A history of bad science by bad scientists

[WillemT]

Relative Risk is een blogger die zich met Lyme bezig houdt. Hij stelt zich in het algemeen zeer kritisch op als het over zgn. lymespecialisten (LLMD's) en activistische groeperingen in de VS gaat.
Hieronder een gedegen stuk, dat een nuttig kijkje in hun ondeugdelijke activiteiten geeft. De titel van het stuk is veelzeggend.

24 August 2013
A history of bad science by bad scientists


I pulled this off the LymeNet Europe board.  It’s a list of publications that have punctured holes in the claims and theories of self-styled “Lyme literate” doctors.  Every time some quack comes up with a new way to diagnose Lyme or tries to associate Lyme with some complex neurological illness competent, credible scientists try to replicate their results…and fail.  That’s how science works, but Lyme activists and their quack doctors don’t much like it. 

I’ve added a few more examples to the original list. 

The recent failure of CDC scientists to replicate the findings of Sapi and the ALS culture methods is just the latest in a consistent history of similar failures.  Each time the Lyme community concocts some new methodology or clinical association related to Lyme disease reality intrudes in the form of irreproducible results, bad technique, and wishful thinking.  And what are the reactions among Lyme activists and their LLMDs to these documented counter-findings?  Outrage.  Accusations. Conspiracy theories.

ALS/Sapi Culture Methods.
Johnson BJ, Pilgard MA, Russell TM.  Assessment of New Culture Method to Detect Borrelia species in Serum of Lyme Disease Patients.  J Clin Microbiol. 2013 Aug 14.

Delong’s reinterpretation of the NIH clinical trials.
Klempner MS, et al.  Treatment trials for post-lyme disease symptoms revisited. Am J Med.2013 Aug;126(8):665-9.

Bransfield’s Autism-Lyme Linkage.
1.  Burbelo PD, et al. Lack of serum antibodies against Borrelia burgdorferi in children with autism. Clin Vaccine Immunol. 2013 Jul;20(7):1092-3.
2.  Ajamian M, Kosofsky BE, Wormser GP, Rajadhyaksha AM, Alaedini A. Serologic markers of Lyme disease in children with autism. JAMA. 2013 May 1;309(17):1771-3.

Stricker’s CD57 Counts.
Marques A, Brown MR, Fleisher TA. Natural killer cell counts are not different between patients with post-Lyme disease syndrome and controls. Clin Vaccine Immunol. 2009 Aug;16(8):1249-50.

Phillips’ “Detroit Water” Cultures.
Marques AR, Stock F, Gill V. Evaluation of a new culture medium for Borrelia burgdorferi. J Clin Microbiol. 2000 Nov;38(11):4239-41.

MacDonald’s Alzheimer Findings.
Marques AR, Weir SC, Fahle GA, Fischer SH. Lack of evidence of Borrelia involvement in Alzheimer's disease. J Infect Dis. 2000 Sep;182(3):1006-7.

Causal relationship between amyotrophic lateral sclerosis (ALS) and Lyme disease.
1. Qureshi, M, Bedlack, RS, and Cudkowicz, ME. Lyme disease serology in amyotrophic lateral sclerosis. Muscle and Nerve 40: 626-628, 2009.
2. The ALSUntangled Group. ALSUntangled update 1: investigating a bug (Lyme Disease) and a drug (Iplex) on behalf of people with ALS. Amyotrophic Lateral Sclerosis 10: 248-250, 2009.

Lyme Urine Assay (LUAT).
Klempner MS, Schmid CH, Hu L et al. Intralaboratory reliability of serologic and urine testing of Lyme disease. Am J Med. 2001;110(3):217-9

Bowen Institute Q-RiBb.
1. Caution regarding testing for Lyme disease. MMWR 2005;54(05):125.
2. Unorthodox and unvalidated laboratory tests in the diagnosis of Lyme borreliosis and in relation to medically unexplained symptoms.  Prof. Brian I. Duerden, Inspector of Microbiology and Infection Control, Department of Health, U.K. 2010.

