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ME/CFS: A disease at war with itself
We can all agree that ME/CFS is a nasty disease, particularly in its severe form, but there are abundant nasty diseases in the world. What is unique and particularly confounding about our disease is that so much controversy surrounds it, and not only surrounds it, but invades it too.
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Famous report of 1934 LA outbreak

Discussion in 'General ME/CFS News' started by Persimmon, Jul 22, 2013.

  1. Forbin

    Forbin Forbin

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    One thing that strikes me about this incident is that the Los Angeles County Hospital facility where it happened had opened just two weeks before the first unusual cases were reported (which was the same time that the first polio cases came through the doors).

    LA County Hospital was (and still is) a huge building. When it opened, many of the nurses lived in cottages surrounding the building. All of that had just been built.

    This makes me wonder about environmental toxins, specifically VOC’s (volatile organic compounds) in the form of paint fumes from the newly constructed facility (and the nurses’ cabins).

    I’ve wondered about this in regard to the many other outbreaks which occurred in institutional settings, including military facilities, where victims might have been exposed to toxic fumes.

    I personally became ill shortly after a terrible case of the flu, but in the brief interval between the flu and the onset of ME I was exposed to strong paint fumes in a poorly ventilated area for several hours. The onset of symptoms occured more than a week later when I was feeling well.

    I’ve heard some speculation that ME is set off by a combination of factors, not just biological but environmental (I think Dr. de Meirleir said this recently). So, might it be that the flu weakens your resistance or opens some pathway that makes you more susceptible to the neurotoxic effects of an environmental factor. I’m not necessarily just talking about paint fumes. I know I’ve seen speculation about organophosphates being a trigger, for example.

    Just wondering if this resonates with anyone.
     
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  2. Sea

    Sea Senior Member

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  3. alex3619

    alex3619 Senior Member

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    From the earlier discussions there were experimental animals being used at the hospital or nearby for pathogen discovery - in possibly encephalitis lethargica, irrc. I do not recall what we discussed though. Such animals may have been hosts to multiple pathogens being investigated.
     
    Valentijn likes this.
  4. Guido den Broeder

    Guido den Broeder *****

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    The CFS definitions are irrelevant since CFS is not ME. The symptoms seem close enough to the ICC-ME, I think. Take into account that the polio virus is not the same as the enteroviruses that are involved in ME today. And any specific outbreak will never exactly match the endemic average anyway.

    Yes, that is interesting, isn't it? Nude mice (recently shown to carry two halves of XMRV) had been introduced in the US shortly before. ;)
     
  5. Mark

    Mark Acting CEO

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    I find this timeline of polio vaccine history quite suggestive in relation to the 1934 and 1955 outbreaks.

    http://www.historyofvaccines.org/content/timelines/polio

    It's quite a coincidence that these outbreaks coincide with the key points at which polio vaccines were being developed and tested. There are many possible reasons for that correlation - perhaps these were evolutions of the polio virus, or perhaps there were experimental prophylactic treatments given to the medical staff at these times which we don't know about - but the correlation does seem fairly remarkable to me.
     
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  6. Mark

    Mark Acting CEO

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    Stiff neck seemed to be a very prominent symptom in that outbreak. That was a key feature for me at onset, but I can't recall any of the definitions or accounts of ME symptoms emphasising that strongly.

    Also note that some of the types described in the paper sound as though they made a partial or full recovery, although others didn't. We can't be confident that those patients really did recover without data on follow-up of those patients but I think it was the case in Royal Free also that many of those affected did recover, and in both outbreaks it was noted at the time that there was a remarkable heterogeneity of symptoms and a lot of variety in the way the disease progressed or remitted. My reading of the 1934 and 1955 accounts doesn't seem to me to support a clear, simple, narrow case definition; it seems more suggestive of heterogeneous responses to the same trigger.
     
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  7. Hip

    Hip Senior Member

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    What I have always wanted to know is why this and other outbreaks of ME/CFS (or similar infectious conditions) are not observed to spread further than the initial town or city they first appear in.

    After all, it only needs on person who caught the infectious pathogen in the initial outbreak to travel to another town or city to then seed a second epidemic in that new locale. So not so long after the original outbreak, you would expect to see secondary outbreaks occurring in satellite towns surrounding the original outbreak "epicenter".

    But in fact these secondary outbreaks are never observed, as far as I understand. The original outbreak somehow confines itself to just one town or city.

    But why is this? You don't find measles or influenza outbreaks confining themselves to only one town or city.
     
  8. Forbin

    Forbin Forbin

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    There was a sort of “city cluster” within 100 miles of Incline Village, but more in the nature of an annual outbreak:

    Incline Village, NV...1984
    Truckee, CA............1985
    Yerington, NV..........1985
    Placerville, CA........1986
    Sonora, CA.............1988
    Roseville, CA..........1989
    Elk Grove, CA.........1990
     
  9. urbantravels

    urbantravels disjecta membra

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    Where are you getting that? From reading the symptom profile, the prominent symptoms at onset were pain and muscle weakness in specific muscle groups - for instance, on one side only or in the legs or some such. There is later reference to "easy fatigue," which is never described in a way that might suggest PEM. On page 24 it says

    Clearly some form of fatiguability is being described here, but not a form that's unique to or particularly characteristic of the disease described in the ICC. Of course there might have been PEM present which was unrecognized as such because they weren't looking for the pattern. But the type of fatiguability that is described can be found in many other illnesses. The problem is similar for many of the other symptoms described - they might be symptoms found in ME/CFS, but they are not unique to ME/CFS.

