The Great Chronic Lyme Mirage – Advocates Gone Wild

Bullying Borrelia: When the Culture of Science is Under Attack
(Full Text PDF)

Paul G. Auwaerter, MD, and (by invitation) Michael T. Melia, MD

Abstract
Although Lyme disease responds to short courses of antibiotics, tick-borne Borrelia burgdorferi has been advanced by some as a frequent explanation for medically unexplained symptoms such as continual fatigue, musculoskeletal pains, and subjective neurocognitive dysfunction.

Often called “chronic Lyme disease” by adherents of this philosophy, it is loosely defined, and practitioners liberally prescribe nostrums, including prolonged antimicrobial therapies, in a belief that this eradicates suspected infection.

Perhaps due to the lack of supportive data, proponents of this theory have developed their own meetings, literature, activist groups, and substantial internet activities to advance their views.

Forces motivating this movement are explored, as are tactics used to advance non-scientific ideas that have included legal action and garnering legislative endorsement.

While neither logical nor evidence-based, “chronic Lyme disease” harnesses corrosive energies that taint modern medicine and society.

…

We know it all too well from ME/CFS: A minority of quack-doctors are proposing valid sounding theories with regards disease mechanisms – which goes hand in hand with cures they claim to have – and some patients and relatives are more than happy to advocate in their name. And when one calls out their lack of evidence, and the likelihood that the supposed cure does in many (if not most) cases harm, one is branded as an enemy. To hell with those malicious patient advocates and malicious patient activists, and to hell with these "LLMD" quack doctors.

And yes, people who supposedly have "Chronic Lyme" are ill with an (in all likelihood) organic disease. But no, it is not "Chronic Lyme" and in most cases it isn't even Post Lyme.

The Great Chronic Lyme Mirage – Herx Edition

Halperin / ALDF:

… Early work indicated that patients with acute, active early Lyme disease, as indicated by the presence of an erythema migrans (EM) skin lesion (when large numbers of spirochaetes are presumably present), sometimes exhibited a Jarisch–Herxheimer-like reaction within 24 h after initiation of treatment (Weber et al., 1988; Maloy et al., 1998).

This led to the notion that any worsening of symptoms during treatment constituted ‘Herxing’, regardless of the duration of symptoms or treatment at the time of the worsening.

The logical in-consistency of postulating that treatment-resistant disease was due to a small number of undetectable bacteria, while at the same time concluding that symptoms arising or worsening during antibiotic therapy were due to the release of large amounts of pharmacologically active bacterial products, was either discounted or never considered.

However, this then completed the very tidy but circular conceptual model.

If patients improved, even transiently, after treatment, this validated the diagnosis and justified further treatment; the possibility of a placebo effect or natural fluctuation in symptom severity was either never considered or completely rejected.

If patients worsened, this was considered to be due to a Jarisch–Herxheimer reaction, similarly validating the diagnosis.

If there were no response to therapy, this validated the assumption that this infection is highly resistant to standard antimicrobial therapy. …

The more I see of these "LLMD" quacks, the more I am sure that "Chronic Lyme" is a quack diagnosis.

The people who are misdiagnosed with "Chronic Lyme" have a disease, no question – and in most if not all cases it is an organic disease – but I am rather sure that it is not a active/persistent/latent ("chronic") lyme infection.

At the same time I believe that a very very small number of people who are misdiagnosed with "Chronic Lyme" might have "Post Lyme", where the bug is gone but the organic damage stays, same as there are Postviral Fatigue Syndromes and other postviral CFS-like diseases.

However, I am certain that no "LLMD" quack would be able to differentiate Post Lyme from Post Mono. These LLMDs see a patient and can only diagnose "Chronic Lyme", it seems …

As Tom Waits once sang:

LLMD always try so hard to look like real doctors
They couldn't catch a cold,
baby don't waste what's left of your health

So unless you have an acute infection and take short term antibiotics for it (for a couple of weeks) stay the hell away from antibiotics if they are given long-term, especially when they give you a long time supposed "Herx" reaction – because a "long-time Herx reaction" is not Herxheimer (due to Lyme "die off"), but the side-effects of antibiotics that are destroying your health.

