Read John Stokes’ book.
A modern review of syphilis
Other resources:
A journal article comparing T. pallidum and B. burgdorferi
Books by Paul Ewald on persisting infections:
Plague Time: The New Germ Theory of Disease
Read John Stokes’ book.
A modern review of syphilis
Other resources:
A journal article comparing T. pallidum and B. burgdorferi
Books by Paul Ewald on persisting infections:
Plague Time: The New Germ Theory of Disease
It gets harder because, real-world, nothing guarantees every disease has to have a clear progression following a neat, concise course. Usually, the easy diseases are acute. You suddenly get sick. You get better in a week or two. The illness matches the textbook description. Your symptoms match those in the textbook.
If you get an infection, both you and your doctor would like it to be one of the easy ones.
But, real-world, some diseases are easy and others not. Lyme disease, more correctly, Lyme borreliosis, is one of the worst. Symptoms can come and go and may vary greatly from one individual to another. Some symptoms can go into a period of quiescence and reappear after an accident or operation. Other microbes can affect the course of the disease. Different individuals have varying responses to treatment.
Unfortunately, nothing messes up a complex disease more than a bad case of politics.
With Lyme borreliosis, the politics are some of the medical world’s most extreme. To summarize a thirty year history in a few words, a small number ideologues—primarily rheumatologists, neurologists, infectious disease researchers and microbiologists—looked at the complexity of the disease in the 1980s and decided their solution was to transform the realities of the infection into a neat package of an ideal infectious disease: easy to diagnose, easy to treat. Reality became a political opponent to be defeated using all means possible, including the production of biased research and censorship of disagreeing experts. Add the fact that many of the researchers were intertwined with a disastrous commercial vaccine effort (GlaxoSmithKline introduced LYMErix in 1999 and removed it from the market in 2002). The result was a distortion of definitions and an unfortunate undercurrent of “blame the patient” that persists to the present. Caught in the middle, between the medical ideologues and the public who experiences something quite different from what the ideologues say, are our everyday doctors, the ones most of us go to when we get sick.
Doctors are pretty much taught a standard way of dealing with medical problems and are required to support that type of medicine if they want to get paid and stay out of trouble. A big part of this model is testing.
In the United States, clinical laboratory testing is estimated to be a $50B a year industry. Testing hits that sweet spot in the medical industry—readily paid for by insurers without question, and not over-utilizing the expensive services of doctors. Tests move doctors away from their rightful subjective decision-making role, a function insurers want under the insurance company’s control. The insurers want everything, especially payout costs (which they refer to as “losses”), as predictable as possible. Predict next year’s payouts, tack on profits, set the premiums accordingly, and insurers have a nice business. A doctor who decides to treat based on knowledge and experience disrupts the whole plan. It is better for insurers to have doctors diagnose based strictly on tests.
Before getting into the specifics of Lyme disease testing, let’s be clear on what we would like from clinical tests for infections. We want a test to produce a positive result 100% of the time in samples taken from subjects infected, producing perfect sensitivity. We want the test to produce a negative result 100% of the time in those uninfected, producing perfect selectivity. Another way of saying this is that sensitivity is the ability to detect the pathogen; selectivity is the characteristic of returning a positive result only for infected subjects. Of course, for many reasons, but primarily because we are dealing with complex biological systems, we never get perfect selectivity and sensitivity. Let’s review what is available in Lyme disease tests.
If a doctor orders a Lyme disease test it will usually be an enzyme-linked immunosorbent assay (ELISA). A blood sample is sent to one of the large clinical laboratory testing corporations such as LabCorps or Quest. You might encounter similar tests such as an enzyme immunoassay (EIA) or Immunofluorescence antibody analysis (IFA), but functionally, these are quite similar to the ELISA. An ELISA is a technique, not specific to Borrelia or any other pathogen until an ELISA test kit or custom assay is designed to detect a particular antibody, hopefully specific to a particular microbe. A key point is that an ELISA looks for antibodies in the blood sample, not the Lyme disease bacteria, Borrelia burgdorferi (Bb). An ELISA is called an indirect test since it does not attempt to detect the bacterium itself, only the antibodies that your body creates to defend against the pathogen.
There are many technical details with several variations, but the basic process is conceptually simple. For a Lyme disease ELISA, a lab strain of Bb is grown in quantities. An extract of the bacteria is then fixed to a plate. Serum from a patient blood sample is washed over the plate and if antibodies are in the sample, they should attach to the Bb antigens on the plate. The antibodies attached to Bb antigen can be detected, after processing, visually or through immunofluorescence. If the antibody-antigen complex is visible at a a predetermined level, the test result is reported as positive. Again, a key point is that the test does not attempt to detect Bb. It looks for antibodies to Bb.
Later in this article, I talk about how well a Lyme disease ELISA works in the real world, but first let’s look at some of the ways an ELISA could produce incorrect results.
Foremost, the test is entirely dependent on the person tested having a well-functioning immune system. Complicating things, the lab strain of Bb used in the test kit could differ from wild strains so greatly that antibodies from patient samples do not attach. Antigen-antibody attachment is not molecularly precise, more of a loose fit, but at some point the mismatch become so great that antibodies do not attach. Attachment will depend upon the strain the test kit manufacturer uses and important differences between wild strains and lab strains may cause antibodies to not attach.
One of the best Lyme borreliosis researchers, Reinhard Straubinger, has become expert at infecting dogs and ponies in his animal studies. His most reliable method is to use wild ticks containing wild strains of Bb. (For those perhaps thinking Lyme disease is rare, note he has no problem reliably collecting ticks carrying Bb.)
There are other subtleties to ELISA technique. The plate should be washed so that only antibody proteins attached firmly to the antigen substrate remain. Wash too vigorously and you wash away the antibody you are trying to detect. Another striking deficiency of a Lyme disease ELISA is that it depends on the blood sample having free antibody molecules available for detection. In a severely sick individual, especially in a person immuno-compromised, they may not be producing excess, free antibodies. Whatever antibodies in the serum are already attached to Bb, making them unavailable to attach to the Bb on the ELISA plate. This is a reasonable explanation for the often observed phenomena where those sickest with Lyme borreliosis and can produce a negative ELISA.
You might encounter some variations in ELISA-type test reporting. Sometimes a numerical titer value is reported. Usually, this means the test antigen, as a reference, is put on a plate in progressively greater dilutions and complexed with the dye molecule as a referene. Rather than just report that a single plate well was positive because it looked, say, pink, the technician looks at the degree of pinkness and compares it to the reference. (More likely an optical density meter and automation is used, but the concept is the same.) If your sample really had a lot of antibodies, it might not turn clear until dilution by a factor of of 1 to 1000. Your titer would be reported as 1:1000. If your sample produces less dye-attached antibodies, the solution might turn clear when diluted 1 to 100. Your reported sample titer would be 1:100. Sometimes labs set a cut-off point. For example, anything above 1:250 is reported positive. Samples 1:250 or less would be reported as negative.
A variation of the whole-cell ELISA is the VlsE C6 peptide ELISA which attempts to detect a specific antibody protein. This test has not proved to offer real advantages and is not often used.
Like the ELISA, the Western Blot (WB) is a technique, not specific to a particular disease. Only when designed to detect the antibody proteins unique (hopefully) to a disease pathogen does it become a diagnostic test. Like the ELISA, a WB for Lyme disease is an indirect test—it does not detect Bb, only proteins of antibodies to Bb. Still, a WB is much more informative than an ELISA, since it attempts to detect antibodies to various components of the Bb bacterium
The basic technique is as follows. Instead of just using a slurry of Bb, the bacterium is first sonicated (busted up with sound waves). The resulting protein fragments are placed on a gel sheet and a current applied. causing the proteins to migrate varying distances down the plate depending on their weight, separating into bands. Proteins are weighed in kDa (kiloDaltons) producing the numerical identification of the bands.
