The Hummingbirds' Foundation for M.E.

The Hummingbirds' Foundation for M.E. (HFME) is fighting for the recognition of M.E.,
and for patients to be accorded the same basic human rights as those with similar
disabling and potentially fatal neurological diseases such as M.S.

An important note:

Before reading the research/advocacy information given in the links below, please be aware of the following facts:

1. Myalgic Encephalomyelitis and ‘Chronic Fatigue Syndrome’ are not synonymous terms. The overwhelming majority of research on ‘CFS’ or ‘CFIDS’ or ‘ME/CFS’ or ‘CFS/ME’ or ‘ICD-CFS’ does not involve M.E. patients and is not relevant in any way to M.E. patients. If the M.E. community were to reject all ‘CFS’ labelled research as ‘only relating to ‘CFS’ patients’ (including research which describes those abnormalities/characteristics unique to M.E. patients), however, this would seem to support the myth that ‘CFS’ is just a ‘watered down’ definition of M.E. and that M.E. and ‘CFS’ are virtually the same thing and share many characteristics.

A very small number of ‘CFS’ studies refer in part to people with M.E. but it may not always be clear which parts refer to M.E. The
A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy paper is recommended reading and includes a checklist to help readers assess the relevance of individual ‘CFS’ studies to M.E. (if any) and explains some of the problems with this heterogeneous and skewed research.

In future, it is essential that M.E. research again be conducted using only M.E. defined patients and using only the term M.E. The bogus, financially-motivated disease category of ‘CFS’ must be abandoned.

2. The research referred to on this website varies considerably in quality. Some is of a high scientific standard and relates wholly to M.E. and uses the correct terminology. Other studies are included which may only have partial or minor possible relevance to M.E., use unscientific terms/concepts such as ‘CFS,’ ‘ME/CFS,’ ‘CFS/ME,’ ‘CFIDS’ or Myalgic ‘Encephalopathy’ and also include a significant amount of misinformation. Before reading this research it is also essential that the reader be aware of the most commonly used ‘CFS’ propaganda, as explained in A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy and in more detail in Putting research and articles on Myalgic Encephalomyelitis into context.

Relevant video: What causes M.E.?

The outbreaks (and infectious nature) of M.E.

From ‘What is M.E.?(on this site):

Myalgic Encephalomyelitis is a debilitating acquired illness which has been recognised by the World Health Organisation (WHO) since 1969 as an organic neurological disorder. ME can occur in both epidemic and sporadic forms (over 60 outbreaks have been recorded worldwide since 1934) and appears to be remarkably similar to post-polio syndrome (an enteroviral triggered disorder). ME can be extremely severe and in some cases the illness is fatal.

Myalgic Encephalomyelitis is an acutely acquired neurological illness (with systemic effects) initiated by a virus infection. This point of view is supported by history (ME epidemics have followed polio epidemics and serological studies have shown that communities affected by an outbreak of M.E. were effectively blocked (or immune) from the effects of a subsequent polio outbreak), incidence (correlation with a flu-like prodromic illness), symptoms (painful lymph nodes, low-grade fever, sore throat), and similarities with other viral ailments, notably mononucleosis and post-polio syndrome. Research also supports a viral causation for the illness.

There is a history of recorded outbreaks going back to 1934, when an epidemic of what seemed at first to be poliomyelitis was reported in Los Angeles. A review of early outbreaks found that clinical symptoms were consistent in over sixty recorded epidemics of M.E. spread all over the world.

Although the illness we now know as Myalgic Encephalomyelitis has existed for centuries, for much of that time it was a relatively uncommon disease. Following the mass polio vaccination programs of the 1960’s cases of polio were greatly reduced and outbreaks of M.E. seemed to be similarly affected. It wasn’t until the late 1970’s that M.E. began (for reasons as yet not fully understood) its dramatic increase in incidence worldwide. Over 20 years later, M.E. is a worldwide epidemic of devastating proportions. Many people have died from M.E. and there are now millions of people severely disabled by this epidemic.

Veteran M.E. specialist Dr Byron Hyde explains that: '[The] prodromal phase is associated with a usually short onset or triggering illness. This onset illness usually takes the form of either, or any combination, of the following, (a) an upper respiratory illness, (b) a gastrointestinal upset, (c) vertigo and (d) a moderate to severe meningitic type headache. These are only the most common onset illnesses or symptoms of which there are several. The onset illness is associated with either a low grade or subnormal temperature, headaches, sometimes persisting and accentuated by movement with intermittent attacks of vertigo or dizziness. Evidence of a previous immune insult [such as a recent immunisation] is found regularly in both epidemic and sporadic cases. The usual incubation period of the triggering illness is 4-6 days. The second and third phases of the illness are usually always different in nature from the onset illness and usually become apparent within 1-4 weeks.'

There appears to be somewhat of an occupational bias towards teachers (students) and health care workers in the incidence of Myalgic Encephalomyelitis cases (and outbreaks). These higher risk groups do not work in environments which are more stressful than the average job, but these are jobs which require higher rates of immunisation than others. This relationship with inoculation is often seen in infectious illnesses.

The main period of infectivity of M.E. peaks at the time just before symptoms appear through to the initial acute phase of the illness (which lasts for several months or in some cases years). M.E. appears to be highly infective but also highly selective. Modes of transmission are thought to include: casual contact (respiratory), salivary transmission (eg. kissing), sexual transmission and transmission through blood products. There is also evidence that asymptomatic carrier of the illness may be able to pass the illness on to others for a brief period following their exposure to the illness. (During the recovery and/or chronic stages of the illness however M.E. does not appear to present a significant infective risk).

The US Centres for Disease Control (CDC) placed 'CFS' on its "Priority One; New and Emerging" list of infectious diseases some years ago; a list that also includes Lyme disease, hepatitis C, and malaria.’ But it seems that is the only real ‘action’ they’ve taken. No real research into transmissibility (or more importantly on reducing infection rates) has been done by the Government despite ample evidence that this is an infectious disease. There have been many well-documented clusters or outbreaks of the illness, reports of 4.5% of people contracting the illness after blood transfusions (or after needle-stick injuries involving the blood of ME patients), evidence of the disease spreading through casual contact amongst family members and so on.

As Dr Elizabeth Dowsett explains: ‘The problem we face is that, in spite of overwhelming epidemiological and technical evidence of an infectious case, the truth is being suppressed by the government and the 'official' M.E. charities as 'too scary' for the general public.’

This pretence of ignorance on behalf of Government has had enormous consequences; only in the UK are people with ME directly banned from donating blood for example. So it is that the number of people infected with ME continues to rise unabated and largely unnoticed by the public.

M.E. is at least as common as Multiple Sclerosis. Children and teenagers are also susceptible to the illness and children as young as five have been diagnosed with M.E. One hundred thousand kids are estimated to have M.E. in the US alone and a recent study in the UK found that M.E. was by far the most common reason for a child’s long term absence from school. Women are affected around three times as often as men, a ratio common in autoimmune disorders (although in children the sexes seem to be afflicted equally). M.E. affects all races and socio-economic groups and has been diagnosed all over the world.

Transmission of M.E. to monkeys has been successfully demonstrated and has produced central nervous system and parasympathetic nervous system injury in at least two separate sets of experiments; in 1934 where ‘cross sections of the spinal cord demonstrated numerous minute haemorrhages in the grey matter’ and in 1949-51 in the Adelaide, Australia epidemic of M.E. where a radiculitis of the sciatic nerve was demonstrated with small punctate lesions of the myelin sheath (Hyde & Jain 1992, p. 40).

