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The Chicago Tribune, “chronic Lyme disease,” and demands for false balance

During the six years of its existence, one frequent complaint I’ve had on this blog, it’s been about how the press covers various health issues. In particular, it’s depressing to see how often dubious and even outright false health claims, such as the claim that vaccines cause autism, that cell phones or powerlines cause cancer, or that various questionable or even quack remedies work for various diseases are reported credulously. Often this takes the form of a journalistic convention that is more appropriate for politics and other issues but not so appropriate for scientific and medical issues, namely telling both sides as though they have equal or similar weight. While this is fine for politics, it’s not so great for discussing, for instance, the scientifically discredited notion that vaccines somehow cause autism. Yet, in such stories, almost invariably there is an anti-vaccine crank like Barbara Loe Fisher, Jenny McCarthy or someone else from Generation Rescue, or someone like Sallie Bernard from SafeMinds cited as though she were on equal footing, scientifically speaking, with scientists who have dedicated their lives to the science of vaccines. Sometimes, the story takes the form of a credulous acceptance of pseudoscientific claims, with a token scientist or skeptic tacked on at the end to give a small quote for “balance.”

One exception to this profoundly annoying pattern (if you’re a skeptic) has been the journalism of Trine Tsouderos, who with Pat Callahan, has produced over the last year or two a number of excellent, science-based stories on the anti-vaccine and its associated “autism biomed” movements, including an expose of Boyd Haley’s “rebranding” of an industrial chelator as an autism treatment. She’s even taken on “America’s doctor,” Dr. Oz. As a result, she’s been demonized by cranks, up to and including having her face crudely Photoshopped into a picture of a Thanksgiving feast in which she and various others whom the merry band of anti-vaccine loons at Age of Autism view as enemies were portrayed as sitting down to a meal of dead baby.

Most recently, Callahan and Tsouderos published an article about the dubious diagnosis that is chronic Lyme disease entitled, appropriately enough, Chronic Lyme disease: A dubious diagnosis, which was subtitled, also quite appropriately, “There’s little good evidence that chronic Lyme disease exists. Yet doctors are treating it with drugs that put patients and the public at risk.” And so there is, and so all too many dubious doctors do. Because this article speaks for itself and is nearly two weeks old, which in blog time is akin to being two years old, I’m not going to discuss it in detail. I will say that it is quite good and lays out the issues better than I’ve ever seen them discussed in a mainstream newspaper or magazine. I’ll also point out that chronic Lyme disease has become such a cause célèbre that in Connecticut the legislature passed a law to protect Lyme quacks from being disciplined by the state medical board for using long term antibiotics to treat chronic Lyme disease. In essence, as Steve Novella pointed out at the time, they carved out an exception to the standard of care and told doctors in Connecticut that they don’t have to worry for not meeting it.

Don’t get me wrong. Lyme disease is real. There does even appear to be a post-Lyme disease syndrome, which is seen in patients who had Lyme disease and now have chronic symptoms (such as fatigue, various pains, and difficulty concentrating) after having been treated. Indeed, this is even referred to as category 4 Lyme disease. What causes this syndrome is a mystery, and there is no doubt that there are patients out there with debilitating symptoms after being treated for Lyme disease, but current scientific and clinical evidence does not support the idea that these symptoms are due to a chronic ongoing infection or that prolonged courses of antibiotics do any good. Steve Novella has written a good treatment of the issues involved (here and here), as have Mark Crislip and Peter Lipson.

As good as Callahan and Tsouderos’ article was, it’s not surprising that it resulted in criticism. One criticism actually appeared in the Knight Science Journalism Tracker’s blog in the form of post written by Paul Raeburn, former senior editor for science at Business Week, former science editor at the Associated Press, author of three science books, and director of a university science journalism program, entitled Chicago Tribune off balance on chronic Lyme disease. For the most part, it’s an article complaining about the journalism of the article. Boiled down to its essence, Raeburn’s complaint is the opposite of what we skeptics, scientists, and supporters of science-based medicine complain about all the time about journalists, namely that Callahan and Tsouderos did not fall into the trap of false balance, did not give undue credence to pseudoscience, and did not “tell both sides” as though they had equal or roughly equal credence. Indeed, Raeburn says just that much in the very last paragraph of the article:

In short, what Callahan and Tsouderos have done is to argue that chronic Lyme disease can’t exist because the people who say it does are nuts.

A far better approach would have been to report the evidence, pro and con, and to quote the most persuasive advocates for and against chronic Lyme disease-not the least persuasive. And to give both sides equal time to speak.

The first sentence, of course, is a massive straw man argument. That is not what Callahan and Tsouderos were doing at all. Seriously. I reread the entire Tribune Lyme article, and nowhere did they say or imply that believers in chronic Lyme disease are nuts. Of course, this is a frequent complaint that people who have been victimized by quackery use: That critics of quackery are calling them crazy. This sort of retort is common whenever it is pointed out that conditions that could well have a strong psychological overlay do, in fact, have a strong psychological overlay; those suffering from it will cry that you’re calling them crazy. Remember when I discussed Morgellon’s disease? Same thing. It’s an easy attack, a veritable cheap shot, though. Yes, sometimes it’s true, but far more often in my experience it’s a cheap shot.

As for the last paragraph, I can’t find a better distillation of the “tell both sides” mantra. Again, in the case of a genuine scientific controversy, this is not an unreasonable approach. However, it is not controversial in medicine that chronic Lyme disease is almost certainly not a result of actual chronic infection and that long term antibiotics don’t do any good and can cause harm.

Raeburn also has a bit of difficulty in defining what does and does not constitute a legitimate medical authority:

Again and again, Callahan and Tsouderos give far more space to advocates making questionable claims than they do to experts who refute those claims, allowing the serious case for chronic Lyme disease, whatever that might be, to be buried under the dubious claims of advocates.

The reporters go on and on impuguning patients and advocates without ever telling us whether there is a debate among legitimate experts about whether Lyme disease might assume a chronic form.

Could it be, perhaps, because there aren’t really any legitimate scientific experts who support the idea that long term chronic antibiotics are useful for the entity that is chronic Lyme disease? Could it be because randomized clinical trials have been done and don’t support the efficacy of long term antibiotics to treat category 4 Lyme disease? Indeed, after pointing out that the nation’s largest organization for specialists in infectious disease concluded that there is “no convincing biological evidence” for a Lyme infection that persists after treatment and continues to sicken and that three panels of experts from the Infectious Diseases Society of America and one panel from the American Academy of Neurology came to the same conclusion, namely that the diagnosis of chronic Lyme disease is suspect at best and that treatment with long term antibiotics is ineffective and risky, Callahan and Tsouderos write:

The evidence against the effectiveness of long-term antibiotic therapy is especially strong — supported by four randomized, double-blind, placebo-controlled clinical trials.

Patients in three trials receiving long-term antibiotic therapy did not do significantly better than those receiving placebos. In one other trial, patients receiving antibiotics felt significantly less fatigued than those receiving the sham treatment, though many of the antibiotic patients figured out they were receiving medicine, a grave flaw in the study.

They also point out:

However, the clinical trials on long-term antibiotic therapy found it can cause serious, even life-threatening problems. In one study, one-fourth of the patients suffered severe problems linked to the treatment, including blood clots, infection and the loss of a gallbladder.

I call B.S. on Raeburn. For a news article written for a mainstream newspaper, this is a very good discussion of the evidence against long term antibiotics for chronic Lyme disease. I mean, jumpin’ Jesus on a pogo stick! They even pointed out that one of the trials had problems with its blinding. What does Raeburn expect? A listing of the randomized, double-blind, placebo-controlled trials, the numbers of patients, the experimental designs, and the statistical analysis? Raeburn was also quite disingenuous in the way he framed this quote:

They then quote chronic Lyme advocates at length before introducing another expert, Dr. Paul Lantos of Duke University, whose quote, in its entirety, is: “Why take needless risks with people’s lives?”

Go back and look at Callahan and Tsouderos’ article, and you’ll note that this quote by Dr. Lantos directly follows the paragraph I cited above about the complications of long term antibiotics observed in clinical trials up to and including the loss of a gallbladder. In context, Dr. Lantos’ quote made perfect sense, particularly given how Callahan and Tsouderos follow that quote by pointing out an example, namely a 52-year-old patient in Minnesota who developed drug-resistant bacteria after 10 weeks of antibiotic treatment for a diagnosis of chronic Lyme disease.

Of course, the problem is that what Lyme advocates have for evidence is the same type of evidence that “autism biomed” advocates have for their woo: Anecdotes and testimonials. The blog Relative Risk describes this quite well as “a strange collection of aging, irrelevant works,” consisting largely of case reports (i.e., anecdotes). And that’s what Callahan and Tsouderos present, anecdotes and testimonials of Lyme advocates. The further problem is that Raeburn recognizes that this is a vastly inferior form of evidence but doesn’t recognize that that’s all Lyme advocates have. Particularly galling to Raeburn appears to be the passages in which Callahan and Tsouderos describe the illegal activities of many doctors pushing the idea of chronic Lyme disease against the standard of care, several of whom have faced legal difficulties. Raeburn appears to be particularly irritated by the singling out of Robert Bradford, founder of the Robert Bradford Research Institute in California, who was quoted as calling Lyme the “potential plague of the 21st century” and likening it to the Black Death, all while making the claim that Lyme disease might be a “contributing factor in as many as half of all cases of chronic illness.” Callahan and Tsouderos pointed out that back in the 1970s, Bradford was convicted of conspiracy to smuggle a “banned cancer treatment.” This actually brings me to one minor quibble I had about the Tribune article, which is that it didn’t specify the banned cancer treatment Bradford got busted for smuggling.

It was Laetrile.

That’s right. Bradford was a Laetrile peddler. How quaint. Perhaps that was so long ago that no one remembers, aside from old codgers like me (and I’m not even that old–yet). In any case, mentioning Bradford’s conviction was completely legitimate, as far as I’m concerned, because it indicates the sorts of advocates of unproven and dubious therapies who associate with chronic Lyme disease and promote all sorts of dubious treatments. Whatever condition patients suffering from the entity described as chronic Lyme disease have, such dubious treatments do them no service.

There’s one other thing about this attack piece by Raeburn that is curious. It was clearly instigated by someone who appears to have an ax to grind. Why, I asked, was Raeburn so annoyed at Callahan and Tsouderos’ article? There’s a hint at the end of Raeburn’s blog post, where which he thanks Pam Weintraub, features editor of Discover Magazine and author of Cure Unknown: Inside the Lyme Epidemic for giving him the heads-up about the Tribune article. I immediately noted that, Weintraub’s book had the contradictory plaudits from the American Medical Writers Association in the form for award for best book, 2009 and from the creator of functional medicine woo, Mark Hyman. Weintraub, it is noted, shows up within three hours of Raeburn’s post’s “going live.” It looks pretty obvious that Raeburn was asked or encouraged to post his hit piece by Weintraub and that he echoed a lot of the same attacks as Weintraub, who in the comments writes:

I am saying that you cannot quote a criminal as counterweight to a scientist, when there are scientists at major universities like Stony Brook, like UC Davis, like UC Irvine, like Berkely, who could be quoted instead, and who could present the the shades of gray and the true context for why there is all this uproar, and what these patients might be like and why they might be sick.

Except that that wasn’t what the story was about. The science is quite clear that the remedies being peddled by many of the doctors cited by Callahan and Tsouderos have been shown to be ineffective in the gold standard of clinical trials: Randomized, double-blind clinical trials. I also looked for a few of these scientists, for instance, doing Pubmed searches for investigators at Stony Brook, UC-Davis, UC-Irvine, and Berkeley. I have to admit, I wasn’t particularly impressed. For example, from Stony Brook, I saw a clinical trial from 2003 that appeared to show that antibiotic therapy was associated with improvement of debilitating fatigue. This study appears to be the very study that Callahan and Tsouderos cited as having had its blinding possibly compromised, as evidenced by the observation that more patients in the treatment group than in the placebo group correctly guessed their treatment assignment. From UC-Davis, there were a couple of mouse experiments, again not very convincing. From UC-Irvine I could find only one review article.

I could find nothing on Pubmed from Berkeley about chronic lyme disease, but maybe I didn’t persist long enough.

