The 1918 Spanish Flu: a grim reminder
“Those who cannot remember the past are condemned to repeat it.” — George Santayana
“In the end, almost no place was spared. When the Spanish influenza virus circled the world in 1918, 1919 and 1920, it missed the Pribilof and St. Lawrence islands in the Bering Sea. Quarantines successfully protected the northern coast of Iceland and American Samoa. Otherwise, nearly every place that man occupied, the virus visited.
Few people alive today remember the Spanish flu firsthand. But the global epidemic lives vividly in the collective memory of medicine and public health. It’s the distant mirror in which today’s epidemic of severe acute respiratory syndrome, or SARS, is reflected.
SARS is caused by a virus, as was Spanish f lu. Both are respiratory illnesses. Both are spread by coughing and close, but casual, contact. Both appear to have arisen from animal viruses that through mutation or genetic reassortment gained the ability to infect human beings.
There are, of course, innumerable differences as well. SARS is deadlier, killing 10 to 15 percent of people who become ill. The Spanish flu exacted a highly uneven toll on different countries and ethnic groups.
In the United States and few other developed countries with good epidemiological records, the mortality rate was about 3 percent of people who became ill. Among poor populations, it appears the death rate may have been as much as 10 times higher.
What the Spanish flu had was extreme contagiousness and a global population almost entirely susceptible to it.
What kind of devastation the SARS virus’s (sic) particular combination of virulence and infectivity might ultimately produce is anyone’s guess. The worst- case scenario, though, is not theoretical. After the Spanish flu ran its course, it had killed at least 50 million people, according to the most recent calculations.
SARS has not yet gone global in an epidemiological sense. Even though 29 countries have reported infections, only in China and Taiwan is it spreading in the general population. Elsewhere, nearly all cases are directly traceable to people who picked up the virus in the disease’s Asian incubator, or had contact with people who did.
The fear, of course, is that SARS will eventually spread stranger to stranger, reaching so many places so quickly that public health officials will be powerless to contain it.
An epidemic’s portrait is painted by both the microbe and host. The Spanish flu’s was painted not only by the peculiar, and still largely mysterious, characteristics of the 1918 virus, but also by the exigencies of war, colonialism and ocean travel.
Some experts today believe the virus came from China — the birthplace of many flu strains. Its first true victim has been lost to history. What is known is that on March 5, 1918, soldiers in Camp Funston, in Kansas, began coming down with inf luenza in large numbers.
Military posts have always been fertile ground for outbreaks of contagious disease. Barracks bring people from many regions into close quarters under high stress. So it wasn’t a surprise that ground zero of the pandemic was a military installation, or that the disease was next reported, on March 18, at Army camps in Georgia. The symptoms were mild, with few deaths. But the numbers of ill were high — 2,900 cases out of 28,586 troops at the Georgia camps.
The epidemic then hopscotched from one military post to another in the East and South, spilled into the civilian population, and reached the West Coast in late April, where an outbreak was recorded at San Quentin Prison.
By then, however, it had already made a bigger and more fateful leap, across the Atlantic Ocean with hundreds of thousands of soldiers going to join the Great War.
Influenza tends to be seasonal, as the virus survives longest in cool, dry air and is most easily spread when people are crowded together — all conditions favored by winter. It was unusual for the first wave of the 1918 pandemic to last as long as it did, and not surprising when things slowed down in August.
Then something happened.
Microbes often adapt and change behavior while epidemics are underway. When slightly different strains are passing from person to person, a strain that kills its victims quickly, before they have time to infect others, may tend to disappear and be replaced by a strain that keeps its victims alive — and transmitting disease — for a longer time.
Stanley Lane, who’d given a false birth date on his enlistment papers, was five days shy of his 17th birthday when influenza struck Camp Mcclellan in Alabama on Sept. 26.
“All I remember about it was I got a little temperature and I went on sick call and the doctor said, ‘Go to the hospital, you got the flu,’” he recalled recently at his home in Silver Springs, Md.
“When I walked in there the nurse says, ‘That’s your bed over there.’ So I went over and sat down. And the greetings I got was from all these other GIS around there telling me: ‘Hey, the guy who just left that bed died,’” Lane, now 101, said with a slight chuckle. “It didn’t bother me. I went to bed.”
He doesn’t recall his illness as being especially severe. In any case, he recovered and went on to spend 32 years in the Army, retiring as a lieutenant colonel. The Spanish flu had an unusual and unexplained predilection for young adults, whom it killed in greater numbers than either children or the elderly. Many of Lane’s fellow soldiers weren’t as lucky as he. About 20,000 died in nine weeks in the United States that fall.
Around the world, wide and cruel variations in mortality were the rule.
As with SARS today, quarantine was the main tool against Spanish flu. A third and fourth wave of Spanish flu began in January 1919, and struck again in 1920.
At some point, on a day as lost to history as the one of its emergence, Spanish flu made a final human being ill and then disappeared.”
“When I walked in there the nurse says, ‘That’s your bed over there.’ So I went over and sat down. And the greetings I got was from all these other GIS around there telling me: ‘Hey, the guy who just left that bed died.’ It didn’t bother me. I went to bed.”
— Stanley Lane