knackers323
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If cfs can be caused by multiple triggers, which seems to be the case, and not just one single type of infection, then how are cfs outbreaks explained?
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Cfs outbreaks explanation
- Thread starter knackers323
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knackers323
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Yes @Badpack your missing my point.
If its any virus, bacteria or fungus that we already know about that is causing cfs and not some new and undocumented 'cfs infection' these outbreakes should statisticly be much more common.
There is a discrepancy here between the two theorys
Theory one. Multiple triggers
Theory two. A single 'cfs infection'
If its any virus, bacteria or fungus that we already know about that is causing cfs and not some new and undocumented 'cfs infection' these outbreakes should statisticly be much more common.
There is a discrepancy here between the two theorys
Theory one. Multiple triggers
Theory two. A single 'cfs infection'
JES
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CFS/ME have more or less been proven to not be triggered by a single infection, at least that's the scientific consensus today. But I do think that it's a bit curious that there were these large documented CFS outbreaks back in the 70's and 80's, but not any today.
One explanation would be that as above poster mentioned, there would be multiple pathogens that would hit the immune system simultaneously, causing the development of CFS/ME. Or there could simply by a common virus and a genetic predisposition that together serve as the trigger. Even in these CFS outbreaks like in Lake Tahoe, not nearly every person got hit, it still was a relatively small number of affected people, compared to say, the swine flu outbreak in 2009.
Obermann
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The meaning of the term ME has shifted. ME originally referred to an epidemic disease resembling the early phase of poliomyelitis. The first known epidemic was in Los Angelses 1934. The term (benign) myalgic encephalomyelitis was coined by Donald Acheson in an unsigned editorial in The Lancet 1956.
It was first believed that most patients recovered, but later recognized that ME often becomes chronic. It was also noted that although many epidemics had been reported in the literature, most cases are endemic. As endemic cases tend to come into contact with the health care system at a later stage, the bulk of cases are patients in the chronic phase. In the 1980s, it was discovered that infection with Epstein–Barr virus may lead to a similar chronic condition as epidemic ME. The interest therefore shifted from the acute phase and epidemics to the chronic phase. This fact also is reflected in the WHO classification of the disease. In ICD-8 (1969) and ICD-9 (1978), ME is located in the section "Inflammatory diseases of central nervous system". In ICD-10 (1994), G93.3 (ME and/or CFS) is located in the section "Other disorders of brain".
The terms ME and/or CFS have been used in the medical literature for the following conditions:
a) an infectious disease that involves the central nervous system and resembles the early phase of poliomyelitis
b) a post-infectious syndrome that is triggered by (a) and primarily characterized by post-exertional malaise, fatigue, autonomic symptoms, and symptoms from the central nervous system
c) a post-infectious syndrome triggered by other pathogens than (a)—notable EBV—but with a similar clinical presentation as (b)
d) a chronic syndrome triggered by non-infectious events or agents, but with a similar clinical presentation as (b) and (c)
e) idiopathic chronic fatigue
ME, CFS, ME/CFS, or CFS/ME now usually refers to a syndrome with the same symptoms as the chronic phase of epidemic ME—regardless of trigger—that is (b), (c), and (d). For example, this is how the Canadian Consensus Criteria from 2003 should be understood. The Holmes and the Fukuda criteria for CFS are flawed attempts to describe (b), (c), and (d). Dr Byron Hyde of the Hummingbird foundation, on the other hand, clearly describes ME as biphasic condition, (a) and (b). The classical description of Melvin Ramsay in his book from 1986 (second edition 1988) also refers to the biphasic condition, (a) and (b). The Oxford criteria for CFS targets a completely different group of patients, (e).
The terminology concerning ME and CFS in the literature can sometimes be confusing.
It was first believed that most patients recovered, but later recognized that ME often becomes chronic. It was also noted that although many epidemics had been reported in the literature, most cases are endemic. As endemic cases tend to come into contact with the health care system at a later stage, the bulk of cases are patients in the chronic phase. In the 1980s, it was discovered that infection with Epstein–Barr virus may lead to a similar chronic condition as epidemic ME. The interest therefore shifted from the acute phase and epidemics to the chronic phase. This fact also is reflected in the WHO classification of the disease. In ICD-8 (1969) and ICD-9 (1978), ME is located in the section "Inflammatory diseases of central nervous system". In ICD-10 (1994), G93.3 (ME and/or CFS) is located in the section "Other disorders of brain".
