this organism--and the exact same thing has happened with pig farming.

One difference between the two is that ST5 causes disease in chickens, whereas ST398 seems to be a very rare cause of illness in pigs. This is likely one reason that ST398 in pigs went undetected until relatively recently--it's simply not much of an economic issue for pig producers, whereas in chickens, S. aureus can cause several nasty diseases (such as bumblefoot and BCO) leading to animal loss (and thus, less money for the farmer).

So, where do we go from here? Clearly studies like this show the utility of using WGST to examine the evolution and spread of these strains. If you look at how spa types are distributed throughout the tree, you can see that those alone don't tell you much about where the strain came from, or if it's fully "human" or a pig-adapted lineage. Ideally, a set of simple markers could be found to distinguish ancestral human strains from livestock strains (as methicillin-sensitive ST398 can also be found in pigs, so methicillin resistance alone isn't enough of an indicator that it's a "pig" strain). We'll be working on this in ST398 and other strains we see being shared between animals and humans, in order to better understand this generous sharing we're doing amongst species.

Reference:

Lance B. Price, Marc Stegger, Henrik Hasman, Maliha Aziz, Jesper Larsen, Paal Skytt Andersen, Talima Pearson, Andrew E. Waters, Jeffrey T. Foster, James Schupp, John Gillece, Elizabeth Driebe, Cindy M. Liua, Burkhard Springer, Irena Zdovc, Antonio Battisti, Alessia Franco, Jacek Å»mudzki, Stefan Schwarz, Patrick Butayej, Eric Jouy, Constanca Pomba, M. ConcepciÃ³n Porrero, Raymond Ruimy, Tara C. Smith, D. Ashley Robinson, J. Scott Weese, Carmen Sofia Arriola, Fangyou Yu, Frederic Laurent, Paul Keima,, Robert Skov, & Frank M. Aarestrup (2012). Staphylococcus aureus CC398: Host Adaptation and Emergence of Methicillin Resistance in Livestock mBio, 3 (1), 305-311 : 10.1128/mBio.00305-11

tsmith Tue, 02/21/2012 - 05:40

Tags

Antibiotic resistance

staphylococcus aureus

Antibiotic resistance

infectious disease

public health

Great article! New research says you can't simply say: MRSA or "Pig MRSA" is caused by the overuse of antibiotics in the pig industry. It seems to be more complicated.

Well, not exactly. Yes, it is more complicated, but note that resistance to several classes of antibiotics were acquired in pigs--so I think the overuse of antibiotics in ag is certainly a large factor in strains of ST398 that are antibiotic-resistant.

Hi Tara, I saw this yesterday and forwarded it to my EID editor in hopes of replacing ref. #10. I see now why one of the reviewers suggested referencing it. It would appear that the MSSA ST398 strains described in the EID paper may be 'ancestral', circulating at low levels in humans as you describe...

Tara, I was reading, "We Beasties," and Kevin was talking about nominations for some sort of science blogging award. He does have some writing I'd like to vote for/nominate. But, I'd like to point out this piece seems pretty solid to me. As well as the one on MRSA in pork products and "antibiotic" free label.

Was just listening to the Quirks & Quarks podcast. Heard this familiar story. Didn't hear Bob say "Tara Smith" until the end. It's your 9:06 of fame?

Very fluent.

http://www.cbc.ca/quirks/episode/2012/03/03/march-3-2012/

I enjoyed the interview on Quirks & Quarks. Sounds like very promising research.
You mentioned animal husbandry practices in Europe but have you seen some of the innovations at places like Polyface Farms in Virginia? They combine animals like pigs and cows or chickens and rabbits to help create less mono-culture environments that help reduce disease. They also move the pens around to spread out the manure around the land and keep a healthier environment for the animals.
http://mulefootpigs.tripod.com/id21.html
http://www.polyfacefarms.com/story/

Pigs with Ebola Zaire: a whole new can o' worms

tsmith — Wed, 18 May 2011 07:00:00 +0000

Pigs with Ebola Zaire: a whole new can o' worms

Ebola has long been associated with wildlife. From the early days, bats were viewed as a potential reservoir (though it wasn't confirmed that they actually harbored the virus until 2005). Contact with wild animals--particularly primates which were butchered for food--was also long thought to be a risk factor, and now we know that primates can become ill with Ebola and pass the virus to humans.

