Triangulating Evidence to Infer Pathways that Influence Ebola Virus Disease–Related Stigma and Clinical Findings among Survivors: An Observational Cohort Study

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  • 1 Department of Epidemiology and Biostatistics, University of California, San Francisco, California;
  • | 2 Institute for Global Health Sciences, University of California, San Francisco, California;
  • | 3 F.I. Proctor Foundation, University of California, San Francisco, California;
  • | 4 U.S. Partnership for Research on Ebola Virus in Liberia (PREVAIL), Monrovia, Liberia;
  • | 5 Division of Biostatistics, University of Minnesota, Minneapolis, Minnesota;
  • | 6 Department of Medicine, University of California, San Francisco, California;
  • | 7 Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland;
  • | 8 A.M. Dogliotti College of Medicine, University of Liberia, Monrovia, Liberia

Visible signs of disease can evoke stigma while stigma contributes to depression and mental illness, sometimes manifesting as somatic symptoms. We assessed these hypotheses among Ebola virus disease (EVD) survivors, some of whom experienced clinical sequelae. Ebola virus disease survivors in Liberia were enrolled in an observational cohort study starting in June 2015 with visits every 6 months. At baseline and 18 months later, a seven-item index of EVD-related stigma was administered. Clinical findings (self-reported symptoms and abnormal findings) were obtained at each visit. We applied the generalized estimating equation method to assess the bidirectional concurrent and lagged associations between clinical findings and stigma, adjusting for age, gender, educational level, referral to medical care, and HIV serostatus as confounders. When assessing the contribution of stigma to later clinical findings, we restricted clinical findings to five that were also considered somatic symptoms. Data were obtained from 859 EVD survivors. In concurrent longitudinal analyses, each additional clinical finding increased the adjusted odds of stigma by 18% (95% CI: 1.11, 1.25), particularly palpitations, muscle pain, joint pain, urinary frequency, and memory loss. In lagged associations, memory loss (adjusted odds ratio [AOR]: 4.6; 95% CI: 1.73, 12.36) and anorexia (AOR: 4.17; 95% CI: 1.82, 9.53) were associated with later stigma, but stigma was not significantly associated with later clinical findings. Stigma was associated with select symptoms, not abnormal objective findings. Lagged associations between symptoms and later stigma substantiate the possibility of a pathway related to visible symptoms identified by community members and leading to fear of contagion.

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Author Notes

Address correspondence to J. Daniel Kelly, Department of Epidemiology and Biostatistics, University of California, 550 16th St., San Francisco, CA 94158. E-mail: dan.kelly@ucsf.edu

Indicates cofirst authors.

‡‡Indicates cosenior authors.

Financial support: J. D. K. was supported by the National Institute of Allergy and Infectious Diseases (K23 Grant number AI135037 to J. D. K.). This funding source had no role in the content of the manuscript nor the decision for publication.

Authors’ addresses: J. Daniel Kelly, Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, Institute for Global Health Sciences, University of California, San Francisco, CA, F.I. Proctor Foundation, University of California, San Francisco, CA, and U.S. Partnership for Research on Ebola Virus in Liberia (PREVAIL), Monrovia, Liberia, E-mail: dan.kelly@ucsf.edu. Moses Badio, Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, and U.S. Partnership for Research on Ebola Virus in Liberia (PREVAIL), Monrovia, Liberia, E-mail: moses.badio@ucsf.edu. Clara Drew, Wayne T. Steward, and Sheri D. Weiser, Division of Biostatistics, University of Minnesota, Minneapolis, MN, E-mails: drewx066@umn.edu, wayne.steward@ucsf.edu, and sheri.weiser@ucsf.edu. Barthalomew Wilson, Joseph B. Cooper, Meekie Glayweon, Kumblytee Johnson, Soka J. Moses, and Dehkontee Dennis, U.S. Partnership for Research on Ebola Virus in Liberia (PREVAIL), Monrovia, Liberia, E-mails: bwilson@prevailcr.org, josephc@liberiaerp.com, meekie.glayweon@prevailcr.org, kumblytee.johnson@prevailcr.org, soka.moses@prevailcr.org, and dehkontee.dennis@prevailcr.org. Jacqueline M. Torres, Catherine Oldenburg, and Chiung-Yu Huang, Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, E-mails: jacqueline.torres@ucsf.edu, catherine.oldenburg@ucsf.edu, and chiungyu.huang@ucsf.edu. Michelle Davidson and George W. Rutherford, Department of Epidemiology and Biostatistics, University of California, San Francisco, CA, and Institute for Global Health Sciences, University of California, San Francisco, CA, E-mails: michelle.davidson@ucsf.edu and george.rutherford@ucsf.edu. Micheal C. Sneller, U.S. Partnership for Research on Ebola Virus in Liberia (PREVAIL), Monrovia, Liberia, and Department of Medicine, University of California, San Francisco, CA, E-mail: msneller@niaid.nih.gov. Cavan Reilly, U.S. Partnership for Research on Ebola Virus in Liberia (PREVAIL), Monrovia, Liberia, and Division of Biostatistics, University of Minnesota, Minneapolis, MN, E-mail: cavanr@biostat.umn.edu. Mosoka P. Fallah, U.S. Partnership for Research on Ebola Virus in Liberia (PREVAIL), Monrovia, Liberia, and Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, MD, E-mail: mosoka.fallah@prevailcr.org.

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