Where did it all begin? Current research traces the likely locus of the outbreak to Haskell county, Kans., near Camp Funston (later, Fort Riley). A review of news sources from January--February 1918 reveals reports of an unusually virulent flu in the county at this time. It is generally believed that the outbreak jumped from the local population to the troops mobilizing at Camp Funston. These soldiers were in turn sent to Europe through the French port of Brest, which was the locus of the outbreak in Europe. Spreading rapidly through the European population, the disease then moved on to Asia and the rest of the world. Spain was particularly hard hit, as is evidenced by the many news reports that referred to the disease as the "Spanish Flu."
A second outbreak of the disease occurred in the latter part of 1918, when American troops returned home through the port of Boston on their way to Fort Devens. At the height of this outbreak, a doctor based at Fort Devens corresponding with a colleague reported that he was recording 100 deaths per day. He noted that the soldiers would "rapidly develop the most viscous type of pneumonia that has ever been seen" and die shortly thereafter. In fact it was the pneumonia that was the actual cause of death. At that time little was known about the infectious agents that cause disease; therefore, doctors had almost no tools to use in fighting the pneumonia. Remedies such as the administration of quinine and hot mineral baths had little effect. In affected areas worldwide, business activity was severely restricted and social gatherings were brought to a halt. People avoided interpersonal contact and began to wear gauze masks.
In an effort to explain why the 1918 flu was so devastating, researchers have conducted tests on tissue samples preserved from victims of the pandemic. The particular virus responsible for the 1918 disease is thought to be of a type originating in birds, an avian flu similar in some ways to the avian flu strains discussed in the news in recent years. Researchers theorize that the virus probably jumped from birds to swine or horses and then passed to humans. Tissue samples reveal that the 1918 influenza contained surface proteins uncommon to human flu strains, both then and now. Because these proteins were foreign to the human immune system, almost none of the human population of 1918 would have had any immune system resistance to the disease, thus accounting for its rapid and universal spread.
Although we now have more tools to treat influenza and even some antiviral medications to treat the cause, we are still at risk. Recent experience with avian flu and severe acute respiratory syndrome (SARS) suggests that humankind is still vulnerable to opportunistic viruses. Indeed, with international travel more rapid and more common than it was at the beginning of the 20th century, we may, in fact, be at greater risk now than we were in 1918.
