Previous works have addressed the idea that infectious disease may manifest in epidemic or pandemic form through processes of amplification through ecological change.1 Despite their analytical shortcomings, Galenic perspectives which specify that chronic poverty and the inequitable distribution of resources function as the principal (if not sole) variable involved in the spread of contagion are currently in vogue.2 Poverty certainly does serve as an amplifier of pathogenic infection, however, it is not alone in this function as other variables, including ecological change, trade, migration, natural disasters,3 and war may also serve as disease amplifiers. This chapter is primarily concerned with the effects of war (both inter-state and intra-state) on the emergence and proliferation of infectious disease. In it I argue that the processes of inter-state war and civil conflict create conditions directly conducive to the emergence, proliferation, and mutation of pathogens among both combatant and civilian populations. Thus war also functions as a “disease amplifier.”
Of the various factors that “amplify” disease, this particular relationship is doubtless the least understood, and it requires the development of a robust theoretical construct of probable paths of causality. The intellectual soil has not remained utterly fallow, as historians have noted this relationship for centuries, and yet such issues remain relatively unexplored within the domain of political science. This chapter explores both historical sources, and the current available empirical data, in order to develop and refine a series of testable hypotheses to inform future work in this neglected area. To empirically establish this relationship I analyze previously unpublished data from the German and Austrian archives regarding the effects of World War I on disease-induced morbidity and mortality.
The causal relationship between conflict and infectious disease is rather complex, often exhibiting both emergent properties and non-linearities. The balance of the evidence presented herein suggests that war has historically functioned as a central catalyst in the propagation of infectious diseases. Conflict spreads contagion between (and within) factions of combatants, and then from the warring parties to the civilian populations that they come into contact with, both during and after the martial engagements in question. A second question, regarding causality, deals with the issue of whether infectious disease can generate conflict within societies, or between sovereign states. There is considerable weight to the proposition that war acts to amplify disease, but there is little current empirical evidence to support the hypothesis that disease fosters war between sovereign states.
Let us engage the first proposition, namely that war functions as a catalytic agent that facilitates the “emergence” of epidemic disease in a given polity or population. What do we then mean by “war” and “conflict”? For the most part the terms are used interchangeably to denote processes of armed aggression between two collectivities or factions of combatants.4 This may manifest in war between two sovereign states (such as France and Germany) or in intra-state conflicts such as civil wars. The processes of conflict often generate the sufficient (although not necessary) conditions for the widespread diffusion of pathogens across the proximate region of conflict, and to those distal regions affected by demobilization. Thus, contagion might be passed from one force to another, and thereafter spread among the civilian populations through which the soldiers passed on their way home. At that point demobilized forces will then inadvertently spread pathogens within their own communities.
But what of the post-modernists who reject a priori any relationship between war and disease? The historian of science Roger Cooter argues that we must focus exclusively on the discourse and socio-historical “construction” of the partnership between war and disease, and ultimately he dismisses the concept of an empirical relationship between the two variables as pure fabrication, as a socially constructed discourse. He implores us to “concentrate on the different socio-political and professionalizing contexts within which the ‘fatal partnership’ between war and disease was fashioned, and eventually deposed, in epidemiology.”5 Such extreme positions ring hollow, as there is no empirical epidemiological basis to Cooter’s assertions. The data presented herein suggest the exact opposite: that an empirical relationship does very much exist, imperfect as the data may be. By denying the relationship between war and disease, post-modern scholars deliberately perpetuate ignorance regarding the relations between such variables, and thereby prevent any meaningful discussion of (and thereby impede the resolution of) these issues. Such obfuscation and denial, in the pursuit of ideology, paradoxically leads to greater harm for all over the long term, particularly the weak and disenfranchised.
Although analyses of the relationship between conflict and disease are novel in the domain of political science, the public health, medical, and historical communities have documented such issues for centuries. In the domain of public health, the epidemiologist Steve Morse has characterized war as a significant historical factor associated with the spread of infectious disease.6 The epidemiologist William Foege concurs in his analysis of war’s proximate and distal effects on population health. Foege argues that “organized violence, as seen in small or large conflicts, has direct and indirect effects on health as it leads to famines, epidemics, social dislocations, and the disruption of public health programs in general.”7 The medical historians Richard Garfield and Alfred Neugut agree, holding that social disruptions associated with the practices of war correlate with increases in the mortality rate among civilian populations. Such practices include “war-induced material deprivations (especially malnutrition), crowding, the breakdown of normal sanitary systems, and shortages of medical care. More casualties may be caused after wars than during wars.”8 The historian of medicine Hans Zinsser also understood this relationship between conflict and pestilence:
. . . war is . . . 75 percent an engineering and sanitary problem, and a little less than 25 percent a military one. Other things being approximately equal, that army will win which has the best engineering and sanitary services. The wise general will do what the engineers and sanitary officers let him. The only reason why this is not entirely apparent in wars is because the military minds on both sides are too superb to notice that both armies are simultaneously immobilized by the same diseases.9
In this chapter I address the mechanisms by which warfare (either between sovereign states, or between factions within them) magnifies the distribution, and often the lethality, of epidemic disease. In 2000, Foege noted this lacuna in the modern literature, stating that “the impact of conflict on infectious diseases in the civilian population remains significant but insufficiently studied.”10 Here I hope to present some remedy to this problem, and to provoke further inquiries.
The medical geographers Matthew Smallman-Raynor and Andrew Cliff argue that conflict contributes to the proliferation of epidemic disease through a variety of biological and social interactions resulting from the ecology of war11:
. . . mobilization heightened mixing of both military and civil populations, thereby increasing the likelihood of disease transmission. Frequently, military personnel were drawn from a variety of epidemiological backgrounds, they were assembled and deployed in environments to which they were not acclimatized, and they carried infections for which the civil inhabitants of the war zones had little or no acquired immunity. For all involved resistance was further compromised by the mental and physical stress, trauma, nutritional deprivation and exposure to the elements. Insanitary conditions, enforced population concentration and crowding, a lack of medical provision, and the collapse of the conventional rules of social behaviour further compounded the epidemiological unhealthiness of war.12
By what mechanisms does war contribute to the emergence, proliferation, and increased lethality of pathogens? Processes of conflict (both intra-state or inter-state) often target, disrupt, and/or destroy public health infrastructure and medical facilities of those affected regions and/ or countries, limiting the civil population’s access to adequate health care and medicines. During war, civilian populations have a rational proclivity to flee zones of conflict, whereupon they may venture into novel regions occupied by certain endemic pathogens to which they may have little or no prior immunity. Conflict may induce widespread famine, or may otherwise dramatically increase the costs of available foodstuffs, both of which result in chronic and acute malnutrition that increases the host’s susceptibility to pathogenic infection. Refugee populations exhibiting immunosuppression due to malnutrition (and psychological stress) may therefore be further victimized through increased levels of pathogenic infection. Further, with their mobility, malnourishment, lack of adequate shelter, and limited access to sufficient medical care, refugees are highly vulnerable to pathogenic colonization.13 And warfare is historically associated with a breakdown in social norms, which typically manifests in an increased incidence of sexually transmitted diseases.
