Did anyone have PEM when they had mono/EBV infection? Or is that just for CFS?

[hunter1899]

I’ve seen people online with mono say they have PEM. Is PEM only for those with CFS or could having only mono/high EBV titers cause PEM also?

 

[Wishful]

PEM isn't well-defined, and there's no clinical test for it, so it's possible for people with other diseases to have something that fits the vague description of PEM. It might be interesting to see if mono PEM has consistent delays or durations that fits ME's PEM.

 

[ljimbo423]

I’ve seen people online with mono say they have PEM. Is PEM only for those with CFS or could having only mono/high EBV titers cause PEM also?

As far as I know PEM is exclusive to ME/CFS. EBV can cause varying levels of fatigue, from mild to extreme. When someone with EBV exercises, they would feel more tired but it wouldn't be delayed as it is in most cases of ME/CFS.

There are many illnesses that cause fatigue and profound exhaustion but they do not cause PEM, to the best of my knowledge. If someone is experiencing PEM, IMO, they do not have EBV or any other virus or illness, they have ME/CFS.

There are many illnesses that "trigger" ME/CFS. They make changes in the body that last even after the viral infection is gone.

Covid 19 is the newest virus that is "triggering" ME/CFS. Many of these people that have been sick with what appears to be ME/CFS for months now have been tested, some multiple times and no longer have covid 19. Some have already been diagnosed with ME/CFS from covid 19.

So these viral infections must be making lasting changes in the body that are causing ME/CFS, even after the viral infection is gone.

This is the definition of PEM from the Center for Disease Control-

Post-exertional malaise (PEM)

Post-exertional malaise (PEM) is the worsening of symptoms following even minor physical or mental exertion, with symptoms typically worsening 12 to 48 hours after activity and lasting for days or even weeks. PEM can be mitigated by activity management (pacing). The goal is to avoid PEM flare-ups and illness relapses by balancing rest and activity.

https://www.cdc.gov/me-cfs/healthca... worsening of symptoms,for days or even weeks.

 

[Rufous McKinney]

mono say they have PEM

Sounds like they are sick with acute mono and they probably feel- low grade fever, lethargic swollen lymph nodes sore throat-

PEM is- a type of poisoning.

 

[wabi-sabi]

There are many illnesses that cause fatigue and profound exhaustion but they do not cause PEM, to the best of my knowledge. If someone is experiencing PEM, IMO, they do not have EBV or any other virus or illness, they have ME/CFS.

This is my understanding as well.

But it is problematic for differentiating diseases or conditions that PEM can be a bit vague, along the lines of feeling worse or symptoms flaring. I had mono so long ago now that I can't remember exactly what it felt like. I almost might prefer plain garden-variety mono to what I've got now. I'm not sure that mono feels quite like ME/CFS.

Some have already been diagnosed with ME/CFS from covid 19.

Has this been published? I'd like to read up on it.

 

[ljimbo423]

But it is problematic for differentiating diseases or conditions that PEM can be a bit vague, along the lines of feeling worse or symptoms flaring. I had mono so long ago now that I can't remember exactly what it felt like. I almost might prefer plain garden-variety mono to what I've got now. I'm not sure that mono feels quite like ME/CFS.

I think it's the consistent delay in the worsening of symptoms, after physical or mental activity that separates ME/CFS from all the other illnesses. Usually a 12-48 hour delay.

Has this been published? I'd like to read up on it.

I don't know of anything that has been published yet. Ron Davis and the OMF are going to be studying the long term effects of covid 19 in triggering ME/CFS because so many people already have symptoms of ME/CFS and no longer have the virus.

Conversion of COVID-19 patients to people with ME / CFS

“We are proud to announce the initiation of a study of patients with COVID-19 to monitor the course of their disease and its sequelae (the medical term for chronic conditions after an illness) to ascertain whether they convert to ME / CFS and if it occurs, to study the molecular transformation.

