Epidemic myalgic encephalomyelitis

There have been at least 75 documented outbreaks of ME and CFS since the 1930s. The true number of clusters and outbreaks is likely vastly higher. Many of these outbreaks occurred in institutions like hospitals and schools, and frequently coincided with outbreaks of poliomyelitis.

The first recorded outbreak of epidemic was in 1934 in Los Angeles and the most recent was putative outbreak was in Arizona in 1996.

History
The first recorded outbreak of epidemic myalgic encephalomyelitis was in 1934 in Los Angeles and was thought to be an outbreak of atypical polio. After the outbreak in Akureyri, Iceland in 1946, the disease came to be called "Akureyri Disease" or Icelandic disease through much of the 1940s and 1950s. It was named myalgic encephalomyelitis after London's Royal Free Hospital outbreak in 1955. Other names included benign myalgic encephalomyelitis and epidemic neuromyasthenia.

After the Incline Village outbreak in Nevada in 1984, the disease came to be called and redefined as Chronic Fatigue Syndrome. The most recent was putative outbreak was in Arizona in 1996.

Symptoms
Reported symptoms could vary considerably from outbreak to outbreak. Common symptoms included:


 * low-grade fever
 * post-exertional malaise ("fatigue on walking short distances and on the least exertion was prominent" )
 * muscle fatigability
 * muscle weakness
 * myalgia and neuralgia
 * tender lymph nodes, spleen and/or liver
 * cognitive symptoms including impaired memory and concentration
 * sleep disturbances
 * sensory symptoms including sensitivity to light and sound, paraesthesiae, hyperaesthesiae
 * autonomic symptoms such as tachychardia, coldness of the extremities, sweating

Findings
Findings varied considerably based on the technology of the time and what tests physicians attending to these outbreaks chose or were able to run:


 * Abnormal electromyogram showing generalized, mild, lower motor neuron changes indicative of a radiculopathy
 * Normal or minimal cerebrospinal fluid findings
 * Autonomic nervous system dysfunction, hypothalamic dysfunction
 * Orthostatic tachycardia
 * Ulnar neuritis or lesion (Iceland, NY State, north of England)
 * Microscopic infiltration of nerve roots with lymphocytes and mononuclear cells; patchy damage to the myelin sheaths and axon swellings (in monkeys infected with unidentified virus from the Adelaide outbreak)
 * Raised urinary creatine excretion (add: NY State 1950)



Epidemiology
Many of these outbreaks occurred at institutions for example, hospitals, schools, army bases or convents. The pattern of spread suggested a highly infectious agent that spread person to person, rather than through contaminated food or drink.

In some outbreaks, women were disproportionately affected. In others, the gender ratio was 1:1. In hospital epidemics, young female nurses were disproportionately affected, but this may have been due to risk factors like higher repeated exposure to the same infection during an epidemic and in some outbreaks, gender-segregated living quarters.

Those most affected tended to be adults in their twenties.

Prognosis
Although many patients improved over time, in follow-up studies, a large percentage were still ill months to years later. Many case studies note long periods of convalescence with relapses following exertion or before or during menstrual periods.

Relationship to polio
Prior to the poliovirus vaccine, several outbreaks of what later came to be called myalgic encephalomyelitis coincided with confirmed outbreaks of poliomyelitis including the 1934 Los Angeles outbreak, the 1948 Akureyri, Iceland outbreak, and 1949 outbreak in Adelaide, Australia. Many outbreaks were initially misinterpreted as clusters of poliomyelitis or abortive poliomyelitis, hence one of ME's earliest names, atypical polio. It is not known whether there is a direct relationship between polio outbreaks and ME or if outbreaks of ME were more likely to be reported when public health authorities were already mobilized for an earlier crisis.

No serological evidence of polio was ever found in these outbreaks and the ultimate pattern of the outbreaks differed in significant ways, chief among them, the tendency to affect adults rather than children, and to result in higher morbidity than poliomyelitis but no mortality. Findings in several outbreaks seemed to suggest that symptoms were caused by an enterovirus distinct from but related to polio including findings of mild, diffuse peripheral nervous system damage in monkeys infected with the virus; a stronger response to polio vaccination in children who had been in epidemic areas; and seasonal patterns of infection resembling polio.

After the Akureyri outbreak, children in areas that had been affected responded to poliomyelitis vaccination with higher antibody titres, as if these children had already been exposed to an agent immunologically similar to poliomyelitis virus.

Controversy
In 1970, a paper by Colin P. McEvedy and AW Beard claimed that the 1955 Royal Free Hospital outbreak was actually mass hysteria.

Learn more

 * "In the Bughouse," The New Yorker by Berton Roueché.
 * Osler's Web by Hillary Johnson