The bottom line is that Weintraub’s complaint is primarily also about how Callahan and Tsouderos didn’t fall for the “tell both sides” mantra that all too many journalists fall prey to when writing about dubious medicine and pseudoscience. I’m not saying that there aren’t criticisms of the Tribune article that aren’t valid, but most would be minor compared to the main messages in their article, which, as far as I was concerned, were spot on: Chronic Lyme disease is, at best, a dubious diagnosis; whatever might be the cause of category 4 Lyme disease, it does not appear to be caused by ongoing infection by the spirochete that causes Lyme disease; and there is no credible evidence that long term antibiotic therapy is effective against category 4 Lyme disease and a lot of evidence that long term antibiotic therapy has the potential to cause harm. These are the key issues, and Callahan and Tsouderos nailed them. Raeburn and Weintraub’s criticisms are nothing more than whines about how, in nailing these essential points, Callahan and Raeburn failed to fall for the trap of false balance.

This entire kerfuffle does bring up a legitimate issue, though. I complain frequently about how journalists fall into the trap of false balance when it comes to scientific and medical issues. However, it’s often difficult to explain this concept to the lay public because on the surface not giving undue voice to advocates of pseudoscience appears to go against commonly believed and taught concepts of fairness. How can a blogger, journalist, or other writer, communicate this concept in a limited space? On my blog, I can write as long or short as I want and have days, weeks, months, and even years to communicate and reinforce this concept to my readers. Journalists don’t have that luxury. I don’t pretend to have the definitive answer. No doubt different topics and different situation will require different approaches. I do know, however, that it is lazy and ultimately unintentionally deceptive to continue letting the mantra of balance result in promoting a false balance when discussing quackery and pseudoscience. As long as you can defend your position with data, science, evidence, and logic, don’t be afraid to defend science and science-based medicine.

By Orac

Orac is the nom de blog of a humble surgeon/scientist who has an ego just big enough to delude himself that someone, somewhere might actually give a rodent's posterior about his copious verbal meanderings, but just barely small enough to admit to himself that few probably will. That surgeon is otherwise known as David Gorski.

That this particular surgeon has chosen his nom de blog based on a rather cranky and arrogant computer shaped like a clear box of blinking lights that he originally encountered when he became a fan of a 35 year old British SF television show whose special effects were renowned for their BBC/Doctor Who-style low budget look, but whose stories nonetheless resulted in some of the best, most innovative science fiction ever televised, should tell you nearly all that you need to know about Orac. (That, and the length of the preceding sentence.)

DISCLAIMER:: The various written meanderings here are the opinions of Orac and Orac alone, written on his own time. They should never be construed as representing the opinions of any other person or entity, especially Orac's cancer center, department of surgery, medical school, or university. Also note that Orac is nonpartisan; he is more than willing to criticize the statements of anyone, regardless of of political leanings, if that anyone advocates pseudoscience or quackery. Finally, medical commentary is not to be construed in any way as medical advice.

To contact Orac: [email protected]

293 replies on “The Chicago Tribune, “chronic Lyme disease,” and demands for false balance”

“Someone named Paul Raeburn” is Paul Raeburn, former senior editor for science at Business Week, former science editor at the Associated Press, author of three science books, director of a university science journalism program. If you had time to do a PubMed search, you had time to Google him. Delegitimizing him by suggesting he has no background or standing doesn’t help your argument.

What difference does it make who Raeburn is? His arguments are no stronger if you know who he is than if you don’t know who he is.

Tsouderos is a clown. Hitch your wagon at your peril. She is nothing but a tool of ASF and big pharma. I am agnostic on the issue of autism and vaccines but, unlike you, understand that “certainty” in science is a dangerous path to embrace.

Very interesting, chronic Lyme disease therapy is a scam I’d not heard of before.

If Trine Tsouderos and Pat Callahan are in need of a new subject to investigate they should look into the CCSVI/Zamboni liberation therapy for multiple sclerosis, a very dubious theory and treatment that has suddenly become very popular thanks to some very poor reporting by a Canadian news channel at the end of last year. As a result of this thousands of people with MS have spent tens of thousands of dollars each to have angioplasty performed on their neck veins…a pointless and potentially dangerous practice.

http://www.ctv.ca/CTVNews/WFive/20091120/W5_liberation_091121/?s_name=W5

http://www.theglobeandmail.com/news/national/paolo-zamboni-a-qa/article1811072/

http://www.ticotimes.net/News/News-Briefs/Costa-Rican-Hospital-Offers-MS-Patients-A-Miracle-_Monday-November-22-2010

CCSVI advocates have been lobbing the usual “pharma shill” accusations (and the occasional death threat) against scientists and doctors who have urged caution or argued against the theory that CCSVI plays an important role in MS, though I suspect that if anyone took a close look at the activities of a companies involved with CCSVI detection and treatment they would uncover some interesting relationships. I’ve also heard that the Italian freemasons are somehow involved, though just how deep the rot runs in the Italian government is not clear.

At the moment the reporting is very biased in favour of the so-called “Liberation therapy”, despite the lack of scientific evidence for CCSVI being a cause of MS, and a lack of clinical evidence for “liberation therapy” having a beneficial effect. It would be good to see this imbalance corrected!

But the certainty of pseudoscience doesn’t bother you one whit, Dadvocate? Give me uncertainty that has a foundation of facts and evidence over certainty based on faith and distrust of authority any day.

Dadvocate: Pharma shill fail.

Raeburn offers little or no evidence to support his claims. Neither do you. Tsouderos and Callahan present the best science available. Not unproven hope shaded as science.

Dadvocate,

If Trina Tsouderos is a tool of big pharma, an article about how long-term antibiotics are a bad thing would just get her fired. It doesn’t make sense that she would write one.

But she did. So maybe she isn’t a tool of big pharma after all?

Wow. Only up for an hour and a half and already you have critics showing up. Is this a record, Orac?

A bit more on topic, Paul Raeburn sounds like the interviewer in Dara O’Briain’s bit:

For the sake of “balance”, we must now turn to Barry, who thinks the sky is a carpet painted by God.

To be fair, the Callahan and Tsouderos article doesn’t do a good job of explaining the difference between “chronic lime disease” and category 4 lime disease. That might have confused some of the critics, who thought they were attacking the idea of category 4 lime disease.

@Alison Cummins

If Trina Tsouderos is a tool of big pharma, an article about how long-term antibiotics are a bad thing would just get her fired. It doesn’t make sense that she would write one.

No. You see, this just throws people off the scent. If she writes the occasional piece that casts doubt on a treatment produced by Big PharmaTM, then people will think that she isn’t tied to them. And you fell for it. Don’t you feel silly now?

@Todd,

this just throws people off the scent.

Keep up exposing that kind of stuff and you will forgo your shill bonus check!

Someone named Paul Raeburn” is Paul Raeburn, former senior editor for science at Business Week, former science editor at the Associated Press, author of three science books, director of a university science journalism program. If you had time to do a PubMed search, you had time to Google him. Delegitimizing him by suggesting he has no background or standing doesn’t help your argument.

I wasn’t “de-legitimizing” him. However, if it bugs you so much, I will change it to say “Paul Raeburn, former senior editor for science at Business Week, former science editor at the Associated Press, author of three science books, director of a university science journalism program.”

So, now that I’ve gotten rid of what appears to be your one and only complaint, can you tell me how I am wrong about the weakness of Raeburn’s arguments?

@MikeMa

Well, you see, by pointing out the tactic, I’m throwing doubt on the tactic. I mean, as a true shill, I wouldn’t be giving away the real tactics. Man. People falling for stuff left, right and center.

Feels like someone complaining that, in a “balanced” article on the Holocaust, someone interviewed David Irving for the counterpoint and he came over as a lunatic. Sometimes even the best and brightest advocates of an idea don’t amount to much.

“Someone named Paul Raeburn” is Paul Raeburn, former senior editor for science at Business Week, former science editor at the Associated Press, author of three science books, director of a university science journalism program. If you had time to do a PubMed search, you had time to Google him. Delegitimizing him by suggesting he has no background or standing doesn’t help your argument.

Before you made this point I’d already forgotten the name “Paul Raeburn.” But now its burned into my long-term memory along with the meme, “that science writer who sold out to the pro-laetril/chronic Lyme crowd for some unknown reason.”

With friends like you…

Now I’m confused. Maryn claims that Orac is “deligitimizing” Raeburn by “suggesting he has no background or standing.”

Yet Orac in his article says “One criticism actually appeared in the Knight Science Journalism Tracker’s blog in the form of post written by Paul Raeburn, former senior editor for science at Business Week, former science editor at the Associated Press, author of three science books, and director of a university science journalism program”.

His background is given due attention – the problem is that he’s misrepresenting Tsouderos’ article and falsely indicating that there’s a serious scientific/medical case for chronic Lyme infection that deserved equal time in Tsouderos’ article.

What Maryn‘s complaint suggests is that she didn’t read Orac’s article and has no good response to its central points – “chronic Lyme disease” as posited by advocates of long-term antibiotic therapy does not have a factual basis, the therapies given have potential harmful effects, and “equal time” is an irresponsible standard for science reporting when one side represents sound science and the other side is a small minority view riddled with quackery.

Actually, I changed that after Maryn’s complaint in order to take away her complaint and force her to focus on substance, rather than superficialities.

Those who call for “balance” are those who would be *excluded* otherwise,while experts-the Orthodoxy”- be they representatives of scientific/medical organizations, governmental agencies, universities, or journals are already compromised by conflicts of interest:indeed they may even challenge the mainstream media itself for similar corporate ties ( Keven Trudeau’s Matrix includes all aforementioned as well as the much-maligned Masons).To which I ask: who, pray tell, is left? Some dude on the internet or radio with a match book school degree selling you over-priced supplements? ( No conflicts of interest there.) Woo-meisters warn about the “cult of the expert”- I wonder why?

These people rabbit on about gold standards when looking at chelation procedures but they never talk about gold standards when it comes to denying the vaccine autism link. That is because the best efforts of the multi billion dollar pharmaceutical industry fall desperately short of gold standards. I would say somewhere around the pits would be more apt.

I have a simple gold standard test for any association between vaccines and autism. Does anyone who was never vaccinated become autistic. Answer no. When my claims that there were no unvaccinated autistic people in Britain were put before the Feb 2004 Federal Vaccines Safety conference in Washington, USA by Professor Boyd Haley the British senior person present Mrs Elizabeth Miller of the Dept of Health didn’t deny the claim. Instead she attacked my arithmetic. Because there are so few unvaccinated children in the UK it would be hard to find the autistic ones amongst them, she said. Wrong and right! There are upwards of two million unvaccinated children (since 1966) in Britain. And its impossible to find the autistic ones amongst them because they don’t exist! It’s all in the minutes of that meeting. Unvaccinated equals unautistic!

Tony Bateson, Oxford, UK.

Thanks for this! I was looking for Crislip’s piece on this and you gave the link! I sent the Trib article to a friend who is personally involved in this as a caretaker for someone who thinks she has “chronic Lyme disease” and guess what she responded? “Thanks, but I guess we can only say that a lot more science needs to be done”. Haven’t I heard that one somewhere before?

So, I’ll send this column as a follow-up, but I am not certain that reason can prevail. Citing Raeburn’s credentials only convinces me that he is a journalist, not a scientist. Journalists need to grasp the concept that the tenets of these two fields collide when the demonstrable facts come into play. The same thing is going on with that book by Devra Davis about cell phones causing cancer. She is touted as a “scientist” because she has some kind of “science studies” (read philosophy of science) degree–from U of Chicago, no less! She is a dedicated New Ager, once you look into it, but I have not seen THAT reported on any of the fluff-piece segments that have been popping up on TV on the subject of her book and cell phones.

Uh, Tony, you need a new shtick. You have been proven wrong so many times it’s scary. Amish autistics exist as do many others in unvaccinated pools.

Often this takes the form of a journalistic convention that is more appropriate for politics and other issues but not so appropriate for scientific and medical issues, namely telling both sides as though they have equal or similar weight.

There being “two sides” is never, alone, justification for reporting two sides. IOW, the press gets this wrong at almost every opportunity, including in politics and other areas.

One wonders whether Tony The Liar even bothers to read posts before responding to them with his lies.

