Pathogens associated with triggering ME/CFS - discussion thread

[AliceLily]

Yeah - oddly, I only started to have night sweats after the initial fever and sore throat had passed. I don't think I'd ever experienced that before. People can break out into a sweat when a fever breaks, but I assume it's pretty much a one time thing reflecting the system's realization that the infection is over and the body needs to cool down - not something that repeats again and again. For me they pretty much went away after just a couple of months, but I remember the times back then when I would wake up with my shirt and hair being just drenched.

@Forbin I always thought it strange that the night sweat for me was only at the chest. It felt like it was coming out right at the centre of chest between the breast area. I'd never experienced this until ME.

Edit. I just remembered I also used to get an unusual groin sweat but this one would come during the day. Right along the sides of the bikini line would be wet. And it is not due to a hot day. I don't know if this one is a ME symptom, but it sure has a similar feel to the night sweat.

 

[chrisb]

I have just recalled those naively innocent days when we thought a cure was just around the corner and the MEA was made up of the official wing believing in PVFS and the provisional wing believing in Candida albicans. The only thing on which they agreed was that the others were undermining their efforts to be taken seriously. (I jest). Perhaps Candida should be added to the list.

One thing that has struck me is that many of those falling ill either side of 1980 seemed to have the unidentified illness of Strauss's chronic EBV, minus the EBV. There are a number of us here. I am sure we have all identified each other. Probably through the obvious psychological vulnerabilities which he ultimately seems to have believed in.

 

[Kitty]

Perhaps Candida should be added to the list.

I don't imagine it's causal, but massive candida overgrowth preceded the onset of my ME by up to a year. I had candida pretty much permanently until the menopause; I still get skin fungus if I eat white bread, though.

 

[rvallee]

So, the fact that there seems to be acute infections involving fevers and sickness behaviour, that can be serious to the point of killing people and result in people lying in bed for a couple of weeks or more but that don't have an associated post-infective 'fatigue' syndrome suggests that the fatigue syndrome isn't (primarily or only) a result of deconditioning or a psychological response to the trauma.

It's not likely that most people will know whether they have a disease with an associated fatigue syndrome before deciding whether to avail of the secondary benefits of ME/CFS. That and the fact that people all over the world who haven't heard of ME or CFS seem to develop it after only specific illnesses suggests that the illness isn't psychogenic.

It suggests that whether a person develops a post-infective 'fatigue' syndrome has something to do with the illness. Of course, not everyone gets the post-infective syndrome after EBV or Q-fever, so there's probably a host-pathogen interaction, but there's something that differentiates the pathogens that cause a post-infective fatigue syndrome from those that don't.

The weird thing is the range of types of pathogens that are associated with a fatigue syndrome - viruses, bacteria, amoeba and even the toxins from dinoflagellates in the case of ciguatera. In the case of amoeba, as I previously noted, I wonder if it's not really the amoeba (e.g. giardia) that causes the fatigue syndrome but another pathogen that infects people at the same time, either from the same contaminated water or even actually inside the amoeba. I saw that the bacteria that causes Q-fever (Coxiella burnetii) can live inside amoeba, as can legionella bacteria.

If we could make a really good list of the pathogens firmly associated with a post-infective fatigue syndrome and those that are clearly not, it might be possible to narrow down the ways that the illness might be causing the CFS.


Re the severity - I'm not sure. In the case of my family, my daughter was hospitalised with severe stomach pains, but for my son and I, from memory it just seemed like a standard gastro-flu. And my daughter was the one less severely affected. I've had worse illnesses before.

What did Jason's prospective EBV Chicago studies find? I think they may have found an association with severity? Did they use any objective rating of severity?

Yesterday there was a report on CBC about the coronavirus that included an interview with a paramedic who had contracted SARS during the epidemic. What he described was pretty much exactly severe ME (not very severe, severe). The message was meant to be a warning to take the new virus seriously, that even if you are healthy and fit it is something to be taken seriously because [describes nearly exactly the symptoms of ME lasting for 2-3 weeks].

It's serious if it happens to you for a couple weeks. If it happens for the rest of your life? No biggie, just ignore and move on. Also no resources will be provided and you will be insulted for asking for help. You useless weakling.

Really frustrating. It usually begins with a viral infection. It strongly resembles a viral infection. By far the closest experience is a typical viral infection. But clearly it must be nothing more than the normal feeling of tiredness being taken out of proportion. Sure. Whatever.

