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Am. J. Trop. Med. Hyg., 73(5), 2005, pp. 977-984
Copyright © 2005 by The American Society of Tropical Medicine and Hygiene

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IDENTIFICATION AND CHARACTERIZATION OF SARCOPTES SCABIEI AND DERMATOPHAGOIDES PTERONYSSINUS GLUTATHIONE S-TRANSFERASES: IMPLICATION AS A POTENTIAL MAJOR ALLERGEN IN CRUSTED SCABIES

ANNETTE DOUGALL, DEBORAH C. HOLT, KATJA FISCHER, BART J. CURRIE*, DAVID J. KEMP, AND SHELLEY F. WALTON
Tropical and Emerging Infectious Diseases Division, Menzies School of Health Research, Darwin, Northern Territory, Australia; Institute of Advanced Studies, Charles Darwin University, Darwin, Northern Territory, Australia; Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia; The Australian Centre for International and Tropical Health and Nutrition, The University of Queensland, Brisbane, Queensland, Australia; Northern Territory Clinical School, Flinders University, Darwin, Northern Territory, Australia

The astigmatid mite Sarcoptes scabiei is the causative agent of scabies, a highly infectious parasitic disease of the skin. Although the mite causes marked hypersensitivity reactions, particularly in crusted (severe) scabies, little is known about the specific scabies mite molecules involved in such immunologic responses. We have identified six genes encoding scabies mite homologues of mu and delta-like glutathione S-transferases (GSTs) as well as novel house dust mite GSTs. A mu class S. scabiei GST was subcloned into a prokaryotic expression system. The purified recombinant protein rSsGST01 reacted strongly with IgE and IgG4 in sera from crusted scabies patients. This response was not observed with control antigens or with ordinary scabies and uninfested patient sera. In addition, the specific IgE response to rSsGST01 did not correlate with the total IgE level of the patient. These results suggest that GST may play a role in the pathophysiology associated with crusted scabies.


Received November 16, 2004. Accepted for publication April 30, 2005.

Acknowledgments: The authors thank Professor Philip Board of the John Curtin School of Medical Research for helpful comments.

Financial support: This work was funded by Australian National Health and Medical Research Council Medical Genomics Grant 219175, Project Grant 137205, Program Grant 290208, and The Channel 7 Children’s Research Foundation.

* Address correspondence to Bart J. Currie, The Menzies School of Health Research, P.O. Box 41096, Casuarina, Darwin, Northern Territory 0811, Australia. E-mail: bart{at}menzies.edu.au

Authors’ addresses: Annette Dougall, Deborah C. Holt, Bart J. Currie, and Shelley F. Walton, The Menzies School of Health Research, P.O. Box 41096, Casuarina, Darwin, Northern Territory 0811, Australia, Telephone: 61 8 89228196, Fax: 61 8 89275187. Katja Fischer and David J. Kemp, The Queensland Institute of Medical Research, P.O. Box Royal Brisbane Hospital, Queensland 4029, Australia, Telephone: 61 7 33620402, Fax: 61 7 33620104.

Reprint requests: Bart J. Currie, The Menzies School of Health Research, P.O. Box 41096, Casuariva, Darwin, Northern Territory 0811, Australia, E-mail: bart{at}menzies.edu.au.




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