The terms ME and/or CFS have been used in the medical literature for the following conditions:
a) an infectious disease that involves the central nervous system and resembles the early phase of poliomyelitis
b) a post-infectious syndrome that is triggered by (a) and primarily characterized by post-exertional malaise, fatigue, autonomic symptoms, and symptoms from the central nervous system
c) a post-infectious syndrome triggered by other pathogens than (a)—notable EBV—but with a similar clinical presentation as (b)
d) a chronic syndrome triggered by non-infectious events or agents, but with a similar clinical presentation as (b) and (c)
e) idiopathic chronic fatigue
ME, CFS, ME/CFS, or CFS/ME now usually refers to a syndrome with the same symptoms as the chronic phase of epidemic ME—regardless of trigger—that is (b), (c), and (d). For example, this is how the Canadian Consensus Criteria from 2003 should be understood. The Holmes and the Fukuda criteria for CFS are flawed attempts to describe (b), (c), and (d). Dr Byron Hyde of the Hummingbird foundation, on the other hand, clearly describes ME as biphasic condition, (a) and (b). The classical description of Melvin Ramsay in his book from 1986 (second edition 1988) also refers to the biphasic condition, (a) and (b). The Oxford criteria for CFS targets a completely different group of patients, (e).
The terminology concerning ME and CFS in the literature can sometimes be confusing.
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Martin aka paused||M.E.
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...or they didn't use the same strict criteria to diagnose ME and there has never been a CFS/ME-outbreak.
Maybe if the people were living in the same area, there was also some common factor, like high toxic load in the environment, problems with mold... Severe toxicity of sth at least seems to be able to weaken the system a lot. Then together with a strong virus/ bacteria, maybe the combination triggered ME in a row of people.
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A map of where ME sufferers live when symptoms manifested may be useful. I think there will be multiple triggers - your immune system must have to be compromised to a certain degree to kick off ME.
I wouldn't t be surprised to find the ground being prepared by living near agricultural / industrial businesses, whether active or not.
There seem to be areas that have clusters.
I wouldn't t be surprised to find the ground being prepared by living near agricultural / industrial businesses, whether active or not.
There seem to be areas that have clusters.
NelliePledge
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If you have post viral fatigue in UK you fall under CFS guidelines. Anti virals specifically excluded from CFS treatment options so GPs not able to be looking at the viral aspect or testing so would they really be able to pick up if there was an outbreak linked to a virus?
Myalgic Encephalomyelitis is the name for a disease that came in epidemics so it can't be a misdiagnosis! CFS was also the name of an epidemic illness but the definition did not match what the patients were suffering from - we were off to a good start there
The patients in the epidemics became worse with exertion. It was noted that the hospital patients became worse by being examined.
The other defining symptoms were a variability over a day, a week, a month, it could relapse and remit chronically and that about 25% became worse and could be house or bed bound.
The epidemics were associated with polio epidemics and ME seemed to give some protection from polio. The most likely culprit was Coxsackie B or one of the other enteroviruses which are all closely related. Polio was obviously the best studied but after the polio vaccine was introduced most of the expertise was lost.
Polio causes a respiratory infection but some people develop a syndrome which is what we call polio and the same thing happened with ME. Like may illnesses, polio is milder in the young and it attacked along exercise lines - tennis players were affected in the arms, football players in the legs.
This uncommon secondary effect of infection, like measles encephalitis, may result from an underlying weakness in the body, or a secondary stress which lets the virus penetrate deep within the system. In the hospital epidemics it was the staff who became ill, very few patients even though the patients' immune systems must have been stressed.
So energy needs were profoundly implicated in the epidemics and I think that they are at the basis of our disease. If there is not enough ATP for the immune system to work properly or keep the nerves firing then there will be downstream effects everywhere.