For those not familiar, Tony has repeatedly been presented with incontrovertible evidence that unvaccinated autistics exist. He then proceeds to deny that such evidence exists. He is either deliberately lying through his teeth, or grossly delusional, and in either case is unworthy of attention.

It is incredibly ignorant to say that there is no science to back up the claim of Chronic Lyme disease. Did you do any research at all before you posted or did you just take Trine and Patrica’s word for it?

ILADS, International Lyme And Associated Diseases Society, releases statement in response to the Chicago Tribune article on Lyme disease- http://www.ilads.org/news/lyme_news/73.html

From the California Lyme Disease Association in response to the Tribune article-
http://www.lymedisease.org/news/lymepolicywonk/609.html

@21

You’ve been giving the same old argument for so long, with no proof and no evidence, and yet when given concrete evidence to the contrary, you still keep rehashing the old argument.

And just what does this have to do with “Chronic lyme disease”?

I am one of the unfortunates that has had to suffer through multiple incidents of Lyme Disease – three separate times, at this point, and I’ll probably pick it up a few more times in the future (due to my many different outdoor activities, including paintball – which puts me in the vicinity of deer ticks, all the freakin’ time).

Each time, I received the recommended course of antibiotics and managed to squelch the infection. I also know of people who had Lyme for years, without realizing it & did progress to the later stages of the disease (and a couple who ultimately died from it). I definitely prefer the hard science to people who “think” something is what it is.

I have a question about Tony Bateson’s insistence that there is no autism without vaccination: does it matter which vaccine? Vaccine come in different types, after all, injected, in hales, swallowed, even scratched on. Some are attenuated viruses, some are inactivated, some are just antigens, not even entire bacteria or viruses. Is it his contention that each and every one of these vaccines has precisely the same impact in terms of causing autism?

If so, how does the body distinguish between an antigen introduced via an accidental scratch or puncture, and an antigen deliberately introduced as a vaccine? It would appear to me that it could not, and thus the ordinary injuries of life would prime unvaccinated people for autism as well.

If some vaccines induce autism and others do not, then wouldn’t it make more sense for Bateson to focus on which is which?

Nothing matters to Tony Bateson, they could find the definite cause and an infallible cure for autism, and he wouldn’t change his mind.

@Mu

Not only that, but he wouldn’t even come back here to see any follow-up comments. He’s little more than a drive-by troll.

Now I have this image of one of those crazy-haired trolls driving around in a Vauxhall or something.

You didn’t find any of the proof of Chornic Lyme or useless blood tests that abounds on pubmed? Ok then, I’ll help you out–I know that you trust these authors.
—————————–
Luft BJ, Gorevic PD, Halperin JJ, Volkman DJ, Dattwyler RJ. A perspective on the treatment of Lyme borreliosis. Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1518-25.
S1519
Par. 1
“In the chronic phase of the illness, B. Burgdorferi is more difficult to isolate or identify in affected tissue[…] localized inflammatory processes may occur in one or more organ systems[…]”

Shadick, Nancy A., Phillips, Charlotte B., Logigian, Eric L. Steere, Allen C., Kaplan, Richard F., Berardi, Victor P., Duray, Paul H., Larson, Martin G. Wright, Elizabeth A.,
Wright, Elizabeth A., Ginsburg. Katherine. S., Katz, Jeffery Z., Liang, Matthew H.
The Long-Term Clinical Outcome of Lyme Disease
A Population-based Retrospective Cohort Study
Annals of Internal Medicine Volume 121, No. 8, (Oct. 15, 1994) pp. 560-567
560
Par. 2
“Some of the late consequences of Lyme disease, such as oligoarticular arthritis, axonal poly- neuropathy, or active encephalopathy, are thought to be caused by persistent spirochetal infection and are amena- ble to antibiotic treatment (6-8).

Par. 4

“…well documented treatment failures have been reported…Weber et. al. [**37***] reported that 27% of patients with EM develop later neurologic or musculoskeletal manifestations of the infection regardless of whether penicillin, tetracycline, or amoxicillin plus clavulante was used.”

U.S.Patent Appli. No. 11/196,475, Unpublished (filing date August 3, 2005)
(Raymond J. Dattwyler; Maria J.C. Gomes-Solecki; Benjamin J. Luft; Dunn, John. J., applicants)
Description
Background of the Invention
Paragraph 3
“Furthermore, patients acutely and chronically infected with B. burgdorferi respond variably to the different antigens, including OspA, OspB, OspC, OspD, p39, p41 and p93. ”

Klempner, Mark S., Norlong, Richard, Rogers, Rick A. Invasion of human Skin Fibroblasts by the Lyme Disease Spirochete, Borrelia Burgdorferi. The Journal of Infectious Diseases Vol. 167, No. 5 (May, 1993) pp.1074-1081
Abstract
“By scanning electron microscopy, B. burgdorferi
were tightly adherent to fibroblast monolayers after 24-48 h but were eliminated from the cell
surface by treatment with ceftriaxone (1 ag/mL) for 5 days. Despite the absence of visible spiro-
chetes on the cell surface after antibiotic treatment, viable B. burgdorferi were isolated from
lysates of the fibroblast monolayers.”
“These observations suggest that B. burgdorferi can adhere to,
penetrate, and invade human fibroblasts in organisms that remain viable.”
———————–

Here’s another helpful hint for you. Don’t go kissing anyone with Lyme Disease. Or sharing there food. According to IDSA author Barbour, mammalian saliva is infectious.

Barbour, Alan G.; Hayes, Stanley F. Biology of Borrelia species. Microbiological Reviews. (Dec 1986) Vol. 50, No. 4. P 381-400.
394
Par. 2
“Although ingestion of spirochetemic blood by an arthropod
and subsequent passage of the borreliae to another
vertebrate host as outlined above is the usual mode of
transfer between animals, direct vertebrate-to-vertebrate
transmission may also occur. The urine of infected animals
can contain viable borrelia (Bosler and Schulze, in press).
Spirochetes in the urine could enter the host through the
mucous membranes of the conjunctiva, mouth, or nose (73).
Borreliae were demonstrated in the milk, and a small proportion
of guinea pigs that consumed milk of an infected
female became infected themselves (222). The demonstration
that rats and dogs can be infected through the consumption
of infected rat brains or other infected organs (132, 149,
158, 215) suggests that a selective advantage could be
conferred upon those strains that are neurotropic and that
infect rodents practicing some degree of cannibalism. Rat
saliva has been found to be infectious, and transmission
through rat bites has been reported (131). Contact transmission
of B. burgdorferi among laboratory-housed field mice
has been documented, but the route of transmission was not
known (64). “

Just how much should you avoid the fluids of patients with Lyme?
393
Par. 2

“A single borrelia of B. turicatae, B. hermsii, or B. durronii is sufficient to produce infection in laboratory animals…in susceptible animals, there may be 100,000,000 borreliae per ml of blood during peak spirochetemias.”

Don’t trust me, though; lymecryme.com, lymeinfo.net, elencook.org, underourskin.com, undertheeightball.com, and ctlymedisease.org . You may want to hop on over to that last sight and look at the original version of the bug’s MSD sheet. (HInt: Laboratory Hazards–“What is wrong with this picture?”)

“but not you…not anymore…”
——————————-

There’s an old adage in medicine. “When you hear hoofbeats, think of horses, not zebras”. There is one lone exception though, and that of course is lyme disease where the adage seems to be “When you hear hoofbeats, think of unicorns, not horses”. In the IDSA’s Alice-In-Wonderland world of lyme disease, if you are bitten by a tick and get a rash and lyme disease symptoms, and have been treated with 10 days of a mild bacteriostatic agent at some point thereafter whether its the day of the tick bite or years later, you are cured.

Your symptoms that persist and get worse after treatment, even though they are the same symptoms as before treatment, are not due to a pathogen. No, this pleomorphic bacteria that can literally outrun the immune system and whose DNA has been found using PCR after months of antiobiotic treatment can’t be causing your symptoms. Instead the IDSA would have us believe its a mysterious and exotic syndrome of unknown etiology, perhaps auto-immune, perhaps psychological, perhaps both, perhaps neither, but in all this uncertainty, they are damn sure of one thing. You don’t have lyme disease. How do they know this? They said so, and even though many patients get better after long-term antibiotic treatment (which is extremely risky and dangerous as evidenced by all the acne ridden teenagers dropping like flies), they have a measly 4 very flawed studies with very small sample sizes to trumpet their conclusions, amid the many showing borrelia persistence post-treatment.

So if you get bitten by a tick and the 10 days of doxycycline doesn’t kill all the borrelia, babesia, ehrlichia, and/or any of the other myriad of blood borne pathogens ticks carry, think unicorns not horses, and feel fortunate that you are the one lone exception to the old medical adage.

Hmmm. I wondered how long it would be before the Lymies showed up. It actually took them longer than I expected; my Google-Fu must not be as strong as I thought.

Now Tony’s just being lazy. At least have the common decency not to cut-and-paste your anti-vaccine ramblings.

Orac, I’d say that 4 1/2 hours is about the going lag time for trolls these days, give or take an hour either way.

The Lymies apparently can’t read. The hypothesis that persistent Borelia infection causes chronic Lyme disease has been tested. Antibiotic treatment does absolutely nothing.

Chronicity

Luft BJ, Gorevic PD, Halperin JJ, Volkman DJ, Dattwyler RJ. A perspective on the treatment of Lyme borreliosis. Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1518-25.
S1518

Abstract
“[…]there has been no standardization of the methodology for measuring either inhibitory or bactericidal levels. Clinical studies have documented the efficacy of antibiotics, but therapy has failed in as many as 50% of cases of chronic infection.”

Par. 2
“Persistent B. Burgdorferi can produce various insidious and chronic dermatolofic, neurologic, and rheumatologic manifestations[…] The pathophysiologic mechanisms involved in the chronic phase of this illness remain incompletely defined.”

S1519

Par. 1
“In the chronic phase of the illness, B. Burgdorferi is more difficult to isolate or identify in affected tissue[…] localized inflammatory processes may occur in one or more organ systems[…]”

S1520
Par.1
“The kinetics of the in vitro killing of B. Burgdorferi are remarkably similar to those for Traponema pallidum [33,34] in that prolongd exposure to antibiotics is necessary for effective killing.”

Par. 2

“…syphilis may also be relevant to Lyme borreliosis [35]. For instance, for eradication of T. pallidum in an animal model, effective levels of penicillin must be maintained[…]beaus slowly multiplying organisms may regenerate…”

Par. 3

“In a randomized, controlled study performed by Steere et. al. […]late complications, such as facial palsies, supraventricular tachycardia, brief episodes of arthritis, fatigue, and lethargy, occurred in 38%-50% of patients irrespective of the treatment regimen. [****2****]”

Par. 4

“…well documented treatment failures have been reported…Weber et. al. [**37***] reported that 27% of patients with EM develop later neurologic or musculoskeletal manifestations of the infection regardless of whether penicillin, tetracycline, or amoxicillin plus clavulante was used.”

“Berger [***38***] reported…six of 16 patients who had more severe illness accompanied by EM and who were treated with 250-500 mg of penicillin required retreatment because of persistent illness.

Par. 6
“Chronic Lyme disease. B-Lactam antibiotics have been the standard therapy for chronic Lyme borreliosis. High-dose intravenous penicillin has not been universally successful. In Studies by Steere et al.[40] of 43 patients treated with either 3 weeks of benzathine penicillin or 10 days of penicillin G, 35% and 55%, respectively, had complete resolution of their arthritis.”

“This efficacy [of treatment in neuroborreliosis] may reflect the breakdown of the blood-brain barrier, which allows high, more sustained levels of penicillin with in the CNS. In several reported cases, acute CNS in infection has progressed during penicillin therapy…”

s1521
Par. 1

“Meningopolyradiculitis does not uniformly respond to treatment with penicillin…”

“Of patients with sever neurologic signs, more than 50% will continue to suffer from disability due to this disease for months to years after treatment….Similarly, antibiotic treament of acrodermatitis atrophicans produces resolution of skin involvement in only ~50% of patients. In addition, ~50% of these patients continue to have etracutaneous manifestation of Lyme disease after therapy [8]…failure rates of >= 50% are being reported in some series for the treatment of chronic rheumatologic, dermatologic, or neurologic disease due to B. Burgdorferi. Clearly, alternative therapies are needed.”

