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Author Notes:

E-mail: katie.mues@gmail.com

Conceived and designed the experiments: KEM MK PJL LMF DGK.

Performed the experiments: PJL.

Analyzed the data: KEM.

Contributed reagents/materials/analysis tools: PJL DA LMF.

Wrote the paper: KEM DGK LMF PJL DA.

The authors have declared that no competing interests exist.

The content is solely the responsibility of the authors and does not necessarily represent the official views of the Centers for Disease Control and Prevention.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Subjects:

Research Funding:

This study was funded by grants from the Office of Women’s Health (http://www.cdc.gov/women/), U.S. Centers for Disease Control and Prevention, Atlanta, Georgia; and the WHO/UNDP/World Bank Special Programme for Research and Training in Tropical Diseases (Filariasis Operational Research Project No. 950568) (http://apps.who.int/tdr/index.html).

KEM was supported in part by Emory University, Laney Graduate School.

Keywords:

  • Lymphedema
  • Antibody response
  • Bacterial pathogens
  • Antibodies
  • Enzyme-linked immunoassays
  • Fungal pathogens
  • Streptococcal infections
  • Candida

Changes in Antibody Levels during and following an Episode of Acute Adenolymphangitis (ADL) among Lymphedema Patients in Léogâne, Haiti

Tools:

Journal Title:

PLoS ONE

Volume:

Volume 10, Number 10

Publisher:

, Pages e0141047-e0141047

Type of Work:

Article | Final Publisher PDF

Abstract:

Introduction Episodes of acute adenolymphangitis (ADL) are often the first clinical sign of lymphatic filariasis (LF). They are often accompanied by swelling of the affected limb, inflammation, fever, and general malaise and lead to the progression of lymphedema. Although ADL episodes have been studied for a century or more, questions still remain as to their etiology. We quantified antibody levels to pathogens that potentially contribute to ADL episodes during and after an episode among lymphedema patients in Léogâne, Haiti. We estimated the proportion of ADL episodes hypothesized to be attributed to specific pathogens. Methods We measured antibody levels to specific pathogens during and following an ADL episode among 41 lymphedema patients enrolled in a cohort study in Léogâne, Haiti. We calculated the absolute and relative changes in antibody levels between the ADL and convalescent time points. We calculated the proportion of episodes that demonstrated a two-fold increase in antibody level for several bacterial, fungal, and filarial pathogens. Results Our results showed the greatest proportion of two-fold changes in antibody levels for the carbohydrate antigen Streptococcus group A, followed by IgG2 responses to a soluble filarial antigen (BpG2), Streptococcal Pyrogenic Exotoxin B, and an antigen for the fungal pathogen Candida. When comparing the median antibody level during the ADL episode to the median antibody level at the convalescent time point, only the antigens for Pseudomonas species (P-value = 0.0351) and Streptolysin O (P-value = 0.0074) showed a significant result. Conclusion Although our results are limited by the lack of a control group and few antibody responses, they provide some evidence for infection with Streptococcus A as a potential contributing factor to ADL episodes. Our results add to the current evidence and illustrate the importance of determining the causal role of bacterial and fungal pathogens and immunological antifilarial response in ADL episodes.

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This is an Open Access work distributed under the terms of the Creative Commons Universal : Public Domain Dedication License (http://creativecommons.org/publicdomain/zero/1.0/).

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