I can't listen to or download the broadcast, too bad there is no transcript. Ortleb seems to be a bit fringe in his theories.
On ME as infectious I would have thought we were well past that with over 80 outbreaks and both horizontal and vertical transmission shown. Healthy patient cells put in ME patient sera become 'sick.'
I had posted many times in the past about both the Tahoe outbreak as well as the 1934 outbreak in five California counties of 'atypical polio.' Tahoe also went on in a series of outbreaks to neighboring communities and down into California in the Bay area over several years.
Each outbreak I think has its own view, Hyde, Bell, Cheney and Peterson will have their own and from each of their outbreak experiences. Ramsey is very significant as the benchmark for when the first definition, diagnostic, and name was given to what was seen at the Royal Free Hospital.
I do think that epidemiology to track back in time, either by 'cellular clock' or 'patient zero' is important, there was a good program which reviewed that for HIV/AIDS (Radiolab). There has been no such epidemiology effort for ME.
It was my experience in reviewing family history that lead me to see that my great grandfather had died in an infectious disease ward in 1934, and my grandfather ill with what was labeled then as 'atypical polio' to find out the other historical events of that time.
I found that five counties in California had an epidemic of that 'atypical polio.' This only two years after a serious outbreak in 1932 of polio that scared the public and put public officials in a panic.
In 1934 medical officials from the Rockefeller Foundation and Yale Medical came to the largest hospital in the world at the time, the Los Angeles County General Hospital. They were greeted with fanfare and were there to run experiments using monkeys to isolate the polio virus and find an effective vaccine.
Meanwhile Dr Brody who had also been funded by the Rockefeller Foundation had the first trial polio vaccine and was crossing the country giving it to thousands of test subjects, often children. He would arrive in California and many lined up to get the vaccine.
What is known is documented by the United States Health Agencies sending out an investigator, his report (Gilliam) was delayed for two years until it was agreed to leave out references to the vaccines. Dr. Hyde decades later also interviewed two of the surviving doctors and some family members of the outbreak victims.
What made the investigation crucial was likely the fact that 198 staff of the Los Angeles County General Hospital became ill and then disabled by the 'atypical polio' illness. They had documented their illness and would win a closed settlement of $6M that would be over $200M currently, 'enough to afford each of them three new homes in a nice Los Angeles suburb' - way more than $200M today.
While the team from Yale had used monkeys, Brody has passaged the virus through the brains of mice 100 times. With what is known today this xenotransplantation of human tissue into animals and back to humans carries risks. The Rockefeller Foundation had an extraordinary withdrawal of $7M at the time of the LACGH staff settlement.
Dr. Paul Offit a modern proponent of vaccination and patent holder would write a paper saying that this history jeopardized the entire future of vaccination. While the risk / benefit of vaccines both in particular and in general remains debated, there was no debate that the early Brody polio vaccine was a disaster, multiple deaths of children in the trial occurred and another polio vaccine trial would not occur for two decades.
From a family history, my great grandfather was a public official in the San Francisco bay area, my grandfather worked in the same office and would be elected to replace him after his death. Later my grandfather was diagnosed with 'post polio syndrome' while never truly having polio, but the odd 'atypical' version.
In retirement he would move in the late 1970s to a small community called Incline Village in Nevada and build a house five blocks from the lake at Lake Tahoe. The local Internist offices of Dr's Peterson and Cheney not more than a mile away would become his medical home. It would be here that visiting my grandparents with my father, both he and I would become ill for months, and my mother later would become ill having tended for us.
My aunt and cousins lived in Tahoe around this time as well and would go on to have classic mysterious neuro immune health issues.
The debate should not be whether ME is an infectious disease, but the origin and nature of the pathogen, an epidemiological analysis would lead one back to the first outbreak, and the first trial of Brody's live attenuated polio vaccine passaged through the brains of mice and injected into thousands of subjects, including LACGH staff, leading to a very large sealed settlement.
Recent publications:
Does the microbiome and virome contribute to myalgic encephalomyelitis/chronic fatigue syndrome?
http://www.clinsci.org/content/132/5/523
" Important clues for the involvement of (viral) infections in the aetiology of ME/CFS can be obtained from historical reports of epidemic or sporadic outbreaks of cases; the first of which was reported in 1934 in a suspected epidemic of poliomyelitis in Los Angeles, California [75,76]. The inconsistent disease pattern observed in patients led doctors to classify this epidemic as atypical; differing from polio cases endemic at the time by the lack of flaccid paralysis, which normally defines poliomyelitis [77]. Additionally, the affected cases were mainly older children and young adults compared with polio which affected infants and children of less than 5 years of age [78]. The disease at the onset consisted of an acute upper respiratory tract infection accompanied by muscle weakness, fever, pain, malaise and photophobia. The patients reported recurrence of fever and other symptoms during recovery, which were at a greater incidence than those in typical epidemic poliomyelitis [76].