Par. 4

“Admission criteria were a history of physician-observed EM and/or evidence of a specific immunologic reactivity to B. Burgdorferi and objective evidence of involvement of two or more of the following organ systems: central and peripheral nervous system, cardiovascular system, and musculoskeletal system.”

“After therapy, five of the ten patients given penicillin (50%) continued to have recurrent oligoarticular arthritis, fatigue, and memory difficulties.”

“One patient with complete heart block was treated with penicillin; his conduction abnormality resolved, but he developed arthritis 2 months after completion of therapy. “

“…of the 13 patients randomized to ceftriaxone…one described ongoing fatigue and memory difficulties and three continued to complain of mild arthralgias.”

Par 5.

“The ceftriaxone arm of the study was extended to an additional 31 patitnts…Overall, 13% of this group of patients failed to respond to therapy. The rates of response to two doses [per day] of ceftriaxone were similar (~85%).

Par. 6-S1522 Par. 1

“Steere et. al. [2, 50] performed several prospective studies…in each treatment study, whether it was concerned with early or late disease, a significant number of treatment failures occurred. For example, in the randomized prospective study evaluating the use of penicillin and tetracycline for the treatment of EM, ~50% of the patients given either regimen subsequently developed “minor” manifestations of disease and several treated with penicillin went on to develop “major” manifestations [2, 51]. For chronic rheumatologic, dermatologic, and neurologic disease, therapy with penicillin has been associated with a failure rate of [>=]50%. Thus, it appears that although tetracyclince and penicillin are clearly efficatious, the are not uniformly effective. Studies for optimization of therapies are certainly warranted.”

Par. 3

“…prolonged exposure (i.e., for as long as 72-96 hours) is necessary for effective killing of B. Burgdorferi [, which] may have important therapeutic implications [32]. Similar kinetics of killing have been noted for T. Pallidum [34,35]; it has been shown in an animal model that T.Pallidum will regrow if penicillin levels are allowed to fall into a subinhibitory range [35]. A similar phenomenon may occur with B. Burgdorferi infection. ”

Par. 4

“Treatment failures with tetracycline has been reported [51].”

S1523
Par. 3

Long-term inves-
tigations are needed to determine whether the pa-
tients treated with ceftriaxone remain in remission.
Although ceftriaxone appears to be promising, it is
still associated with a 15?% failure rate [52]. A topic
for further research is whether a more prolonged
course of therapy would be useful in decreasing this
rate of relapse. In addition, the efficacy of various
antimicrobial agents for the treatment of the differ-
ent manifestations of early and chronic Lyme bor-
reliosis must be assessed

U.S.Patent Appli. No. 11/196,475, Unpublished (filing date August 3, 2005)
(Raymond J. Dattwyler; Maria J.C. Gomes-Solecki; Benjamin J. Luft; Dunn, John. J., applicants)
Description
Background of the Invention

Paragraph 3
“Furthermore, patients acutely and chronically infected with B. burgdorferi respond variably to the different antigens, including OspA, OspB, OspC, OspD, p39, p41 and p93. ”

Paragraph 5
“Currently, Lyme Disease is treated with a range of antibiotics, e.g., tetracyclines, penicillin and cephalosporins. However, such treatment is not always successful in clearing the infection. Treatment is often delayed due to improper diagnosis with the deleterious effect that the infection proceeds to a chronic condition, where treatment with antibiotics is often not useful. One of the factors contributing to delayed treatment is the lack of effective diagnostic tools.”

Klempner, Mark S., Norlong, Richard, Rogers, Rick A. Invasion of human Skin Fibroblasts by the Lyme Disease Spirochete, Borrelia Burgdorferi. The Journal of Infectious Diseases Vol. 167, No. 5 (May, 1993) pp.1074-1081

Abstract

“By scanning electron microscopy, B. burgdorferi
were tightly adherent to fibroblast monolayers after 24-48 h but were eliminated from the cell
surface by treatment with ceftriaxone (1 ag/mL) for 5 days. Despite the absence of visible spiro-
chetes on the cell surface after antibiotic treatment, viable B. burgdorferi were isolated from
lysates of the fibroblast monolayers.”

“These observations suggest that B. burgdorferi can adhere to,
penetrate, and invade human fibroblasts in organisms that remain viable.”

1074
Par. 2

“Despite an immune response to multiple borrelial anti-
gens, B. burgdorferi can establish a persistent infection in
humans and animals. Organisms have been isolated from
weeks to years after the initial infection from skin [2-5], cere-
brospinal fluid [5, 6], synovial tissue [7], the flexor retinacu-
lum [8], the eye [9], myocardium [10], blood [1 1], and syno-
vial fluid [12, 13].”

This blog post and other protests by non-journalists reminds me of patients going to medical journal sites to protest the scientific method. If you don’t like the results, just change the methodology to get what you want.

Likewise, at the Knight Science Journalism Tracker, the most credible and important source of science journalism peer review, not a single journalist agreed that the story in question represented appropriate journalistic practice,or met the standards of good journalism. Not a single classically trained journalist disagreed with Paul Raeburn, the reviewer, who is himself one of the finest and most credentialed science journalists in the United States.

The site was then invaded by voices with knowledge in medicine but zero credentials,training, or experience in journalism, who rushed in to impugn the standards of good journalistic practice endorsed by the journalist peer reviewers, and to insist there was another, better way of doing things: their way, which would rewrite the ethics and guidelines of journalism practice, whole cloth. To wit, these non-journalists feel that they should be enfranchised to peer review journalism along with journalists themselves –and that while they are at it, they should change good journalistic practice to suit themselves.

This is absurd: There is a lot of bad journalism practiced, for instance, the journalism in the Tribune story, but the profession still has standards, still has ethics, still has requirements, for those who care to practice with care.

I don’t want to respond much on the science because to me, this is an issue of journalism, pure and simple: Any story done in this fashion, no matter what the topic, would have the same journalistic flaws and would violate the kind of journalistic practice we require at Discover and most other quality national magazines.

However, on the science I will say this: I thought that the recent conference on Lyme and Tick-borne Disease: The State of the Science, organized by the Institute of Medicine, with presenters that included the top experts in the world, gave nuanced insight into the issues these journalists ignored. I wish the Tribune journalists had bothered to watch the webcast, at least, and to quote some of the academic scientists presenting –and that they had enriched their story with the sort of context one gets from a meeting like that.

Pamela Weintraub
Features Editor
Discover Magazine

Chronicity

Luft BJ, Gorevic PD, Halperin JJ, Volkman DJ, Dattwyler RJ. A perspective on the treatment of Lyme borreliosis. Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1518-25.
S1518

Abstract
“[…]there has been no standardization of the methodology for measuring either inhibitory or bactericidal levels. Clinical studies have documented the efficacy of antibiotics, but therapy has failed in as many as 50% of cases of chronic infection.”

Par. 2
“Persistent B. Burgdorferi can produce various insidious and chronic dermatolofic, neurologic, and rheumatologic manifestations[…] The pathophysiologic mechanisms involved in the chronic phase of this illness remain incompletely defined.”

S1519

Par. 1
“In the chronic phase of the illness, B. Burgdorferi is more difficult to isolate or identify in affected tissue[…] localized inflammatory processes may occur in one or more organ systems[…]”

S1520
Par.1
“The kinetics of the in vitro killing of B. Burgdorferi are remarkably similar to those for Traponema pallidum [33,34] in that prolongd exposure to antibiotics is necessary for effective killing.”

Par. 2

“…syphilis may also be relevant to Lyme borreliosis [35]. For instance, for eradication of T. pallidum in an animal model, effective levels of penicillin must be maintained[…]beaus slowly multiplying organisms may regenerate…”

Par. 3

“In a randomized, controlled study performed by Steere et. al. […]late complications, such as facial palsies, supraventricular tachycardia, brief episodes of arthritis, fatigue, and lethargy, occurred in 38%-50% of patients irrespective of the treatment regimen. [****2****]”

Par. 4

“…well documented treatment failures have been reported…Weber et. al. [**37***] reported that 27% of patients with EM develop later neurologic or musculoskeletal manifestations of the infection regardless of whether penicillin, tetracycline, or amoxicillin plus clavulante was used.”

“Berger [***38***] reported…six of 16 patients who had more severe illness accompanied by EM and who were treated with 250-500 mg of penicillin required retreatment because of persistent illness.

Par. 6
“Chronic Lyme disease. B-Lactam antibiotics have been the standard therapy for chronic Lyme borreliosis. High-dose intravenous penicillin has not been universally successful. In Studies by Steere et al.[40] of 43 patients treated with either 3 weeks of benzathine penicillin or 10 days of penicillin G, 35% and 55%, respectively, had complete resolution of their arthritis.”

“This efficacy [of treatment in neuroborreliosis] may reflect the breakdown of the blood-brain barrier, which allows high, more sustained levels of penicillin with in the CNS. In several reported cases, acute CNS in infection has progressed during penicillin therapy…”

s1521
Par. 1

“Meningopolyradiculitis does not uniformly respond to treatment with penicillin…”

“Of patients with sever neurologic signs, more than 50% will continue to suffer from disability due to this disease for months to years after treatment….Similarly, antibiotic treament of acrodermatitis atrophicans produces resolution of skin involvement in only ~50% of patients. In addition, ~50% of these patients continue to have etracutaneous manifestation of Lyme disease after therapy [8]…failure rates of >= 50% are being reported in some series for the treatment of chronic rheumatologic, dermatologic, or neurologic disease due to B. Burgdorferi. Clearly, alternative therapies are needed.”

Par. 4

“Admission criteria were a history of physician-observed EM and/or evidence of a specific immunologic reactivity to B. Burgdorferi and objective evidence of involvement of two or more of the following organ systems: central and peripheral nervous system, cardiovascular system, and musculoskeletal system.”

“After therapy, five of the ten patients given penicillin (50%) continued to have recurrent oligoarticular arthritis, fatigue, and memory difficulties.”

“One patient with complete heart block was treated with penicillin; his conduction abnormality resolved, but he developed arthritis 2 months after completion of therapy. “

“…of the 13 patients randomized to ceftriaxone…one described ongoing fatigue and memory difficulties and three continued to complain of mild arthralgias.”

Par 5.

“The ceftriaxone arm of the study was extended to an additional 31 patitnts…Overall, 13% of this group of patients failed to respond to therapy. The rates of response to two doses [per day] of ceftriaxone were similar (~85%).

Par. 6-S1522 Par. 1

“Steere et. al. [2, 50] performed several prospective studies…in each treatment study, whether it was concerned with early or late disease, a significant number of treatment failures occurred. For example, in the randomized prospective study evaluating the use of penicillin and tetracycline for the treatment of EM, ~50% of the patients given either regimen subsequently developed “minor” manifestations of disease and several treated with penicillin went on to develop “major” manifestations [2, 51]. For chronic rheumatologic, dermatologic, and neurologic disease, therapy with penicillin has been associated with a failure rate of [>=]50%. Thus, it appears that although tetracyclince and penicillin are clearly efficatious, the are not uniformly effective. Studies for optimization of therapies are certainly warranted.”

Par. 3

“…prolonged exposure (i.e., for as long as 72-96 hours) is necessary for effective killing of B. Burgdorferi [, which] may have important therapeutic implications [32]. Similar kinetics of killing have been noted for T. Pallidum [34,35]; it has been shown in an animal model that T.Pallidum will regrow if penicillin levels are allowed to fall into a subinhibitory range [35]. A similar phenomenon may occur with B. Burgdorferi infection. ”

Par. 4

“Treatment failures with tetracycline has been reported [51].”

S1523
Par. 3

Long-term inves-
tigations are needed to determine whether the pa-
tients treated with ceftriaxone remain in remission.
Although ceftriaxone appears to be promising, it is
still associated with a 15?% failure rate [52]. A topic
for further research is whether a more prolonged
course of therapy would be useful in decreasing this
rate of relapse. In addition, the efficacy of various
antimicrobial agents for the treatment of the differ-
ent manifestations of early and chronic Lyme bor-
reliosis must be assessed

U.S.Patent Appli. No. 11/196,475, Unpublished (filing date August 3, 2005)
(Raymond J. Dattwyler; Maria J.C. Gomes-Solecki; Benjamin J. Luft; Dunn, John. J., applicants)
Description
Background of the Invention

Paragraph 3
“Furthermore, patients acutely and chronically infected with B. burgdorferi respond variably to the different antigens, including OspA, OspB, OspC, OspD, p39, p41 and p93. ”

Paragraph 5
“Currently, Lyme Disease is treated with a range of antibiotics, e.g., tetracyclines, penicillin and cephalosporins. However, such treatment is not always successful in clearing the infection. Treatment is often delayed due to improper diagnosis with the deleterious effect that the infection proceeds to a chronic condition, where treatment with antibiotics is often not useful. One of the factors contributing to delayed treatment is the lack of effective diagnostic tools.”