This will involve the collection of body fluid samples at frequent intervals, continuous health monitoring via wearables, and symptom data recorded at many separate time points over two years. The expected outcome is that some will develop ME / CFS, as many other viruses serve as triggers for the disease.

The COVID-19 pandemic is an unprecedented opportunity to study the biological factors that may determine or predict the development of ME / CFS.

In a significant percentage of patients, severe viral infection preceded their development of ME / CFS. In this current COVID-19 pandemic, it seems likely that COVID-19 may also be a trigger, and that many people will develop ME / CFS.

It is thought that up to 11% of patients who had severe infections from Epstein-Barr virus (EBV), Q fever (Coxiella burnetii), or Ross River virus (RRV), and others, develop ME / CFS. Other studies following SARS and MERS suggest an even higher proportion (50%) develop ME / CFS or Fibromyalgia.

After COVID-19 patients recover from the acute phase of their disease, they may be at significant risk for a prolonged period of post-viral fatigue, which may last six months or more before returning to their previous normal state. However, for some patients, their fatigue may fail to resolve or become even more profound over these initial six months and continue indefinitely, converting to ME / CFS.

A detailed genomic, metabolic, and proteomic analysis over time will likely provide tremendous insights to understand how to identify those pathways that can be useful to predict, diagnose, or treat ME / CFS.

The world is intensely focused on COVID-19 at the moment. The likely conversion of thousands of patients to a disease that causes life-long suffering provides a unique opportunity for the world to finally pay appropriate attention to ME / CFS.”

Source

 

[wabi-sabi]

@ljimbo423

Yes, I'd seen the OMF announcement that they were studying COVID to ME/CFS conversion, which I think is tremendously exciting, but I was wondering if there was more news or updates yet. I guess it's still early days.

 

[ljimbo423]

@ljimbo423

Yes, I'd seen the OMF announcement that they were studying COVID to ME/CFS conversion, which I think is tremendously exciting, but I was wondering if there was more news or updates yet. I guess it's still early days.

None that I'm aware of. I wish there was. It is very exciting!

 

[Wishful]

I think it's the consistent delay in the worsening of symptoms, after physical or mental activity that separates ME/CFS from all the other illnesses. Usually a 12-48 hour delay.

I couldn't remember if consistency in delay was universal for PWME. Do you recall it being official?

My physically-induce PEM had a consistent 24 hr delay, but my cerebrally-induced PEM was less consistent and much shorter (within hours, maybe even under an hour). The C-PEM was harder to identify the start of, which doesn't help with identifying consistency. Maybe we need a poll for PEM delay, for both P-PEM and C-PEM?

My C-PEM wasn't blocked by cumin, so I think the two types have different pathways. One hypothesis I have is that the P-PEM involves IFN-g, produced about 24 hrs after physical exertion, which triggers the brain's immune system. Cerebral activity might bypass the IFN-g delay and trigger the glial cells more directly.

 

[ljimbo423]

I couldn't remember if consistency in delay was universal for PWME. Do you recall it being official?

I don't know if it's official, just that it happens to most of us. But as you point out, not all of us. This illness is consistently inconsistent!

Cerebral activity might bypass the IFN-g delay and trigger the glial cells more directly.

This sounds like you might be on to something.

 

[Hip]

Covid 19 is the newest virus that is "triggering" ME/CFS. Many of these people that have been sick with what appears to be ME/CFS for months now have been tested, some multiple times and no longer have covid 19. Some have already been diagnosed with ME/CFS from covid 19.

So these viral infections must be making lasting changes in the body that are causing ME/CFS, even after the viral infection is gone.

That's a conclusion that does not follow from the evidence. The coronavirus PCR test is done on the patient's saliva; now just because the virus is no longer found in the saliva, it does not prove it is not present in all other parts of the body, such as the brain.

There are plenty of examples where a viral infection is found in specific organs, but is not found in other parts of the body, and is not found in the blood.

This logic is analogous to someone looking for his lost keys: he searches the living room and cannot find them there, and so he concludes the keys cannot be anywhere in the house. Obviously that logic is not correct.

