Pathogens associated with triggering ME/CFS - discussion thread

[Hutan]

This is what I drafted in response to the list.

I think the authors have confused diseases associated with the acute onset of ME/CFS with diseases that have been discussed as possibly being part of the cause of ME/CFS. For example, Human Herpesvirus 7 almost always infects people in infancy, but ME/CFS is typically diagnosed from late childhood onwards. It has been proposed that there is a reactivation of the latent HHV7, possibly at the time of infection with another disease. Anyway, that's detail that the GPs don't really need.

I would avoid giving a list, as there is quite a number of illnesses associated with ME/CFS onset. An obvious omission from the list is SARS CoV-2. A large percentage of the people with persisting symptoms following Covid-19 meet ME/CFS diagnostic criteria.

So, I’d replace the section with simply ‘Relatively sudden onset of the disease is typical, often associated with a preceding infection such as Epstein-Barr virus and SARS-CoV-2.’

 

[Hutan]

My question would be why is someone writing a list like this if they are not well-informed on the matter?

Par for the course when it comes to the development of ME/CFS information resources.

 

[Ash]

Par for the course when it comes to the development of ME/CFS information resources.

…No word of a lie.

 

[Mij]

Some have suggested to have common cellular and molecular pathological mechanisms in post infectious diseases, so between onset and progression only time will tell if all roads lead to Rome or delayed PEM.

 

[alktipping]

I don't know anyone ('in real life') who claims their illness was caused by the flu either. There was the Norwegian study that found excess CFS cases, but it was rare, with 227 reported cases for 113,979 influenza diagnoses (though only 13054 cases were laboratory-confirmed - side note, it shows how much more seriously lab-testing is considered for COVID-19 compared to seasonal influenza.)
https://pubmed.ncbi.nlm.nih.gov/26475444/

0.23% is a far cry from what we see from EBV/CMV/enterovirus/Q Fever, or SARS-Cov-2 for that matter.

My illness symptoms started with Beijing flu which i caught immediately after recovering from a week long stomach bug . all the symptom hit like a truck after the near two week long fever . After 6 months of not recovering i was diagnosed with M E.

 

[Amw66]

My illness symptoms started with Beijing flu which i caught immediately after recovering from a week long stomach bug . all the symptom hit like a truck after the near two week long fever . After 6 months of not recovering i was diagnosed with M E.

A double tap.
I think it's likely not one thing , but a combination.
An assault by a tag team....

 

[Amw66]

My illness symptoms started with Beijing flu which i caught immediately after recovering from a week long stomach bug . all the symptom hit like a truck after the near two week long fever . After 6 months of not recovering i was diagnosed with M E.

Does this suggest a blindsided immune response ?
Was the stomach bug inducing a response which made a viral infection more lethal ?
Hmmm

 

[SNT Gatchaman]

That sounds valid to me. If a viral infection, eg as seen with SARS-CoV-2, causes metabolic reprogramming that leaves the immune system dysregulated for a period [1], then a second hit could be the nail in the coffin. Perhaps two hits are not required in everyone but maybe the majority?

We've learned that a significant number of Covid infections are asymptomatic [2].
The second hit could be an immune challenge that doesn't specifically require a further infection - viral or otherwise. Perhaps major surgery, physical trauma or some other inflammatory process.

Perhaps that underlies the 10%? non-infective ME onset histories. I suspect I had an asymptomatic infection in Aug 2020. In late Nov I had single-leg varicose vein sclerosing, which required daily 40 minute walks. The amount of swelling/inflammation in that leg was surprisingly excessive although settled after a few weeks. But by Dec things were going off and I crapped out in mid Jan. Not that I could have been forewarned in the circumstances, but I'm a bit suspicious that the combination may have done me in where either by itself may not have. Maybe.

