Pathogens find themselves most commonly in the presence of plants other than their hosts. Under such circumstances, a pathogen fails in its ef forts tooinitiate infection. What is it that renders a plant's environment in hospitable to a pathogen except in that rare instance when the plant hap pens to be a susceptible host? It is this question which we propose to an swer by our hypothesis that, in many instances of pathogenesis by bacteria or fungi, it is an interaction between the pathogen and the carbohydrates of the host which determines the pathogen's ability to produce enzymes capa ble of degrading the host's cell walls. The production of these enzymes, then, determines whether or not a successful infection will be initiated. It ' should be stressed that only the initiation of the infective process is consid ered in this hypothesis. Once the plant actively responds to the presence of a pathogen, the ensuing metabolic responses are known to be both complex and varied.
EVIDENCE FROM SYSTEMS NOT DIRECTLY RELATED TO PHYTOPATHOLOGYAt the most fundamental level, a disease syndrome represents a summa tion of the interactions between molecules which are characteristic of two or more types of cells. This interpretation of the disease process is perhaps best described by illustration. Several systems will be considered in which interactions of molecular structures on the cell surface determine the estab lishment of a morbid state.A classic example of the involvement of surface polysaccharides in pathogenesis is the requirement for Pneumococcus (Diplococcus pneumo niae) to possess capsular polysaccharides in order to initiate successfully bacterial pneumonia in animals (38). A more recent demonstration of the involvement of cell surface elements in disease comes from studies of the relative virulence of Escherichia coli strains. E. coli is a weakly virulent 1 Supported in part by a grant from the United States Atomic Energy Com mission