General M.E. Quotes
Quotes by M.E. sufferers
Quotes from M.E. political discussion groups
On so-called 'fatigue' in M.E...
On the supposed role of 'stress' in M.E...
Quotes on the outbreaks (and infectious nature) of M.E.
Quotes from M.E. sufferers on the negative effects of CBT and GET
M.E. vs MS quotes
Quotes on 'Are we just marking time?'
Quotes on the problems with the so-called "Fair name" campaign
Quotes on the problems with the use of 'ME/CFS' by M.E. advocates
Quotes on the topic of 'Who benefits from 'CFS' and 'ME/CFS'?'
Before reading these quotes, please be aware of the following facts:
1. Myalgic Encephalomyelitis and ‘Chronic Fatigue Syndrome’ are not synonymous terms. The overwhelming majority of research (and articles) 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/articles as ‘only relating to ‘CFS’ patients’ (including those which describe 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/articles 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/advocacy.
Note that the inclusion of a quote on this site does not necessarily denote support for all parts of the article it was taken from, or support for the terminology used in this article, nor total support for all articles created by this author.
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. and that M.E. activism also focuses entirely on M.E. The bogus, financially-motivated disease category of ‘CFS’ must be abandoned.
2. The research and articles 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. For more information see A warning on ‘CFS’ and ‘ME/CFS’ research and advocacy and the more detailed paper Putting Research and Articles on Myalgic Encephalomyelitis into Context.
From ‘What is M.E.?’ and M.E: The Medical Facts (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 M.E. 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 up to three times more common then Multiple Sclerosis. It is also more common than lung cancer, breast cancer, or HIV (in women) with an estimated 2 million sufferers in the US, 250 000 sufferers in the UK and around 36 000 in Australia and many more worldwide. 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.
A significant number of the world’s leading M.E. experts believe that M.E., like Polio, is caused by an enterovirus. The evidence which exists to support this theory is compelling, for example: 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. See the qoutes below for more information.
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.
The Clinical and Scientific Basis of ME Dr Byron Hyde p. 115
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.
The Clinical and Scientific Basis of ME Dr Byron Hyde p. 115
To suggest that ME 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!
Redefinitions of ME - a 20th Century Phenomenon 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.
Research into ME 1988 - 1998 Too much PHILOSOPHY and too little BASIC SCIENCE! 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"
Dr Elizabeth Dowsett
'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.'
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.) by Dr Byron Hyde 2006
'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.'
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.) by Dr Byron Hyde 2006
'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.'
The Nightingale Definition of Myalgic Encephalomyelitis (M.E.) by Dr Byron Hyde 2006
"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."
Jane Colby in 'M.E. The New Plague'
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)
'In 1984-85, a large number of people living in Incline Village, Nevada, were devastated by a mysterious, debilitating disease, now known to be Chronic Fatigue Syndrome. After a cursory investigation of the outbreak, the Centers for Disease Control (CDC) and the National Institutes of Health (NIH) have made little effort to aggressively research the disease. It was not until 1995--ten years later--that scientists at the CDC gave CFS a "Priority 1" listing among their "New and Re-emerging Infectious Diseases" category, thus officially recognizing it as a bona fide disease. Despite including CFS in this category, these agencies continue to insist there is no evidence that CFS is infectious.'
Hillary Johnson (author of Osler's Web)
"Is CFS contagious? In a 1992 research paper on the Nevada outbreak, Harvard researchers pointed out that there was enough evidence to "suggest the possibility of an infectious agent transmissible by casual contact." Anecdotal reports from doctors who have specialized in the care of people with CFS report that some proportion of their patients come down with CFS after blood transfusions. A nurse who worked in a CFS-dedicated clinic acquired the disease after accidentally sticking herself with a needle used to draw blood from a CFS patient."
Hillary Johnson (author of Osler's Web)
"Is CFS an epidemic? An epidemic is defined as an unusual occurrence of disease. What is so remarkable and disturbing about this one is that it is an epidemic hiding in plain sight. Despite clear evidence that CFS is an epidemic, the government health agencies responsible for tracking and curbing disease outbreaks have continually minimized this threat with bland reassurances to the public."