The virologist Paul Ewald has also noted the empirical association between warfare and infectious disease, and concurs with the argument that epidemics may exhibit war-induced “emergent properties.” “Although the association between disease and warfare has long been recognized,” Ewald writes, “it has been attributed solely to increased spread of pathogens and increased vulnerability of hosts. The possible effects of war on the evolution of pathogen characteristics has long been overlooked.”14 Ewald argues that the processes of conflict actually force the pathogens within the human host population to develop novel genetic attributes.
In 1916, the German medical historian Friedrich Prinzing argued that warfare was a proximate and direct cause of pathogenic infection, not only of military forces, but of civilian populations too.15 The historian Paul Slack notes that historical archives are replete with accounts of epidemic diseases that afflicted and/or were distributed by military forces,16 although the precise etiology of these pestilences remains indeterminate, hindered by the lack of diagnostic capacity in earlier eras. The historian J. N. Hays argued that military forces function as exceptionally effective conduits (vectors) of pathogenic dissemination, not only to other combatants but also to civil populations:
[As vectors] the armies of late medieval and early modern Europe afforded nearly ideal conditions: they contained large masses of unwashed and illnourished people living an undisciplined life in which they foraged over the countryside and lived in close proximity to others. And not only did armies propagate typhus; warfare disrupted whatever public health measures might be attempted. Not only did (the military) practice direct violence . . . it remained basically unwashed, itinerant, and promiscuous, a powerful agent for the diffusion of disease. And its enhanced destructive powers made it all the more likely that its incursions could completely break down the fabric of a community it attacked, including whatever provisions for health and sanitation existed.17
Let us examine the historical record in order to construct testable hypotheses regarding the diachronic relationship between conflict and contagion. Given that pathogens interact with the human ecology in different manners, particularly in the context of violent conflict, we conduct this inquiry by examining the role of individual pathogens.
The first of the recorded “war pestilences” was the “plague” of Athens18 (430-425 BC), which arose in Piraeus during the second year of the Peloponnesian War, shortly after the Peloponnesian invasion. According to Thucydides, trade and the conditions of war—particularly the flows of war refugees who were driven into Athens (and the resulting exceptional population densities)—played pivotal roles in the rise of the epidemic.19 Ergo, a contributing factor to the outbreak of contagion would seem to be massive population movements from rural to urban centers (in this case Athens), generating exceptional population densities that were epidemiologically permissive to the pathogenic colonization of the population. Zinsser concurs, and attributes the pathogen’s emergence directly to the conditions associated with the ongoing conflict, such as dense military encampments and the movement of materiel from Africa.20 Moreover, once the contagion was established within Athens, the Athenian military apparently served as an efficient vector for diffusion of the pathogen, even as it was simultaneously depleted by the disease. Zinsser notes that “the pestilence followed the Athenian fleet, which was attacking the Peloponnesian coast, and prevented the carrying out of the objectives for which the expedition had been organized.”21
Notwithstanding the nascent body of genetic evidence that typhus visited Greece during the Peloponnesian War, it appears to have burned itself out or gone into hibernation, as it was some time before it revisited European societies. Hays argues that the next confirmed appearance of typhus on European soil (after the Peloponnesian War) occurred in 1489-90, during (and perhaps resulting from) the Spanish conflict with the Moors over the possession of Granada.22 The historian William McNeill concurs with the temporal frame of typhus’ introduction into European societies (circa 1490), but he offers a different explanation of the pathogen’s geographic origins. Typhus, he writes, “made its debut on European soil in 1490, when it was brought to Spain by soldiers who had been fighting in Cyprus. Thence it came into Italy with the wars between Spaniards and French for dominion over that peninsula. Typhus achieved a new notoriety in 1526 when a French army besieging Naples was compelled to withdraw in disarray due to the ravages of the disease.”23 From this point on, typhus became endogenized within the European human ecology, and its proliferation became associated with violent conflict.
