Any recent ME/CFS outbreaks?

[Murph]

I'm a fan of @Hip's double hit theory. Viral infection plus a second situational factor that makes you susceptible to the virus affecting you in an unusual way.

I don't know what specifically the other thing is but I got sick at a point in my life I was really burning the candle at both ends - lots of sport, lots of partying and ensuing hangovers, poor nutritition (I was a vegetarian who ate terribly), not enough sleep, stress.

 

[Moof]

But what I am saying is that many hospitals are likely the same in terms of their work ethic, so you thus would expect to see hospital ME/CFS outbreaks everywhere and all the time, every time an ME/CFS virus arrived at a hospital.

Sure, but they're clearly uncommon, and for the time being most people are no longer susceptible to one of the main suspects...but I'm not betting any actual money that outbreaks of diseases like polio won't re-emerge in Westernised countries, given the astounding willingness to deny the obvious in the anti-vax movement!!

 

[heapsreal]

Ebv outbreaks happen in high schools and why its called the kissing disease. So ebv is possible.

Alot of viruses are never diagnosed, more likely your GP would say you have the flu or just a virus. I think because they dont really have treatments outside of bed rest, keep fluids up and take paracetamol, we may never know how many of these are ebv cmv or hhv6 or some other type of virus altogether. Usually by the time someone is still feeling sick from a virus like ebv, a few weeks have passed before the dr sends someone for a blood test and they may have lost their igm new infection antibidies and now produce igg antibodies.

Im sure this happens in other countries too but in australia antibody levels arent tested, its either positive or negative. If you have positive igg antibodies they say it may have been ebv or the test can be indicating you have had it in the past. So getting a test to say you have a particular active virus would be rare unless you became septic and were hospitalised and if tested early on the infection and had positive igm antibodies indicating a new viral infection or they did a spinal tap and found the actual virus in your spinal cord fluid.

So i guess by the time someone sees a dr about their symptoms it can be several weeks for many of us and testing becomes less accurate. Dont forget the 6 month waiting period to diagnose cfsme.

Other basic immune tests like lymphocyte and neutrophil tests on a full blood count can indicate a viral infection but they cant tell us what the virus is or it could also be bacterial.

Until theres good , cheap and easy technology to detect a particular ongoing viral infection, its either a guess, an educated guess or you have done a treatment trial and improved on a particular anti infective drug.

 

[Marylib]

@alex3619

I'm shocked that today for the first time I'm reading about post polio syndrome.

https://en.wikipedia.org/wiki/Post-polio_syndrome

Seems widely known and respected and at least partially understood. We should be so lucky.

Apparently post polio syndrome can come on decades after the original polio infection. This makes me think about those people who say they had no ME/CFS trigger or a gradual onset. It might have been a virus they didn't even notice, from years before...

Yes I have a couple of friends with Post Polio - for both of them, it struck years later when least suspected. And apparently the existence of post polio syndrome was denied for years. This I learned on a separate occasion at a Post Polio Conference. The atmosphere was congenial - seems everyone realized that they might be the last generation of Post Polio patients. So they were having a good time together. Despite their considerable pain and physical limitations, they far outlasted me in terms of energy.

 

[FMMM1]

Myself, I cannot imagine how an outbreak like the classic ME/CFS outbreaks of the past would be overlooked today. Many of the historical outbreaks were localized to an institution like a hospital, and the incidence of ME/CFS in institution (the attack rate) was very high, often above 10%.

If you are running a hospital and suddenly a substantial portion of your staff develop ME/CFS, you are going notice.

@JenB wrote a good MEpedia article on the historical ME/CFS outbreaks.



Note also that unlike enterovirus, which often causes viral outbreaks in general, EBV almost never produces outbreaks, so you will not normally find EBV epidemics, let alone EBV epidemics causing ME/CFS.

The historical outbreaks of ME/CFS would have to have been caused by a virus that is capable of creating outbreaks. That excludes EBV, cytomegalovirus and HHV-6 which never create viral outbreaks.

@Hip I tagged you in another post. It may be relatively easy to resolve your questions about virus's. Check out Bhupesh Prusty's talk at last months NIH Conference. HHV6A has learned the trick of evading the immune response by fragmenting mitocondria (using microRNAs). Bhupesh states that other virus/bacteria have probably also developed this strategy; I suspect he already knows this! Possibly by testing exosomes for microRNAs, using mass spectrometry, you would be able to identify which virus/bacteria was responsible (I assume each has a slightly different microRNA).