Hillary Johnson (author of Osler's Web)
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.
Jane Colby in’ ME: The New Plague’ (p35)
"I had no idea that my place in epidemiological and cultural history would play a giant role in the was my illness was perceived. I simply collided with a pathogen. In 1992, on a day in May, the sky started spinning"
Peggy Munson in 'Stricken'
"In 1995 I called the CDC and asked them for data from the polio epidemics in the 1950s, year by year, and discovered that the attack rate of M.E. was about fifteen times higher in the late 1980s-early than the attack rate of polio in the early 1950s. We don't get paralyzed in the formal sense; we just drop out and disappear"
Hillary Johnson, author of 'Osler's Web'
"An infectious pathogen can and will infect a multitude of people--but only a few get symptoms, and only a few of them actually become seriously ill. This is how infectious diseases work. If all were immunologically vulnerable to every infectious pathogen, the human race would never have survived. No species would. So given this information, you would have to say, this is a huge disease and remarkably common"
Hillary Johnson, author of 'Osler's Web'
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.
Research into ME 1988 - 1998 Too much PHILOSOPHY and too little BASIC SCIENCE! by Dr Elizabeth Dowsett
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).
THE IMPACT OF PERSISTENT ENTEROVIRAL INFECTION Dr Elizabeth Dowsett
In 1948(3), the year in which polio viruses 1,2,3 were first grown in the cells of human or animal tissues (“tissue culture”), Coxsackie viruses (typical of some 12 species of “non polio” enteroviruses with potential to attack neurological tissues in the same way as polio viruses 1-3) were isolated during an epidemic of poliomyelitis in Coxsackie, New York State, USA from 2 boys with typical symptoms.
In 1955(4), an epidemic of neurological illness (later called myalgic encephalomyelitis) affected some 300 members of the staff at the Royal Free Hospital, London causing encephalitis accompanied by paresis but without permanent paralysis.
However, many nurses remained chronically disabled and unfit for strenuous hospital duties for the rest of their lives. Some 15 years after this outbreak (1970) two psychiatrists (McEvedy & Beard)(5) studied the case histories of these sufferers and, without seeing or examining a patient, declared the whole incident to be an example of “mass hysteria”. Unfortunately, this opinion was to have a profound affect upon the fate of future generations of sufferers from the same illness in the 1980-1989 pandemic. As for McEvedy, he went on to declare an outbreak of “winter vomiting disease”, affecting a boy’s school, to be another example of “mass hysteria”. By this time further advances in technology (e.g. the electron microscope) clearly indicated a common virus infection to be at fault.
THE IMPACT OF PERSISTENT ENTEROVIRAL INFECTION Dr Elizabeth Dowsett
Some studies have shown genetic linkages, however, genetic basis is not consistent with the epidemiology of ME Genetic diseases slowly increase in the population over time, not as a sudden explosion of cases, as happened with ME in the early-mid 1980s.
Jill McLaughlin
"Fatigue is not a disease. It is a symptom of many diseases. Since there is no single underlying condition behind fatigue, by equating [ME eqivalent] C.F.S. with unexplained fatigue, federal officials can say that there is no single underlying condition behind C.F.S."
Hillary Johnson in 'Osler's Web'
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.’
"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 Committee for Justice and Recognition of Myalgic Encephalomyelitis
'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.'
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
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.
Hillary Johnson in ‘Osler’s Web’ p 438
M.E. is different in clinical presentation from other chronic fatigue syndromes. The evidence speaks for itself. Other postviral fatigue states are clinically in contrast to the three cardinal features of M.E. [M.E. is not the same illness as post-viral syndromes caused by glandular fever/mono, Q fever, etc.]
What is M.E.? What is CFS? INFORMATION FOR CLINICIANS AND LAWYERS: Eileen Marshall, Margaret Williams and Professor Malcolm Hooper
The term myalgic encephalomyelitis (means muscle pain, my-algic, with inflammation of the brain and spinal cord, encephalo-myel-itis, brain spinal cord inflammation) was first coined by Ramsay and Richardson and has been included by the World Health Organisation (WHO) in their International Classification of Diseases (ICD), since 1969. It cannot be emphasised too strongly that this recognition emerged from meticulous clinical observation and examination.