M.E. is an infectious neurological disease and represents a major attack on the central nervous system (CNS) by the chronic effects of a viral infection. A significant number of the world’s leading M.E. experts believe that M.E., like poliomyelitis, is caused by an enterovirus. (This includes doctors such as A. Gilliam, A. Melvin Ramsay and Elizabeth Dowsett, John Richardson of Newcastle-upon-Tyne, W.H. Lyle, Elizabeth Bell of Ruckhill Hospital, James Mowbray of St Mary’s, Peter Behan and also the brilliant Byron Hyde of Canada.) The evidence which exists to support this theory is compelling (Hyde 2007, [Online]) (Hyde 2006, [Online]).

Enterovirus infections are able to cause:

  1. a chronic host infection
  2. major or no cardiac disease depending on the virulence of the subtype
  3. cardiac injury dependent upon the sex of the patient and of the level of physical activity of the patient during the acute or infectious stage
  4. cardiac disease depending upon the immunological variability of the host (Hyde & Jain 1992a, p. 40).

An enterovirus would also explain the; age variation, sex variation, obvious resistance of some family members to the infection and the effect of physical activity (particularly in the early stages of the illness) in creating more long-term/severe M.E. illness in the host (Hyde & Jain 1992a, p. 40). There is also the evidence that; M.E. epidemics very often followed polio epidemics, M.E. resembles polio at onset, serological studies have shown that communities affected by an outbreak of M.E. were effectively blocked (or immune) from the effects of a subsequent polio outbreak, evidence of enteroviral infection has been found in the brain tissue of M.E. patients at autopsy, and so on (Hyde 2007, [Online]) (Hyde 2006, [Online]) (Hyde 2003, [Online]) (Dowsett 2001a, [Online]) (Dowsett 2000, [Online]) (Dowsett 1999a, 1999b, [Online]) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43) (Hyde et al. 1992, pp. 25-37) (Dowsett et al. 1990, pp. 285-291) (Ramsay 1986, [Online]) (Dowsett & Ramsay n.d., pp. 81-84) (Richardson n.d., pp. 85-92) (Richardson 1999, [Online]).

M.E. expert Dr Elizabeth Dowsett writes about Myalgic Encephalomyelitis that: ‘This illness is distinguished from a variety of other post-viral states by an unique clinical and epidemiological pattern characteristic of enteroviral infection. Prompt recognition and advice to avoid over-exertion is mandatory’ (Dowsett et al. 1990, pp. 285-291).

See below for more information.

The Clinical and Scientific Basis of Myalgic Encephalomyelitis Edited by Byron Hyde, M.D. , Nightingale Research Foundation, Ottawa, Canada

‘It is a fact that the majority of M.E. patients are not in high-stress occupations as the popular press frequently suggests, but are teachers, nurses, physicians, and other health care workers. This group represents those most closely related to infectious illness, frequent immunisations and those most frequently immunised.’

‘Up to 1955, recognised M.E. was clearly previously associated with poliomyelitis. The viruses that cause paralytic poliomyelitis are some of the same viruses that cause M.E. But these enteroviruses that are capable of causing paralysis attach to more than one set of tissue receptors. These other receptors are found on different cells in the brain and spine as well as in other body areas. The symptoms described by M.E. sufferers are due to injury to these other cells.’

Note: This book contains an enormous amount of information on the epiemics of M.E. (and many other aspects of M.E.) that is simply not available anywhere else. Each epidemic is listed and many are gone into in great detail, information is given on transmissibility, onset and on the historical facts of each outbreak (for example; the links with Polio and how sufferers of one early outbreak were actually paid to keep silent about what had happened to them!). This book is essential reading for anyone with an interest in M.E.

The Nightingale Definition of Myalgic Encephalomyelitis (M.E.)  by Dr Byron Hyde 2006

'Under epidemic and primary M.E. there is no consensus as to the viral or infectious cause. Much of this lack of consensus may be due to the non-separation of acute onset from gradual onset patients in the M.E. and CFS groups of patients. Primary M.E. is always an acute onset illness.

Doctors A. Gilliam, A. Melvin Ramsay and Elizabeth Dowsett, John Richardson of Newcastle-upon-Tyne, W.H. Lyle, Elizabeth Bell of Ruckhill Hospital, James Mowbray of St Mary’s and Peter Behan all believed that the majority of primary M.E. patients fell ill following exposure to an enterovirus (Poliovirus, ECHO, Coxsackie and the numbered viruses are the significant viruses in this group).

I share this belief. Unfortunately, it is very difficult to recover polio and enteroviruses from live patients. Dr. James Mowbray developed a test that demonstrated enterovirus infection in many M.E. patients but I do not believe he qualified his patients by acute or gradual onset type of illness. In my tests in Ruckhill Hospital in Glasgow, I found confirmation of enteroviral infection only in acute onset patients and not in any gradual onset [ie. CFS] patients. Few physicians realize that almost all cases of poliovirus recovered from poliomyelitis victims came from cadavers. At the very least, these enteroviruses must be recovered from patients during their onset illness and this has rarely been done. An exception is in the case of the Newton-le-Willows Lancashire epidemic where Dr. W. H. Lyle’s investigation recovered ECHO enterovirus. Recent publications by Dr. J. R. Kerr have also identified the fact that enteroviruses are one of the most likely causes of M.E. If this belief is correct, many if not most of the M.E. illnesses could be vanquished by simply adding essential enteroviral genetic material from these enteroviruses to complement polio immunization.'

'It has become obvious to me that we are dealing with both a vasculitis and a change in vascular physiology. Numerous other physicians have supported this finding. Dr. David Bell, who rediscovered the work of Dr. David Streeten and his book, Orthostatic Disorders of the Circulation: Mechanisms, Manifestations and Treatment, New York: Plenum Medical, 1986, advanced this understanding of M.E. The work of Dr. Vance Spence and his colleagues in Scotland have started to nail this CNS-vascular relationship down even further with a series of major research papers. The recent interpretation of the cause of Multiple Sclerosis (MS) as an injury of the microvasculization causing the injury of the schwann cells that in turn causes the demyelination injuries of MS has been added to that of paralytic poliomyelitis as an essential vascular injury. Paralytic poliomyelitis was thought to be a primary injury to the anterior horn cells of the spinal cord but is now recognized as a vasculitis injuring the circulation to the anterior horn cells. Poliomyelitis is generally a non-progressive, specific site injury, although post-polio syndrome has challenged that belief. MS is a recurrent more fulminant physiological vascular injury.

M.E. appears to be in this same family of diseases as paralytic polio and MS. M.E. is definitely less fulminant than MS but more generalized. M.E. is less fulminant but more generalized than poliomyelitis. This relationship of M.E.-like illness to poliomyelitis is not new and is of course the reason that Alexander Gilliam, in his analysis of the Los Angeles County General Hospital M.E. epidemic in 1934, called M.E. atypical poliomyelitis.'

'M.E. is a clearly defined disease process. CFS by definition has always been a syndrome. At one of the meetings held to determine the 1994 U.S. Centers for Disease Control and Prevention (CDC) definition of CFS, in response to my question from the floor, Dr. Keiji Fukuda stated that numerous M.E. epidemics—he cited the Los Angeles County Hospital epidemic of 1934, the Akureyri outbreak of 1947-48 and the 1955-58 Royal Free Hospitals epidemics-- were definitely not CFS epidemics. Dr. Fukuda was correct.'


Are Myalgic Encephalomyelitis and Chronic Fatigue Syndrome Synonymous Terms? by Byron Hyde MD

Byron M. Hyde, M.D. Presented at 1998 International ME Conference, Sydney

A Record of Myalgic Encephalomyelitis Epidemics: A basic factor about ME throughout its history is that it does occur in epidemics. This fundamental aspect is essential. This fact conveys, among other things, the infectious and contagious nature of our disease. These characteristics of our disease are strictly avoided by the health agencies. It could be said that a strategic aspect of the health agency policies has been to conceal the history of ME.