After the test gel is made, the rest of the technique is similar to an ELISA. Serum from the sample is washed over the plate to see if there are antibodies that stick to the separated Bb protein fragments on the plate. An added feature of WBs is that usually the sample antibodies are first separated out by weight into IgM and IgG antibodies and separate results reported. (It is thought that IgM antibodies develop early in an infection and that IgG antibodies develop later, providing long-term immunity, but with Lyme borreliosis, often new IgM antibodies are detected late in the disease.) After washing and staining the result is something that looks like this:
 |
There is a lack of consistency in how the bands are labelled and often there is no clear separation of the bands. But, generally, results are reported like this:
BAND INTENSITY: Low +, Medium ++, High +++, Equivocal +/-
18 kDa +/-
22 kDa -
23-25 kDa +/-
28 kDa -
30 kDa -
31 kDa +/-
34 kDa +/-
37 kDa -
39 kDa +
41 kDa ++
45 kDa —
58 kDa +
66 kDa +/-
73 kDa -
83 kDa -
93 kDa +/-
Sometimes, all you get is a positive or negative result on a report instead of a listing of bands. Results are highly dependent on the technician reading the blot. What could be an “indeterminate” for one technician could be a “+” for another. As one treating doctor has asked, what does indeterminate mean anyway? Certainly, they see something there or they would not report it.
Generally, patients find WBs impressive. Finally, they think, in the course of this confusing disease, they have a lab report with some hard numbers and all this precise data must mean something. We can only wish.
The same group of ideologues who worked years to convince the world that Lyme disease was easy to diagnose and easy to treat, specified to the world what those Western blot numbers mean. The Centers for Disease Control (CDC), rubber-stamped or directed (depending on one’s level of cynicism) which bands mean a positive result. The detailed list of bands, used to this day, was based on a single study of 74 people, endorsed by a 1994 committee sponsored by The Association of State and Territorial Public Health Laboratory Directors, CDC, the Food and Drug Administration, the National Institutes of Health, the Council of State and Territorial Epidemiologists, and the National Committee for Clinical Laboratory Standards: 2 of 8 IgM bands from this list: 18, 21, 28, 37, 41, 45, 58, and 93 kDa; 5 of 8 IgG bands from this list: 18, 21, 28, 30, 39, 41, 45, 58, 66 and 93 kDa.
The CDC is always quick to add that this list is only to be used for surveillance, not for clinical diagnosis, and reported positive only when coupled with specific symptoms. The official stance is that Lyme disease is a clinical diagnosis not dependent on tests. But, de facto, most doctors insist on a surveillance quality positive test before they will diagnosis and treat. The word on the street, or back office, since the mid-1980s has been that “good” doctors only diagnose the most obvious Lyme borreliosis infections and then if they do find a positive case, get someone else to treat it.
An especially interesting detail of the WB band criteria is that the highly diagnostic 31 kDa band is omitted from the list. Many of the researchers influencing the list were involved with GlaxoSmithKline , developer of the disastrous LYMErix vaccine which was on the market from 1999 to 2002. Lymerix was based on injecting the 31 kDa protein. Leaving it off the list was an attempt to ensure Lymerix did not contribute to creating positive test results, an unwanted effect of a vaccine. GlaxoSmithKline surely did not want their vaccine to change a patient’s negative test into a positive test. In reality, LYMErix did much worse, crippling many of those vaccinated and sometimes causing neurological disease. Additionally, for reasons not adequately explained, LYMErix produced another unexplained Lyme borreliosis anomaly: the vaccine often turned all the bands in a WB into a continuous dark blob.
Both the ELISA and WB, tests that look for antibodies, are referred to as serologies.
A seldom performed test, primarily because of cost, is a Bb PCR. This test looks for Bb DNA, typically in a blood sample, but sometimes in a tissue sample. It is highly insensitive, most likely because Bb has a tendency to sequester in fibrous tissue, such as the skin and nerve cells, rapidly clearing the bloodstream. While a Bb PCR is rarely positive, a positive test is a nearly certain indication of infection. Still, ideologues often claim positive PCR tests are detecting only dead Bb. Plus, as an exception in the infectious disease world, the CDC does not count a person with a positive PCR for Bb as a surveillance case, nor do doctors feel compelled to treat PCR-positive patients. Remember, prevailing ideology says to deny as many cases as possible.
Unlike many bacteria which are routinely cultured to diagnose infection, the Bb spirochete is quite difficult to culture and cultures are only performed in a research setting. Note that the spirochete that causes syphilis, Treponema pallidum, has never been cultured outside of living mammals, so any claim that Bb does not exist in a patient or group of patients because it cannot be cultured in a lab is the logical equivalent of saying syphilis does not exist.
Everyone wants Lyme disease tests to be more than they actually are. Doctors want some objectivity and certainty and so does the public. But we don’t get it. Instead, we get the ideology, dominating and often censoring the discussion. Medical journals and popular media usually report and conform to the ideologues advocacy. Sick and disabled people become especially interested in the precise-sounding band numbers in the Western Blots. All those numbers, they think, finally some precision and confirmation to this confusing, mutable illness. People post their Western blot results on forums and there is continuing speculation as to what the bands actually mean.
Exacerbating the testing problem are everyday doctors who are more familiar with HIV testing, where an ELISA seems to work as an effective screening test, and confirmation is made with the more accurate WB. Doctors assume Lyme disease ELISAs and WBs work just as well as HIV ELISAs and WBs, when there has never been any science performed that remotely indicates this. In Lyme disease testing, the two-tier testing, using an ELISA for a screen and a WB for confirmation does not meet acceptible standards for detection. For one thing, often studies show a sample that tests negative on a Bb ELISA produces a positive WB in a significant number of cases, meaning the ELISA is an invalid screening test. This is yet another Lyme borreliosis anomaly.
What is almost jaw-droppingly irresponsible is that ideologues like Gary Wormser, who wish to deny as many Lyme borreliosis infections as possible, state that doctors should throw out a positive WB result when coupled with a negative result on the cheaper, less precise ELISA. The responsible approach, since studies show the ELISA is less sensitive, would be to skip the ELISA entirely. Money keeps most doctors from ordering WBs. An ELISA cost about $50 versus the WB’s $250.
What do the published studies tell us about the accuracy of Lyme borreliosis tests? It seems as though it would be straightforward to evaluate tests. A committee associated with the World Health Organization recently published recommendations for evaluating clinical tests. Indicative of the distortion of clinical Lyme disease research, the few available evaluations of Lyme borreliosis testing seldom, if ever, follow established procedure.
Good science involves details and data, so only by looking somewhat closely at a single study can we see the distortions of routinely published clinical Lyme disease research. In 2004, I worked as a contract researcher for Dr. Joseph Jemsek, the doctor shown being persecuted by the North Carolina Medical Board in the documentary film Under Our Skin. Patients were telling him that Johns Hopkins had some new tests that were 100% sensitive for detecting Lyme disease. It was easy to see why the patients were saying this— there were readily available early copies of a study abstract quoting impressive sensitivity statistics like 100% and 92% that practically jumped off the page.
The Johns Hopkins study looked at 86 people who were classified primarily by EM rashes as being "probable", "possible", and "unlikely" cases of Bb infection. All subjects had symptoms of Lyme borreliosis. There was no comparison to healthy controls. As an aside, there has never been an study objectively determining the prevalence of the supposed hallmark symptom of Lyme disease, the EM rash, so its validity as a study determinant is highly suspect.