Persistent conflicts between European forces and the Ottoman Empire facilitated the spread of typhus throughout Europe during the 1500s. Prinzing argues that in the latter years of the fifteenth century Hungary was destabilized by typhus, which had been brought to that country as a result of the protracted conflict with the Ottoman Empire:
. . . hitherto prosperous Hungary, by endless wars with Turkey . . . was brought to the very edge of ruin. . . . the utter lack of sanitation, increased the baneful effects of camp life. Dirt and refuse accumulated in heaps, vermin multiplied so rapidly that it was impossible to get rid of them, corpses were inadequately buried, while enormous numbers of flies and gnats molested the soldiers and did a great deal toward spreading infectious diseases. The hospitals were in a pitiable condition . . . [and] the soldiers . . . gave themselves over to a most dissolute life. . . . A large part of the German troops never once faced the enemy, for the reason that they succumbed beforehand to “Hungarian disease” (i.e. typhus), which killed more of them than the swords of the Turks. Hence Hungary was called at that time the “Cemetery of the Germans.”24
The war-induced diffusion of typhus facilitated the first pan-European epidemic of the pestilence in 1566, as the disease became ubiquitous during the war between Maximilian II and the Turks, then spread into western lands. “After the dispersion of the (Habsburg) army,” Prinzing writes, “the discharged soldiers carried the disease in all directions. Vienna was hit very hard. . . . The returning Italians brought the disease first to Carinthia . . . and then to Italy. In the same way it was carried to Bohemia, Germany, Burgundy, Belgium, and Spain.”25
In the seventeenth century the spread of typhus was also greatly facilitated by the horrid conditions of the Thirty Years’ War (1618-1648), by troop movements, and by the widespread conflict-induced famine that eroded the immunological vigor of affected populations. “In the history of this calamitous war,” the Prussian historian Friedrich Seitz wrote, “we see typhus fever like a malignant specter hovering over the armies wherever they go, in their camps, on their marches, and in their permanent quarters, and preparing an inglorious end for thousands of valiant warriors. Its ravages among the non-belligerent population in town and country caused the inhabitants of many provinces to remember with hatred and loathing the departed soldiers. . . .”26 Prinzing concurs: “. . . epidemics of dysentery, typhus fever, and bubonic plague followed at the heels of armies (and thus) were borne from place to place, . . . the great depopulation of Germany during the Thirty Years’ War was chiefly caused by epidemics of typhus fever and bubonic plague.”27 Typhus would also seem to have contributed to the destruction of French forces during Napoleon’s withdrawal of the Grand Armée from Russia in 1812.28 Indeed, typhus was one of the numerous infections that beset Napoleon’s forces as they marched toward Moscow from their bases in Central Europe during the summer of 1811:
After the battle of Smolensk (August 14-18, 1811) . . . typhus fever and other diseases . . . continued to spread throughout the army. The most common disease even in Moscow was typhus fever. . . . When Napoleon’s army withdrew from the city it left behind several thousand typhus fever patients, almost all of whom died. . . . The horrors of the return march are well known. . . . The number of sick soldiers was enormous, and typhus fever raged more and more extensively. In pursuing the French army the Russians also suffered severely from diseases. . . . between October 20 and December 14, 1812, they lost 61,964 men, most of whom died of “nerve fever” (typhus fever).29
Thus, both the Napoleonic and the Russian army served as primary vectors of contagion, and their movements subsequently generated epidemic typhus in the cities that lay in the path of the combatants (e.g., Vilnius, Warsaw, and St. Petersburg). According to H. A. Goden, a physician in the French forces, the military hospitals (lazarets) of the time also functioned as effective nodes of pestilential diffusion in the wake of the dispersing Grand Armée.30 The Prussian physician Heinrich Haser corroborates this description of disbanded troops, and their military hospitals, serving as highly effective vectors of transmission throughout Central Europe:
French soldiers returning from Russia . . . spread the contagion of various diseases over a large part of Central Europe. Almost naked, or clothed in . . . rags, without shoes . . . and their frozen limbs covered with festering sores, they marched through Poland and Germany. Typhus fever and other diseases . . . marked their course. The inhabitants of the country were forced to house the sick; but teamsters also conveyed the infection to villages which the soldiers did not visit. The disease raged most furiously in the hospitals.31
The contagion also appears to have visited the Americas, and it became particularly pernicious during the hostilities associated with the American Revolutionary War (1775-1783). The US medical historian Ted Woodward noted that during the American Revolution typhus infected, and debilitated, approximately one-third of the New York Army of General Nathaniel Greene in 1776, immediately before a confrontation with British forces.32
Modern skeptics may certainly argue that much of this argument is based on anecdotal evidence, or may otherwise question the validity of such accounts. However, the German medical archives of World War I, as prepared by German military physicians, provide us with solid empirical data to support the hypothesis that conflict can act as a mechanism of transmission of epidemic typhus. In this case the onset of the war initiated a massive outbreak of typhus among the German armed forces in the months immediately after the initiation of hostilities. (See figure 7.1.)
During the years 1916-1918, medical innovations resulted in the reduction of incidence and typhus-induced mortality. Despite the increasing capacity of the Germans to control the spread of typhus, it spread inexorably eastward in the months that followed the formal cessation of hostilities in November 1918. Consequently, the pestilence infected millions throughout Eastern Europe and Russia, with estimated civilian and military mortality exceeding 100,000. The military physician Brown notes that during this period approximately one-third of physicians in the Soviet Red Army contracted typhus, and 20 percent of those perished of the disease.33 This dynamic of post-conflict diffusion followed the pattern of earlier epidemics as demobilizing forces again served as agents that transmitted the louse vector, and therefore Rickettsia, throughout a vast area.
During World War II the incidence of typhus in European forces declined dramatically as military units made hygiene a priority. However, that war temporally coincided with epidemic outbreaks in those geographic regions where public health capacity was greatly diminished as a result of the hostilities. Specifically, the physician Bavaro notes that “during and immediately after the war hundreds of thousands of cases of typhus, with up to 10 percent mortality rates, appeared in civilian populations in Egypt, French North Africa, Naples, Germany, Japan, and Korea.”34 The manifestations of the illness, and the impact on both military and civilian populations were far more pronounced in the Pacific theater of operations. “In that preantibiotic era, the disease sometimes caused more casualties than actual combat, with mortality rates exceeding 27 percent. There were more than 20,000 cases among Japanese forces and 16,000 cases among Allied troops, including more than 7,300 cases and 331 deaths among US troops.”35 The last major recorded outbreak of conflict-induced typhus occurred during the Korean War. Although typhus was largely contained within the military populations of the UN alliance, the material deprivation and destruction of public health infrastructure resulting from the war spawned an outbreak of typhus that resulted in approximately 32,000 cases and 6,000 deaths among South Korean military and civilian populations.36
Variola established itself in East Asia after the Chinese General Ma-Yuan employed military forces to suppress a Wuling revolt in Hunan province in the years 48-49 AD. The historian Donald Hopkins writes:
The general led his army into a district where an epidemic was in progress. The result was that more than half of the Chinese expeditionary force, including General Ma-Yuan, succumbed to the disease. The remnants of Ma-Yuan’s army returned home with their prisoners, bringing “captives pox,” or “barbarian pox” into China.37