What hadn't been examined until 2008 were pigs. I mean, it's not exactly the animal you associate with central Africa, where many of the Ebola cases have been concentrated. However, pigs are much more plentiful in the Philippines, where another Ebola subtype--Ebola Reston--is thought to lurk. The Reston strain actually was first documented in the United States, where twice it was associated with outbreaks in primates originating from the Philippines. When the facility in the Philippines was closed down in 1997, Reston disappeared for 11 years--until it surfaced in pigs in 2008.

The ecology of Ebola Reston in the Philippines isn't known--unlike African Ebola strains (and their cousin, Marburg), no bats have been caught in that country and tested positive for the virus, though they probably serve as a reservoir of the virus in the Philippines just as they do in Africa. So it was a huge surprise when pigs from that country tested positive for Ebola Reston--and so did 6 of their human caretakers, suggesting cross-species transmission. (I should note here that the Reston strain has yet to be linked to any symptomatic infections in humans--the pig farmers who tested positive probably had no idea they'd been infected and did not show any clinical signs of illness). Pigs hadn't previously been linked to any Ebola infection, so this brought in a whole other wrinkle when it came to Ebola transmission--the possibility of being exposed to Ebola via contaminated food, and the potential for pig populations to harbor the filovirus (and transmit it to their caretakers, as we have seen with outbreaks of Nipah and Hendra viruses).

A new study delves further into Ebola in pigs. Instead of using the Reston strain, they use the much-more-deadly Zaire strain. This is the one that movies are made about; the one which can cause outbreaks so nasty that they kill up to 90% of those who are infected. Why use Zaire instead of the Reston strain--the one which has actually infected pigs in nature? Well, the researchers wanted to find an animal that's easier to work with than primates (there are all kinds of very strict regulations when it comes to working with non-human primates), so if pigs could work as a good model for human Ebola disease, that would make studying the virus just a bit easier. (In any case, for any live Ebola work, it still needs to be done in a biosafety level 4 environment, meaning complete spacesuits and the whole works).

The authors did 2 studies. In the first, they inoculated 6 pigs with Ebola Zaire, via a combination of intranasal, intraocular, and oral routes of infection. (Interestingly, no injection, which can be a key way Ebola is spread). They had an additional 2 pigs that they inoculated the same way with a saline solution, and housed them separately from the Ebola-inoculated animals. The goal of this experiment was to look at the pathogenesis of a virulent Ebola strains in the pig model. The infected animals all developed fevers and respiratory disease, with some internal hemorrhaging and evidence of airway replication by Ebola. Infectious virus was found at low levels in nasal washes and oral and rectal swabs; one animal also had a low level of virus in the blood. Higher levels of virus were found in various organs, including the heart and bladder, while the highest levels were found in lung tissue.

In the second experiment, they inoculated 3 new pigs in the same fashion, but then added in 4 additional (uninoculated) animals to stay with them, and kept 2 additional control animals in a separate area so that they could investigate pig-to-pig transmission of the virus. They did find viral RNA from the mucosa of all contact animals, and infectious virus was detected from 2 of 4, demonstrating that the virus can be passed among pigs. Not stated in the article was if the authors thought this was due to direct contact with respiratory secretions among the pigs, or via airborne transmission (a much more concerning route of transmission, as in humans, Ebola Zaire doesn't seem to transmit well via air--typically it's spread via close direct contact and bodily fluids).

Notably, pigs didn't seem to develop severe systemic disease from Ebola, as primates do--the main symptoms exhibited were respiratory, which the pathology supports (finding little virus in the blood, but a lot in the lungs). This suggests that even for Ebola Zaire, infection in a pig could be mistaken for other respiratory diseases, such as influenza or PRRS virus (porcine respiratory and reproductive syndrome virus, which the initial pigs in the Phillipenes were co-infected with). So, Ebola may be circulating even more than we realize in the pig population, disguised by its commonplace symptoms.

A commentary published in tandem with the research article ponders the issue of foodborne Ebola, suggesting that this is a remote possibility and noting that butchering infected animals in the wild in Africa has certainly spread the virus. However, solely eating meat as a means of infection hasn't been reported, and cooking likely destroys any risk (similar to influenza viruses). Like influenza virus, Ebola doesn't seem to survive long in most environments, but it's also noted that differences in African food storage (with little refrigeration) versus more typical cold storage may affect that as a risk factor, possibly prolonging the life of the virus when held in the cold. I think foodborne transmission is unlikely, but it can't be completely ruled out right now.

