Recent evidence suggests that the 1918 influenza was in fact an H1N1 variant, and therefore genetically similar to the virus currently spreading throughout avian populations in East and Southeast Asia. The 1918 virus likely originated in avian species, crossed over into the human ecology through processes of zoonotic transmission, then continued to evolve and mutate within human populations. This helps to account for the three waves of the pandemic that circled the world in 1918, each progressively more lethal, and likely intensified by the conditions of World War I.

The orthodox epidemiological history traces the origins of the pandemic to Camp Funston (near Fort Riley, in Kansas) during March 1918, after which it appeared at Camp Oglethorpe in Georgia and then at Camp Devens in Massachusetts.22 With troop transport vessels serving as vectors of both incubation and distribution, the flu then supposedly traveled to the battlefields of Europe, whereupon it infected thousands of soldiers during the spring of 1918. During this initial phase, the pathogen exhibited significant morbidity, with slightly elevated mortality, and then entered a period of relative dormancy during the summer months that followed. Late August of 1918 saw the second wave of the epidemic erupt with much greater lethality, appearing simultaneously in France, Sierra Leone, and the United States (with its epicenter in Boston).

The third and most virulent wave of the epidemic appeared in the fall of 1918, attacking the military forces of both the United States and the Central Powers and overwhelming field hospitals, transports, and lazarets in the rear with fevered, debilitated, and dying young men. According to the microbiologist Paul Ewald, throughout these three increasingly lethal waves of infection, the influenza virus progressively mutated to take advantage of the densely packed populations and of the mobility of soldiers, resulting in the emergence of a highly communicable and lethal strain. Ewald notes that the mobility of forces acted as a "cultural vector" to distribute the virus from infected host populations to uninfected populations:

Soldiers in the trenches were grouped so closely that even immobile infecteds could transmit pathogens. When a soldier was too sick to fight, he was typically removed by his trenchmates. But by that time trenchmates often would have been infected.23

Thus, the malign ecological conditions associated with a protracted ground war allowed the virus to mutate in order to become more infective (and increasingly lethal) to the young adult populations that served as hosts in the theater of war, and resulting in the unusual W-shaped mortality distribution. Ewald writes:

The increased mortality in the trenches due to fighting or the other infectious diseases that typically accompanied such warfare should have, if anything, also favored a high level of virulence. Any deaths of recovered immune individuals would result in the transport of replacements into the trenches who would often be susceptible to the strains circulating in the trenches. In addition, one of the costs that a pathogen may incur from extremely rapid reproduction is a shortened duration of infection due either to a more rapid immune response or to host death.24

Thus, the epidemic was a product of the pernicious ecology of war, with high population densities of combatants, poor sanitation, stress, and the movement of forces collectively serving as remarkably efficient vectors of transmission around the world. However, the pandemic may have also affected the course of the war, to some degree, through its successive waves of debilitation and destruction of human life. Thus, we may understand the relationship between war, pathogenic emergence, and outcome of the war as a complex feedback mechanism. I shall explore this concept in greater detail below.

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Swine Influenza

Swine Influenza

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