Who said: 80% of ME is post-infectious

I've heard it said and I see it on ME-pedia's main page for ME... but it's not cited.

This is something that's hard to search for. Anyone know where this figure comes from? Is it for real? And how was it determined?

 

Possibly this?

The Evengård et al study says 80%.

https://www.ncbi.nlm.nih.gov/pubmed/12839515

 

I'd caution not to conflate post-infectious with solely following acute illness. There is nothing to say that gradual onset is not also post-infectious.

 

YES.

https://academic.oup.com/cid/article-pdf/36/5/671/1244019/36-5-671.pdf may also be a source; if you add up all of their post-infectious triggers (including mold) it ends up being 75.5% or thereabouts. Found by @Hip

 

Doesn't really sound like a solid claim for the main page on ME. Thanks for those looking into it.

 

The relative number of cases that are triggered by an infection is typically in the interval 70–80%. Wessely states 72%, Evengård 80% (2003), and the NIH workshop 78%. There is a study by Palacios among nurses in the US where only 19% of the cases are triggered by infection. I don’t know why this study differs from the other.

Wessely S, Powell R. Fatigue syndromes: a comparison of chronic "postviral" fatigue with neuromuscular and affective disorders. J Neurol Neurosurg Psychiatry. 1989;52(8):940–8.

Evengård B, Jonzon E, Sandberg A, et al. Differences between patients with chronic fatigue syndrome and with chronic fatigue at an infectious disease clinic in Stockholm, Sweden. Psychiatry Clin Neurosci. 2003;57(4):361–8.

State of the Knowledge Workshop. Myalgic Encephalomyelitis/Chronic FatigueSyndrome (ME/CFS) Research: Workshop Report. Bethesda: National Institutes of Health; 2011.

Palacios N, Fitzgerald KC, Komaroff AL, et al. Incidence of myalgic encephalomyelitis/chronic fatigue syndrome in a large prospective cohort of U.S. nurses. Fatigue. 2017;5(3):159–66.

 

I thought ME Action were the ones claiming the 80% figure. It's in the educational video by David Kaufman.

Good to check these things. Had a quick look (without reading the full studies) and found these:

2018 Jason study: "The majority of participants (93%) from the qualitative sample reported that a virus or infection was the cause of or partial cause of the ME or CFS onset."

I think Ray et al. (1998) also found that around 90% of ME/CFS patients report an infectious trigger at onset (but without it being considered the sole cause).

Salit et al. (1997) reported that "CFS started with an apparently infectious illness in 96 (72%) but a definite infection was only found in seven of these 96 (7%). "

Naes et al. (2010) reported that "Initial infection was reported by 77%."

De Beker et al. (2002): "If all infectious onset events were totalled (flu-like illness, viral and other infections, upper respiratory tract infection) almost 60% of the CFS patient group had a potentially infectious etiology."​

Haven't read these studies in full, so I hope somebody does to check if they are reliable.

Some studies refer to acute onset as if it's the same thing as an infectious onset, so that can be confusing. I think initially specialists saw a patient sample in which around 70-80% reported an acute onset but that later epidemiological studies brought this figure back to 50%.

 

Interesting. My wife had a nasty flu bug appear the day after having an operation (so the bug was presumably already taking hold when she had the op). So we tend to think that it was maybe that double-hit that tipped over the edge into ME. But of course that is purely conjecture. The ME onset was rapid, in that my wife seemed like she was not recovering properly from the operation, whereas in fact it was the ME kicking in concurrently with recovering from the op.

ETA: In fact, is that significant in any way, and is it commonplace? That after the triggering infection, the person never fully recovers, and that the ME becomes established before the person gets the chance to fully recover from the bug (and maybe from the op and the anaesthetic)? Is that of any relevance? And just in case any BPS'ites are lurking, no my wife did not fall into a period of inactivity to provoke deconditioning! She was getting back on her feet as best she could within a couple of days, which is, and always has been, her way.

 

Presumably unless there is confirmation that the patient had a specific infectious agent, we can not be certain that all onsets associated with an episode of 'flu-like' symptoms are the result of an infection, as one of the common symptoms of ongoing ME is 'flu-like' without any identified ongoing infection. There is a danger here of inferring an infection as a cause just from symptoms that may be a feature of the condition.

My first onset was associated with an identified infection with the Epstein-Barr virus, but my second 'onset' or relapse was associated with what seemed like a bad dose of flu, but the presence of a virus was never formally confirmed, just assumed from the symptoms.

Often for me PEM is associate with cold or flue like symptoms, and it is only possible to tell them apart from the onset of an acute infection of some sort by seeing if the symptoms go away with rest or if they devlop into an apparent full blow infection despite rest. However I can not conversely rule out that these short lasting symptoms are not in fact a mild short lived infection.

Presumably this confusion can get even worse with gradual onset of ME. So presumably there is an element of unreliability deciding retrospectively if the onset was associated with an active infection or not.