Unorthodox applications and interpretations of immunoblots.
1. Halperin JJ, Logigian EL, Finkel MF et al. Practice parameters for the diagnosis of nervous system Lyme borreliosis. Neurology 1996;46(3):619-27
2. V. Seriburi, N. Ndukwe, Z. Chang, M. E. Cox and G. P. Wormser. High frequency of false positive IgM immunoblots for Borrelia burgdorferi in Clinical Practice. Clin Microbiol Infect.2012 Dec;18(12):1236-40.
3. Notice to Readers: Caution Regarding Testing for Lyme Disease.  MMWR.  February 11, 2005 / 54(05);125.
4. Johnson, BJ.  Laboratory Diagnostic Testing for Borrelia burgdorferi Infection. In Lyme Disease: An Evidence-based Approach, (ed. J.J. Halperin). CAB International 2011.

WillemT

[Tulipano]

Willem, dit is geen forum voor anti Lyme propagandisten. Als je onderstaande quote van R.R. even doorneemt dan begrijp je misschien wat ik bedoel. Voor jou kunnen de beweringen van R.R. veelzeggend zijn, veel (chronische) Lymepatiënten denken daar waarschijnlijk anders over.

The Web already is full of their nonsense about B. burgdorferi and Lyme disease. According to the gigabytes of data dumped into the WWW, Lyme is:

fatal
Causes autism, faked diseases (Morgellons), suicides, rage, and other anti-social behaviors,Is contagious,


But that is the goal of Lyme activists and their quack enablers: to turn a common bacterial infection that is antibiotic-responsive, non-fatal, non-communicable, and seasonally- and geographically-limited into the Andromeda Strain of the 21st century.

One would think that with such a monstrous plague on the loose Lyme activists would be screaming for a preventive vaccine. And they did. Once. Until they realized that it might lead to less hysteria, fewer people claiming to have Lyme disease and therefore fewer followers, and an evidence-based definition of Lyme disease instead of the undefined catch-all, “chronic Lyme disease”. Now they’re screaming to stop any idea of a second Lyme vaccine.


And isn’t that odd? A deadly, unstoppable, incurable plague sweeping across the collective imaginations of the activists, but they don’t want a vaccine that might ameliorate said plague. Imagine AIDS or cancer activists making such nonsensical demands. The only consistent demands the Lyme activists have made to date concern money and power. Sound familiar?

They want someone else to pay for their various ineffective treatments. In effect: a transfer of wealth from insurers and their customers to a small cadre of quacks, many of whom have been sued by their own patients, jailed for fraud or patient endangerment, and censured by medical boards. And they want disability payments, which amounts to another transfer of wealth from the taxpayer to the allegedly infected. Finally, they want political control of federal spending for Lyme disease in order to prevent prevention in the form of vaccines, punish the well-known researcher they have spent decades hating, and reward the quacks who re-enforce their anti-science, anti-vaccine beliefs.

Sounds like a run-of-the-mill scheme for money and power. It’s just that this one, strangely enough, involves a common bacterial infection that is antibiotic-responsive, non-fatal, non-communicable, and seasonally- and geographically-limited. Who would have guessed?

http://relative-risk.blogspot.nl/2014/0 ... to-be.html

R.R. kan zich beter niet met Lyme bezighouden want ondanks alle kritiek komt hij/zij zelf niet met iets beters. Derhalve geeft het gewauwel van deze blogger mijn inziens geen enkele toegevoegde waarde.

Off Topic!

[Foetsie]

I pulled this off the LymeNet Europe board

Die Relative Risk is zeker net zo'n troll als die Willem T.
De hele dag alle berichten van iedereen zitten nakijken terwijl je zelf nieteens ziek bent.
Volgens mij ben je dan niet helemaal goed.
Of misschien worden ze er voor betaald?




Als hobby zou ik dan iig toch iets anders verwachten, vooral van mensen die zichzelf zo intelligent vinden.