The Great Chronic Lyme Mirage

I found some interesting comments by Phillip J. Baker (who seems to be associated with the American Lyme Disease Foundation) underneath an otherwise not recommendable article & discussion (or rather an article & discussion which can only be recommendable as a negative example for the display of confirmation biases and cognitive dissonances).

Especially this comment by Phillip J. Baker struck a chord with me:

Believe what you will, Phyllis, but you are wrong. Ceftiofur and ceftriaxone are chemically different in structure. Embers et al. have provided no assurances in their work that they have similar PK and PD properties, let alone the same MIC. It is incumbent upon them to provide such data, as well as to show that therapeutic regimen used was adequate to clear the huge inoculum that was used to produce a disseminated infection. Obviously, their experimental design did not mimic the Klempner study, which is what Mario was initially funded to do. Why he chose to use ceftiofur is for him to explain, not me. As I said before, ceftiofur has not been approved by the FDA for use in humans and there are no published data showing that it is effective for treating borreliosis in animals, let alone humans. There is one report showing that it is not effective for treating borreliosis in ponies.

Phillip J. Baker
on February 24, 2012 at 1:52 pm

http://lymedisease.org/news/lymepolicywonk/lymepolicywonk-was-this-important-lyme-study-hidden-for-12-years.html#comment-3798

He goes on to notice in another comment:

I must say that I find it strange that the term ceftriaxone is used throughout the Embers et al. paper, and it is only in the first paragraph on page 9 that it is first mentioned that ceftiofur was actually used. I find that very strange indeed.

So to claim that Lyme is still active despite anti-biotics, Embers et al. have to pull these two tricks:

1. Use a "huge inoculum" to intruduce an amount of pathogens not encountered in the wild, causing an "massive disseminated infection" not encountered in the wild.
2. Use an antibiotic that (most likely) is not effective in clearing the pathogen (let alone in this massive disseminated infection) – and hide that as good as you can.

What Phillip J. Baker describes are the tactics of quacks.

No wonder anybody with at least a couple of working brain cells left*, who looks into the matter comes to the conclusion that "Chronic Lyme" is a BS quack diagnosis.

And just for the record: I do think that these patients have an organic disease, which severely affects their lives – however there is no evidence** that this disease is Lyme. There are many many diseases that can cripple your live, and possibly some of which are yet of unknown.

* As to so called "Lyme Literate Medical Doctors" ("LLMD"):
They do not seem to have any working brain cells left. My (purely anecdotal and not evidence based) advise is to stay away from medical doctors who have no working brain cells. LLMD? Just say no. Choose a doctor instead with working brain cells, this is usually better for your health.

** As to any non-standard tests used to detect "Chronic Lyme": I can offer you an even more reliable Lyme test! I will match any price, just give me a call!

IGeneX's Robert Giguere about their Lyme tests

After the wonderful world of lies fraud story-telling by Mikovits/Lombardi/WPI/VIPdx and their worthless wonderful XMRV test, I am very very very skeptical about any tests, especially when I read that the lab "uses additional markers for Lyme under which some people test positive who have been negative" and Giguere's presentation style reminds me more than a little about the way my dear friend Mikovits throws sand in patients eyes – for me this is reminiscent of the XMRV rip off disaster. So take take the following presentation with lots and lots of grains of salt:

IGeneX, Inc. - Lyme testing discussion
Robert O. Giguere, director of sales for IGeneX, Inc., explains Lyme disease testing at a talk in Fishkill early this month. The Palo Alto, Calif., company uses additional markers for Lyme under which some people test positive who have been negative.

One more thing, his anthropomorphic descriptions – like the Lyme bug as "smart" and that it tries to "evade" the immune system – seem more like woo than like science.

[UPDATE] I could not find anything published by the good Robert Giguere (and I haven't seen any references to anything published so far in the video), so everything he tells seems to be secret knowledge only passed on orally – this is a major red flag for me since Mikovotis the non-publisher (with her colorful and fact-pacted talks). And what's lovely is the "hides in tissue" fear-mongering we have seen with Mikovits. 50% of tests are positive, "If you get a positive result, you have active infection", "no false positives but false negatives" (keep testing until you are positive), same fear-mongering as we have seen with Mikovits. They use PCR in strange ways (50 cycles), Mikovits used PCR in strange ways (nested).