---
[1]
Long COVID manifests with T cell dysregulation, inflammation and an uncoordinated adaptive immune response to SARS-CoV-2 (2024, Nature Immunology)

Post-COVID exercise intolerance is associated with capillary alterations and immune dysregulations in skeletal muscles (2023, Acta Neuropathologica Communications)

Major alterations to monocyte and dendritic cell subsets lasting more than 6 months after hospitalization for COVID-19 (2023, Frontiers in Immunology)

Impaired ketogenesis ties metabolism to T cell dysfunction in COVID-19 (2022, Nature)

Host metabolic reprogramming in response to SARS-CoV-2 infection: A systems biology approach (2021, Microbial Pathogenesis)

[2]
Persistent symptoms after COVID-19 are not associated with differential SARS-CoV-2 antibody or T cell immunity (2023, Nature Communications)

A common allele of HLA is associated with asymptomatic SARS-CoV-2 infection (2023, Nature)

 

[Wyva]

Interesting, I also believe I had a sort of double infection. The first one was just some nasty cold, it gave me a cough that kept going away and coming back, it was really annoying but I kept going on with my life. Then I recovered from that and a while later EBV knocked me out and I've never been the same since. I believe I was probably infected at the same time by the same person. It is clear that I got the cold from the guy I was dating at the time but I probably also got the EBV from him together with the cold, as EBV has a much longer incubation time (it can be more than a month). And you can't catch EBV very easily, it spreads through saliva etc. So it kind of checks out.

Edit: of course, EBV in itself may have been my trigger and the other virus may very well be just a red herring, I have no way to tell.

 

[Mij]

Does this suggest a blindsided immune response ?
Was the stomach bug inducing a response which made a viral infection more lethal ?
Hmmm

In my case I suspect I had asymptomatic h pylori infection for a while and was activated when I got hit by a sudden viral onset. I think it was 2 hits. First was the hit and run virus, and the second hit was the underlying activated h pylori that lingered on for the next 5 years until I was tested and treated.

 

[forestglip]

For completeness, I'll add that the Swedish Dr. Gottfries in Sweden said he had an influx of patients in the 1950s during the "asian flu" H2N2 pandemic.

https://s4me.info/threads/immune-st...ococcus-toxoid-vaccine-bcg.41358/#post-568807

Yeah, it's rather peculiar because I'm a professor of psychiatry, and chronic fatigue syndrome is not a psychiatric disorder. And I'm treating the patients with vaccines, and that's not a useful treatment in psychiatry either.

The reason [...] it was 1957 and 1958. At that time, the Asian Flu ravaged in Sweden. I had many patients in my psychiatric unit who came there because they were so tremendously tired. They couldn't work, and internal medicine couldn't find any explanation to their fatigueness, so they then refer them to the psychiatric unit, assuming this was some kind of psychiatric disorder. I investigated them carefully [...] and found that they were quite normal people, and they complained of tiredness. And in almost all of them, they said "I had the Asian Flu a couple of months ago" and since then I have felt so tired that I can't work any longer.

I got the Asian flu myself, and was rather ill for one week. and experienced the same thing as my patients.

Though I'm not sure he was checking for PEM back then. He says he used Fukuda until CCC came around, but Fukuda didn't even appear until 1994.

 

[forestglip]

This might be useful. Though while the thread is about trigger infections, I don't think they were necessarily testing them for pathogens during onset, but later when the condition was established, so I'm not sure if there's a better thread.

This correspondence from John Chia and his son Andrew Chia lists suspected causes of ME/CFS in "the first 200 patients with CFS who we evaluated for viral etiologies". They said over half (109) were probable enterovirus based on high antibody titers and/or presence of enteroviral RNA. In second place with 18 patients was Chlamydia pneumoniae based on high antibody titer and response to macrolide therapy.

