Any recent MECFS outbreaks?

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There was an interesting talk at the Emerge conference on chronics Q Fever and Q fever fatigue syndrome. Seems like the Q fever outbreak was well known by epidemiologists and public health officials which helped the post-Q fever illnesses to be understood and labeleled with the specific label rather than beig bundled as ME/CFS


Some good discussion in the Q&A about the late Dr Marmion of Adelaide who found bacteria or bits of bacteria in the bone marrow of QFS patients. Theory being that caused perpetual immune activation. Such studies have never been repeated, apparently.
 
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There was an interesting talk at the Emerge conference on chronics Q Fever and Q fever fatigue syndrome. Seems like the Q fever outbreak was well known by epidemiologists and public health officials which helped the post-Q fever illnesses to be understood and labeleled with the specific label rather than beig bundled as ME/CFS


Some good discussion in the Q&A about the late Dr Marmion of Adelaide who found bacteria or bits of bacteria in the bone marrow of QFS patients. Theory being that caused perpetual immune activation. Such studies have never been repeated, apparently.
I also found Dr. Raijmakers' talk very interesting. And the theory of a perpetual immune activation surely has not been ruled out.

There is also the small (n=253) prospective Australian Dubbo study which included Q-fever, EBV, and Ross River virus infections and reported that 6 months post-infection 11% of patients met diagnostic criteria for ME/CFS (I don't remember which criteria), and this 11% seemed mostly explained by the severity of the infection and not by which infection it was.

So this all fits with Murph's point that we might not see recent epidemics of ME/CFS if they are all being labeled post-Q-fever fatigue or post-EBV fatigue or post-anything-else fatigue.

Also at the eMErge meeting, I talked to Cathie Powell, MPH, CEO of an Adelaide group called Bridges and Pathways, which aims to help patients and caregivers dealing with ME. She says they still see outbreaks of ME/CFS in Adelaide, but they are smaller. She sees clusters from individual high schools - perhaps 5-12 new ME/CFS patients at a time. This came up because, in making my point about epidemics and common mutations, I used the example of the famous 1949 Adelaide epidemic of ME/CFS, which was, at the time, called atypical polio and might today be called post-poliovirus fatigue.
 
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I also found Dr. Raijmakers' talk very interesting. And the theory of a perpetual immune activation surely has not been ruled out.

There is also the small (n=253) prospective Australian Dubbo study which included Q-fever, EBV, and Ross River virus infections and reported that 6 months post-infection 11% of patients met diagnostic criteria for ME/CFS (I don't remember which criteria), and this 11% seemed mostly explained by the severity of the infection and not by which infection it was.

So this all fits with Murph's point that we might not see recent epidemics of ME/CFS if they are all being labeled post-Q-fever fatigue or post-EBV fatigue or post-anything-else fatigue.

Also at the eMErge meeting, I talked to Cathie Powell, MPH, CEO of an Adelaide group called Bridges and Pathways, which aims to help patients and caregivers dealing with ME. She says they still see outbreaks of ME/CFS in Adelaide, but they are smaller. She sees clusters from individual high schools - perhaps 5-12 new ME/CFS patients at a time. This came up because, in making my point about epidemics and common mutations, I used the example of the famous 1949 Adelaide epidemic of ME/CFS, which was, at the time, called atypical polio and might today be called post-poliovirus fatigue.
I think we have to agree outbreaks are ongoing but they are not perceived so much as ME/CFS outbreaks anymore.

nb. I laughed at hearing the crowd all yell DUBBO! when you pronounced it Dubeau. :)
 

Hip

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I think we have to agree outbreaks are ongoing but they are not perceived so much as ME/CFS outbreaks anymore.
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.
 
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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.
Going off Jen's list, hospital-based MECFS outbreaks were common in the first part of last century but became relatively rare. A handful after 1960? That's infrequent enough that you wouldn't expect them too often - one or two every decade, perhaps. Improved handwashing and infection practice in hospitals might make them even rarer now.
 

debored13

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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%.
Many but not all outbreaks in hospitals. Tahoe and lundonville notable exceptions. And that could have been due to an environmental factor present in those hospitals that no longer is as present, a chemical or mold (maybe current day hospitals have better ventilation/cleaning.
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
so hhv-6 can’t cause outbreaks? I thought cheney ans Peterson suspected it as causative agent.

