2009 Lyme Articles-4
Danbury Hospital readies Lyme registry
By Robert Miller, Staff Writer
December 18, 2009
DANBURY -- Take one Lyme disease case. Multiply that by a thousand, or more, and you may be able to glean some vital information about this complex disease from all the gathered information.
That's what Danbury Hospital plans to do, beginning early next year, when it opens its Lyme disease registry for the region.
But for it to work, the public must be willing to sign up.
"We really want to engage the Lyme community,'' said Dr. Ramin Ahmadi, the hospital's director of graduate medical education and research. "If the community supports it and participates in it, it will be wildly successful. If it doesn't, the project won't go very far.''
[snip]
Since then, Ahmadi said, the hospital has gone through all the complicated work that needed to be done to get an undertaking this complex off the ground. The hospital's own institutional review board, which rules on research projects, had to approve it. The project's leaders then had to find ways to link it with the hospital's electronic record system.
This work Ahmadi said, established the methods the project will use to protect the privacy and anonymity of the people who enter their case histories into the register.
[snip]
Ahmadi said the project will require that any patient involved with the registry have a doctor's certification that the patient has been diagnosed with Lyme disease.
However, the registry won't ask people to have a positive blood test for Lyme before joining the registry. For years, Lyme disease advocates have complained that because blood tests for Lyme can be inaccurate, depending on them as the sole diagnosis is highly unreliable.
Jennifer Reid of the Ridgefield Lyme Disease Task Force said requiring a doctor's report confirming Lyme disease is a good thing, since it relies on the observation of clinical symptoms, not just blood tests.
[This is where things begin to fall apart. Unless the registry contains actual cases and patient samples from current or prior infection the data will be a hodge-podge of misleading and probably useless information. It’s a case of “garbage in, garbage out.”]
Reid said the participation of the Lyme disease patients in the area, as well as advocacy groups, will depend on how well the hospital explains the objectives of the registry.
[ Good luck there. The Lymeland community has a long history of demanding more research and trials, but not actually coming forward to participate in those efforts. EvenFallon had trouble scaring up actual Lyme patients for his own NIH-funded trial.]
"What we all want to hear is how the registry will be designed,'' she said. "But we all understand the need for great research into tick-borne diseases. This is a very good opportunity to do that.''
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Posted by Relative Risk at 07:25 0 comments Links to this post
Labels: Lyme disease
From a poster on the LymeNut Forum:
"I spent the better part of a day researching online and called the following doctors within 2 hours of NYC."
Dr Raxlen in NYC (a friend of ours went to him and did not have a positive experience though she did not elaborate)
- $900 initial fee + labs
- No insurance accepted
- No appts before Feb
Dr Leigner in Armonk, NY
- No insurance accepted
- Only nurse practitioners are seeing new patients
- $1065 for an initial 3 hr appt
- 2nd week of Jan availability
Dr Fein in West Caldwell, NJ
- Have not been able to speak to anyone
Dr Cameron in Mt Kisco, NY
- Accepts her insurance (HealthNet)
- Available appointment for next Monday.
Dr Streit in Howell, NJ
- do not take HealthNet (may take other insurance)
- Appts avail 2nd week of Jan
- $300 initial visit
Dr Horwitz in Hyde Park, NY
- No insurance accepted
- $975 for 2 hour initial consult
Dr Eiras in Jackson, NJ
- No insurance accepted, but they said testing is usually covered
- $300 new patient appt, followups $100-115
- No appts before Feb
The last time I saw a doctor it cost me $15.00.
Posted by Relative Risk at 13:52 0 comments Links to this post
Labels: Cameron, Lyme disease
Antimicrob Agents Chemother. 2009 Dec 7.
Ineffectiveness of Tigecycline Against Persistent Borrelia burgdorferi.
Barthold SW, Hodzic E, Imai DM, Feng S, Yang X, Luft BJ.
An interesting--but complicated--paper about the persistence of borrelial infections in mice during and after antimicrobial treatments. Some of the paper’s important points are noted below. (Note: Tigecycline is a structural analog of minocycline that avoids tetracycline resistance mediated by…efflux…and ribosomal protection…)
Management of Lyme disease patients with antibiotics is based upon evidence based clinical guidelines.
[That’s the IDSA guidelines.]
What is not known is whether or not antibiotic treatment completely eradicates the infection….
[We do know more antibiotic treatments don’t help persisting symptoms.]
Antibiotics are likely to kill most B. burgdorferi organisms, but the immune system is needed to fully eliminate the remaining spirochetes. However, therein lies the challenge, since Borrelia burgdorferi has evolved to persistently infect fully immunocompetent hosts.
[Of course, this is true of most successful pathogens that have evolved over time. Until very recently, humanity had nothing else to rely on but a robust immune response. One lived or died depending on the genetic quality of that inherited immune system.]
These results challenge prevailing dogma about [the] effectiveness of antibiotics for eliminating B. burgdorferi infection….
[This is a critical point that Lyme activists and their enabling quacks are going to overlook because it runs counter to their personal and financial beliefs that more antibiotics are the key to treating so-called “chronic” Lyme disease. So much for the dogma of ILADS, the LDA, the CALDA, and other activist groups.]
Earlier studies on antibiotic treatment of laboratory mice that were based upon culture of tissues as a read-out, showed effective elimination of infection, and this was essentially confirmed with standard PCR assays. With the advent of more sensitive real-time PCR, PCR-positive, culture-negative evidence for spirochete persistence after antibiotic treatment has been increasingly recognized, using the mouse model….
[Yes, using the mouse: the natural host of this annoying little bug. Perhaps it’s not too surprising that the mouse (the host) and the borrelia (the parasite) would negotiate some kind of “immuno-pathogenic” compromise over time, allowing each other to exist and function without too much immunologic or pathogenic interference. The question is, have humans done the same thing or are we still sitting at the negotiating table hammering out boundaries of disease, inflammation, and stabilizing immunity.]
In the present study, tick transmission to SCID mice was confirmed, and spirochetes in the ticks survived molting into the adult tick stage. Furthermore, transmission of infectious spirochetes was shown to occur following transplant of tissues from antibiotic treated mice into SCID mice. The enhanced success of transplant-related infection in the current study was based upon observations that heart base and joint tissue were the most likely tissues to contain residual spirochetes….
[Interesting, but can it be done in fully immunocompetent mice?]
This parallels human clinical experience, in which treatment is generally more effective when administered during early Lyme disease.
[Again, this tends to be true of all infectious and non-infectious diseases You don‘t want to wait ‘til the last minute to treat TB or pancreatic cancer.]
…none of the samples tested from antibiotic-treated mice indicated transcription of flaB (flagellin), which is generally considered to be constitutively expressed by B. burgdorferi. The down-regulation of genes involved in nonessential functions, such as flagellin, has been noted in persistent forms of E. coli following antibiotic exposure.
[Well, there goes the activist conspiracy theory that no one is using the flagella antigen for diagnosis because it would show too many cases of Lyme disease and “chronic“ Lyme disease. A perfectly good conspiracy theory ruined by a little bit of genetic reality.]
Collectively, results from previous studies and the current study indicate persistence of low numbers of non-cultivable spirochetes, detected by real-time PCR, following antibiotic treatment. For at least 3 months after cessation of antibiotic, these non-cultivable forms can be acquired by ticks (xenodiagnosis), transmitted by ticks, survive the molts between larvae to nymphs to adults, infect recipient mice by tissue transplant, transcribe RNA, and express antigen in ticks and tissues in the form of morphologically identifiable spirochetes. The fact that these forms are unable to be cultured does not negate their viability.
It remains uncertain if non-cultivable spirochetes are present during the normal course of persistent infection, or if they are induced in response to antibiotic. Despite their persistence, previous studies and the current study indicate that antibiotic treatment results in a significant decline in antibody titers to B. burgdorferi suggesting that the persisting spirochetes remain sequestered or occult to immune surveillance.
The significance of antibiotic persisting B. burgdorferi has also been challenged, because no disease was evident in SCID mice infected with these organisms. That conclusion is not valid, since inflammation does not necessarily correlate with presence of spirochetes. Inflammation requires invasion of specific tissue types, such as synovium, and no inflammation is found in many other tissues (in fact the majority) infected with B. burgdorferi.
[So what’s driving post-infection/post-treatment inflammation and other symptoms?]
Tolerance to lethal concentrations of various antibiotics, even after prolonged treatment, has been observed in a wide variety of bacteria and clinical conditions. It is not clear whether these persisting forms of B. burgdorferi occur in human patients after treatment, or give rise to chronic disease later in life.
________________________
So we’re left with a lot of questions about the nature of “post-infection” or “post-treatment” pathologies associated with prior infection by B. burgdorferi. Not to mention the nature of persisting, non-cultivable borrelia themselves.
It would be helpful to do some of these same experiments on people. Fortunately, there’s a huge population of alleged “chronic” Lyme patients. Maybe some of them would like to volunteer for a little xenodiagnosis or donate some tissue samples? Probably not. They weren’t too eager to volunteer for antibiotic treatment trials (Science 1999;283(5407):1431). Hard to imagine many of them sitting still for biopsies and tick-feedings.
So questions persist…as do symptoms…and complaints…and conspiracy theories….so it’s back to the bench.