Klempner, Mark S., Norlong, Richard, Rogers, Rick A. Invasion of human Skin Fibroblasts by the Lyme Disease Spirochete, Borrelia Burgdorferi. The Journal of Infectious Diseases Vol. 167, No. 5 (May, 1993) pp.1074-1081

Abstract

“By scanning electron microscopy, B. burgdorferi
were tightly adherent to fibroblast monolayers after 24-48 h but were eliminated from the cell
surface by treatment with ceftriaxone (1 ag/mL) for 5 days. Despite the absence of visible spiro-
chetes on the cell surface after antibiotic treatment, viable B. burgdorferi were isolated from
lysates of the fibroblast monolayers.”

“These observations suggest that B. burgdorferi can adhere to,
penetrate, and invade human fibroblasts in organisms that remain viable.”

1074
Par. 2

“Despite an immune response to multiple borrelial anti-
gens, B. burgdorferi can establish a persistent infection in
humans and animals. Organisms have been isolated from
weeks to years after the initial infection from skin [2-5], cere-
brospinal fluid [5, 6], synovial tissue [7], the flexor retinacu-
lum [8], the eye [9], myocardium [10], blood [1 1], and syno-
vial fluid [12, 13].”

Steere, AC.; Dressler, F..; Yoshinari, NH. The T-Cell Proliferative Assay in the Diagnosis of Lyme Disease. Ann Intern Med. 1992 Apr 1;116(7):603.
Abtract
Measurements and Main Results

“Nineteen of 42 patients with Lyme arthritis or chronic neuroborreliosis and 4 of 77 patients with other diseases had positive T-cell proliferative responses to B. burgdorferi antigens. The sensitivity of the proliferative assay was 45% (95% Cl, 30% to 60%) and the specificity was 95% (95% Cl, 87% to 99%). Twelve of 27 patients with active Lyme arthritis, 7 of 15 patients with chronic neuroborreliosis, 4 of 16 patients with inactive Lyme disease, 4 of 9 healthy Borrelia laboratory workers, and 0 of 9 healthy subjects had positive responses. Three of five patients with Lyme disease who had negative or indeterminant antibody responses by ELISA had positive T-cell proliferative

Steere, Allen C., Schlesinger, Peter A.; Duray, Paul H.; Burke, Barbara A.; Stillman, Thomas. Maternal-Fetal Transmission of the Lyme Disease Spirochete, Borrelia burgdorferi. Annals of Internal Medicine . (July 1, 1985) vol. 103, no.1, p. 67-68.

67
Par. 1

“We report the case of a woman who developed Lyme disease during the first trimester of pregnancy…Her infant, born at 35 weeks gestational age, died of congenital heart disease during the first week of life. Istologic examination of autopsy material showed the Lyme diseae spirochete in the spleen, kidneys, and bone marrow.”

Par. 8

“The Lyme disease spirochete may also spread transplacentally to the organs of the fetus.”

68
Par. 1

“…because the fetus is likely to have been infected during cardiovascular organogenesis, a teratogenic effect of the spirochete cannot be excluded.”

Par. 2

“Women who acquire Lyme disease while pregnant sould be treated promptly with penicillin, or if allergic, erythromycin…At te time of childbirth, the placenta should be examined for histologic abnormalities and for spirochetes, as in congenital syphilis (10.) If the infant is ill, the diagnosis of Lyme disease should be considered.”

This blog and other protests by non-journalists reminds me of patients going to medical journal sites to protest the scientific method. If you don’t like the results, just change the methodology to get what you want. Likewise, at the Knight Science Journalism Tracker, the most credible and important source of science journalism peer review, not a single journalist agreed that the story in question represented appropriate journalistic practice, or met the standards of good journalism. Not a single classically trained journalist disagreed with the reviewer, Paul Raeburn, who is himself one of the finest and most credentialed science journalists in the United States.
The site was then invaded by voices with knowledge –and especially, by set positions– in medicine, but zero credentials,training, or experience in journalism. These people rushed in to a space reserved for journalist peer reviewers, to impugn the standards of good journalistic practice endorsed by the journalist peer reviewers, and to insist there was another, better way of doing things: their way, which would rewrite the ethics and guidelines of journalism practice, whole cloth. To wit, these non-journalists feel that they should be enfranchised to peer review journalism along with journalists themselves –and that while they are at it, they should change good journalistic practice and write new rules to suit themselves. This is not going to happen: There is a lot of bad journalism practiced, for instance, the journalism in the Tribune story, but the profession still has standards, still has ethics, still has requirements, still has a set of guidelines to differentiate good work from bad.
I don’t want to respond much on the science because to me, this is an issue of journalism, pure and simple: However, I will say this: I thought that the recent conference on Lyme and Tick-borne Disease: The State of the Science, organized by the Institute of Medicine, with presenters that included the top experts in the world, gave nuanced insight into issues these journalists ignored. I wish the Tribune journalists had bothered to watch the webcast, at least, and to quote some of the academic scientists presenting –and that they had enriched their story with the sort of context one gets from a meeting like that.

Pamela Weintraub
Features Editor
Discover Magazine

“This is absurd: There is a lot of bad journalism practiced, for instance, the journalism in the Tribune story, but the profession still has standards, still has ethics, still has requirements, for those who care to practice with care.”

Do those ethics require you to give Holocaust deniers equal voice in all stories dealing with the Holocaust? You will find plenty of ‘experts’ who will proide you with ‘evidence’ that, by your standards, would seem to require balanced reporting.

Der Ricther Spricht, we got it the first couple of times. Do you have anything that’s peer-reviewed (patent application doesn’t count) and less than fifteen years old?

Do those ethics require you to give Holocaust deniers equal voice in all stories dealing with the Holocaust? You will find plenty of ‘experts’ who will proide you with ‘evidence’ that, by your standards, would seem to require balanced reporting.

I purposely avoided this example because I knew that if I used it someone, somewhere would claim that I was calling Lyme advocates and those claiming to suffer from CLD Nazis, when I most definitely am not. However, now that someone else has brought it up, I can agree that it is a perfect example to illustrate the principle of false balance. Whenever a journalist writes about the Holocaust, should she be required to interview “experts” on the “other side,” for instance countering an interview with noted Holocaust historian Deborah Lipstadt with an interview with Holocaust denier David Irving?

Or, to bring it to science, suppose a journalist is doing a story about a perpetual motion machine, which all of physics tells us to be impossible. Should the journalist feel obligated to interview and “expert” who claims that such a device is possible?

Personally, I think Weintraub is using the “balance” complaint as an intellectually lazy way of not having to think too hard about the issue and make judgments.

In addition to the use of “false balance,” another problem with the official journalism formula is the heavy use of anectdotes. Nearly every article (good or bad) starts with an anecdote. This falsely sets up the thesis of the journalist. It also reinforces the popular perception that anecdotes are as good if not better than data. What is the proper use and role of anecdotes in scientific journalism?

Ms. Weintraub,

In your comments here and at the Knight Science Journalism Tracker post you’ve made several assertions of your expertise in the ethics and quality-control of science journalism, including a necessarily balanced discussion. Instead of diverging into a No True Scotsman/Science Journalist vein of commentary, would you please outline how a journalist is supposed to properly weigh differing opinions, particularly when there is a clear imbalance in the level of support for one claim over another?

—————————-

Recovery of Lyme spirochetes by PCR in semen samples of previously diagnosed Lyme disease patients
Gregory Bach, DO, International Scientific Conference on Lyme Disease, April 2001
Objective
Lyme disease, being a spirochete with pathology similar to syphilis, is often found difficult to treat due to the spirochete invading sanctuary sites and displaying pleomorphic characteristics such as a cyst (L-form). Because a significant portion of sexually active couples present to my office with Lyme disease, with only one partner having a history of tick exposure, the question of possible secondary (sexual) vector of transmission for the spirochete warrants inquiry. Additionally, sexually active couples seem to have a marked propensity for antibiotic failure raising the question of sexually active couples re-infecting themselves through intimate contact.
Methods
Lyme spirochetes/DNA have been recovered from stored animal semen. Recovery of spirochete DNA from nursing mother’s breast milk and umbilical cord blood by PCR (confirmed by culture/microscopy), have been found in samples provided to my office.

Results
Surprisingly, initial laboratory testing of semen samples provided by male Lyme patients (positive by western blot/PCR in blood) and the male sexual partner of a Lyme infected female patient were positive approximately 40% of the time. PCR recovery of Lyme DNA nucleotide sequences with microscopic confirmation of semen samples yielded positive results in 14/32 Lyme patients (13 male semen samples and 1 vaginal pap).

ALL positive semen/vaginal samples in patients with known sexual partners resulted in positive Lyme titers/PCR in their sexual partners. 3/4 positive semen patients had no or unknown sexual partners to be tested.

These preliminary findings warrant further study. Current a statistical design study to evaluate the possibility of sexual transition of the spirochete is being undertaken. Our laboratory studies confirm the existence of Lyme spirochetes in semen/vaginal secretions. Whether or not further clinical studies with a larger statistical group will support the hypothesis of sexual transmission remains to be seen.

A retrospective clinical study is also underway. We are reviewing the medical records, collecting semen samples of patients who were previously diagnosed with current and previously treated Lyme disease are being asked to provide semen,pap and blood samples for extensive laboratory testing.

Conclusion
With the initially impressive data, we feel the subsequent statistical study on the sexual transmission of the Lyme spirochete will illuminate a much broader spectrum of public health concerns associated with the disease than the originally accepted tick borne vector.
—————————————–
So the question now becomes, Orcac et al,

Why do you want your fellow human being–Homo sapiens sapiens– who has never even heard of you or seen you, let alone tried to rob you of your ability to have a wife, a husband, a child, to wonder why you raised an eye to see, a ear to hear, or a finger to touch the world–
to have an incurable, contagious brain infection?
What joy can you possibly derive when you make a feeling, wondering, laughing, crying, dancing, dreaming person back into an animal or into dirt? Take someone whose only goal may be to better name their world and maybe even repair it a little, or help another human being do so, if they ever try to act on any of these intentions, mutilators, debasers, and even murderers? Is it that you feel a little more like God when you make it so easy for good people to do something so terrible…

@Pamela “…gave nuanced insight into the issues these journalists ignored.”

Nuanced insight. *crickets*

There is a reason why scientists rush in to help you journalists with reporting science: we’re pretty good at it, we follow a method, we must have a falsifiable hypothesis, and we collect data that either supports or fails to support a hypothesis – we don’t prove things.

What you describe as the journalistic MO sounds like a textbook definition of groupthink.

This link says it all. When it comes to the possibility of persistent borrelia burdorferi infection despite seemingly adequate antibiotic therapy, there is a legitimate scientific debate between credible researchers and physicians on both sides.

It would be in your best interest to understand the nuances of the subject as well as all of the studies regarding persistent infection before applying your cynicism.

Link: https://acrobat.com/app.html#d=sbb-EmpQrQTgrPoezLGreg

Pamela Weintraub:

I don’t want to respond much on the science because to me, this is an issue of journalism, pure and simple

Fair enough — now, would you mind explaining in what way the Chicago Tribune piece was bad journalism? In your post, you justified your position with nothing more than “a bunch of authorities in journalism agreed it was bad”, and then launched into a diatribe about how bloggers aren’t proper journalists. Now, most journalists have degrees in communication or English or another topic which will train them how to communicate clearly. I do not see how this diatribe supports your thesis that the Chicago piece was bad journalism. Instead, it seems like a bit of poisoning the well. You don’t even explain why THIS blog post is bad, speaking instead in generalities.

So come on — you see there’s a problem. Would you mind pointing it out?