 

[Hutan]

There's some discussion on this thread about what characteristics of some flu infections seem to lead to ME:
CFS/ME is associated with pandemic influenza infection, but not with an adjuvanted pandemic influenza vaccine, 2015, Magnus, Hornig, Lipkin et al

 

[Annamaria]

EBV has by far the most published evidence that ME/CFS can follow after an acute infection:

https://www.ncbi.nlm.nih.gov/pubmed/19564299
https://www.ncbi.nlm.nih.gov/pubmed/9926075
https://www.ncbi.nlm.nih.gov/pubmed/20819961
https://www.ncbi.nlm.nih.gov/pubmed/16950834

Enterovirus has by far the most published evidence that it can exist as a chronic active infection in the tissues of ME/CFS patients:

https://me-pedia.org/wiki/List_of_enterovirus_infection_studies


I've never come across any of the following viruses being linked to triggering ME/CFS, or being found as possible active infections in ME/CFS patients:

norovirus, adenovirus, HHV-8, rotavirus, rhinovirus.

In the first months I tested positive for adenovirus and toxoplasma but these were dismissed as 'self-limiting'. I didn't improve though and wasn't re-tested.

 

[Hip]

In the first months I tested positive for adenovirus and toxoplasma but these were dismissed as 'self-limiting'.

Depending on the test, "positive" can mean several things: if it was an adenovirus antibody test, positive can mean that you caught adenovirus in the past, but the infection is now under control and dormant.

 

[NelliePledge]

As gradual onset only getting diagnosed approx 10 years after my health started deteriorating noticeably I’ve got a few possible triggers

none of which were followed by anything that seemed to be anything approaching ME symptoms

first bad gastroenteritis followed 3-4 weeks later by chicken pox age 28

i had what in retrospect may have been bullseye rashes on holiday in Sri Lanka. Didn’t follow up as I just thought I’d had a bad reaction to mozzie bites. mid 30s

a further holiday gastro virus with full on projectile vomiting mid 30s

Then I had a spell of a few years when I had regular flu like illness and bouts of laryngitis early 40s - I still get sore throats as part of flare ups. This was the time when my health started to cause problems with sick absences from work and also reduced socialising. I acquired depression diagnosis as a parent had died and everything got attributed to the physical effects of being depressed for around 10 years......

 

[Peter T]

For me, a combination of the flu jabs, caused extra deterioration, on top of the graded exercise therapy I did at the beginning of my illness. In hindsight I wish I hadn’t had them as I can track my deteriorations each time I had them. However, I do also know people with ME who get them who have not had any reaction whatsoever to them. It’s again one of those things that I wish would be researched thoroughly.

I agree, we lack a good ‘natural history’ or quantitive description of ME and its variation between individuals or over time within an individual.

There are a number of immune related phenomenon that are not yet adequately described let alone understood:
- are there some pathogens that never trigger ME?
- why do different pathogens differentially trigger ME, for example why does the Epstein Barr Virus commonly trigger ME whilst say the measles virus does not?
- do the geographically located ‘ME’ outbreaks, eg Lake Tahoe and Royal Free, just represent clusters of ME or do they differ in any way for ME ordinarily arising in the general population?
- can we be certain that no virus was involved in those cases where onset was not associated with any obvious infection, given it is possible to have symptomless viral infections
- is ME thought not to be triggered by any pathogen the same as ME triggered by a virus?
- do some people with ME genuinely get every bug going, whilst others never get colds or flue or is this a subjective misinterpretation related to differential exposure?
- objectively do some people with ME have a negative reaction to vaccines whilst others do not, or could this be explained by something else such as an intolerance to the vaccine’s medium?

It could be that we are not just looking at the right variables? Over time various concepts have helped me makes sense of the variation in my condition: PEM, food intolerances causing delayed reactions, orthostatic intolerance. Do we just need to identify the variables that define other variation?

 

[spinoza577]

I'm interested in understanding what pathogens have been found to reliably be associated with the onset of ME/CFS and/or post-viral fatigue syndrome.

This is an important question, I would say.

