English names: Potato Wart Disease
Nordic names: Kartoffelbrok (DK), Perunasyöpä (FI), Potetkreft (NO), Potatiskräfta (SE)
Estonian name: Kartulivähk
Major host plants
Potatoes are the only cultivated host, but wild Solanum spp. can be infected.
Galls are produced on tuber initials and tubers, but not on the roots. In tubers, the eyes are infected; they develop into characteristic, warty, cauliflower-like protuberances. The galls vary from pea-size up to 8 cm in diameter; they are initially whitish or green if exposed to light, but gradually darken and eventually rot and disintegrate. The whole tuber may be entirely replaced by the warty proliferation. Similar warts occur on stem basis and stolons.
Aerial symptoms are not usually apparent, although there may be a reduction in plant vigour. Small greenish warts may form in the position of the aerial buds at the stem. Leaves may also be attacked.
S. endobioticum originates in South America, from where it was introduced into Europe in the 1880s. It spread widely in Europe, but statutory measures finally restricted its distribution and it has spread only to a limited extent to other parts of the world.
A map can be downloaded from EPPO's website. See instructions here.
The disease is favored by cool, wet soils. The fungus produces sporangia containing 200-300 motile zoospores. In the spring, at temperatures above 8°C and sufficient moisture, the long-lived winter sporangium in decaying warts germinates and releases zoospores in the soil. The zoospores are able to move in soil water and reach and invade the living host. The host cells become enlarged and the enclosed fungus forms a short-lived summer sporangium, from which numerous zoospores are rapidly dispersed. The zoospores reinfect the surrounding cells which again produce summer sporangia. Warts are formed when the tissue are stimulated to divide and enlarge.
Under certain conditions of stress, such as water shortage, the zoospores may transform within the host cell to the resistant, thick-walled resting sporangium. This matures and is released into the soil from rotting warts. Resting sporangia can remain viable for at least 30 years and are found at depths of up to 50 cm.
Many pathotypes (strains) of the fungus exist, defined by their virulence on differential potato cultivars.
S. endobioticum has a very limited capacity for natural spread. The pathogen is primarily carried in infected potato tubers or in soil. The sporangia resist digestion by animals, and can thus be spread in faeces.
Detection and inspection
Symptoms associated with Potato Wart Disease may appear similar to some of the symptoms caused by Powdery Scab (Spongospora subterranea f. sp. subterranea), Potato Smut (Thecaphora solani), and ‘Pseudo-wart,’ a proliferation of eyes that may be a physiological or varietal response or, alternatively, induced by chemical factors. Full confirmation of Potato Wart Disease requires a laboratory diagnosis.
Pest status and importance
Potato Wart Disease was the most serious disease in potatoes and quarantine legislations have been in force for nearly 100 years throughout the world. Once the pathogen has been introduced into a field, the whole crop may be unmarketable; moreover the fungus is so persistent that potatoes cannot be grown again for many years, nor can the land be used for any plants intended for trade and export.
Pathotype 1 is controlled by use of resistant cultivars. New pathotypes of the fungus, capable of attacking potato varieties that were previously resistant, have developed in several European countries. It is most important to prevent the spread of these new pathotypes.
Source of information
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Author: Jorma Räutapaa