Diverse Etiologies for Chronic Fatigue Syndrome (Chia et al, 2003, Clinical Infectious Diseases)


Some more information on C. pneumoniae in this paper they cited:

Chronic Chlamydia pneumoniae Infection: A Treatable Cause of Chronic Fatigue Syndrome (Chia et al, 1999, Clinical Infectious Diseases)

Over the past 3 years, we encountered 10 of 171 patients with symptoms of chronic fatigue who had elevated titers of antibody to C. pneumoniae long after initial respiratory infection. Most patients had favorable clinical and serological responses to a 1- to 2-months course of azithromycin therapy, although relapse was common.

One example of a woman that developed ME/CFS or something like it after an EBV infection. Three years later blood tests indicated presence of C. pneumoniae and antibiotic treatment helped.

A 32-year-old female developed pharyngitis, cough, cervical lymphadenopathy, low-grade fevers, severe fatigue, and myalgia in January 1993 (patient 1). A medical evaluation showed a normal complete blood cell count and normal results of thyroid function test and serum chemistry analysis. IgG antibody to Epstein-Barr virus was positive. During the following 3 years, the patient had frequent relapses of severe fatigue, diffuse myalgia, night sweats, pharyngitis, headaches, insomnia, and painful, swollen cervical lymph nodes (especially following exertion) that resulted in total disability.

Repeated evaluation in August 1996 revealed small nontender anterior cervical lymph nodes. Results of routine laboratory studies and serologies for several viruses were unremarkable. The titer of IgG antibody to C. pneumoniae was 1:256. Magnesium sulfate injections and salt loading failed to alleviate symptoms. One month later, when the patient was having increasing fatigue, the titer of antibody to C. pneumoniae rose to 1:1,024. Azithromycin (500 mg) was administered by mouth the first day, followed by 250-mg doses for the subsequent 4 days. The patient’s condition improved by day 3 of therapy, although her symptoms relapsed 12 days later.

Similar improvement and relapse followed a second 5-day course of azithromycin treatment. Thereafter, 250 mg of azithro- mycin was given daily for a total of 30 days; this therapeutic course resulted in a marked decrease in her symptoms. She re- turned to full-time work as a manager at her company and main- tained an energy level of 8 –9 of 10 for the next 2 years. Follow-up antibody titers are shown in table 1.

 

[forestglip]

Thread: Increased risk of chronic fatigue syndrome following infection: a 17-year population-based cohort study, 2023, Chang et al

"The study defined CFS as ICD-9-CM 780.7 and ICD-10-CM G93.3, R53.8."

ICD-9-CM 780.7 being "Malaise and fatigue", ICD-10-CM G93.3 is "Postviral and related fatigue syndromes" and ICD-10-CM R53.8 is "Other malaise and fatigue".

Those with VZV (aHR = 1.09, 95% CI 1.04–1.14), Mycobacterium tuberculosis (aHR = 1.45, 95% CI 1.34–1.57), E.coli (aHR = 1.17, 95% CI 1.05–1.3), Candida (aHR = 1.43, 95% CI 1.37–1.48), enterovirus (aHR = 1.86, 95% CI 1.29–2.67), Salmonella (aHR = 1.41, 95% CI 1.19–1.67), Staphylococcus aureus (aHR = 1.38, 95% CI 1.09–1.74) and influenza virus (aHR = 1.67, 95% CI 1.63–1.71) had significantly higher risk of CFS than did those without these pathogens (p < 0.05).

Various antibiotics appeared to decrease risk of the fatiguing conditions. Everything they tested except Clarithromycin. Though the sample size is small for these at only about 15-30 patients taking these meds.

Patients with dementia (aHR = 0.65, 95% CI 0.42–0.98) and those taking doxycycline (aHR = 0.1, 95% CI 0.07–0.15), azithromycin (aHR = 0.07, 95% CI 0.05–0.1), moxifloxacin (aHR = 0.05, 95% CI 0.04–0.08), levofloxacin (aHR = 0.04, 95% CI 0.03–0.06), or ciprofloxacin (aHR = 0.51, 95% CI 0.31–0.83) had a significantly lower risk of CFS than patients in the corresponding control group.