33 



critically by the different soil treatments. In fumigated soils in 



which the pathogen was added every 7 days and in nonfumigated soils, 

 pathogen population and infection incidence were related. The inoculum 

 density of the pathogen was not related to infection incidence when the 

 pathogen was maintained in fumigated, nonamended soils; in fumigated, 

 amended soils; or in fumigated soils in which recolonization by other 

 organisms was inhibited. The ability of the pathogen to infect the 

 host decreased with time in fumigated, nonamended soils. Although the 

 pathogen population increased, the incidence of infection did not in- 

 crease. In fumigated, nonrecolonized soils the incidence of infection 

 was nearly lOOfo during the duration of the experiments. The high infec- 

 tion incidence was attributed to the high efficiency of the pathogen for 

 host infection in the absence of competing organisms. The decrease of 

 the pathogen population in the nonrecolonized soil probably was due to 

 the exhaustion of nutrient sources or to the accumulation of toxic metab- 

 olites. At present, it is not possible to explain the results obtained 

 when the pathogen was maintained in fumigated, amended soils. The path- 

 ogen population was relatively stable, but the infection incidence in- 

 creased and then decreased with time. The low incidence of infection k 

 days after fumigation, when the pathogen and antagonists were first 

 added, may have been due to antagonisms by A. ochraceus , which was the 

 predominant antagonist at that time. Perhaps the population of T. 

 harzianum , which was dominant when the incidence of infection was high, 

 was not as capable of restricticting the pathogenic activities of the 

 pathogen. The decrease in infection incidence with time may have been 

 due to increased antagonism as the combination of populations of P. 

 restrictum and T. harzianum increased during the later stages of succes- 

 sion. 