What we need is the funding for science i.e. to resolve these issues.

ME Action are lobbying for the delivery of a diagnostic test and treatments
https://www.meaction.net/2019/02/26/announcing-millionsmissing-2019-join-us/

@JaimeS @Murph

 

[kday]

It might be but its more likely its several. However CFS is probably a huge number of illnesses, all lumped together. Certainly there are a huge range of triggering pathogens, though the usual culprits are either EBV or an enterovirus.

Evidence shows that it's a very dinstinct syndrome with very distinct and specific abnormalities. This enough is evidence that there may be a singular cause. I haven't seen any good evidence of heterogeneity unless you incorporate poorly selected cohorts and misdiagnosed patients into this pool of heterogeneity. If it's more than one thing, I'd bet the causative factors are a small handful of things that exert the same or very similar biological consequence. Different triggers doesn't mean the illness is heterogeneous. It only means that different risk factors can cause the same display of illness.

I was reading research about the lab abnormalities in Norwegian patients in the giardia outbreak and I cringed because the research shows they may not have the same syndrome at all. No NK Cell functional deficiency? Different inflammatory cytokinesis? How bout call it something else and keep it and their Rituximab in Norway? I think it's time that American scientists stop inviting them to our events.

Though doctors don't seem to be good at DDX's these days so I wouldn't be surprised if a large amount or even the majority are misdiagnosed. ME/CFS should be diagnosed with a combination of history, laboratory testing, and other testing (like VO2 max exercise testing and autonomic testing), but our poor guidelines don't lay out what these very useful tests are.

And because of this, you can end up with false heterogeneity. And I think that's exactly what is happening. Obfuscation of a distinct medical entity until it's not longer distinguishable.

 

[Murph]

Evidence shows that it's a very dinstinct syndrome with very distinct and specific abnormalities. This enough is evidence that there may be a singular cause. I haven't seen any good evidence of heterogeneity unless you incorporate poorly selected cohorts and misdiagnosed patients into this pool of heterogeneity. If it's more than one thing, I'd bet the causative factors are a small handful of things that exert the same or very similar biological consequence. Different triggers doesn't mean the illness is heterogeneous. It only means that different risk factors can cause the same display of illness.

I was reading research about the lab abnormalities in Norwegian patients in the giardia outbreak and I cringed because the research shows they may not have the same syndrome at all. No NK Cell functional deficiency? Different inflammatory cytokinesis? How bout call it something else and keep it and their Rituximab in Norway? I think it's time that American scientists stop inviting them to our events.

Though doctors don't seem to be good at DDX's these days so I wouldn't be surprised if a large amount or even the majority are misdiagnosed. ME/CFS should be diagnosed with a combination of history, laboratory testing, and other testing (like VO2 max exercise testing and autonomic testing), but our poor guidelines don't lay out what these very useful tests are.

And because of this, you can end up with false heterogeneity. And I think that's exactly what is happening. Obfuscation of a distinct medical entity until it's not longer distinguishable.

I see what you're saying. But also: if you take this argument to its extreme you have what they call the "no true scotsman" fallacy: you define me/cfs as non-heterogenous - so if anyone finds heterogeneity you're able to say they didn't only choose me/cfs patients.

 

[Hufsamor]

Post Polio patients. So they were having a good time together. Despite their considerable pain and physical limitations, they far outlasted me in terms of energy

Well yes, some have.
But my mother have this, and she would never ever be joining such a conference. Due to lack of energy.
The post polio hits differently. And for some of them, there are a considerable lack of energy.
I've read that post polio is the one sickness closest to me/ cfs

 

[FMMM1]

Evidence shows that it's a very dinstinct syndrome with very distinct and specific abnormalities. This enough is evidence that there may be a singular cause. I haven't seen any good evidence of heterogeneity unless you incorporate poorly selected cohorts and misdiagnosed patients into this pool of heterogeneity. If it's more than one thing, I'd bet the causative factors are a small handful of things that exert the same or very similar biological consequence. Different triggers doesn't mean the illness is heterogeneous. It only means that different risk factors can cause the same display of illness.