I think that you have a point about hospital outbreaks not going unnoticed but w/ any other outbreak I would not think it would necessarily be noticed. There are many social factors that might prevent clusters of illness going unnoticed in this day and age. I think if really thorough epidemiological mapping was done we would notice geographical patterns. I still think at least a large factor is environmental , although viruses obviously play a role.
Jen brea recently commented on Twitter about Palo Alto feeling really bad outdoors for her. And this has been reported by others. There are people that find the whole Bay Area intolerable!!
 

roller

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does anyone know if vaccine batch + vaccinated person (+ shipping location) are electronically stored ?
if so, from what year on, what countries ... ?

...... wondering because ...

would a vaccine contamination be detected (in the logistics system) for epidemics/diseases like
- mecfs
- autoimmunity
- (others possibly)
?
(or were vaccines (or vaccine contamination) definitely ruled out as a cause already?)

not necessarily that there was THAT pathogen in it, but perhaps something that later e.g. together with EBV/bacteria/prions... causes disease (or some similar process).
 
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Hip

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Going off Jen's list, hospital-based MECFS outbreaks were common in the first part of last century but became relatively rare. A handful after 1960? That's infrequent enough that you wouldn't expect them too often - one or two every decade, perhaps. Improved handwashing and infection practice in hospitals might make them even rarer now.
It's still quite extraordinary how the attack rate was so high when you had these ME/CFS outbreaks in hospitals and other institutional buildings; but as soon as the virus spread beyond the institution into the population at large (as a virus will inevitably do), then it lost most of its ability to trigger ME/CFS.

As mentioned earlier, it suggests that some factor present within the building was working in tandem with the virus to trigger ME/CFS. The dual factor theory of ME/CFS triggering.


Not on the MEpedia's comprehensive list of outbreaks is the 1990 Gulf War Illness outbreak of ME/CFS — the largest ever outbreak. I suspect the Gulf War ME/CFS was due to a viral infection passing among the troops, along with the known exposure to organophosphates. Again a dual factor trigger.



so hhv-6 can’t cause outbreaks? I thought cheney ans Peterson suspected it as causative agent.
Some viruses are just not able to create infectious outbreaks. Viruses that do not cause outbreaks are just acquired sporadically.

You hear of norovirus outbreaks, adenovirus outbreaks, measles outbreaks (among the unvaccinated), Coxsackie virus outbreaks, etc, but you never get, for example, cytomegalovirus outbreaks.


HHV-6 was discovered in 1986, just after the 1984 Lake Tahoe ME/CFS outbreak, so maybe they did not know much about HHV-6 when they were investigating this outbreak. But we now know HHV-6 is usually acquired at a very young age (usually before 2), and nearly 100% of adults have it.
 

i-lava-u

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the 1990 Gulf War Illness outbreak of ME/CF
This is not related to the GWI, nor ME/CFS necessarily, but interesting as an example of what exposure to environmental stressors can do...and @HTester this may be of interest to you? Or not :xeyes:

My husband was born on the Camp Lejeune marine corps base in mid 70's. There is now well known documentation of water contamination and long term health effects from it showing up many years later.

https://www.publichealth.va.gov/exposures/camp-Lejeune/
https://en.wikipedia.org/wiki/Camp_Lejeune_water_contamination

His parents both lived on base, himself, an older and younger sister (there are 7 children now in my husbands family)

My mother in-law was not able to breastfeed so all of the 3 babies received contaminated tap water with their formula. They all bathed, drank, washed clothes and dishes, cooked and cleaned with contaminated water.

About 10 years ago my mother-in-law was diagnosed with Lupus, Addison's and many other autoimmune issues since. His older sister, also about the same time, was diagnosed with Rheumatoid arthritis and Celiac disease. His younger sister, about 15 years ago was diagnosed with primary progressive MS. Last year, my father-in-law was diagnosed with Parkinson's disease. My husband miraculously does not have any autoimmune issues, but I worry that he may also, at some point, develop them.

So, 4 out of the 5 that were in that environment have developed serious medical issues. The other 4 out of 4 not exposed have no significant health impairments. I do not find this accidental or a fluke.

The government studies have shown the detrimental effects of being exposed to the pollutants. Many, many more people that lived and worked there are also very ill.

This was just one incident of many more bases that also have or have had contaminated water.
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ETA: I couldn't fall asleep last night when writing this, late at night, so brain fog. :pem: :xeyes: The reason I shared this is that this is an example of how an exposure to something harmful can cause issues many years down the line. There was not an immediate "outbreak", but there have been many, many people that were exposed, to go on and develop serious health repercussions later on (the water was contaminated from 1953 to 1987)

I find it very interesting that there are sudden onset and gradual onset ME/CFS occurrences.
 