 

[ljimbo423]

That's a conclusion that does not follow from the evidence.

The evidence is the virus is not being found in these post covid 19 patients, that it's gone. Not that it is somewhere else in the body.

This logic is analogous to someone looking for his lost keys: he searches the living room and cannot find them there, and so he concludes the keys cannot be anywhere in the house.

Your post assumes the keys (the virus) is somewhere else in the house (the body) without evidence and it also assumes that if the virus is somewhere else in the body it's causing there ME/CFS symptoms, again without evidence.

To assume the virus is still present and causing symptoms in civid 19 long haulers is a complete hypothesis when the virus hasn't been found and is baseless at this point. Where as the evidence so far shows the virus is no longer present.

If research shows the virus is still present in these covid 19 long haulers and is causing their symptoms, I will change my view. But that's not what the evidence is showing.

EDIT- I think the more research that is done, the more it will show that covid 19 is just another virus, one of many, that "triggers" ME/CFS but is not the root cause. This is from the OMF-

In a significant percentage of patients, severe viral infection preceded their development of ME / CFS. In this current COVID-19 pandemic, it seems likely that COVID-19 may also be a trigger, and that many people will develop ME / CFS.

It is thought that up to 11% of patients who had severe infections from Epstein-Barr virus (EBV), Q fever (Coxiella burnetii), or Ross River virus (RRV), and others, develop ME / CFS. Other studies following SARS and MERS suggest an even higher proportion (50%) develop ME / CFS or Fibromyalgia.

Source

 

[Hip]

@ljimbo423 in your above post, you said:

So these viral infections must be making lasting changes in the body that are causing ME/CFS, even after the viral infection is gone.

The possibility that ME/CFS might be caused by a virus making some lasting changes or creating some hit and run damage during the acute infection is a hypothesis that has been around for a long time.

Similarly, the possibility that ME/CFS might be caused by an ongoing viral infection hidden in the body is another hypothesis that has been around for a long time.

These two possibilities are not facts, they are hypotheses.

But you stated the first hypothesis as if it were a fact. That's why I pointed out that the evidence does not support this.

Your post assumes the keys (the virus) is somewhere else in the house (the body) without evidence and it also assumes that if the virus is somewhere else in the body it's causing there ME/CFS symptoms, again without evidence.

No it does not assume that. I am making the point that if you cannot find something in just one room in the house, you cannot conclude it is not in the house. You have to search all rooms before you can reach that conclusion.

If research shows the virus is still present in these covid 19 long haulers and is causing their symptoms, I will change my view. But that's not what the evidence is showing.

That research can only come from post-mortem studies, where the brain tissue from long haul COVID patients is tested for viruses. It is very difficult to get such post-mortem studies done, for obvious reasons.

But we do know that in mouse models, SARS-CoV-1 can infect the brain.

 

[Wishful]

It is very difficult to get such post-mortem studies done, for obvious reasons.

I don't see the difficulty. They don't scream or struggle like live subject do.

 

[ljimbo423]

The possibility that ME/CFS might be caused by a virus making some lasting changes or creating some hit and run damage during the acute infection is a hypothesis that has been around for a long time.

Similarly, the possibility that ME/CFS might be caused by an ongoing viral infection hidden in the body is another hypothesis that has been around for a long time.

These two possibilities are not facts, they are hypotheses.

But you stated the first hypothesis as if it were a fact. That's why I pointed out that the evidence does not support this.

That is my conclusion based on the evidence I've seen in post covid 19 patients testing negative for the virus and having ME/CFS symptoms. EDIT- And not seeing conclusive evidence for other ongoing viral infections causing ME/CFS.

I apologize for not stipulating that it is my opinion.

There are plenty of examples where a viral infection is found in specific organs, but is not found in other parts of the body, and is not found in the blood.

I'm trying to understand your view but don't really get it.