An important chapter in the Encyclopaedia of Myalgic Encephalomyelitis contains a very fundamental disclosure of ME by documenting the outbreaks from 1934 to 1990. This chapter is the result of work carried out over many years by Drs. Acheson, Henderson, Shelokov and Parish. We are profoundly grateful to these doctors and their vigilance over the years to evaluate and keep track of these outbreaks.

"It is thus important that those that attempt to define any disease or illness to have long term clinical experience with patients with this illness. There is simply no place for the bureaucrat in defining illness. All definition of epidemic or infectious illness must be based upon persistent clinical examination of the afflicted patient, an understanding and exploration of the environmental factors producing that illness, and pathophysiological examination of tissue from those patients. For similar reasons, I believe that the inclusion of psychiatrists in the defining of an epidemic and obviously disease of infectious origin, simply muddies the water for any serious understanding of that disease. The UK definition of CFS was developed by a panel of physicians who were primarily psychiatrists, with few if any clinicians who had ever looked at an epidemic of CFS. A serious attempt must be made to look at epidemic disease as and where that disease starts. This has not been done by those who have defined CFS in the USA nor in the United Kingdom and this factor alone is probably the single greatest reason why we know so little about CFS today that we did not know in 1984."

Myalgic Encephalomyelitis (M.E.) This is a term used to describe an epidemic and sporadic disease process that is associated with a chronic debilitating illness of children and adults. Variants of this term M.E. were first used following a series of repeating epidemics starting in May 1955 in the Royal Free Hospital in London England. New outbreaks of this illness continued until 1958 in various London area hospitals. M.E. and these epidemics are well described by A. Melvin Ramsay in his book Myalgic Encephalomyelitis and Post-Viral Fatigue States.

Dr. A. Melvin Ramsay followed many of those who fell chronically ill during this 1955-1958 epidemic period for up to 34 years, until he died in 1989. This type of epidemic continuity proved to be quite characteristic of the M.E. epidemics that occurred in Akureyri in 1947-1949, in the Royal Free epidemics and in the North American epidemic period that extended from 1984 to 1988 (In 1983 in New Zealand where this pan-epidemic may have originated. All of these epidemics occurred in the late summer and autumn, decreasing in winter, with a new small peak of new female cases at Christmas in the Northern Hemisphere. The numbers of new cases would then rapidly fall off as the winter months progressed, only to reappear in the late summer again.

Monthly pattern of onset of new M.E. illness. This M.E. type of epidemic that was first observed and documented in detail in the summer of 1934, Los Angeles County General Hospital Epidemic by Dr. Alexander (Sandy) Gilliam, is not uncommon. Over 60 similar but often less known epidemics have been documented by Dr. J. Gordon Parish.

These epidemics have been associated with certain particular characteristics. Onset can be at any season but most frequently occurs in summer or autumn. There appears to be a high prevalence of epidemics or clusters in schools, hospitals and institutions involving hospital staff. The usual incubation period of the triggering illness is 4-6 days. The second and third phases of the illness are usually always different in nature from the onset illness and usually become apparent within 1-4 weeks.’

A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome by Dr Byron Hyde 2006

[This paper discusses several of the epidemics]

‘Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. Though CFS is based upon a typical M.E. epidemic, in my opinion it has always been a confused and distorted view of reality. The invention of Chronic Fatigue Syndrome has to be one of the most curious cases of inventive American scientific imperialism that one could imagine. It is my opinion that the CDC 1988 definition of CFS describes a non-existing chimera based upon inexperienced individuals who lack any historical knowledge of this disease process. The CDC definition is not a disease process.’

M.E. is not caused by the HHV6 virus: 'This virus was not associated with CFS until after the 1990 period. HHV6 is the virus that causes the benign childhood illness, Roseola. By 1986 HHV6 was already known to have an incubation period of 9 days due to human experimentation when the actual virus was injected into several children. See (Gorbac, Second Edition, Infectious Diseases, page 1335). When acquired by random infection, the incubation period of HHV6 Roseola was more like 12 days. So once again anyone with access to a library or a computer would have soon dispelled any view that HHV6 was a cause of M.E. epidemics where the incubation was approximately 7 days or less.'

M.E. is not caused by the Epstein Barr virus (or mononucleosis/glandular fever): 'The Lake Tahoe epidemic that started in August 1984 also started amongst students. In this case the epidemic began in a high school girls' basketball team that was travelling in a bus to play various other teams. The epidemic spread rapidly with an incubation period of approximately a week. As in many of the other epidemics, it then spread to the general community. After the epidemic started it then involved three high schools, both students and teachers and ultimately spread to the community. For some reason it was considered to be an epidemic of infectious mononucleosis. This is an illness caused by a virus Epstein Barr Syndrome. Associating the Lake Tahoe epidemic with Epstein Barr Syndrome was frankly ridiculous and you will see why almost immediately. Anyone who realizes that infectious mononucleosis is caused by the herpes family virus, Epstein Barr Virus (EBV), and that the incubation period of this illness is approximately 40 days, should have realized that you simply cannot have a rapidly spreading viral epidemic with a virus with a latent period of 40 days. Neither Dr Straus nor Dr Holmes, senior government physicians, should have fallen into such a trap. They only had to go to the excellent CDC library to realize that rather than spending half a million dollars or so on a publication that they should have known would not have incriminated EBV. Yet this epidemic somehow spread the myth that this illness was caused by EBV. Today, as I write this short history of M.E. the vast majority of physicians and the public still associate Epstein Barr Virus with [M.E.]. Such is the perseverance of error.'

'The incubation period from time of contact with the infection until the appearance of the illness is approximately 4-7 days. In its epidemic form M.E. was most commonly seen in (a) Health Care Workers, (b) children and older students in residential schools, nurses residences and hospitals, (c) in military barracks where students or soldiers were housed in close proximity further supporting the belief in its infectious nature. Although M.E. was not caused by poliovirus in the Akureyri epidemic, infection with M.E. somehow protected the patients from the polio epidemic that swept though Iceland in the 1950s. Polioviruses represent three of approximately 100 different enteroviruses. This was the reason why many in the UK believed that some of these epidemics were probably caused by a less lethal non-polio form of enteroviruses such as ECHO, Coxsackie, the numbered and new enteroviruses.'


The Nightingale Definition of Myalgic Encephalomyelitis (M.E.) by Dr Byron Hyde 2006


Since the Nightingale Research Foundation's publication in 1992 of its textbook, The Clinical and Scientific Basis of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome, there has been a tendency by some individuals and organizations to assume that M.E. and CFS are the same illness. Over the course of two International Association of Chronic Fatigue Syndrome (IACFS, formerly the American Association of CFS) conferences, there have been suggestions that the name CFS be changed to M.E., while retaining the CFS definitions as a basis for such change. This does not seem to me to be a useful initiative: it would simply add credence to the mistaken assumption that M.E. and CFS represent the same disease processes. They do not.

M.E. is a clearly defined disease process. CFS by definition has always been a syndrome

At one of the meetings held to determine the 1994 U.S. Centers for Disease Control and Prevention (CDC) definition of CFS, in response to my question from the floor, Dr. Keiji Fukuda stated that numerous M.E. epidemics he cited the Los Angeles County Hospital epidemic of 1934, the Akureyri outbreak of 1947-48 and the 1955-58 Royal Free Hospitals epidemics-- were definitely not CFS epidemics. Dr. Fukuda was correct.

I believe it essential to define clearly Myalgic Encephalomyelitis. That is what the Nightingale definition of M.E. sets out to do


M.E. Definition Booklet, September 2011, by Dr Byron Hyde (PDF format)

This document is an excellent and timely antidote to the scientifically unsupportable ICC.This is the latest unhelpful CFS redefinition being endlessly promoted by 'ME/CFS' advocates.Dr Hyde's new booklet is highly recommended by HFME.