Posted by Relative Risk at 17:49 0 comments Links to this post
Labels: Lyme disease
I keep reading these complicated imagining studies involving people who may have had Lyme disease, but it’s still hard to know what they mean or of what value they may be to the patient or the treating physician. It might be more interesting at this point to see what other infectious diseases patients (e.g., HIV, TBE, West Nile, EEE, Neisseria, CSD ) look like under SPECT.
And for all the complicated work, it doesn’t seem like the Lymees who funded this center and some of this work (below) are getting back what they hoped for. But then that’s science: favored opinions, hopes and beliefs ruined by uncooperative data.
Regional Cerebral Blood Flow and Metabolic Rate in Persistent Lyme Encephalopathy
Brian A. Fallon
(REPRINTED) ARCH GEN PSYCHIATRY/VOL 66 (NO. 5), MAY 2009
While most patients recover fully when treated with antibiotics soon after infection, patients who are treated months after the initial infection may sustain ongoing problems with fatigue, cognition, and pain despite receipt of a standard course of antibiotics. These patients have been described as having chronic Lyme Disease or post treatment Lyme disease syndrome.
The purpose of this study was to address the lack of systematic data regarding rCBFand rCMR in patients with persistent Lyme encephalopathy, a type of chronic Lyme disease characterized by cognitive deficits that persist or return after antibiotic treatment. In this study, carefully characterized patients were compared with age-, sex-, and education matched healthy volunteers (controls) using a series of PET scans in both resting and hypercapnic conditions to obtain full quantification of regional cerebral blook flow (rCBF) and regional cerebral metabolic Rate (rCMR) in the same subjects.
These patients reported that their cognitive symptoms emerged after contracting Lyme disease and that their symptoms either returned or persisted despite prior treatment.
…compared with controls, the patients had substantial differences in specific brain regions
of blood flow and metabolism.
…there was no evidence in this study that the patient group was characterized by an excess of extreme values.
Some of the dysfunction in neurologic Lyme disease may result from inflammatory changes in CNS blood vessels—a hypothesis supported by case reports of diffuse or focal vasculitides and strokes attributed to Lyme disease and by perivascular inflammation noted in brain biopsies of patients with Lyme disease.
…the patients and controls did not differ in global CBF during the hypercapnic assessment.
This study does not address whether the imaging abnormalities reflected persistent B burgdorferi infection as opposed to a postinfectious process. We also cannot prove that the imaging abnormalities might not be accounted for by another unexamined variable in which the groups differed.
….although patients reported developing cognitive problems only after getting Lyme disease, we cannot be certain that the identified brain regional abnormalities were not present prior to infection.
Although helpful in confirming objective central nervous system abnormalities in a patient with a history of Lyme disease, this pattern of hypofunction is nonspecific and cannot be used to make the diagnosis of Lyme encephalopathy.
In conclusion, this study demonstrates that patients with persistent encephalopathy after treatment for Lyme disease have objective neurobiological dysfunction.
Financed in part by: the Columbia University Lyme and Tick-borne Diseases Research Center established by Time for Lyme, Inc, and the Lyme Disease Association.
Posted by Relative Risk at 19:49 0 comments Links to this post
Labels: diagnostics, Lyme disease
A Tale of Two Spirochetes: Lyme Disease and Syphilis.
Halperin JJ.
Neurol Clin. 2010 Feb;28(1):277-291.
Two spirochetal infections hold fascinating positions in the history of infectious diseases. Numerous historic and literary figures were believed to have neurosyphilis, which consequently has been blamed for otherwise inexplicable developments in Western European history. More recently, Lyme disease has served as a focal point for the divide between evidence-based medicine and traditional experiential approaches, highlighting issues of physician autonomy in an era of guideline development, and epitomizing the tension between patient advocacy and scientific medical care.
Most significant is the societal context in which these diseases first appeared. Syphilis invaded Europe when biologic understanding of disease was limited. In the absence of knowledge of other diseases, and with few tools to diagnose syphilis unequivocally, all manner of clinical phenomena were blamed on this infection. Lyme disease was described at a time of far greater scientific understanding. However, the inaccurate notion that this is a novel infection for which diagnostic tools are limited, and the availability of the Internet to enable widespread but uncritical proliferation of information have contributed to an unfortunate degree of misunderstanding. At a time when the population is inadequately scientifically literate but simultaneously suspicious of organized medicine and sympathetic to populist outpourings, this has allowed the widespread acceptance of scientifically invalid information, culminating in state legislatures passing laws requiring insurance companies to pay for treatment that has been shown to be irrelevant, unhelpful, and, in fact, harmful.
Diagnosis
False-positives are a concern and fall into two groups. Some organisms, T pallidum, T denticola (an organism responsible for periodontal disease), and Borrelia responsible for relapsing fever, are so antigenically similar that differentiation can be difficult. Fortunately, little geographic overlap exists between relapsing fever and Lyme disease; syphilis can usually be differentiated using tests to measure reaginic antibodies, such as the venereal disease research laboratory (VDRL) or rapid plasma reagin (RPR) assays. These anticardiolipin antibodies are almost always produced in syphilis and are rarely if ever demonstrable in Lyme disease. More common is cross-reactivity caused by more global B-cell stimulation. Patients who have lupus, subacute bacterial endocarditis,12 parvovirus, and other disorders develop a significant polyclonal gammopathy that can result in cross-reactive false-positives on many serologic assays. This cross-reactivity can be most easily differentiated using a Western blot….
Clinical
Contrary to assertions of some internists and hapless candidates at the Neurology Board examination, Lyme disease does not cause every imaginable neurologic disorder.
Patients who have active Lyme infection, particularly with evidence of active inflammation such as arthritis, often experience ongoing fatigue and malaise, and perceive cognitive and memory difficulties. These symptoms are identical to the toxic metabolic encephalopathies seen in innumerable other chronic infections or inflammatory states.25 Unfortunately, some have asserted that these cognitive symptoms, in isolation, are strongly suggestive of Lyme disease, with or without laboratory support for the diagnosis. Because population studies indicate that these same symptoms occur for unexplained reasons in a significant number of individuals, even being sufficient to disrupt daily activities in a meaningful fashion in 2% of the otherwise healthy population,26 this assumption is clearly inappropriate.
Treatment
B burgdorferi is sensitive to common antibiotics; meaningful antimicrobial resistance has not been shown.7 For most patients, oral regimens with doxycycline, amoxicillin or cefuroxime axetil given for between 2 and 4 weeks are highly effective (grade A evidence). Numerous studies in the European literature indicate that oral treatment with doxycycline is highly effective (grade A evidence, meta-analysis) in individuals who have Lyme meningitis, cranial neuritis, and radiculitis.29 This treatment has not been tested in the United States but, in light of the known biology of the organism and its different strains, similar results seem likely.
SUMMARY
Because neurosyphilis and neuroborreliosis share similar biologic characteristics, these two spirochetal infections have several of the same distinct clinical themes. Both can readily seed the nervous system and cause prolonged infections, despite the presence of an obvious humoral immune response. Both are readily diagnosed primarily using serologic tests, which are excellent but imperfect. In both, CNS infection is most readily confirmed through CSF examination. Both infections remain readily responsive to straightforward antimicrobial regimens. However, each has acquired a distinct mystique, leading to its being blamed for a broad range of unrelated disorders. Hopefully the final common thread will be that, just as increased scientific understanding resulted in clarification of the true biology of syphilis, continued development of understanding of Lyme disease, and the dissemination and acceptance of this information, will similarly result in its demystification.
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Posted by Relative Risk at 11:50 0 comments Links to this post
Labels: Lyme disease
Some notes from a recent paper on pregnancy outcomes should come as no surprise to many scientists, be a great relief to many pregnant women, and be dreadful news to Lyme activists who have used fantastic tales of child deaths and deformities to frighten the public.
Maternal Lyme borreliosis and pregnancy outcome
Andra Lakos, Norbert Solymosi
Int J Inf Dis, Nov 2009 (In Press)
With the exception of some publications, most early case reports have described patients with adverse outcomes following their pregnancies. Incidence and cross-sectional studies on populations of 1000–5000 pregnant women and/or their offspring found hardly any cases of Lyme borreliosis and, therefore, remained inconclusive with respect to risk for adverse pregnancy outcome.
The Center for Tick-borne Diseases, Budapest was opened in 1986 under the leadership of one of the authors (AL). Since then, 8149 erythema migrans (EM) patients have been seen, including 97 cases in which Borrelia burgdorferi s.l. infection was clinically evident during pregnancy. Here we report our experience with these cases.
From the 97 registered cases of gestational Lyme disease, we were able to analyze 95. Two women were lost to follow-up before delivery. All women were seen by the same examiner (AL). The following criteria for inclusion were used: (1) EM rash during pregnancy, as defined by the CDC and EUCALB criteria (n = 72). (2) Patients were included if they visited the center after delivery, with EM that had commenced before or during pregnancy (n = 17); in many of them the inflammation had already resolved at the time of the first visit to the center (n = 12). The condition for the inclusion of these latter patients was a definitive description of the EM made by the family doctor or another institute. (3) Those with clinically diagnosed acrodermatitis chronica atrophicans (ACA), with signs of inflammation still present15 after delivery, which had commenced before or during the pregnancy (n = 3) were included. (4) Patients with facial palsy beginning during pregnancy with preceding EM or with the presence of intrathecal Borrelia antibody production16 (n = 3) were also included.
The onset of the first clinical symptom (starting point) and the first day of the antibiotic treatment (end point) were used to calculate the length of the Borrelia infection during pregnancy.
