Patient perceptions of infectious illnesses preceding Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, 2021, Jason et al

Abstract

Objectives
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is often reported to be caused by an infectious agent. However, it is unclear whether one infectious agent might be the cause or whether there might be many different infectious agents. The objective of this study was to identify self-reported infectious illnesses associated with the onset of ME/CFS.

Methods
The present study involved data from multiple sites in several countries. 1773 individuals diagnosed with either ME, CFS or ME/CFS provided qualitative data concerning infectious triggers which were coded and classified for analysis.

Results
60.3% of patients report a variety of infectious illnesses some time before onset of ME/CFS. The most frequently reported infectious illness was Mononucleosis, which occurred in 30% of infections. However, over 100 other infectious illnesses were mentioned.

Discussion
The findings suggest that many infectious agents might be associated with the onset of ME/CFS.

Paywall: https://journals.sagepub.com/doi/10.1177/17423953211043106

 

One problem is that if you want to find a cause of something and there's no way to prove or disprove the cause, it's fairly easy to find something to blame. I had a tetanus booster some months before I developed ME. Was that the cause? There's no way to test that. Did I sneeze at least once in the several months before ME? Was that the viral cause? Did I visit a building that had possible mold?

If you asked the questions appropriately, I think 60% of the patients would report sighting yellow vehicles, or eating junk food, or getting rained on, or any number of other factors that can't be proven to not be the cause of ME. Pointless research IMO.

 

their is also the problem of many people who have asymptomatic infections .

 

I think that there will be varying degrees of uncertainty from person to person and onset to onset.

For me my ME began with an acute episode of glandular fever (EBV), there was 100% overlap in symptoms between the glandular fever and the subsequent ME and no obvious way of distinguishing where one ended and the other began. Obviously of itself EBV is not sufficient to fully explain to explain developing ME, otherwise why do so many people have EBV infections but not develop ME and how can many disparate viruses, or even no obvious viral infection, trigger the same condition ie ME. However I can not believe that coincidence could sufficiently explain the relationship between my ME and my glandular fever.

There must be some relationship between the body’s response to an acute viral infection and ME. My own experience indicates it is not a simple one as I believed I had subsequently recovered from ME, but then in association with a presumed season flue infection (the virus was not formally confirmed) I had a total relapse, again it is not obvious where the acute flue infection ended and the ME relapse began. Over the subsequent years I have had less complete remissions and more serious relapses, not associated with any obvious viral infections, and new symptoms have emerged such that my ME now is markedly different to the initial glandular and seasonal flue related conditions. So I also believe that my ME is a condition in itself beyond any viral triggers.

Though association is not of itself sufficient to demonstrate causation, I find it very hard to imagine my two sudden onsets, with a 100% overlap of symptoms with the associated viral infections and no way of defining a point of transition from acute viral infection to the chronic ME are not at least causally contributing factors.

That there are others whose experience is less clear cut, means any full answer is more complex than a simple causal relationship between viral infections and ME onset, but for some such as me it is very hard conceive that viral infections were not contributing causally.

 

Words matter. I hate that they chose the word ‘perception’ in the title. My infectious onset is documented. Clinically it was just as clear. I remember in my own words telling my doctor ‘I have felt that the flu is coming for over a week now, you know, sore throat, sore lymph nodes, exhausted, sore muscles, but i have no respiratory symptoms’

I understand that not everyone went to their dr, and may have missed the acute phase window, but perception of infection is very muddy.

 

My onset was very rapid, but I can’t associate it with any variety of infection. The same was true for my daughter, 8 years later, when we were living in a different house in a different state. There was no acute phase for either of us. We both were just abruptly very ill. Subclinical infection is possible, but I am far more inclined to think that there has to be a genetic connection.

 

My ME also started with ‘I have felt that the flu is coming'. The muscle aches/body tenderness and overall malaise seemed identical to previous flu infections. However, the next day I felt fine again. Then a week later, the same feeling occurred, and this time I felt feverish and really awful the next day or two ... and then it passed. Then I drank some orange juice, and the same feelings arose, and I remembered that I'd eaten oranges the day before each of the previous episodes. A bit more experimentation showed that I was having a consistent 48-hr delayed reaction to oranges. Eventually I learned about type IV delayed food sensitivity, which clearly fit. Type IV is t-cell mediated, similar to viral infections. After 2.5 years, I managed to accidentally cure my type IV sensitivity, but the same symptoms (ME) remained.

So, from your experiences and my experience, my hypothesis is that t-cell activation triggers ME, regardless of what triggers the t-cell response. I don't know whether activation of other immune systems (IgE, IgA, glial) can also trigger ME. It's up to immunology experts to figure out what about t-cell activation might be triggering ME.