A few quotes:

"One has to cease believing that M.E. resembles or is the same as CFS. One has to cease believing those who patent virus and infectious agents for profit are necessarily going to tell the truth. If one looks only at M.E. and the diagnostic principles outlined above it is obvious that only one group of viruses can fit the picture as the causal agent of M.E. and those are the enterovirus family. There are no known patents on this group of viruses."

"Although the illness can occur at any time of the year, epidemics and endemic cases in the North Temporal zone tend to peak in the late summer. Epidemics when they occur, (if they
are followed) may grumble on for 2-4 years or longer in the general community.

This (i) biphasic nature of M.E., the (ii) short incubation period of 4-5 days, and the (iii) peak period in late summer, (iv) lack of prior immunity in the over 20 age group excludes most viruses."

"As in all infectious diseases, this virus causes a wide degree of injury from:
• Non-symptomatic and/ or infectious carrier states,
• Mild: in which the patient recovers without any sequellae, is never investigated and is usually given the diagnosis of mild "flu",
• Chronic: where the patient is diagnosed with M.E. or
• Death: in an autopsy the pathological diagnosis is given and the cause of severe M.E. is missed. In at least four published M.E. epidemics deaths has occurred."

"I know of only one viral family that can typically provoke all of the above findings, and that is the enterovirus family."

"If one observes:
a. All three North American M.E. epidemics occurred at the same time, in the late summer of 1984 during the known peak phase of entero-viral infection. Originally, those who described their regional epidemic were not aware of the other two epidemics that occurred at the time; b. All three epidemics has similar if not the same features consistent with an enterovirus cause, c. The cohort diseases mentioned above were noted in one or all of the three epidemics are consistent with known enteroviral illnesses, It is hard to dismiss the enteroviral family as probable cause of this illness. But there are other reasons to believe this epidemic was due to enteroviruses.

This same epidemic & endemic occurred all over North America and Ontario during the same time period. In Canada we have free health care and free testing. Hundreds of Ontario doctors, independently observing seriously ill individual M.E. patients, initially assumed they were due to EBV and ordered EBV virus testing. Some may have picked up on the EBV theories already promulgated by Stephen Straus and his associates. Yet in the thousands of tests verified by Dr Bernadette McLaughlin at the Ontario Viral Centre, collectively she did not find any percentage increase in EBV recovery from these patients during the 1984-1989 period. During this period, Dr McLaughlin routinely sent the thousands of samples for a spectrum of other viral tests. Unfortunately testing was performed only during the endemic period from 1983-1989, at which time the Ontario Government stopped authorizing enteroviral testing as a cost saving measure. During this endemic period Dr McLaughlin found only one viral group responsible for the surge in fatigue and encephalitis related illnesses. The significantly increased viral recoveries were only enteroviruses."

"It is of interest that we supplied the Ruchill team with 100 of our endemic and epidemic Ottawa patients. Our sample consisted of 60 gradual onset CFS type patients and 40 acute onset M.E. type patients. We found NO enteroviral association in any of the gradual onset CFS patients. In the 40 acute onset patients the Ruchill group found that 20 of the 40 acute onset, or 50% diagnosed as acute onset M.E. were positive for enterovirus by PCR."

"We believe that CFS illness usually represents missed major disease that would be diagnosed if a proper total body organ total system investigation were conducted. We also found that the Ruchill group failed to recover enterovirus in our previously positive same patients when they were tested several years later. Obviously with time, there is an increasing difficulty in recovering enteroviruses. However, positive virus results or not this group of M.E. patients were not significantly better."

"When a gastric biopsy of one of the severely M.E. positive Ruchill Ottawa/Quebec patients (Pierre M) was sent for analysis to Dr John Chi in California in 2010, his tissue sample was found to be highly positive for chronic enterovirus infection."

"The pathologies of acute onset M.E. patients as a group differ significantly from gradual
onset patients CFS patients, whom I refer to as CFS and not as M.E. Gradual onset CFS patients tend to be misdiagnosed as M.E. and as a group have major and multiple missed organ and system pathologies rather than having typical M.E. Many CFS have no observable CNS findings."

"At the first meeting on the 27th of October 2005, the Chairman of the Joint Committee, Dr Ian Gibson, asked me to prepare a report and definition that might assist the committee in its further deliberations. The following are my original recommendation. Dr Bruce Carruthers, who chaired the 2003 Canadian Clinical Case Definition for M.E./CFS, was also present when I gave this definition. I strongly disagreed with Dr Caruthers in the merging the definitions of M.E. and CFS since on the basis of the physical total body assessment of both M.E. and CFS patients; these two names represent two entirely different spectrums of illnesses."

It is increasingly obvious that too much importance was being placed upon the definitions of Chronic Fatigue Syndrome (CFS), and not enough upon the actual disease, Myalgic Encephalomyelitis (M.E.). These two illness spectrums are not the same and should not be considered to be the same. Nor is there any doubt in my mind that the various definitions of CFS actively impede physicians' ability to make a rapid and rational diagnosis as well as a scientific confirmation of any testable illness. Such is not true of M.E. where a rapid and rational diagnosis can be made that can be confirmed by laboratory and other technological testing.'

"We propose that the diagnosis of Chronic Fatigue Syndrome (CFS) should be limited to gradual onset fatigue syndromes and that all of these gradual onset CFS patients should be carefully investigated for major organ or system pathology. In our experience gradual onset CFS patients tend to have significant missed pathology that may be correctable if a diagnosis is made early in their disease process. In our investigations, because CFS represent so many serious and very different disease processes, it is of limited value to take seriously any uniform viral theory of cause or any uniform treatment when referring to CFS."

Enteroviral Myalgic Encephalomyelitis - EvME: A treatise on EvME by Dr Irving Spurr

"Myalgic Encephalomyelitis is recognised by the WHO as a neurological disease. It is well annotated in medical literature, from the Polio epidemics in 1930s-40s [Gilliam]. Defined by Melvyn Ramsay in the 1950s - Royal Free Disease and in the 1960s by Luis Leon Sotomayor. In 1970 the BMA published a paper by two psychiatrists. Dr C P McEvedy and Dr A W Beard which concluded that the Royal Free outbreak was largely due to hysteria. The effect on medical opinion was far reaching and still prevails. The effect on patients was and remains catastrophic.

The enteroviruses, ubiquitous in nature, are responsible for a variety of human diseases ranging from mild gastroenteritis to fulminating multi-organ failure. They are the cause of Myalgic Encephalomyelitis and it is no surprise that this disease has multi-organ involvement with protean manifestation.

Enterovirus genus is comprised of Polioviruses, Coxsackieviruses A&B, Echoviruses and E71. They are members of the Picornaviridea family. The Picorna family is marked by its extremely small size. The virion is a naked icosahedron about 30 nm in diameter. The genome is comprised of single-stranded monopartite RNA. While Poliomyelitis has virtually been eradicated in the Western world, others of the genera have filled the vacuum so created [E71]. Enteroviruses, as the name implies, persist in the gut and are remarkably resistant to its harsh conditions. They mutate slowly, en passage, to re-challenge host resistance; pandemics occurring every 2-4 years. Diseases can range from relatively minor gastrointestinal upset to paralysis, meningitis, encephalitis, cardiac damage and birth defects. Sub clinical and mild infections are by the far most common."

Reference Index Of Papers Published On Epidemics of ME 1934-80 (collected by Dr J. Gordon Parish)

Redefinitions of ME - a 20th Century Phenomenon by Dr Elizabeth Dowsett

‘To suggest that ME/CFS is merely one subgroup amongst this heterogenous collection of physiological and pathological states, makes thus making any attempt at differential diagnosis between them impossibly expensive to pursue; to suggest that diagnosis must be delayed for 6 months, vitiates any real attempt at virus investigation, especially among the young. It has to be remembered that these "Fatigue" definitions were devised specifically for research, not clinical purposes; that they exclude variations in children and adolescents and that scientists in the USA (their main country of origin) are now foremost in seeking a more descriptive name than that of "Chronic Fatigue [Syndrome]" for this illness!’