We registered 23 adverse outcomes in 20 (21.1%) of the 95 offspring….
Our findings demonstrate a statistically significant association between untreated Lyme borreliosis and adverse pregnancy outcome. The association between the untreated Lyme borreliosis and first visit only after delivery was expected.
We should stress that adverse pregnancy outcome is a combination of several perinatal and neonatal indicators with different degrees of severity.
It appears that a specific syndrome representing ‘congenital Lyme borreliosis’ is unlikely.
However, spontaneous abortion, stillbirth, and preterm birth have frequently been identified in other published studies and were also found in our series.
We frequently observed hemangioma, a hitherto unpublished symptom coincidental with maternal Borrelia infection. In contrast, cardiac abnormalities were not found; these have been the most frequently published consequence of maternal Lyme borreliosis in other reports
It is striking that of the three pregnancies where the mothers had late Lyme borreliosis (i.e., ACA) and in which the infection was acquired long before conception and remained untreated before and during the whole period of pregnancy, none resulted in any fetal or newborn harm. Patients with late Lyme borreliosis, especially with ACA, always produce a strong antibody reaction against B. burgdorferi, while most EM patients usually have faint antibody titers. The intensive immune response of ACA patients may play a role in preventing Borrelia spread and transmission to the placenta or fetus.
Placentas and offspring were not tested for Borrelia by PCR or culture in our study. Therefore, it cannot be concluded that the adverse outcomes were a result of a Borrelia invasion of the fetus or placenta. The adverse outcome may have been a consequence of damage to the placenta or a maternal reaction to the infection. There are animal studies that have demonstrated maternal–fetal transmission but others have not supported this conclusion.
Ideally, a prospective, multicenter study should be conducted, enrolling sufficient numbers of women, in order to adequately address these research questions.
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Posted by Relative Risk at 13:20 0 comments Links to this post
Labels: Lyme disease
Insciences.OrgPublished on 18 November 2009New Haven, Conn. — A protein found in the saliva of ticks helps protect mice from developing Lyme disease, Yale researchers have discovered. The findings, published in the November 19 issue of Cell Host & Microbe, may spur development of a new vaccine against infection from Lyme disease, which is spread through tick bites.Traditionally, vaccines have directly targeted specific pathogens. This is the first time that antibodies against a protein in the saliva of a pathogen’s transmitting agent (in this case, the tick) has been shown to confer immunity when administered protectively as a vaccine.The Lyme bacterium known as Borrelia burgdorferi is transmitted by ticks. When it moves through the tick, it is coated with a tick salivary protein known as Salp15. The Yale team injected Salp15 into healthy mice and found that it significantly protected them from getting Lyme disease. When combined with outer surface proteins of B. burgdorferi, the protection was even greater.
[snip]
Several years ago there was a Lyme vaccine on the market that utilized just the outer surface proteins of the bacteria. It was taken off the market in 2002, and to date no other antigen has been tested in phase III clinical trials.
The authors believe this new strategy of targeting the saliva - the “vector molecule” that a microbe requires to infect a host - may be applicable not just to Lyme disease but to other insect-borne pathogens that also cause human illness. “We believe that it is likely that many arthropod-borne infection agents of medical importance use vector proteins as they move to the mammalian host,” Fikrig explained. “If so, then this paradigm, described with the Lyme disease agent, is likely to be applicable to these illnesses. Currently, we are working to determine if this strategy is likely to be important for West Nile virus infection, dengue fever, and malaria, among other diseases.”
This isn’t a new idea—others have been working on a tick-based vaccine for a number of years—but it is a promising approach to the problem of protecting against multiple infectious agents carried by a single vector. You can develop half a dozen separate vaccines or develop one single vaccine against the vector itself. There is already one working model of such a vaccine: the Boophilus tick vaccine used to protect cattle in Cuba, Brazil and Australia.
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Posted by Relative Risk at 10:15 0 comments Links to this post
Labels: Lyme disease, vaccines
ScienceDaily (Nov. 17, 2009) — Using a powerful microscopic live imaging technique, a research team led by Dr. Justin Radolf, professor in the Departments of Medicine and Genetics and Developmental Biology at the University of Connecticut Health Center, has discovered the way ticks transmit Lyme disease to humans is different than previously thought. The research is published online in the Journal of Clinical Investigation.
Radolf and researchers Star Dunham-Ems and Melissa Caimano tried a novel approach. They genetically modified a virulent strain of B. burgdorferi to express green fluorescent protein (GFP). "This bacterium glows and can be followed in the living state as it migrates through the tick to the mouse during feeding," explains Radolf. "Then using a powerful microscopic technique called confocal microscopy, we discovered that the transmission process unfolds quite differently than previously believed."
Spirochetes in culture are highly motile, and it is widely believed that during feeding, the spirochetes in the midgut rapidly move through the wall of the midgut. But Radolf and his team found that during much of the feeding period, the spirochetes do not move. They actually divide and surround the cells of the midgut lining or epithelium, forming tight networks. "We also found that the reason they don't move is that the tick midgut secretes molecules that actually inhibit the motility of the spirochetes," explains Radolf.
Eventually, spirochetes in the networks reach the base of the epithelium by completely surrounding the epithelial cells. At this point, they become motile, detach, and completely penetrate the midgut, although in very small numbers. These few bacteria then swim to the salivary glands, which they penetrate en route to the mouse. "So rather than being entirely motility-driven, dissemination of spirochetes within ticks actually happens in two phases," says Radolf, "which is something we didn't know before.
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Posted by Relative Risk at 22:34 0 comments Links to this post
Labels: Lyme disease
Clinical Infectious Diseases 2009;49:1733–1735
BRIEF REPORT
Blood Cultures for Patients with Extracutaneous Manifestations of Lyme Disease in the United States
John Nowakowski, et al. Department of Medicine, Division of Infectious Diseases, New York Medical College
The findings of the present study document that spirochetemia can be detected in 20% of US patients with extracutaneous Lyme disease, including patients with neurologic, cardiac, or musculoskeletal manifestations. Positive blood culture results, however, were closely associated with having a concomitant erythema migrans skin lesion and with having a short duration of illness. Thus, the findings suggest that spirochetemia is principally found in patients with Lyme disease who have relatively early infection. These results are consistent with the observations made in studies involving rhesus monkeys in which positive blood culture results could only be detected for 6 weeks after inoculation of the spirochete. Similarly, in immunocompetent rodents, positive blood culture results are more frequently observed during the first 30 days after infection, although in certain strains of mice, spirochetemia has been detected in some animals at much later times (360 days).
[And from the “I’m shocked!” Department….]
Our findings are strikingly different from those of Phillips et al, [quacks from ILADS] who reported that B. burgdorferi was yielded by blood culture for 43 (91%) of 47 patients who had received or were receiving prolonged antibiotic therapy for putative “chronic Lyme disease.” Several follow-up studies, however, have been unable to reproduce the findings (without a single positive blood culture result). In fact, the novel culture medium used by Phillips et al was unable to support the growth of B. burgdorferi when the spirochete was directly introduced into it. [Probably all killed by that secret ingredient:Detroit tap water.]
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Posted by Relative Risk at 17:02 0 comments Links to this post
Labels: diagnostics, Lyme disease
There’s been some excitement over at LymeNut about a press release from Johns Hopkins. Johns Hopkins .. yes.. HO HO Hopkins... has just made a discovery that Lyme disease can be in the L-form and.... have admitted the following..."Not only are L-form bacteria difficult to culture and therefore study, but this "fried egg" cluster is part of what makes the L-form bacteria resistant to antibiotics, in addition to the fact that they do not have cell walls for commonly used antibiotics to disintegrate."
"It is ground breaking and VERY significant!" "Now the IDSA can't say we are not infected after getting the treatment." "They obviously let this slip out. I can't imagine they intended this to be out there."
This is some non-scientist’s interpretation of a press release, which is a writer’s interpretation of a journal article. A lot gets lost in the interpretations. Apparently, some of the Lymee activists got excited about this press release because it seemed to offer a reason for their lingering pains and their appetite for expensive antibiotics.
But anyone taking the time to read the actual journal article will find that it has nothing to do with Lyme disease—it’s not even mentioned—and not much to do with in vivo L-form pathogens either. Rather, it has a lot to do with the genetics of bacteria surviving without cell walls.
Insights into the molecular basis of L-form formation and survival in Escherichia coli.
Glover WA, Yang Y, Zhang Y.
PLoS One. 2009 Oct 6;4(10):e7316.
"Despite the discovery of L-form bacteria in 1935, the molecular mechanisms underlying L-form formation and survival have remained obscure. This lack of progress is mainly because of the unstable nature of L-form bacteria, the variability of the models used for their generation, and the unavailability of modern molecular biology tools before the 1980s when L-form research was largely abandoned. In this study, we took advantage of microarray technology and an E. coli deletion mutant library. These tools were used to perform whole genome-wide gene expression analysis and mutant library screens to provide insight into the molecular basis of L-form formation using the E. coli L-form as a model. The major findings of this study are the identification of pathways and genes involved in cell envelope stress, DNA repair, iron homeostasis, outer membrane biogenesis, and drug efflux/ABC transporters being involved in L-form formation and survival. This study represents the first systematic genetic analysis of L-form bacteria and provides important insights into the molecular basis of L-form bacteria."