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debored13

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I suspect the Gulf War ME/CFS was due to a viral infection passing among the troops, along with the known exposure to organophosphates. Again a dual factor trigger.
I read that Saddam planned to use aflatoxin in shells in the gulf war but apparently never got around to it? But also apparently there were bad Cyanobacteria exposures in gulf war troops in Kuwait which later manifest in higher rate of Alzheimer’s in Troops
 

debored13

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Bad news and fear gets clicks. (Alex Jones is a great example!). Epidemics of dangerous unknown diseases would get huge clicks. If one outlet declined to cover that another outlet would jump on it. (My bona fides: I work in the media and editors never interfere with my stories. I got a big story on me/cfs into a rupert murdoch outlet a couple of years ago.)

We also have bloggers and social media. It would be very hard, I believe, to hide news of outbreaks
Well, this is not exactly true. CFS is a devastating disease. It’s a living death. But it’s not usually fatal. That makes it less of a good tabloid story than many other infectious diseases. But also, the tone for this disease was fairly successfully set by straus et al, who, when initially frustrated at the outbreak not fitting their chronic ebv theories, decided to name it “chronic fatigue syndrome” which of course sounds trivial , and discard the references to immune dysfunction in the name and definition. There’s not a conspiracy exactly in terms of an organized, secret movement to discredit the disease, but it is still a political problem. Also it’s a disease that’s disabling and not rare and doesn’t lead to death usually so it leads to a ton of insurance payouts and disability payouts if it is considered serious and experimental treatments are approved. Many chronic diseases of comparable or even lower severity have a higher death rate
The ties between the DWP, New Labour, private insurers, and all the PACE researchers are all well documented. No conspiracy.
 

debored13

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As far as outbreaks that involve the same pathogen going around and disabling a group of people, I don’t think we have that incredibly common anymore. 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??
 

Moof

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It's still quite extraordinary how the attack rate was so high when you had these ME/CFS outbreaks in hospitals and other institutional buildings; but as soon as the virus spread beyond the institution into the population at large (as a virus will inevitably do), then it lost most of its ability to trigger ME/CFS.

As mentioned earlier, it suggests that some factor present within the building was working in tandem with the virus to trigger ME/CFS. The dual factor theory of ME/CFS triggering.
I guess it's possible that the dual factor could have been high levels of stress and the inability to take appropriate rest? For instance, in a hospital caring for people with a dangerous infectious disease – especially given the fierce workplace discipline of the 1950s – staff would have been under immense pressure to carry on working extremely hard regardless of how well they were themselves. This would tie in with Nancy Klimas's finding that GWI is much more prevalent in veterans who received multiple vaccines and toxic exposures when they were already in theatre, as opposed to those who received them beforehand.
 

Hip

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I guess it's possible that the dual factor could have been high levels of stress and the inability to take appropriate rest? For instance, in a hospital caring for people with a dangerous infectious disease – especially given the fierce workplace discipline of the 1950s – staff would have been under immense pressure to carry on working extremely hard regardless of how well they were themselves.
Workplace stress might I guess play a minor role, would not have thought it would be a major factor in these hospital ME/CFS outbreaks, because such stress would be present in all hospitals.

Given that that the enteroviruses linked to ME/CFS are common viruses in general circulation, if workplace stress were a major factor, then every time one of these common viruses entered a hospital environment, it would trigger an ME/CFS outbreak. But we don't see that in reality.



Going off Jen's list, hospital-based MECFS outbreaks were common in the first part of last century but became relatively rare. A handful after 1960? That's infrequent enough that you wouldn't expect them too often - one or two every decade, perhaps. Improved handwashing and infection practice in hospitals might make them even rarer now.
It's certainly possible that hand washing and other modern hygiene practices might reduce the spread of a virus a hospital.
 

Moof

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Workplace stress might I guess play a minor role, would not have thought it would be a major factor in these hospital ME/CFS outbreaks, because such stress would be present in all hospitals.
I didn't explain myself very well – what I meant was the pressure to keep on working, even though they were ill themselves with an ME-associated pathogen. Many current patients feel that not stopping to rest soon enough, and for long enough, was a factor in their own (endemic) cases; if acute lack of rest was teamed with a particularly risky infectious trigger, it may go some way to explaining the outbreaks.

