Barley, oat and wheat were used as both inappropriate hosts (IH) and appropriate hosts (AH) for three formae speciales of the fungus Blumeria graminis, the causal agent of powdery mildew disease. Treatment with either the glucose analog 2-deoxy-D-glucose (DDG) or with D-mannose dramatically suppressed penetration resistance in IH and to a much lesser extent in AH combinations. Other effects of DDG and D-mannose were strikingly dissimilar. DDG greatly reduced localized autofluorescence at fungal attack sites on epidermal cells, and prevented hypersensitive epidermal cell death (HR). D-mannose had little effect on autofluorescence or HR. DDG arrested the development of fungal haustoria and apparently prohibited biotrophy leading to secondary hyphae. D-mannose allowed haustorial development and functional biotrophy leading to the production of elongating secondary hyphae. This suggests that B. graminis is in some way capable of utilizing D-mannose as a carbon substrate. Results with IH combinations paralleled those of known mlo-barley responses to DDG and D-mannose. Results are discussed in relation to specific physiological processes known to be influenced by either DDG or by D-mannose, or by both compounds. (C) 2003 Elsevier Science Ltd. All rights reserved.