Professor Malcolm Hooper 2006
"Outbreaks of M.E. 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."
Jane Colby in 'M.E. The New Plague'
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 M.E.
Jane Colby in’ M.E.: The New Plague’ (p35)
"In 1995 I called the CDC and asked them for data from the polio epidemics in the 1950s, year by year, and discovered that the attack rate of M.E. was about fifteen times higher in the late 1980s-early than the attack rate of polio in the early 1950s. We don't get paralyzed in the formal sense; we just drop out and disappear"
Hillary Johnson, author of 'Osler's Web'
"An infectious pathogen can and will infect a multitude of people--but only a few get symptoms, and only a few of them actually become seriously ill. This is how infectious diseases work. If all were immunologically vulnerable to every infectious pathogen, the human race would never have survived. No species would. So given this information, you would have to say, this is a huge disease and remarkably common"
Hillary Johnson, author of 'Osler's Web'
"Suppose that, in the 'bad old days' before polio vaccination, a parent whose child had died had been told: "She stopped breathing on purpose you know." A public outcry would surely have ensued. And imagine if the next remark had been: "Tell me, did you encourage her in this belief that she couldn't breathe?" The mere idea of such an attitude, quite properly, takes the breath away. Yet children with severe M.E., unable to walk or even to eat, are often considered to be shamming and all sorts of bizarre startegies have been used to try to expose this".
Jane Colby in 'M.E.: The New Plague' (p22)
"The crucial differentiation between ME and other forms of postviral fatigue syndrome lies in the striking variability of the symptoms not only in the course of a day but often within the hour. This variability of the intensity of the symptoms is not found in post viral fatigue states"
Dr Melvin Ramsay, President, UK ME Association. ME Association Newsletter, Winter 1989: 20-21)
When Holmes et al. 1988 was written - the condition which they were trying to define was Chronic Epstein Barr Virus. The principal symptom was 'fatigue'. It is interesting to note that those who were familiar with M.E. on the committee refused to sign off on this definition - as they pointed out that it was not a definition of M.E.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
In all M.E. epidemic or endemic patients the patients represent acute onset illnesses. The fatigue criteria listed here can be found in hundreds of chronic illnesses and clearly defines nothing.
Dr Byron Hyde 2006
Recently an M.E. patient's spine has been examined in the UK and the inflammatory nature was also discovered. Myalgic Encephalitis is a diffuse inflammatory injury of the capillaries at the level of the basement membrane of the brain. It makes no sense to rename the horse and call it Myalgic Encephalopathy. All brain pathologies involving brain tissue are encephalopathies. Let us stop fussing around and get back to the real problem and that is investigating the patients.
Dr Byron Hyde 2006
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.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
We believe it is also our duty to alert the general public that this devastating disease epidemic shows no sign of ending, which means that all our fellow citizens are at risk to be its next victim. Therefore we will promote patient and public understanding of ME, and demand that the national health agencies end the policies and practices of deliberate roadblocks, distraction and dishonesty. These policies have had enormous consequences and continue to extract a tragic toll.
Many people have died from Myalgic Encephalomyelitis and there are now millions disabled by this epidemic. It is time to put an end to the cover-up of this epidemic.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
The outbreak in Los Angeles, California in 1934 is most cited as the first well documented outbreak of ME. The 1934 outbreak, like most eventually affected a wide area, and for years afterward sporadic cases were reported. However, the official reports focused on the 200 staff members of the Los Angeles County General Hospital who were affected. As with many of the other outbreaks it occurred during a local polio epidemic, had a high incidence among hospital staff and resembled a polio illness.
The US Surgeon General undertook a major investigation of the Los Angeles outbreak and Dr Alexander Gilliam published the extensive report about this illness: US Public Health Bulletin 1938. This was a landmark effort as it extensively described the illness, and for the first time made it clear that there was a new disease present: while this illness was Polio-like it was not Paralytic poliomyelitis. The landmark US Public Health Bulletin referred to the new disease, with features of a chronic polio encephalitis, as "Atypical Polio".
