Host–pathogen interactions modulated by heat treatment

Abstract

Prestorage heat treatment appears to be a promising method of postharvest control of decay. Heat treatments against pathogens may be applied to fresh harvested commodities by hot water dips, by vapour heat, by hot dry air or by a very short hot water rinse and brushing. Heat treatments have a direct effect slowing germ tube elongation or of inactivating or outright killing germinating spores, thus reducing the effective inoculum size and minimising rots. Heat treatment can also indirectly affect decay development via physiological responses of the fruit tissue. These responses include inducing antifungal-like substances that inhibit fungal development in the fruit tissue, or enhancing wound healing. Heat treatment can induce PR proteins such as chitinase and β-1,3 glucanase, stabilise membranes, elicit antifungal compounds, or inhibit the synthesis of cell wall hydrolytic enzymes (polygalacturonases), and delay the degradation rate of pre-formed antifungal compounds that are present in unripe fruit. Additionally, curing, as a heat treatment can cause the disappearance of wax platelets normally present in untreated fruit and make the fruit surface relatively homogeneous. Thus, cuticular fractures, microwounds and most stomata are partially or completely filled, and early-germinated spores are encapsulated and inactivated by molten wax. The occlusion of possible gaps for wound pathogens as well as the encapsulation and inactivation of early-germinated spores have been considered as additional factors in fruit protection against decay.