As for L-forms being a common source of chronic infections or persisting inflammatory processes, the paper’s authors throw some cold water on those notions.
"Since their discovery by Emmy Klieneberger in 1935, L-forms, named in honor of the Lister Institute where she worked, have been suspected to be causative agents of disease underlying chronic and persistent infections. Although numerous publications exist characterizing their morphologies, growth requirements, and isolation from humans and animals with chronic infections the role of L-forms in disease has been difficult to ascertain. This, in part, is due to lack of understanding of the basic biology of L-forms and the circumstances favoring the transition of classical bacteria into L-forms."
"Additionally, the fact that L-forms can be obtained in vitro by multiple methods which can influence subsequent analyses and that multiple types of L-forms appear to exist, have made the design of a definitive study implicating these forms as causative agents extremely challenging. More importantly, difficulty in establishing standardization within the field has contributed to the lack of clarity in the field, which ultimately led to neglect and abandonment of research on these forms until recently."
The moral of this story: don’t assume too much from a press release. Read the original source before jumping up and down with excitement.
Posted by Relative Risk at 08:34 0 comments Links to this post
Labels: Lyme disease
An excellent review of Lyme disease diagnosis and treatment for continuing medical education in Europe. The summary conclusions are listed below.
Lyme Disease—Current State of Knowledge
Roland Nau, Prof. Dr. med., Hans-Jürgen Christen, Prof. Dr. med., and Helmut Eiffert, Prof. Dr. med. Dr. rer. nat.
Geriatrisches Zentrum, Evangelisches Krankenhaus Göttingen-Weende; Abteilung für Neurologie, Universitätsklinikum Göttingen
Kinderkrankenhaus Auf der Bult, Hannover
Abteilung Medizinische Mikrobiologie, Universitätsmedizin Göttingen
Background
Lyme disease is the most frequent tick-borne infectious disease in Europe. The discovery of the causative pathogen Borrelia burgdorferi in 1982 opened the way for the firm diagnosis of diseases in several clinical disciplines and for causal antibiotic therapy. At the same time, speculation regarding links between Borrelia infection and a variety of nonspecific symptoms and disorders resulted in overdiagnosis and overtreatment of suspected Lyme disease.
Conclusions
After appropriate antibiotic therapy, the outcome is favorable. In approximately 95% of cases neuroborreliosis is cured without long-term sequelae. When chronic borreliosis is suspected, other potential causes of the clinical syndrome must be painstakingly excluded.
Causative organisms
Acute and chronic infection in human beings can be caused by Borrelia burgdorferi sensu lato, of which the main types are Borrelia burgdorferi sensu stricto, B. garinii, and B. afzelii.
Probability of transmission
The probability of transmission to a person bitten by a tick is low in the first 24 hours of tick adhesion and then becomes markedly higher.
Antibiotics
The routine administration of antibiotics is not recommended after tick bites. It is currently debated whether antibiotics should be given under certain exceptional circumstances, e.g., multiple bites in a highly endemic area, but the necessary duration of antibiotic treatment has not yet been adequately studied in clinical trials.
Clinical entity
Lyme disease can affect many organs. The frequency of the individual clinical manifestations varies depending on the age of the patient, the infecting species, and other factors.
Acrodermatitis chronica atrophicans of Herxheimer (ACA)
Six months to several years after the tick bite, inflammatory skin lesions can develop, primarily on the extensor surfaces of the limbs, which undergo a transition to an atrophic stage of ACA.
Establishing the diagnosis
Lyme disease is a clinical diagnosis, i.e., clinical criteria (the history, symptoms, and physical findings) play the decisive role in the establishment of the diagnosis and the interpretation of serological findings.
The interpretation of serological findings
The less specific the patient’s symptoms, the lower the predictive value of a positive serological finding.
Neuroborreliosis
Clinically suspected neuroborreliosis is confirmed by the demonstration of CSF pleocytosis and of intrathecally formed specific antibodies (antibody index). The Borrelia-specific antibody index (AI) is determined for both IgG and IgM.
The inflammatory process in the central nervous system
The Borrelia-specific antibody index (AI) can still be negative in early stages of the disease. The criterion for the activity of the inflammatory process in the central nervous system is CSF pleocytosis.
Treatment
Lyme disease has a good prognosis. Most of its clinical manifestations are self-limited.
Serology
Because the serological findings vary widely, and because antibodies (including those formed in the central nervous system) persist for a long time, serological follow-up testing is not a suitable method for judging the adequacy of treatment.
Immunity
An infection with B. burgdorferi sensu lato is not followed by permanent immunity. Conclusively documented cases of clinically manifest reinfection have been described.
The choice of antibiotic
The choice of the antibiotic drug, its mode of administration, and the duration of treatment depend on the stage of the disease, the clinical manifestations, and the age of the patient.
Antibiotic treatment in children
Tetracyclines are contraindicated for children under 9 years old, because they can cause yellow discoloration of the teeth. Children in this age group with skin or joint manifestations are usually treated with amoxicillin.
"Post-Lyme borreliosis"
According to the findings of controlled studies, symptoms such as impaired performance, fatigability, impaired concentration, or chronic pain apparently do not arise any more frequently in persons who have had unambiguously documented Lyme disease than they do in normal control individuals.
Borrelia as a cause of rheumatic disease?
Current research is addressing the question whether a Borrelia infection can induce an autoimmune reaction of rheumatic type that persists after the elimination of the causative organism.
Sequelae
Persisting symptoms in the aftermath of Borrelia burgdorferi infection must be treated symptomatically (e.g., with anti-inflammatory agents or antidepressants).
Internet addresses for further information.
• Quality Standards for the Microbiological Diagnosis of Infectious Diseases (MIQ) from the German Society for Hygiene and Microbiology
• Guidelines of the German Neurological Society
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Posted by Relative Risk at 09:25 0 comments Links to this post
Labels: Lyme disease
JOURNAL OF WOMEN’S HEALTH
Volume 18, Number 10, 2009
Gary P. Wormser, M.D. and Eugene D. Shapiro, M.D.
Evidence from a variety of sources indicates that the term ‘‘chronic Lyme disease’’ is a misnomer and is often improperly used to diagnose patients who have illnesses completely unrelated to Borrelia burgdorferi infection. Our study found that patients with chronic Lyme disease were significantly more likely to be female than were patients reported to the Centers for Disease Control and Prevention (CDC) with Lyme disease (odds ratio [OR]=2.42, 95% CI 1.98-2.94, p<0.0001) or than were those with ‘‘post-Lyme disease syndrome’’ (OR=2.32, 95% CI 1.62-3.34, p<0.0001). These results suggested the likelihood that nonspecific illnesses with a female predominance, such as fibromyalgia, are being misdiagnosed as chronic Lyme disease. A recent publication by Hassett et al. corroborates both the findings and the conclusions of our report.
[snip]
In their letter, Stricker and Johnson [sorry, but I’m not directing readers to this crap.] hypothesize that the reason for the male predominance in Lyme disease is that the evidence-based interpretative criteria for immunoblot testing recommended by the CDC are in some way biased against women. This is a specious argument for many reasons.
First, a recent study explicitly demonstrated that there is no effect of gender on the results of serological testing for Lyme disease. Moreover, to our knowledge, gender bias in serological testing for infectious diseases is unprecedented.
Second, Stricker and Johnson appear to have overlooked the fact that>70% of Lyme disease cases reported to the CDC are based on the occurrence of erythema migrans (EM) only and, thus, are unrelated to any immunoblot result.
Considering only patients with EM, there is still a male predominance in reported cases (Paul Mead, CDC, personal communication, 2009). A similar male predominance is seen in a wide variety of other tick-borne and mosquito-borne diseases, consistent with an increased risk of exposure to arthropod bites among men.
In addition, in contrast to what Stricker and Johnson state, seropositivity was not in fact a requirement in the Krupp et al. study or in one of the two Klempner et al. trials. Contrary to what Stricker and Johnson assert, evidence convincingly shows that the alternative immunoblot criteria used by Donta to diagnose chronic Lyme disease are insufficiently specific to be useful clinically. Furthermore, the putative relationship of a decrease in CD57 natural killer cells to post-Lyme disease symptoms has been shown to be invalid.
Another day, another correction to the letter-writing antics of Stricker and Johnson.
Posted by Relative Risk at 12:11 0 comments Links to this post
Labels: Lyme disease, Stricker
"Searching for Persistence of Infection in Lyme Disease" is a highly innovative Bench-to- Bedside research project that could have an extraordinarily significant impact on the field of Lyme disease. Although antibiotic therapy is clinically effective in treating the symptoms of Lyme disease for most patients early in the course of disease, a significant number of patients who receive therapy report persistent symptoms. A range of theories have been proposed for why this occurs. Moreover, commonly available tests for human Lyme disease are not able to determine persistent infection after antibiotic therapy.
Program Director, Linden Hu, MD (Associate Professor of Medicine, Tufts University School of Medicine and Associate Professor of Microbiology, Sackler School of Biomedical Graduate Sciences) has begun an unconventional study examining whether xenodiagnosis (the feeding of uninfected Ixodes ticks on infected animals) can be used to determine when persistent infection occurs in humans. Xenodiagnosis has been used for other difficult to diagnose diseases such as Chagas disease and can sometimes definitively identify the presence of an organism in animals where other techniques cannot. Whether xenodiagnosis is effective in humans is unknown.