I had begun to investigate, for now I am not going to put the tiny bit of literature, leaving it for later when I will have cleared up my situation. But the tiny bit what I had on the cards is this, by memory:

1. Causing high manganese levels in the cells. Borrelia may be able to accumulate huge levels of manganese and will release high packages into the blood when dividing. Coxilla burnetti cannot be destroyed by sequestering manganese and is therefore able to survive the phagosome. The vitamin D receptor (VDR) encodes for the manganese exporter ZnT10, so any pathogen blocking it may be in line here.
2. EBV is blocking the VDR. This goes also for an A strain of the enteroviruses, though only the B strains are associated with CFS. (I think also influenza, which is in Australia quit a CFS factor, has an action on the VDR?). Other viruses may not have been investigated (it´s not intelligent not to publish negative results), but I found for a lot of them a tiny association, be it qua autoimmune disease (CFS than maybe having an autoimmune component), or be it qua telomeres. On PR I made a thread on it (percyval577 - I was reluctant to use the name again as I am not English, which I wasn´t aware ...)
3. Four of the triggers have been found to alter ion currents, but all in a different way. EBV alters potassium currents.
4. I think: metal distribution
5. and distribution of Vit B´s (probably both not investigated at all)

The question is further on:

1. are there any pathways which stay altered, on their very level?
2. is there any structure which could get transiently disturbed and would not find back to normal although everything functions like normal? Interesting may be the funnel structure of the nucleus caudatus.

I think that vulnerable in general are the basal ganglia and the non-specific thalamus. In the particular point, manganese can accumulate near cellular nuclei in the substantia nigra, possibly disturbing the nucleus intralaminares (my own thought and search, havn´t already googled for it). I think waves are important, coded by neurons.

 

[Arnie Pye]

I was diagnosed with a Group B streptococcal infection after I got bits of me swabbed and cultured because of a recurring rash. This is allegedly only dangerous to newborn babies, the elderly, and people with compromised immune systems. Since I wasn't in that group of at-risk people I was treated as if I just had a minor infection that needed a week of low dose antibiotics.

I was prescribed erythromycin, an antibiotic that I could never remember being prescribed before. The first time I was given the prescription I got completely better. I felt well and energetic for the first time in decades and I could think - all my brain fog had gone. I told the doctor how much better I felt before I'd even finished the course and I asked if I could get the original course of antibiotics extended without a gap. But the wheels of the NHS grind really slowly. By the time I got another prescription I had already run out of the original prescription several days before. And during that gap my symptoms had come roaring back, as if they had never been away and the new prescription was too late to get me back to where I felt completely well again. Although I tried erythromycin several times after that I never got the same amazing effect again. I actually wonder what would have happened if I had been given a higher dose and a longer course of the pills at the very start.

I did some brief research into how erythromycin worked and discovered that they were "bacteriostatic agents" according to wikipedia. This means that they don't kill bacteria they just reduce their ability to reproduce. I also discovered that I was prescribed the smallest dose and the shortest course that is recommended by the NHS. And when I looked up info on this antibiotic from drugs.com (info from the USA) the minimum dose was a bit bigger than the NHS thought was necessary. So as far as I can tell I was doomed from the start. I don't beg for this antibiotic any more - I've realised that my bugs are now completely immune to it and I get no benefit from it at all.

 

[Mithriel]

When I read the descriptions of the Royal Free Epidemic it matches what I had better than many other things. There was an overlap between the survivors of the epidemic and new cases and there did not seem to be any differences. After CFS, the patient base became much bigger, especially in the US where CFS was seen as a disease of mainly EBV and a compromised immune system and the UK where ME was seen as a disease of enteroviruses and an unusual adverse response to exertion.


The initial illness with enterovirus was often felt to be fairly trivial so gradual onset may simply be a gradual deterioration from an illness that has been forgotten.

I know when I got infected because I was never quite right afterwards, but I was far from ill for years, just having attacks I now know were PEM induced neurological problems. It was when I took flu after 4 years that I first began losing time off university and another flu made things worse and seriously overexercising brought me to a wheelchair. Then I got caught in a vicious loop where I have to overdo things just to do anything at all and am never able to rest enough to get an improvement.

 

[Hoopoe]

The initial illness with enterovirus was often felt to be fairly trivial so gradual onset may simply be a gradual deterioration from an illness that has been forgotten.

Interesting because I have at times doubted the ME/CFS diagnosis because the turning point appeared to be only a trivial flu-like illness that didn't even cause fever. Something that wouldn't be attributed any real significance if infections weren't known to be connected to ME/CFS.

