Helminthosporium solani is a fungal plant pathogen responsible for the plant disease known as silver scurf. Silver scurf is a blemish disease, meaning the effect it has on tubers is mostly cosmetic and affects "fresh market, processing and seed tuber potatoes." There are some reports of it affecting development, meaning growth and tuber yield. This is caused by light brown lesions, which in turn change the permeability of tuber skin and then it causes tuber shrinkage and water loss, which finally causes weight loss. The disease has become economically important because silver scurf affected potatoes for processing and direct consumption have been rejected by the industry. The disease cycle can be divided into two stages: field and storage. It is mainly a seed borne disease and the primary source of inoculum is mainly infected potato seed tubers. Symptoms develop and worsen in storage because the conditions are conducive to sporulation. The ideal conditions for the spread of this disease are high temperatures and high humidity. There are also many cultural practices that favor spread and development. There are multiple ways to help control the disease.
Signs and symptoms
Silver scurf is a plant disease of potato, which is caused by the anamorphic ascomycete fungus, Helminthosporium solani. Potato tubers are the only known host of Helminthosporium solani. It is a highly specific pathogen which does not have a secondary host or alternate host. A common symptom of this disease is blemishing on the surface of the potato tubers. These blemishes are tan and/or gray due to a loss of pigment, and they are usually irregularly shaped. Also, a post-harvest symptom can be shrinkage and shriveling of the outer tissue of the potato due to water loss. Black spots can also be found on the surface of infected tubers, which are a sign of the disease. These are made up of conidia and conidiophores of the pathogenic fungus. The conidia are characterized by being very darkly melanized and having multiple pseudosepta. Another characteristic of this fungus is the absence of motile spores. Like with many other fungal plant diseases, a diagnosis can be made by looking for the specific sexual structures of the fungus and observing them for the specific characteristics of silver scurf. Another way that silver scurf can be diagnosed is through molecular techniques, such as PCR and sequencing to identify the presence of the pathogen. The primer pair, HSF19-HSR447, has been generated to be specific for amplifying only a section of Helminthosporium solani DNA. Currently, no known host factors have been identified that have been linked to increase susceptibility or development of the disease. It seems as though the environmental conditions are what plays a major role in severity of the disease.
Disease cycle The disease cycle of silver scurf can be divided in two phases (field and storage). The primary source of inoculum is infected potato seed tubers. This inoculum is then transferred to the daughter tubers through an unknown mechanism, although indirect evidence suggests it happens when they come in direct contact or close proximity to daughter tubers. Conidia produced on the surface of seed tubers are dispersed by rain or irrigation to uninfected tubers. These conidia germinate and infect tubers. The pathogen enters through the periderm or lenticels. After that, the pathogen colonizes the periderm cells in the tuber. Infection may happen when tubers are formed and can continue in the season. In harvest (mostly in summer), silver scurf symptoms are not too apparent. However, the symptoms develop and worsen due relatively humid and warm temperatures in storage, since these conditions are conducive to sporulation. Secondary inoculum is produced by conidia, which can spread in storage by wind of ventilation while the tubers are in storage. When a seed tuber from this storage is planted, this can then carry inoculum to the field. It was believed that overwintering soil-borne inoculum wasn’t important in the disease cycle, but recent studies suggest H.solani may survive in the soil for a short period of time, which can cause more infection. This is an imperfect fungus and its teleomorph has not been described. Disease symptoms appear on tubers, but not on the haulm (vine) or roots, and are limited to the periderm, composed of phellem, phelloderm and cortical layers that replace the epidermis of the tuber. See next section (Environment) to understand the occurrence and severity of the different stages of the life cycle mentioned here.
Environment There are a number of conditions that favor the spread and development of H. solani. Usually, the temperature range of 15 – 32 °C combined with high humidity increase conidial germination. In addition to this, there are many cultural practices which affect the conditions that favor disease spread and development. These practices include: the level of H. solani present on the seed, planting and harvesting dates, crop rotations and warehouse management. It has been demonstrated that later harvest dates increase the development of the disease. It has also been demonstrated that the disease was more severe when planting densities were higher. All of these factors combined have an effect of disease spread and development.
Pathogenesis The spores can still infect and cause disease in daughter tubers in the soil for about two years. It is also possible for the pathogen to spread by growing through the roots of a potato plant to the developing tubers and cause infection. H. solani conidia are found on the outside of potato tubers, and the hyphae enter the tuber to cause disease. The pathogen can enter the tissue through wounds or natural openings, as well as being able to directly penetrate the periderm with the use of an appressorium and penetration peg. The fungus is contained in the outer layers of the potato and cannot infect very deep into the tuber. The discoloration on the periderm of the potato is formed from the loss of pigmentation caused by extreme dryness of the cell and suberin deposition. Not much is currently known about the molecular aspects of the mechanism for spread and infection of the disease, but there is currently ongoing research on this pathogen to gain a better understanding.
Disease control
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