Incidentally, you’re an editor for Discover Magazine. While that is a pop magazine, it is a pop *science* magazine, and time was, that meant something. If you think some ill-defined “journalistic ethics” is more important than actual honesty, that may explain why the quality of Discover Magazine has declined so much since I was a subscriber. Time was, journalists investigated and reported on stories. Now, it seems prominent editors will openly castigate (while signing with the name of their employer!) journalists who dare to adhere to the old standards of journalistic ethics.

That’s the first time I’ve heard it claimed that journalistic ethics require the journalist to ignore truth and disregard facts. I was kind of under the impression that accuracy was the central requirement of journalistic ethics. Yet here Pamela is blasting an accurate article, and demanding that it should have included falsehoods in order to be ethical.

Orac, you wrote: “Could it be, perhaps, because there aren’t really any legitimate scientific experts who support the idea that long term chronic antibiotics are useful for the entity that is chronic Lyme disease?” As Pamela Weintraub wrote, there certainly are legitimate expert researchers who are looking into that very question, and evidence is mounting in its favor. As to the randomized clinical trials, if you would read them, as I did, you would find that the patient cohort was quite narrow (for one thing, they had already failed the very IV antibiotic treatment for which they were tested), and the findings should not be generalized to the entire Lyme population. The research had to start somewhere, but it is incomplete. I am glad that you recognize that some patients go on to be symptomatic (and with much more than aches, fatigue, and trouble concentrating). Is it damage? auto-immune? co-infections? persistent infection? or a combination of all of these? Let’s let the science play out, and in the meantime, let fully-informed patients decide what they need to get their lives back.

More on that “imbalance of evidence:”

Borrelia Burgdorferi –Material Safety Data Sheet. Canadian Office of Biosafety Information edited by the Colorado State University Office of Biosafety; June 16 1998.
Section VI) Laboratory Hazards
“PRIMARY HAZARDS: Accidental parenteral inoculation and exposure to infectious aerosols.”
[Compiler’s note: The implications of this, given that B.b. has been found in urine and that toilets have been shown to produce aerosols , are disturbing.]

Aguero-Rosenfeld, Maria E.; Nowakowski, John; McKenna, Donna F.; Carbonaro, Carol A.;
Wormser, Gary P.
Serodiagnosis in Early Lyme Disease
Journal of Clinical Microbiology, Dec. 1993.
Vol. 31, No. 12
p. 3090-3095
3093
Par. 2
“In our patient
population, the frequency of prior tick bite (24%)…”

Burgess, Elizabeth C.; Amundson, Terry E.; Davis, Jeffrey P.; Edelman, Robert.
Experimental Inoculation of Peromyscus spp. With Borrelia burgdorferi: Evidence of Contact Transmission
Am. J. Trop. Med. Hyg., 35(2), 1986, pp.355-359
[Compiler’s note: While this study is not by any members of the 2006 IDSA guidelines panel, it is included because Burgess, Amundson, and Davis worked at, respectively, UW-Madison’s School of Veterinary Medicine, Wisconsin DNR, and Wisconsin Division of Public Health at the time they published the study.

Abstract

“To determine if B. burgdorferi was being transmitted by direct contact, 5 uninfected P. leucopus and 5 uninfected P. maniculatus were caged with 3 B. burgdorferi infected P. leucopus and 3 infected P. maniculatus, respectively. Each ofthese contact-exposed P. leucopus and P. maniculatus developed antibodies to B. burg dorferi, and B. burgdorferi was isolated from the blood of 1contact-exposed P. maniculatus 42 days post-initial contact. These findings show that B. burgdorferi can be transmitted by direct contact without an arthropod vector.”

358
Par. 3

“Since the contact mice had developed antibodies by day 14 and there was no evidence of fighting among the mice it is Un likely that B. burgdorfrri was transmitted via blood.”

“Transmission of other spirochetes by infected animals have been documented to occur through the urine (as with B. recurrentis),’6 or venereally as with T. pallidum.17 Actual infection with spirochetes could occur by the oral route as in B. anserina infection in birds.”

Par. 5

“Spirochete transmission without a tick vector could be an explanation for some human cases of Lyme disease with no known tick exposure.”

Dattwyler, Raymond J.; Volkman, David J.; Luft, Benjamin J.; Halperin, John J.;
Thomas, Josephine; Golightly, Marc. Seronegative Lyme Disease.
N Engl J Med 1988; 319:1441-1446December 1, 1988

Abstract
“The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients.

We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls.

The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean (±SEM) stimulation index of 17.8±3.3, similar to that (15.8±3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1+0.5; P<0.001).

We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in sero-negative patients with clinical indications of chronic Lyme disease.”

US Patent Appl. 10/222,566 (Aug. 13, 2004)
VMP-like sequences of pathogenic borrelia
Noris, Steven J.; Zhang, Jing-Ren; Hardham; John M.; Howell; Jerrilyn K.;
Barbour; Alan G.; Weinstock; George M.

Other References

“Persing et al., “Genetic stability of Borrelia burgdorferi recovered from chronically infected immunocompetent mice,” Infect. Immun., 62:3521-3527, 1994.”

“Schutzer et al., “Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease,” Lancet., 335:312-315, 1990. .
Schwan and Simpson, “Factors influencing the antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete,” Scand. J. Infect. Dis., 77:94-101, 1991. .
Schwan et al., “Changes in antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete, during persistent infection in mice,” Can. J. Microbiol., 37:450-454, 1991.”
“Stevenson et al., “Expression and gene sequence of outer surface protein C of Borrelia burgdorferi reisolated from chronically infected mcie,” Infect. Immun., 62:3568-3571, 1994. .”

2.1 Methods of Treatment

“An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed.”

@LW:
This study looks plenty peer-reviewed to me. Steere himself says that it’s chronic and they can’t test for it. And its publication date should be acceptable to you as well (not that you can actually infer ANYTHING about the validity of an argument or study >>directly < 1 month”

Par. 7

“In summary, PCR testing can detect B. burgdorferi DNA in CSF in some patients with acute or chronic neuroborreliosis. This method represents an advance over culture, which is usu-ally negative in patients with neuroborreliosis. However, for the PCR test to be of routine diagnostic value, greater sensitivity is needed.”

Par. 3

“In this study, B. burgdorferi DNA was detected in CSF in 3807o of patients with acute neuroborreliosis and 2507o of those with chronic neuroborreliosis…when the results of blinded determinations were analyzed, the PCR results corre-lated with the duration of previous intravenous antibiotic ther-apy, and all control samples were negative. This distribution of results would be unlikely if the samples had been contaminated..”

Par. 4

“We believe that low numbers or absence of spirochetal plasmids in CSF is a more likely explanation for the insensitivity and limited reproducibility of the CSF assay than contamination of samples during testing.”

More on that “imbalance of evidence:”

Borrelia Burgdorferi –Material Safety Data Sheet. Canadian Office of Biosafety Information edited by the Colorado State University Office of Biosafety; June 16 1998.
Section VI) Laboratory Hazards
“PRIMARY HAZARDS: Accidental parenteral inoculation and exposure to infectious aerosols.”
[Compiler’s note: The implications of this, given that B.b. has been found in urine and that toilets have been shown to produce aerosols , are disturbing.]

Aguero-Rosenfeld, Maria E.; Nowakowski, John; McKenna, Donna F.; Carbonaro, Carol A.;
Wormser, Gary P.
Serodiagnosis in Early Lyme Disease
Journal of Clinical Microbiology, Dec. 1993.
Vol. 31, No. 12
p. 3090-3095
3093
Par. 2
“In our patient
population, the frequency of prior tick bite (24%)…”

Burgess, Elizabeth C.; Amundson, Terry E.; Davis, Jeffrey P.; Edelman, Robert.
Experimental Inoculation of Peromyscus spp. With Borrelia burgdorferi: Evidence of Contact Transmission
Am. J. Trop. Med. Hyg., 35(2), 1986, pp.355-359
[Compiler’s note: While this study is not by any members of the 2006 IDSA guidelines panel, it is included because Burgess, Amundson, and Davis worked at, respectively, UW-Madison’s School of Veterinary Medicine, Wisconsin DNR, and Wisconsin Division of Public Health at the time they published the study.

Abstract

“To determine if B. burgdorferi was being transmitted by direct contact, 5 uninfected P. leucopus and 5 uninfected P. maniculatus were caged with 3 B. burgdorferi infected P. leucopus and 3 infected P. maniculatus, respectively. Each ofthese contact-exposed P. leucopus and P. maniculatus developed antibodies to B. burg dorferi, and B. burgdorferi was isolated from the blood of 1contact-exposed P. maniculatus 42 days post-initial contact. These findings show that B. burgdorferi can be transmitted by direct contact without an arthropod vector.”

358
Par. 3

“Since the contact mice had developed antibodies by day 14 and there was no evidence of fighting among the mice it is Un likely that B. burgdorfrri was transmitted via blood.”

“Transmission of other spirochetes by infected animals have been documented to occur through the urine (as with B. recurrentis),’6 or venereally as with T. pallidum.17 Actual infection with spirochetes could occur by the oral route as in B. anserina infection in birds.”

Par. 5

“Spirochete transmission without a tick vector could be an explanation for some human cases of Lyme disease with no known tick exposure.”

Dattwyler, Raymond J.; Volkman, David J.; Luft, Benjamin J.; Halperin, John J.;
Thomas, Josephine; Golightly, Marc. Seronegative Lyme Disease.
N Engl J Med 1988; 319:1441-1446December 1, 1988

Abstract
“The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients.

We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls.

The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean (±SEM) stimulation index of 17.8±3.3, similar to that (15.8±3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1+0.5; P<0.001).

We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in sero-negative patients with clinical indications of chronic Lyme disease.”

US Patent Appl. 10/222,566 (Aug. 13, 2004)
VMP-like sequences of pathogenic borrelia
Noris, Steven J.; Zhang, Jing-Ren; Hardham; John M.; Howell; Jerrilyn K.;
Barbour; Alan G.; Weinstock; George M.

Other References

“Persing et al., “Genetic stability of Borrelia burgdorferi recovered from chronically infected immunocompetent mice,” Infect. Immun., 62:3521-3527, 1994.”

“Schutzer et al., “Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease,” Lancet., 335:312-315, 1990. .
Schwan and Simpson, “Factors influencing the antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete,” Scand. J. Infect. Dis., 77:94-101, 1991. .
Schwan et al., “Changes in antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete, during persistent infection in mice,” Can. J. Microbiol., 37:450-454, 1991.”
“Stevenson et al., “Expression and gene sequence of outer surface protein C of Borrelia burgdorferi reisolated from chronically infected mcie,” Infect. Immun., 62:3568-3571, 1994. .”

2.1 Methods of Treatment

“An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed.”

@LW:
This study looks plenty peer-reviewed to me. Steere himself says that it’s chronic and they can’t test for it. And its publication date should be acceptable to you as well (not that you can actually infer ANYTHING about the validity of an argument or study >>directly < 1 month”

Par. 7

“In summary, PCR testing can detect B. burgdorferi DNA in CSF in some patients with acute or chronic neuroborreliosis. This method represents an advance over culture, which is usu-ally negative in patients with neuroborreliosis. However, for the PCR test to be of routine diagnostic value, greater sensitivity is needed.”

Par. 3

“In this study, B. burgdorferi DNA was detected in CSF in 3807o of patients with acute neuroborreliosis and 2507o of those with chronic neuroborreliosis…when the results of blinded determinations were analyzed, the PCR results corre-lated with the duration of previous intravenous antibiotic ther-apy, and all control samples were negative. This distribution of results would be unlikely if the samples had been contaminated..”

Par. 4

“We believe that low numbers or absence of spirochetal plasmids in CSF is a more likely explanation for the insensitivity and limited reproducibility of the CSF assay than contamination of samples during testing.”

This article is incredible! I wish I saw journalism like this more often!

I’ve got distant relations with “Chronic Lyme disease” out in Manitoba. It’s frustrating. I have so many relations who fall for woo.

Concerned Scientist @4 said

If Trine Tsouderos and Pat Callahan are in need of a new subject to investigate they should look into the CCSVI/Zamboni liberation therapy for multiple sclerosis, a very dubious theory and treatment that has suddenly become very popular thanks to some very poor reporting by a Canadian news channel at the end of last year.

