Brown Recluse Spider Bite Mediated Hemolysis: Clinical Features, a Possible Role for Complement Inhibitor Therapy, and Reduced RBC Surface Glycophorin A as a Potential Biomarker of Venom Exposure

The venom of Loxosceles reclusa (Brown Recluse spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosi...

Full description

Saved in:
Bibliographic Details
Published inPloS one Vol. 8; no. 9; p. e76558
Main Authors Gehrie, Eric A., Nian, Hui, Young, Pampee P.
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 27.09.2013
Public Library of Science (PLoS)
Subjects
Online AccessGet full text
ISSN1932-6203
1932-6203
DOI10.1371/journal.pone.0076558

Cover

More Information
Summary:The venom of Loxosceles reclusa (Brown Recluse spider) can cause a severe, life-threatening hemolysis in humans for which no therapy is currently available in the USA beyond supportive measures. Because this hemolysis is uncommon, relatively little is known about its clinical manifestation, diagnosis, or management. Here, we aimed to clarify the clinical details of envenomation, to determine the efficacy of the complement inhibitor eculizumab to prevent the hemolysis in vitro, and to investigate markers of exposure to Brown Recluse venom. We performed a 10-year chart review of cases of Brown Recluse spider bite-mediated hemolysis at our institution. We also designed an in vitro assay to test the efficacy of eculizumab to inhibit hemolysis of venom exposed red blood cells. Finally, we compared levels of CD55, CD59 and glycophorin A on venom exposed versus venom-naïve cells. Most victims of severe Brown Recluse spider mediated hemolysis at our institution are children and follow an unpredictable clinical course. Brown Recluse spider bite mediated hemolysis is reduced by 79.2% (SD=18.8%) by eculizumab in vitro. Erythrocyte glycophorin A, but not CD55 or CD59, is reduced after red blood cells are incubated with venom in vitro. Taken together, our laboratory data and clinical observations indicate that L. reclusa venom exposure results in non-specific antibody and complement fixation on red blood cells, resulting in complement mediated hemolysis that is curtailed by the complement inhibitor eculizumab in vitro. Glycophorin A measurement by flow cytometry may help to identify victims of L. reclusa envenomation.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
Competing Interests: The authors have read the journal's policy and have the following conflicts: 1) The study was funded in part by a grant from Alexion Pharmaceuticals, the manufacturer of eculizumab, to EG and PPY. This does not alter the authors' adherence to all of the PLOS ONE policies on sharing data and materials. Dr. HN has declared that no competing interest exists for her contribution.
Conceived and designed the experiments: EG PYY. Performed the experiments: EG. Analyzed the data: EG PYY HN. Contributed reagents/materials/analysis tools: EG PYY HN. Wrote the manuscript: EG PYY HN.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0076558