Out of the Trenches

Boxcars were labeled “8 horses or 40 men.

In 1918, chickens were still pecking around the barnyard. Industrial chicken factories didn’t take off until after the second World War. How then could a pandemic virus of such ferocity have arisen? Nobody knows for certain, but evolutionary theory allows us to speculate. The development of extreme virulence is thought to require an overcrowding of susceptible hosts who cannot escape from one another. Otherwise, the virus needs to restrain itself. If a bird flu virus gets too vicious, if the bird gets too ill too fast, the virus is less likely to infect others…unless the next beak is just inches away. That wasn’t the case in 1918. There were no reports of mass bird die-offs, nor would one expect any since the 1918 virus was H1, and only H5 and H7 viruses are thought capable of mutating into highly pathogenic forms in chickens. In 1918, there were no stress-compromised chickens teeming with virus crammed into enclosed spaces en masse. In 1918, the virus didn’t learn how to kill humans crowded in filthy chicken sheds. Instead, it may have gotten that education in the trenches of World War I. In 1918, the soldiers may have been the chickens.

Military medical historian Carol Byerly argues in her 2005 book Fever of War: The Influenza Epidemic in the U.S. Army During World War I that the 1918 virus built up its virulence in the transport ships, trains, and trenches of the Great War.¹⁶⁰¹ Millions of young men were forced together in close quarters where there was no escaping a sick comrade. Instead of battery cages of egg-laying chickens, battery units of infantry dug themselves into festering trenches. Instead of ammonia to irritate the respiratory tracts of chickens and predispose them to infection, residues of poison gases like chlorine saturated the Western Front.¹⁶⁰² The unspeakable conditions, the theory goes, led to the perfect breeding ground for influenza superstrains: a population of “physically compromised” individuals under intense confinement undergoing mass troop movements, not unlike live animal transports. In both cases, fodder for slaughter.¹⁶⁰³ Boxcars were labeled “8 horses or 40 men.”¹⁶⁰⁴ Evolutionary biologist Paul Ewald agrees that the crowded, stressful, unhygienic WWI conditions could have favored the evolution of a “predator-like virus” that otherwise may have killed too quickly to spread with peak efficiency under normal conditions.¹⁶⁰⁵

If this controversial theory is correct, how might the virus have gotten into the trenches in the first place? There are a number of competing theories as to the true origin of the virus, all of them contentious.¹⁶⁰⁶ University of Hong Kong’s Shortridge thinks it may have originated in Asia, conveyed to the front by Chinese laborers brought in to dig trenches for the Allies.¹⁶⁰⁷ Contemporary accounts have the workers speaking the Cantonese dialect of Guangdong Province (then Canton), the region harboring domesticated ducks for centuries alongside the highest concentration of people, pigs, and poultry in the world.¹⁶⁰⁸ The 1918 U.S. Surgeon General’s report on the Spanish flu indeed alluded to an Asian origin.¹⁶⁰⁹ An avian virus may have smoldered in the Chinese population before serendipitously finding itself in the trenches, like a duck virus in a broiler chicken shed.¹⁶¹⁰

Royal London Hospital’s John Oxford, on the other hand, points to declassified military medical records showing excessive numbers of deaths from respiratory infection in French military camps before the Chinese laborers arrived.¹⁶¹¹ The “heliotrope cyanosis” (bluish-purple skin discoloration) described in these reports does share a resemblance to the millions of cases that were soon to come.¹⁶¹² He suggests that the virus arose in the battlefield.