    Localized muscle groups being affected might suggest a disease attacking peripheral nerves, but that doesn't exclude the possibility that the central nervous system wasn't affected as well. The description of many patients having fits of crying is interesting, since that can be caused by neurological disease or injury.
     
  10. Hip

    Hip Senior Member

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    That's very interesting. Do you know if the symptoms of the outbreaks in the other towns were the same symptoms observed in the original Incline Village outbreak. If so, that would indicate it was the same pathogen that had travelled to these surrounding towns.

    Even so, why did the epidemic soon die out, and not travel further than those towns? The Incline Village outbreak was devastating, so the pathogen involved must have been a nasty one. Yet that pathogen did not seem to travel far and wide and conquer the world like for example influenza outbreaks do.

    I think the answer to this question might throw light on the nature and etiology of ME/CFS.




    Here is a list of emerging enteroviruses and enteroviral disease outbreaks (focusing on the enteroviruses: coxsackievirus B and echovirus) that have occurred in the last few decades.
     
    Last edited: Nov 19, 2013
  11. urbantravels

    urbantravels disjecta membra

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    Not all viruses are equally easily transmitted from person to person. And viruses don't necessarily evolve toward higher transmissibility. Some of them just peter out and some become highly transmissible.

    ETA: This is why new strains of bird flu are always emerging, but only sometimes do they evolve to a form that transmits easily from person to person. Often a strain will emerge that jumps from chickens to people, but not from person to person, so such strains are carefully monitored to see if they start going from person to person rather than just infecting people who have been in direct contact with poultry.

    Since we're talking polio, polio is not so transmissable that it just sweeps across the countryside. Outbreaks were localized throughout the early 20th century, almost always occurring in the summer. Newspapers of the period always have reports of outbreaks in various towns and cities across the country, some not so big. See

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1473032/
     
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  12. Hip

    Hip Senior Member

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    Sure, not all viruses have equal transmissibility.

    The answer to this question of limited spread is likely connected to the fact that both poliovirus, and the coxsackievirus B and echoviruses that Dr Chia thinks cause ME/CFS, are enteroviruses, and enteroviruses are known to exhibit sporadic outbreaks. That is to say, enteroviruses will spontaneously break out in a local epidemic, but then rather than spreading wider, the outbreaks just disappears again. Though I understand the reason for these sporadic outbreaks of enterovirus epidemics is not known.

    It is possible I guess that the seasons play a role in terminating an outbreak. This article looks into that possibility.
     
  13. Mark

    Mark Acting CEO

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    A very thought-provoking article. This quote is particularly interesting:




    This may perhaps explain inconsistencies between different studies of immune markers in ME/CFS: the date and latitude at which the various samples were taken may well make a difference, it would seem crucial that the patient and control samples are taken at the same place and time (time of day also being potentially significant), and I doubt that study design and analysis of the literature has typically taken that into account.
     
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  14. Forbin

    Forbin Forbin

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    I think that’s probably the case. Dr. Komaroff has said that he’s never seen delayed PEM in any disease other than ME/CFS, so it’s not a symptom most doctors, and certainly none in 1934, would have suspected.

    When I became ill in the 1980’s, I felt so bad all the time that it took me 3-4 years to recognize that I felt worse 24 hours after exertion. I think I only recognized this after some of the initial symptoms had lessened. At the time, I had never heard of ME and “CFS” did not yet exist. When I told people about this symptom, they were pretty incredulous.

    Dr. Melvin Ramsay did describe days long recovery after exertion as a “sheet anchor” symptom in his 1986 definition of ME, although I don’t think he described it as being at its worst 24 hours after exertion. This “delayed peak” seems to be correlated with increased gene expression results in this 2009 paper by the Lights http://www.co-cure.org/Light.pdfs which says that the increases "were highly correlated with symptoms of physical fatigue, mental fatigue, and pain."

    So, I guess what I’m saying is that you really have to look at these reports through the lens what physicians would have been looking for, and what patients would have reported, 80 years ago. Among other things, the reports may simply be from too early in the illness for patients to have recognized PEM, which, at that point, may have been too difficult to pick out of the swamp of other symptoms, particularly if it's delayed and there is no precedent or nomenclature for it.
     
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  15. alex3619

    alex3619 Senior Member

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    I read a study years ago in which enteroviruses can induce a polio-like syndrome in mice. They may be different, but it is suspected that enteroviruses can indeed induce polio, its just that the likelihood is very low, and it may be atypical polio.

