4. BACKGROUND
This section sets out background information on the symptoms of the disease and its likelihood of survival and transmission in different circumstances. It should be noted that the factors affecting survival and transmission differ from those applicable to potato brown rot, caused by Ralstonia solanacearum. Although both are bacterial quarantine diseases of potato, they behave differently and should not be confused.
4.1 Symptoms
Symptoms are more likely to be seen in tubers than in aerial parts of the plant.
Symptoms in the potato plant
4.1.1 The earliest symptom is wilting of the leaf margins, especially on the lower leaves and often on only one side of the plant. Wilting often occurs in discrete sectors bounded by leaf veins. High temperatures during the day may cause temporary wilting with recovery at night. The symptoms may easily be mistaken for rhizoctonia, blackleg or drought. The affected areas of leaves typically appear dull and greasy. Leaves curl and progressively lose their shine with the onset of yellowing, browning and eventual necrosis (see Fera's illustrated leaflet for pictures)
4.1.2 When infected stems are cut close to ground level, discoloration of the vascular tissue is not obvious but it may ooze a creamy bacterial slime. Whole stems can wilt and die, but it is unusual for all the stems on a plant to be killed.
4.1.3 Varietal differences in reaction, as well as the lateness of expression of symptoms in the season make growing crop inspections specifically to detect the disease inappropriate.
Symptoms in the potato tuber
4.1.4 For routine screening of stocks, potato tubers should be cut transversely close to the heel (stolon) end. However, if suspicious symptoms are found in a stock, some tubers should be cut longitudinally through the heel end to check for symptoms. In the early stages the tissue around the vascular bundles appears semi-translucent, glassy and water-soaked. As the infection progresses the vascular ring becomes discoloured and the tissue around it degrades and develops colourless rot with a paste-like consistency. If the cut tuber is squeezed a pale creamy, cheese-like ooze emerges. Later, the vascular discoloration becomes a more distinct brown and the necrosis can extend into the surrounding tissue.
4.1.5 In advanced stages, the outer cortex separates from the inner cortex and the bacterium can ooze from the heel end and eyes. This may result in reddish-brown, slightly sunken and star-shaped lesions on the skin from which bacteria may ooze, causing soil particles to adhere. External symptoms are not common but advanced vascular infections can cause slightly sunken lesions to form below the skin. Secondary bacterial infections would normally result in the total breakdown of the tuber. In some interceptions, rapid rotting of the central part of the tuber has been seen to accompany rotting of the vascular ring (again, see Fera's illustrated leaflet).
4.2 Transmission and survival
4.2.1 Spread of ring rot is most common via clonal multiplication links, for example by planting infected seed. Ring rot infection can pass through one or more field generations without causing symptoms in stems and tubers. Experience from Belgium suggests that the spread of the disease in latently infected tubers is therefore very important in the case of this pathogen. Seed traceability, in the event of an outbreak, should therefore always be up (parent stock), sideways (sister stocks) and down (daughter stocks), and restrictions will need to be placed on these stocks and the premises where they have been grown.
4.2.2 Another important method of spread for potato ring rot is by physical contact from tuber to tuber, either directly or by contact with contaminated containers, equipment and premises during handling, grading, processing etc. Cross infection from stock to stock can occur, most commonly via superficial damage to tubers through direct physical contact with infected tubers or through contact with contaminated machinery, storage containers, sacks, bags or wash water. Seed tuber cutting is an ideal means of spreading ring rot within and between potato stocks.
4.2.3 In the field, spread of the disease from plant to plant is unlikely, although movement of machinery through a crop with infection in the haulm could potentially spread infection (via ooze or infected sap). There is experimental evidence that some insects (including Colorado beetle, leafhoppers and aphids) can transmit it. The risks associated with survival of the bacterium in soil are poorly defined but are usually considered to be low.
4.2.4 The pathogen can survive in de-ionised water for more than a month and there is clear evidence that contaminated wash water from infected tuber lots can transmit the pathogen to subsequent lots washed in the same water.
4.2.5 Ring rot is not known to be spread long distances by water.
4.2.6 Ring rot survives longer on dry surfaces than wet and longer at low relative humidity than at high relative humidity. The bacterium will survive in a desiccated state on equipment or machinery and in dust in stores for several years. However, once wetted or at high relative humidity the bacterium does not survive for as long in the absence of potato host material. In wet soil it can survive for several months. In drier soil, survival can be for more than a year.
4.2.7 The bacterium can survive for at least a month on machinery and considerably longer if the machinery dries rapidly and is kept under dry conditions after contamination.
4.2.8 All those involved in growing, packing or processing potatoes should be aware that the use of the same equipment to grade/process ware and seed potatoes poses a very high risk of cross-infection. This is especially the case where the stocks are from different growers, and where ware from outside the UK is handled. Regulation 6 of the Seed Potatoes (Scotland) Regulations 2000 prohibits any contact between seed and ware potatoes, except where these were produced on the same unit, unless the business concerned holds an exemption from the Scottish Government.
4.3 Other hosts
4.3.1 There was some evidence from the USA in the 1980s that sugar beet can act as a symptomless carrier of Cms, but this has not been confirmed by recent research. The risk is probably minimal for modern varieties and so no special measures are required for this crop.
4.3.2 It is clear from inoculation experiments involving wounding that some weeds, such as couch, may have the potential to act as hosts or symptomless carriers, but it is not known if weeds can act as hosts or can harbour the pathogen in natural outbreak situations. There is no known aquatic weed host to build up inoculum levels in watercourses. No specific measures are therefore required for weeds in the event of an outbreak.