Study of Insect-borne Infections in ME patients planned

[Research 1st]

This looks an interesting idea, mainly because of viruses in insects which looks like a totally novel idea in ME and CFS.

Questions:

1) Are Simmaron really not testing a very common CFS pathogen found by Lyme physicians (Chlamydia Pneumoniae)? and the not uncommon Mycoplasma Pneumoniae or Bartonella Henselea/Quintana) too? Maybe this was just missed in the blog?

2) Are all known pathogenic strains of Borrelia being tested? (CDC B31 Burgodferi strain is the original disease). What about Borrelia Garinii, Borrelia Bavariensis, Borrelia Miyamotoi, Borrelia Lonestari, Borrelia Afzelli?


Before we get excited lets run over the basics that hobble us so much in actively over-turning our demise:

1) Is this a genuine probable ME cohort study (neurological signs and damage such as autoimmunity/POTS?) or a Fukuda CFS study or Canadian CFS study?

2) If so, what % of the 'CFS' blood samples meet each criteria? Fukuda is not a disease, so you'd need at minimum all patients meet Canadian CFS criteria when looking at people for consequence of chronic infections - not simple fatigue.

3) If so, were the 'CFS' patients vetted before the blood was drawn by a doctor who are claimed to meet this criteria?

4) If not using fresh samples, how old is the blood (if frozen) and how is it stored and in what tubes? Does freezing or other storage conditions affect accuracy of the tests? You may remember a group 'accidentally' did this in the past with Mycoplasma - thus there was no link to 'CFS', as the Mycoplasma would be destroyed in the tube. NB: This can easily happen again if people don't think before using the wrong type of collection tube preservative for the blood.

The above are important points to consider for a studies possible legitimacy when published, and possible claimed relevance to ME or CFS even if negative. So far Dr Lipkin has failed to find any pathogens in 'CFS', despite people on this forum testing positive for the infections Dr Lipkin cannot find (in people without ME) and endless CFS studies also finding these pathogens - thus his 'CFS' samples are not people with immune suppression = no infection and not Organic CFS or ME. In contrast Dr Montoya finds infections and finds high levels of cytokines in more severe patients - the opposite finding of Dr Lipkin and the psychiatrist he's done 40 papers with before.

This is why criteria are so important in pathogen studies, sample storage and handling, and having patients with a 'clinical diagnosis' well vetted by an ME expert to be called an 'ME patient' when it comes to validity of scientific papers using the word Myalgic Encephalomyelitis in their title.

 

[msf]

Yersinia, Salmonella and Campylobacter.

 

[sarah darwins]

Yersinia, Salmonella and Campylobacter.

msf, you seem like someone who would know ... ;-) I've tried searching for the current state of thinking on borrelia etc and other 'insect' vectors, such as mosquitoes, but can't find anything other than dodgy looking websites. Do you know if anyone credible has anything to say on this?

I ask because I've lived in some very mosquito rich parts of the world and been bitten more times than I could possibly count. I eventually developed a very bad allergy-type reaction to mozzie bites.

 

[msf]

No, sorry, there was a poster who knew about this stuff, but I can´t remember who, unless it was Brenda.

 

[duncan]

My understanding is that mosquitoes can harbor Bb, but there is little evidence - other than anecdotal - they can transmit.

Of course, if no one is looking for the connection anymore...

Check out Magnarelli and Anderson in 1988 Journal of Clinical Microbiology "Ticks and Biting Insects Infected with the Etiologic Agent of Lyme Disease, Borrelia Burgdorferi". The infected hamster had to get those Bb antibodies from somewhere.

 

[sarah darwins]

Check out Magnarelli and Anderson in 1988 Journal of Clinical Microbiology "Ticks and Biting Insects Infected with the Etiologic Agent of Lyme Disease, Borrelia Burgdorferi".

Thanks, Duncan. I will.

 

[msf]

Research1st, the article says that they will use spare XMRV samples. In the first part of Cort´s report, he quoted Hornig saying that Peterson had classified his samples into infectious onset and other, so hopefully they will use the infectious ones from his patient group, not sure whether they can distinguish between the two for the other patient groups.

 

[Hutan]

The plague (with fleas as a vector) caused some pretty good outbreaks.

Bartonella (often spread by fleas) does seem to cause outbreaks in families and presumably could cause similar outbreaks in people living in an institution or community. The presentation below suggests that there are many vectors for Bartonella - it is suggested that one family may have been infected by spider bites with the spiders having fed on Bartonella-infected insects.

e.g.

(it's long, start at 9 minutes)

The study below found a much higher incidence of rickettsial exposure in people with CFS vs healthy controls. They were even able to isolate rickettsial DNA from some people with CFS.

Markers of exposure to spotted fever rickettsiae in patients with chronic illness, including fatigue, in two Australian populations

N. UNSWORTH1, S. GRAVES1, C. NGUYEN1, G. KEMP2, J. GRAHAM3 and J. STENOS1​

In my family's case, three of us became ill with ME following what we think was a gastro-flu. My daughter has essentially recovered. She has had much less exposure to arthropod-borne illnesses than my son and I - and we remain ill. I have tested positive to rickettsias at a level that could indicate an ongoing infection. Other tests (eg Ehrlichia, Anaplasma) are pending. Our pet dogs developed Ehrlichia (as diagnosed by a vet from looking at slides of blood) following tick bites from the forest around our house.

One of my hypotheses is that the viral illness (and a genetic susceptibility) initiated the ME. But the inability of my son and I to recover as my daughter did may be because of a higher burden of (intra-cellular) pathogens.