[UPDATE] If anybody can show the world a published study demonstrating sensitivity and specificity (false negatives and false positives) of these tests, then that would be fabulous.

"The phenomenon of 'chronic Lyme'; an observational study."

The phenomenon of 'chronic Lyme'; an observational study.
Ljøstad U, Mygland A.

Department of Neurology, Sørlandet Hospital, Kristiansand, Norway Institute of Clinical Medicine, University of Bergen, Bergen, Norway Department of Habilitation, Sørlandet Hospital, Kristiansand, Norway

Abstract

Purposes:
To chart clinical, laboratory, and psychometric profiles in patients who attribute their complaints to chronic Lyme disease.

Methods:
We assessed the patients by clinical examination, laboratory tests, and questionnaires measuring fatigue, depression, anxiety, health-related quality of life, hypochondriasis, and illness perceptions.

Results:
We found no evidence of ongoing Borrelia burgdorferi (Bb) infection in any of the 29 included patients using current diagnostic guidelines and an extended array of tests.

Eight (28%) had other well-defined illnesses.

Twenty-one (72%) had symptoms of unknown cause, of those six met the suggested criteria for post-Lyme disease syndrome.

Fourteen (48%) had presence of anti-Bb antibodies.

The patients had more fatigue and poorer health-related quality of life as compared to normative data, but were not more depressed, anxious, or hypochondriacal.

Their beliefs about the illness were characterized by negative expectations.

Conclusion:
Our patients, who all attributed their symptoms to chronic Lyme disease, were heterogeneous.

None had evidences of persistent Bb infection, but whether current diagnostic criteria are functional in patients with longstanding complaints is controversial.

Other well-defined illnesses or sequelae from earlier Lyme disease were probable as main explanatory factor in some cases.

The patients were not more depressed, anxious, or hypochondriacal than the normal population, but they had poorer health-related quality of life, more fatigue, and negative expectations about their illness.

Unforutnatly only the abstract is available. The other "well-defined illnesses" would be interesting to collect.

And about half(!) of the patients who were seen by these doctors supposedly with "chronic Lyme" did actually not have anti-bodies against Borrelia Burgdorferi - and none had evidences of persistent infection! There are certainly some Quacks out there diagnosing people with "Chronic Lyme". And only "six met the suggested criteria for post-Lyme disease syndrome".

NIAID on Chronic Lyme and long-term Antibiotic use

NIAID on Chronic Lyme:

The first clinical trial, which included two studies conducted at multiple research sites, provided no evidence that extended antibiotic treatment is beneficial (New Engl J Med 345: 85-92, 2001). In those studies, physicians examined long-term antibiotic therapy in patients with a well-documented history of previous Lyme disease, but who reported persistent pain, fatigue, impaired cognitive function, or unexplained numbness. Patients were treated with 30 days of an intravenous antibiotic followed by 60 days of treatment with an oral antibiotic.

These studies did reinforce the evidence that patients reporting PLDS symptoms have a severe impairment in overall physical health and quality of life. However, prolonged antibiotic therapy showed no benefit when compared with groups who received placebo.

In another study, published in 2003, researchers examined the effect of 28 days of intravenous antibiotic compared with placebo in 55 patients reporting persistent, severe fatigue at least 6 months following treatment for laboratory-diagnosed Lyme disease. Patients were assessed for improvements in self-reported fatigue and cognitive function (Neurology 60: 1923-30, 2003).

In that study, people receiving antibiotics did report a greater improvement in fatigue than those on placebo. However, no benefit to cognitive function was observed. In addition, six of the study participants had serious adverse events associated with intravenous antibiotic use, and four patients required hospitalization. Overall, the study authors concluded that additional antibiotic therapy for PLDS was not supported by the evidence.

More recently, a study supported by the National Institute of Neurological Disorders and Stroke (NINDS), also a part of the National Institutes of Health, again showed that long-term antibiotic use for Lyme disease is not an effective strategy for cognitive improvement (Neurology 70(13): 992-1003, 2008). Researchers compared clinical improvement following 10 weeks of intravenous ceftriaxone versus intravenous placebo. The patients were treated for Lyme disease and presented with objective memory impairment tests. In a complicated statistical model, the ceftriaxone group showed a slightly greater improvement at 12 weeks, but at 24 weeks, both the ceftriaxone and the placebo groups had improved similarly from baseline. In addition, adverse effects attributed to intravenous ceftriaxone occurred in 26 percent of patients. The authors concluded that because of the limited duration of the cognitive improvement and the risks involved, 10 weeks of intravenous ceftriaxone was not an effective strategy for cognitive improvement in these patients, and more durable and safer treatment strategies are still needed.

