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Antimicrobial Agents and Chemotherapy, February 2003, p. 475-479, Vol. 47, No. 2
0066-4804/03/$08.00+0 DOI: 10.1128/AAC.47.2.475-479.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Departments of Medicine,1 Pathobiology, University of Washington, Seattle, Washington,2 Cerus Corporation, Concord, California3
Received 24 June 2002/ Returned for modification 26 June 2002/ Accepted 28 October 2002
Trypanosoma cruzi, the protozoan pathogen that causes Chagas' disease, can be found in the blood of infected individuals for their entire life span. This presents a serious challenge in safeguarding blood products. Transmission of T. cruzi from blood products is a frequent occurrence in Latin America, where Chagas' disease is endemic. This study was designed to determine whether T. cruzi could be inactivated in human platelet concentrates and plasma by a photochemical treatment process with long-wavelength UV A light (UVA, 320 to 400 nm) plus the psoralen amotosalen HCl (Cerus Corporation). Units of platelet concentrates (300 ml) and plasma (300 ml) were intentionally contaminated with approximately 106 T. cruzi trypomastigotes, the T. cruzi form found in the bloodstream, per ml. The viability of T. cruzi after photochemical inactivation was determined by their ability to replicate in 3T3 fibroblasts. Controls, including treatment with 150 µM amotosalen or 3 J/cm2 UVA alone, did not lead to reduction of the viability of T. cruzi in plasma or platelet concentrates. However, treatment with 150 µM amotosalen plus 3 J/cm2 UVA inactivated T. cruzi to undetectable levels in plasma and platelet concentrates. This represented a >5.4-log reduction of T. cruzi in platelet concentrates and >5.0-log reduction of T. cruzi in plasma. We conclude that the amotosalen plus UVA photochemical inactivation technology is effective in inactivating high levels of protozoan pathogens, such as T. cruzi, in platelet concentrates and plasma, as has been previously shown for numerous viruses and bacteria.
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