 

[Forbin]

It does give me pause to think that I went on a long hike in the Santa Monica Mountains, some of it off trail, only two weeks before coming down with the "flu" that preceded ME. My friend and I were literally pushing our way through brush. It was the one and only time I ever went on a wilderness hike like that - and I'd not hiked at all for several years prior. Never saw a rash, though.

This was only a couple of years after the causative agent in Lyme was discovered in 1981, so I doubt there even was a test available at that time. Certainly, none of my doctors ever mentioned Lyme disease as a possibility back then.

M.E. is like a mystery novel with too many suspects.

 

[justy]

I suppose that clusters could be caused for example by infections spread by mosquitoes? Also Lyme is now at epidemic proportions in certain areas.

Not looking at more strains of BB seems weird and NO Bartonella??? Bart is a big problem just on its own as the video @Hutan added above shows. It is a long talk but please do watch it...we all talk about Lyme...but that talk opened my eyes when I first saw it. Not enough work is being done to make people aware of the dangers of Bartonella infection. I have Bart and treating it when you have had it a long time can be VERY hard.

 

[ukxmrv]

If the clusters could be explained by insect or other bites would someone not have noticed that the patients had all been bitten?

 

[Gijs]

This study has nothing to do with ME/CFS. If some would have Lyme then they don't have ME/CFS. It makes no sense at all.

 

[duncan]

@Gijs, that is like saying if some have EBV then they cannot have ME/CFS. Or if some have an active enterovirus they cannot have ME/CFS.

A theory is that Lyme - in some people - triggers an autoimmune or immune dysfunction known as ME/CFS, or interacts with a pre-existing pathogen/condition to galvanize ME/CFS.

 

[MeSci]

MeSci, if Borrelia can only be transmitted by ticks - I'm not saying that is true - how can clusters occur?

Presumably because there is a high concentration of the ticks' preferred hosts and/or infected hosts, e.g. mice or deer.

My brain is rather foggy at the moment, but I think that this abstract explains it to some extent.

Parasitised or infected animals often seek out the next hosts by various means. For example, parasitised prey animals sometimes lose their fear of predators, which appears to be an evolutionary mechanism developed by the parasite to enable it to pass to the next host/life stage.

 

[msf]

So Gijs, you already know what ME is, since you can already tell us what it isn´t? Please tell us!

Also, the fact that they are using the XMRV samples means that, if they test positive for TBIs, some percentage of the population characterised as having ME actually have TBIs. These people could then say that the subset with pure autoimmune disease haven´t got ME, they have an autoimmune disease. The important thing is to work out what those people who are labelled as having ME actually have. Then we can argue about who has the ´real´ ME.

 

[MeSci]

If the clusters could be explained by insect or other bites would someone not have noticed that the patients had all been bitten?

No - it is easy to be bitten by a tick without noticing. This page says:

ticks are very small, and often do not hurt when they bite so it is quite easy to have a tick bite without noticing. Many people who develop Lyme disease cannot remember being bitten by a tick.

 

[duncan]

@MeSci , what you propose is possible. I think in terms of probabilities it is highly unlikely, although I could not qualify how improbable.

It would have to be a perfect storm. Not only would a very high portion of the ticks have to be infected, enough would have to transmit the disease - in only a very small geographic area - to infect all those individuals...then abruptly stop once a certain radius is achieved. Few of those people if any reported a rash, right? Also, this isn't how persistent Lyme usually unfurls. Typically, you have a flu-like episode, and then you improve as the body and/or abx resolve most of it...and then it comes back and presents much in the same way as ME/CFS.

It's not even the symptoms. It's primarily that only a few ticks in a very limited geography transmit to so many people. Ticks don't typically disperse this way. This is extremely unusual and difficult to explain.

So, this perfect storm I suppose could happen, but I think the conditions would be so extreme to reduce the probabilities to a very low amount.

But could it then happen again? And again? And still again?

A caveat here, though: If the assumed mode of transmission has been wrong all these years, or the vectors different, that might change everything.

 

[ukxmrv]

No - it is easy to be bitten by a tick without noticing. This page says:

Thanks for that. Other thing I was thinking was along the lines of the (possible) ME outbreaks being in the Summer when Polio was rife.

Could that fit in with a possible insect or similar vector? Was the Plague (good point @Hutan ) more common in the Summer?

 

[Gijs]

@Gijs, that is like saying if some have EBV then they cannot have ME/CFS. Or if some have an active enterovirus they cannot have ME/CFS.

A theory is that Lyme - in some people - triggers an autoimmune or immune dysfunction known as ME/CFS, or interacts with a pre-existing pathogen/condition to galvanize ME/CFS.

That is not what i am saying at all. I believe that some patiënts could have Lyme (misdiagoses) but there symptoms are much more objective then in ME. If you don't treat Lyme and it goes to your heart you will have serious heart problems which doctors can see as carditis. Also you can have serious seizures and be paralized. These objective symptoms doesn't occure in ME/CFS.

 

[ukxmrv]

@Gijs, that is like saying if some have EBV then they cannot have ME/CFS. Or if some have an active enterovirus they cannot have ME/CFS.

A theory is that Lyme - in some people - triggers an autoimmune or immune dysfunction known as ME/CFS, or interacts with a pre-existing pathogen/condition to galvanize ME/CFS.

Lyme disease was listed as an exclusion on the original CFS Criteria by the CDC. So that needed to be ruled out before the dx was made.

So "pure" Lyme disease cannot be CFS.

Then we get to the practical problems of many CFS patients being given tests that other doctors tell us could not rule this out at all.