Yet another problem making the Johns Hopkins study difficult to apply to clinical practice was that the researchers devoted a good deal of attention to culture, a test not available to the general public. The study’s prominent Figure 1 showed “NO EVIDENCE OF LYME DISEASE” for about half of the subjects tested and I had difficulty discerning how the data were created. I wrote to the journal asking for clarification and the response from the lead investigator gave me enough information to figure out how the data were reported. Consistent with the politics, the lead investigator used the opportunity to pontificate and get in an unrelated dig in at IGeneX, a specialty lab that had been a long-time target of the ideologues, primarily for performing more sensitive tests than those a typical commercial lab uses. To cut to the chase (more details), what the Johns Hopkins researchers were doing , astoundingly, was using the same tests they were evaluating to determine what was a true positive test. In other words, they assumed the tests were always right and then began their analysis. Unsurprisingly, the tests were determined to be 100% sensitive.
In their analysis, if a test came back positive it was assumed it was 100% accurate: the subject had Lyme disease. If a test came back negative, it was assumed it was 100% accurate: the subject did not have Lyme disease, even though a lot of those samples came from CDC-positive surveillance cases (which usually don’t depend on tests). Look at the tests, the study asserted, assume they are 100% sensitive, and then our analysis concludes they are 100% sensitive.
Taken to the logical extreme, using their methodology, flipping coins, reading tea leaves, and throwing darts, would all in combination show 100% sensitivity for detecting Lyme disease, just as they had for serology, PCRs, and culture. Moving into the world of clinical realities, a CDC-positive surveillance case in a citizen of Lyme, Connecticut, who had six Bb-PCR-positive ticks attached for three days, resulting in a 30 cm EM rash observed by a physician, coupled with severe Bell’s palsy, fever, and arthritis in one knee, where symptoms resolved after antibiotics; this subject would be classified in the Johns Hopkins study as having “NO EVIDENCE OF LYME DISEASE”, just because the subject had a negative ELISA.
I made numerous requests to the authors for disclosure of their basic data—counts of how many in their three study cohorts tested positive or negative—and received no information, only multiple promises the data were forthcoming. The editors of the journal and peer reviewers have never required these data either.
How did the the tests regular doctors use almost exclusively, ELISA followed by WB, perform? Without data, we have to guess at whether test positives came from the probable, possible or unlikely groups, but in total, only 36 of the 84 subjects tested (43%) were positive. I suspect that the researchers found that many gold-standard cases, those with positive PCRs or cultures, came from the group they deemed “Unlikely”. This would have encouraged a discussion ideologues do not seem to want to engage in. Once I knew how the data were presented I wrote to the editor of the journal pointing out that even in its obscure presentation the study data showed…
if a physician required a positive test for diagnosis and only used the two-tier ELISA followed by Western Blot testing procedure (currently these are the only tests routinely ordered in clinical settings), 11 cases of certain infection would be entirely missed in the 86 subjects. Those 11 (13%) were positive by our present day gold standards, culture and PCR results, yet had negative serologies. This statistic furthermore ignores all subjects not positive on any test, a number not stated in the study as presented, but quoted in the abstract as 49/86 (57%). If only 20% of these subjects (who were selected because they exhibited symptoms suggestive of Lyme disease) were truly infected, the physician relying on two-tier serology testing would miss 21/86 (24%) cases of a potentially disabling or fatal disease.
This letter was promptly and summarily rejected by the journal’s chief editor even though I had some support from hands-on editors. Ironically, at about the same time a study submitted by Dr. Jemsek to the same journal was rejected. In Jemsek’s study, rather than just make the absurd assumption all Lyme tests are always correct and equally valid, Jemsek selected from 550 patients the gold-standard cases, those with positive PCRs. Only 27% of these definite Lyme cases, when concurrently tested, produced a positive Western Blot by standard CDC-endorsed criteria. So, in response to the protest voiced repeatedly for the last thirty years, that if the treating doctors are seeing something that differs from the published ideology they should report it, Jemsek’s study was censored.
Soon, after reading much more, equally dubious, clinical Lyme disease research, I stopped relying on what medical journals said about Lyme disease. I am not the only one who has lost faith:
It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine.
From Dr. Marcia Angell, The New York Review of Books, Volume 56, Number 1. January 15, 2009 Drug Companies & Doctors: A Story of Corruption. (Dr. Angell resigned as editor-in-chief of The New England Journal of Medicine in June, 2000.)
If you have read even a few parts of this article, you may suspect Lyme disease tests are not acceptably accurate. We do not even have a good estimate of test accuracy because there have not been any credible studies evaluating test accuracy of which I am aware. But that is not to say the tests are useless.
Lyme borreliosis is complex and the tests are obviously not definitive. Possibly, they miss 90% or more of those infected. Patients want the tests to mean more. Doctors often insist that they mean more. That does not mean they do.
I’ve studied Lyme borreliosis for over ten years. My guess is that if you have a Western Blot that is positive for any band other than 41, this is highly indicative of Bb infection. Another guess is that if you have a ELISA for Lyme disease that comes back negative, there is still significant probability you have a Bb infection. I won’t even hazard a guess at a percentages—everything depends on your history and entire clinical picture. You should be especially concerned if you have a set of symptoms that are not typically expected in combination. Be particularly concerned if the symptoms developed about the same time without other plausible explanation.
Most importantly, if you are negative on every Lyme tests you have ever had and you have symptoms, consider that there is still a good chance you have a Bb infection.
I’ve come to put more confidence in another test of sorts: how someone responds to antibiotics. A significant reaction, either good or bad, strongly suggests a bacterial infection. An anonymous treating doctor writing in an excellent blog agrees with me.
Tests are only part of a responsible diagnosis. Get one or more tests, talk to a doctor not constrained by the prevailing ideology, and take someone with you whose judgement you trust. Decide what is important to you and do it.
"Case Definitions for Infectious Conditions Under Public Health Surveillance. Centers for Disease Control and Prevention." MMWR. Recommendations and reports : Morbidity and mortality weekly report. Recommendations and reports / Centers for Disease Control , no. 46 (1997): 1-55.
Coulter, Peggy, Clara Lema, Diane Flayhart, Amy S Linhardt, John N Aucott, Paul G Auwaerter, and J Stephen Dumler. "Two-Year Evaluation of Borrelia Burgdorferi Culture and Supplemental Tests for Definitive Diagnosis of Lyme Disease." Journal of clinical microbiology 43, no. 10 (2005): doi:10.1128/JCM.43.10.5080-5084.2005.
Dressler, F, J A Whalen, B N Reinhardt, and A C Steere. "Western Blotting in the Serodiagnosis of Lyme Disease." The Journal of infectious diseases 167, no. 2 (1993): 392-400.
Latov, Norman, Anita T Wu, Russell L Chin, Howard W Sander, Armin Alaedini, and Thomas H Brannagan. "Neuropathy and Cognitive Impairment Following Vaccination with the Ospa Protein of Borrelia Burgdorferi." Journal of the peripheral nervous system : JPNS 9, no. 3 (2004): doi:10.1111/j.1085-9489.2004.09306.x.
Straubinger, R K, B A Summers, Y F Chang, and M J Appel. "Persistence of Borrelia Burgdorferi in Experimentally Infected Dogs After Antibiotic Treatment." Journal of clinical microbiology 35, no. 1 (1997): 111-6.
Wormser, G P, C Carbonaro, S Miller, J Nowakowski, R B Nadelman, S Sivak, and M E Aguero-Rosenfeld. "A Limitation of 2-Stage Serological Testing for Lyme Disease: Enzyme Immunoassay and Immunoblot Assay Are Not Independent Tests." Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 30, no. 3 (2000): doi:10.1086/313688.
Minor edits added August 6, 2011
]]>“There are all sorts of reasons we default to being quiet,” she said. “It is general etiquette not to correct another adult, especially when this is their profession. But when the consequences are so grave, you have to summon up your courage.”
