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

Firestormm

Senior Member
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5,055
Location
Cornwall England
Eur J Neurol. 2012 Mar 15. doi: 10.1111/j.1468-1331.2012.03691.x. [Epub ahead of print]

The phenomenon of 'chronic Lyme'; an observational study: http://www.ncbi.nlm.nih.gov/pubmed/22416947

Ljstad U, Mygland A.

Source

Department of Neurology, Srlandet Hospital, Kristiansand, Norway Institute of Clinical Medicine, University of Bergen, Bergen, Norway Department of Habilitation, Srlandet 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.'
 

oceanblue

Guest
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1,383
Location
UK
Thanks, firestormm, very interesting.

There seems to be a lot of debate over whether 'chronic' Lyme Disease is real in most cases or whether it might be another case of post-infectious fatigue syndrome

from http://relative-risk.blogspot.co.uk/2012/03/yes-we-have-no-chronic-lyme.html on this paper:
We found no differences in symptoms between patients with and without anti-Bb antibodies. On the other hand, patients with symptoms of unknown cause had more fatigue and less vitality than those with well-defined illnesses. The majority of the patients with symptoms of unknown cause met the criteria for chronic fatigue syndrome.
It's worth noting that this study only had 29 particpants, some of whom had no physician diagnosis and it's not clear if all patients originally had confirmed Lyme disease.

Still, it's interesting the authors reject a 'functional' explanation. One author is a neurologist, the other is based in an institure of Clinical Medicine and a dept of 'Habilitation'.
 

WillowJ

คภภเє ɠรค๓թєl
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4,940
Location
WA, USA
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.


does this say something about the "suggested criteria for post-Lyme disease"? or not necessarily since one could have had Lyme, recovered, and then gotten something else? or does that not meet Occam's razor?

also I agree that the pt or dr suspected Lyme isn't a very useful cohort; usually something is done when a given illness is suspected, to clarify whether that is or isn't the case.

one doesn't study suspected cases to verify or deconstruct an illness construct; one studies the best cases--those with a history of tick bite or rash, confirmed coinfection, stuff like that. In other words, only the 14 with anti-Bb antibodies are relevant here.

14 is not a very highly-powered study to make decisions by, especially considering that larger studies do find evidence of ongoing infection in patients more carefully selected:

http://www.ncbi.nlm.nih.gov/pubmed/8923044
The presence of Borrelia burgdorferi DNA was established by PCR from urine samples of 97 patients clinically diagnosed as presenting with symptoms of chronic Lyme disease. All patients had shown erythema chronica migrans following a deer tick bite.
Of the 97 patients, 72 (74.2%) were found with positive PCR and the rest with negative PCR. The 62 healthy volunteers were PCR negative. It is proposed that a sizeable group of patients diagnosed on clinical grounds as having chronic Lyme disease may still excrete Borrelia DNA, and may do so in spite of intensive antibiotic treatment.

also see a cerebrospinal fluid study
http://www.ncbi.nlm.nih.gov/pubmed/1734321
PCR detected B burgdorferi OspA DNA in CSF of
(1) 10 of 11 patients with Lyme encephalopathy - patients with immunologic evidence of systemic B burgdorferi infection and clinical manifestations suggestive of CNS dysfunction,
(2) 28 of 37 patients with inflammatory CNS disease - seronegative patients with clinical disorders consistent with Lyme borreliosis,
(3) seven of seven seronegative patients with Lyme-compatible disorders - patient and contamination controls, and
(4) zero of 23 patient controls. Zero of 83 additional contamination controls were PCR-positive.

In eight patients from whom we obtained CSF before and after parenteral antimicrobial therapy, PCR results invariably predicted clinical outcome accurately.

(I rearranged some elements for clarity and added paragraph breaks)

Once again, epidemiology may be the key.