Because of the respiratory symptoms, does this mean Ebola could enter the population via meat from animals that farmers don't consider very ill, or put butchers at a heightened risk of infection during slaughter? This to me is more concerning than simple foodborne transmission. With Reston, at least no human symptoms have been observed, but if pigs (and potentially other animals?) can present with Ebola Zaire as a rather generic respiratory infection...well, that could spell trouble in a lot of different ways. It means that telling individuals to simply avoid sick-looking primates (and bats) is going to be even more woefully inadequate than it already is. Plus, it raises the remote-but-not-completely-outside-the-realm-of-possibility of someone intentionally spreading the virus via animals that are infected in this manner.

Science fiction? Maybe. Probably. Hopefully. But this research opens the door on many new lines of investigation and once again, raises even more questions.

Kobinger GP, Leung A, Neufeld J, Richardson JS, Falzarano D, Smith G, Tierney K, Patel A, & Weingartl HM (2011). Replication, Pathogenicity, Shedding, and Transmission of Zaire ebolavirus in Pigs. The Journal of infectious diseases PMID: 21571728

tsmith Wed, 05/18/2011 - 03:00

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Weekly Dose of Cute: Teacup Pigs

cwilcox — Tue, 13 Oct 2009 12:49:00 +0000

Weekly Dose of Cute: Teacup Pigs

Ok, I really tried not to post about this. But come on - they're just so cute. I want ten of them.
And to really make you squeal, some video:

(it's all your fault, Rick. Ever since you posted this on your facebook I couldn't stop thinking about them!)

cwilcox Tue, 10/13/2009 - 08:49

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When I leave to Mexico I'm so getting one, and she/he will be my new bestiie foreva! So exited :)

Ebola found in pigs (thankfully, it's the one harmless type)

edyong — Thu, 09 Jul 2009 12:00:38 +0000

Ebola found in pigs (thankfully, it's the one harmless type)

As the world is now painfully aware, pigs can act as reservoirs for viruses that have the potential to jump into humans, triggering mass epidemics. Influenza is one such virus, but a group of Texan scientists have found another example in domestic Philippine pigs, and its one that's simultaneously more and less worrying - ebola.

There are five species of ebolaviruses and among them, only one - the so-called Reston ebolavirus - doesn't cause disease in humans. By fortuitous coincidence, this is also the species that Roger Barrette and colleagues have found among Philippine pigs and even among a few pig farmers.

The team were called in last July by the Philippine Department of Agriculture to identify a mystery illness that was sweeping across the country's pigs, infecting their lungs and airways and causing miscarriages. Barrette's group collected tissue samples from five groups of pigs throughout the island and through a battery of tests, they gradually ruled out their list of potential candidates - foot-and-mouth disease, African swine fever, and others.

The first positive hit was an infection known as blue ear disease, or to give it its formal name - porcine reproductive and respiratory syndrome virus (PRRSV). It was already the primary suspect for the pig illness, and the Philippine strain was genetically similar to one that was sweeping through China at the time. It seemed like the mystery was solved. But not so - when Barrette incubated an infected lymph node with monkey cells that are immune to PRRSV, the cells still started dying. There was another virus.

To identify it, Barrette used a powerful tool called a "panviral microarray" - a small slide that contains the genetic signatures of tens of thousands of viruses, neatly arranged in a grid. Similar tools have already proved their worth in viral detective work - the closely related Virochip was used to identify the SARS virus in 2002. This time, the technique brought up a strong hit for Reston ebola.

Samples of the virus were sent to the CDC, who confirmed through a battery of tests that REBOV was infecting the Asian pigs. Barrette clinched the diagnosis by sequencing the genomes of viruses isolated from his samples. He even managed to take a snapshot of the virus under an electron microscope.

Ebolaviruses, and their close relatives the Marburgviruses, belong to a viral family called filoviruses, which were first discovered in 1967. In the 40 years since, outbreaks of the disease have cropped up across the world seemingly at random. The high fatality rates of most infections have prompted scientists to search for wild animals that could act as living headquarters from which the viruses could seed infections in the human populace. African fruit bats have emerged as one such reservoir for both Marburg and the particularly lethal Zaire strain of ebola.

But until now, the Reston species, or REBOV, has only ever been found in monkeys. In fact, it was first identified in 1989 when a shipment of crab-eating macaques carried the virus to the US from the Philippines. No fewer than three separate outbreaks in the 1990s, in the US and Italy, were traced back to a single facility in these islands.

Nonetheless, it seems that the virus has been circulating in pigs for a while. Barrette found that the viruses form various Philippine sites are genetically further from each other than they are to the 1989 monkey strain that was the first to be discovered. And when the modern pig strains are added to a family tree of ebolaviruses, they don't clump together neatly.