The Antonine Plague that ravaged the Roman Empire in 166-168 AD exhibited symptoms that bore a close resemblance to smallpox. According to Prinzing, the contagion was the result of military vectors transporting the pathogen from the Levant back to the Empire. Specifically, General Avidius Cassius (preceding Verus) was deployed to Syria in order to suppress rebellious local factions, and Variola appeared during the capture of Seleucia. From that point “it was borne by the troops back to Rome, where, after the triumphal procession of 166, it spread far and wide. . . . The plague spread from Italy to Gaul, to the very banks of the Rhine, and a large part of the province was significantly depopulated—decayed and deserted villages were found everywhere.”38
Variola appears to have been firmly established in the Arab world around 622 AD, and the vectors and conditions associated with warfare accelerated the spread of the pathogen throughout that region. “After Alexandria,” Hopkins writes, “the Arab armies swept across western Asia, North Africa, and conquered Spain before they were stopped at Constantinople in 717, and at Poitiers, France, in 732. Smallpox went with them, into Syria, Palestine, Sicily, Mauritania, Spain, and France.”39 Furthermore, the Crusades in the twelfth and thirteenth centuries apparently reintroduced and facilitated the spread of Variola across European societies. “Pox houses” became ubiquitous along the paths trod by Crusaders returning from the Levant to England via Germany.40
In later years, smallpox influenced the outcome of the conflict between the nascent United States and the Dominion of Canada. During the American Revolutionary War, the contagion played a role in debilitating the US Army. Benedict Arnold led a massive force of colonial troops against the British colony, and after the capture of Montreal the contagion entered the ranks of the American forces en route to Quebec City. American forces buried their dead in mass graves as they retreated in disorder.41 “Of the 10,000 troops in the attack, 5,500 developed smallpox. There were not enough tents to shelter even the desperately sick men. The moans of the sick and dying could be heard everywhere. Pits were opened as common graves and filled day after day with corpses as the men died like flies.”42 Thomas Jefferson later commented that Variola had been “sent into our army designedly by the (British) commanding officer in Quebec,” although such claims have never been empirically verified.43 According to Oldstone’s analysis, approximately 55 percent of US forces in this particular campaign developed smallpox and were killed, nullifying the United States’ capacity to project military power within this theatre and allowing the continuation of British rule within North America.44 Fenn notes that after the disastrous campaign against Quebec the demobilizing US forces were highly effective vectors for the spread of the contagion throughout New York, Connecticut, and Pennsylvania.45
Prinzing argued that the Franco-Prussian War operated as the central epidemiological catalyst that generated the devastating smallpox epidemic of 1870-71. This contagion was the scourge of both Prussia’s and France’s populations (military and civilian) and resulted in approximately 300,000 fatalities.46 The French physician Andre Laveran noted that this particular epidemic of smallpox began in France and circulated throughout French military forces before their deployment against Prussia.47 Prinzing speculated that field soldiers in general and French prisoners of war in particular served as agents of pathogenic transmission to Prussian populations. In particular, the prisoner-of-war camps in Prussia functioned as nodes in a network of pathogenic distribution that facilitated the spread of smallpox to the Prussian civilian population. The medical historian James Rolleston concurs, stating that “the epidemic would seem to have originated in France, but then mutated into a haemorrhagic form as it was spread by French troop vectors into the states of Prussia and its allies.”48 This explosion of smallpox mortality temporally coincided with the onset of hostilities, whereupon the mortality associated with the pathogen increased by an order of magnitude. (See figure 7.2.) Smallpox subsequently continued its pattern of diffusion into the civilian population, persisting well beyond the formal cessation of hostilities in 1871. The mortality induced by the war-pestilence reached its zenith in 1872, and thereafter declined in equally dramatic fashion.
The historian Richard Evans observed that soldiers returning to Hamburg from the Franco-Prussian war served as effective conduits of transmission, resulting in the deaths of 4,043 residents of Hamburg by Variola in 1871. Such mortality generated a mortality rate of “15.4 per 1000, which made the smallpox outbreak of 1871 the greatest of all epidemics in nineteenth-century Hamburg. . . . 9,055 victims were hospitalized, of whom 908 died. If this ratio of deaths to cases held good for those not treated in hospital, then there may have been 40,000 cases. . . . 29 percent of all deaths in Hamburg in 1871 were caused by smallpox.”49
Smallman-Raynor and Cliff argue that Prinzing was indeed correct in his assertions that the geographical diffusion of smallpox during the Franco-Prussian War was very much facilitated by the network of prisoner-of-war camps. In conducting their analysis, Smallman-Raynor and Cliff employ data originally collected by the Prussian medical statistician Albert Guttstadt.50 The analysis involved geospatial multivariate regression, in order to determine that the war directly contributed to the proliferation of smallpox among the Prussian military and civilian populations. Smallman-Raynor and Cliff argue that smallpox “spread through the civil system of urban centres as a mixed diffusion process with a dominant hierarchical component. Contrary to expectation, however, this process . . . was determined by the system of POW camps that had developed around the urban system during the course of the war.”51 They conclude that “the exigencies of war may result in a fundamental reconfiguration of epidemic diffusion processes in civil settlement systems.”52
Hans Zinsser argued that pathogenic co-infectivity during a protracted conflict exhibited enormous complexity and variation over time. He argued that it is possible to divide the biological history of the Thirty Years’ War (1618-1648) into two distinct epidemiological periods, with typhus reigning from 1618 to 1630. Thereafter, from 1630 to 1648, bubonic plague rose to become the premier scourge of those countries party to the conflict. On an epidemiological level this succession of contagion makes sense as those exposed to typhus would either have been killed, or thereafter acquired some immunity to the pathogen, clearing the way for the ascension of a pathogen to which they had little or no prior immunity (Yersinia pestis). However, during this epic era of societal chaos and inter-state war, various and diverse pathogens; dysentery, typhoid fever, smallpox, and scarlet fever, all interacted with typhus and plague.
Once again soldiers proved to be highly efficient vectors of pathogenic distribution. After the return of bubonic plague in 1630, it “traveled with the rapidly moving armies, remaining behind when the soldiers departed, and spreading from innumerable foci into the surrounding country.”53 It is noteworthy that even into the nineteenth century, the disease continued to be problematic for military forces, and the conduct of martial campaigns. August Hirsch observed that the conflict between Russian and Turkish forces in Wallachia in 1828-29 generated the last significant outbreak of Bubonic Plague in the European theatre.54
Thereafter, the incidence of plague in the European population diminished markedly as sanitary measures improved. Yet Yersinia pestis would continue to afflict societies in East Asia for some time to come. Hays notes that the armed rebellion of 1855 in Yunnan province of China facilitated the spread of the pathogen throughout the entire region: “The great Muslim rebellion that began in 1855 resulted in nearly two decades of internal turmoil in Yunnan, in which plague epidemics coincided with military massacres, famine, and considerable emigration. . . . Troop movements and emigration may have spread plague to other areas of China.”55 This association between war and plague continued into the twentieth century as a significant outbreak of plague struck down thousands of Vietnamese citizens from 1966 to 1974, primarily as a result of the atrocious conditions associated with the war; including the destruction of health infrastructure, and breakdown of hygiene and sanitary measures.56 Antibiotic prophylaxis has proved to be crucial to the containment of Yersinia pestis, yet the pathogen remains endemic at low levels throughout some regions of the world, including the American Southwest.