Of course there's also this, but I think Lyme Arthritis is not the same as chronic Lyme (LA seems to be autoimmune and could theoretically be related to dead unfamiliar DNA or certainly other matter from the Bb; while that doesn't necessarily rule out CLD as having an active infection component--however, it is possible that something similar could be going on; Lupus (SLE) patients can also have neurological symptoms):
B burgdorferi mRNA, a marker of spirochetal viability, was detected in 8 of 10 skin samples from EM patients, but in none of 11 SF samples from LA patients, even when obtained prior to antibiotic administration. Moreover, the median ratio of spirochetal rRNA to DNA, a measure of ribosomal activity, was 160 in the 10 EM skin samples, but only 0.15 in the 3 LA SF samples with positive results.

B burgdorferi in the skin lesions of EM patients were active and viable, whereas those in the SF of LA patients were moribund or dead at any time point. Thus, detection of B burgdorferi DNA in SF is not a reliable test of active joint infection in Lyme disease.
http://www.ncbi.nlm.nih.gov/pubmed/21590753

Then again, there's this (discussing LA):
However, studies such as those in non-human primates suggest that bystander inflammatory responses to the persistently infective pathogen may explain more clearly the CNS complications of this disease [120122].
in http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2665673/?tool=pubmed (paper on infections, including Bb, in autoimmune disease, including LA)

Here is a recent free full text paper on how Bb might develop a chronic presence in the body:
http://www.frontiersin.org/Microbial_Immunology/10.3389/fmicb.2012.00104/abstract

(I have not read it all, but the full text appears to discuss mainly chronic untreated infections, while leaving such topics as CLD to others and claiming quite good effectiveness from presumably standard antibiotic treatment, in most cases, even if treatment commences many years after initial infection)

We developed a mathematical model describing the bacterial growth and the immune response against Borrelia burgdorferi in the C3H mouse strain that has been established as an experimental model for Lyme disease....

The mathematical model predicts that Borrelia recovers from the strong initial immune response by the regrowth of an immune-resistant sub-population of the bacteria.

The chronic phase appears as an equilibration of bacterial growth and adaptive immunity. This result has major implications for the development of the chronic phase of Borrelia infections as well as on potential protective clinical interventions.
 

Snow Leopard

Hibernating
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5,902
Location
South Australia
There are a variety of alternative explanations:

(1) a tick-bourne coinfection
A number of other tick bourne pathogens (not Lyme) have been associated with CFS in Australia.

(2) the infection could cause dysregulation of gut flora, perhaps reactivating another pathogen.

(3) Chronic Lyme is CFS.

Perhaps a better name is post-Lyme disease.
 
Messages
13,774
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.


does this say something about the "suggested criteria for post-Lyme disease"? or not necessarily since one could have had Lyme, recovered, and then gotten something else? or does that not meet Occam's razor?

I does seem a bit of a coincidence.

One other possibility is that Lyme disease can do damage which leaves one less able to deal with other problems? So chronologically, the Lymes diseased does not immediately precede disability, but still plays a role?
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
Perhaps a better name is post-Lyme disease.

Hi Snow Leopard, this has precedence - post-Polio syndrome is also almost identical to CFS and ME - the major difference being a verified (though probably not in all cases) poliomyelitis infection. Similarly we could speak about post-EBV disease and post-Coxsackie disease. This still leads to the question: while the symptoms and pathophysiology do differ between CFS and post-Lyme, is the underlying perpetuating biochemistry substantially the same? We still don't know.

Bye, Alex
 

Firestormm

Senior Member
Messages
5,055
Location
Cornwall England
And then you come up with the question: are the same treatments appropriate in all cases? Ta da! The conundrum of CFS or ME criteria. Symptoms may present similarly post-acute phase of infection, but in chronic-mode but we're all in the 'pot' together.

Post Viral Fatigue Syndrome is a 'catch-all' and always has been. Anyone can join. But the way out might not be the same for everyone. Who knows? Who's looking?

Maybe scientists should only be looking at those who fit the bill e.g. who presented with coxsackie or paravirus etc. and work on those little 'pots' separately. Maybe they have and still aren't getting anywhere.