 

[Kitty]

There are a number of immune related phenomenon that are not yet adequately described let alone understood:
- are there some pathogens that never trigger ME?
- why do different pathogens differentially trigger ME, for example why does the Epstein Barr Virus commonly trigger ME whilst say the measles virus does not?
- do the geographically located ‘ME’ outbreaks, eg Lake Tahoe and Royal Free, just represent clusters of ME or do they differ in any way for ME ordinarily arising in the general population?
- can we be certain that no virus was involved in those cases where onset was not associated with any obvious infection, given it is possible to have symptomless viral infections
- is ME thought not to be triggered by any pathogen the same as ME triggered by a virus?
- do some people with ME genuinely get every bug going, whilst others never get colds or flue or is this a subjective misinterpretation related to differential exposure?
- objectively do some people with ME have a negative reaction to vaccines whilst others do not, or could this be explained by something else such as an intolerance to the vaccine’s medium?

There are some important questions here, and you're right that we don't know nearly enough to approach answering them.

I'd also add the 'multiple hit' possibility. For instance, my parents told me I was never quite the same again after being very ill with measles when I was eight; I then (gradually) developed ME in my late teens. There are lots of stories like that, but we have no idea whether they have some basis in fact or are just retrospective attempts to make the pieces fit.

 

[JES]

I agree, we lack a good ‘natural history’ or quantitive description of ME and its variation between individuals or over time within an individual.

There are a number of immune related phenomenon that are not yet adequately described let alone understood:
- are there some pathogens that never trigger ME?
- why do different pathogens differentially trigger ME, for example why does the Epstein Barr Virus commonly trigger ME whilst say the measles virus does not?
- do the geographically located ‘ME’ outbreaks, eg Lake Tahoe and Royal Free, just represent clusters of ME or do they differ in any way for ME ordinarily arising in the general population?
- can we be certain that no virus was involved in those cases where onset was not associated with any obvious infection, given it is possible to have symptomless viral infections
- is ME thought not to be triggered by any pathogen the same as ME triggered by a virus?
- do some people with ME genuinely get every bug going, whilst others never get colds or flue or is this a subjective misinterpretation related to differential exposure?
- objectively do some people with ME have a negative reaction to vaccines whilst others do not, or could this be explained by something else such as an intolerance to the vaccine’s medium?

It could be that we are not just looking at the right variables? Over time various concepts have helped me makes sense of the variation in my condition: PEM, food intolerances causing delayed reactions, orthostatic intolerance. Do we just need to identify the variables that define other variation?

Lots of the things are obviously not yet known and I agree that several factors could be necessary for triggering something like ME/CFS. At least for the cases that are triggered by an (acute) infection, it still strikes me that the explanation that requires the least amount of assumptions (which is usually the correct one) would be that this virus is still the driving cause for the later chronic symptoms. This also doesn't go against the idea that only certain viruses trigger ME/CFS, because we know viruses behave very differently. EBV for example does live in B-cells unlike other herpesviruses, which makes it quite a bit special in that sense.

COVID-19 is another good example of a virus that seems to mess around with a huge number of host immune response processes. If we didn't have the technology to detect COVID-19, I reckon many of the post COVID-19 infection symptoms would be looked at as something else than COVID-19, some of them are that bizarre. It does worry me something similar could be going on in ME/CFS and we are just not able to detect the pathogen which could be causing an array of symptoms.

@spinoza577 It's an interesting idea and probably the case that pathogens mess with various metabolic pathways, etc. I still wonder though, IF that is the case, wouldn't the best treatment then still be to directly target the pathogen (borrelia, etc.)? Trying to fix dysregulated pathways caused by a pathogen is a bit like trying to put out the fire by water, but never getting rid of the fuel that's still burning.

 

[Hutan]

A number of posts about flu vaccinations have been moved to
Whether to have a flu vaccination

 

[spinoza577]

@JES thank you.

I might need to beg your pardon. The approach doesn´t require the pathogens to be present, maybe they are virulent, maybe they are under control, or maybe they only left their footprint.

In my case, I indeed have been tested positive for borrelia after I had begun an intervention (on my own) against them, funnily, only then. Meanwhile I think they may have been only an impact back some time, and this impact may only have become an impact important enough together with other impacts. This goes together that until now no infection could be confirmed, also the disease itself may look pretty autonomous.