To recap:

• The people are ill 
• Long-term antibiotics do most certainly not cure
• Long-term antibiotics have dangers
• Diagnose is done through "a well-documented history of previous Lyme disease"

As far as I am concerned, there is no evidence that "Chronic Lyme" or "post-Lyme disease syndrome" (PLDS) is anything else then just another pathogen that can cause CF(S) or PVFS.

Different pathogens can cause CFS-like illness

After two studies popped up recently (Naess et al. 2012 and Morroy et al. 2012), I thought I'll collect here some of the studies implicating different pathogens. Interesting is that the finding of Hickie et al. 2006 (to paraphrase: "Initial illness severity predicts duration of chronic fatigue") was found in Morroy et al. 2012, albeit reported inversely (as paraphrased: "the majority of persons with mild illness recover spontaneously within a few weeks"). The report of David Bell on patients of the Lyndonville outbreak after 25 years seem to go in a similar direction, that those who got hit the hardest, stayed the most ill.

Some things are missing. First of all, I have no measure of the quality of most of these studies. Hickie 2006 seems solid. John Chia's finding of Enterovirus seems intriguing (and jives well with previous findings of researchers on the British Isles), yet I'm cautious. If half of the people presenting with CF(S) at John Chia's office have persistent Enterovirus infections, then Ian Lipkin will find a comparable number.

Then another thing that is missing is (Chronic) Lyme and other pathogens like Mycoplasma.

And the third thing to keep in mind is that local outbreaks can skew any numbers, as obviously an outbreak increases the number of people who have the same pathogen in that region. Giardia cases may or may not be common now in Haukland, Norway – the incidence of Giardia in CF(S) cases in e.g. California may or may not be neglectable.

So here we go:

Hickie et al. 2006: a prospective cohort study on Epstein-Barr virus (glandular fever), Coxiella burnetii (Q fever), or Ross River virus (epidemic polyarthritis) in Australia:

Post-infective and chronic fatigue syndromes precipitated by viral and non-viral pathogens: prospective cohort study

Ian Hickie 1, Tracey Davenport 1, Denis Wakefield 2, Ute Vollmer-Conna 3, Barbara Cameron 2, Suzanne D Vernon 4, William C Reeves 4, Andrew Lloyd 2

Cite this as: BMJ 2006;333:575
Degenerative joint disease Drugs: CNS (not psychiatric) Epidemiologic studies

1 Brain and Mind Research Institute, Sydney University, Sydney, NSW 2050, Australia,
2 School of Medical Sciences, University of New South Wales, Sydney, NSW 2052,
3 School of Psychiatry, University of New South Wales,
4 Division of Viral and Rickettsial Diseases, Centers for Disease Control and Prevention, Atlanta, GA 31033, USA

Correspondence to: A Lloyd

Abstract
Objective To delineate the risk factors, symptom patterns, and longitudinal course of prolonged illnesses after a variety of acute infections.

Design
Prospective cohort study following patients from the time of acute infection with Epstein-Barr virus (glandular fever), Coxiella burnetii (Q fever), or Ross River virus (epidemic polyarthritis).

Setting
The region surrounding the township of Dubbo in rural Australia, encompassing a 200 km geographical radius and 104 400 residents.

Participants
253 patients enrolled and followed at regular intervals over 12 months by self report, structured interview, and clinical assessment.

Outcome measures
Detailed medical, psychiatric, and laboratory evaluations at six months to apply diagnostic criteria for chronic fatigue syndrome. Premorbid and intercurrent illness characteristics recorded to define risk factors for chronic fatigue syndrome. Self reported illness phenotypes compared between infective groups.