There were many similar outbreaks of ME over the years. Some were well-known, such as the Iceland epidemic of '48 and the outbreak at the London hospitals in 1955, where the well known infectious disease specialist Dr A Melvin Ramsay began his detailed investigations. Again the epidemics focused attention, and the medical journals reported on the outbreaks and examined the similarities with Poliomyelitis. While the principal differences were a broader array of symptoms, absence of poliovirus, a prominence of myalgia and a chronic course in many, nevertheless it was consistent with an encephalomyelitis. The term Myalgic Encephalomyelitis has been used since that time.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
Children Fall Ill with Myalgic Encephalomyelitis: Knowing about the Akureyri epidemic and the Cumberland epidemic, it is curious that there should be any debate in the UK or anywhere else that M.E. is also a disease of children. All of these children, and the medical and scientific community as well, could benefit if funds were dedicated for the complete and integrated physical and technological examination of these [M.E.] victims. I call them victims since I believe the medical community as a whole have abandoned them, both children and adults. Lack of progress in developing both scientific and medical understanding and treatment protocols are what I believe to be the result of medical and psychiatric arrogance
Dr Byron Hyde
Although ME and the outbreaks have been known and described for some time, on the broad landscape of disease ME was a rare infection. After the mass polio vaccination programs by the 1960's, polio vastly diminished and cases of ME seemed to have decreased as well. Yet by the late 70's an increasing incidence of ME had begun. By the early 80's, there were many community clusters and the dramatic worldwide spread of ME was in full swing. For some reason, the rare disease, Myalgic Encephalomyelitis, had exploded into a worldwide epidemic. Many millions worldwide are now disabled by ME.
The very alarming and most disturbing aspect of this disease is that amid this epidemic explosion of disease, the national public health agencies failed to act, and ignored the pleas from doctors in affected communities. In the USA, the Centers of Disease Control and Prevention (CDC) at first ignored the reports, then without any need for evidence immediately declared that there were no outbreaks, then acted to delay any investigation. Subsequently the CDC responded by obscuring the evidence, and confusing the medical community and the public regarding the nature, history and identity of this disease.
This unnatural response became formal policy in 1988 when the CDC controlled panel renamed this disease CFS, over the vehement objections of the experienced medical specialists, who advised that what was being observed was a widespread reemergence of Myalgic Encephalomyelitis. In effect a group of government employees invented Chronic Fatigue Syndrome and disregarded the medical experts. Pursuant to this policy to conceal the identity of ME, medical journals were encouraged to never again publish reports about Myalgic Encephalomyelitis but only articles that discussed fatigue.
Much of this history suggests that the CDC knew something that the medical community did not. Rather than investigating this epidemic, the CDC appears to be acting to cover it up, with a clear disregard for the consequences, the many fatalities and the huge numbers of disabled citizens.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
Infectious diseases often occur in epidemics and the investigation of epidemics has been the most important tool to discover the nature and origins of disease. This most valuable science has not been undertaken regarding the ME outbreaks. In fact the CDC has never investigated an ME epidemic.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
Every person is at risk and the public is entitled to a vigorous program and mobilization of public resources to investigate and proceed to control this epidemic. The public deserves to know the truth.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
ME is best understood in context, with detailed study of the outbreaks. Even though most cases today are considered sporadic, we also must recognize that the outbreaks continue and this report of the recent Arizona epidemic provides a wealth of information and insight.
The Committee takes note that while the CDC takes great pride and stimulates major media attention to their vigorous pursuit of even potentially contagious outbreaks of illness, when it comes to outbreaks of ME they decidedly avoid any investigation. In the Arizona outbreak we see another example of this policy to avoid investigating these outbreaks, just as they had done in the 1980’s at the beginning with the outbreaks in Tahoe and Lyndonville.
The Committee has indications of renewed waves of escalation of ME, particularly in certain regions. We want to hear from you to help collect any reports of recent or new community outbreaks.
The Committee for Justice and Recognition of Myalgic Encephalomyelitis
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."
Jill McLaughlin
A CDC official advised an inquiring ME 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.
Jill McLaughlin
ME 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. [4.5% of M.E. sufferers became ill after a blood transfusion.]