A similar apparent epidemic of poliomyelitis appeared in Akureyri, Iceland between 1948 and 1949. There were striking similarities between this outbreak of atypical poliomyelitis and the one recorded in Los Angeles in 1934, including both overlapping symptoms and occurrence of relapse. This disease was named Iceland (or Akureyri) disease [79]. Sixty-one other outbreaks of a similar disease were reported worldwide between 1934 and 1990 [75]. The most significant outbreak was in 1955 at the Royal Free Hospital in London, where 292 hospital staff were affected by the illness. The disease when fully developed showed features of a generalized infection with involvement of the lymphoreticular system, and widespread involvement of the central nervous system. The mysterious polio-like illness (including the disease at the Royal Free Hospital) was renamed ME and later extended to CFS (ME/CFS) to include a seemingly identical disease [80,81]. "
Myalgic encephalomyelitis, chronic fatigue syndrome: An infectious disease
http://www.clinsci.org/content/ppclinsci/132/5/523.full.pdf
www.medical-hypotheses.com/article/S0306-9877(15)00382-5/fulltext
"
Occurrence of cluster outbreaks
ME/CFS is globally endemic as sporadic cases and occasional cluster outbreaks. The names, myalgic encephalomyelitis and chronic fatigue syndrome were coined to describe two outbreaks of an infectious disease in London, UK in 1955 [37] and a clinically similar disease in Nevada, USA in 1984 [6]. Sixty-one other outbreaks of a similar disease were reported worldwide between 1934 and 1990 [10]. Different names were given to these outbreaks: e.g., epidemic diagnosed as poliomyelitis, Los Angeles, USA, (1934); Iceland disease, Iceland, (1948); Royal Free disease, London, UK, (1955), (later named benign myalgic encephalomyelitis); epidemic neuromyasthenia, Florida, USA, (1957); Tapanui flu, New Zealand, (1983); chronic Epstein Barr virus syndrome (later named chronic fatigue syndrome), Nevada, USA, (1984); Lyndonville outbreak, NY, USA, (1985) [10]. A further outbreak occurred in Bergen, Norway, (2004) in 5% of patients who had previously been infected in an epidemic of Giardia enteritis [38]. Most physicians only see patients with sporadic ME/CFS, and most research studies have only included patients with sporadic ME/CFS and the occurrence of outbreaks of ME/CFS has often been forgotten or ignored. The occurrence of cluster outbreaks implies an infectious disease and outbreaks may occur when the virulence of the pathogen is increased or population (herd) immunity is decreased. "
" Pathogens are more likely to be found when actively replicating. This usually occurs early in the disease, in a relapse and possibly in extremely debilitated patients. The presence of confounding, secondary,
opportunistic or reactivated latent infections are less likely early in the disease. Early diagnosis is possible only in patients in cluster outbreaks. Cluster outbreaks can be identified by the occurrence of more than the expected number of patients with similar symptoms and signs in a geographic area, during a limited time period. Physicians and public health authorities need to be educated about the characteristics of cluster outbreaks and encouraged to report suspected outbreaks to appropriate public health agencies. A new case definition for cluster outbreak patients should be created [110], as the various case definitions for sporadic ME/CFS patients are not useful. Patients may be very ill and it may not be possible e.g., to determine post-exertional symptoms. The requirement for symptoms to be present for six months is
inappropriate.
The search for a pathogen might also include healthy patient contacts who have immune system changes similar to those found in patients with ME/CFS. These healthy patient-contacts may also carry the causal pathogen and may be less likely to harbor confounding secondary infections and activated latent viruses. They could also be studied to determine which immune system responses are correlated with symptoms and which are not.
Conclusions
Substantial epidemiological, clinical and immunological evidence supports the hypothesis that ME/CFS is an infectious disease. ME/CFS is globally endemic, with occasional cluster outbreaks, implying an infectious agent. The clinical illness starts abruptly with a viral-like syndrome in outbreak patients and many sporadic patients and this onset is followed by symptoms characteristic of ME/CFS. Immune system changes in sporadic ME/CFS resemble the changes found in other infectious diseases. Evidence of contagion is shown by secondary cases in outbreaks and suggested by the higher prevalence of ME/CFS in patients’ genetically unrelated family members than in the community. The chronic phase of the
disease does not appear to be particularly infective. Healthy patient-contacts and healthy people from the community surrounding an outbreak showed immune system changes similar to those found in patients, suggesting exposure to the same antigen (a pathogen). The causal pathogen appears to be transmitted by
casual contact. The chronicity of symptoms and immune responses suggest that the pathogen persists in patients. An apparent population of healthy carriers may be able to shed the pathogen. Only a minority of close patient-contacts develop the illness. Factors found to increase host susceptibility include: being a family member of a patient; age; female gender; race; rest/exercise; exposure to stress or toxins; recent previous illnesses; and occupational exposure of healthcare professionals. Confirmation of the hypothesis
requires identification of the causal pathogen. Future research should include a search for known and unknown pathogens. "