Dowd talks mostly about getting doctors to wash their hands, not exactly a controversial or complex medical issue. But, if people are so reluctant to confront a doctor about something so simple and obvious, just how will the patient-doctor encounter go for a complex and less obvious subject? And, how much will the sick or injured pay if they don’t?
With more difficult medical subjects, we usually get the mysterious, technical, definitive sounding language doctors use. It convinces patients that, well, this medical stuff is just too much for regular people to understand. To cut right to a fundamental problem, we have the absolute, legal monopoly that medical doctors have worked to establish for the last one-hundred years. Medical societies regularly campaigned to get doctors elected to state legislatures in the 1880s to write laws to drive out the competition. Their efforts continue through closed state boards. They do this either because they are certain, absolutely certain, that other practitioners are harming patients and they needed sole responsibility for our health—or possibly, MDs want more money and no competition from others who could demonstrate the MDs’ deficiencies. Take your pick.
This could be interpreted as terribly cynical, but then, everyone has their own medical story. Dowd certainly has hers. Whenever I tell, or hear someone else tell, of a medical problem that was left untreated for years because a doctor, or a series of doctors, clung to their medical school diagnosis rather than probe, think, and treat logically, some listener usually chimes in with something like, “Certainly, no doctor is going to send a patient home sick or harm them! They do the best they can!”. But then, a few seconds later comes their own story. It usually goes like this—a neighbor went in for routine orthopedic surgery and got a horrible infection. Or, someone’s foot was broken and hurt like hell for a year because the doctor didn’t order an MRI (probably because his group gets compensated more by the insurance company for ordering fewer and cheaper tests). Or, someone went to the emergency room with severe abdominal pain and they got a good dose of narcotics that didn’t do anything except clear the ER doc of immediate responsibility and get the patient out the door. (I have heard each of these stories, directly from the person affected.)
Because we are a nonprofit looking at ignored and under-treated infectious diseases, the stories we often hear involve Lyme disease, more correctly called Lyme borreliosis. I used to say Lyme borreliosis is a disease with the symptoms of syphilis, treatments like cancer’s, and the politics of AIDS. But, the last few years, I have changed this message, particularly the political part. Lyme politics often seems worse than AIDS politics. As one example, doctors are frequently sanctioned by state medical boards for testing too often for Lyme borreliosis. I have yet to hear of a doctor losing his license for ordering too many HIV tests.
Lyme borreliosis has a long and complex history, medical and political, but don’t even start down the road of saying we need to step back and rely solely on science. Particularly in medicine, and especially with borreliosis, science is often just a tool used by commercial and political forces for pushing an agenda. I am all for science that helps us understand our world, but science used to manipulate society for political power and corporate profit is despicable. Unfortunately, that is about all the science we are getting for borreliosis.
The other big problem is how the press reports on Lyme disease. Presenting it as a war between fractious doctor groups fits the current donnybrook reporting model, but does little to educate or inform. And, when the press, and readers, assess the accuracy of an opinion by the celebrity or position of the speaker rather than substance, we all lose, except maybe for the medical politicians working to distort the picture.
Like Dowd, people do have their stories. With Lyme borreliosis, the story is distressingly repetitive: suddenly got sick; went to the doctor; told they were crazy or lazy with nothing really wrong; then, diagnosed with MS, ME/CFS, lupus, or fibromyalgia; became sicker and sicker; saw more and more doctors; finally stumbled upon someone who knew about Lyme borreliosis and associated infections; got treated; and, depending on how long the disease had been neglected and how good the treating doctor was, got better to varying degrees.
I have been asked to write more about some of the specifics of Lyme borreliosis by the Lyme Disease Awareness group here at dKos. We need to remember that specific diseases are but a single manifestation of the disaster of medical care in the U.S. We need a better discussion of complex medical issues than I have seen lately, too.
Good for Maureen Dowd, from her New York Times bully pulpit, for suggesting we need to be more assertive with our doctors. Now the challenge is to shed light on more complicated issues like Lyme borreliosis, a difficult systemic infection like syphilis, hard to treat and hard to understand. Citizens need to ask the right things and assert the obvious at the doctor’s office. They need to report what they experience there, too. Our online world lets us do it. It is a good place to start.
(Cross-posted on Daily Kos.)
]]>We don’t feel focusing on one condition is going to do much. Disease factionalism is a tool, used intentionally or not, that keeps those not wanting reform in control. So, if we have an agenda, it is to get this changed. But, here is where a goal can sabotage the most expedient tactics. Most people, reading something like the previous paragraph, will click onto a new website page before finishing the second sentence. A story about a sick child down the street who needs a $20,000 operation, on the other hand, captivates most people’s attention. Yes, some of us have family members with health problems. I have health problems. Yes, some of us have been treated for Lyme borreliosis and associated infections, with dramatic results. No, the treatments have not been entirely curative. Yes, we are convinced if our medical systems were not sleep-walking through a fantasy world we would be much better. A single person’s medical problems can be quite interesting, especially if you think you have the same thing. And, especially then, it often elicits a response. But, all these self-identifying condition and disease groups are not going to get most people’s, maybe not anyone’s, problems fixed. It will take unified action from all the medically ignored and mistreated.
We have heard individual accounts of stories almost identical to ours hundreds, maybe thousands of times. As we show on our website, there are millions with persisting conditions who probably could be helped by treatment for under-treated infections. As to how one gets the overwhelmed, unmotivated public interested, there probably is not a single answer except that it it going to take some courage, consideration, and hard work. Would we be doing what we do if family members had not gotten sick? I would like to think perhaps that I am such a decent, informed, and compassionate person that the answer is yes, but realistically, probably no.
I hear stories of how efforts of a few people can make a big difference. I think it was Malcolm Gladwell who wrote recently that a few high school friends started the lunch counter sit-ins that resulted in major civil rights changes. He also pointed out that it took an intense personal relationship to get them started, something increasing rare with our digital technologies. I am convinced that getting help for one person, one disease, one deprived group, maybe even one country, is not going to fix the disastrous state of medical care. We are quite interested in getting the best citizen activists available together to work on this.
]]>In October, 2009, researchers published a paper demonstrating a correlation between xenotropic murine leukemia virus-related virus (XMRV) and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). They found 67% of ME/CFS suffers were positive for XMRV and only 4% of healthy subjects were positive.
Government agencies, particularly the Centers for Disease Control, would be expected greet news like these reports with their full support and resources. But something much different happens—almost invariably.
Current estimates of the number Americans with MS are about 400,000. Estimates of U.S. prevalence of ME/CFS are about four million. Both of these diseases can rapidly become disabling and persist for years or decades. Any plausible suggestion of a pathway to cure or remission should obviously be investigated to its fullest by our best and most insightful researchers. But this rarely happens. Usually, government/academic/corporate machinery kicks into gear to smother the most innovative, perceptive research.
We can guess at reasons why, but in a secretive and manipulative system it gets hard to determine true causes.
It could be as simple as an agency, medical specialty, or corporation unwilling to admit they have been embarrassingly wrong for a long time. It could be the unwillingness of the medical doctor culture to deviate from their medical textbooks or professional group guidelines.
More cynically, it could be that medical resistance to new ideas comes from entrenched investment by drug companies, medical device manufacturers, and medical specialities profiting substantially from the status quo.
Health insurers could be the real cause of the problem. They like predictability. They would rather have a disease classified as incurable with predictable costs than have it be curable with unpredictable costs. This is particularly true if the innovation has a one-time, fairly substantial cost that does not entirely guarantee immediate payback in reduced insurance company payouts. Insurers only want to pay for things they build into the premiums they charged the previous three years.