Results
Prolonged illness characterised by disabling fatigue, musculoskeletal pain, neurocognitive difficulties, and mood disturbance was evident in 29 (12%) of 253 participants at six months, of whom 28 (11%) met the diagnostic criteria for chronic fatigue syndrome. This post-infective fatigue syndrome phenotype was stereotyped and occurred at a similar incidence after each infection. The syndrome was predicted largely by the severity of the acute illness rather than by demographic, psychological, or microbiological factors.

Conclusions
A relatively uniform post-infective fatigue syndrome persists in a significant minority of patients for six months or more after clinical infection with several different viral and non-viral micro-organisms. Post-infective fatigue syndrome is a valid illness model for investigating one pathophysiological pathway to chronic fatigue syndrome.

Naess et al. 2012 on Giardia in Norway:

Chronic fatigue syndrome after Giardia enteritis: clinical characteristics, disability and long-term sickness absence.
Halvor Naess, Morten Nyland, Trygve Hausken, Inghild Follestad and Harald I Nyland

Institute of Clinical Medicine, Department of Neurology, and Unit for Gastroenterology, Department for Medicine, Haukeland University Hospital, N-5021 Bergen, Norway

BMC Gastroenterology 2012, 12:13 doi:10.1186/1471-230X-12-13

Abstract (provisional)
Background
A waterborne outbreak of Giardia lamblia gastroenteritis led to a high prevalance of long-lasting fatigue and abdominal symptoms.

The aim was to describe the clinical characteristics, disability and employmentloss in a case series of patients with Chronic Fatigue Syndrome (CFS) after the infection.

Methods
Patients who reported persistent fatigue, lowered functional capacity and sickness leave or delayed education after a large community outbreak of giardiasis enteritis in the city of Bergen, Norway were evaluated with the established Centers for Disease Control and Prevention criteria for CFS.

Fatigue was self-rated by the Fatigue Severity Scale (FSS).

Physical and mental health status and functional impairment was measured by the Medical Outcome Severity Scale-short Form-36 (SF-36).

The Hospital Anxiety and Depression Scale (HADS) was used to measure co-morbid anxiety and depression.

Inability to work or study because of fatigue was determined by sickness absence certified by a doctor.

Results
A total of 58 (60%) out of 96 patients with long-lasting post-infectious fatigue after laboratory confirmed giardiasis were diagnosed with CFS.

In all, 1262 patients had laboratory confirmed giardiasis.

At the time of referral (mean illness duration 2.7 years) 16 % reported improvement, 28 % reported no change, and 57 % reported progressive course with gradual worsening.

Mean FSS score was 6.6. A distinctive pattern of impairment was documented with the SF-36.

The physical functioning, vitality (energy/fatigue) and social functioning were especially reduced.

Long-term sickness absence from studies and work was noted in all patients.

Conclusion
After giardiasis enteritis at least 5% developed clinical characteristics and functional impairment comparable to previously described post-infectious fatigue syndrome.

Morroy et al. 2012 Q-fever (Coxiella burnetii) in The Netherlands:

Self-reported sick leave and long-term health symptoms of Q-fever patients

Gabriella Morroy 1,2, Hans H. J. Bor 2, Johan Polder 3, Jeannine L. A. Hautvast 2, Wim van der Hoek 4, Peter M. Schneeberger5 and Clementine J. Wijkmans 1,2

1 Department of Infectious Disease Control, Municipal Health Service Hart voor Brabant, ‘s-Hertogenbosch, The Netherlands
2 Academic Collaborative Centre AMPHI, Department of Primary and Community Care, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
3 Department Tranzo, Tilburg University, Tilburg, The Netherlands
4 Centre for Infectious Disease Control, National Institute for Public Health and the Environment, Bilthoven, The Netherlands
5 Laboratory of Medical Microbiology, Jeroen Bosch Hospital, ‘s-Hertogenbosch, The Netherlands

Abstract

Background:
In The Netherlands, 1168 Q-fever patients were notified in 2007 and 2008.

Patients and general practitioners (GPs) regularly reported persisting symptoms after acute Q-fever, especially fatigue and long periods of sick leave, to the public health authorities.

International studies on smaller Q-fever outbreaks demonstrate that symptoms may persist years after acute illness. Data for the Dutch outbreaks were unavailable.

The aim of this study is to quantify sick leave after acute Q-fever and long-term symptoms.