This implies that the virus made its way into pigs on several occasions, rather than one strain accounting for all the modern infections. It's entirely possible that REBOV "spilled over to monkeys and swine from an as yet unidentified host". Given their affinity with ebolaviruses, fruit bats are a possible candidate.

Worryingly, there are signs that the virus may have made the jump from pigs to people. Barrette tested 141 people and found six who tested positive for antibodies against REBOV, all of whom either worked on pig farms, or with pig products. As with previous outbreaks of the virus, there are no signs of any actual disease in the infected people.

Even so, REBOV has the potential to evolve into an emerging human disease. Michael McIntosh, who also worked on the study, says, "The question is what level is that risk. The fact that it is in domestic pigs, an animal species that is intimately connected to humans, increases the risk significantly. However, there is simply no way of knowing if the virus will cause or contribute to disease in pigs or humans at this time." Given our recent experiences with both swine flu and MRSA, it pays to be careful.

McIntosh adds, "While the WHO suggests that the risk of disease caused by REBOV in healthy humans is low, it would be premature to say that it is currently harmless."An immediate concern is to work out how the virus might affect people suffering from weakened immune systems or other diseases. In pigs, it seems that REBOV only infects animals that were already suffering from blue ear disease, just as the original monkey strains were found in conjunction with another virus - simian haemorrhagic fever. Although REBOV is capable of infecting monkeys on its own, the fact that it has now been found in the company of other viruses in two different hosts is most intriguing.

Already, a surveillance programme is being put into place to monitor the virus and there's still a lot of work to do to understand how it's transmitted, what its reservoirs are and how common it is. The World Health Organization has posted a factsheet on the web regarding the emergence of Reston ebolavirus in domestic swine, which includes recommendations for pork processing and consumption in the Philippines.

Reference: Science 10.1126/science.1172705

Images: Macaque from Chris Huh and virus from Science/AAAS

More on ebola and other pig-transmitted viruses:

edyong Thu, 07/09/2009 - 08:00

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Haha! I saw this story in my GoogleNews 'virus' bar-- and was annoyed that it was the harmless type. RAGE to the journalists that played on the obvious bait-switch, but as usual, kudos to you :)

The Buzz: MRSA is Back and Badder Than Ever

amillikan — Thu, 29 Jan 2009 10:39:53 +0000

The Buzz: MRSA is Back and Badder Than Ever

A notorious bacterial foe has made its first documented appearance in the U.S. and is jumping species around the farm scene. First, MSRA—methicillin resistant Staphylococcus aureus— was found in chickens. Just recently, research conducted by ScienceBlogger Tara Smith from Aetiology found that ST398, a strain found in pigs, was also found in many of the humans who came into contact with the pigs at a large food production farm in Iowa. While this strain seems to spread readily between animals and humans, its potential for lethal infections is still unclear.

MRSA in pigs and pig farmers

edyong — Fri, 23 Jan 2009 18:39:26 +0000

MRSA in pigs and pig farmers

Methicillin-resistant Staphylococcus aureus (MRSA) is very difficult to kill. This notorious "superbug" can withstand a broad and growing range of antibiotics, and is the leading cause of hospital infections in many countries. But it's not restricted to hospitals. According to studies coming in from all over the world, MRSA has found a new route into our bodies -piggyback.

Pig farms throughout the world have become breeding grounds for strains of MRSA that can jump from swine to humans. These strains have already been isolated in the Netherlands, Denmark and Canada, and now, the latest study adds the USA to that list. The research was led by Tara Smith from the University of Iowa, who I know as a Scibling and who many of you will recognize as the author of the excellent Aetiology blog.

Smith found widespread traces of MRSA in two different production systems in the states of Iowa and Illinois. Within the nostrils of 49% of pigs and 45% of pig farmers, her team detected traces of the "superbug" (although it's worth noting that none of the farmers had experienced any actual infections). Piglets had the highest rates of infection and in fact, every single pig under the age of 12 weeks harboured MRSA colonies.

The high levels of the bacterium in both man and pig suggest that it can spread readily between the two species. To MRSA, both four leg and two legs are good...

The link between MRSA and pigs was first discovered a few years ago in the Netherlands. Dutch hospitals have little to fear from MRSA - aggressive "search-and-destroy" policies and restricted antibiotic use have controlled the bug to such an extent that hospitals list "treatment in foreign hospitals" as a risk factor for infection!

But in 2003, Dutch researchers started to find unexpected cases of MRSA in pig farmers and eventually identified the culprit as a new strain that became known as ST398, or non-typeable MRSA (NT-MRSA). It's this same strain that Smith found in the Iowan pigs.