I've only read up the Royal Free outbreak in any detail, but a high proportion of those who became sick were female nurses and auxiliaries. Many of them would have had caring responsibilities in addition to their jobs, putting even greater pressure on them to keep working despite being ill. The women presumably took the infectious trigger home to husbands, children and friends; but if they were not under the same physical and psychological stress from nursing people with a potentially deadly disease, it might explain why they didn't also develop ME.

However – to undermine my own case – it's reported that at least some of those 1955 epidemic patients developed brain or spinal lesions that are not unusually seen in endemic ME. It may be a different disease, in the same way that GWI appears similar but is nevertheless distinct.
 

Hip

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I didn't explain myself very well – what I meant was the pressure to keep on working, even though they were ill themselves with an ME-associated pathogen.
I do understand what you are saying, and it could play a role. 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.
 
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It's still quite extraordinary how the attack rate was so high when you had these ME/CFS outbreaks in hospitals and other institutional buildings; but as soon as the virus spread beyond the institution into the population at large (as a virus will inevitably do), then it lost most of its ability to trigger ME/CFS.
@Hip Two things about this short paragraph... Obviously, I agree with you that these high attack rates are extraordinary, but you know a lot about virology that I don't and I wonder if you think the virologist-on-the-street would also find these attack rates extraordinary. If so, why?

Second, it seems possible that the virus, once it spread beyond the institution, didn't lose most of it's ability to trigger ME/CFS - what it lost was the institutional environment, and the second, third, or fourth "hit" all of which were required parts of that particular trigger.

There was a large attack rate in Adelaide in 1949, but most (maybe all) of those patients were seen in a single hospital. Could they have acquired the virus, gone to the hospital, and there encountered the "rest" of a ME/CFS trigger?
 
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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.
Does this argument imply that every ME/CFS outbreak includes a virus as part of its trigger? Are you further suggesting that EBV, CMV and HHV-6 could be triggers for sporadic cases, just not for outbreaks?

If I recall correctly, EBV was one of the infections in the DUBBO infection outcome study and that 11% of patients seemed to have CFS six months after infection, independent of which virus they had.

Isn't it possible that outbreaks need not depend on a viral trigger? What's required is a localized appearance of an effective trigger. Many triggers appear to include a virus, but are you thinking a virus is a necessary part of all triggers? Are you also thinking that a virus capable of viral outbreaks is a necessary part of the etiology of an ME/CFS epidemic?
 

Hip

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but you know a lot about virology that I don't and I wonder if you think the virologist-on-the-street would also find these attack rates extraordinary. If so, why?
I wish I did know a lot about virology, but in fact I've just picked up a few bits of knowledge on the main viruses associated with ME/CFS, but don't really have any broad understanding, unfortunately.

I think the attack rate of the viruses in these institutional outbreaks is not extraordinary per se, but extraordinary in relation how these viruses normally behave at large. If you consider that the prevalence of ME/CFS in the general populace is around 0.2%, but in these institutions you might find 10% or more of the staff suddenly being hit with ME/CFS as the virus circulates, that's a factor of 50 difference in the prevalence.

So something in the institutional environment was making it easier for the virus to trigger ME/CFS.



Second, it seems possible that the virus, once it spread beyond the institution, didn't lose most of it's ability to trigger ME/CFS - what it lost was the institutional environment, and the second, third, or fourth "hit" all of which were required parts of that particular trigger.
Yes, that's what I believe may be the case. My hunch is that in general, an ME/CFS-associated virus like coxsackievirus B or Epstein-Barr virus will not often cause ME/CFS on its own; but when the virus is combined with certain other factors (like perhaps an immune-modifying environmental chemical or biotoxin), those factors facilitate the virus to trigger ME/CFS much more readily.

One interesting bit of evidence for this comes from Dr John Chia's discovery of the corticosteroid + acute viral infection combination trigger of ME/CFS. Dr Chia found out that literally hundreds of his ME/CFS patients had developed ME/CFS after being inadvertently prescribed corticosteroids during an acute viral infection.

In a probably over-simplistic and naive way, I interpret this as perhaps the immune weakening effect of corticosteroids allowing the virus during its acute infection phase (when you have the highest level of virus in the blood) to more deeply insinuate itself into the body or into important tissue compartments such as the brain.

Or perhaps the weakened immunity creates an abnormal immune response, and it's that abnormal response that then becomes the basis of the ME/CFS.

I also think this may explain the known chronic stress connection to ME/CFS: chronic stress also weakens immunity by raising cortisol, so if you were unfortunate enough to catch an ME/CFS virus during a period of chronic stress, maybe your weakened immunity allows the virus to insinuate itself more deeply in the body. That I think could explain the published studies showing that major chronic stress increases the risk of ME/CFS.