Canadian Expert Consensus Panel Clinical Case Definition for ME/CFS
ME occurs in both epidemic and sporadic forms.
Canadian Expert Consensus Panel Clinical Case Definition for ME/CFS
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.
Dr. P.O. Behan, Prof. Neurology, in: Critical Reviews in Neurobiology, 1988, vol 4
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. [Click on link to see list of epidemics; at bottom of the page]
"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."
Byron M. Hyde, M.D. Presented at 1998 International ME Conference, Sydney
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.
Byron M. Hyde, M.D
[The] prodromal phase [of M.E.] 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 is found regularly in both epidemic and sporadic cases.
Byron M. Hyde, M.D
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.
Byron M. Hyde, M.D
Documented deaths have occurred in several M.E. epidemics, but are best documented in the Cumberland epidemic and were well known in the Akureyri epidemic. All of these deaths involved CNS injury.
Byron M. Hyde, M.D
This M.E. definition is important in that unlike the CDC definitions of Chronic Fatigue Syndrome, the Wallace and Ramsay definitions of M.E. observes the importance the initial acute variable infectious type illness associated with subnormal temperatures. They then note the important secondary and resulting chronic illness characterized by CNS and the autonomic nervous system features and intellectual and muscle dysfunctions and their chronic persistence.
Byron M. Hyde, M.D
Definitions are not diseases, they are often simply the best descriptions that physicians and researchers can offer, with their always imperfect knowledge, to describe a disease. Good definitions are good because they correspond closely to the disease state being described. 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 ME'. 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 ME today that we did not know in 1984.
Byron M. Hyde, M.D
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?
Paralysis from polio occurred in about 1 percent of those that contracted the polio virus. At the time that polio epidemics were studied many of the herpes viruses had not been discovered, were they there then contributing to these plagues. Do certain herpes viruses have a special relationship with the polio viruses in the same way HIV and HHV6 work together.
We may never know if the government continues to cover up the existence of ME by calling it fatigue and confusing the public and doctors and fostering mythical subgroups. Confusing the understanding of this disease by opening the door for the inclusion of a multitude of unexplained fatigue conditions and somatic syndromes that will choke off the support and investigation of Myalgic Encephalomyelitis.
Much reported controversy surrounds the public health agencies and their handling of investigation into the disease Myalgic Encephalomyelitis. Surely the most advanced nations with legions of medical scientists would be motivated to meet the challenge and discover the cause of an epidemic striking down its citizens, which leaves large numbers permanently disabled. Yet the response of the public health agencies has caused particular skepticism. This has raised many questions.
Now this question may sound very odd, but consider: How would you Disguise a Disease ? I doubt there could be too many ways . . . But if that were your intent, Let's see, where would you start –
Camouflage! First declare it is a New illness. (Brilliant!) Declare that there is no epidemic! (Tremendous) Spread the word it is not serious. (Spectacular!!!) Create a smokescreen by using a vague definition so that you can mix in many non-cases, and thus claim it is very hard to identify; then
Cover your tracks! Give the Disguised Disease a variety of New names. (Yes, a trivial absurd name, splendid!) Disassociate it from its previous established name, research, case studies, descriptions and diagnostic ICD classification. (Fantastic) Lets see what else could we do to disguise a disease
Create Confusion! We could tell Drs that this disease is "mysterious" and that there is no need to investigate, "Don't do any testing" (you won't find anything) Its a Mystery.
What else... Oh, yeah, Confuse some more, Rewrite the definition every few years. While expanding the inclusion of non-cases and making the whole field more frustrated.
My god, that should be enough? Wait, also we could use the stall tactic. You know, wait several months before allowing Drs to even consider the vague criteria, surely by that time there won't be much of the originating virus left to find. Once the acute phase and fevers are gone, so will most of the evidence.
Sophisticated Investigation, or How to Disguise a Disease Cesar Quintero
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.
Erich D. Ryll, M.D.
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.
I was appointed chairman of a committee to investigate the outbreak. Fearing that some people might die, I asked that the CDC (Communicable Disease Center of Atlanta, Georgia) to become involved. An epidemic intelligence officer of the CDC spent one week in residence, and an epidemiologist from the California State Department of Health, Berkeley, came for a day.