So I think, already the impact - I think manganese - might have lasted, until later another impact stirred up, regardless of the presence of the borrelia. And here I cannot judge if there are pathways altered in themselves, say in a time and dose dependent way (eg in the substantia nigra), or if only a bigger structure had been shot at.


The consequence would be, to reverse the impacts, and I think a bit this will not be possible without paying attention to a bigger structure (which I have in mind, basal ganglia and non-specific thalamus).

 

[Simbindi]

My mum insisted I was 'never the same' after getting glandular fever just after my 17th birthday (she insisted the GP come to the house and take the blood to test for this from my bed as I was so ill, so it was a confirmed diagnosis). After 'recovering' from the PVFS I did continue to need a lot more sleep than my peers and was very susceptible to colds, ear infections and tonsillitis, so may have had very mild M.E. However, I was able to complete my Gold D of E 6 day expedition over Dartmoor during the hottest week of 1983, as well as able to continue cycling and mountain walking within 6 months of getting over the initial fever.

I've personally put my M.E. onset to a severe upper respiratory infection, the worst I'd had to date, back in 1992 when I was 26. I had a toddler and was breast feeding my youngest at the time, as well as attending a part-time (1.5 day a week) art course in the city (I lived out in the suburbs). Like many Covid-19 long term sufferers, I originally thought I was getting better but kept getting worsening symptoms including the chronic muscle fatigue and pain, dizziness, nausea etc. after my respiratory symptoms had completely cleared up.

I thought stopping breast feeding would lead to an improvement but instead I quickly became bed bound, often struggling just to get to the toilet. After about 6 months I started getting an extremely itchy spot on the front of my throat. About a year later (whilst still mostly bed bound) my GP did blood tests and picked up hypothyroidism (including having antibodies to my thyroid). Putting me on thyroxine enabled me to start getting out of bed, but I still had moderate M.E. (the PEM being very obvious once I was able to be up and about - prior to that I must have been in permanent PEM).

 

[Mij]

@Simbindi

We have some similarities with our thyroid onset. In 1991 I had 'extremely' elevated anti-thyroid antibodies during onset and was sent for a thyroid scan by my GP. My thyroid function was fine. The Endo told me it was viral and that the anti-bodies would eventually go back to normal, but it could take several months. They eventually went back to normal. I started feeling much better after 9 months, well enough to return to work, but I relapsed shortly after.

The pathogen was of no importance to the ME specialist I saw in 1992, but my onset history and relapse was the reason I was dx with atypical ME or PVFS/CFS. I didn't experience PEM until 10 years later when I started exercising again.

 

[Simbindi]

@Simbindi

We have some similarities with our thyroid onset. In 1991 I had 'extremely' elevated anti-thyroid antibodies during onset and was sent for a thyroid scan by my GP. My thyroid function was fine. The Endo told me it was viral and that the anti-bodies would eventually go back to normal, but it could take several months. They eventually went back to normal. I started feeling much better after 9 months, well enough to return to work, but I relapsed shortly after.

The pathogen was of no importance to the ME specialist I saw in 1992, but my onset history and relapse was the reason I was dx with atypical ME or PVFS/CFS. I didn't experience PEM until 10 years later when I started exercising again.

My thyroid test at the time included measuring antibody levels, T3 and T4. Although I noticed the itchy throat when I first became bed bound I didn't have the thyroid testing until 18 months after the upper respiratory infection when I finally agreed to see a doctor, so my GP didn't link it to any viral cause (although I believe it was triggered by the M.E. as none of my family has ever had the problem). In the meantime (while bedridden) I had got my husband to buy and set up a multi-gym in the bedroom as I really believed that trying to exercise would help me get better (this was because I had been so active and going to the gym 3 times a week once my youngest hit 10 weeks old, not on the advice of any health professional). Needless to say, I never managed to use the home gym, even once - I finally sold it 10 years later!

My GP diagnosed me with M.E. once she had got my thyroid hormones back to the normal levels and it was obvious I was still very ill. She had sent me to an arrogant chest consultant who announced I just had 'CFS or PVFS', would get well soon as he'd never known anyone to suffer from it for more than 18 months (by the time I saw him I'd already been ill that long). He then wrote to my GP telling her to stop the thyroxine (which she didn't do as she had seen the difference it was making in my test results). I didn't know what he meant by CFS or PVFS until he said these were the 'same as M.E.' However, my GP at the time always referred to it as M.E.