This two-year project seeks to test the utility of xenodiagnosis for identifying persistence of B. burgdorferi, the spirochetal bacteria that cause Lyme disease, after antibiotic treatment of the disease. Dr. Linden's team will test subjects with elevated C6 antibody levels or persistent symptoms after antibiotic therapy and patients with Lyme arthritis. Evidence that B. burgdorferi can be identified by xenodiagnosis after antibiotic therapy in subjects with continued symptoms would significantly change the current paradigm for potential mechanisms of disease and provide researchers and clinicians with a novel tool for identifying patients with persistent infection.
Well, activists have been whining for a better diagnostic test, but I wonder how many of them will be signing up for this one:
“We will perform biopsies of the EM site after completion of antibiotics and then allow 25-30 larval Ixodes ticks to feed on the subject. Repleted ticks will be collected, allowed to molt to their nymphal stage and then fed on severe combined immunodeficiency (SCID) mice. The repleted nymphal ticks and the SCID mice will be tested for the presence of B. burgdorferi by PCR and culture. Evidence of acquisition of bacteria by xenodiagnostic ticks in specific aim #1 would provide proof of principle that B. burgdorferi are able to persist after antibiotic therapy.”
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Posted by Relative Risk at 13:22 0 comments Links to this post
Labels: diagnostics, Lyme disease
One seldom mentioned problem with the National Academy of Sciences is that it’s full of elderly scientists who once upon a time did something interesting or important or both. Long past their prime, they continue to hang around the seminar rooms, pushing pet theories and waving their membership privileges like an AARP discount card.That seems to explain the famous (but elderly) Lynn Margulis and her recent spate of strange papers published with O. Brorson, the Norwegian scientist for whom every bleb and speck of debris spotted under a microscope is evidence of a spirochete doing something extraordinary. Here’s why he and Margulis are published in a recent issue of PNAS:
Now, at PNAS Three Papers in Question:
The science journal Proceedings of the National Academy of Sciences (PNAS) offers special publication privileges to members of their Academy, a group of elite scientists chosen by other esteemed scientists based on their unique contributions to science research. Now the editorial board has retracted some of those privileges in light of papers that recently appeared in the journal.
Nature News reported on a "row" caused when PNAS published research that didn't meet the journals' standards for peer review. The dispute is now heating up. The controversy began in August when one article published on-line at PNAS forwarded a theory by author Donald Williamson, all about what he called "larval transfer hypothesis".
[snip]
So how did the research get published, they asked, incredulous? The tale gets even more interesting. ...Lynn Margulis, an editor at PNAS who shepherded Williamson's work through the peer-review and publishing process.
[snip]
It turns out that Lynn Margulis "communicated" Williamson's paper to PNAS, a method of publishing offered to Academy members that differs from "submissions". Via this method, members can suggest for publication papers by non-members, along with reviewers selected by the member. PNAS recently announced it will eliminate this "Track I" publishing in 2010. In the meantime PNAS editors will not publish Williamson's paper in print edition pending further discussion with Margulis about the review process.
But now it's not just that paper. Another PNAS paper by Margulis and co-authors that's being questioned apparently proposes a treatment for Lyme disease that's "800" times more effective than doxycycline -- "it is very important to get this paper published", co-author Oystein Brorson told Nature.
A third paper in question is a computational biology paper by an adjunct professor of the Margulis lab. PNAS has asked Margulis to withdraw that paper because of problems with the methods. Margulis told Nature she would do no such thing.... The three PNAS papers all circle themes that Margulis has been pursuing for decades -- Spirochetes, desiccation, spores, symbiosis and more symbiosis than you'd ever believe, and disease.
Another 2009 paper has been published on-line in the (less well-known) journal Symbiosis (another journal that Margulis edits), by the same authors -- Hall, Brorson, Margulis and others. This "position paper" [an incredible piece of garbage thinking] proposes that antibiotic treatment of Lyme and Syphilis, both caused by Spirochetes, induces the formation of cysts, or "round bodies", that then revert to their original Spirochete form in a favorable (antibiotic free) environment, causing secondary infections, long-term human symbioses, and compromised immunity.
Although the abstract is pretty straight-forward, the paper quickly leaps out on a limb to suggest that AIDS is not caused by HIV but by Spirochete round bodies. Again, there's no evidence.
[snip]
The PNAS controversy is interesting, although it wouldn't leap out at everyone so much if the papers in question weren't so blatantly ludicrous. PNAS's publication "favoritism" is far from unusual in the science world. And really, Margulis has been publishing these ideas for years, drawing connections based on thin research (often foreign, often Russian, somehow lost on Americans), and asking the science community to run some experiments to test her ideas.
[snip]
Margulis: “All I ask is that we compare human consciousness with spirochete ecology." [What the f___?]
"All I ask". That was in 1991. But the gulf between what she "asks" and a warm reception from scientists has grown as science has advanced.
[snip]
Margulis has always published in PNAS. Some of the labs' older papers have similar themes and a little research. But it's a different world now. Margulis still has the prestige to gather a cast of characters around her in symbiotic relationships, to continue to push ideas out, and to entertain admirers like PZ Myers and his followers. But while her fame draws admirers and moths it also draws vipers, many of whom are now online.
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Posted by Relative Risk at 13:13 0 comments Links to this post
Labels: Lyme disease
From: Amyotrophic Lateral Sclerosis. 2009;10:248-50.
Lyme Disease Testing and Treatment
Background: A number of websites claim a causal link between ALS and Lyme disease. The websites are often sponsored by ‘‘Lyme literate clinics’’ specializing in the treatment of chronic Lyme, or by the sellers of products for Lyme, which they state can cause hundreds of misdiagnosed illnesses. The evidence for their proposed link between Lyme and ALS comes from poorly documented case reports or small series in which there is either insufficient evidence provided to establish a diagnosis of ALS in the first place, or inadequate follow-up to establish a true improvement in the ALS coincident with Lyme treatment. These Lyme literate clinics often state that the current standard of testing for Lyme (ELISA followed, if positive, by Western Blot) is inadequate, and they offer Lyme testing which they claim is better. We have seen no data to support the claim of superior testing.
Investigation: Ten ALS clinician-scientists from across the United States and Ireland have thus far shared their experiences with Lyme disease testing and treatment. All those weighing in use standard testing for Lyme, as is recommended by the American Academy of Neurology, the Center for Disease Control and the Association of State and Territorial Public Health Laboratory Directors. Only 3 clinician-scientists have routinely tested most or all newly diagnosed patients with ALS for Lyme, the other 7 test it only when there are other symptoms or signs of possible Lyme, or when a patient asks for it. In all, more than 4,000 newly diagnosed people with ALS (PALS) have been tested for Lyme by our group, with only 30 having had positive Elisa and Western Blot tests. Thus, in our experience, the incidence of positive Lyme disease testing in PALS is less than 1%, which is similar to the background incidence positive testing in people without ALS across the United States. Of the 30 PALS with positive Lyme tests, most were treated with intravenous antibiotics effective against Lyme for recommended durations, and none was ever seen to improve.
Recommendation: There is no convincing evidence that ALS can be caused by Lyme disease. PALS who exhibit symptoms of co-morbid Lyme disease can request standard, CDC-approved testing for Lyme from their neurologist, with the understanding that treatment of a positive Lyme test will not reverse their ALS. Until Lyme literate clinics can provide reasonable data supporting their claims, we do not recommend that PALS pursue evaluation or treatment in such clinics.
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Posted by Relative Risk at 06:18 0 comments Links to this post
Labels: diagnostics, Lyme disease
Hudson: Bad reaction to hysteria over swine flu
By Rev. J.F. Hudson, Spiritually Speaking
Thu Oct 15, 2009
[Excerpt]
Four years ago, I contracted Lyme disease. My doctor shared the blood test results with me, and then patiently and compassionately laid out my treatment. Then he took down one of his medical textbooks from the shelf, showed me where he had marked an article on Lyme disease and its causes and cures, and then handed the tome to me. “If you have any questions, call me or read this book. Do not go on the Internet!” Of course I did surf the Net when I got home and was immediately buried under thousands of sites, a few legitimate, but most created by “experts” offering many more scary opinions that true facts. So then I decided to listen to my doctor. I read the book. I took my medicine. And I got better.
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Posted by Relative Risk at 08:03 0 comments Links to this post
Labels: Internet, Lyme disease
I saw this little note posted on the LymeNut forum the other day. It’s from one of the moderators worrying about the fate of a webcast video from the recent IDSA hearing on the treatment guidelines for Lyme disease.
“I want to know if a copy of the video webcast is going to be made available to anyone but IDSA. Copies of it need to be held, so that it does not disappear.”
Why would it disappear? Probably all of the reviewers on the panel have copies for reference. As do a number of reporters. Yet this statement seems emblematic of the Internet-connected nuts who think they are plagued with a permanent infection that limits their social and financial lives to sitting in front of their computers and trolling the Internet for Lyme-related information 18 hours a day.
It reminds me of the Lyme activist who called my house one night and started the conversation with this question: “You’re not taping this are you?” To which I answered, “Ahh, you called me. I don’t pick up the phone with one hand and a tape recorder with the other.”
Yet, it’s common paranoia in LymeLand. They are always worrying about Internet trolls, imagining someone is hacking their computers, searching for their names, reporting their doctors to state licensing boards, and keeping tabs on everything they say and do and plan.
