Malaria Paradoxes of the U.S. Civil War

ABSTRACT.

The U.S. Civil War (1861–1865) pre-dated modern understanding of malaria. Yet, malarial diseases (remittent fever, intermittent fever, typho-malarial fever) were frequently reported as causes of morbidity and mortality in soldiers. Modern readers find Civil War-era descriptions of malaria contradictory or paradoxical. For example, although the concept of race-specific immunity to tropical diseases was widely accepted, malaria mortality rates were reportedly more than three times higher among Black than White Union soldiers (16/1,000/year versus 5/1,000/year). Also, malaria rates were reportedly lower among prisoners of war at the infamous Andersonville, GA, prison camp than among Confederate soldiers in the same area. Literally tons of quinine were given prophylactically to Union soldiers deployed in the southern United States, but blackwater fever was not reported by medical officers. All three paradoxes have reasonable modern explanations that give credence to the astute clinical observations of our scientific predecessors during the U.S. Civil War.

Throughout history, malaria has been a decisive determinant of the courses of military operations, including during the U.S. Civil War (1861–1865), which was largely conducted in southern states, which were then endemic for malaria. During that war, malaria-related morbidity and mortality were reportedly high; however, diagnoses fell into unfamiliar categories such as remittent fever, intermittent fever, and typho-malarial fever.¹ This disconnection from current concepts of malaria is unsurprising because the Civil War pre-dated the emergence of modern understanding of malaria, which began with Laveran’s discovery of the blood parasite in 1880 and Ross’s discovery of mosquito transmission in 1897.

When reading the huge Medical and Surgical History of the War of the Rebellion, one encounters descriptions of cases and events that raise doubts regarding the ability of Civil War-era medical officers to reliably discern malaria.² Three seeming paradoxes illustrate the point: first, malaria mortality rates were reportedly much higher among Black than White soldiers; second, malaria rates were reportedly lower among Union prisoners of war than their Confederate captors; and third, blackwater fever was not reported while quinine was widely used for prophylaxis. These apparent three inconsistencies have explanations consistent with current understandings of malaria but only after detailed examinations of relevant data.

The Medical and Surgical History of the War of the Rebellion documents that throughout the war, Black soldiers were much more affected by “malarial fevers” than White soldiers. Of note, during midsummer peaks of malaria activity, mean monthly prevalences were approximately 50% higher among Black (mean prevalence in August: 112 cases/1,000) than White (mean prevalence in July: 74/1,000) soldiers (Figure 1). Overall, malaria-related mortality rates were more than three times higher among Black (16.3 malaria deaths/1,000 person/years) than White (5.0 deaths/1,000 person/years) soldiers, and the case fatality rate was approximately twice as high among Black (estimate 2%) than White (estimate 1%) soldiers.^1,3 Similar comparisons could not be made for the Confederate Army because Black men were enslaved laborers but not soldiers.

Figure 1.

Malaria prevalence (remittent fever, intermittent fever, typho-malarial fever) in Union soldiers during the U.S. Civil War (1862–1865) expressed as rates/1,000 soldiers divided by racial group (White and Black).¹

The racial dichotomy in malaria incidence during the Civil War fits poorly with modern understandings of malaria susceptibility factors, particularly genetic resistance factors such as hemoglobin S for Plasmodium (P.) falciparum and Duffy negativity for P. vivax typically found in Black populations. The race-based disparities in risk also belied the prejudices of the time that held that Black soldiers were inured to tropical diseases and, in contrast to their White counterparts, could be used in tropical areas with relative impunity. Such thinking may explain, at least in part, the racial differences in malaria-related morbidity and mortality in the Union Army. Black soldiers were accepted into the largely White Union Army to meet the large need for manpower; however, Black and White soldiers were not treated equally. Black troops primarily conducted garrison and military labor (“rear echelon”) duties, often in the relatively malarious areas of the Ohio and Mississippi river valleys and along the Gulf Coast. Black soldiers were preferentially used in such places, as White soldiers actively avoided such static duties away from the battlefield.⁴ The major diagnostic category of “typho-malarial fever,” promoted by Dr. Joseph Woodward, forthrightly indicated that one could not clinically distinguish between the two diseases, especially prior to the knowledge that microorganisms caused disease.⁵ As such, it is likely that many of the febrile illnesses reported as malaria during the Civil War were caused or complicated by other or additional pathogens.³ Regardless of the natures or degrees of misclassifications of diagnoses, however, it is unlikely that acute febrile illnesses were reported differently in relation to patients’ races by the Union Army medical officers who treated them. Although one cannot authoritatively ascertain medical officers’ attitudes toward their soldier patients, if there were racial biases it would seem likely that it would have required Black soldiers to be more sick than White soldiers to be excused from duty or sent to the hospital. As such, differences in malaria-related morbidity and mortality in relation to race more likely reflect differences in the physical environments in which soldiers served and the natures of their activities rather than intrinsic genetic differences in susceptibility.

