1949-53 Adelaide outbreak

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From 1949 to 1953 in Adelaide, Australia, there was an outbreak of a disease resembling poliomyelitis, during and after a poliomyelitis epidemic. In August of 1949, cases of myalgic encephalomyelitis began to appear and continued to be seen until 1951, by which time 800 patients had been admitted to Northfield Infectious Diseases Hospital.

Patients had slight, diffuse muscle weakness mainly affecting the legs. In some, weakness appeared for the first time up to three months after the onset of the initial symptoms.[1] Dr. R.A. Pellew, of Adelaide, believed that most of the 3,130 polio cases during this period suffered from a mild form of polio (i.e., abortive poliomyelitis, atypical poliomyelitis).[2]

Onset[edit | edit source]

Onset was either gradual or sudden, often in the form of an upper respiratory tract infection and/or gastrointestinal distress with low-grade fever. Sudden onset was often accompanied by severe headache.[3] Pellew describes the initial symptoms as indistinguishable from poliomyelitis: "bursting headache, stiff back, stiff neck, aching limbs, pain behind the eyes, upper respiratory tract infection, mild muscle weakness, and a fever followed by lysis over a period of three days."[4]

Also noted was a rise in temperature between the seventh and tenth days, with a recurrence of symptoms.[4]

Symptoms[edit | edit source]

  • headache
  • muscle weakness
  • cognitive dysfunction (lack of concentration, depression, irritability, emotional instability)[4]
  • sound sensitivity
  • pain behind the eyes[3]
  • hyperaesthesia

"Muscle weakness - generally slight and diffuse in distribution - occurred more commonly in the legs than in the arms. Where paralysis was severe, rapid recovery generally ensued. Two noteworthy features of the muscle involvement in this disease were as follows: the pain frequently persisted in various muscles for periods up to six months after the acute illness; in some cases the onset of muscle weakness was delayed for several months.[5]

Findings[edit | edit source]

As with other epidemics, no virus was isolated and there was an absence of abnormal findings in cerebrospinal fluid[3] However, there were some interesting finding in animal studies.

Pellew collected throat washings, feces, and cerebrospinal fluid from a subset of patients and inoculated rhesus monkeys, mice, and hen eggs. Several monkeys displayed sluggishness and subnormal body temperature. One died. On autopsy, two monkeys showed red spots along the sciatic nerves and microscopic damage:

"There were lesions in the nerve roots and in the sciatic nerves. In the nerve roots close to their point of exit from the spinal canal there was pronounced infiltration with lymphocytes and mononuclear cells, and in a percentage of the nerve fibres were found vacuoles in the myelin sheaths and axon swellings. In the sciatic nerves there were small localized infiltrations with inflammatory cells associated with exudation of a few red blood corpuscles. The only abnormality in the skeletal muscle was the presence of sarcoporidiosis in all sections from one animal; but examination of the heart muscle of the monkey which had died showed severe myocarditis with widespread infiltration mainly with lymphocytes and mononuclear cells."[4]

Epidemiology[edit | edit source]

The male : female ratio was 1: 1.[1]

Age distribution in the Adelaide outbreak[3]
Age set Percentage
< 5 15%
5-9 20%
10-15 10%
15-20 10%
20-25 10%
25-30 10%
30-65 25%
> 65 none

During the Adelaide outbreak of atypical polio, while the number of reported polio cases increased in New South Wales and Queensland, and remained constant in the rest of Australia, there was a 43% reduction in typical polio cases in South Australia (where Adelaide is located).[6] This may have been indirect evidence of cross-immunity, that is, partial immunity to poliovirus acquired via exposure to a related enterovirus.

A similar phenomenon was observed in Iceland, when children from an area that had recently had an outbreak of epidemic myalgic encephalomyelitis had a stronger response to poliovirus vaccination, with higher antibody titers.[1][7] Conversely, in a study of children exposed to live and inactive poliovirus vaccines in Estonia and Finland,[8] where those who had been exposed to the live polio vaccine had a stronger antibody response to Coxsackievirus B4.

Prognosis[edit | edit source]

Pellew followed up with five cases, three years after onset.

See also[edit | edit source]

Learn more[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 Parish, JG (1978). "Early outbreaks of 'epidemic neuromyasthenia'". Postgraduate Medical Journal. 54: 711–7.
  2. "Conference on Polio" "The Advertiser, Adelaide Australia, 01 February 1952
  3. 3.0 3.1 3.2 3.3 Dr R.A. Pellew, "A Clinical Description of a Disease resembling Poliomyelitis, seen in Adelaide, 1949-1951" Medical Journal of Australia, Medical Journal of Australia 1951, June 30 Vol. 1 No. 26 pp. 944-6
  4. 4.0 4.1 4.2 4.3 Pellew, R.A.A. (September 24, 1955). "Further Investigations on a Disease Resembling Poliomyelitis Seen in Adelaide". The Medical Journal of Australia. 2: 480–2.
  5. Dr R.A. Pellew, "A Clinical Description of a Disease resembling Poliomyelitis, seen in Adelaide, 1949-1951" Medical Journal of Australia, Medical Journal of Australia 1951, June 30 Vol. 1 No. 26 pp. 944-6
  6. "Poliomyelitis in 1953" Bulletin of the World Health Organization. 1955;12(4):595-649.
  7. Sigurdsson, B (February 15, 1958). "Response to poliomyelitis vaccination". The Lancet. 1: 370–1.
  8. Juhela, S (July 1999). "Comparison of enterovirus-specific cellular immunity in two populations of young children vaccinated with inactivated or live poliovirus vaccines". Clinical & Experimental Immunology. 117: 100–105.