HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by DOUGALL, A. Articles by WALTON, S. F. Search for Related Content PubMed PubMed Citation Articles by DOUGALL, A. Articles by WALTON, S. F. Related Collections Scabies Immunology

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

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.

This article has been cited by other articles:

				S. F. Walton and B. J. Currie Problems in Diagnosing Scabies, a Global Disease in Human and Animal Populations Clin. Microbiol. Rev., April 1, 2007; 20(2): 268 - 279. [Abstract] [Full Text] [PDF]

				C. WILLIS, K. FISCHER, S. F. WALTON, B. J. CURRIE, and D. J. KEMP SCABIES MITE INACTIVATED SERINE PROTEASE PARALOGUES ARE PRESENT BOTH INTERNALLY IN THE MITE GUT AND EXTERNALLY IN FECES. Am J Trop Med Hyg, October 1, 2006; 75(4): 683 - 687. [Abstract] [Full Text] [PDF]