Methods:
Our study targeted 898 acute Q-fever patients, notified in 2007 and 2008 residing in the Province Noord-Brabant.

Patients from the 2008 cohort were mailed a questionnaire at 12 months and those of the 2007 cohort at 12–26 months after onset of illness.

Patients reported underlying illness, Q-fever-related symptoms and sick leave.

Results:
The response rate was 64%.

Forty percent of the working patients reported long-term (>1 month) sick leave.

Pre-existent heart disease odds ratio (OR) 4.50; confidence interval (CI) 1.27–16.09), hospitalization in the acute phase (OR 3.99; 95% CI 2.15–7.43) and smoking (OR 1.69; 95% CI 1.01–2.84) were significant predictors for long-term absence.

Of the patients who resumed work, 9% were—at the time of completing the questionnaire—still unable to function at pre-infection levels due to fatigue or concentration problems.

Of the respondents, 40% reported persisting physical symptoms at the time of follow-up.

Fatigue (20%) was most frequently reported. Daily activities were affected in 30% of cases.

Conclusions:
Q-fever poses a serious persisting long-term burden on patients and society.

In 2007, the Netherlands began a large, drawn-out outbreak of Q fever, which resulted in thousands being infected and a dozen or so fatalities.

In a study just released in the European Journal of Public Health, Dutch researchers show that many of those infected with Coxiella burnetti previously, now face chronic fatigue syndrome and other physical symptoms.

1,168 Q-fever patients were notified in 2007 and 2008 in the Netherlands. The study targeted 898 acute Q-fever patients, notified in 2007 and 2008 residing in the Province Noord-Brabant. Patients from the 2008 cohort were mailed a questionnaire at 12 months and those of the 2007 cohort at 12-26 months after onset of illness. In the questionnaire, patients reported underlying illness, Q-fever-related symptoms and sick leave.

Some of the key results found in the study include:

• Forty percent of the working patients reported long-term (greater than 1 month) sick leave.
• Daily activities were affected in 30% of cases.
• 20% of respondents reported issues with fatigue.
• 9% of those who did return to work reported they were (up to 2 years post-Q fever infection) still unable to function at pre-infection levels due to fatigue or concentration problems.

Based on the results of the study, the authors conclude that Q-fever poses a serious persisting long-term burden on patients and society.

Q fever is caused by the obligate intracellular pathogen, Coxiella burnetii. The disease is usually transmitted to people through either infected milk or through aerosols.

This disease is found on most continents with the reported incidence probably much lower than the actual because so many cases are so mild.

Animal reservoirs of C. burnetii include sheep, cattle, goats, dogs and cats. In areas where these animals are present, Q fever affects veterinarians, meatpacking workers, and farmers.
…

The mortality rate for acute Q fever is low (1–2%), and the majority of persons with mild illness recover spontaneously within a few weeks although antibiotic treatment will shorten the duration of illness and lessen the risk of complications.

John Chia 1999 about Chronic Chlamydia Pneumoniae:

Chronic Chlamydia pneumoniae infection: a treatable cause of chronic fatigue syndrome.

John K. S. Chia and Laura Y. Chia

Torrance Memorial Medical Center, Torrance, California

…
Over the past 3 years, we encountered 10 of 171 patients with symptoms of chronic fatigue who had elevated titers of antibody to C. pneumoniae long after initial respiratory infection. Most pa- tients had favorable clinical and serological responses to a 1- to 2-months course of azithromycin therapy, although relapse was common. The clinical symptoms of and titers of antibody to C. pneumoniae for our 10 patients over the course of treatment are summarized in table 1.
…

The spontaneous rise of titers for several patients correlated with an increased severity of fatigue and a concomitant increase in respiratory symptoms. This observation suggests that relapses of symptoms could be due to persistent infection with periodic reac- tivation rather than reinfection. All of the patients with relapses responded to additional azithromycin treatment.
…

Collectively, these results suggest that C. pneumoniae is an uncommon yet treatable cause of chronic fatigue. The sensitivity, specificity, and interlaboratory variability of the DNA test will need to be better defined.…

And John Chia 2003 again, this time with his son, about many different pathogens, but obviously implicating Enteroviruses:

