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Infection and Immunity, December 1999, p. 6637-6642, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Germ Tubes and Proteinase Activity Contribute to Virulence of Candida albicans in Murine Peritonitis

Marianne Kretschmar,1 Bernhard Hube,2 Thomas Bertsch,3 Dominique Sanglard,4 Renate Merker,5 Meike Schröder,1 Herbert Hof,1 and Thomas Nichterlein1,*

Institute of Medical Microbiology and Hygiene1 and Institute of Clinical Chemistry,3 Faculty of Clinical Medicine Mannheim, University of Heidelberg, 68167 Mannheim, Institute for General Botany, Applied Molecular Biology III, University of Hamburg, 22609 Hamburg,2 and Department of Electrical Engineering IEE, University of Technology, 01062 Dresden,5 Germany, and Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, CH-1011 Lausanne, Switzerland4

Received 7 June 1999/Returned for modification 6 July 1999/Accepted 27 August 1999

Peritonitis with Candida albicans is an important complication of bowel perforation and continuous ambulatory peritoneal dialysis. To define potential virulence factors, we investigated 50 strains of C. albicans in a murine peritonitis model. There was considerable variation in their virulence in this model when virulence was measured as release of organ-specific enzymes into the plasma of infected mice. Alanine aminotransferase (ALT) and alpha -amylase (AM) were used as parameters for damage of the liver and pancreas, respectively. The activities of ALT and AM in the plasma correlated with invasion into the organs measured in histologic sections and the median germ tube length induced with serum in vitro. When the activity of proteinases was inhibited in vivo with pepstatin A, there was a significant reduction of ALT and AM activities. This indicates that proteinases contributed to virulence in this model. Using strains of C. albicans with disruption of secreted aspartyl proteinase gene SAP1, SAP2, SAP3, or SAP4 through SAP6 (collectively referred to as SAP4-6), we showed that only a Delta sap4-6 triple mutant induced a significantly reduced activity of ALT in comparison to the reference strain. In contrast to the Delta sap1, Delta sap2, and Delta sap3 mutants, the ALT induced by the Delta sap4-6 mutant could not be further reduced by pepstatin A treatment, which indicates that Sap4-6 may contribute to virulence in this model.

* Corresponding author. Mailing address: Institute of Medical Microbiology and Hygiene Mannheim, Faculty of Clinical Medicine, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. Phone: (49) 0621/383 2695. Fax: (49) 0621/383 3816. E-mail: thomas.nichterlein{at}imh.ma.uni-heidelberg.de.

Infection and Immunity, December 1999, p. 6637-6642, Vol. 67, No. 12
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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