[WillemT]

Willem, dit is geen forum voor anti Lyme propagandisten

Beste Tulipano,
Kennelijk wil je bepaalde opvattingen niet toelaten. Dat heet censuur.
Ik wordt gekwalificeerd als “anti-Lyme propagandist. Ik vind dit een rare uitdrukking, alsof je voor of tegen een ziekte kunt zijn.
Vermoedelijk bedoel je dat ik het bestaan van de ziekte die op dit forum meestal wordt aangeduid als “chronische Lyme” in twijfel trek. Dat klopt en de redenen daarvoor zijn zeer voor de hand liggend.
Er bestaat geen definitie van de ziekte van Lyme. Ook degenen die wel in het bestaan van “chronische Lyme” geloven, zoals zgn. lymespecialisten kunnen geen definitie geven, zie bijvoorbeeld de ILADS richtlijn. Ook op dit forum valt geen definitie ervan te lezen
Als er geen definitie van “chronische lyme” bestaat kan er logischerwijs ook geen diagnose worden gesteld.
Een therapie voor “chronische lyme” die vervolgens wordt toegepast is dus gebaseerd op een onjuiste diagnose. Dat is dus verkeerd.
Een groot misverstand is dat de betrokkenen patiënt geen gezondheidsprobleem zou hebben: het deugt niet als gezegd wordt :“ hij/zij stelt zich aan, hij/zij heeft een ingebeelde ziekte” etc. Het gevaar bestaat dat de verkeerde therapie schadelijk voor de patiënt is, bijvoorbeeld langdurig, bovenmatig gebruik van antibiotica
Het “geloof” in het bestaan van “chronische lyme” wordt zo krachtig mogelijk in stand gehouden door de zgn. lymespecialisten. Dat is begrijpelijk omdat zij een direct groot belang hebben bij het in stand houden van dat geloof.
De literatuurbronnen die in het stukje van Relative Risk genoemd verwijzen alle naar serieus onderzoek naar de ondeugdelijkheid van hun claims.

WillemT

[Tulipano]

Beste Willem,

Een anti Lyme propagandist is voor mij iemand die de Lymepatiënt niet serieus neemt en er de gek mee steekt zoals blogger R.R. doet. Als je het door mij gequote stukje aandachtig leest en een beetje objectief, bent, dan zul je dit toch moeten toegeven.

Hoe kun je stellen dat de ziekte van Lyme/Borreliose een doodgewone bacteriële infectie is die zeer goed te bestrijden is met antibiotica terwijl er al d.m.v. diverse studies is aangetoond dat Lyme persisteert na een antibiotica behandeling (ik refereer nu o.a. aan de Embers apenstudie en de Barthold muizenstudie maar er zijn ook studies met patiënten bekend waarbij dit is aangetoond zoals de discutabele xenodiagnose studie die je hier op 'wetenschap' kunt terugvinden).

Hoe kun je stellen dat Lyme niet fataal is en niet kan leiden tot zelfmoord als we er inmiddels al diverse schrijnende voorbeelden van hebben! Heb je het topic al gelezen Willem? viewtopic.php?f=5&t=8253

Hoe kun je stellen dat de Lymepatiënt graag een diagnose 'chronische Lyme' krijgt zodat hij dan een uitkering kan aanvragen terwijl er talloze hondsberoerde patiënten dolgraag aan de slag zouden willen maar het fysiek en mentaal eenvoudigweg niet meer kunnen opbrengen? Was mr./mrs. R.R. die beruchte avond misschien ook aanwezig in het Denkcafe te Rotterdam?

Hoe kun je je beklag doen dat Lymepatiënten anderen willen laten opdraaien voor de kosten van hun (niet effectieve) behandelingen en een kostenplaatje vertegenwoordigen voor de belastingbetalers?
Op de eerste plaats zijn Lymepatiënten ook belastingbetalers en op de tweede plaats hebben zij niet voor niets een zorgverzekering afgesloten.

Mr./Mrs. R.R. zou zich beter druk kunnen maken om het geld dat de schijnheilige Amerikaanse overheid uit haar burgers heeft gezogen om zinloze oorlogen te kunnen voeren en om de corrupte banken overeind te houden die het spaargeld van diezelfde belastingbetalers hebben weggesluisd in louche beleggingen en foute formules waardoor niet alleen de Amerikaanse doorsnee burger maar ook de Europeanen verzeild zijn geraakt in een ongekende economische malaise!

