Bacterial infections often upregulate the plasma kinin-forming cascade of the host (the 'contact system') which is triggered by adsorption of high molecular mass kininogen (HK), coagulation factor XII (FXII) and prekallikrein (pHPK) on the host or pathogen cell surfaces. A possible activation of the contact system upon infection of the human host by major fungal pathogens of Candida species has not been extensively explored until a recent report of tight binding of HK to the cell walls of these fungi. In the current study, the adsorption of the other contact system components to the cell surfaces of Candida albicans and Candida tropicalis was characterized. FXII was found to be tightly bound by Candida germ tube forms, to a level 5-fold higher than that for HK. In contrast, pHPK bound poorly but its additional amounts could dock to the cell wall through the surface-bound HK. It was also shown that within the complex of these proteins assembled on the cell walls of fungal hyphae, pHPK could be activated by FXIIa and the active HPK effectively produced kinins from HK. It is suggested that kinins, released at the Candida cell wall, can promote host colonization by the pathogen and the development of infection.