As Ludwig Fleck explained in Genesis and Development of a Scientific Fact the medical profession is filled with uncertainties. When doctors encounter a new medical phenomenon there is a period of chaos where all sorts of explanations and recommendations are suggested. Then, at some point, a version of the phenomena is included in a vade mecum (handbook) that becomes the reality doctors use. (Yes, this is similar to points raised in Thomas Kuhn’s The Structure of a Scientific Revolutions. Kuhn acknowledged reading Fleck, but did not feel significantly influenced by his writings.)
Regardless of motivation, there is a pattern of behavior among our government backed researchers that is not good.
We see it in recent government-academic-corporate handling of CCSVI.
Zamboni published his first paper on CCSVI and MS in April,2009 (web availability December, 2008). Without the efforts of patient advocates, the news might have gone unnoticed. In February, 2010 Canadian news media picked up the story and in June, 2010 The New York Times published a fairly balanced article.
From the article:
“In my view the evidence is quite scanty and the biological plausibility is low,” said Dr. Stephen L. Hauser, the chairman of neurology at the University of California, San Francisco. Many neurologists agree. Dr. Hauser said there was much stronger evidence that the disease arose from genetic variations affecting the immune system.
Neurology specialists want to own MS. They prescribe expensive, injectable drugs that generally make patients feel worse and only produce improved symptoms about a third of the time. Science has little to do with this. Their popular theory of genetic differences in the immune system causing MS, were recently refuted in an extremely rigorous study in identical twins. There was no indication of genetic causation, nor has there ever been, but that does not change neurologists’ minds.
In a National Post article, in January, 2010, Dr. Mark Freedman states “I think there are going to be millions of dollars spent now to follow a hoax…. If I thought for one instant there was substance to this, I’d be all over it,”. Freedman is head of U. of Ottawa’s MS program.
Dr. Zamboni has always presented his observations with the great caution, saying only that we need to find out more. The vitriol directed at him is unwarranted, almost spectacular, and, depending on the career strategy of the journalist, either reported reasonably, or as vitriol confirmation.
With CCSVI, U.S. government agencies have yet to join the discussion. The CDC is, at its heart, primarily an infectious disease agency and does not look that closely at therapies not involving acute infections. The CDC has historically discounted infection as a possible cause of MS.
But what about CDC response to a new possible cause and treatment for ME/CFS? The CDC has been actively trying to suppress evidence of infectious causes of ME/CFS since the mid-1980s. In October, 2009, Dr. Judy Mikovits reported in Science that her research group found evidence of XMRV in 68 of 101 patients (67%) as compared to 8 of 218 (3.7%) in healthy controls. The CDC immediately began research to show Mikovits wrong and show themselves right, advancing their advocacy of CFS as a psychological condition, just as they had for the last 25 years. And, the CDC’s study saw nothing, absolutely nothing. Their study tested 51 persons with CFS and 56 healthy persons. All had completely negative tests.
But outside the CDC, researchers just weren’t with the CDC’s program of XMRV suppression. A National Institutes of Health/Food and Drug Administration (NIH/FDA) study showed a significant correlation between ME/CFS and the XMRV retrovirus.
Both papers were approved for publication, but once word got out there was a disagreement, both sides agreed to put their papers on hold. Right here, we have a problem. If researchers were doing real science, data should be a data and any observations, if legitimate, should published as soon as possible.
Despite the detente agreement, the CDC paper, denying a correlation between XMRV and ME/CFS was published July 1, 2010. The NIH/FDA paper confirming the correlation was put on hold.
But this week there is news. On August 24, 2010, the NIH/FDA paper was released. Not only does it give remarkably good evidence for a correlation between XMRV-like viruses and ME/CFS, but it explains how the XMRV denialists might have produced their negative results.
Clinical medical research has become something much different from real scientific research motivated by desire to understand our world. It is mostly a propaganda tool using the whitewash of prestigious universities, institutes and agencies to give it credibility.
Marcia Angell resigned as editor of the New England Journal of Medicine in June, 2000. In 2009, in The New York Review of Books she says:
It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine.
Sharon Begley recently wrote in Newsweek of how little useful comes from NIH sponsored medical research despite the $31B a year it costs taxpayers. This is a really bad thing. But what is worse is the sizable portion spent to stifle possible innovations that could help disabled and dying citizens. As with virtually everything political in the U.S. these days, everyday citizens end up financing corporate malfeasance. We pay for it in insurance premiums, drug prices, and taxes.
Maybe we don’t need to speculate on why this is going on. Maybe we just need to stop doing it. We can sort through which senators and reps support this medical cartel and get them to change or get them out of office. XMRV and CCSVI are just recent examples coming to light. How many other medical problems are waiting for unbiased research and solutions?
(Cross posted on Daily Kos. You might want to read comments there.)
]]>While staffing our table, yet again we were struck by the number and similar arc of people’s stories: health problems unresolved for years, a chance event that led them to the proper diagnosis of Lyme borreliosis, and successful treatment, usually out of state.
Also, yet again we were struck by a disconnect: the CDC’s reporting of six to eighteen Lyme disease cases in Oregon each year and a movie house in Portland, Oregon on a sunny afternoon with over 250 people, most knowing several people diagnosed with Lyme disease.
The world hears about the eighteen CDC Lyme disease cases in 2008 and nothing from the hundreds not meeting CDC criteria or process hurdles. We are encouraged by the people we talked to before and after the film that asked to participate in our census. Only by getting an accurate count of who has had L. borreliosis will proper diagnosis, treatment, and research be realized.
Whether you have attended Under Our Skin or not, if you know anyone who has or had Lyme disease or unresolved condition possibly related, please help us get them counted. We particularly need to count those who have received treatment and improved. Our census uses a survey that most people can complete online in less than twenty minutes. (Other ways to take the survey are available.) We issue controlled invitations; just send an email message to info@seranogroup.org or click here. Those of you who provided your email addresses at the Under Our Skin showing should receive your invitation soon.
Awareness of the size and severity of L. borreliosis is essential to getting the problem fixed. We appreciate your attention and help.
]]>Dr. Marcia Angell, The New York Review of Books, Volume 56, Number 1. January 15, 2009 Drug Companies & Doctors: A Story of Corruption. (Dr. Angell resigned as editor-in-chief of The New England Journal of Medicine in June, 2000. The Klempner study of a Lyme disease treatment was published in June, 2001.)
Klempner joined the editorial board of The New England Journal of Medicine after Dr. Angell resigned. You can read our evaluation of Klempner’s study here.
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We don’t know why Audrey Longhurst, LN Yaddanapudi and the Online Distributed Proofreading Team pulled John Stokes’ book on syphilis off the shelf of Cornell University and put it into Project Gutenberg, but we are glad they did.
Reading Stokes’ book, we were struck by several things:
Without modern tests, drugs, and insurance codes, early twentieth century medical practice seemed to have the freedom to be perceptive, intelligent, and artful. Granted, syphilis and Lyme borreliosis are different diseases, but the similarities are great. Both are caused by spirochetes, bacteria that branched off early from other bacteria in the evolutionary tree. Both often start with a skin lesion and go into an indeterminate, often lengthy, period of quiescence which can quickly convert to active disease. Both have a special affinity for attacking the nervous system. Both left untreated can have devastating effects, producing many of the same symptoms: severe heart disease, plaques in various blood vessels and organs, dementia, crippling arthritis, pain syndromes, extreme fatigue, and general malaise. Both can cause blindness and deafness. Both can be fatal.
The big difference between the two is that Treponema pallidum, the spirochete that causes syphilis, lives only in humans, unable to tolerate temperature variation more than a few degrees from 98.6º F. It is completely dependent on the chemical and physical environment the human body provides. Borrelia burgdorferi, (Bb), the spirochete that causes L. borreliosis, moves readily between cold-blooded arachnids (ticks) and a wide variety of mammals, birds, and reptiles. With some effort researchers can grow Bb in test tubes, but In contrast the syphilis spirochete can be cultured only in live lab mammals. No one has ever been able to grow it in a test tube or Petri dish.