The patients in the epidemics became worse with exertion. It was noted that the hospital patients became worse by being examined.
The other defining symptoms were a variability over a day, a week, a month, it could relapse and remit chronically and that about 25% became worse and could be house or bed bound.
The epidemics were associated with polio epidemics and ME seemed to give some protection from polio. The most likely culprit was Coxsackie B or one of the other enteroviruses which are all closely related. Polio was obviously the best studied but after the polio vaccine was introduced most of the expertise was lost.
Polio causes a respiratory infection but some people develop a syndrome which is what we call polio and the same thing happened with ME. Like may illnesses, polio is milder in the young and it attacked along exercise lines - tennis players were affected in the arms, football players in the legs.
This uncommon secondary effect of infection, like measles encephalitis, may result from an underlying weakness in the body, or a secondary stress which lets the virus penetrate deep within the system. In the hospital epidemics it was the staff who became ill, very few patients even though the patients' immune systems must have been stressed.
So energy needs were profoundly implicated in the epidemics and I think that they are at the basis of our disease. If there is not enough ATP for the immune system to work properly or keep the nerves firing then there will be downstream effects everywhere.
Murph
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This is an excellent question and the epidemiology is pretty quiet on how you could get the Royal Free outbreak and the incline village outbreak, but afterward the disease seems sporadic and with a genetic component. It's a genuine mystery and I think if one of the hypotheses above explains it that's mostly by luck.
Hip
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With localized ME/CFS outbreaks such as the Royal Free Hospital outbreak, or the Lake Tahoe outbreak, you have to explain two things: why the virus causes such a very high incidence of ME/CFS in the locale, but then causes very little further problems as the virus spreads to people outside of that locale.
The only logical explanation I can see is a dual causal factor theory of ME/CFS, with this disease being triggered by an ME/CFS-associated virus in combination with another pernicious factor that is only present in that locale. That explains why the rate of ME/CFS is so high in the locale, but as the virus spreads outside the locale, it produces very little new cases of ME/CFS.
If you consider the Lake Tahoe outbreak, we know that during the outbreak, there was a large toxic algae bloom on the lake (and biotoxins such as toxic algae or mold can cause disease just on their own — Dr Shoemaker's CIRS illness is due to these biotoxins). There was also some known issues of mold problems in certain municipal building in the Lake Tahoe area.
In the Royal Free Hospital, we don't have any information about any possible biotoxins or other localized pernicious factors; but my personal theory is that there may have been water damage and a toxic mold growth in communal staff rooms or staff canteens in one or more of the hospital buildings, which in combination with the virus, caused the Royal Free outbreak. This theory would also explain why it was only the staff, but not the hospital patients, who were hit with the ME/CFS (because only the staff would go into the mold-infested staff rooms or staff canteens).
I posted some info about this dual causal factor theory of ME/CFS during outbreaks in this post.
One fact that tends to corroborate this dual causal factor theory is Dr John Chia's discovery that an acute viral infection + corticosteroids often causes ME/CFS (see this thread). Dr Chia investigated thousands of ME/CFS patients' case histories, and noted that ME/CFS was often triggered in these patients when corticosteroids were prescribed during the course of an acute infection. Corticosteroids weaken the immune response, so it seem that when the immune response is weakened during the time of an acute infection when you first catch a virus linked to ME/CFS, that creates the conditions necessary for the virus to trigger ME/CFS.
So with acute viral infection + corticosteroids, we see another example of the dual causal factor theory of ME/CFS.
I think to toxic algae or mold may have analogous immunosuppressive effects to corticosteroids, weakening the immune response in such a way that allows the virus to trigger ME/CFS.
The only logical explanation I can see is a dual causal factor theory of ME/CFS, with this disease being triggered by an ME/CFS-associated virus in combination with another pernicious factor that is only present in that locale. That explains why the rate of ME/CFS is so high in the locale, but as the virus spreads outside the locale, it produces very little new cases of ME/CFS.