En jij wilt stellen dat deze blogger zich kritisch opstelt? Laat me niet lachen Willem. Voor mij is iemand kritisch als hij het lef heeft om toe te geven dat de partij waarvoor hij/zij zelf staat ook steken laat vallen en tot nu toe met niets beters of concreets is komen aankakken. Voorlopig moeten we dealen met onbetrouwbare two tier testen en een groot aantal artsen die nog steeds geen fatsoenlijke kennis hebben van onze ziekte waardoor patiënten het risico lopen om, jawel, CHRONISCHE lyme te ontwikkelen.

Dat er kwakzalvers zijn geef ik grif toe. Maar ook een overheid en/of artsen die onbetrouwbare testen in stand houden zijn kwakzalvers. In plaats van het investeren in betere diagnostiek worden er kosten nog moeite gespaard voor de ontwikkeling van een Lymevaccin. Want dat brengt pas goed geld in het laatje. Jammer dat de (chronische) Lymepatiënt daar niets aan heeft. En zeg nou zelf Willem, waarom een vaccin ontwikkelen (met al z'n mogelijke bijwerkingen) voor wat volgens mr./mrs. R.R. een 'doodgewone' bacteriële infectie is die zo goed op antibiotica reageert en niet chronisch kan worden?

Jij hebt geen Lyme Willem en ik ben blij voor je. Maar wij zijn helaas de ervaringsdeskundigen. Jammer dat dit er zo moeilijk in wil bij het groepje dat mogelijk door jou wordt geclassificeerd als 'good scientists'.

(P.S. Willem, heb diverse linkjes beschikbaar van studies die chronische Lyme bevestigen, mocht je het op prijs stellen. Oh ja, en probeer niet het slachtoffer te spelen door het woord 'censuur' te gebruiken. Wie in werkelijkheid gecensureerd worden zijn de lymepatiënten die niet serieus worden genomen.)

[RobertF]

WillemT schreef
Als er geen definitie van “chronische lyme” bestaat kan er logischerwijs ook geen diagnose worden gesteld.

Wat een onzin kraam je uit.!!!!

De ziekte van Lyme of liever borreliose is een infectie met de borrelia bacterie. Het is heel goed mogelijk om een voortdurende chronische infectie aan te tonen.

Omdat het geen naam heeft bestaat het niet, wat een redenatie.!!!!

Het laat weer eens zien dat jouw bijdrage hier op het forum niets toevoegt. Dus

[Tulipano]

Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and both define tertiary neurosyphilis or tertiary Lyme neuroborreliosis. The use of chronic and late Lyme neuroborreliosis as different entities is inaccurate and can be confusing.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3551238/

[savan]

De grootste KWAKZALVERS zijn vooralsnog degenen die zichzelf op de maak van de richtlijnen gestort hebben.
Misschien kan het CBO ook even HLA DR-1, HLA DR-2, en HLA DR-4 uitsluiten voordat de kwek opengaat.

In Berlijn zijn ze allang bekend met dit gegeven:

http://www.imd-berlin.de/leistungsschwe ... ostik.html

[WillemT]

In het onderstaande stuk, eveneens afkomstig van de weblog van RelativeRisk, wordt meer gedetailleerd de stelling dat "chronische lyme" niet bestaat toegelicht.

Chronic Lyme disease: the controversies and the science.
Expert Rev. Anti Infect. Ther. 9(7), 787–797 (2011)
Paul M Lantos, Departments of Internal Medicine and Pediatrics, Duke University Medical Center.