This begs an obvious question: Which of these spirochetes is more likely to end up causing a human infection—the extremely fussy and dependent syphilis spirochete or the extremely adaptable L. borreliosis spirochete? The resourceful L. borreliosis spirochete, in addition to its single chromosome, has more than twenty plasmids, functioning chunks of DNA that it can shed to facilitate genetic recombinations making it extremely adaptable.. It can turn genes on and off in complex patterns to confuse and evade out our immune systems. The spirochete causing syphilis does not have plasmids. It has evolved to prosper solely in the human host, remaining there for years in the individual and for millennia in the species,
It is not in the best interest of parasitic or commensal bacteria—pick the adjective best reflecting you current opinion of the microbe—to kill their host before they have propagated sufficient copies in other hosts for species survival. By necessity, they evolve a life cycle that gives them opportunity to spread to other hosts. For the syphilis spirochete, it needs its host to stay alive long enough to spread to their newborns and sexual partners. L. borreliosis requires a similar lengthy life cycle. If nothing else, it has to make sure its vertebrate host stays alive long enough to infect next years ticks. Ticks are born sterile.
This is a much shorter life cycle than that of the microbial diseases that dominate CDC press releases. Pneumococci bacteria do not have to wait for childbirth or sexual unions to spread to more humans. A sneeze or a crowded elevator ride can do the trick. They live fast and furious lives. The syphilis and Lyme borreliosis spirochetes require slower, more persistent lifecycles spanning years, rather than days, to proliferate. (See Paul Ewald’s works listed below for details.)
That the L. borreliosis spirochete has evolved a strategy of proliferation definitely utilizing ticks, and sexual partners, and offspring is not surprising.
Europeans studied and pondered syphilis for 500 years, from the time Columbus’s sailors brought it to Italy from the New World until Alexander Fleming discovered penicillin, which did a pretty good job of keeping its worst effects dampened. Then, we pretty much forgot about syphilis and stopped paying it much attention. A side note: some recent research is beginning to ask what is going on with syphilis in our twenty-first century world of AIDS and a microbial ecosystem transformed by sixty years of antibiotic use. As just one issue, did syphilis really almost vanish when the AIDS epidemic appeared or did we just stop looking for it?
The important point is that researchers stopped observing and thinking much about spirochetes after 1950. They did finally investigate a borreliosis epidemic in the 1970s near Old Lyme, Connecticut, but it took a German expatriate researcher familiar with syphilis, Willy Burgdorfer, to identify its spirochetal cause. Unfortunately, the initial academic researchers followed standard medical-scientific procedure: simplify case definition, promote rote treatment, and devote research to supporting foregone conclusions. Little true insight has been gained since. L. borreliosis was force-fit into the modern model of assembly-line medicine where medical-industrial complex wants to treat doctors like technicians. Doctors are told to run a blood test and prescribe the drug indicated by the test results. If that does not work, they are pressured to extract themselves from the case at hand.
A commercial vaccine or test kit, hopefully one generating a continuous revenue stream, would have been another solution fitting into the modern medical model. But test development and vaccine attempts which dominated L. borreliosis research have been colossal failures. The tests are not acceptably accurate and the vaccines did not keep people from getting sick. In fact, they often made people sick. As for the tests still in use, doctors just assume they mean more than they actually do. None meet acceptable standards for sensitivity.
Very few researchers have closely studied humans with L. borreliosis. Fewer still have applied sufficient critical, comprehensive thinking to the problem.
John Stokes closely studied humans with syphilis. His analysis and insight teaches expands what we know about spirochetal disease. Read past his discussion of mercury and arsenic treatments, substituting "antibiotics" and you will learn much. Apply Stokes knowledge and insight of syphilis to L. borreliosis. and you will come away with a clear-minded, rational concept of spirochetal infections, something much different from what today’s textbooks say about Lyme disease.
Read John Stokes’ book.
A modern review of syphilis
Other resources:
A journal article comparing T. pallidum and B. burgdorferi
Books by Paul Ewald on persisting infections:
Plague Time: The New Germ Theory of Disease
Although on that day my reaction was uneasiness with the doctor’s rigidity and close-mindedness, and despite knowing better, for the most part I used his standard for deciding what to believe about borreliosis for several years. If information was not coming from a journal indexed in PubMed or a similar source, for me it was questionable information. I was so biased that when shopping for a book on a medical subject, I generally would not buy it unless the author was an MD.
Biology, medicine, and health are subjects with some science and a great deal of uncertainty. We would like to defer to science to sort what is real from what is not. But this is hard, especially in medicine and health, because there are few absolutes and great potential for manipulation by people driven by forces other than a quest for knowledge and promotion of societal good.
I wanted validated information, too. The easiest, and seemingly best way to get it was to rely on journal editors and reviewers for the vetting process.
Then, reality descended when I actually read a few papers in medical journals instead of just their abstracts or summaries. These papers were in journals of good reputation, and often on subjects related to borreliosis. It was disheartening—more than disheartening. At times I felt like a child realizing there really was no Santa Claus.
Behind all the fine print and grandiose academic language, usually there was very little information, logic, or analysis. The greatest offenders were often the journals with the best reputations. The most unreliable authors were often those affiliated with the most prestigious institutions and universities. Regarding Lyme borreliosis, the oft-quoted Klempner study on a treatment for persisting borreliosis was a dreadful piece of work.
Even so, to this day, despite my many disappointments, I still give a knee-jerk deference to papers published established medical journals. Unlike the MD of my first Lyme disease conversation, however, I have been able to step back and become open to other sources. I no longer limit my information sources to medical journals or textbooks. Not that this made things easy. It takes some discipline to read a paper, focus on substance, and set aside automatic deference to a supposed authority.
To illustrate the wrong way of doing things—an expedient and professionally acceptable way to evaluate is by a process like this: if information is printed in JAMA assume it is true and accurate; if it is posted on a blog assume it is unreliable and not worth your time; For everything else, judge it by where it falls on this scale.
Automatic acceptance of papers in medical journals is bad policy. Much printed in journals is unscientific advocacy dressed up in obscure academic language and accompanied by obtuse graphics—impressive on the surface, but manipulative in its intent and content.
It is probably easier for me to transition than the typical medical professional reader. I never joined, or wanted to join, any of their clubs. My undergraduate biology department was diverted by an arrangement where medical students from Rush Medical College in their first year could choose to spend it at my college. I saw an informal club form that I did not want to join, fighting for the first row of classroom seats. That club continued on to medical school and became the MD club. Most then joined a medical specialty club. I did not join any of those clubs and I certainly did not join the medical academics club.
But still, I want to read those prestigious medical journals, or maybe just their abstracts, and accept and believe them. If it is that hard for me, it must be harder for doctors who joined those clubs. But really—we all need to grow up.
Scientific method is not all that difficult to understand. Most of us leave grade school knowing its essence. That said, it takes time and mental effort to read a journal paper and analyze what is really being said, undistracted by journal name, authors names, and self-promotions in the abstract, introduction, and conclusions. We all need to make the effort, particularly with medical subjects. Put simply, it is irresponsible to accept journal papers uncritically or rely on editors and reviewers for qualification.
Evaluating a medical study does not restrict readers to be completely logical and linear, discarding their prior knowledge and observations. It is entirely appropriate for a reader to use what they know about the authors, their past history, and motivations. Just be certain you have your facts straight.