Cultures were obtained for all known viruses, bacteria, mycoplasma, and rickettsiae, and all were found to be negative. The disease was apparently due to an unknown agent, presumably a virus.
Erich D. Ryll, M.D.
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 were always in association with a polio outbreak. And that those who came down with ME 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.
Erich D. Ryll, M.D.
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.
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.
Multiple Family Member Illness: There is a patient folklore that there are a large number of nuclear families with multiple individuals ill with M.E. However, it is my opinion that the finding of twins and a mother in the same family with a history of M.E. is unusual. In an unpublished epidemiological study of 1,826 M.E. patients who had contacted our office, less than 5 % had unconfirmed multiple family members ill with M.E. in the same household. The real figures are probably lower since many of these multiple cases were not subject to verification. This type of frequency would correspond quite closely to historical records of multiple poliomyelitis illness in the same family.
You can then compare this bar graph to the number of poliomyelitis cases per family and observe their similarity. This is yet another suggestion of a possible enterovirus association to M.E.
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.
WHAT IS ME?
a. ONSET: It is a syndrome (a group of linked symptoms) initiated by one or more of a related group of enteroviruses which circulate annually in the community in summer and autumn in temperate climates, but all the year round in tropical areas.
b MINOR ILLNESS: The majority of encounters with these viruses are asymptomatic but some subjects, more commonly teenagers and adults, suffer a seemingly trivial minor illness, usually described as a non specific summer 'flu accompanied by gastrointestinal upset, sore throat and occasionally by generalised glandular enlargement.
c. SECONDARY PHASE: The minor illness is self-limiting in 90% of adults. However, some 5-10% of all age groups exposed, may progress to a more significant episode ~ severe headaches and vertigo, a stiff neck and back and generalised muscle pain, signifying that the central nervous system has now become involved with a possible progression to viral meningitis and encephalitis(3). Clinical recovery at this stage is normally possible, but does not preclude further effects of the illness in later years. It has to be remembered that ME is a life-long disability where relapse is always possible.
d. FINAL STAGE(1,2) After a variable interval, a multi-system syndrome may develop, involving permanent damage to skeletal or cardiac muscle and to other "end organs" such as the liver, pancreas, endocrine glands and lymphoid tissues, signifying the further development of a lengthy chronic, mainly neurological condition with evidence of metabolic dysfunction in the brain stem. Yet, stabilisation, albeit at a low level, can still be achieved by appropriate management and support. The death rate of 10% occurs almost entirely from end-organ damage within this group (mainly from cardiac or pancreatic failure). It has to be said that suicide in younger patients and in earlier stages of the disability is related to the current climate of disbelief, rejection of welfare support and loss of educational and employment prospects. It is an additional and potentially avoidable factor.
WHAT IS THE EVIDENCE THAT THE LATE EFFECTS OF ME AND THE POST-POLIO SYNDROME CAN BE CAUSED BY ENTEROVIRUSES OTHER THAN POLIO VIRUSES 1-3?
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.
There has been little government interest or support for patients suffering from the late effects of ME or from the post-polio syndrome. It is generally expected that survivors of polio will gradually disappear because of successful immunisation or the UK population 40 years ago. However the fact that "Post-polio", by any other name, can arise from currently circulating enteroviruses has not been taken into account. The Chief Medical Officer's Working Party on ME (set up in 1999 and funded privately by the Linbury Trust) has made it clear that its remit is only with management, and that all discussion about the cause, epidemiology and social benefit requirements of these patients is ruled out. It seems that it will be difficult to advise on rational management in the absence of such vital information.
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.
A. Melvin Ramsay M.A. M.D.
‘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.’
Dr Byron Hyde MD
Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. The CDC definition is not a disease process. It is (a) a partial mix of infectious mononucleosis /glandular fever, (b) a mix of some of the least important aspects of M.E. and (c) what amounts to a possibly unintended psychiatric slant to an epidemic and endemic disease process of major importance.
Dr Byron Hyde
M.E. is not caused by the HHV6 virus: 'This virus was not associated with ME 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.'
Dr Byron Hyde
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.'
Dr Byron Hyde
'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.'
Dr Byron Hyde