Malaria Relapses Following Parasite-Free Blood Transfusions in the U.S. Army during the Korean War

G. Dennis Shanks Australian Defence Force Malaria and Infectious Diseases Institute, Enoggera, Australia;
University of Queensland, School of Public Health, Brisbane, Australia

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Michael Waller University of Queensland, School of Public Health, Brisbane, Australia

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ABSTRACT.

Latent Plasmodium vivax parasites in the liver known as hypnozoites activate causing malaria relapses months after the original infection. The putative initiation signal is unknown. Plasmodium falciparum infections appear to trigger P. vivax relapses and initiation of relapse may be triggered by hemolysis or fever. The U.S. Army hospital records from the Korean War (> 500,000 individual records) were used to determine whether there was an association between blood transfusion and vivax malaria relapse. Importantly, blood for transfusion was collected in the United States, so the risk of transmission of malaria parasites was minimal. Blood transfusion (largely for combat trauma) was a risk factor for subsequent vivax malaria (relative risk 2.54, 95% CI 2.15–2.99, P < 0.0001). As expected, blood transfusion was not a risk factor for subsequent dysentery, but transfusion was a risk factor for subsequent hepatitis. Blood transfusion causing an increased heme delivery to the liver and a subsequent redox signal within hepatocytes may partially explain hypnozoite activation leading to relapses of vivax malaria.

Author Notes

Address correspondence to G. Dennis Shanks, Australian Defence Force Malaria and Infectious Diseases Institute, Weary Dunlop Dr., Gallipoli Barracks, Enoggera, 4051 Queensland, Australia. E-mail: dennis.shanks@defence.gov.au

Financial support: G. D. S. is an employee of the Australian Defence Organization and a retired U.S. Army Medical Corps Officer. No specific funding was given for this epidemiological study.

Disclaimer: The opinions expressed are those of the authors and do not necessarily reflect those of the Australian Defense Force or the U.S. Department of Defense.

Authors’ addresses: G. Dennis Shanks, Australian Defence Force Malaria and Infectious Disease Institute, Gallipoli Barracks, Enoggera, Queensland, Australia, and University of Queensland School of Public Health, Brisbane, Queensland, Australia, E-mail: dennis.shanks@defence.gov.au. Michael Waller, University of Queensland, School of Public Health, Herston, Queensland, Australia, E-mail: m.wallter@uq.edu.au.

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