If you consider the Lake Tahoe outbreak, we know that during the outbreak, there was a large toxic algae bloom on the lake (and biotoxins such as toxic algae or mold can cause disease just on their own — Dr Shoemaker's CIRS illness is due to these biotoxins). There was also some known issues of mold problems in certain municipal building in the Lake Tahoe area.
In the Royal Free Hospital, we don't have any information about any possible biotoxins or other localized pernicious factors; but my personal theory is that there may have been water damage and a toxic mold growth in communal staff rooms or staff canteens in one or more of the hospital buildings, which in combination with the virus, caused the Royal Free outbreak. This theory would also explain why it was only the staff, but not the hospital patients, who were hit with the ME/CFS (because only the staff would go into the mold-infested staff rooms or staff canteens).
I posted some info about this dual causal factor theory of ME/CFS during outbreaks in this post.
One fact that tends to corroborate this dual causal factor theory is Dr John Chia's discovery that an acute viral infection + corticosteroids often causes ME/CFS (see this thread). Dr Chia investigated thousands of ME/CFS patients' case histories, and noted that ME/CFS was often triggered in these patients when corticosteroids were prescribed during the course of an acute infection. Corticosteroids weaken the immune response, so it seem that when the immune response is weakened during the time of an acute infection when you first catch a virus linked to ME/CFS, that creates the conditions necessary for the virus to trigger ME/CFS.
So with acute viral infection + corticosteroids, we see another example of the dual causal factor theory of ME/CFS.
I think to toxic algae or mold may have analogous immunosuppressive effects to corticosteroids, weakening the immune response in such a way that allows the virus to trigger ME/CFS.
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Dr Maureen Hanson seems to have a theory about this which she alluded to in her recent talk but didn't elaborate on it. I'm just copying this from the notes I made from the recording at the time. She was asked a question from the audience
"Why no outbreaks since 1990 ?
The pathogenic virus could be weaker OR these viruses are now out in the general population and it's now sporadic and there is some immunity, OR our health system could be better now
Interesting that outbreaks tracked with HIV/AIDS she says"
I think that the early ME outbreaks were also said at the time to relate to the polio ones
"Why no outbreaks since 1990 ?
The pathogenic virus could be weaker OR these viruses are now out in the general population and it's now sporadic and there is some immunity, OR our health system could be better now
Interesting that outbreaks tracked with HIV/AIDS she says"
I think that the early ME outbreaks were also said at the time to relate to the polio ones
Obermann
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My comment above was a bit out of sync with other comments because of moderation. I would like to add that the evidence is strong for a pathogen as causal agent to the epidemics of ME, although no such agent has been isolated. Evidence from several epidemics suggest spread by person-to-person contact and an incubation time of half a week up to a week. The disease was transferred to rhesus monkeys in animal experiments in Australia (Pellew et al, Med J Aust, 1955). Three of the infected animals were dissected, and two of them showed histological signs of inflammation in the peripheral nervous system (lesions and minute red spots in the sciatic nerves).
This does not necessarily imply that the post-infectious chronic phase of epidemic ME—i.e. what we nowadays mean by ME/CFS—is an infection. It was demonstrated in the Australian Dubbo study, that 11% of the patients that were infected with Epstein–Barr virus, Coxiella burnetii, or Ross River virus fulfilled the criteria for CFS after six months. The infectious agents may trigger other pathological processes that cause the chronic phase of the illness.
Epidemic ME interfered with poliomyelitis on several occasions, and two polio epidemics (Australia and Iceland) changed into epidemic ME. Coxsackie B is an enterovirus that fits some of the expected qualities of a viral agent for epidemic ME, and it has the capability to suppress poliomyelitis. However, Coxsackie B was considered and rejected at the Royal Free epidemic, so it is probably not the cause.
This does not necessarily imply that the post-infectious chronic phase of epidemic ME—i.e. what we nowadays mean by ME/CFS—is an infection. It was demonstrated in the Australian Dubbo study, that 11% of the patients that were infected with Epstein–Barr virus, Coxiella burnetii, or Ross River virus fulfilled the criteria for CFS after six months. The infectious agents may trigger other pathological processes that cause the chronic phase of the illness.