Frankly, I can’t think a more boring thing to do, but perhaps it makes them feel important or powerful if they imagine people are thinking about them and plotting against them. After all, Lyme disease is--to them--a vast conspiracy so there must be conspirators.
Paranoia aside, there’s also the near pathological use by activists of superlatives to describe the doctors who fleece…I mean treat…them. They are always described as “world- renowned,” “experts,” “noted experts,” a “nationally renowned Lyme disease expert,” a “leading Lyme doctor,” a “renowned Lyme expert and medical researcher,” “a leading authority,” “a renowned physician,” “a nationally renowned expert,” and “the world's leading Lyme pediatric specialist.” Their research--which is seldom published, almost never funded by federal agencies, is occasionally conducted in home basements, and is never reproducible--is described as “pioneering work,” and “pioneering research.”
Yet these quacks remain little known to people outside of the activist community and various state prosecutors and medical licensing boards. Their “research” is often paid for by activist organizations, is presented at activist meetings and is “published” in activist newsletters. (But then, so are their legal bills.) So why the superlatives? Why the outrageous accolades? I’m not sure. Maybe the activists and patients do it to make themselves feel better; to imagine associating themselves with someone and something better; simply to flatter; and maybe to lure more patients and members to the Lyme Movement with promises of expert advice and care. Whatever the motives, it’s all still delusion and deceit.
Finally, there are the lies.
It’s hard to find any accurate and honest information about Lyme disease on a Lyme-related website. Aside from spelling “Lyme” correctly, most of the information provided on activist and quack sites is repeatedly, regularly, consistently falsified. I’m thinking specifically of information about the sensitivity and specificity of diagnostic tests, the geographic limits of Lyme disease, the statements of Blumenthal regarding the settlement with the IDSA, and the IDSA’s recent statements about that settlement and the recent re-review of the IDSA treatment guidelines. Many of these activist statementsare easily dismissed with a quick review of the literature or the published statements of Blumenthal and the IDSA. But I guess they expect no one will check, and many of their backers won’t care. Still, a lie is a lie, and one wonders what the harm would be in occasionally admitting, “Yes, that’s true.”
Maybe that’s why right-wing radio and TV are so popular among society’s fringe: it’s the feel-good noise and not the factual basis that matters. The Right focuses on a limited target audience. I guess the Lyme Movementis doing the same, and any reality could only undermine that feel-good, self-righteous focus.
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Posted by Relative Risk at 01:53 0 comments Links to this post
Labels: Anti-science, LDA, Lyme disease
Hurrying home from work one night, I stopped at a Park St. station newspaper box to buy a paper to read on the T. I dropped in my coins, yanked open the door, and discovered I'd just bought a copy of the Boston Herald instead of the Globe. I closed the door and walked away sans newspaper.
By Boston Herald Editorial Staff
Thursday, September 24, 2009 - Added 1d 14h ago
We’re all in favor of reforming the medical malpractice system but not on a state-by-state, disease-by-disease basis.
So we can’t think of a less efficient way to ensure that Lyme disease patients in Massachusetts get proper treatment than by passing a state law that would shield doctors from disciplinary action or lawsuits if they happen to prescribe long-term antibiotics to their patients.
Talk about a special pleading. Can’t Beacon Hill just leave the doctoring to the doctors?
Yes, on Tuesday lawmakers took testimony on a bill that would protect those physicians who deviate from the recommendations of the Infectious Diseases Society of America when treating patients with Lyme.
The society recommends against long-term antibiotic treatment, according to the State House News Service, but some advocates say it’s sometimes the best option.
OK, fine, so there’s disagreement within the medical community over the best course of treatment for these patients.
But just how deeply into the weeds are Massachusetts lawmakers willing to go?
What about legislation for pediatricians who say it’s OK for children to watch a little television?
Or a whole separate law to protect the cardiologist who says the occasional cheeseburger won’t kill you?
Medical malpractice reform is urgently needed, but this doesn’t get us anywhere close.
Posted by Relative Risk at 11:35 0 comments Links to this post
Labels: Lyme disease, Politics
Debate continues over whether Lyme disease is a threat in Texas
September 21, 2009
By LINDSAY KALTER / The Dallas Morning News
Experts who say Lyme disease poses little threat in Texas are doubted by some patients, researchers and doctors in the area.
[snip]
Kocurek, 60, a lifelong Texas resident who lives in Colleyville, serves as officer and treasurer of the Texas Lyme Disease Association. He and many physicians believe that the risk of contracting Lyme disease in Texas is vastly underestimated. But other experts – representing mainstream thinking and backed by well-known medical journals – confidently say that it presents little or no threat to Texas residents.
[snip]
Dr. Justin Radolf, a professor at the University of Connecticut Health Center who previously worked at UT Southwestern Medical Center, is among the experts who say the risk in Texas is insignificant.
The key factor, he says, is that Texas does not have enough animals from which the disease-bearing ticks feed, or areas for them to reside. "You just don't have many wooded areas in Texas," he says. "It's very open. The vegetation is different than what's normally required to support the bacterium."
Durland Fish, professor of epidemiology at Yale School of Public Health, agrees. He says that even in the wooded areas of East Texas, the chance of getting Lyme disease is minimal. While deer ticks in the Northeast feed on humans, they have been shown to prefer reptiles in the South. And tests that seek nymphal-stage ticks – the main carriers of the bacterium – "hardly ever" collect them in the South.
The CDC classifies Texas as a low-to-no-risk area and reports that in-state cases have not exceeded 100 since 2002.
But Phillip Williamson, director for tick-borne disease research at the University of North Texas Health and Science Center in Fort Worth, sees two problems with those estimates. First, he says, standard methods of predicting Lyme disease are based on the number of deer ticks, which are rare in Texas. Williamson says this underestimates the actual risk.
[What? I hope for Williamson’s sake the reporter got this wrong because if the vector is rare, the bacteria must also be rare, and therefore locally-acquired cases of Lyme must also be rare.]
Secondly, for people to qualify as Lyme patients by the CDC, Williamson says they must register positive on two separate tests that he considers largely unreliable: the Enzyme-Linked Immunosorbent Assay (ELISA), which measures concentrations of a particular antibody, and the Western blot, which helps determine the molecular weight of a protein and measure amounts of the protein present. He argues that both tests look for antibodies to the Lyme bacterium, which he says is good at evading the immune system and changes often, producing antibodies that tests might miss.
[So he’s dismissing 30 years of research, not to mention the well-characterized immune responses to stable, conserved borrelial proteins. This is why serology looks at a number of different proteins or lipoproteins that provoke immune responses. B. burgdorferi is not B. hermsii, and even variable lipoprotein VlsE contains conserved sequences.]
Dr. Bessie Owens, a doctor of osteopathic medicine in Rowlett, says she sees about five Lyme disease patients each day, although she goes beyond standard methodology to identify the disease: In addition to using the Western blot, she tests for a vitamin D deficiency, which she says is common in Lyme patients. She also checks for a low natural killer-cell count; some doctors believe the production of these infection-fighting cells is suppressed by the Lyme bacterium.
[And she’s diagnosing “chronic” Lyme disease, and probably using Igenex in California. (August 23, 2005 NYT, Unproved Lyme Disease Tests Prompt Warnings. By DAN HURLEY and MARC SANTORA). And she’s seeing 5 patients a day? Strange. Texas has only had 37 reported cases so far this year. In 2008 the state had a grand total of 68. Maybe she only works 12 days a year.]
She says she has personal experience with the illness: In 2007 she was found to have degenerative arthritis and given steroid injections in her hands, which worsened her condition. Like Kocurek, she researched potential illnesses until she concluded that Lyme disease best explained her symptoms. She tested negative the first time around on the Western blot, but a later test came back positive. She is on three antibiotics and said her health is improving. Kocurek, who just finished up five years of antibiotics treatment, said he is nearly recovered.
[Amazing. Five years. Not even XDR-TB and Leprosy take five years to eradicate. What’s wrong with these people (mentally) and how much money does it take to buy five years worth of antibiotics?]
[snip]
Backed by established research, Radolf calls the natural killer-cell and vitamin D tests that Owens relies on "baloney." He believes there are doctors who loosely hand out Lyme diagnoses for the benefit of their practices.
But Owens says the exact opposite is true. "Lyme patients are very high-maintenance."
[I think she means they’re attention-seeking hypochondriacs who are easily exploited by doctors with “high-maintenance” practices.]
[spin]
Although the debate in Texas has not made headlines, controversy about Lyme disease has raged nationally.
Dr. Allen Steere, professor of rheumatology at Harvard University, is credited with discovering the disease in the late 1970s in Lyme, Conn. Radolf says that the controversy surrounding Lyme disease began in the late 1980s and reached a new level in the early 1990s, when Steere and colleagues said it was over-diagnosed. The backlash included death threats against Steere.
Each camp agrees that the chance of reconciling the differing viewpoints is nil.
Fish said there will always be sick people who wrongly believe that they are infected with Lyme. "They still have the Flat Earth Society," he says. "You can't argue with that kind of illogic."
Kocurek, who says his symptoms affected him socially and professionally for nearly his entire life, says too much emphasis in medical science has been on prevention, and insufficient research has been conducted on prevalence and treatment. "The most disturbing thing is that some of these physicians are absolutely brilliant, but they are so entrenched in dogma that they don't look at the literature critically."