It’s not just one TV news channel, it’s in the newspapers, the internet news magazines, the glossy news magazines, the fussy household decorating magazines… it’s thick as zombies in the mall here in Canada. I’ve got older family and family friends with MS who are flying to back-alley clinics in Latin America to get this “Liberation treatment” despite my protests that it has scant and highly suspect “evidence” and is linked to a recent spat of deaths.

Health Canada agrees with me. Kiss of death, right there. The Feds agree with me, so of course I must be a Killer Robot Space Jew. Austa la bar mitzvah, baby. Call Dana Scully and Fox Mulder.

I wish I could sit people down with a box set of The X Files and convince them that if what they’re being told ever resembles a plot from the show, slow down and quadruple check all the facts, because it’s bound to be fiction. Sadly, no dice. I’m not getting anywhere.

More on that “imbalance of evidence:”

Borrelia Burgdorferi –Material Safety Data Sheet. Canadian Office of Biosafety Information edited by the Colorado State University Office of Biosafety; June 16 1998.
Section VI) Laboratory Hazards
“PRIMARY HAZARDS: Accidental parenteral inoculation and exposure to infectious aerosols.”
[Compiler’s note: The implications of this, given that B.b. has been found in urine and that toilets have been shown to produce aerosols , are disturbing.]

Aguero-Rosenfeld, Maria E.; Nowakowski, John; McKenna, Donna F.; Carbonaro, Carol A.;
Wormser, Gary P.
Serodiagnosis in Early Lyme Disease
Journal of Clinical Microbiology, Dec. 1993.
Vol. 31, No. 12
p. 3090-3095
3093
Par. 2
“In our patient
population, the frequency of prior tick bite (24%)…”

Burgess, Elizabeth C.; Amundson, Terry E.; Davis, Jeffrey P.; Edelman, Robert.
Experimental Inoculation of Peromyscus spp. With Borrelia burgdorferi: Evidence of Contact Transmission
Am. J. Trop. Med. Hyg., 35(2), 1986, pp.355-359
[Compiler’s note: While this study is not by any members of the 2006 IDSA guidelines panel, it is included because Burgess, Amundson, and Davis worked at, respectively, UW-Madison’s School of Veterinary Medicine, Wisconsin DNR, and Wisconsin Division of Public Health at the time they published the study.

Abstract

“To determine if B. burgdorferi was being transmitted by direct contact, 5 uninfected P. leucopus and 5 uninfected P. maniculatus were caged with 3 B. burgdorferi infected P. leucopus and 3 infected P. maniculatus, respectively. Each ofthese contact-exposed P. leucopus and P. maniculatus developed antibodies to B. burg dorferi, and B. burgdorferi was isolated from the blood of 1contact-exposed P. maniculatus 42 days post-initial contact. These findings show that B. burgdorferi can be transmitted by direct contact without an arthropod vector.”

358
Par. 3

“Since the contact mice had developed antibodies by day 14 and there was no evidence of fighting among the mice it is Un likely that B. burgdorfrri was transmitted via blood.”

“Transmission of other spirochetes by infected animals have been documented to occur through the urine (as with B. recurrentis),’6 or venereally as with T. pallidum.17 Actual infection with spirochetes could occur by the oral route as in B. anserina infection in birds.”

Par. 5

“Spirochete transmission without a tick vector could be an explanation for some human cases of Lyme disease with no known tick exposure.”

Dattwyler, Raymond J.; Volkman, David J.; Luft, Benjamin J.; Halperin, John J.;
Thomas, Josephine; Golightly, Marc. Seronegative Lyme Disease.
N Engl J Med 1988; 319:1441-1446December 1, 1988

Abstract
“The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients.

We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls.

The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean (±SEM) stimulation index of 17.8±3.3, similar to that (15.8±3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1+0.5; P<0.001).

We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in sero-negative patients with clinical indications of chronic Lyme disease.”

US Patent Appl. 10/222,566 (Aug. 13, 2004)
VMP-like sequences of pathogenic borrelia
Noris, Steven J.; Zhang, Jing-Ren; Hardham; John M.; Howell; Jerrilyn K.;
Barbour; Alan G.; Weinstock; George M.

Other References

“Persing et al., “Genetic stability of Borrelia burgdorferi recovered from chronically infected immunocompetent mice,” Infect. Immun., 62:3521-3527, 1994.”

“Schutzer et al., “Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease,” Lancet., 335:312-315, 1990. .
Schwan and Simpson, “Factors influencing the antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete,” Scand. J. Infect. Dis., 77:94-101, 1991. .
Schwan et al., “Changes in antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete, during persistent infection in mice,” Can. J. Microbiol., 37:450-454, 1991.”
“Stevenson et al., “Expression and gene sequence of outer surface protein C of Borrelia burgdorferi reisolated from chronically infected mcie,” Infect. Immun., 62:3568-3571, 1994. .”

2.1 Methods of Treatment

“An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed.”

@LW:
This study looks plenty peer-reviewed to me. Steere himself says that it’s chronic and they can’t test for it. And its publication date should be acceptable to you as well (not that you can actually infer ANYTHING about the validity of an argument or study >>directly < 1 month”

Par. 7

“In summary, PCR testing can detect B. burgdorferi DNA in CSF in some patients with acute or chronic neuroborreliosis. This method represents an advance over culture, which is usu-ally negative in patients with neuroborreliosis. However, for the PCR test to be of routine diagnostic value, greater sensitivity is needed.”

Par. 3

“In this study, B. burgdorferi DNA was detected in CSF in 3807o of patients with acute neuroborreliosis and 2507o of those with chronic neuroborreliosis…when the results of blinded determinations were analyzed, the PCR results corre-lated with the duration of previous intravenous antibiotic ther-apy, and all control samples were negative. This distribution of results would be unlikely if the samples had been contaminated..”

Par. 4

“We believe that low numbers or absence of spirochetal plasmids in CSF is a more likely explanation for the insensitivity and limited reproducibility of the CSF assay than contamination of samples during testing.”

What an amazing, wonderful world it is when “fringe lunatic quack idiots” are your biggest thread. What a truly wonderful world.

Re your comment, I work with many scientists, in fact many of the greatest in the world, and have for decades. I don’t think anyone could accuse me of being an intellectually lazy journalist. In my opinion the story was a poor job of journalism because it painted a broad, black-and-white picture when the reality of the situation is complex –it missed the real story for its own hype, and did so by putting forth great opinion but little data. For all the reasons Raeburn pointed out, I feel this was a broad, sloppy, heavy-handed job that did not meet the journalistic standard to which I have been trained and that we hold to at Discover If you think this story represents a thoughtful, intellectual tour de force, or that it is appropriately balanced –or that it represents good or great journalism, well, what can I say? You may be a doctor, but you are not an expert on Lyme disease –and you certainly are no expert on journalism. Sometimes people must agree to disagree, and I certainly disagree with you.

Psm Weintraub,
Features Editor
Discover

More on that “imbalance of evidence:”

Borrelia Burgdorferi –Material Safety Data Sheet. Canadian Office of Biosafety Information edited by the Colorado State University Office of Biosafety; June 16 1998.
Section VI) Laboratory Hazards
“PRIMARY HAZARDS: Accidental parenteral inoculation and exposure to infectious aerosols.”
[Compiler’s note: The implications of this, given that B.b. has been found in urine and that toilets have been shown to produce aerosols , are disturbing.]

Aguero-Rosenfeld, Maria E.; Nowakowski, John; McKenna, Donna F.; Carbonaro, Carol A.;
Wormser, Gary P.
Serodiagnosis in Early Lyme Disease
Journal of Clinical Microbiology, Dec. 1993.
Vol. 31, No. 12
p. 3090-3095
3093
Par. 2
“In our patient
population, the frequency of prior tick bite (24%)…”

Burgess, Elizabeth C.; Amundson, Terry E.; Davis, Jeffrey P.; Edelman, Robert.
Experimental Inoculation of Peromyscus spp. With Borrelia burgdorferi: Evidence of Contact Transmission
Am. J. Trop. Med. Hyg., 35(2), 1986, pp.355-359
[Compiler’s note: While this study is not by any members of the 2006 IDSA guidelines panel, it is included because Burgess, Amundson, and Davis worked at, respectively, UW-Madison’s School of Veterinary Medicine, Wisconsin DNR, and Wisconsin Division of Public Health at the time they published the study.

Abstract

“To determine if B. burgdorferi was being transmitted by direct contact, 5 uninfected P. leucopus and 5 uninfected P. maniculatus were caged with 3 B. burgdorferi infected P. leucopus and 3 infected P. maniculatus, respectively. Each ofthese contact-exposed P. leucopus and P. maniculatus developed antibodies to B. burg dorferi, and B. burgdorferi was isolated from the blood of 1contact-exposed P. maniculatus 42 days post-initial contact. These findings show that B. burgdorferi can be transmitted by direct contact without an arthropod vector.”

358
Par. 3

“Since the contact mice had developed antibodies by day 14 and there was no evidence of fighting among the mice it is Un likely that B. burgdorfrri was transmitted via blood.”

“Transmission of other spirochetes by infected animals have been documented to occur through the urine (as with B. recurrentis),’6 or venereally as with T. pallidum.17 Actual infection with spirochetes could occur by the oral route as in B. anserina infection in birds.”

Par. 5

“Spirochete transmission without a tick vector could be an explanation for some human cases of Lyme disease with no known tick exposure.”

Dattwyler, Raymond J.; Volkman, David J.; Luft, Benjamin J.; Halperin, John J.;
Thomas, Josephine; Golightly, Marc. Seronegative Lyme Disease.
N Engl J Med 1988; 319:1441-1446December 1, 1988

Abstract
“The diagnosis of Lyme disease often depends on the measurement of serum antibodies to Borrelia burgdorferi, the spirochete that causes this disorder. Although prompt treatment with antibiotics may abrogate the antibody response to the infection, symptoms persist in some patients.

We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls.

The patients had a vigorous T-cell proliferative response to whole B. burgdorferi, with a mean (±SEM) stimulation index of 17.8±3.3, similar to that (15.8±3.2) in 18 patients with chronic Lyme disease who had detectable antibodies. The T-cell response of both groups was greater than that of a control group of healthy subjects (3.1+0.5; P<0.001).

We conclude that the presence of chronic Lyme disease cannot be excluded by the absence of antibodies against B. burgdorferi and that a specific T-cell blastogenic response to B. burgdorferi is evidence of infection in sero-negative patients with clinical indications of chronic Lyme disease.”

US Patent Appl. 10/222,566 (Aug. 13, 2004)
VMP-like sequences of pathogenic borrelia
Noris, Steven J.; Zhang, Jing-Ren; Hardham; John M.; Howell; Jerrilyn K.;
Barbour; Alan G.; Weinstock; George M.

Other References

“Persing et al., “Genetic stability of Borrelia burgdorferi recovered from chronically infected immunocompetent mice,” Infect. Immun., 62:3521-3527, 1994.”

“Schutzer et al., “Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease,” Lancet., 335:312-315, 1990. .
Schwan and Simpson, “Factors influencing the antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete,” Scand. J. Infect. Dis., 77:94-101, 1991. .
Schwan et al., “Changes in antigenic reactivity of Borrelia burgdorferi the lyme disease spirochete, during persistent infection in mice,” Can. J. Microbiol., 37:450-454, 1991.”
“Stevenson et al., “Expression and gene sequence of outer surface protein C of Borrelia burgdorferi reisolated from chronically infected mcie,” Infect. Immun., 62:3568-3571, 1994. .”

2.1 Methods of Treatment

“An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed.”

@LW:
This study looks plenty peer-reviewed to me. Steere himself says that it’s chronic and they can’t test for it. And its publication date should be acceptable to you as well (not that you can actually infer ANYTHING about the validity of an argument or study >>directly < 1 month”

Par. 7

“In summary, PCR testing can detect B. burgdorferi DNA in CSF in some patients with acute or chronic neuroborreliosis. This method represents an advance over culture, which is usu-ally negative in patients with neuroborreliosis. However, for the PCR test to be of routine diagnostic value, greater sensitivity is needed.”