If there are other medical or even scientific areas where the literature has been manipulated as greatly as it has in Lyme disease, I do not know of them. All indications are that a small group of misguided individuals looked at the realities of Borrelia burgdorferi infections in the 1980s and decided their careers would go better if they promoted and campaigned for a paradigm that satisfied what they wanted from the world instead of advancing what is known about the disease. There was no a conspiracy, but something much more insidious: the transition of extreme, irresponsible policy into everyday business.
We know it is hard to give up cherished, ingrained beliefs. But we are optimistic about the possibilities of transformation. The Serano Group intends to work to transition professionals away from the false comfort of uncritical acceptance of medical journal articles and rote repetition of flawed dogma. Making this transition is a responsibility you owe yourself and everyone else.
Resources
Many papers in Nature and BMJ have obvious and significant errors.
]]>The CDC and IDSA advocate underdiagnosis of Lyme borreliosis, ignoring much of the available science. A few quotes, some from guideline authors themselves, show the irrationality of requiring an EM rash or positive antibody tests (ELISA or Western Blots) for diagnosis.
"The absence of significant antibody titers to B. burgdorferi is not uncommon in Lyme disease, especially in early disease. ...Although it was initially believed that patients with neurologic Lyme disease generally have antibodies to B. burgdorferi, this may not always be the case. ...We would advise that in an endemic area, the differential diagnosis of nonspecific muscle and joint aches without rash should include Lyme disease—even in the absence of antibodies to B. burgdorferi."
Nadelman RB, Pavia CS, Magnarelli LA, Wormser GP. Isolation of Borrelia burgdorferi from the blood of seven patients with Lyme disease. Am J Med. 1990 Jan;88(1):21-6. PMID: 2294761 (Abstract)
Since coauthoring this paper, Gary Wormser has become a medical politician for the view that Lyme borreliosis is overdiagnosed. He regularly supports the opinion that antibody tests for B. burgdorferi are important, if not required, for diagnosis, contrary to his own research.
Research since 1990 continues to confirm the inadequacy of common Lyme disease tests:
"Lyme borreliosis patients who have live spirochetes in body fluids have low or negative levels of borrelial antibodies in their sera.”
Tylewska-Wierzbanowska S, Chmielewski T. Limitation of serological testing for Lyme borreliosis: evaluation of ELISA and western blot in comparison with PCR and culture methods. Wien Klin Wochenschr. 2002 Jul 31;114(13-14):601-5. PMID: 12422608 (Abstract)
Similary, research has never established an EM rash as a predominant symptom:
"In our series, only 27% of children with neurologic abnormalities due to LD had a history of EM or arthritis."
Bingham PM, Galetta SL, Athreya B, Sladky J. Neurologic manifestations in children with Lyme disease. Pediatrics. 1995 Dec;96(6):1053-6. PMID: 7491220 (Abstract)
Why does the CDC endorse EM rash or antibody tests as nearly essential for Lyme disease diagnosis? ]]>
Steven J. Dumler did a 2-year evaluation of Lyme disease tests. He divided subjects into three classes based on symptoms and history: probable, possible, and unlikely for Lyme disease. The Journal of Clinical Microbiology let him publish without disclosing the test results of the three groups. Through a convoluted scheme, he obscured the fact that he threw out all the subjects with negative results and only analyzed subjects having positive tests, completely disassociated from any real-world phenomena other than the fact they produced a positive test. He has refused numerous requests to disclose who tested positive and who tested negative in his study. The journal editor, Andrew Onderdonk, supportive of the IDSA ideology, has refused to ask Dumler for his results. Dumler’s study would classify a person bitten during the summer outside of Old Lyme, Connecticut by an identified Ixodes scapularis tick having DNA evidence of Bb, who left the tick attached three days, who had a flu-like episode and a physician-observed a 20 cm EM rash, followed by a swollen knee, as having NO EVIDENCE OF LYME DISEASE, just because the person had a single test and it was negative. He does not hide this detail, but does not bother to mention it, either.
Mark Klempner was chief investigator on one of the most quoted (particularly by insurance companies) studies on persisting Lyme disease. He made numerous measurements pre-treatment and, if he made these measurements post-treatment, he has never reported them. The only result he analyzed came from a general questionnaire where each patient self-rates their physical and mental health. This questionnaire, the SF-36, generates eight scores, each on a scale from 0 to 100. Klempner has refused to disclose these scores for the groups studied. Instead, he used mathematically derived summary scores that one of the principals of the company who licenses the SF-36, Mark Kosinski, has stated never to use without disclosing the eight underlying scales. Maybe Kosinski decided to quiet his objections when Klempner made him a co-author of the paper in the prestigious New England Journal of Medicine.
Eugene Shapiro is quoted in a letter to a journal that he cannot provide the results from one of his papers because the results were “in storage”. Doesn’t Yale University use computers? Maybe the results were “in storage” in a far corner of a disk drive, too far away for Shapiro to get to. And, don’t you put your results in storage so you can get them out to answer challenges and questions?
In 1991, organizers of a Lyme disease conference had to be ordered to allow submission of papers whose views and research contradicted IDSA ideology. Durland Fish was unhappy. (No link because the journal Science still wants $15 to display the article, Science 5 June 1992: 1384-1385) Since 1992, the IDSA faithful convene regularly at private Gordon conferences where dissenting opinions and research are not permitted.
Gary Wormser has disclosed his financial interest in Diaspex, which he describes, in entirety, as a company having no products or services. We applaud Dr. Wormser for providing full disclosure. But, in April, 2009, Dun & Bradstreet gives the same address for Diaspex as for Cenogenics, listed as a manufacturer of medical diagnostic products including “syphylis (sic) serology reagents”. Gary Wormser’s company that, remember, has no products or services is listed as providing Noncommercial Research and Development in the Social Sciences and Humanities.
In 2005, Justin Radolf attacked the innovative and perceptive treating physician Dr. William Harvey in The Dallas Morning News saying Harvey was “making up his own rules”. In 2003, Radolf had been found guilty of falsifying data to get research grants. After that, he repeatedly sued the University of Connecticut for using his admitted fraud as a reason not to allow him to receive grants. (In this case, the legal system got it right. Radolf’s suits were unsuccessful.) He’s back to getting NIH grants and being quoted as a Lyme disease authority.
In the mid-1980s, Lyme borreliosis researchers began finding their research routinely censored. The Lyme Disease Foundation created their own journal in 1994 to provide an uncensored forum for research. The LDF received some NIH funding support and has been vehemently attacked by IDSA ideologues ever since. The journal ceased publication in 2002.
The fifth edition of the textbook Infectious Diseases of the Fetus & Newborn Infant, edited by Jack S. Remington, Philadelphia : Saunders, 2001, had a balanced and comprehensive 100-page chapter on congenital Lyme borreliosis. This chapter was excised and replaced with a few pages of Eugene Shapiro dumbing down the whole subject to a few pages non-scientific IDSA ideology in the 2006 edition. (Thank you to Dr. David Martz for finding this.)
Alan Steere has so many secrets, it is hard to pick just a few. Writing up his version of what citizens explained to him was going on in Old Lyme, Connecticut, he cited at least 15 literature references on EM rash in June, 1977. Why didn’t he stress that EM rashes respond to antibiotics? Why did he try so hard in 1977, and for the next 30 years to turn borreliosis into a new disease, preferably a rheumatologist’s disease? Secrecy was the standard operating procedure for Steere’s clinical trial for the Lymerix borreliosis vaccine failure which had 10,936 participants in 1995. Participants were informed of symptoms of borreliosis and asked to look for signs during the trial. They were told to call their doctor if they observed symptoms. Of the 1,917 that called in and were evaluated, 269 were determined to have borreliosis. What was wrong with the other 1,648? How many of them were infected? Remember: if you are conducting a vaccine trial, you want nobody to have the disease going in and certainly nobody to have the disease after the shot. Would a vaccine manufacturer want over-diagnosis or under-diagnosis? (Online access to the paper costs $31.50. Systemic symptoms without erythema migrans as the presenting picture of early Lyme disease, Am J Med. 2003 Jan;114(1):58-62.)