Does chronic Lyme disease exist?
Most patients who are diagnosed with chronic Lyme disease have prolonged somatic and/ or neurocognitive symptoms, such as fatigue, arthralgias or memory impairment, but usually lack the objective findings classically associated with Lyme disease.  The term ‘chronic Lyme disease’ implicitly suggests that these symptoms are caused by infection with B. burgdorferi, and it is often argued that infection with this organism may become persistent despite antimicrobial therapy. These assumptions, however, have not translated to any accepted clinical, pathologic or microbiologic definition of the term.  One clinical practice guideline devoted to the management of chronic Lyme disease included a provisional definition so broad that Lyme disease could not be differentiated from the myriad other medical conditions [ILADS].  Without a definition, the term lacks meaning and it becomes fruitless to debate about whether or not ‘chronic Lyme disease’ exists as such.

Unable to precisely say what chronic Lyme disease is, we must next examine the features of patients referred for Lyme disease to discern whether there emerges a subset who have verifiable Lyme disease, and who appear to have chronic, treatment-refractory infection.  In seven studies conducted in endemic areas, comprising a total of 1902 patients referred for suspected Lyme disease, only 7–31% had active Lyme disease and 5–20% had previous Lyme disease.  Among the remainder, 50–88% had no evidence of ever having had Lyme disease.  Most of these patients had either an alternative medical diagnosis or a functional somatic syndrome such as chronic fatigue syndrome or fibromyalgia.

A substantial number were diagnosed with Lyme disease based on an inability to make an alternative diagnosis – referred to in one paper as ‘diagnosis of Lyme disease by exclusion’. Primary psychiatric diagnoses, psychiatric comorbidity and psychological traits such as catastrophization and negative affect are also common.  Many had symptoms of long duration and had received multiple courses of antibiotics directed at Lyme disease. Similar observations were made in Vancouver, British Columbia, where Lyme disease is very rare; of 65 patients referred for Lyme disease, 61 had either an alternative medical diagnosis or a functional somatic syndrome, and nine had a primary psychiatric diagnosis.

Post-Lyme disease syndromes
The designation ‘post-Lyme disease syndromes’ has been proposed to describe patients who experience prolonged subjective symptoms following Lyme disease.  It is more properly thought of as a means of categorizing this patient cohort, rather than describing a clinical diagnosis.  The case definition of post-Lyme disease syndromes differs from ‘chronic Lyme disease’ chiefly in its requirements that patients have: unequivocal documentation of appropriately-treated Lyme disease; and persistent subjective symptoms that cannot be explained by other medical illnesses. The definition contains abundant exclusion criteria.

The rarity of post-Lyme disease syndromes is exemplified by the great difficulty three investigative teams had in recruiting subjects for clinical trials investigating this condition. Of 5846 patients screened over several years, only 222 (3.8%) could ultimately be randomized, a striking finding given that most of the 20,000 annual cases of Lyme disease occur in the region where these studies are conducted.  The dominant reason for this is that very few of the screened patients had documentation of prior Lyme disease. This suggests that the attribution of chronic symptoms to Lyme disease is grossly out of proportion to its actual occurrence.

Biological plausibility
No adequately controlled, hypothesis-driven study using a repeat­able method has demonstrated that viable B. burgdorferi is found in patients with persistent post-Lyme symptoms any more frequently than in those with favorable outcomes.  In three clinical trials, com­prising more than 150 subjects with strictly-defined post-Lyme disease symptoms, no patient was found to have positive culture or PCR of cerebrospinal fluid.  However, these studies were unique in that they investigated evidence of persistent B. burgdorferi infection in a prospectively defined group of chronically ill subjects.  Other sources of data include case reports and case-series, which however compelling are inherently incapable of testing a hypothesis. Advocates of chronic Lyme disease contend that our ability to detect the organism is hampered by current technology and an incomplete scientific understanding of B. burgdorferi, and that conventional diagnostic testing misses patients with chronic Lyme disease.  However, this begs the question of on what microbiologic basis we assume that chronic B. burgdorferi infection exists at all.