I was reading research about the lab abnormalities in Norwegian patients in the giardia outbreak and I cringed because the research shows they may not have the same syndrome at all. No NK Cell functional deficiency? Different inflammatory cytokinesis? How bout call it something else and keep it and their Rituximab in Norway? I think it's time that American scientists stop inviting them to our events.

Though doctors don't seem to be good at DDX's these days so I wouldn't be surprised if a large amount or even the majority are misdiagnosed. ME/CFS should be diagnosed with a combination of history, laboratory testing, and other testing (like VO2 max exercise testing and autonomic testing), but our poor guidelines don't lay out what these very useful tests are.

And because of this, you can end up with false heterogeneity. And I think that's exactly what is happening. Obfuscation of a distinct medical entity until it's not longer distinguishable.

Prusty's work, showing mitocondrial fragmentation may support your comments [NIH Conference last month]. Seems like a number of virus's/bacteria can fragment mitocondria i.e. to evade the immune response - same outcome different causes. However, we need large scale testing of patients to resolve whether it's "same outcome different causes" or "different outcomes different causes".

ME Action are lobbying for the development of a diagnostic test and treatments.

 

[kday]

I see what you're saying. But also: if you take this argument to its extreme you have what they call the "no true scotsman" fallacy: you define me/cfs as non-heterogenous - so if anyone finds heterogeneity you're able to say they didn't only choose me/cfs patients.

But this is happening. Studies co-authored by the well-known expert clinicians (many at it since the 80's) are generally pretty consistent. I am one who also fits the general findings of those studies.

Now if I dive into the pool of heterogeneity by looking at scientific publications thaf are not co-authored or signed off by the expert clinicians with a lot of clinical experience, it can sometimes even look as if ME/CFS isn't a real syndrome at all because of the inconsistencies.

I think the moral of the story is to not trust any PhD and any non-expert clinician to select cohorts of patients for studies.

When searching PubMed, I can put in a list of trustworthy names across the world. People that understand the science and history of the syndrome. And the science is pretty consistent.

I don't think it's a logical fallacy. You may call it bias that I have a "trusted" list of names. But these scientists have been around the block and have witnessed the history of the syndrome. They know what they are looking at. You could call this bias, or appeal to authority fallacy, or some other fallacy, but I think not immediately giving too weight much weight to studies not co-authored by expert clinicians is just smart. But if the studies not co-authored by ME/CFS expert clinicians are consistent with the studies co-authored by expert clinicians and/or are consistent with the history of the syndrome, I think it's perfectly reasonable to give them more weight. I believe this approach to be very scientific as well. You have to know how to filter out the junk no matter what area of science you are looking at. Filtering like this is just good science.

I particularly like Peterson. He'll put his name on a lot of papers. But generally not bad ones and generally not any ones that obfuscate or do not accurately represent the syndrome. I don't think he wanted to be part of the XMRV thing for example, because his researcher and clinician instincts knew it didn't fit with the syndrome. And he was quick to put his name on papers debunking it.

So yeah, I don't think I am falling in any type of logical fallacy trap. There are plenty of true scotsmen. I think many others are in an obfuscation trap though as they don't know how to filter out the science that causes a false sense of heterogeneity. If you include any science unbiasedly for the sake of inclusion, all it does is attempt to redefine what the syndrome is by including cohorts with abnormalities that do not align with historical findings.

 

[Rufous McKinney]

Until theres good , cheap and easy technology to detect a particular ongoing viral infection

Meanwhile: they plan flights to mars? But can't find a virus?

Also Jen Brea and some other mcas patients have mentioned they feel awful in Palo Alto.

Seen this comment about Palo Alto before. I assume this relates to: people going to Stanford University for ME CFS help...Are they visiting other towns around the San Francisco Bay area?

1) generally- its going to be moldy humid around there;
2) Stanford has: major particle accelerators and physics experiments.....
3) the whole bay Area is: going to have alot of chemical exposure

 

[frozenborderline]

Seen this comment about Palo Alto before. I assume this relates to: people going to Stanford University for ME CFS help...Are they visiting other towns around the San Francisco Bay area?

There’s a famous cfs doctor in Palo Alto—David kaufman

 

[frozenborderline]

1) generally- its going to be moldy humid around there;
2) Stanford has: major particle accelerators and physics experiments.....
3) the whole bay Area is: going to have alot of chemical exposure

Many people have speculated that the combination of biotoxins from outdoors mold or Cyanobacteria combined with exposures to various toxins involved in industry, has resulted in some outdoor toxins that are particularly problematic for many ill people.