Research into ME 1988 - 1998 Too much PHILOSOPHY and too little BASIC SCIENCE! by Dr Elizabeth Dowsett

‘The term "Myalgic encephalomyelitis" (ME) was henceforth used in the UK, Canada and Australasia to define an illness which, following a virus infection, leads to multisystem involvement of cardiac and skeletal muscle, liver, lymphoid and endocrine organs but which is primarily due to central nervous system dysfunction and subsequent breakdown in bodily homoeostasis. Confirmation of this hypothesis was supported by electrical tests of muscle and of brain function (including the subsequent development of PET and SPECT scans) and by biochemical and hormonal assays.’

‘In the mid 1980’s, the incidence of ME had increased by some seven times in Canada and the UK, while in the USA a major outbreak at Lake Tahoe (wrongly ascribed at first to a herpes virus) led to calls for a new name and new definition for the disease, more descriptive of herpes infection. This definition based on "fatigue" (a symptom common to hundreds of diseases and to normal life, but not a distinguishing feature of myalgic encephalomyelitis) was designed to facilitate research funded by the manufacturers of new anti-herpes drugs. However, a "fatigue" definition (which also omits any reference to children) has proved disastrous for research in the current decade.’

Differences between ME & CFS by Dr Elizabeth Dowsett

ME is a systemic disease (initiated by a virus infection) with multi system involvement characterised by central nervous system dysfunction which causes a breakdown in bodily homoeostasis (The brain can no longer receive, store or act upon information which enables it to control vital body functions, cognitive, hormonal, cardiovascular, autonomic and sensory nerve communication, digestive, visual auditory balance, appreciation of space, shape etc). It has an UNIQUE Neuro-hormonal profile"

‘The problem we face is that, in spite of overwhelming epidemiological and technical evidence of an infectious case, the truth is being suppressed by the government and the 'official' M.E. charities as 'too scary' for the general public.’

Recent Epidemics: Why are the Epidemics so important The Committee for Justice and Recognition of Myalgic Encephalomyelitis

"We encourage patients to learn about ME, its history and the epidemics and the modern research. Do not be confused by the deceitful propaganda about a "new disease". No CFS definition defines a neurological disease. All definitions which wear the 'f' word (ie. fatigue) in their name are not ME nor neurological. They are definitions of fatigue conditions. And when these definitions were written it was not neurological ME which they were attempting to define.'

'The CDC history and their record with the ME epidemic, and experiences of ME patients, strongly suggests that in order to help save lives the CDC must be prohibited from any further involvement with any decisions about our disease. It is clear to us that there is a fundamental conflict between the interests of the large and growing patient community disabled by ME with their desire for progress, and the program of the CDC, which has been to delay and derail the search for the cause and cure.'

‘ME outbreaks and sporadic disease has been documented for many decades. ME appeared most commonly during local polio outbreaks, and at a high rate among hospital personnel. At onset ME resembles polio, and for many years was considered a variant of polio and classified as Atypical poliomyelitis.

Although Myalgic Encephalomyelitis had been reported in the medical journals many times over the past century it was considered a rare disease. Despite this profile, during the 1980’s ME exploded into an alarming worldwide epidemic. For example during the last 20 years ME progressed from a rare disease to now claim over a million victims in the USA alone.

Upon this background of alarming community outbreaks, pleas from doctors, a contagious pattern and an expanding epidemic spread, the government health agencies did not act in a straightforward manner to determine the nature, cause, and extent of the epidemic, nor to alert and protect the public.

As the leading example, in the USA, the Centers for Disease Control (CDC) is the agency entrusted to actively investigate precisely this type of major health hazard. Rather than fulfilling its mandate, for some reason, the CDC abandoned their duty and proceeded to avoid its investigation. They then proceeded to develop and implement policies designed to disguise the disease, and confuse the medical community and the public. The centerpiece of this program of confusion and distraction was forged by changing the name of ME to CFS, interpreted by all as an innocuous, unexplainable fatigue condition. This instantly cut off the disease from its history and prior medical investigations and reports. Replacing knowledge with ignorance.

These actions rendered doctors ignorant of the history and the established neurological infectious nature of this epidemic disease. This new name distracted doctors and the research investigators with a major effort that proclaimed a "new illness" and focused all attention on fatigue. These policies of concealment even go so far as to advise doctors not to investigate patients for the infectious causes. Many other governments immediately followed the same model. These policies have not diminished this epidemic, or protected the public, or sought to determine the cause of this disease. These policies reveal a clear pattern of malfeasance and disregard for the public’s health.’

Note: This article lists many of the more than 60 individual outbreaks

ME: The New Plague by Jane Colby

"Outbreaks of ME can be linked with outbreaks of different enteroviruses right back to 1948, when they were first grown in tissue culture and could be identified. Doctors would often diagnose polio but eventually conclude they were seeing 'an unusual' poliovirus. Their clinical acumen was spot on, even though they lacked our present technology."

‘Right back in 1970, it was shown by Gatmaitan, Chason and Lerner that when mice infected with Coxsackie B3 were forced to swim in a warm pool, the virulence of the virus was drastically augmented. In fact, viral replication was augmented 530 times. This did horrendous things to the animals' hearts. We all know that to play squash with the flu can lead to heart attacks. Much the same danger can be courted by undertaking hard exercise with ME. ‘

Osler's Web by Hillary Johnson

Hillary Johnson, author of a book which documented the mid-eighties M.E. outbreak in the US (Osler’s Web), explains that the name was selected: [By] a small group of politically motivated and/or poorly informed scientists and doctors who were vastly more concerned about cost to insurance companies and the Social Security Administration than about public health. Their deliberate intention – based on the correspondence they exchanged over a period of months – was to obfuscate the nature of the disease by placing it in the realm of the psychiatric rather than the organic. The harm they have caused is surely one of the greatest tragedies in the history of medicine. ... The Government’s choice of names was so inept, in fact, that many observers came to view it as a deliberate effort to defuse the potentially panic-inducing issue of the eruption of a life-altering infectious disease. "CFS" after all, hardly sounded "catching". (1996, p.219)

‘Cheney was not particularly interested in a patient’s level of ‘fatigue.’ He graded the disease instead by its progressive phases which be believed began with a mononucleosis-type illness and an up-regulated or hyperactive immune system. Then over the years it progressed to a neuralgic, MS like illness, with mild to severe dementia and an AIDS-like or down-regulated immune system. Cheney selected his patients based on their neurological signs and symptoms. All of this was a departure from the CDC’s criteria, which essentially looked for one thing – disabling, unexplained fatigue – and excluded patients who exhibited unambiguous signs of disease.’ (p 438)


‘By 1972, a distinguished group of clinicians and scientists had set out to share information, form research groups and hold national and international conferences related to the problems of ME. Following successful vaccination against the three polio viruses during the early 1960s over 60 epidemics of atypical, non paralytic polio had been recorded in the UK alone. It was obvious that (since Nature abhors a vacuum) the non polio enteroviruses were naturally filling the gap(6), and demonstrating their potential for inducing a serious neurological disease of considerable chronicity, mainly affecting school children and middle aged adults in the most important and productive years of their lives. Most of the famous London teaching hospitals were involved, at that time in investigating epidemics and in subsequent research while links were forged with international institutions in USA, Canada, Europe and Australasia, facing the same problems.