Par. 3

“In this study, B. burgdorferi DNA was detected in CSF in 3807o of patients with acute neuroborreliosis and 2507o of those with chronic neuroborreliosis…when the results of blinded determinations were analyzed, the PCR results corre-lated with the duration of previous intravenous antibiotic ther-apy, and all control samples were negative. This distribution of results would be unlikely if the samples had been contaminated..”

Par. 4

“We believe that low numbers or absence of spirochetal plasmids in CSF is a more likely explanation for the insensitivity and limited reproducibility of the CSF assay than contamination of samples during testing.”

@pweintraub

Ms. Weintraub, I’m curious about your response to Roadstergal’s comment at #42 and Orac’s at comment #44. What are your thoughts?

Re your comment, I work with many scientists, in fact many of the greatest in the world. I don’t think anyone could accuse me of being an intellectually lazy journalist. In my opinion the story you are boosting paints a broad, black and white picture with little real reporting and an abundance of opinion, tripping over its own, overblown hype. There isn’t a doctor in the world who could tell me this is good reporting. It violates the journalistic standard, and by touting this as an example of what we should strive for, you are trying to reinvent journalism as invective, as screed. Do you really think I would take journalistic advice from a doctor who tells me to do journalism like this? I don’t think we’ll be doing it your way at Discover Mag any time soon. But good luck with it –at least you have your own blog.
Pam Weintraub,
Features Editor
Discover

Ms. Weintraub, science main purpose is to paint things black and white, that is, get a definite answer to a question. While there might be a gray area of “what causes CDL syndrom”, there’s no gray left in the question of “does long term antibiotics do any good”. The question has been answered. No amount of “it’s journalism, not science” gets you around that.

The site was then invaded by voices with knowledge in medicine but zero credentials,training, or experience in journalism, who rushed in to impugn the standards of good journalistic practice endorsed by the journalist peer reviewers, and to insist there was another, better way of doing things: their way, which would rewrite the ethics and guidelines of journalism practice, whole cloth. To wit, these non-journalists feel that they should be enfranchised to peer review journalism along with journalists themselves –and that while they are at it, they should change good journalistic practice to suit themselves.

False Equivalence
The qualifications for a journalist are much lower than the qualifications of a scientist. Scientists like Ed Yong can do journalism a lot better than journalists can do science.
This may be confirmation bias, but it seems that every time a read a new story that covers a field where I have any expertise, they get stuff wrong.

Ms Weintraub is also making the unwarranted assumption that “appropriate journalistic practice” is good journalistic practice. We need only to look at how the petroleum industry has managed to confuse the public with regard to AGW by gaming the system of “appropriate journalistic practice” to see how broken the current journalistic practice is.

Instead of using Holocaust denial as example, I wonder if a sports reporter is supposed to interview a drunk Riders fan staggering out of the stadium who thinks Saskatchewan won the 2010 Grey Cup (Canadian Football Championship) in order to provide journalistic balance. After all, I am sure there are plenty of people in Africa wearing Saskatchewan Roughriders 2010 CFL Champions T-Shirts

There isn’t a doctor in the world who could tell me this is good reporting.

Bullshit – I can think of at least one. Hint – he is a surgeon specializing in breast cancer and a research oncologist. Care to try anymore demonstrably false statements.

Yikes, always knew Chronic Lyme disease was complete woo. It’s called an anxiety disorder, get your meds. Even acute Lyme disease is looking to be a bit far fetched, now I am far from an expert but it seems a little bit out of a sci fi novel for a tick to harbor some strange virus, who proved this and what experimental data did they have? What were the experiments that prove that some tick borned virus is the cause of a human disease in the first place?

@pweintraub,
RE: “I don’t think anyone could accuse me of being an intellectually lazy journalist.”

This looks like lazy commenting and writing.

Perhaps you’d like to rephrase that to “I don’t think anyone would be justified in accusing me of being an intellectually lazy journalist.”, since you were responding to just such an accusation.

Obviously someone could accuse you of being intellectually lazy because someone just did so.

RE: “There isn’t a doctor in the world who could tell me this is good reporting”

Again, your journalistic writing skills fail you. You are responding to a blog post in which an MD/PhD (A surgical oncologist and research scientist- a double doctor) has said exactly that.

Such demonstrably false hyperbole does not demonstrate your writing skills as a journalist to any good effect. If your comments here are any indication of the skill with which you construct and edit news features, I would suggest that the intellectually lazy label seems appropriate.

Pamela Weintraub said: “Not a single classically trained journalist disagreed with the reviewer, Paul Raeburn, who is himself one of the finest and most credentialed science journalists in the United States.
The site was then invaded by voices with knowledge –and especially, by set positions– in medicine, but zero credentials,training, or experience in journalism. These people rushed in to a space reserved for journalist peer reviewers, to impugn the standards of good journalistic practice endorsed by the journalist peer reviewers”

The very idea! People who aren’t “trained” and “credentialed”* journalists “invading” a forum to give opinions on what constitutes good journalism?!

Ms. Weintraub’s high dudgeon at these acts of lese majeste reminds me of instances where physicians have been offended that non-M.D.s dare to challenge their ideas or competency, and are rightly ridiculed in news stories. The difference here, of course, is that medicine is a specialized field requiring a great deal of training, board certification and continuing education, while journalism…hmmm, I don’t recall there being any similar standards required for reporters. Nor should there necessarily be. Having a journalism degree does not equate to having the necessary skills to be a good reporter.

I admire Ms. Tsouderos’ reporting, in particular her avoidance of the box that lazy reporters fall into, of treating stories like the vaccine manufactroversy and “chronic Lyme disease” as a battle between the cold ivory tower physicians and the brave but misunderstood patient advocates – and giving “equal time” to both a scientist who’s devoted his/her career to the field and some pressure group spokesperson who cherry-picks their “knowledge” from Google searches. “Expert” is not a dirty word in Ms. Tsouderos’ reporting.

For Ms. Weintraub’s benefit, my perspective on this is based on experience both as a physician and a working reporter whose beat included science and medical issues.

Although theoriginalihaveaches didn’t mean it this way, it seems to me that that comment points up why long term antibiotic use in this case is a bad idea.

Suppose that Lyme disease *can* be sexually transmitted. Suppose further that A gets infected and passes the disease to B before getting treated. B perhaps has a milder case that goes unrecognized, so B isn’t treated and reinfects A. As a result, A keeps developing symptoms, is diagnosed with chronic Lyme disease, and is put on long term antibiotics. Doesn’t that set up both A and B for antibiotic-resistant Lyme disease? Not to say that Lyme disease is in fact sexually transmitted — I wouldn’t know that — but that this is a logical possibility.

theoriginalihaveaches accuses Orac and others here of wanting to hurt people and cause them to suffer an incurable brain infection, but that’s precisely what Orac and others *don’t* want, and that why they call for research instead of jumping to conclusions.

pweintraub,

Re your comment, I work with many scientists, in fact many of the greatest in the world, and have for decades. I don’t think anyone could accuse me of being an intellectually lazy journalist.

Be that as it may, both of your posts here have been intellectually lazy; you’ve stated many assertions and opinions but given not a single bit of evidence to back them up. If the “journalistic standard” today is to forgo supporting one’s arguments, then no wonder the quality of science journalism is so bad.

This blog and other protests by non-journalists reminds me of patients going to medical journal sites to protest the scientific method. If you don’t like the results, just change the methodology to get what you want.

But the scientific method has been repeatedly tested and it works. The Journalism that you are advocating has repeatedly failed. It fails with evolution, it fails with global warming, it fails with the vaccine-autism crankery, it failed with “cold-eaze”, ….

Your method is broken and needs to be fixed. Interviewing “experts” and quoting all of them in a way that gives the impression that their views are equally valid is simply nonsensical.

Speaking of lazy commenting, this probably wasn’t an optimal turn of phrase: “The site was then invaded by voices with knowledge –”. I paused at the break to savor the image of Ms. Weintraub and her colleagues aghast at the people with actual *knowledge* invading their knowledge-free demesne. Man the barricades!

The rest of the comment didn’t do much to dispel that image, either.

I assume pweintraub is a genuine editor at Discover and not a troll. If so, I think she would be best served by reviewing the principles of logical fallacy. There are about a half-dozen I count in her two posts. If I were executive editor of Discover magazines, I would be humiliated to have a senior editor at my science publication wandering around the internet posting with ignorance of these obvious fallacies.

As others have pointed out, her favorite crutch appears to be Argument From Authority with no coherent arguments as to why a marginal and unproven (and apparently disproved) medical theory deserves any kind of serious recognition in quality science journalism.

I suspect pweintraub is a troll, I would expect no one with any serious experience with writing could muster such drop dead stupid phrases as “Not a single classically trained journalist disagreed with the reviewer” and “The site was then invaded by voices with knowledge “

@LW

Given what is known about Relapsing Fevers (Borrelioses)–that circulating spirochete levels can again become quite after their post-acute stage dropoff (there is even documentation of Bb in the urine of asymptomatic horses), that even during treatment, “survival forms” of the organism lacking cell walls persist in the circulation– the infected at this point need to proceed as if they will >>always<< be infectious until research proves otherwise or the cure is found. The risks of not doing so are simply too profound. ( http://docs.google.com/viewer?a=v&q=cache:JhhFVGoDt7MJ:www.stcatherines.chsli.org/lifecyclepaper.pdf+fowl+spirochetes+infective+granule&hl=en&gl=us&pid=bl&srcid=ADGEESh32xsLuK8pNDDHPpKBt3j4hWT12GOGqfC5G-NjtMvH2s67B_SGSquAhLLdwDr8co3Kwnjn86N-qHyyjBK9evdCrgCX29GtrDFiEfz4LGu6ZHymwcSp4Blmx14pz0WDD9VcYgB2&sig=AHIEtbQOiTlQi_vGypr_uS8kF55oOFfliQ)

(http://www.jvdi.org/cgi/reprint/10/2/196.pdf)

(http://www.lymecryme.com/Japans_Secret.pdf–READ THIS EVERYONE. It is a WWII-era primary source discussing at length the above-mentioned filtrable “survival” forms and their significance in efforts stretching to create–!Weaponized Borrelia!–and sheds much light on the true nature of the coverup of Chronic Lyme. If you’re really feeling intrepid, check out filedropper.com/lymeshow for a download of a radio show that was just done on Lyme, Gulf War Illness, and the assassinations of 99 microbiologists since 9/11. Also elenacook.org)

Re-the issue of “antibiotic-resistant Lyme:”
The research on this is extremely limited, and what I’ve been able to find has all been about in vitro phenomena.
What we do know, though, is that persistence via intracellular sequestration, encystment, biofilm formation, antigenic variation–mechanisms that have nothing to do with classical “antibiotic resistance”–have been proven, and that that the resistance you speak of is thus, if anything, simply a necessary risk (which, incidently, lyme-treating clinicians are finding ways to minimize with multi-drug therapy.)One never, hears, for instance, of withholding treatment from leprosy patients, who the WHO recommends be treated for up to 2 years, because they might develop a resistant strain.

(http://aac.asm.org/cgi/content/abstract/54/2/643)

Your argument about what it being an STD implies re: treatment doensn’t make sense to me. The possibliltiy of reinfection that you speak of would imply that it’s curable (which we know it’s not) and thus preclude the possibility of any resistance; in the case of each of A’s infections, once A had been treated and recovered, there’d be nothing there to become resistant. The infection A had given to B before treatment and then gotten back couldn’t be resistant, as B’d have received no treatment, and A and B could just take the initial treatment A’d received.

Even this is academic, though, as it depends on the assumption that Lyme is curable, which we know that, once it is disemminated, it is not. Furthermore, given what is known about Syphilis and Leptospirosis, it seems likely that if anything, long-term treatmend would reduce to potential for transmission.

(http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=8913478&ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum)

Human-human transmission possibilites should be the #1 thing being studied now. As the infective dose can be 1 germ, at least when its put right into the blood (though it can also be as high as many millions, depending on many different factors), and spirochetes in all forms are filtrable (a google search for filtrable treponema tells you much abuot this–the granule can be .1 microns across, which is also the diameter of the spiral form), condoms, while obviously indescribably better than nothing, may not always stop it.

(http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1044897/)
(http://www.ncbi.nlm.nih.gov/pubmed/1411838)

“Waiting for more research” while people are dying from a proven infection and none of said “research” has really been done in the 30 years the disease has been epidemic is simply not an option. We have to do all we can now.

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