As with other cases of epidemics across history, from Justinian’s Plague to the Black Death, it is almost impossible for historians to trace the origins of the ‘Spanish flu’. Initial research carried out by Edwin Oakes Jordan in 1927 traced the origins of the flu to three locations: British military camps in Great Britain and France (1916–17), Haskell, Kansas (March 1918), or, surprise, surprise, China (winter 1917–18). Most historians or virologists have accepted that Spanish flu emerged from one of these three areas, but from precisely which area, there has been no consensus.

For many years, the Chinese hypothesis has been dismissed by scholars as German wartime propaganda.The Chinese Labour Corps (CLC) was a force of workers recruited by the British and the French governments, with the tacit agreement of the Chinese government, to aid the Allied effort on the Western Front. Some 140,000 Chinese, mainly from Shandong Province, served on the Western Front from early 1917 onward. German propaganda linked the arrival of the CLC with the start of the epidemic in Europe. Ironically, recent research has proposed this was exactly what happened.

From Chinese newspapers such as the North China Herald, we know that a contagious disease began to spread in northern China from November 1917. The Chinese government refused to classify it as a plague, claiming a low case-fatality rate as proof that it was merely a form of ‘winter sickness’. No quarantines and travel restrictions were set up. Later investigations by both Chinese and western doctors proved that the disease was indeed, not plague. However, the disease reemerged in autumn 1918, reported to have caused 20 to 30 deaths a day in some towns.

Despite this, Christopher Langford has shown that the epidemic in China was much less virulent as compared to the rest of the world. In Shanghai, the observed mortality was actually lower than expected: 12.8 in 1918 and 14.3 in 1919 per 1,000 persons, 12.4 per cent and 2.2 per cent below the expected average. Hong Kong officials reported that it was an

extremely noteworthy fact that Hong Kong enjoyed an astonishing immunity to influenza during the worldwide pandemic of the closing months of 1918 … Had the disease prevailed in Hong Kong in similar form and with the same intensity as it did in many parts of British India, the mortality that it would have caused in the crowded parts of Hong Kong City is terrible to contemplate.

In comparison,

New York mortality rates rose by 24.8 per cent in 1918 from an expected rate of 13.62 per 1,000 persons (1913–17) to 18.1 deaths per 1,000. In England and Wales the average number of deaths for the eight-year period preceding the pandemic was 14.04 deaths per 1,000 persons. In 1918 it rose 18.8 per cent to 17.3 deaths per 1,000. In Sri Lanka the death rate rose 17.3 per cent in 1918 from an average of 28.2 per 1,000 persons (1913–17) to 34.1 per 1,000. In Bombay, the average mortality for the period 1910 to 1917 was 32.83 deaths per 1,000 persons. In 1918 those numbers climbed 82 per cent to 59.61 deaths per 1,000; in 1919 they were higher still at 113 percent of expected mortality.

To explain why Chinese mortality rates were lower, Langford proposed that the epidemic originated from China - the Chinese had previous exposure to the influenza, which gave them relative immunity to the virus. According to this hypothesis, the epidemic spread from the trans-oceanic voyages of the CLC. From Weihaiwei in Shandong, CLC forces were initially transported via Singapore, Durban, and Cape Town, or through the Mediterranean via the Suez Canal, to the Western Front. Afterwards, the CLC was moved via Vancouver, across Canada to Halifax, then to France across both the Pacific and the Atlantic. Telegrams from recruiting officers in Weihaiwei confirm the existence of the disease among the CLC:

1,600 coolies are ready to embark at Chengyang in Conconada. Recruiting there is stopped by plague. At Weihaiwei there are 2,480 coolies not yet free from infection and probably ready to embark in about six weeks time.

In France, the epidemic continued among the Chinese workers, not helped by the commanding officer of Number 3 Native Labour General Hospital, Colonel Gray, who was more interested in the temperature of his stove than in the ill Chinese workers who filled his hospital, as recorded in the hospital’s official daily war diary. From there, the epidemic spread to British and French forces stationed in France and Belgium. Meanwhile, from Plymouth, England, which was a major stopping point for ships transporting the CLC to France, the disease spread out across the UK. American ships moving across the Atlantic ferrying American troops to the front, most likely brought the Spanish flu to the US, with the first signs of infection located at the port of Boston.

The Chinese hypothesis is therefore extremely attractive, for it explains the spread of the disease better than both the European or American hypothesis. It also explains why the Spanish flu did not have as great an impact on China as compared to other countries. However, due to the scarcity of data from China, we have no way of confirming or estimating the number of epidemic fatalities in China, and indeed, no way of fully confirming that the Spanish flu originated from China.

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Sources:

Xu, Guoqi, Strangers on the Western Front: Chinese workers in the Great War (Cambridge, Mass., 2011).

Morens, David M., and Anthony S. Fauci. "The 1918 Influenza Pandemic: Insights for the 21st Century." The Journal of Infectious Diseases 195, no. 7 (2007): 1018-1028.

Patterson, K. David, and Gerald F. Pyle. "The Geography and Mortality of the 1918 Influenza Pandemic." Bulletin of the History of Medicine 65, no. 1 (1991): 4-21.

Humphries, Mark Osborne. “Paths of Infection: The First World War and the Origins of the 1918 Influenza Pandemic.” War in History 21, no. 1 (2014): 55–81.

The Spanish flu pandemic of 1918: new perspectives, edited by Howard Philips and David Killingray (London, 2001).

Langford, Christopher. “Did the 1918–19 Influenza Pandemic Originate in China?” Population and Development Review 31, no. 3 (2005): 473-505.