Research first published in 1975(7) indicated that the enteroviruses (which triggered the illness) belonged to a vast group of viruses (many of them at that time yet to be discovered) which were able to survive persistently in the human body as an uncoated form of intracellular genetic material, thus avoiding direct challenge from the immune system. Simple (indirect) laboratory confirmation of their presence based on blood tests, was available in most NHS laboratories without let or hindrance, while the European enterovirus reference centre at Ruchill Hospital in Glasgow, provided expert identification. It was clear from their work that epidemics occurred at 10 year intervals and pandemics (world wide spread) were approximately 20 years apart. By 1987, famous research workers, including Drs Ramsay, Richardson and (from Canada and the USA) Byron Hyde and David Bell, Professors Mowbray and Banatvala and scientists of the status of Len Archard and (from the USA) Roger Loria and Richard Bruno and Nancy Frick, were able to enlighten and to back up the hundreds of GPs and NHS consultants dealing with an ever increasing number of seriously disabled patients. The potential of this disease to disable children and interrupt their education was realised(8) and (in the early 1980’s) the late effects of polio were rediscovered (earlier reports dated from the late 19th century).’

A Public Statement to Government Health Ministers and an ALERT to citizens worldwide The Committee for Justice and Recognition of Myalgic Encephalomyelitis

Worldwide Epidemic/Over 1 Million in U.S. 

Atypical Polio, Myalgic Encephalomyelitis, Gulf War Syndrome Vaccines and Toxic Chemicals Government Agencies Obscuring the Evidence

The Committee for Justice and Recognition of Myalgic Encephalomyelitis

The Tahoe Outbreak The Committee for Justice and Recognition of Myalgic Encephalomyelitis

Polio and ME  The Committee for Justice and Recognition of Myalgic Encephalomyelitis

Canadian Expert Consensus Panel Clinical Case Definition for ME/CFS

‘ME/CFS has developed following a blood transfusion. Within days or weeks of the initiating event, patients show a progressive decline in health and develop a cascade of symptoms.’

‘ME/CFS occurs in both epidemic and sporadic forms.’

Dr. P.O. Behan, Prof. Neurology, in: Critical Reviews in Neurobiology, 1988, vol 4

'Epidemic myalgic encephalomyelitis has attracted increasing attention during the last 5 years, leading to a clearer definition of its clinical and laboratory features. The illness occurs both sporadically and in epidemics, with cases being reported from all over the US, Europe, Australasia, and South Africa. Single cases may continue to appear after the epidemic has ended. Thus, it is stressed that the syndrome is an endemic disease with periodic outbreaks of epidemic prevalence.'

Three Babuska Clusters of Enteroviral-Associated Myalgic Encephalomyelitis by Byron Hyde MD

‘Unique Enterovirus Association Although physicians associated with Nightingale have been studying both M.E. and CFS patients since 1984, it was only in 1995 that we began to include in the investigation of each new Nightingale M.E. patient, an evaluation by PCR for chronic persisting enteroviral infection. The material employed was frozen blood serum that was evaluated by the research team of the viral laboratory of Ruchill Hospital in Glasgow. These patients were re-evaluated approximately once or twice a year for a period of three years. Blood serum from control patients of similar age and sex were submitted with serum from M.E. patients. Blood from other patients with various autoimmune diseases or neurological illnesses were also submitted along with our samples. The names were changed in repeat samples. The serum received at Ruchill Hospital was divided into reserves and two blinded samples of this serum were investigated by PCR in different laboratories. Only when each sample source was found to be positive for the same enteroviral code was the serum accepted as having a specific circulating enterovirus.

When possible, patients with a positive enterovirus confirmation had their serum resubmitted over a period of up to three years. Due to distance this was not always possible for some patients.

Among this group of M.E. patients we found that in those who had been ill for (1) less than 3 years, and (2) who had fallen ill abruptly, we were able to demonstrate a high recovery of persisting enterovirus. Approximately 40% of the acute onset M.E. group were positive for enterovirus by PCR. Patients with slow onset disease or who had been ill for over 5 years had infrequent positive enterovirus assays. Most important, in no case have I found a persisting positive enterovirus in two or more assays in normal controls. It is of interest that two of the few controls that were positive for enterovirus PCR both had had massive transfusions, related to either cardiac surgery or to obstetrical emergencies.’

‘There is an increasing evidence from our investigations, that one of several new and unique enterovirus PCRs can be recovered in the serum of a significant number of patients who fell ill acutely with M.E. There appears to be an extended period of up to 3-4 years during which this virus family can be recovered and it is possible that evidence of enteroviral PCR begins to disappear from the circulating serum.’

The Complexities of Diagnosis by Byron Hyde MD 2003

(Taken from: Handbook of Chronic Fatigue Syndrome by Leonard A. Jason, Patricia A. Fennell and Renée R. Taylor)

‘The term myalgic encephalomyelitis was based on clinical descriptions of an illness that has occurred both sporadically among the general population and in clusters, or epidemics, usually in hospitals or schools. Over 60 such epidemics have been described in the medical literature (Acheson, 1992; Henderson & Shelokov, 1992; Hyde, 1992) since Sandy Gilliam, Assistant Surgeon General of the United States and later Dean of Medicine at Johns Hopkins, first described the 1934 epidemic in the Los Angeles County General Hospital (1938). B. Sigurdsson et al. (1950) in Iceland, D. A. Henderson, and A. Shelokov, in the United States (1959a, 1959b); A. Wallis, in 1955, and A. M. Ramsay, in 1988, and John Richardson, in England (1992); and P. Behan, in Scotland (Behan & Behan, 1988; Behan, Behan, & Bell, 1985), have all added to this growing literature.

Those who are most injured or die are easily recognized at disease onset or shortly after as CNS, cardiovascular, or organ injury. Because of their overwhelming illness and the specificity of the end-organ injury, they are never diagnosed as ME except in epidemic or cluster situations.’

How to disguise a disease by Cesar Quintero

‘ME has had a long association with Poliomyelitis. It should also be taken into account that when ME and Polio were described as being similar it was done at a time when Drs were often very experienced with polio cases and knew its features.

In 1938 the U.S. Asst. Surgeon General, Dr A Gilliam published a major report about this Polio-like illness detailing the epidemic of 1934 at Los Angeles California. This was a landmark to the understanding of this disease. The primary importance of this work was to alert the medical world that this was a different disease yet polio-like it was not polio. Accordingly it would be difficult for Drs today to acknowledge the similarities to polio, a disease they have never had any experience with.

The question remains today. Is ME a different expression of polio? Were there other viruses that were present along with the wave of the polio epidemics? Did polio and its companions mutate after the polio vaccine?’

‘In the fifties there was an epidemic in Iceland, also associated with a polio outbreak - but again, recognized to be a new disease. It was found that patients who developed [M.E.] became immune to polio. [M.E.] has occurred more or less world-wide. Epidemics have been described in closed, contained populations such as schools, military barracks, convents, monasteries, and especially hospitals.’

Information on Myalgic Encephalomyelitis (M.E.)/Chronic Fatigue Syndrome (CFS) by Jill McLaughlin

‘Some studies have shown genetic linkages, however, genetic basis is not consistent with the epidemiology of ME/CFS Genetic diseases slowly increase in the population over time, not as a sudden explosion of cases, as happened with ME/CFS in the early-mid 1980s.’

‘There have been many recorded outbreaks of ME during the 20th century, which in the U.S. were initially referred to epidemic neuromyaesthenia. In 1959 a comprehensive review paper was published by Dr. Donald Henderson (a CDC epidemiologist) and Dr. Alexis Shelakov (an NIH epidemiologist) in the New England Journal of Medicine describing several outbreaks. Dr. Henderson noted, "The pattern of the epidemic, the absence of any common exposure factors and the high incidence among medical and hospital personnel were consistent only with an infectious disease transmitted from person to person."’

‘A CDC official advised an inquiring ME/CFS patient to refrain from donating blood or organs until the cause or mode of transmission is better understood. It has been shown that patients may harbor infectious agents in their blood.’

 1970’s ME Epidemic at California Hospital Erich D. Ryll, M.D.

