Mechanisms for the infection of potato tubers by the soft rot organism Erwinia carotovora var, atroseptioa (van Hall) Holland, and associated defence mechanisms

Abstract

The increasing losses of potato tubers in storage due to soft rot spoilage have emphasised the need for detailed studies of the entry and spread of the pathogen and the action of the defence mechanisms of the potato at an ultrastructural level.

The studies have shown that the tuber may be infected through fresh wounds or lenticels under conditions of high relative humidity, providing sufficient inoculum is present and, in the case of lenticels, the conditions before inoculation have been suitable.

The effects of the environment on the physical barriers and consequently bacterial spread are complex. Observation of the formation of suberin and melanin at the infection interface have shown that the former may hinder bacterial spread: the role of the latter is more obscure.

Light microscopy has shown that the pattern of initial colonisation is highly temperature dependant. Colonisation through lenticels is quicker at first than through fresh wounds probably due to the differences in anatomy, although quantitatively large amounts of inoculum are involved in the latter under most conditions.

Once inside the tuber the bacterium spreads through the storage parenchyma as zoned colonies aligned in one direction during the early stages, but after the host cells have been macerated the cells of the pathogen become uniformly distributed between the potato cells.

Vascular spread is less common, and the bacteria are enclosed in the xylem and phloem by the suberised, closely packed cells of the vascular parenchyma, although some pectolysis and subsequent melanin formation occurs outside the bundles for distances of up to 500 µm.

Tissue degradation involves the destruction of the cytoplasm, as well as the cell wall. Characteristically membrane rupture is associated with the enlargement of microbodies. Although cells containing calcium oxalate monohydrate are colonised intracellularly, the crystals do not appear to be utilised.

The significance of these findings in relation to the disease as a whole are discussed, and possible practical implications for the grower and user of potatoes are considered.

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