The diffusion of Vibrio was also often associated with the movements of troops who carried it to vulnerable populations. Such conflict-induced epidemics were certainly not confined to European soil, as war proved to be the pivotal vector of the transmission of cholera from its reservoirs in South Asia (i.e. India) to Europe. Evans argues that one of the first of such transmissions occurred when, “the Marquess of Hastings fought a military campaign against the Marathas in 1817, losing 3,000 out of 10,000 troops to the disease in the process.” From that point the contagion traveled via various routes, through other proximate military campaigns, until it reached England.57 William McNeill concurs: “British troops fighting a series of campaigns along India’s northern frontiers between 1816 and 1818 carried the cholera with them from their headquarters in Bengal, and communicated the disease to their Nepalese and Afghan enemies. Military movements connected with Russia’s wars against Persia (1826-28) and Turkey (1828-29) . . . carried the cholera to the Baltic by 1831, whence it spread by ship to England.”58 Hirsch supports this line of argument as well, noting that the spread of cholera throughout Poland and the Baltic region during the 1830s was very much related to conflict, stating that the “military operations of the RussoPolish War contributed materially to its diffusion.”59
It was from this foothold in Eastern Europe that cholera began its inexorable march across the fertile and immunologically naive populations of Europe. Evans concurs that Russian military actions to thwart the Polish rebellion in 1831 created the pre-conditions, abetted by conflict-induced waves of Polish refugees, that allowed for the rapid spread of Vibrio to Central and ultimately Western Europe. Furthermore, he argues that the Crimean War also contributed to the pathogens diffusion throughout the Continent and Asia Minor: “In 1854 French troops embarking for Gallipoli and Varna at Marseilles and Toulon carried cholera with them and ensured that a major outbreak occurred when they finally reached the theatre of war in the Crimea.”60 Finally, the destabilization induced by the Austro-Prussian War of 1866 appeared to have contributed directly to the rise of epidemic cholera in AustriaHungary, which induced approximately 165,000 deaths in that year.61
Few modern empirical studies have tested the empirical relationship between war, and vectors of pathogenic diffusion, in the domain of cholera. The most revealing (and methodologically sophisticated) medical-spatial regressions to date have been conducted by SmallmanRaynor and Cliff, who examined the dynamics of the diffusion of epidemic cholera in the Philippines during the Philippine-American War (1902-1904). They consequently determined that “the mass population movements associated with the war had the effect of speeding up the geographical propagation of cholera as compared with peace,” although the fundamental geographical channels of disease spread remained in effect.62
McNeill suggests, correctly, that the horrific conditions generated during the course of World War I, and contact between troops of disparate geographical origins, may have accelerated the evolution of a lethal and highly transmissible pandemic influenza that killed millions in 1918-19.63 Oxford et al. concur that the influenza pandemic of 1918 was likely facilitated and indeed intensified by the conditions of the protracted war in Europe.64 It does seem reasonable to argue that the epidemiologically malign conditions of the western front, notably the exceptional population densities associated with trench warfare, contributed to the evolution of increasingly lethal waves of the pandemic as it circled the world, with troop movements serving as vectors. Perhaps the best empirical argument to support the notion of the 1918 pandemic as exhibiting emergent properties deriving from World War I is proffered by the virologist Paul Ewald:
One of the best examples of an evolutionary increase in virulence is the influenza pandemic of 1918. The environmental conditions associated with the trench warfare of World War I could hardly have been more favorable for the evolution of increased virulence of airborne pathogens like influenza. Soldiers in the trenches were grouped so closely that even immobile infecteds could transmit pathogens. The sick individuals were generally moved between a succession of crowded rooms by a succession of crowded vehicles. The severely sick and badly wounded were then sent within a few hours by trucks to one or more evacuation hospitals and then eventually by railcars to base hospitals. Additional new susceptibles would be transported to the trenches to take the place of ill people who had been removed. As the trenchmates infected by an already removed soldier became ill, the process continued. In the camps away from the trenches, the high densities of soldiers and transport of sick and susceptible soldiers may have contributed to increased virulence by a similar mechanism. 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. If the conditions and activities at the western front were responsible for the enhanced virulence of the 1918 pandemic, the timing and spatial pattern of virulent disease should accord with virulence enhancement at the western front. . . .65
The data presented by Alfred Crosby appear to support Ewald’s hypothesis that the war, and the activities on the western front in particular, served as an amplifier of the contagion, accelerating its proliferation among susceptible hosts, and thereby increasing its lethality.66 The only caveat to Ewald’s argument is that, as I have argued above, the first manifestations of a highly lethal influenza may have actually appeared in Austria during the spring of 1917, reinforcing Oxford’s hypothesis that the influenza emerged and evolved within the European theatre before its apparent emergence in highly lethal form in Kansas during the spring of 1918. Ewald’s argument does help to explain how the lethality of the virus intensified in the horrid conditions of the western front, and was augmented in each of the three waves as it circled the world, propelled by the continual movements of troops serving as highly efficient vectors.
The “White Plague” has been the bane of human societies for millennia, and it continues to debilitate and kill millions per year, even in the era of antibiotics. The association of tuberculosis with conflict is an area that is rather unexplored, yet the association makes intuitive sense. Theoretically, soldiers under stress will experience weakened immune systems, and malnourishment will further compromise immunity. Significant population densities in military camps and trenches would certainly facilitate the communication of the pathogen between susceptible troops, and one would expect that the processes of war would increase the incidence of, and perhaps the mortality associated with tuberculosis. Again, the German medical records from World War I illustrate this relationship, and provide preliminary empirical evidence to support this association. (See figure 7.3.) One can certainly discern an increase in tuberculosis-induced mortality from 1914 until 1916, whereupon the mortality rate appears to plateau and thereafter decline somewhat toward the end of the war. This suggests that the onset of the war had a moderate effect on increasing both the incidence and the mortality associated with the pathogen in German forces.
