Rhizoctonia solani

Rhizoctonia solani (teleomorph: Thanatephorus cucumeris) is a plant pathogenic fungus with a wide host range and worldwide distribution. It was discovered more than 100 years ago. R. solani frequently exists as thread-like growth on plants or in culture, and is considered a soil-borne pathogen. R. solani is best known to cause various plant diseases such as collar rot, root rot, damping off, and wire stem. R. solani attacks its hosts when they are in their early stages of development, such as seeds and seedlings, which are typically found in the soil. The pathogen is known to cause serious plant losses by attacking primarily the roots and lower stems of plants. Although it has a wide range of hosts, its main targets are herbaceous plants. R. solani would be considered a basidiomycete fungus if the teleomorph stage were more abundant. The pathogen is not currently known to produce any asexual spores (conidia), though it is considered to have an asexual lifecycle. Occasionally, sexual spores (basidiospores) are produced on infected plants. The disease cycle of R. solani is important in management and control of the pathogen. In 1858, Julius Kuhn observed and described a fungus on diseased potato tubers and named it Rhizoctonia solani. Rhizooctonia is from Ancient Greek, ῥίζα (rhiza, 'root') + κτόνος (ktonos, 'murder'). Solanum, Latin for nightshade, is the genus of the potato. The disease caused was well known before the discovery and description of the fungus. R. solani causes a wide range of commercially significant plant diseases. It is one of the fungi responsible for brown patch (a turfgrass disease), damping off (e.g. in soybean seedlings), black scurf of potatoes, bare patch of cereals, root rot of sugar beet, belly rot of cucumber, sheath blight of rice, and many other pathogenic conditions. The fungus, therefore, has a wide host range and strains of R. solani may differ in the hosts they are able to infect, the virulence of infection, selectivity for a given host ranges from nonpathogenic to highly virulent, the temperature at which infection occurs, the ability to develop in lower soil levels, the ability to form sclerotia, the growth rate, and survival in a certain area. These factors may not always show up given the environment and host that Rhizoctonia attacks. R. solani primarily attacks seeds of plants below the soil surface, but can also infect pods, roots, leaves, and stems. The most common symptom of Rhizoctonia is 'damping off', or the failure of infected seeds to germinate. R. solani may invade the seed before it has germinated to cause this pre-emergent damping off, or it can kill very young seedlings soon after they emerge from the soil. Seeds that do germinate before being killed by the fungus have reddish-brown lesions and cankers on stems and roots. Various environmental conditions put the plant at higher risk of infection due to Rhizoctonia, the pathogen prefers warmer, wet climates for infection and growth. Postemergent damping off is a further delay in attack of R. solani. The seedling is most susceptible to disease in its early stages. Cereals in regions of England, South Australia, Canada, and India experience losses caused by R, solani every year. Roots are killed back, causing plants to be stunted and spindly. Other noncereal plants in those regions can experience brown stumps as another symptom of the pathogen. In England, this is called purple patch. R. solani can also cause hypocotyl and stem cankers on mature plants of tomatoes, potatoes, and cabbages. Strands of mycelium and sometimes sclerotia appear on their surfaces. Roots turn brown and die after a period of time. The best known symptom of R. solani is black scurf on potato tubers, which are the sclerotia of the fungus. R. solani can survive in the soil for many years in the form of sclerotia. Sclerotia of Rhizoctonia have thick outer layers to allow for survival, and they function as the overwintering structure for the pathogen. In some rare cases (such as the teleomorph) the pathogen may also take on the form of mycelia that reside in the soil, as well. The fungus is attracted to the plant by chemical stimuli released by a growing plant and/or decomposing plant residue. The process of penetration of a host can be accomplished in a number of ways. Entry can occur through direct penetration of the plant cuticle/epidermis or by means of natural openings in the plant. Hyphae come in contact with the plant and attach to the plant by which through growth they begin to produce an appressorium which penetrates the plant cell and allows for the pathogen to obtain nutrients from the plant cell. The pathogen can also release enzymes that break down plant cell walls, and continues to colonize and grow inside dead tissue. This breakdown of the cell walls and colonization of the pathogen within the host forms the sclerotia. New inoculum is produced on or within the host tissue, and a new cycle is repeated when new plants become available.The disease cycle begins as such: The pathogen is known to prefer warm, wet weather, and outbreaks typically occur in the early summer months. Most symptoms of the pathogen do not occur until late summer, thus most farmers do not become aware of the diseased crop until harvest. A combination of environmental factors has been linked to the prevalence of the pathogen, such as presence of host plant, frequent rainfall/irrigation, and increased temperatures in spring and summer. In addition, a reduction of drainage of the soil due to various techniques such as soil compaction are also known to create favorable environments for the pathogen. The pathogen is dispersed as sclerotia, and these sclerotia can travel by means of wind, water, or soil movement between host plants.