Abstract
Over the years several hypotheses have been put forward to account for the “fungistatic” action of phosphite against Phytophthora, but biochemical detail is scarce. The complexity of the interaction between host and pathogen is such that no single aspect of phosphite chemistry is able to explain all the various effects of phosphite that have been observed. For instance, why does the temporal efficacy of phosphite vary up to ten-fold between horticultural and native plants? And how can this observation be reconciled with the fact that pathogen growth in vitro is not inhibited by the concentration of phosphite that gives disease control in planta? This talk will outline a biochemical model that explains how and why phosphite has the effects on Phytophthora that it has. However, when considering models of phosphite action it should be noted that “Essentially, all models are wrong, but some are useful” (George Box), and within this context “usefulness” can be defined as increased disease control and better management of Phytophthora dieback. The model suggested that the efficacy of phosphite in controlling disease caused by Phytophthora may be enhanced by maintaining high levels of extracellular calcium. Results from a glasshouse trial confirmed this, and showed that although phosphite and calcium are not lethal to the pathogen, combined treatments of soil calcium supplementation and foliar phosphite application were synergistic in controlling infection caused by Phytophthora cinnamomi in Banksia leptophilia. Rigorous biochemical testing is needed to confirm that inhibition of the calcium-dependent ATPase by phosphite does in fact cause the synergistic effect. However, in the absence of evidence to the contrary, the suggested model of phosphite action has proved useful.