A comparison of the German military data with the Austrian records of tuberculosis-induced civilian mortality in Vienna is expedient. The Austrian data provide us with a prewar baseline of 4,924 deaths in 1912, peaking at 9,650 deaths in 1917, and declining to 8,539 deaths in 1919. The data clearly indicate that the onset and progression of the war is directly associated with the dramatic increase in tuberculosis-induced mortality in Vienna. Furthermore, the epidemic of tuberculosis intensifies in the latter years of the war, and indeed this pattern persists into the postwar period. Another point to consider is that the increasing mortality associated with tuberculosis in 1919 may reflect the destructive effects of the 1918 influenza pandemic, which certainly weakened the lung tissues and immune systems of survivors, making them vulnerable to secondary bacterial infections of which tuberculosis would be a prime candidate. This further illustrates the complex interactivity and connectivity of pathogens in the context of the human ecology.
In more recent times, the attenuated conflict in Afghanistan between United States and newly resurgent Taliban forces has apparently amplified the incidence of tuberculosis in that country. The epidemiologists Ibrahim Khan and Ulrich Laaser argue that the war has directly contributed to the increasing incidence of the disease among the general population, with attendant increases in mortality.67 Aside from generating the preconditions that facilitate pathogenic diffusion and colonization of hosts, the war has also impeded efforts by international organizations (e.g., the WHO), and non-governmental organizations (e.g., Medicins Sans Frontiers) to bring the contagion under control. Specifically, the diffuse conflict has impeded comprehensive epidemiological surveys of the population, such that only sporadic surveys are possible. It has also resulted in the erosion of the endogenous public health infrastructure, or prevented the establishment of such infrastructure in highly impoverished areas. Moreover, the nature of the conflict has impeded the delivery of effective medical treatment to those suffering from infection. This requires the consistent provision of medicines to those infected, who must in turn follow a prolonged regimen of treatment. Khan and Laaser elaborate:
War extremely reduces the chance of regular therapy among patients and limits access to regular health care in every conflict area. . . . Over one third of the country has no routine immunization program. . . . Dormant tuberculosis bacilli can spring back to life and cause illness when people are especially stressed, not adequately nourished, immunocompromised, or in close contact with the infection source. The circumstances in refugee camps are extremely poor and there is a high risk of infection and re-infection.68
Moreover, refugees also serve as conduits of infection to other proximate countries. In this particular case, it would appear that the war has exacerbated the prevalence of endemic tuberculosis, which is now spreading from its reservoir in Afghanistan through population movements (primarily civilians fleeing conflict) to neighboring Pakistan.69 In this manner we see the interactivity between war and disease, with the former reinforcing the latter. In this sense then the global public bad of war clearly serves to exacerbate another public bad, the tuberculosis pandemic.
The spread of malaria is related to many factors, including poverty, but it is also very much related to environmental change, specifically changes in land use, changes in water use (i.e., dams and irrigation) and transportation infrastructure that permitted the migration of the plasmodium through human vectors. It should not come as a surprise then that the conditions associated with conflict might contribute to epidemics of malaria in immunologically naive populations, and even to establish the disease in those geographic zones where it had not been previously endemic. Evidence of the latter comes from the highlands of Western Kenya, which were free of malaria for much of their recorded history. In this case, changes in land use and transportation infrastructure, such as the extension of the railroad from the coast in 1901, allowed for the gradual establishment of the plasmodium in the regional ecology. However, epidemic malaria was only first reported in the region in the second decade of the twentieth century. The epidemiologist Mark Malakooti and his co-workers conclude that troop demobilization after World War I was the premier factor in establishing malaria throughout that region: “The first reported epidemic was in 1918 to 1919 when local soldiers returned from Tanzania after World War I. Two epidemics were recorded in the 1920s and four in the 1930s. After the military camp in the area was disbanded in 1944, the local outbreaks ceased, but highland malaria continued to be a serious public health problem until the late 1950s. . . .”70
As was noted above, war is often characterized by interaction between various pathogens. Aside from the smallpox induced by conditions of the Franco-Prussian War, numerous other diseases were transmitted during the course of that campaign including dysentery which generated an extraordinary level of morbidity among the troops. “Of the German field-army,” Prinzing writes, “38,975 men, all told, contracted dysentery (47.8 per 1,000 of the average number of troops under arms), and of these 2,405 died. Of the average number of French prisoners taken to Germany 41.7 percent contracted the disease. . . .”71 McNeil concurs: “. . . in even the best-managed armies, disease was always a far more lethal factor than enemy action, even during active campaigns. In the Crimean War (1854-56), for example, ten times as many British soldiers died of dysentery as from all the Russian weapons put together. . . .”72 Data collected by the German medical services indicate that the incidence of dysentery (described as “Ruhr” in the German records) in the German forces increased dramatically as the war continued, peaking in 1918. This pattern of increase is consistent with the reports of poor nutrition and declining health infrastructure throughout the country. (See figure 7.4.)
Armies have also functioned as optimal vectors for the transmission of syphilis and other sexually transmitted diseases. The historical appearance of syphilitic infection in European populations closely followed on the heels of the Columbian “discovery” of the Americas. Indeed, Crosby posits that syphilis was imported to Europe by Iberian troops during the initial phases of the conquest of the Americas.73 Anthropological evidence suggests that syphilis (Treponema pallidum or Treponema S), which is genetically similar to yaws (Treponema Y), was imported to Europe from the Americas by the Spaniards during and after 1492.74 “The disease,” Watts argues, “then mutated in their bodies . . . to become the Treponema pallidum which suddenly was so much in evidence among the French mercenary army which invaded Italy in 1494.”75 The virulence of the syphilis epidemics that swept Europe in the fifteenth and sixteenth centuries was of such magnitude that it suggests the bacterium was devastating a population that had acquired no prior immunity through exposure to the pathogen. In other words, European populations were apparently immunologically naive. War had a now familiar role to play in the subsequent diffusion of syphilis across the Continent. During the siege of Naples by the French armies of Charles VIII in 1494, the latter’s troops bore the contagion of syphilis with them. “There the French army gave itself over to the most unbridled licentiousness, and the result was that [syphilis] spread rapidly in both the French and Italian armies. The disbanding of Charles’s army caused the disease to spread far and wide in Europe.”76 McNeill concurs, arguing that syphilis made its first appearance in epidemic form during the long series of FrancoItalian conflicts in the period 1494-1559: “[Syphilis] broke out in epidemic fashion in the army that the French king, Charles VIII, led against Naples in 1494. When the French withdrew, King Charles thereupon discharged his soldiers, who thereupon spread the disease far and wide to all adjacent lands.”77 Thereafter, syphilis became an endemic pathogen that colonized European populations, its virulence declining through mutual pathogen-host adaptation. It persists to this day all over the world.