Are you saying that all the many different triggers of ME/CFS, like Giardia, Q-fever, EBV, Ross River virus, SARS and MERS viruses, etc, are all still present in ME/CFS patients that had their illness triggered by them but they are hiding out somewhere in the body causing their ME/CFS?

 

[Hip]

That is my conclusion based on the evidence I've seen in post covid 19 patients testing negative for the virus and having ME/CFS symptoms. I apologize for not stipulating that it is my opinion.

I appreciate it can be tricky to use language in the correct way when discussing scientific facts and hypotheses.

Scientists themselves are careful not to call something a fact when it is just a hypothesis. Even if a scientist personally really believes his hypothesis is true, he will still be careful to call it a hypothesis, and not a fact.

But scientists are used to using language in a very precise way in their careers.

I'm trying to understand your view but don't really get it.

Are you saying that all the many different triggers of ME/CFS, like Giardia, Q-fever, EBV, Ross River virus, SARS and MERS viruses, etc, are all still present in ME/CFS patients that had their illness triggered by them but they are hiding out somewhere in the body causing their ME/CFS?

With chronic diseases in general (not just ME/CFS), there is a hypothesis that these may be caused by ongoing infection in the body.

Infections can reside in just one organ in the body, and may cause a disease as a result. We know in type 1 diabetes that the pancreas is infected with enterovirus, and there is a theory (hypothesis) that enterovirus is causing the diabetes.

 

[Tammy]

Infections can reside in just one organ in the body,

Why isn't it possible for infections to reside in more than one organ?

 

[ljimbo423]

Even if a scientist personally really believes his hypothesis is true, he will still be careful to call it a hypothesis, and not a fact.

Sometimes I get overly enthusiastic with my opinions and present them as fact because that's how they feel to me. That's a good way to offend people though and I really don't want to do that.

 

[Hip]

Why isn't it possible for infections to reside in more than one organ?

They can, they can reside in more than one organ.

The point I am making is that low-level infection can be localized to certain organs of the body.

So you may only be able to detect that infection if you cut off a tissue sample from the organ (cut off a bit of the organ by biopsy) and test the actual tissues for infection.

If you test the blood, you may not find the infection, because the infection may only be found in specific organs.

Sometimes I get overly enthusiastic with my opinions and present them as fact because that's how they feel to me. That's a good way to offend people though and I really don't want to do that.

It's nice to hear people's theories and hypotheses, as well as the hypotheses of various ME/CFS researchers that people might want to present, especially if presented in an enthusiastic way.

It's also nice to discuss and criticize theories, to see if there are any holes or flaws in the theory, and understand the ramifications of the theory.

It is always good idea though to point out that they are theories/hypotheses, and not facts. Eventually a theory might be proven true, and then it's appropriate to call it a fact. But while it is still unproven, it's called a hypotheses.

I know it can be hard to do this. Researchers are experts in using language in way that differentiates theory/hypothesis from fact.



In my case, I am very interested in the theory that most chronic diseases may be caused by chronic low level infection. I think it would be wonderful if this turns out to be the case, because then humanity might be able to eliminate most chronic diseases just by developing vaccines to protect against the pathogens involved.

So then humanity might enjoy a golden era of health. If it works out that way, it will take at least 50 ot 100 years to happen, so it's not something our generation will benefit from. But it may be great for future generations, who may be able to live in a largely chronic disease-free world. That's if it turns out to be true that pathogens are a major cause of chronic disease.

But I understand that it is only a hypothesis that pathogens are a major cause of chronic disease. So in spite of my enthusiasm, I will never present this as a fact, only as a theory.

 

[Tammy]

The point I am making is that low-level infection can be localized to certain organs of the body.

So you may only be able to detect that infection if you cut off a tissue sample from the organ (cut off a bit of the organ by biopsy) and test the actual tissues for infection.

If you test the blood, you may not find the infection, because the infection may only be found in specific organs.

Agreed...................that's why I think the whole viral testing bit isn't giving an accurate picture.