By Meagan Iott
PP 728 Soilborne Plant Pathogen Class Project
Helminthosporium solani is the fungus known to cause Silver Scurf on potato. The fungus causes a cosmetic effect on the tubers in the form of a surface blemish which gives a dirty look to the tuber. The fungus may also cause weight loss in the potatoes as the severity increases while in storage. Sloughing of the periderm, or skin, can be a point of entry for other pathogens as well (5). While the infection first occurs in the field, the most damage occurs during storage of the potatoes. Due to the blemish effect, the most economic loss is occurred on those cultivars meant for the fresh market (3). However, economic loss is seen in processing and seed tuber potatoes as well (2). It was first introduced in the United States in 1908 but was not thought to be a major issue until the 1990s (3, 5).
H. solani is only known to have potatoes as its host. It is known to occur worldwide. However, it is thought to be of greatest economic importance in areas that possess temperate climates where tubers stored for extended periods of time. The Pacific Northwest is a location in the United States where this disease is of great importance (7).
Incubation of infected tubers or tissue under high relative humidity can produce conidia for isolation (2). Conidia aseptically picked from sporulating tissue may be spread and grown on V8 medium/agar (177 mL V-8 juice per liter), at 20-25 degrees Celsius (1). The fungus can be then maintained on V8 medium/agar.
Inoculum of the pathogen can be obtained by taking 3 mm disks from the margin of active cultures on V8 medium and transferring the disks to sterile rye grains in a flask. Grains are then incubated at 20-25 degrees Celsius for 6 weeks. Every 3 days, the flask is shaken to prevent clumping. Rye grains are prepared for culturing by soaking in an equal volume of water for 16 hours. Excess water is then removed and the rye grains autoclaved for 30 minutes on 2 consecutive days (1). Rye grain cultures also can be used for long-term storage.
Isolation from the soil is more difficult. The process involves trapping the fungus on potato tubers, washing them, and collecting the run-off. Run-off is placed in a flask with oil making the conidia rise above the oil emulsion. Molten PDA can then be added to the emulsion for plating or to make slides for observation (2).
H. solani belongs to the Moniliales order of imperfect fungi (2). It is closely related to the saprophytic species found on tree bark. The fungus is a slow growing, asexual fungus that sporulates on infected tubers in high humidity (7).
H. solani has septate, branched, and hyaline mycelium that turn from green to brown as it gets older. Its conidiophores are unbranched and septate (7). Conidiophores arise from beneath periderm of the infected lesions but not from the hyphae on the surface (2). Conidia are borne in whorls from the distal ends of the cells and have up to eight septa. The conidia are dark brown, round at the base, and pointed at the end (7). Conidia range from 15 to 64 µm in length and from 4 to 8 µm in width. Lesions with the most sporulation are brown to tan while mature lesions are silver in color (2).
Figure 1. Helminthosporium solani cultures (A) and H. solani colony with Acremonium strictum (C) ( Rivera-Varas, et al. (5)(With permission Phytopathology).
Figure 2. Scanning electron micrograph of Helminthosporium solani’s whirling conidia from conidiophores (Rivera-Varas, et al. (5)(With permission Phytopathology).
Symptoms and Signs:
Symptoms of the disease include an irregular metallic discoloration of the periderm on the tubers of the potatoes (4). The lesions may look tan to gray depending on their age and are usually contained within the periderm at the stolon end of the tuber. Lesions tend to start small but grow to cover considerable amount of the tuber’s surface area (7). As the disease progresses, parts of the periderm may slough off and cause weight loss in storage. Sloughing of the periderm can be a point of entry for other pathogens as well (5). Symptoms can be seen at harvest and will increase in severity during long-term storage of the tubers. Increased severity is due to the lesion expansion and repeated sporulation and infection cycles (4).
Symptoms are not limited to variety of potato (white, red-skinned, or russet) though they are less noticeable on russet potatoes (7). With the infection of red-skinned varieties, the skin can become partially or completely discolored (6).
3. Silver scurf originating from the
4. Silver scurf on red potatoes
5. Silver scurf following second
infection in storage
There are two phases to H. solani’s life cycle: the field and storage phase.
Tubers become infected through lenticels and directly through the periderm before harvest. The mycelium colonizes the periderm both intercellularly and intracellularly (7). The primary source of inoculum comes from infected seed tubers from the year before (2), though H. solani is thought to survive in the soil as a saprophyte (7). Low levels of inoculum can come from a previous potato crop in the field (2).
Once harvested and placed in storage, the lesions on the tubers begin to expand. Spore production and dispersal occurs causing reinfection of surrounding tubers. The humidity and temperature of these storage areas are favorable to the fungus for sporulation (7). Lack of air movement in the pile and condensation in the storage area will result in an increase in sporulation and secondary infection of tubers (6). Seed potatoes from these storage areas are then planted in the field becoming a new source of inoculum (2). Secondary infections in storage are usually seen four to five months after storage time begins, and lesions are not restricted to the stolon end of the tuber (6).
Figure 6. Life cycle for Helminthosporium solani.
There are few post-harvest fungicides available for effective control over H. solani. Thiabendazole (TBZ) has been the most widely used fungicide to control the pathogen. However, increased resistance of TBZ has caused the use of alternative forms of control mostly in the form of cultural management (2).
One of the most important management strategies is to plant disease free seed potatoes and use appropriate seed treatments to reduce the amount of inoculum being introduced into the soil (7). Adjustment of planting dates can also be a cultural management tool. The less time in the soil from planting to harvest, the less amount of infection on tubers will occur. This also results in fewer infected in storage and thus less secondary infection in the storage. Resistant cultivars for the pathogen are not available although the disease is not as severe on russet-skinned potatoes (5). Maintaining clean cutting and handling equipment is key to prevent the spread of inoculum. Storage facilities should be cleaned of all soil and plant material before and after potato storage to prevent the pathogen from overwintering or reproducing in storage areas. Crop rotation should also take place with at least two years between potato crops (3).
Storage management is a crucial tool to controlling the amount of disease. If possible, storage temperatures need to be cooled to 10 degrees Celsius as quickly as possible and then cured for 2 to 3 weeks. The holding temperature should then be lowered to 5-7 degrees Celsius. This temperature is less optimal for the pathogen to sporulate and disperse. The relative humidity should be maintained at 90-95 percent but without condensation which promotes pathogen growth. However, depending on the market conditions, these management strategies may not be available to the grower. Continual ventilation on low and frequent cycles can help to maintain optimal temperatures and a low level of condensation in the pile (6).
Figures 3-5 are from Silver Scurf Management in Potatoes (PNW 596), Oregon State University. Used by permission.
1. Dhingra, O.D., and Sinclair, J.B. 1995. Basic Plant Pathology Methods, second edition. Lewis Publishers, Boca Raton, FL.
2. Errampalli, D., Saunders, J.M., and Holley, J.D. 2001. Emergence of silver scurf (Helminthosporium solani) as an economically important disease of potato. Plant Pathology, 50:141-153.
4. Hervieux, V. Yaganza, E.S., Arul, J., and Tweddell, R.J. 2002. Effect of organic and inorganic salts on the development of Helminthosporium solani, the causal agent of potato silver scurf. Plant Disease, 86:1014-1018.
5. Rivera-Varas, V.V., Freeman, T.A., Gudmestad, N.C., and Secor, G.A. 2007. Mycoparasitism of Helminthosporium solani by Acremonium strictum. Phytopathology, 97: 1331-1337.
7. Stevenson, W.R., Lora, R., Franc, G.D., and Weingartner, D.P. 2001. Compendium of Potato Diseases, second edition. APS Press, St. Paul, MN.