As of the time of writing (2008), two clades of the human immunodeficiency virus have become endogenized within the human ecology, with HIV-1 exhibiting global diffusion whereas HIV-2 has become widespread predominantly throughout western Africa. In their analysis of the distribution of HIV-1, Smallman-Raynor and Cliff determined that the distribution of the pathogen in Central and East Africa is highly correlated with the distribution of conflict, and with recruitment vectors in the region. Specifically, they argue that “both the spread of HIV 1 infection in the 1980s, and the subsequent development of AIDS to its 1990 spatial pattern, are shown to be significantly and positively correlated with ethnic patterns of recruitment into the Ugandan National Liberation Army (UNLA) after the overthrow of Idi Amin some ten years earlier in 1979.” Their data suggest that both the “truck-town” hypothesis (according to which transportation vectors determine the distribution of the pathogen) and the “migrant labor” hypothesis (according to which the pathogen is diffused from urban centers of labor demand to rural areas that possess a supply of labor) are inaccurate in predicting the present pattern of pathogenic diffusion. Specifically, multivariate regressions that analyze the spatial distribution of the epidemic indicate that the Ugandan civil war of 1979-1985 is the greatest predictor of the distribution of the pathogen.78
A team of geneticists and demographers led by Philippe Lemey reconstructed the evolution of the HIV-2 epidemic from its established locus of origin in Guinea-Bissau. They found that the virus shifted from endemic to epidemic status in the period 1955-1970, which coincides with that country’s war of independence from Portugal. Lemey et al. write:
Our demographic estimates suggest that an event enabled HIV-2 subtype A to switch to epidemic growth sometime around 1955-1970. An initiation of the epidemic at this time coincides with the time frame of the independence war (1963-1974) in Guinea-Bissau. . . . There is evidence that both sexual and blood-borne HIV-2 transmission markedly increased during this period. Epidemiological linkage of HIV-2 with Portugal, established during the presence of the colonial army, was recognized when the first reported cases of HIV-2 in Europe were Portuguese veterans who had served in the army during the independence war.79
According to the military analyst Lindy Heinecken, a significant proportion of African military forces exhibit HIV seroprevalence rates ranging from 40 percent to 60 percent.80 Although this estimate may be elevated, there are few solid empirical data to refute it, as many states have defined such data as classified. The political scientist Stefan Elbe has written extensively on the role of soldiers as highly effective vectors of HIV transmission, particularly in the context of sub-Saharan Africa. He notes that soldiers are “of a sexually active age; they are highly mobile and away from home for long periods of time; they often valorize violent and risky behavior; they have greater opportunities for casual sexual relations; and they may seek to relieve themselves from the stress of combat through sexual activity.”81 Martin Schonteich concurs, but further argues that armed conflict often leads to an increased frequency of sexual coercion, often to the rape of civilians by military personnel.82 In this vein of inquiry, Elbe presents convincing evidence that “war-rape” is increasingly used as deliberate weapon of war. He states that “the deliberate transmission of HIV/AIDS has been used in Africa at a minimum as a psychological weapon of war to induce further anxiety among females in societies that have become war zones. Preliminary evidence suggests that the HIV prevalence rate among rape survivors is high. Two-thirds of a recent sample of 1,200 Rwandan genocide widows tested positive for HIV.”83 Elbe continues: “. . . appropriations of HIV/ AIDS by armed forces in Africa reflect the virus’s increasing significance as a weapon of war. Combatants have sought to use the psychological and lethal effects of HIV/AIDS to gain strategic advantage over their opponents.”84 It is difficult to state definitively that this is a departure from past practices, as soldiers infected by pathogens have engaged in practices of sexual coercion and rape of civilians throughout recorded history. The difference in this case is that such practices are apparently being used in deliberate and strategic fashion to undermine the morale and social cohesion of the enemy.
As was noted above, one analytical problem is the issue of the coinfection of troops and civilian populations by multiple pathogens. It is certainly reasonable to assume that over the span of an attenuated conflict (such as the Thirty Years’ War) that the forces and populations involved experienced a succession of epidemics, often with multiple sources of infection. World War I saw the infection of German and Austrian populations by influenza, which then opened the way for subsequent epidemics of pneumonia and tuberculosis. This makes any such strict accounting of influenza-induced mortality rather problematic, in that the secondary effects of the pandemic persisted for some time. This reinforces the position taken by the political scientist Hazem Ghobarah et al. that the public health costs of wars (and complex emergencies) are likely complex, attenuated, and difficult to estimate.
Disease-induced mortality data from the US Civil War provide us with some idea of the relative aggregate mortality from disease vs. battlefield injuries. The mortality statistics on Union troops compiled by US SurgeonGeneral Barnes in 1870-1888 are the best available data on causes of death during that conflict.85 The data indicate that deaths from infectious diseases vastly exceeded battlefield deaths and deaths from wounds suffered in action. (See figure 7.5.) It is instructive to compare aggregate battlefield and wound-induced mortality (93,443) against deaths from infectious disease. The ratio of disease-induced mortality to battlefield/ wound-induced mortality is a significant 1.9928:1, suggesting that disease was very much a security issue to American forces during this era. But such data were not disaggregated into mortality by specific pathogen, and so (aside from anecdotal records) we have little empirical evidence to indicate which specific pathogens accounted for what proportion of that aggregate mortality.
