1949-53 Adelaide outbreak

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 has 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. 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).

Onset
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.

Symptoms

 * headache
 * muscle weakness
 * cognitive dysfunction (lack of concentration, depression, irritability, emotional instability)
 * sound sensitivity
 * pain behind the eyes
 * 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.

Findings

 * Absence of abnormal findings in cerebrospinal fluid

Epidemiology
The male : female ratio was 1: 1. 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). This may have be 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. 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.