Using his long experience, Dr. Ryll describes Myalgic Encephalomyelitis and the history of a California Hospital Outbreak during the 1970’s. This report is a valuable page in ME history and provides additional perspective about this infectious disease. Further illustrating the continuous trail of ME epidemics and discussion of the diverse complex of symptoms and pathology. Patients often find his description of the illness very realistic.

‘In the spring and summer of 1975 there occurred a major, severe epidemic of a communicable, apparent viral disease at the Mercy San Juan Hospital in Carmichael, a suburb of Sacramento, California. The first two cases became ill in February; the bulk of the cases fell ill between July and November of 1975. Several cases tailed out to 1978. The epidemic spread to all departments of the Hospital. It was equally severe in all departments.’

‘So what causes IVN/ME? A specific viral agent has not yet been identified. It does not appear to be anything common. It could be a viral agent very difficult to cultivate. It could be what is called a partial virus. Could it be due to two viruses? As yet there has been no association with the retrovirus that has been proven. The previous finding of a retrovirus has not been able to be repeated by experiments and is invalid. But suppose that all, or nearly all of us, carry an unknown retrovirus in our genes. And then another viral agent infects and the two in combination produce the disease? Or could this illness be due to a virus that escapes immune surveillance. This is, that our immune system is unable to detect it as a foreign invader?

There is a very interesting illness called the post-polio syndrome. Patients who have had polio 20-30 years before acquire an illness that closely resembles [M/E.]. Could this syndrome be due to a mutant polio virus that escapes immune detection? Earlier I said that the early epidemics of ME/ENM/CFS were always in association with a polio outbreak. And that those who came down with ME/ENM/CFS were immune to polio.

It is very important for you to have a firm diagnosis. If you know what you are up against, it is half the battle won.’

The Late Effects Of M.E. Dr Elizabeth Dowsett


In 1948, the year in which polio viruses were first cultured, specimens from 2 children with clinical poliomyelitis, yielded a non- polio enterovirus, (eponymously called Coxsackie after the neighbourhood in which they lived). This finding opened a Pandora's box of some 70 previously undiscovered enteroviruses of which 14 strains were later found to have neurogenic potential equal to that of polio viruses.

From the late 1940s, studies in the USA indicated that outbreaks of major or minor enteroviral illness (eg. Paralytic or non paralytic and non specific summer 'flu") could be caused by varying proportions of virulent and non virulent polio viruses combined with other neurogenic enteroviruses, for example in Akron and Cincinnati, Ohio (1947) Delaware and Connecticut (1949).

In the UK, an outbreak of poliomyelitis affecting an Edinburgh housing estate from August 1961- February 1962 (a period when polio immunisation with the Salk (injectable) vaccine had recently been introduced) provided evidence that a "mosaic" of enteroviruses, including Polio type 3, Coxsackie viruses B2 and B4, Echo viruses 5 and 15 could act in combination to enhance virulence in individual patients, to block the spread of polio virus type 3 and to interfere with vaccine efficiency. Each virus type appeared sequentially until the arrival of Echo virus 5 in November which ended the outbreak by the following February (as indicated by serial sampling of the local school sewer). It has to be remembered that a sudden change in the virulence and spread of enteroviruses in the 20th century has been due to alterations in human hygienic behaviour rather than to viral mutations.’

(Note that while terms such as 'CFS' and 'ME/CFS' are used by Dr Chia, it is certain that at least part of his research relates to authentic M.E. patients. The evidence for enteroviral causation of M.E. is overwhelming. It is unfortunate however that Dr Chia seems unaware in many ways of the vast difference between M.E. and 'CFS' and the political and financial motivations behind 'CFS' and so on, as his research mixes M.E.and 'CFS' unfortunately and confuses the terms and definitions. Jodi Bassett)

Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach John kai-sheng Chia 1* and Andrew Y Chia 11 EV Med Research, United States. To whom correspondence should be addressed.

J Clin Pathol. Published Online First: 13 September 2007. doi:10.1136/jcp.2007.050054 Copyright 2007 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.


Aims The aetiology for chronic fatigue syndrome remains elusive although enteroviruses have been implicated as one of the causes by a number of studies. Since most CFS patients have persistent or intermittent gastrointestinal (GI) symptoms, we evaluated the presence of viral capsid protein 1(VP1), Enterovirus RNA and culturable virus in the stomach biopsies of CFS patients.

Methods165 consecutive CFS patients underwent upper GI endoscopies and antrum biopsies. Immunoperoxidase staining was performed using enterovirus-specific monoclonal antibody (mAb) or a control mAb specific for cytomegalovirus. RT-PCR ELISA was performed on RNA extracted from paraffin sections or samples preserved in RNA-later. Biopsies from normal stomach and other gastric diseases served as controls. 75 samples were cultured for enterovirus.

Results135/165 (82%) biopsies stained positive for VP1 within parietal cells, whereas 7/34 (20%) of the controls stained positive (P ɘ.000001). CMV mAb failed to stain any of the biopsy specimens. Biopsies taken from 6 patients at the onset of the CFS/abdominal symptoms, and 2-8 years later demonstrated positive staining in the paired specimens. EV RNA was detected in 9/24 (37 %) paraffin-embedded biopsy samples, and 1/21 controls had detectable EV RNA (pɘ.01). 1/3 patient had detectable EV RNA from two samples taken 4 years apart. 5 patient samples demonstrated transient growth of non-cytopathic enteroviruses.

Conclusion Enterovirus VP1, RNA and non-cytopathic viruses were detected in the stomach biopsies of CFS patients with chronic abdominal complaints. A significant subset of CFS patients may have chronic, disseminated, non-cytolytic form of enteroviral infection, which could be diagnosed by stomach biopsies.


"An estimated 80 - 90% of our 1400 CFS patients have recurring gastrointestinal symptoms of varying severity, and epigastric and/or lower quadrant tenderness by examination, compared to only 3/100 control subjects (authors unpublished observations). Finding enterovirus VP1 protein in 82% of stomach biopsy samples seems to correlate with the high percentage of CFS patients with GI complaints."

"Finding enteroviral protein in some of the control subjects could be explained by the high prevalence of enterovirus infections throughout the year, affecting as many as 50 million Americans per year, or 17-25% of the population.4 Viral shedding in stool can persist for weeks after acute infections. It is probable that the control subjects had an asymptomatic or self-limited enterovirus infection within the preceding months. More careful screening of the control subjects may increase the specificity of this test in future studies."

"Enterovirus infection initiated the GI symptoms and CFS, and the persistence of the virus years later likely was responsible for the patients symptoms."

"Endomyocardial biopsy taken from patients with viral myocarditis demonstrated persistence of enteroviral genome in almost one-third of the samples 1 year after acute infection.31 Muscle biopsy specimens taken from CFS patients, and postmortem examination of brain tissues from one CFS patient, years after the initial infection, also demonstrated the persistence of enteroviral genome.69 32 Collectively, these findings clearly support the concept of viral persistence in human tissues."

"Taken together, the findings of enteroviral protein, RNA and the growth of non-cytopathic viruses in the stomach tissue of CFS patients, years after initial infection, suggest a strong association between enteroviral persistence/infection and CFS."

"By inference, a significant subset of CFS patients may have a chronic, disseminated, non-cytolytic form of enteroviral infection, which can lead to diffuse symptomatology without true organ damage. If confirmed, stomach biopsies could be used as a test to document viral persistence, and serve as an objective means to follow the response to antiviral therapy, in addition to quantitation of subjective complaints."