Diverse Etiologies for Chronic Fatigue Syndrome

John K. S. Chia and Andrew Chia

I D Med, Torrance, California

Clinical Infectious Diseases 2003;36:671–2
…

Probable cause	Criteria for inclusion	No. of patients (n = 200)
Chlamydia pneumoniae infection	High antibody titer compared with control subjects from the community; response to macrolide therapy	18
Epstein-Barr virus infection	Whole blood (at 1:1000 dilution) or urine sample positive for EBV DNA; response to Val or iv Cid therapya	6
Cytomegalovirus infection	Surveillance of acute infection for a period 16 months; positive culture results; response to iv Cid or IVIG therapy	3
Recurrent VZV infection	Recurrent lesions; response to antiviral drugs	6
Recurrent HHV6-like disease	Recurrent roseola-like illness for a period of 3 years; response to iv Cid therapy	1
Parvovirus B19 infection	Test results positive for IgM or viral DNA	3
Hepatitis C	Resolution of symptoms after interferon/ribavirin therapy	3
Neurocardiogenic hypotension	Initial flulike illness; tilt test positive for NMS; response to midodrine therapy	2
Toxic mold exposure	Documented cultures of environmental samples positive for toxic mold; 11 household member was affected; symptoms improved after leaving the house	2
Postvaccination	Received pneumovax, MMR, or influenza vaccine	3
Enterovirus infection	Persistent, significantly elevated levels of neutralizing antibody for coxsackievirus B or high echovirus titer compared with controls from the community; PBMC sample positive for enteroviral RNAb	109
Unknown	—	44

Chia's study is surely not made to gold standards and any numbers should be taken not to be poured in concrete. Chia claims here to have found enteroviral RNAb in PBMCs, while later he opted to search for enteroviral protein VP1 in gut biopsies - something that seems to me to be unnecessarily complicated. If there is actual enteroviral RNAb in PBMCs in the majority of CFS patients, then Ian Lipkin will find it.

Taken together, it looks like there is a clear indication that different pathogens are likely invovled in different CF(S) subgroups and that there is not one single cause involved in all nor even most CF(S) cases – and though the group of likely pathogens is small, it is not exhaustive. While I am hopeful that it is possible to establish the etiology for a considerable portion of CF(S) cases within the next years, I am pessimistic and think that in the foreseeable future a substantial part of CF(S) patients will remain without a established etiology.

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

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

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.

More woo from the WPI

This is old news, but needs to reposted.

As the battle is waged on the scientific front, it is with great joy that I am able to announce that we will begin to see patients at the WPI on August 1. It will close the circle necessary to be a true translational research center with synergy between disciplines. Dr. Chitra Bhakta is a Family Practitioner with a private practice in Orange County where she treats ME/CFS and autism.

So let's look at Chitra Bhakta.

Chitra Bhakta is a DAN! practitioner (more info on DAN!) and apparently a Chronic Lyme True believer (more info on 'Chronic Lyme').She is a wooer, not a family doctor.
Posted by: ERV | June 20, 2011 11:58 AM

We haven fallen in with cranks and cuckoos.

ME/CFS Differential Diagnosis Gotchas: Lyme

I was dx'd with ME/CFS for 17 years before finding out I had Lyme, Bartonella and Babesia last November. Since being on treatment for the last 7 months, my life is returning. I am getting my life back after 17 years. My passion now is to ask all of my ME/CFS friends to consider getting retested for Lyme Disease. Even if you had tests and they were negative (mine was three times from 1993-2004), and/or even if you cannot recall being bit by a tick, or think you cant have it because you don't live in a "Lyme" state. Lyme tick distribution in the US is growing past the old borders on the east coast. And there is evidence that Lyme can be gotten in other ways (See the page "First things first..." question #1 on the web site)

The standard (CDC's of course) test given (the ELISA test) to test for Lyme is 50-59% wrong Always. You need to get a western blot test at a reputable Lyme lab to accurately test you.

.

It's critical for you to get a Western Blot Lyme Disease and it's Co-infections test. This is performed by many labs, but some of the labs have different standards of interpreting the tests. In order to get the most accurate results, there are reputable Lyme labs you should consider getting tested from. IGeneX, Fry labs and a few more are listed on this blogs Good Lyme Lab Page:

Good Lyme Labs