The reason IDSA supporters repeatedly cite for the failure of the Lymerix vaccine is “poor sales”, which is a little like a football coach saying his team lost because the other team scored more points. Perhaps the failure of the vaccine was due to its inability to protect against borreliosis and its tendency to make well recipients sick or crippled, something rarely reported but fairly well-known to the participants. We do not think this was patient hysteria. Class-action lawyers became involved not when contacted by patients, but when a group of doctors, worried they would be sued for malpractice after giving people the vaccine, went to the lawyers seeking protection.
Just perhaps, the IDSA Lyme disease guideline authors are completely accurate and ethical. Maybe they have nothing to hide. Perhaps they just have personality quirks that compel them to behave furtively, acting almost like criminals. Another explanation is they might have some facts in hand that contradict their religious-like dogma. You can decide. It might help if you talk to any of the hundreds of thousands of citizens and their doctors who have experienced something completely different from what the IDSA says is true.
]]>Even some of the most staunch Lyme disease ideologues like Gary Wormser know this: Survival of Borrelia burgdorferi in human blood stored under blood banking conditions. Nadelman RB, Sherer C, Mack L, Pavia CS, Wormser GP. Transfusion. 1990 May;30(4):298-301. PMID: 2349627 (Note that the big shift in turning Lyme borreliosis into a hard-to-catch, easy-to-cure dogma did not swing into full force until the early 1990s. Fortunately, the National Library of Medicine keeps records of pre-dogma papers.)
Jumping into the historical timeline, we see Eugene Shapiro, the same guy seen in the film Under Our Skin harassing treating physicians and making outrageous statements, already cranking up the denialism campaign in 1994:
The risk of acquiring Lyme disease or babesiosis from a blood transfusion. Gerber MA, Shapiro ED, Krause PJ, Cable RG, Badon SJ, Ryan RW.J Infect Dis. 1994 Jul;170(1):231-4. PMID: 8014507
We have not analyzed this paper, but from the abstract it seems the authors are basing their conclusions on testing for antibodies to Bb six weeks after a transfusion and using clinical assessments by doctors with a bias toward diagnosing as few cases of Lyme disease as possible. Six weeks is pretty early to expect seroconversion from Bb infection and certainly only a weak indication patients were Bb-free. Antibody testing has been repeatedly shown to miss cases of culture- and DNA-positive infection. Shapiro’s entire case is weak, certainly less evidence than what a responsible doctor would like to see for assurance that Bb is not transmitted by blood trasnfusion. And, by the way, his study showed Babesia, a borreliosis coinfection that can cause serious disease, can be transmitted by infusion.
(This is the same Eugene Shapiro quoted in a medical journal that he cannot provide data from one of his studies because he keeps his data “in storage”.)
There is a startlingly small number of published scientific studies that look at blood transfusion transmission of Bb. Readers can look at the literature and decide whether the question has been answered with enough certainty. Keep in mind it is extremely hard to culture Bb or find DNA-RNA evidence, our most definitive indicators of Bb infection, so not finding that type of evidence is typical.
The NIH should be investing taxpayer money to assure the blood supply is safe from Bb instead of funding commercial interests trying to make a Lyme disease vaccine. A Lyme borreliosis vaccine is highly unlikely to ever be successful because of the complexities of borreliosis and the increasing evidence indicating that Bb immunity will not come from a vaccine. Efforts to produce Lyme disease vaccines in the 1990s were abysmal failures.
Before looking at other probable ways that Bb is transmitted, it might help to look at Dr. William Harvey’s paper that asks the right questions and deals directly with the reality of illness from borreliosis. Often, it is best to start by acknowledging broader realities, as Dr. Harvey does.
In summary, Dr. Harvey relates how multiple members of families were being diagnosed with multiple sclerosis in his area. Multiple sclerosis is a condition that is difficult to tell from Lyme disease and has no reliable test for diagnosis. Often, what one doctor calls multiple sclerosis can just as easily be diagnosed as Lyme disease and the patient responds dramatically to antibiotics. This begs an obvious question…
Are there any indications that Bb can be transmitted by close, non-sexual contact?
In 1986, the NIH, working with other researchers, put uninfected mice in a cage with Bb infected mice. All of the uninfected mice had evidence of Bb infection 42 days later.
It is well established that Bb is found in urine. Willy Burgdorfer, the discoverer of Borrelia burgdorferi, unfortunately got Lyme borreliosis when urine from an infected rabbit splashed into his eye. As with blood transfusions, not enough research has been done on transmission by other body fluids.
Syphilis, another spirochetal disease closely related to Lyme borreliosis, is. of course, sexually transmitted. Bb has been found in human semen. In April, 2001, Dr. Gregory Bach presented a paper at the International Scientific Conference on Lyme Disease showing that in 42 tested Lyme borreliosis patients, 14 had DNA evidence of Bb in semen or vaginal fluids. These results were not published in a medical journal, probably because of censorship, pervasively common at that time, or perhaps because of lack of funding for treating physicians doing research.
On April 27, 2009, the National Library of Medicine listed 8576 medical journal papers related to Lyme disease. They listed one paper regarding sexual transmission of Lyme disease, and that was a chance mismatch of a word combination. Searching “sexual transmission Borrelia” produced three results: two of them duplicates and all concerning ticks having sex with ticks.
For quite some time, we wanted to get most, if not all, of our information on borreliosis from medical journals. Gradually, we found that the journals routinely censor valid work, often publish sloppy and illogical papers, and their peer review consists mostly of an if-you-approve-my-paper-I-will-approve-yours system. This was a disappointment, because we really believe good science can help society answer questions.
Most of the foregoing are details of a big subject. This article is not trying to make the best scientific case for non-tick transmission of Bb; that would be the subject of a book, maybe several books. We are only trying to explain why we do not spend much time or effort talking about ticks here. Bottom-line, tick transmission of borreliosis has been covered pretty well elsewhere while we see almost no research evaluating the risks of non-tick transmission.
Many people concerned about the environment advocate use of the precautionary principle: if an action or policy might cause severe or irreversible harm to the public or to the environment, in the absence of a scientific consensus that harm would not ensue, the burden of proof falls on those who would advocate taking the action or endorsing the policy. Since the policy of endorsing denial of non-tick transmission of Bb definitely has potential to cause severe or irreversible harm to the public, the precautionary principle applies.
Of course, be ever-vigilant about tick bites. You can certainly contract severely disabling, possibly fatal, diseases from a tick bite. What precisely you should do after a tick bite is still an open question. Most of the research on this subject has been done by some of the least reliable Lyme disease researchers. But, no one, especially not public health officials, should assume you can get Lyme disease only from a tick.
]]>The budget of the state of Connecticut wasn’t sufficient to take on so large a battle, so the AG agreed to a compromise that lets the IDSA review their deeply flawed guidelines using IDSA members to review what other IDSA members swear to. Yes, it was a little hard for us to be optimistic about the outcome. We did not plan to submit anything.
But, David Volkman, Ph.D., M.D. Emeritus Professor of Medicine and Pediatrics SUNY, Stony Brook, NY submitted a startlingly honest statement to the IDSA review panel. We had already done a fair amount of work looking into the IDSA’s bad science (only to be censored), so we thought it only right to support Dr. Volkman.
Let all hope that some members of the IDSA, especially those reviewing the egregious guidelines, get up some morning and decide to acknowledge reality. Take a look.
]]>Some of the academic-speak, particularly in the abstract, might discourage you, but give this paper a close reading. It deserves the time invested.
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