As there is a lack of evidence that post-Lyme disease patients remain infected with B. burgdorferi, it is perhaps not surprising that the duration of initial antibiotic therapy does not influence the persistence of subjective symptoms.  A prospective trial of therapy for 180 patients with early Lyme disease found that after 30 months, neuropsychologic deficits were equally common among patients treated for 10 versus 20 days.  In a retrospective study of 607 patients treated for early Lyme disease, 99 ± 0.2% of patients were well after 2 years of follow-up, regardless of whether they had received less than 10, 11–14 or greater than 14 days of therapy. In a randomized, open-label trial of therapy for late Lyme disease, patients treated for 14 days were no more likely to have severe symptoms than those treated for 28 days – despite the fact that objective treatment failures were significantly more likely in the 14‑day arm. Lengthy courses of antibiotics, meant to prevent the development of persistent symptoms, are no more effective than conventional courses.  Following 3 weeks of parenteral cef­triaxione, an additional 100 days of oral amoxicillin was no better than placebo at improving cognitive and somatic outcomes. 

Conclusions
Two important research gaps are: what pathophysiologic mech­anisms underlie chronic pain and chronic fatigue?; and what nonantibiotic modalities are helpful for patients with post-Lyme disease syndromes?  The former is an area of tremendous gen­eral interest given the ubiquity of such symptoms in the general population.  The latter is a puzzlingly understudied field, but it has promise to improve the lives of many who suffer chronic symptoms attributed to Lyme disease – whether or not a history of Lyme disease is ultimately to blame.  Furthermore, these may be far safer than prolonged antibiotics and indwelling vascular access devices. A variety of such interventions have proved use­ful in patients with functional pain syndromes, chronic fatigue syndrome and other debilitating chronic medical illnesses.  These include antidepressants,pregabalin and gabapentin, analgesics, biofeedback and complementary and alternative medicine. To date, the only published study is a small open-label trial that found that gabapentin reduced pain in 9/10 and improved qual­ity of life in 5/10 patients with chronic post-Lyme neuropathic pain.  Until the medical community has better explanations and therapies for the millions who suffer unexplained chronic symptoms, some patients looking for answers will still come to blame Lyme disease for their illness.  This is likely to remain the case 5 years from now.


NOTE:  In September 2010, a Dutch trial began randomizing patients with post-Lyme disease syndromes to receive 12 weeks of doxycycline, clarithromycin plus hydroxychloroquine, or placebo following an initial course of ceftriaxone. The primary outcome measure will be the SF-36 medical outcomes scale at week 14, as well as repeated assessments that include fatigue and neuropsycho­logic testing up until week 40.  This will be the first prospective, placebo-controlled trial of post-Lyme disease syndromes con­ducted in Europe.

WillemT

[Tulipano]

Enkele voorbeelden (het officiële artikel openklikken voor details over hoe de studies werden uitgevoerd) :

http://www.ncbi.nlm.nih.gov/pubmed/20508824

Proof That Chronic Lyme Disease Exists

Daniel J. Cameron

Abstract


The evidence continues to mount that Chronic Lyme Disease (CLD) exists and must be addressed by the medical community if solutions are to be found. Four National Institutes of Health (NIH) trials validated the existence and severity of CLD. Despite the evidence, there are physicians who continue to deny the existence and severity of CLD, which can hinder efforts to find a solution. Recognizing CLD could facilitate efforts to avoid diagnostic delays of two years and durations of illness of 4.7 to 9 years described in the NIH trials. The risk to society of emerging antibiotic-resistant organisms should be weighed against the societal risks associated with failing to treat an emerging population saddled with CLD. The mixed long-term outcome in children could also be examined. Once we accept the evidence that CLD exists, the medical community should be able to find solutions. Medical professionals should be encouraged to examine whether: (1) innovative treatments for early LD might prevent CLD, (2) early diagnosis of CLD might result in better treatment outcomes, and (3) more effective treatment regimens can be developed for CLD patients who have had prolonged illness and an associated poor quality of life.

http://www.plosone.org/article/info%3Ad ... ne.0029914

Persistence of Borrelia burgdorferi in Rhesus Macaques following Antibiotic Treatment of Disseminated Infection

Monica E. Embers, Stephen W. Barthold, Juan T. Borda, Lisa Bowers, Lara Doyle, mir Hodzic, Mary B. Jacobs, Nicole R. Hasenkampf, Dale S. Martin, Sukanya Narasimhan, Kathrine M. Phillippi-Falkenstein,
Jeanette E. Purcell, Marion R. Ratterree, Mario T. Philipp