[Mr. Kocurek is in no position to comment on the professional literature. He’s an amateur with an opinion based on hope and hype and misguided belief. It’s him, his fellow “patients” and their doctors who have a dogma and an agenda, and a distain for science and evidence. No doubt Mr. Kocurek wants to be better, to be free of whatever ails him, but he‘s unwilling to face the fact that might not ever feel any better than he does today and he‘s not willing to make that emotional leap to adjust, to cope, to carry on. Modern medicine isn‘t perfect. It can‘t fix every problem, every ache and pain--Christ, I wish it could--but that‘s no reason to embrace quackery and witchcraft.]
Radolf says while there are professionals who can respectfully disagree, the debate is becoming increasingly "nasty and contentious."
"It's reached a new peak of ferocity," he said.
[Well, the greed of these so-called “Lyme Literate“ physicians and the mental illness affecting people who think they have a chronic--if not permanent--infection will do that.]
Posted by Relative Risk at 11:32 0 comments Links to this post
Labels: Lyme disease, Politics
Well, it’s only been a few days since some ILADS priest has issued a polemic denouncing evidence-based medicine in general and the Infectious Diseases Society of America in particular.
This time ILADS quack, Elizabeth Maloney, has written “The Need for Clinical Judgment in the Diagnosis and Treatment of Lyme Disease” in the house organ of a right-wing medical group, the AAPS.
It’s the same old crap thinly disguised as reasoned analysis and argument.
First off, she attacks the insensitivity of serology in early stage Lyme disease. Well, yes, you need time to make antibody before you can measure antibody. Don’t blame diagnostics or the IDSA; blame Mother Nature. That’s just how the world--and immunology--works.
Then she’s on to the alleged insensitivity and specificity of current diagnostics in late stage Lyme, citing a couple of 15-year-old papers about Lyme testing. No mention of the diagnostic changes following the 1994 Dearborn Conference or the multitude of papers on serology and assays that followed. (Centers for Disease Control and Prevention. 1995. Recommendation for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR. 44:590-591.)
Next up, some arguments and citations suggesting long-term antibiotics and i.v. antibiotics are safe. But again, no mention of the cases of antibiotic-associated biliary complications among people with suspected Lyme disease or the horrific death of one individual at the hands of some clumsy, incompetent “Lyme Literate” doc (refs below).
Ceftriaxone-Associated Biliary Complications of Treatment of Suspected Disseminated Lyme Disease -- New Jersey, 1990-1992.
January 22, 1993. MMWR. 42(02);39-42
Clin Infect Dis. 2000 Oct;31(4):1107-9.
Death from inappropriate therapy for Lyme disease.
Patel, R et al.
No mention either of the 142,000 annual ER visits due to antibiotic adverse events, or the 20,000 annual community-acquired C. difficile infections caused by overuse or improper use of antibiotics.
Her best excuse for pumping antibiotics into people who think they have Lyme disease: “there is no test of cure.” Well, I’m hard pressed to think of a ‘test of cure’ for anything. Why not keep cancer patients on chemo indefinitely? Why not irradiate people indefinitely? Why not pump INH and rifampicin into TB patients for years and years beyond the standard 6-9 month timeframe? After all, there’s no definitive test to show that they’re free of every single cancer cell or mycobacterium.
The whole point of this paper--and every other op-ed, letter, commentary, and piece of fiction from ILADS and their patient supporters--is to again make the demand that “physicians should be free to act without interference….” Well, I’d like that right too. And I’m sure the police would too. And the FBI. And oil executives. And politicians. And Wall St. financiers….Oh, wait. They had that right, but it didn’t turn out too well for anyone but them.
Given their track record of patient lawsuits, federal sanctions, criminal charges, and license suspensions, I’m sure all these “Lyme Literate” quacks would like to be free of all legal, professional, financial and moral modes of interference. But that’s not going to happen. Ever.
Maloney laments the shortcomings of medical guidelines in general and the IDSA guidelines for Lyme disease in particular. So why is she a member of a group that bootstrapped their own treatment guidelines for Lyme disease? Better yet, why isn’t she advocating those ILADS guidelines instead of complaining about the IDSA guidelines? Why not try to promote the alternative guidelines? Is it because those guidelines are little more than a fig leaf for physicians to “act without interference?”
Maloney signs off noting she’s a physician from a “Lyme disease endemic area in Minnesota.” She can’t be very busy. According to last week’s MMWR there have been 67 cases of Lyme reported in Minnesota to date. In all of 2008, there were 330. Did she happen to treat all 330 last year or has she just neglected to report all her cases to the CDC like a good doc should?
Posted by Relative Risk at 11:27 0 comments Links to this post
Labels: diagnostics, ILADS, Lyme disease, Politics
Lyme disease patients rally for better diagnostic tests
Updated Sun. Sep. 20 2009
CTV.ca News Staff
Canadian Lyme disease patients are calling for better doctor training and more accurate tests so sufferers can be diagnosed and treated quickly before their side effects become crippling and chronic.
[snip]
This has always been a curious argument for me. Lyme patients want better Lyme diagnostics. But they’re already calling themselves Lyme patients so they or their doctors must have decided they have Lyme. Why do they need better diagnostics for a conclusion they have already reached?
Regarding the current diagnostics--which often show self-diagnosed Lyme patient they don’t have Lyme disease--most Lyme patient/activists insist the diagnosis of Lyme disease is a “clinical diagnosis” and not a laboratory diagnosis. So again, why the insistence on better diagnostics if the diagnosis is clinical and not laboratory-based? (The current serology-based assays are pretty sensitive and specific....once patient antibody begins to form. CID 2008:47 (15 October):1113)).
Ironically, any improved assays for Lyme are likely to show that most people claiming to have so-called “chronic” Lyme disease do not in fact have Lyme disease…and never did. What then? Most of the activist/patient groups are committed to a belief in chronic B. burgdorferi infections and the belief that all of their physical and emotional problems are the result of that chronic infection. What do they say in the absence of additional laboratory evidence?
Paging Dr. Hassett.
Posted by Relative Risk at 11:24 0 comments Links to this post
Labels: diagnostics, Lyme disease
Filmmaker revives discussion of Lyme diseaseSan Francisco Chronicle Sunday, September 13, 2009The first question filmmaker Andy Abrahams Wilson hears about his latest documentary: Lyme disease? Really?
Well, that’s probably because the things portrayed in his propaganda film bear no resemblance to the common bacterial infection called Lyme disease.
[snip]
"If this were HIV or West Nile virus," Wilson said, "we'd be doing everything we could."
So 30 years of federally funded research, clinical trials, education campaigns, and tens of millions of dollars spent is not enough? What, I wonder, would be enough? Especially, when you consider Lyme is non-fatal, non-communicable, geographically- and seasonally-limited and readily responses to common antibiotic treatments. As for HIV, it’s a communicable, ultimately fatal, viral infection currently ravaging large swaths of the developing world, and adding great expense to the healthcare costs of the developed world. West Nile is a usually mild viral infection (only 20% of infected people will show symptoms) that can sometimes cause serious post-infectious sequelae in older patients (West Nile Poliomyelitis, for example). As of September 8 this year, there have been 196 cases of WNV reported to CDC, and 6 deaths. Strange examples to compare with Lyme disease.
[snip]
As Wilson learned, patients are often misdiagnosed with maladies ranging from chronic fatigue syndrome to multiple sclerosis to Lou Gehrig's. Making the disease more difficult to identify, as many as 50 percent of all Lyme tests are inaccurate, and patients are often told their case is psychosomatic. Because there's no cure (antibiotics are an early treatment), many sufferers are left to treat their symptoms with no hope of solving the disease. "I uncovered a whole world of untold suffering," Wilson said. "And what seemed to me like a medical fraud."
No, patients are often misdiagnosed as having Lyme disease, thus delaying proper treatment of more serious conditions. Yes, there is a cure: antibiotics. But no, there is no cure for post-infection cartilage, nerve, or tissue damage. But then that’s true of all infections; no one grows back a toe lost to gangrene, no matter how many antibiotics they continue to swallow. As for “medical fraud,” well, there’s plenty of that among the private practice quacks who prey on people who think they have “chronic” Lyme disease. Wilson’s propaganda has probably greatly enriched them by bring more confused and worried patients to their offices.
[snip]
Wilson came to a multipronged conclusion. First, because Lyme is not easily defined and diagnosed, it's difficult to find a singular cure. Second, the best treatment can be antibiotics, which generate little profit for the big pharmaceuticals.
"But there is a lot of money in keeping people chronically ill," Wilson said, noting that steroids, painkillers and a slew of drugs can treat the symptoms of Lyme.
Wilson sounds like a idiot. Big Pharma isn’t treating patients, doctors are. They can order up all the generic antibiotics they want. And charge whatever they want. But most don’t knowing that persistent symptoms following an infection are usually the result of permanent damage from that infection. Treatment then may involve common anti-inflammatory agents and pain meds such as gabapentin.
The only people getting rich from Lyme disease are the so-called “Lyme Literate MDs” heroically portrayed in Wilson’s cinematic commercial for their services. And maybe Wilson myself. His film seems to be advertised on the web sites of most Lyme activists and predatory quacks.
[snip]
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Posted by Relative Risk at 11:49 0 comments Links to this post
Labels: Film, Lyme disease, Quackery
September 10th, 2009
(PhysOrg.com) -- Lyme disease has become a major public health issue in the northeastern United States since it was first identified in Connecticut in the 1970s. But the scientific community is uncertain as to why the risk of Lyme disease is so much higher in the northern part of the country than elsewhere.