Dr Joseph Brewer's study suggested that mold biotoxins (from water-damaged buildings) may be another environmental risk factor for ME/CFS.



There was a large attack rate in Adelaide in 1949, but most (maybe all) of those patients were seen in a single hospital. Could they have acquired the virus, gone to the hospital, and there encountered the "rest" of a ME/CFS trigger?
I've not read about the Adelaide outbreak, though in cases of a city-wide outbreak, as a guess, perhaps a more likely scenario might be enteroviral contamination of the water supply.

It does not seem feasible that a whole city would be affected by some environmental chemicals (that's more feasible in an institution or a village), so something like a viral contamination of the water supply might be a possible explanation. Enterovirus is often found in lakes, and enteroviruses can be detected even in treated drinking water supplies. Ref: 1


I am not sure if a quick visit to a hospital would be enough to expose a virally-infected person to the "rest" of the ME/CFS triggering factor (but I guess that would depend on the nature of the factor). If there is say an toxic environmental chemical in the hospital, it may perhaps require months or years of daily exposure before it causes ill effects to health, making you more susceptible to getting ME/CFS from a virus.

It's interesting that in the Royal Free Hospital outbreak, the hospital patients did not usually get hit with ME/CFS, mainly just the staff. Since most patients will only be in the hospital for a short time, but the staff will be there permanently, that suggests that at least in the Royal Free case, it required months or years of exposure to the environment. Perhaps there was some sort of bioaccumulative chemical toxin in the Royal Free, that slowly build up in the body tissues over months or years.



Are you further suggesting that EBV, CMV and HHV-6 could be triggers for sporadic cases, just not for outbreaks?
Yes, I would think the herpesviruses would only be capable of causing sporadic cases, whereas enteroviruses I would think could cause both sporadic and epidemic.

For EBV there are several studies (Dubbo is just one of them) demonstrating that about 10% or more of patients with mononucleosis will go on to get ME/CFS. Although one study found that after around 2 years, many with mono-triggered ME/CFS recover, and the final figure 2 years after mono is around 4% still with ME/CFS. Those studies are here: 1 2 3 4

There isn't the same evidence for HHV-6, cytomegalovirus, coxsackievirus B and echovirus triggering ME/CFS; for these viruses there is evidence of ongoing infection in ME/CFS patients (especially for enteroviruses, which are found by PCR in the muscles, brain and stomach tissues of patients).

I would say that in terms of published studies of triggering ME/CFS, EBV has the strongest evidence base; whereas in terms of studies demonstrating low-level ongoing infection, enterovirus has the strongest evidence base.

In the case of HHV-6, I am unsure if this virus could ever be a trigger of ME/CFS, as this virus is present in virtually 100% of adults, and is usually first caught early in infancy. Though once present in the body it could play a role in ME/CFS, once ME/CFS manifests.

However, cytomegalovirus can be first caught at any time in life, so I imagine this could be a trigger virus. Likewise with coxsackievirus B and echovirus, these can be caught anytime during life, and there are several serotypes of CVB and echovirus linked to ME/CFS, so even if you have already caught one enterovirus earlier in life, you can catch another and that may trigger ME/CFS.



Isn't it possible that outbreaks need not depend on a viral trigger? What's required is a localized appearance of an effective trigger. Many triggers appear to include a virus, but are you thinking a virus is a necessary part of all triggers? Are you also thinking that a virus capable of viral outbreaks is a necessary part of the etiology of an ME/CFS epidemic?
Does this argument imply that every ME/CFS outbreak includes a virus as part of its trigger?
@JenB may be the best person to answer this question, as she trawled through about a quarter of all the published papers on the ME/CFS outbreaks, in order to write the MEpedia ME/CFS outbreaks article. I've only really looked at the Royal Free Hospital and the Lake Tahoe outbreaks in any detail.

But as far as I know an infectious agent was always involved. Even though in most cases no infectious agent was found, it's usually clear that you have an infectious outbreak on you hands, because of the acute symptoms that will hit one person at a time over many months (acute symptoms such as a short flu-like illness, gastrointestinal illness, sore throat, etc, which will then be followed by ME/CFS in a certain percentage of cases).

As the MEpedia article says:
The pattern of spread suggested a highly infectious agent that spread person to person, rather than through contaminated food or drink or exposure to a single toxic agent.
 
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