Perhaps the most informative epidemiologic studies of malaria during the U.S. Civil War were conducted by a Confederate medical officer, Major Joseph Jones.⁶ Dr. Jones noted peaks of febrile illnesses beginning in May and of deaths shortly thereafter (Figure 2A),⁷ especially in the Confederate heartland of South Carolina, Georgia, and Florida. The recurring epidemics of deadly febrile illnesses caused immense casualties among Confederate soldiers, and the death tolls were exacerbated by shortages of quinine caused by Union blockades of Confederate ports. After learning of extreme mortality rates in Union prisoners of war (POWs) at the Andersonville, GA, camp, Jones investigated. He noted that the compound was dangerously overcrowded and had a single, contaminated, water source; not surprisingly, prisoner mortality was largely due to gastrointestinal illnesses. Less understandably, Jones found that the prison guards who lived outside the compound were more affected by malaria than the prisoners.⁷

Figure 2.

Military malaria morbidity and mortality in the southern United States during the U.S. Civil War. (A) Malaria rates in the Confederate Army in South Carolina, Georgia, and Florida during 1862–1863 (no data from 1864) expressed as cases and deaths/1,000 soldiers.⁷ (B) Union prisoners of war in Andersonville (Fort Sumpter), GA, March 1864 to January 1865, as cases of malaria fever/1,000 soldiers and individual deaths ascribed directly to remittent fever.^1,7

He further observed that malaria rates began to increase in May among both the prisoners and the Confederate soldiers but, among the prisoners, the increase in rates was short lived and there were relatively few deaths (particularly compared with the thousands of deaths due to diarrheal diseases) (Figure 2B). Jones could not explain the findings; but he did note, analogously, that crowded cities were generally not centers of significant malaria activity.⁷

Note that in the midst of a mortality crisis induced by poor field sanitation, an astute medical officer discerned differences in malaria risk between the POWs and their guards.⁸ However, Jones’s observations did not lead to his understanding of the underlying mechanisms of malaria disease occurrence. Relapsing P. vivax malaria without local transmission is one key to the epidemiologic findings (and may have modern echoes in tropical refugee camps). However, principles of germ theory, insect vector transmission of disease, and relapsing P. vivax malaria still lay decades in the future. Our current knowledge of the pathophysiology and epidemiology of malaria illuminates the mysteries of Jones’s perplexing findings. Relapsing malaria cases were consistently observed in soldiers in the United States before the mosquito transmission seasons during the 1920s.⁹ The initial cases each year were in April–May and were likely relapses from liver hypnozoites obtained the previous years. Based on experiences of soldiers in the southern United States in the 1920s,³ it is reasonable to assume that during the Civil War, soldiers during field campaigns were heavily exposed to malaria, most likely predominately P. vivax.

If Anopheline mosquitoes did not breed efficiently in the fecally contaminated environment of the prison camp, local transmission of malaria among the prisoners would have been inhibited. In contrast, if mosquito propagation flourished in the woodlands outside the camp where the Confederate guards were quartered in cabins, they would have been at significant malaria risk.¹⁰

The authors of the Medical and Surgical History of the War of the Rebellion that was published in the 1880s noted the absence of blackwater fever (hemorrhagic malaria) among Union soldiers during the war. In the 1880s, blackwater fever was a “new” clinical manifestation of malaria that was being reported from southern states postwar.¹ From the first descriptions of blackwater fever by the French colonial army in Africa (Fievre Bilieuse Melanurique), the relationship between the distinctive clinical entity and prophylactic quinine use was recognized.¹¹ One of the Union Army’s most successful medical interventions was the use of prophylactic quinine, usually mixed into whiskey to ameliorate its bitter taste and enhance its palatability.¹²

It is a credible inference that blackwater fever did not affect Union soldiers during the war. Importantly, it is inconceivable that clinical expressions of malaria that included black urine, if they occurred, would have gone unnoted by Union Army medical officers.² Despite the great postwar interest in blackwater fever, Union medical officers attested to its absence during the war: “Haemorrhagic malaria fever…does not seem to have been observed in our soldiers.”¹

Literally tons of quinine were used by the Union Army in southern states during the Civil War. However, Union blockades of southern ports denied the South comparable access to the life-saving drug. Even today, blackwater fever cannot be pathologically defined, only described; among clinical hallmarks of cases are prophylactic quinine and suppressed falciparum malaria, sometimes with glucose-6-phosphate dehydrogenase deficiency.¹³

Blackwater fever was largely limited to the tropics, indicating that it was mostly associated with P. falciparum.¹⁴ It is likely that most of the malaria affecting Union soldiers was due to P. vivax and they were therefore not at increased risk of blackwater fever. To the extent they were debilitated and unable to perform military duties, soldiers with chronic malaria were evacuated North to a “better climate.” It is unlikely that many Union soldiers had chronically suppressed falciparum malaria, unlike their Confederate counterparts, who remained in endemic areas and were denied access to quinine.

The medical officers of the U.S. Civil War were largely limited to clinical observation and had very restricted perspectives regarding disease mechanisms and treatments. As such, they deserve admiration and respect for their careful clinical observations and their empirical approaches to diagnosing and treating diseases. The malaria paradoxes of the Civil War all have reasonable explanations even if the facts remain obscure. Intellectual humility and professional respect are warranted, especially when contemplating the judgments of future scientists of our work.