Despite the assertions of F. G. Crookshank (1919), Rudolf von Jaksch (1923), and others that 1918 influenza was the principal cause of encephalitis lethargica, leading researchers of the 1920s, such as E. O. Jordan (1927) and A. J. Hall (1924), judged the relationship between influenza and encephalitis to be so inconsistent and confusing that they stated the etiology of encephalitis lethargica to be "unknown." But now, 60 and more years after the pandemic, from research done in Seattle and Samoa by R. T. Ra-venholt and W. H. Foege (1982), the etiology of encephalitis lethargica seems clear. Death records in Seattle show a characteristic modal lag of approximately a year from influenza-pneumonia death peaks to onset of encephalitis lethargica clusters terminating in death (Figure VIII.46.1), providing strong evidence that encephalitis cases previously thought to have occurred independently of influenza were actually late sequelae.

The Samoan Islands were chosen as another site for study because the sharply contrasting experience of Western and American Samoa with respect to the 1918 influenza epidemic provided a unique basis for study of its pathological effects. As stated by Jordan:

In no part of the world did influenza exact a more crushing toll than in the islands of the South Sea. In Western Samoa the steamer Talune from Auckland introduced the disease on November 7,1918, into the islands of Upolu and Savaii. As a result there were nearly 8,000 deaths, the population during the two months ended December 31, 1918, being reduced from 38,178 to 30,636.

Meanwhile, American Samoa, just 70 kilometers away, and inhabited by the same racial stock, managed to exclude the infection with strict quarantine measures and good fortune.

During May 1982, American Samoa records stored in the National Archives and Records, in San Bruno, California, along with death records for American Samoa maintained by the Lyndon B. Johnson Tropical Medicine Center on Tutuila, and death records for Western Samoa available in the Registrar's Office at Apia were analyzed. Although the rudimentary nature of the death records in Western Samoa limited the comparative studies that could be made of mortality patterns in American and Western Samoa during the 1920s, it was clear that whereas Western Samoa suffered heavily from both influenza-pneumonia and encephalitis lethargica during the years 1918-22, American Samoa was remarkably free of both these diseases during those years. The evidence, then, is compelling that the pandemic of influenza beginning in 1918 and the pandemic of encephalitis lethargica generally beginning the following year had a common etiology. Both pandemics were globally distributed and were closely related in time, and only one etiologic agent (swine influenza virus) has been reliably identified.

Local, regional, and national influenza-pneumonia epidemics ordinarily (perhaps invariably) preceded local, regional, and national epidemics of encephalitis lethargica. A large proportion of individual encephalitis lethargica cases during the early years of the pandemic had had clinical influenza. Later, as influenza and encephalitis occurrence patterns shifted from massive epidemic to sporadic endemic, the relationship between these two diseases became progressively obscured.

Seasonal and global occurrence patterns of encephalitis lethargica rule out the possibility that this pandemic was caused by an arbovirus or any known nonrespiratorily spread infection. Moreover, although influenza-pneumonia was highly communicable from person to person, encephalitis lethargica was remarkably noncommunicable from person to person by any known route.

Analogous pandemics of encephalitis have been recorded in close association with other influenza epidemics, although none as severe as that in association with the 1918 influenza pandemic. Guillain-Barr6's disease following inoculation with swine influenza antigen suggests a neurotoxic effect of this organism, even in the killed state. Likewise occurrence of parkinsonism during convalescence from influenza and/or encephalitis and during many years and decades thereafter demonstrates the extraordinary neuropathogenic qualities of the causative agent - now identified as the 1918 (swine) influenza virus.

Swine Influenza

Swine Influenza

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