Abstract


The persistence of symptoms in Lyme disease patients following antibiotic therapy, and their causes, continue to be a matter of intense controversy. The studies presented here explore antibiotic efficacy using nonhuman primates. Rhesus macaques were infected with B. burgdorferi and a portion received aggressive antibiotic therapy 4–6 months later. Multiple methods were utilized for detection of residual organisms, including the feeding of lab-reared ticks on monkeys (xenodiagnosis), culture, immunofluorescence and PCR. Antibody responses to the B. burgdorferi-specific C6 diagnostic peptide were measured longitudinally and declined in all treated animals. B. burgdorferi antigen, DNA and RNA were detected in the tissues of treated animals. Finally, small numbers of intact spirochetes were recovered by xenodiagnosis from treated monkeys. These results demonstrate that B. burgdorferi can withstand antibiotic treatment, administered post-dissemination, in a primate host. Though B. burgdorferi is not known to possess resistance mechanisms and is susceptible to the standard antibiotics (doxycycline, ceftriaxone) in vitro, it appears to become tolerant post-dissemination in the primate host. This finding raises important questions about the pathogenicity of antibiotic-tolerant persisters and whether or not they can contribute to symptoms post-treatment.

http://www.ncbi.nlm.nih.gov/pubmed/22889796

SPECT Brain Imaging in Chronic Lyme Disease.

Donta, Sam T. MD *; Noto, Richard B. MD +; Vento, John A. MD
[Article] Clinical Nuclear Medicine. 37(9):e219-e222, September 2012.

Objectives: Lyme disease is an infectious disease that frequently involves the central nervous system, leading to cognitive and/or mood dysfunction. The basis for these symptoms remains to be defined but may be the result of a vasculitis or metabolic abnormality secondary to the infection. SPECT scans of the brain might provide an objective measure of abnormalities present in patients with otherwise difficult to objectify clinical findings. The objective of this study was to determine the frequency, location, and severity of abnormalities in SPECT scans of the brain of patients with chronic Lyme disease.

http://www.ncbi.nlm.nih.gov/pubmed/18316520

Persistence of Borrelia burgdorferi following Antibiotic Treatment in Mice


Emir Hodzic, Sunlian Feng, Kevin Holden, Kimberly J. Freet, and Stephen W. Barthold*

Abstract.

The effectiveness of antibiotic treatment was examined in a mouse model of Lyme borreliosis. Mice were treated with ceftriaxone or saline solution for 1 month, commencing during the early (3 weeks) or chronic (4 months) stages of infection with Borrelia burgdorferi. Tissues from mice were tested for infection by culture, PCR, xenodiagnosis, and transplantation of allografts at 1 and 3 months after completion of treatment. In addition, tissues were examined for the presence of spirochetes by immunohistochemistry. In contrast to saline solution-treated mice, mice treated with antibiotic were consistently culture negative, but tissues from some of the mice remained PCR positive, and spirochetes could be visualized in collagen-rich tissues. Furthermore, when some of the antibiotic-treated mice were fed on by Ixodes scapularis ticks (xenodiagnosis), spirochetes were acquired by the ticks, as determined based upon PCR results, and ticks from those cohorts transmitted spirochetes to naïve SCID mice, which became PCR positive but culture negative. Results indicated that following antibiotic treatment, mice remained infected with nondividing but infectious spirochetes, particularly when antibiotic treatment was commenced during the chronic stage of infection.

http://www.ncbi.nlm.nih.gov/pubmed/23346260

Chronic or Late Lyme Neuroborreliosis: Analysis of Evidence Compared to Chronic or Late Neurosyphilis