 

[marlunette]

As far as geographical clusters?? I noted w interest that Ron said he found out there were a few severe ME patients on his same block, when they started doing the study. Perhaps that’s explainable by chance, I’m not great w math. But I found it interesting. Also Jen Brea and some other mcas patients have mentioned they feel awful in Palo Alto.
It would be very interesting to do a low budget but thorough epidemiological map even just in the US of ME/CFS patient locations by severity , perhaps color coded. Difficult project labor wise but no lab work so maybe doable? Maybe something the OMF could do??

I thought the same thing when Ron Davis said he found multiple patients within a few blocks. Since we don't really know how frequently ME/CFS occurs in the population, I think it would be hard to calculate the odds of that happening.

There are free or low-cost digital mapping options that allow people to put pins on maps and add ratings anonymously. An org with the capacity to get the word out could potentially get people to volunteer their info anonymously and ask people at a block level so it's not too personal. It wouldn't be super rigorous but it would probably help researchers figure out whether or not this is worth pursuing further.

 

[Hip]

Since we don't really know how frequently ME/CFS occurs in the population, I think it would be hard to calculate the odds of that happening.

We do know how frequently it occurs in the general population, as a result of various studies which have estimated the prevalence. 0.2% is the normally quoted prevalence.

 

[marlunette]

We do know how frequently it occurs in the general population, as a result of various studies which have estimated the prevalence. 0.2% is the normally quoted prevalence.

Oops. I thought there was some uncertainty around the percentage but I must be wrong. I have seen higher numbers quoted, maybe due to the different criteria being used.

 

[FMMM1]

Oops. I thought there was some uncertainty around the percentage but I must be wrong. I have seen higher numbers quoted, maybe due to the different criteria being used.

My understanding is that a commonly quoted figure is "approx 0.4%" just below the upper limit of the definition of a "rare disease" (0.5%). Bear in mind that there is no biomedical diagnostic test, so these really are estimates.

Random search online [https://www.ncbi.nlm.nih.gov/pubmed/12860574/ ]:
"RESULTS:
The overall weighted point prevalence of CFS, adjusted for nonresponse, was 235 per 100,000 persons (95% confidence interval, 142-327 per 100,000 persons). The prevalence of CFS was higher among women, 373 per 100,000 persons (95% confidence interval, 210-536 per 100,000 persons), than among men, 83 per 100,000 persons (95% confidence interval, 15-150 per 100,000 persons). Among subjects nonfatigued and fatigued for less than 6 months, the 1-year incidence of CFS was 180 per 100,000 persons (95% confidence interval, 0-466 per 100,000 persons)".

 

[frozenborderline]

There are free or low-cost digital mapping options that allow people to put pins on maps and add ratings anonymously. An org with the capacity to get the word out could potentially get people to volunteer their info anonymously and ask people at a block level so it's not too personal. It wouldn't be super rigorous but it would probably help researchers figure out whether or not this is worth pursuing further.

I did mention this to OMF ans they said they couldn’t pursue that at this time. Feel like some basic epidemiology hasn’t been done in this illness and would reveal a lot. Recently found out someone got severe me/cfs on the same block as me (in a tiny rural town) a few years back, without me knowing.

 

[frozenborderline]

We do know how frequently it occurs in the general population, as a result of various studies which have estimated the prevalence. 0.2% is the normally quoted prevalence.

So what are the odds of that many severe patients on the same block ? And I know I could be fooled by randomness here but it does seem odd and noteworthy

 

[Hip]

So what are the odds of that many severe patients on the same block ? And I know I could be fooled by randomness here but it does seem odd and noteworthy

Well if you had a block containing say 5,000 people, since the general prevalence of ME/CFS is normally quoted at 0.2%, then you might expect 0.2% x 5,000 = 10 people to have ME/CFS in that block.

If you had more than that, say 20 people with ME/CFS in this block, and you want to calculate the odds of that happening just by chance, I think you would need to use the formulas from a branch of mathematics called "permutations and combinations" to find your answer. I don't think it would be a difficult calculation, but I find anything mathematical hard going with brain fog.