Epidemic ME interfered with poliomyelitis on several occasions, and two polio epidemics (Australia and Iceland) changed into epidemic ME. Coxsackie B is an enterovirus that fits some of the expected qualities of a viral agent for epidemic ME, and it has the capability to suppress poliomyelitis. However, Coxsackie B was considered and rejected at the Royal Free epidemic, so it is probably not the cause.
ljimbo423
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Robert Naviaux's theory of the cell danger response (CDR) could explain it. Anything that overwhelms the cells ability to maintain enough metabolic balance, can cause the CDR and therefore symptoms and the different assaults from different agents - viral, bacterial, toxins, stress, etc. are cumulative.
http://www.sciencedirect.com/science/article/pii/S1567724913002390
It could be that the people that developed CFS in these outbreaks already had a high enough level of potential triggers of the CDR and/or genetic predisposition. That the viral, bacterial, parasitic infection etc. in the outbreak was enough to fully trigger the CDR and CFS.
So it really wasn't just one infection in these outbreaks that triggered the CFS. It was probably many factors over many years and the outbreak infection was the straw that broke the camels back.
Jim
Hip
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Something changed in the world of ME/CFS during the 1980s, because there was an apparent 5- to 8-fold increase in the incidence of ME/CFS during this decade. See this thread:
Fivefold to eightfold increase in the incidence of ME from 1980 to 1989
One speculation is that the introduction of the poliovirus vaccine decades earlier may have caused this huge increase in incidence. Because natural poliovirus infection may confer some immunity to the enteroviruses linked to ME/CFS, once natural poliovirus in the wild was eradicated by the vaccination program, we may have lost that protection. See here.
In any case, by the end of the 1980s, something in the dynamics of ME/CFS in the world had changed. I wonder whether this could be related to the lack of ME/CFS outbreaks since 1990.
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Obermann
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I think that dr Dowsett's statement of a sevenfold increase in the incidence of ME during the 80s should be interpreted with some caution. She makes that statement in a short article on the webpage of the Hummingbird foundation. There is no epidemiological data to back up her assertion. In the list of ME epidemics by Parish and Hyde, there are 29 epidemics in the 50s, 6 in the 60s, 6 in the 70s, and 12 in the 80s. It seems that the big peak was in the 50s. There have been some speculations that the decline in ME epidemics is related to polio vaccines. Large scale vaccination started in the 50s.
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Hip
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No epidemiological studies on ME/CFS were performed in that era, so we have to fall back on records kept by doctors and other professionals involved with ME/CFS. There are statements and documents from several key experts in the ME/CFS world: Dr Elizabeth Dowsett, Dr John Richardson, Professor Malcom Hooper and Dr Byron Hyde in Canada. Richardson also provides a graph here showing a large increase in incidence of viral diseases in the 1980s.
There is corroborating data from disability insurance company UNUM, who reported claims for disability resulting from ME/CFS had increased 500% from 1989 to 1993. This massive increase in claims likely explains why the disability insurance teamed up with people like Simon Wessely, to try to portray ME/CFS as an "all in the mind" condition rather than a real disease, in order that these insurance companies could withhold disability payments to ill ME/CFS patients.
If it had not been for this massive apparent increase in the incidence of ME/CFS, we might never had had this sorry episode of the disability insurance industry colluding with people like Wessely to make ME/CFS look as if it were an "all in the mind" condition.
But people typically don't start getting ME/CFS until their teenage years and later, so if large scale poliovirus vaccination did increase the incidence of ME/CFS, then you would expect the increased incidence to occur say 2 decades after the introduction of large scale vaccination, which would be around about the 1980s.
That closely fits the coxsackievirus B incubation period, which is 3 to 5 days.
It does not fit Epstein-Barr virus, as the incubation period for mononucleosis is 4 to 8 weeks. In any case, Epstein-Barr virus, HHV-6 and cytomegalovirus do not usually cause epidemics, whereas coxsackievirus B and echovirus infections are known to appear in epidemic outbreaks. So enteroviruses are the likely virus behind these ME/CFS epidemics, rather than herpesviruses. I think the herpesviruses can only be responsible for sporadic cases of ME/CFS.
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