Journal of Clinical Pathology 2005;58:1126-1132; doi:10.1136/jcp.2004.020255 © 2005 by BMJ Publishing Group Ltd & Association of Clinical Pathologists

REVIEW The role of enterovirus in chronic fatigue syndrome J K S Chia Correspondence to: Dr J K S Chia CEI Research Center, 23560 Crenshaw Blvd 101, Torrance, CA 90505, USA;


ABSTRACT Two and a half decades after coining of the term chronic fatigue syndrome (CFS), the diagnosis of this illness is still symptom based and the aetiology remains elusive. Enteroviruses are well known causes of acute respiratory and gastrointestinal infections, with tropism for the central nervous system, muscles, and heart. Initial reports of chronic enteroviral infections causing debilitating symptoms in patients with CFS were met with skeptism, and had been largely forgotten for the past decade. Observations from in vitro experiments and from animal models clearly established a state of chronic persistence through the formation of double stranded RNA, similar to findings reported in muscle biopsies of patients with CFS. Recent evidence not only confirmed the earlier studies, but also clarified the pathogenic role of viral RNA through antiviral treatment. This review summarises the available experimental and clinical evidence that supports the role of enterovirus in chronic fatigue syndrome.

Taken together, these data suggest that enterovirus can initiate and perpetuate the immunological response often seen in patients with CFS. Smouldering viral infection of various cells of the body with continuous expression of double stranded RNA and viral antigens could result in a chronic inflammatory state in the local tissues and account for the diverse symptoms reported by these patients.

The mechanism of viral persistence reconciles the two seemingly opposing observations of the past two decades: absence of live virion in chronically infected patients and animals and the finding of enteroviral RNA in the blood or other tissues. The finding of double stranded RNA is consistent with the clinical symptoms of patients with CFS. Without forming double stranded RNA, our patients with HIV or hepatitis B/C infections are usually not symptomatic, even though the measurable viraemia often exceeds 104?/ml. In contrast, patients with CFS and the presence of viral RNA in peripheral blood leucocytes or in tissues, but without true viraemia, have debilitating symptoms; the severity of the symptoms correlated with the frequency of finding enteroviral RNA in the peripheral blood leucocytes (J Chia and A Chia. Detection of double-stranded RNA in the peripheral blood leukocytes of patients with the chronic fatigue syndrome. Abstract T-101. In: Program of the 104th General Meeting for the American Society of Microbiology. New Orleans: Louisiana, 2004). In most of the patients with CFS, the cyclic nature of low grade febrile illness and severe exacerbation after physical activity would be consistent with a cyclical pattern in the viral replicative activity.

It is probable that viral RNA found inside cells, in a stable double stranded form, can dissociate and replicate using viral RNA replicase; some of the positive strands, although restricted in replication,51 are translated to viral proteins during active metabolic states (for instance, exercise), which subsequently perpetuates the immunological response, including but not limited to synthesis of specific neutralising antibody. Consistent with this hypothesis, a recent study on Sjögren’s syndrome clearly detected enteroviral RNA and VP1 protein in minor salivary gland biopsies from these patients, but not in controls.52 From the available data in the literature, however, it is not possible to exclude with complete certainty the possibility that a few virions are actually formed and sequestered in membrane vesicles within the infected human cells.

Among other immunostimulatory effects, double stranded RNA is a potent inducer of interferon synthesis, which activates intracellular RNase, with resultant degradation of excessive single stranded RNA. The finding of a higher level of RNase L activity in the mononuclear cells of patients with CFS is consistent with this paradigm.53,54 However, enough positive and negative strands probably recombine to form stable double stranded RNAs, which are resistant to RNAse L inactivation, and the life cycle will start again when the pressure of the immune response decreases. Ironically, the continuing inflammatory response towards persistently infected cells/tissues to halt viral infection may be partially responsible for the difficulty in finding viral genomes in these patients, and may also be responsible for the symptoms.

Take home messages

  • A severe flu-like illness occurs in most cases of chronic fatigue syndrome (CFS), suggesting that an infection triggers and possibly perpetuates this syndrome


  • Common viral infections and unusual causes of CFS could be diagnosed based on the details of the initial flu-like illness, if present, epidemiological history, and early virological testing


  • Different laboratories from Europe and recently from the USA have found enteroviral RNA in the tissues, including peripheral blood mononuclear cells and muscles, of patients with CFS


  • Viral persistence through the formation of stable double stranded RNA reconciles the two opposing observations of the past two decades: (1) the absence of live virion in chronically infected patients and animals and (2) the presence of enteroviral RNA in the blood or other tissues


  • Smouldering viral infection of various cells with continuous expression of double stranded RNA and viral antigens could result in a chronic inflammatory state in the local tissues, accounting for the diverse symptoms


  • Interferon {alpha} and {gamma} act synergistically against enterovirus in vitro, and preliminary studies suggest that this combination may be an effective treatment for patients with chronic enteroviral infection


Self replicating double stranded RNA molecules (replicons) have been well studied and are currently used as vectors for DNA vaccines and drug susceptibility assays.55,56 Double stranded RNAs can be extremely potent adjuvants for immune responses or, alternatively, these molecules with certain sequences may silence our genes by blocking our mRNA,57 although the evidence for this last mechanism is not yet available for CFS.

"Ironically, the continuing inflammatory response towards persistently infected cells/tissues to halt viral infection may be partially responsible for the difficulty in finding viral genomes in these patients, and may also be responsible for the symptoms"

The paradox remains, however, that despite an ongoing immune response, these viral RNA infected cells are not eradicated. It is possible that viruses hide in long living, immunologically privileged cells, including but not limited to, macrophages, muscles, myocardial cells, and neurones,28�� although these cells are unable to produce much live viruses, perhaps, in part, because of the pressure from local interferon and high concentrations of neutralising antibody—a form of cryptic infection. Viral antigen has been identified in tissues by virus specific monoclonal antibodies but positive staining did not allow the differentiation between membrane bound viral proteins and sequestered virions.58,59 Persistent infection of B cells and monocytes/macrophages, the cells initially responsible for the uptake/transport of virus, has been well described for other intracellular pathogens.60 Recently, we have found enteroviral RNA in the bone marrow samples of two patients with CFS and cyclic neutropenia (JK Chia, unpublished observation, 2004), suggesting that stem cells in the bone marrow could be a source of ongoing viral infection, as reported in animal models of enteroviral infection.59

Thus, renewed interest is needed to study further the role of enterovirus as the causative agent of CFS. Many aspects of this research need to be addressed but there are three urgent priorities.

(1) To overcome the technical difficulties associated with the enteroviral RNA detection assay, because a reliable and reproducible measurement of cell associated viral RNA will provide a marker for antiviral treatment and provide conclusive evidence of chronic infection.

(2) To perform a proof of concept, randomised, double blinded, placebo controlled clinical trial investigating the efficacy of the combination of interferon {alpha} and {gamma}.

(3) To develop inhibitors for viral RNA replicase, the main mechanism for RNA replication, which allows the persistence of the viral genome in infected cells. In the future, a well designed, randomised, controlled trial of antiviral treatment will ultimately provide crucial information on the pathogenic role of enterovirus in patients with CFS and other chronic diseases.

The laboratory work was supported by the Chu-Lee Tu memorial research fund.

© 2005 by BMJ Publishing Group Ltd & Association of Clinical Pathologists

ME and CFS, The Definitions  A. Melvin Ramsay M.A. M.D.

‘The clinical course of the Myalgic Encephalomyelitis syndrome is consistent with a virus type of infection. It most commonly commences with an upper respiratory tract infection with sore throat, coryza, enlarged posterior cervical glands and a characteristic low-grade fever with temperatures seldom exceeding 101°F. Alternatively there may be a gastro-intestinal upset with diarrhoea and vomiting. In 10% of the 53 cases we reported between 1955 and 1958 the onset took the form of acute vertigo often accompanied by orthostatic tachycardia.

The prodromal phase is characterised by intense persistent headache, paraesthesiae, blurring of vision and sometimes actual diplopia. Intermittent episodes of vertigo may occur at intervals both in the prodromal and later phases of the disease.’