 

On reflection, I had a sudden onset of symptoms, literally between 1 and 2pm on a Wednesday afternoon at a regional communication technology special interest group. Some weeks later presence of the Epstein Barr markers was established. Everyone assumed that my symptoms were acute glandular fever, and over six to eight months of improving, getting back to work, relapsing, etc ME was diagnosed.

However although I can say my ME had a sudden onset and everyone assumed it was associated with an acute infection, can I be certain of this? It is theoretically possible, even if unlikely, that I had a subclinical infection prior to my onset that was the reason for testing positively for Epstein Barr.

 

"Lurking BPS'ites", @Barry, great phrase!

Excellent point about getting back to activity right away. This has always been my method as well, and doubtless most others with ME.

There are many, many stories about pwME struggling to maintain work, fitness, and all other obligations until the disease progresses to the point where they can't.

 

Interesting, this is very similar to my experience. I also improved after the 6-8 month period and returned to work, only to relapse within a month and get a diagnose of ME. The virus was never identified, but I did have 'extremely' elevated anti-thyroid antibodies and vertigo attacks.

 

There is also the reverse consideration: since the pathogens associated with ME/CFS can be caught asymptomatically, without showing any initial symptoms (or only mild symptoms no more than a few sniffles), the ~20% of patients who did not observe an infectious onset may well have had their ME/CFS appear after an infection, but a "silent" infection which caused no acute symptoms.

 

The problem is there are many infections out there and we don't have specific tests for many of them. The conclusion isn't necessarily that these cases aren't due to infection, we can however conclude that the specific infectious pathogen does not seem so important.

 

ME/CFS is associated with a range of viruses and certain bacteria, but I would not say that the specific infectious pathogen is not important.

If we take the case of norovirus for example (which is pretty contagious and typically creates outbreaks on cruise ships), norovirus produces a similar gastrointestinal illness to enteroviruses like coxsackievirus B, but there is no known association between norovirus and ME/CFS.

That is to say, when you get these norovirus outbreaks, you don't find a certain percentage of infectees coming down with ME/CFS.

Adenovirus is another that creates outbreaks, typically in military barracks. But again you don't find ME/CFS appearing as a sequelae.



Many viral medical conditions are caused by a specific range of viruses, but not caused by viruses outside that range. Viral myocarditis for example can be caused by certain viruses, but not others.

So you might expect the same thing with ME/CFS: certain viruses may cause or trigger ME/CFS, whereas other viruses are likely completely uninvolved.

 

Right, but there are more people at #MEAction than just me! I asked where the figure had come from at #MEAction HQ, but most are already turning off notifications for the holiday season.

 

Do we really know that? The problem is we don't regularly test for Norovirus and we haven't done a prospective study to see if people with such infections develop ME.

I think the primary risk factor associated with the infection is how long the infection sticks around for increases the risk of ME. EBV for example, sticks around for a long time, so...

 

I don't think there is any absolute proof that norovirus does not cause ME/CFS.

But I believe norovirus outbreaks are generally quickly identified. So if someone developed ME/CFS after a norovirus infection picked up during an outbreak, they would usually know it was norovirus. But I have never once seen a patient on an ME/CFS forum or blog say, "my ME/CFS appeared after a norovirus infection". Nor have I seen any research papers, or doctors' reports, suggesting that norovirus might be linked to ME/CFS.


Furthermore, norovirus is an RNA virus, and unlike DNA viruses (like the herpesvirus family), RNA viruses are generally not capable of latency. So norovirus I believe would not be able to stick around long-term in the body after the acute infection is cleared by the immune response, as it cannot hide away in cells in a latent state.

To me it is no coincidence that all the pathogens linked to ME/CFS are ones that can, by latency or some other means, stick around in the body.

You never find ME/CFS appearing after a common cold infection with rhinovirus, because rhinovirus cannot enter latency and is completely cleared from the body by the immune system.

If it was merely the immune response to any old infection that could trigger ME/CFS, then we would observe people coming down with ME/CFS after a cold. Which we don't see.

That fact tells you something. It tells you that it's unlikely to be the generic effect of any old infection that triggers ME/CFS, but more likely to be caused by the continued chronic presence of pathogens that are able to persist in the body.




By the way, enterovirus is also an RNA virus, and these are unable to create latency states and thus normally unable stick around to form a chronic presence in the body. Enteroviruses are normally thought of as producing acute infections only.

However, we now know that certain enteroviruses can undergo genomic mutations in the body that transform it into a different viral quasi-species that is able to persist long-term as an intracellular infection (that different species is called non-cytolytic enterovirus).

There are dozens of different enteroviruses, but the only ones linked to ME/CFS are the enterovirus B species — which is the only enterovirus species known to form chronic infections. Coincidence? I think not.

 

Lots of people claim a non-specific infectious trigger. I don't see the big deal. The fact they didn't name it is because the infection wasn't characterised. This is a clear bias.

 

I am not really following your statement.

If you are trying to suggest that because some patients were not able to identify their triggering infection, that that implies that any infection can trigger ME/CFS, well that does not follow logically.