Judith Miklossy*

Abstract
Whether spirochetes persist in affected host tissues and cause the late/chronic manifestations of neurosyphilis was the subject of long-lasting debate. Detection of Treponema pallidum in the brains of patients with general paresis established a direct link between persisting infection and tertiary manifestations of neurosyphilis.
Today, the same question is in the center of debate with respect to Lyme disease. The goal of this review was to compare the established pathological features of neurosyphilis with those available for Lyme neuroborreliosis. If the main tertiary forms of neurosyphilis also occur in Lyme neuroborreliosis and Borrelia burgdorferi can be detected in brain lesions would indicate that the spirochete is responsible for the neuropsychiatric manifestations of late/chronic Lyme neuroborreliosis.
The substantial amounts of data available in the literature show that the major forms of late/chronic Lyme neuroborreliosis (meningovascular and meningoencephalitis) are clinically and pathologically confirmed. Borrelia burgdorferi was detected in association with tertiary brain lesions and cultivated from the affected brain or cerebrospinal fluid. The accumulated data also indicate that Borrelia burgdorferi is able to evade from destruction by the host immune reactions, persist in host tissues and sustain chronic infection and inflammation. These observations represent evidences that Borrelia burgdorferi in an analogous way to Treponema pallidum is responsible for the chronic/late manifestations of Lyme neuroborreliosis.
Late Lyme neuroborreliosis is accepted by all existing guidelines in Europe, US and Canada. The terms chronic and late are synonymous and both define tertiary neurosyphilis or tertiary Lyme neuroborreliosis. The use of chronic and late Lyme neuroborreliosis as different entities is inaccurate and can be confusing. Further pathological investigations and the detection of spirochetes in infected tissues and body fluids are strongly needed.

http://www.nejm.org/doi/full/10.1056/NE ... 1223232102

Chronic Neurologic Manifestations of Lyme Disease

Eric L. Logigian, M.D., Richard F. Kaplan, Ph.D., and Allen C. Steere, M.D.

Abstract


Lyme disease, caused by the tick-borne spirochete Borrelia burgdorferi, is associated with a wide variety of neurologic manifestations. To define further the chronic neurologic abnormalities of Lyme disease, we studied 27 patients (age range, 25 to 72 years) with previous signs of Lyme disease, current evidence of immunity to B. burgdorferi, and chronic neurologic symptoms with no other identifiable cause. Eight of the patients had been followed prospectively for 8 to 12 years after the onset of infection.

Conclusions.

Months to years after the initial infection with B. burgdorferi, patients with Lyme disease may have chronic encephalopathy, polyneuropathy, or less commonly, leukoencephalitis. These chronic neurologic abnormalities usually improve with antibiotic therapy.

http://journals.lww.com/jneuro-ophthalm ... _an.1.aspx

First Isolation of Borrelia burgdorferi from an Iris Biopsy

Preac-Mursic, V. M.D.; Pfister, H. W. M.D.; Spiegel, H. M.D.; Burk, R. M.D.; Wilske, B. M.D.; Reinhardt, S. M.D.; Böhmer, R. M.D.

Abstract

The persistence of Borrelia burgdorferi in six patients is described. Borrelia burgdorferi has been cultivated from iris biopsy, skin biopsy, and cerebrospinal fluid also after antibiotic therapy for Lyme borreliosis. Lyme Serology: IgG antibodies to B. burgdorferi were positive, IgM negative in four patients; in two patients both IgM and IgG were negative. Antibiotic therapy may abrogate the antibody response to the infection as shown by our results. Patients may have subclinical or clinical disease without diagnostic antibody titers. Persistence of B. burgdorferi cannot be excluded when the serum is negative for antibodies against it.
(C) Williams & Wilkins 1993

Zie ook: https://sites.google.com/site/virginial ... 2013-study

@Willem,

Het is dus maar net welke artikelen je van Pubmed plukt. Maar hoogst waarschijnlijk worden bovenstaande publicaties door mr./mrs. R.R. geclassificeerd als 'bad science written by bad scientist'. Ik denk dat je beter de blog van Camp Other kunt raadplegen. Die is ook kritisch maar gelukkig een stuk genuanceerder, misschien omdat hij/zij zelf ook Lyme heeft!

Jammer trouwens dat ik geen inhoudelijke reactie van je kreeg op mijn vorige post Willem. Maar ja, dat is per slot van rekening niet de eerste keer.