    Enteroviruses are still my leading candidate as a cause of ME currently. Autoimmune, autoinflammation, gut permeability, detox and cognitive issues may all be secondary consequences (and involve secondary risk factors), though involve other important mechanisms that can be targeted.

    Almost every argument I have ever heard against enteroviruses being causal for ME disappear under current scientific knowledge of enteroviruses. We have been presuming simple behaviour from them, and though a virus is tiny what they are doing is not simple.
     
  16. alex3619

    alex3619 Senior Member

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    On easy fatiguability and PEM, in 1934 would anyone have had even the vaguest idea that it was important to distinguish between fatigue, delayed fatigue, and delayed fatigue associated with an increase in other symptoms? I seriously doubt it, and given that fatigue is often considered trivial today, it might have been considered trivial back then and so subtle distinctions would have been easy to miss.
     
  17. urbantravels

    urbantravels disjecta membra

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    Actually, the specific form of localized muscle fatiguability described in the report sounds quite a bit like myasthenia gravis. Which, like Guillain-Barre, is an autoimmune disease that attacks the peripheral nerves that innervate the muscles.

    Note I'm not saying that this disease WAS Guillain-Barre or myasthenia gravis, because it doesn't seem to quite fit the onset profile for either of those; but I do think that we have to recognize that many of the symptoms being described are found in other autoimmune diseases, while they aren't characteristic of ME. Why is the argument for it being ME automatically stronger than the argument that it was some other neuroimmune and/or autoimmune disease, which may or may not be known today?
     
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  18. Forbin

    Forbin Forbin

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    This isn't going to settle anything, but I suppose the best way to investigate why the 1934 Los Angeles outbreak was considered consistent with later outbreaks would be to read the original papers that made those comparisons:

    So far as I know, that would be these two papers from 1959:

    Early Outbreaks Of 'Epidemic Neuromyasthenia'
    J. Gordon Parish
    American Journal of Medicine, Vol. 26, Issue 4, Pages 569–595, Copyright (1959)
    http://www.name-us.org/DefintionsPages/DefinitionsArticles/Acheson1959.pdf

    and

    Epidemic Neuromyasthenia; Clinical Syndrome.
    Henderson Da, Shelokov A
    N Engl J Med - Apr 9, 1959
    http://www.ncbi.nlm.nih.gov/pubmed/13644582

    Unfortunately, at the moment, I can not find a copy of the second paper. An earlier 1957 paper, also by Shelokov, makes the comparison as well, though I can only find the first page.

    Epidemic Neuromyasthenia — An Outbreak of Poliomyelitis-like Illness in Student Nurses
    Alexis Shelokov, M.D., Karl Habel, M.D., Elizabeth Verder, Ph.D., and William Welsh, M.D.
    N Engl J Med - August 22, 1957
    http://www.nejm.org/doi/full/10.1056/NEJM195708222570801

    That first page says that the Los Angeles 1934 outbreak bore "more than a superficial resemblance" to a 1953 cluster among nurses at a Rockville, Maryland psychiatric hospital.

    However, a 1959 editorial reviewing the first two papers says this…

    http://journals.lww.com/smajournalonline/Citation/1959/06000/Epidemic_Neuromyasthenia.27.aspx

    My onset initiated with a more severe flu than described, but, other than that and the "projectile vomiting" part, that’s quite an accurate description from 1959 of how it began for me in the mid 1980's.
     
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  19. akrasia

    akrasia Senior Member

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    Whatever else M.E. represents, it is another epic fail for the CDC's claim to represent state of the art epidemiology and a history of lost opportunities. The Holmes definition opened the door to the farrago of assertions that Chronic Fatigue Syndrome was a condition of compromised recuperation driven by neurotic tendencies

    Both Parish and Shelokov were involved, initially, in the first CDC definition.

    From CFS Untied quoting Byron Hyde:


    According to Dr. Byron Hyde’s A Brief History of Myalgic Encephalomyelitis and an Irreverent History of Chronic Fatigue
    Syndrome, there were three Myalgic Encephalomyelitis- literate doctors present at the Committee meeting – Dr. Byron Hyde, Dr.
    Alexis Shelokov, and Dr. J. Gordon Parish.

    “It was obvious that most of the assembly associated this epidemic disease with Epstein-Barr Virus and infectious Mononucleosis,
    what the British refer to as glandular fever. It was immediately apparent that the consensus was going to be highjacked by this
    majority. Dr. Shelokov and Dr. Parish decided that this meeting was going nowhere and so decided to leave before it terminated. I
    followed them knowing full well that if I was going to learn anything credible about this disease process then I had to understand their
    incredible knowledge base that had been developed for over 20 years.








     
  20. lansbergen

    lansbergen Senior Member

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    "projectile vomiting"

    Glad to see somebodyelse noticed it.

    That is how I named it in the animals and now that I have improved enough I think I know what happens.

    Towards the end of a flareup the stomachwall secretes very fast in a short time a lot of gastric acid. I can feel it happen. That has to be ejected. Usely one go is enough, sometimes the secretion does not stop quick enough and a second emptying follows. After that the flareup end is nearby.

    During flareups mucosa are to dry
     

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