1948-49 Akureyri outbreak

The Akureyri outbreak was an outbreak of myalgic encephalomyelitis in Northern Iceland during the winter of 1948-1949. It lasted for three months and a total of 488 cases were reported in Akureyri, and a total of 1,090 across Iceland. The outbreak may have been related to the earlier 1946-47 Iceland outbreak. It was after this outbreak that the term Icelandic disease, an early name for myalgic encephalomyelitis, was coined.

Onset
Initial symptoms involved pain the neck and back accompanied by a rise in temperature. The estimated period of incubation was five to eight days.

Symptoms
The systemic form of the illness was present in 70% of patients with the characteristic low fever, muscle tenderness and marked lassitude. 30% had muscle weakness. Infectious disease testing failed to find evidence of poliovirus, Coxsackie or other known encephalitis viruses.

Epidemiology
In town, the incidence was 6.7%. In rural areas, it was 0.8%. While the incidence among adults was significantly higher for females, there was no significant difference in incidence between sexes among those under twenty.

Rates of infection were highest among those 15-19 years of age. Multiple cases were often found in the same household and schools, with the exception of the elementary school, were heavily struck.

No toxic, food, or waterborne agent was found. The dairy in Akureyri pasteurised the milk and did not appear to have spread the illness to other communities served by it. When infections spread beyond Akureyri, the first cases appeared along the main land transportation route from Akureyri to Reykjavik, suggesting person-to-person transmission. Ultimately, 1,090 cases were reported, with the majority (70%) coming from three districts: Akureyri, Saudarkrokur and Isafjordur.

Course & prognosis
In 1955, neurologist Kjartan Gudmundsson reexamined 39 patients affected by the outbreak. He found that 31% were free from objective clinical signs and only 13% considered themselves completely recovered.

Of the most severely affected, only 25% had completely recovered, 52% had residual muscle tenderness, and 65% had objective neurological signs. Many patients still complained of nervousness, abnormal fatiguability of muscles, muscle pain, sleeplessness and loss of memory. Of those mildly affected in 1948 only 44% had fully recovered, 50% had muscular tenderness, and 19% had residual objective neurological signs. There were no deaths.

In 1988, Byron Hyde published a long term follow-up in the Lancet, 40 years after the initial outbreak. He managed to examine 10 patients, of which only 2 reported a full recovery.

Polio vaccine
In a study of children in Iceland vaccinated against polio in 1956, Sigurdsson, et. al found significant differences in antibody response to vaccination depending on where the children lived. Children in Egilsstadir had only a slight antibody rise to type 2 and type 3 poliovirus, while children in Thorshofn, which had recently had an outbreak of epidemic myalgic encephalomyelitis, had a much stronger antibody response response to the polio vaccine. Sigurdsson postulated that this might be explained by "the existence of basic immunity acquired through a related infection."

Indirect evidence of cross-immunity was also seen in the outbreak in Adelaide, Australia, where there was a 43% reduction in polio cases following an ME outbreak. Conversely, in a study of children exposed to live and inactive poliovirus vaccines in Estonia and Finland, where those who has been exposed to the live polio vaccine had a stronger antibody response to Coxsackievirus B4.