In 2007, Albert de Neeling and Xander Huijsdens found ST398 in 39% of pigs and 81% of local pig farms, suggesting again that the bacteria was jumping from pigs to humans. In the same year, Huijsdens, together with Inge van Loo, found further proof for this theory. By comparing 35 people with ST398 to 76 people carrying other strains, they found that the ST398 carriers were 12 times more likely to have come into close contact with pigs and 20 times more likely to have come into contact with cattle. On a map, they saw that the distribution of ST398 uncannily matched the spread of pig and cattle farms.

ST398 is a newcomer. By reviewing a national MRSA database, Dr Huijsdens and Dr van Loo found that the strain was non-existent in 2002 but now accounts for over one in five human infections. Its origin is unclear. It almost certainly jumped from pigs to humans, but the researchers think that this was just the return part of a round-trip. They think the bacteria may have originally jumped from humans to pigs.

In their new porky hosts, the bacteria developed new antibiotic resistances and returned, stronger than ever. Unlike other strains, ST398 strongly withstands tetracyclines, a group of antibiotics that is heavily used to medicate livestock. Unnecessary antibiotic use has been blamed for the evolution of MRSA strains in humans and the same could apply to pigs, especially since the farming industry uses more antibiotics than hospitals. Under such heavy assault, it is almost inevitable that bacteria, which reproduce quickly and swap beneficial mutations, will develop resistance.

So far, it is not clear if ST398 is spreading beyond pig farms or if it causes so-called community-associated MRSA, which occurs outside the hospital setting. For the moment, people who frequently come into contact with pigs or cattle, including vets, have the highest risk of infection. The bacteria could also spread to their friends and family by hitching a ride on clothes or skin.

Even the food chain is not entirely safe. Van Loo detected ST398 in 2 out of 79 meat samples from Dutch supermarkets and butchers, but only at low levels that are unlikely to cause disease if food is properly prepared. For the general population, there's no need to panic over ham and bacon but the risks could be higher for people who handle meat directly, or those with weakened immune systems. At least one hospital outbreak began when an immunocompromised patient ate contaminated meat. Even though this was a different MRSA strain, it set a dangerous precedent.

The problem is not confined to the Netherlands either. Pigs are heavily exported around the world and ST398 may have stowed away inside them. It has already been detected in France, Singapore and Denmark. Scott Weese from the University of Guelph in Ontario found the Dutch strain in a quarter of local pigs and more worryingly, in a fifth of pig farmers. Human cases of ST398 are extremely rare in Canada but that could change as it spreads among the pig population.

And as we've seen, the US is affected too. As the largest importer of Canadian pork, their farms could have become contaminated by swine brought in from their northern neighbour, but only further studies can confirm that. It's also unclear how widespread ST398 is in the US, but Iowa alone accounts for a quarter of all the swine raised within its borders.

It is clear that we need more research and better monitoring to fully understand the scale of the MRSA epidemic in pigs and the role that agricultural antibiotics have played in it. Only then we recommend the right control measures to protect farmers and the wider population.

Reference: Tara C. Smith, Michael J. Male, Abby L. Harper, Jennifer S. Kroeger, Gregory P. Tinkler, Erin D. Moritz, Ana W. Capuano, Loreen A. Herwaldt, Daniel J. Diekema (2008). Methicillin-Resistant Staphylococcus aureus (MRSA) Strain ST398 Is Present in Midwestern U.S. Swine and Swine Workers PLoS ONE, 4 (1) DOI: 10.1371/journal.pone.0004258

More on drug resistance:

Image: My MRSA GiantMicrobe, with enormous thanks to Rebecca Skloot

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edyong Fri, 01/23/2009 - 13:39

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C'mon tell the truth, it's killing people!, or you harbour the bacteria and it's resistance until something else kills you, just like AIDS! I'm surprised this is not at the forefront of medical academia. Pretty scarey stuff.

http://www.nytimes.com/2009/03/12/opinion/12kristof.html?em

Yes, it is killing people... this is epidemic. It is too late to stop or control this bacteria. The damage is done (overuse of ABx). My baby and I survived MRSA without using conventional treatment (no ABx). Instead, we used stable allicin (garlic) which was developed and tested with Dr. Ronald Culter from University of London. We also take probiotics everyday and drastically changed the way we eat. Would love to have everyone's input on my new website: MRSAsupportgroup.com. If you or anyone you know is suffering from MRSA, I'd be happy to help... have them contact me through my site.
Carrie
info@MRSAsupportgroup.com

An ounce of prevention: http://www.infectioncontrolservice.com

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