Such problems of co-infection persist into the modern era. According to Grant and Jorgenson, who studied the mortality patterns of Soviet troops in Afghanistan during the 1980s, disease played a significant role in mortality. Specifically, they report that less than 3 percent of casualties resulted directly from combat, yet approximately 76 percent of Soviet casualties resulted from infectious diseases, including malaria, plague, typhus, hepatitis, and various forms of dysentery.86
The economist Paul Collier notes that collapsed states, often as the result of civil war, act as the epicenters of disease and regional turbulence.87 In this sense, state failure can be also seen as a public bad, which then generates further externalities such as pathogens, which may then function to afflict a specific region, or indeed come to burden the entire world. Toole et al. comment that the civil war in Bosnia during the early 1990s “revealed extensive disruption to basic health services, displacement of more than 1 million Bosnians, severe food shortages in Muslim enclaves in eastern Bosnia, and widespread destruction of public water and sanitation systems. War-related violence remains the most important public health risk; civilians on all sides of the conflict have been intentional targets of physical and sexual violence.”88 Moreover, the extensive empirical analysis of Ghobarah confirms that contiguous civil wars are significantly associated with the spread of HIV in neighboring territories.89 Furthermore, Garenneand et al. argue that during the civil war in Central Mozambique in the 1990s “mortality from infectious diseases increased dramatically during the civil war.”90 Interestingly, Ghobarah concludes that “the most common impact [of civil war] is through infectious diseases. . . . In fact, by t value, five of the 25 groups most impacted by civil wars are from the increased incidence of malaria. The three other most affected disease groups are tuberculosis, respiratory infections, and other infectious diseases. . . .”91
Civil wars in the modern era are associated with generating significant flows of refugees and internally displaced persons. Since the mid 1980s, the turbulent Western Upper Nile region of the Sudan has seen the emergence of epidemic visceral leishmaniasis, and massive mortality of the local population. Seaman et al. note that the epidemic began in 1983, when the civil war between the Nilotic peoples of the South and the Arab-African populations of the North began again in earnest, as a result of the introduction of the parasite through troop vectors from its regions of endemicity. This low-intensity but protracted civil war has resulted in complete disruption of the health-care infrastructure in the area, in increased malnutrition, and in huge population movements of both combatants and civilians. According to Seaman, “movement to escape the fighting and to search for food . . . has probably increased the rate of transmission and facilitated the spread of the epidemic within [the western upper Nile region] and beyond. Agriculture and cattle rearing have been disrupted by the war, resulting in more persistent malnutrition which has probably contributed to a higher conversion rate to clinical disease . . . and hence to high mortality.”92 Moreover, the hostilities have disrupted both coherent epidemiological surveillance of the epidemic and the provision of treatment to the infected, as expatriate medical staff are often evacuated because of the fighting.93 As a result, this conflict-induced epidemic has resulted in catastrophic mortality throughout the region: “Between 38 percent and 58 percent of the population reportedly died, and up to 70 percent in the most affected areas. . . . 80,000-136,000 people who might otherwise have been expected to live, have died since 1984.”94
Rey et al. note that refugees returning to Kosovo after the conflict with the Serbs in 1998 generated an epidemic of hepatitis (HAV and HEV, specifically) in that region.95 The displacement of populations as a result of civil war has also been associated with recent outbreaks of epidemic typhus in sub-Saharan Africa. According to the epidemiologists J. Ndihokubwayo and D. Raoult, Burundi’s lengthy civil war of 1993-2006 forced a significant proportion of the population to “live in the cold, promiscuity, and malnutrition of makeshift refugee camps.” They conclude that “political unrest as well as numerous civil wars are now epidemiological factors favor[ing] outbreaks of epidemic typhus at any time.”96 Toole and Waldman concur, noting that war generates conditions of stress, malnourishment, lack of sanitary facilities, and lack of access to public health provision that contribute directly to the spread of communicable diseases within densely populated refugee camps.97 Ghobarah concurs:
Prolonged and bloody civil wars are likely to displace large populations, either internally or as refugees. Epidemic diseases—tuberculosis, measles, pneumonia, cholera, typhoid, paratyphoid, and dysentery—are likely to emerge from crowding, bad water, and poor sanitation in camps, while malnutrition and stress compromise people’s immune systems. [Furthermore] the camps become vectors for transmitting disease to other regions. Prevention and treatment programs already weakened by the destruction of health-care infrastructure during civil wars become overwhelmed as new strains of infectious disease bloom. For example, efforts to eradicate Guinea worm, river blindness, and polio—successful in most countries—have been severely disrupted in states experiencing the most severe civil wars.98
Smallman-Raynor and Cliff conclude that civil war can affect the spread of epidemic disease through various mechanisms of diffusion: “. . . the population movements engendered by the Cuban Insurrection (1895-98) and the Philippine-American War (1899-1902) were found to be associated with a strengthening of the geographical corridors of epidemic transmission that would ordinarily be witnessed in peacetime.”99 Przeworski et al. argue that political disruption generates persistent and negative effects on economic growth rates in affected polities.100 Thus, the economic shortfall induced by political instability typically results in a reduction of government revenues available for expenditure on public goods such as health care, clean water, and sanitation, which in turn greatly facilitates the proliferation of pathogens in a society. The pernicious effects of war on capital (both fiscal and human), particularly as they affect the provision of public health, are very much in need of further empirical investigation.
War may be seen as malign not only in and of itself but also in its role as the progenitor and disseminator of disease. Consequently, war should be understood as amplifying disease through its contribution to contagion as a function of emergent properties. Thus, even regional wars may generate the circumstances for pathogenic emergence (and further evolution) that contribute to the spread of global public bads in the form of pandemic diseases. “If we fail to recognize the evolutionary changes in pathogen virulence that our activities may inadvertently cause,” Ewald warns, “then we will pay the price in sickness and death not just until our activities change the environment back to a state that favors the benign forms, but rather until the evolutionary change toward benignness is completed.”101 Collectively, such preliminary evidence reinforces the hypothesis that war and disease may operate synergistically as symbiotic externalities wherein the former extensively reinforces the latter, with this malign nexus operating at domestic, regional, and global levels.
In summation, the following factors, generated or exacerbated by conflict, contribute directly to the emergence and/or proliferation of pathogens:
increased population density (combatants and civilian)
famine-induced malnourishment, compromising immunity
conflict-related mobility or vectors (troops and refugees)
lack of hygienic conditions (water, etc.)
destruction of health infrastructure
lack of access to health services
impediments to treatment
poverty (induced or exacerbated)
inhibition of effective public health surveillance
sexual coercion and commercial sex
physical and psychological stress, compromising host immunity.