“Wounded survivors of gas contaminated battlefields gather in the Great City British Army Camp of Etaples in northern France,” Oxford explains, “in close proximity with each other, with geese and poultry markets of the area and even pig farms installed right into the army camp itself.”¹⁶¹³ On any one day, the army base crowded 100,000 soldiers into tents and temporary barracks, a ripe setting for a respiratory virus. Survivors from the trenches crossed paths with more than a million men from England on their way to the Western Front in the Etaples camp alone. Combine the population density with the geese, chickens, and pigs raised for slaughter in the camps, Oxford notes, and “[t]hose conditions mimic what naturally occurs in Asia.”¹⁶¹⁴ In the absence of air travel, the virus may have simmered for months or years in such a camp, relying on the demobilization in the fall of 1918 for rapid global dispersal.¹⁶¹⁵

Others think the pandemic 1918 virus was made in the USA. The American Medical Association sponsored what many consider to be the most comprehensive of several international investigations into the pandemic. Written by the editor of the Journal of Infectious Disease, the AMA report was published in 1927. The intervening years were spent reviewing evidence from around the world. The AMA concluded that the most likely site of origin of the 1918 virus was Haskell County, Kansas.¹⁶¹⁶

The first wave of the pandemic in the spring of 1918 was so mild that it did not merit special mention in the medical journals of the time.¹⁶¹⁷ The virus still had a lot to learn. The AMA was able to track the spread of this mild spring wave from the first recorded case on March 4, 1918,¹⁶¹⁸ at Camp Funston (now Fort Riley) in Kansas. Patient zero was a soldier recorded cleaning pig pens prior to his infection.¹⁶¹⁹ Maybe a Canadian goose flew the virus to Kansas, infecting a pig, who infected a man. We will probably never know. From the Midwest, the flu virus spread along the rail lines from Army camp to Army camp,¹⁶²⁰ then into the cities, and finally traveled with the troops to Europe.¹⁶²¹ The virus found itself not in Kansas anymore.

An equally authoritative multivolume British analysis of the pandemic agreed with the AMA: “The disease was probably carried from the United States to Europe.”¹⁶²² A Nobel Laureate who spent most of his research career studying influenza also concluded that the available evidence was “strongly suggestive” that the virus started in the United States and spread with “the arrival of American troops in France.”¹⁶²³

Over the summer of 1918, the virus mutated into a killer.¹⁶²⁴ Just as low-grade influenza viruses may infect free-range fowl, so too may they infect free-range Frenchmen. The highly unnatural wartime conditions may have allowed the virus to achieve its full lethal potential. The critical component, Ewald argues, “is something that chicken farms have in common with the Western Front: large numbers of hosts packed so closely that even immobilized hosts can transmit the virus to susceptibles.”¹⁶²⁵ Once the ability of the virus to spread no longer depends on the host feeling well enough to move around in order to infect others, there may be little Darwinian limit to how fierce the virus can get.¹⁶²⁶

In the wild, if a bird gets too sick, too fast, the virus isn’t going anywhere. Stick a sick chicken in a broiler shed, though, or a sick soldier in a troop transport, and the uninfected can no longer escape their sick companion. The key to the evolution of virulence may be the packing together of the infected with the uninfected, beak-to-beak or shoulder-to-shoulder.¹⁶²⁷ Ewald is uncompromising on this point:

[W]e will continue to get severe influenza epidemics in chicken farms so long as the conditions in chicken farms, like the conditions at the Western Front, allow transmission from immobile chickens. This prediction has been confirmed by the lethal outbreaks of H5N1 in Asia and H5N2 in Mexico. Anyone who dismisses this analysis as speculation does not understand how the scientific process works or what scientific theory actually is, at least with regard to evolutionary biology.¹⁶²⁸

The author of Fever of War emphasizes the uniqueness of the conditions that led to the pandemic. “The 1918 flu epidemic most likely will not happen again,” she said, “because we won’t construct the Western Front again.”¹⁶²⁹ She fails to take into account that the same stress, filth, and crowding of trench warfare exists in nearly every industrial egg farm and chicken facility the world over. Even Ewald, though convinced that the overcrowding of intensive poultry production made H5N1 into the killer it is today,¹⁶³⁰ seemingly fails to recognize the newfound genetic similarities between chickens and humans that make viral evolution in the egg farm and the broiler house a sobering concern for us all.¹⁶³¹ The idiosyncratic likeness between the viral binding capacity to both chicken and human respiratory linings may allow chickens to stand in as our surrogates for the evolution of human transmissibility. Though millions fought along the Western Front, we keep birds in the trenches by the billions.