To examine the reasons for the unexpected geographic distribution of the disease, theNational Science Foundation has awarded a four-year, $2.5 million grant to scientists from a consortium of five universities including the University of Rhode Island.
“These ticks are on the move,” says Dr. Jean Tsao of Michigan State University, who will lead the study. “As ticks expand into new areas, more people will likely become infected.”
Findings from this study will help public health agencies develop better prevention strategies for Lyme disease, which the Centers for Disease Control and Prevention reports infects more than 20,000 people in North America each year.
[snip]
The researchers plan to study ecological and disease factors affecting the Lyme disease cycle by applying standardized survey methods at twelve sites in states ranging from Georgia to Massachusetts. “Lyme disease is a major public health problem, and the reasons for its changing geographical distribution raise serious questions,” said Howard Ginsberg, a research ecologist for the U.S. Geological Survey and professor-in-residence at URI. “The questions are medical, but the answers are ecological. The knowledge to be gained from this project will help us better predict the future distribution of this disease, and lower the risk to human health.”
A number of hypotheses have been put forward to explain why the disease agent is rare in southern tick populations. “Some scientists think that the tick’s lifecycle differs in the southern climate in ways that interfere with disease transmission,” said URI Entomology Professor Roger LeBrun. “Others point to the abundance of lizards in the south. The ticks love the lizards, but many of them are unsuitable hosts for the Lyme bacteria. Furthermore, southern ticks differ genetically from their northern cousins. Any of these factors might contribute to disease distribution, but it will take a lot of work to sort them out.”
[snip]
Posted by Relative Risk at 11:53 0 comments Links to this post
Labels: Emerging Infections, Lyme disease
Exactly what you’d expect a bunch of self-selected, like-minded people to say when asked leading questions.
Below is part of a comment by Lorraine Johnson, a Lyme disease activist and apparent lawyer, about an online survey put together to collect meaningless responses from Internet-connected Lyme activists and patients.
Ask the Lyme community a question, or two or 30 and they answer! When we asked for input before the IDSA Lyme hearing, we had 3,600 completed surveys within 2 months—that’s astounding! I want to thank everyone who participated. The survey results provide very important information for the Lyme community and will be useful to describe the extent of the problem that patients have being timely diagnosed, treated, reimbursed, seriously ill and the devastating effect the guidelines have on patients health.
Those of you who listened to my speech before the IDSA review panel know that I used the survey data to reinforce key points. This survey should be a powerful tool with public policy makers trying to understand the devastating impact these guidelines have on patient care and the need for curb the effects of these guidelines through legislative and other means. The full results of the survey can be downloaded by clicking on the attachment at the end of this blog post.
Once again, she is confusing the opinions of like-minded people with evidence. I’ve discussed this before and the central problem is people like Johnson and her activist cohort simply do not believe in evidence. Her survey is not a tool, it’s not evidence, it’s not data. It’s opinion. It’s belief. It’s useless except perhaps as a feel-good exercise in delusion.
The problem may be compounded by the fact that Johnson is a lawyer. This is a profession in which people are trained to ignore evidence, to question evidence, to distort evidence, but to never accept what the scientific and medical community regards as evidence. Otherwise, what would be the point of having lawyers?
(Interestingly, her usual pamphleteering partner, Ralph--Want a bigger penis--Stricker, also has some difficulties with evidence as indicated by an earlier NIH finding on scientific misconduct. Maybe he helped draft the survey.)
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Posted by Relative Risk at 11:39 0 comments Links to this post
Labels: Anti-science, Internet, Lyme disease, Quackery
Lyme Literate Physician Recommends Taking a Photograph of Any Unusual or Bulls-Eye Rash to Assist in Proper Lyme Disease Diagnosis and Testing
Havertown, PA (PRWEB) September 9, 2009
Lyme disease is often called the great pretender because early symptoms may seem like the flu. That's why it's important to stay on the alert for the classic Lyme bulls-eye rash, or any other unusual rash", advises Lyme expert Domenic Braccia D.O, "if you see an unusual rash, take a photograph and make an appointment to see your physician. Taking a wait-and-see attitude before reporting the tell tale "bulls-eye" rash of the deer tick bite can be dangerous".
This is part of an online PR piece from the Haverford Wellness Center. Sounds like good advice, though you might want to keep the cameras and mics rolling during your visit. The Center seems to have the kind of press attention that no amount of self-promotion can paper over.
For starters, there’s former inmate Dr. Lionetti. Then there’s not-quiet-Dr. Kane. I like the CBS Philadelphia affiliate report about her: “I-Team Follow-Up: False Hope. There are major developments in the wake of CBS 3 I-Team Investigation of a local woman who calls herself a doctor.”
Posted by Relative Risk at 09:00 0 comments Links to this post
Labels: Lyme disease, Quackery
Thursday, September 10, 2009
Scam artists used Lyme disease to scare victims, feds allege
The U.S. Attorney for Kansas says a California woman, Carole E. Bradford, has been indicted in an alleged Lyme disease scam that also included others, including her husband. Here's how it reportedly worked:
The 20-count superseding indictment alleges Carole E. Bradford and the other defendants conspired to violate the federal Food, Drug and Cosmetic Act by conspiring to sell a microscope that supposedly would diagnose Lyme disease, as well as drugs that supposedly would cure the disease.
They distributed marketing materials making false claims that Lyme disease was “the plague of the 21st century” and was a contributing factor in 50 percent of all chronic illness including Chronic Fatigue Syndrome.
Carole E. Bradford’s husband, Robert W. Bradford, claimed to be a “doctor” and a “professor” even though he was not a physician and had no science degrees from an accredited university in the United States. He was the inventor of what he called “the Bradford Variable Projection Microscope,” which he claimed could be used to identify Lyme disease.
Toth, who was a licensed medical doctor in Kansas, used Bradford’s microscope and treatments, charging patients approximately $100 for each use of the equipment and approximately $320 for a series of injections he called “antimicrobial treatment.” In March 2008 in Shawnee County District Court, Toth was sentenced to 32 months in prison after pleading no contest to a state charge of reckless involuntary manslaughter in the death of a patient, Beverly A. Wunder.
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Posted by Relative Risk at 08:56 0 comments Links to this post
Labels: Lyme disease
I was never much interested in taxonomy so I’m not surprised to have lost track of new developments in Borrelia nomenclature. Fortunately, the blog, Spirochetes Unwound(Blogging about those twisty bacteria known as spirochetes) has a brief update. Here’s some of it:
The number of named species of B. burgdorferi sensu lato found worldwide now stands at 14:
• B. burgdorferi sensu stricto
• B. garinii
• B. afzelii
• B. andersonii
• B. bissettii
• B. californiensis
• B. carolinensis
• B. japonica
• B. lusitaniae
• B. sinica
• B. spielmanii
• B. tanukii
• B. turdi
• B. valaisiana
Posted by Relative Risk at 04:03 0 comments Links to this post
Labels: Lyme disease
Posted on the wackjob website, LymeNet:
I saw my LLMD today and we discussed many things but for now i wanted to pass along that she told me that Columbia University had indentfied the Lyme strain/surface protein that causes Chronic Lyme. She was emphatic about this news.
She expects testing for this strain to be available in weeks!!!! I checked the website and this news is not published yet. My doctor would have an inside track as she supported this research and had candidates blood drawn at her office.
Stands to reason if you can isolate the strain than a more narrow scope of research for a cure can be conducted. More to follow ...but she fully excepcts the test to be available by my next visit in October.
Right. This is how major research findings are released by universities: Someone tells someone else who whispers it to an ignorant patient who posts it on the Internet. I’m sure this how the results of the Kenyan malaria vaccine trials will be revealed, along with CERN’s discovery of the Higgs Boson.
There’s just so much wrong with this “exciting news” I don’t know where to begin. Let’s just skip the analysis and jump to the conclusion that this quack he’s seeing is setting him up for some expensive new tests, fake diagnostics and some more expensive treatments for an undefined condition called “chronic Lyme disease.”
But maybe “chronic Lyme disease” is a win-win situation for both the patient and the doctor. The patient does not get better or worse. The doctor collects a lot of money. The patient gets the attention he or she craves….at least until the money runs out. I guess by then they’re cured.
Waiting breathlessly for further word from Columbia.
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Posted by Relative Risk at 01:37 0 comments Links to this post
Labels: diagnostics, Lyme disease
Reminder: Don't confuse a common infection with a fatal neuromuscular disease.
Muscle Nerve. 2009 Aug 20.
Lyme disease serology in amyotrophic lateral sclerosis.
Qureshi M, Bedlack RS, Cudkowicz ME.
Neurology Clinical Trials Unit, Massachusetts General Hospital, Harvard Medical School, 13th Street, Building 149, Room 2274, Charlestown, Massachusetts
Lyme disease is sometimes part of the differential diagnosis for amyotrophic lateral sclerosis (ALS). Herein we report on 414 individuals with ALS at the Massachusetts General Hospital who underwent laboratory testing for Lyme disease. Twenty-four (5.8%) were seropositive, but only 4 (0.97%) had confirmed past immunoreactive infection. Two of these patients received ceftriaxone for 1 month without clinical improvement. Lyme disease was rare in 414 patients with ALS and is not likely to be causative.
Posted by Relative Risk at 01:33 0 comments Links to this post
Labels: diagnostics, Lyme disease