Thanatephorus cucumeris is a basidiomyceteous fungus, the anamorph Rhizoctonia solani belongs to the Agonomycetales which do not produce conidia. R. solani is considered to be an aggregate species including different (host-specific) entities which may be differentiated by anastomosis grouping (AG). It is a plant pathogenic fungus with a wide host range and worldwide distribution. This plant pathogen was discovered more than 100 years ago. Rhizoctonia solani frequently exists as thread-like growth on plants or in culture, and is considered a soil-borne pathogen. Rhizoctonia solani is best known to cause various plant diseases such as collar rot, root rot, damping off and wire stem.
Rhizoctonia 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 in seedlings, as well as 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 Rhizoctonia solani may differ in the hosts they are able to infect, the virulence of infection, selectivity for a given host ranges from non-pathogenic 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, the survival in a certain area. These factors may or may not show up given the environment and host that Rhizoctonia attacks.
Rhizoctonia 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. Rhizoctonia 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.
There are various environmental conditions that put the plant at higher risk of infection due to Rhizoctonia, the pathogen prefers warmer wet climates for infection and growth. Post-emergent damping off is a further delay in attack of Rhizoctonia solani. The seedling is most susceptible to disease in its juvenile stage.
Cereals in regions of England, South Australia, Canada, and India experience losses caused by Rhizoctonia solani every year. Roots are killed back, causing plants to be stunted and spindly. Other non cereal plants in those regions can experience brown stumps as another symptom of the pathogen. In England, this is called purple patch. Rhizoctonia solani can also cause hypocotyl and stem cankers on mature plants of tomatoes, potatoes and cabbage. Strands of mycelium and sometimes sclerotia appear on their surfaces. Roots will turn brown and die after a period of time. The best known symptom of Rhizoctonia solani is black scurf on potato tubers which are the sclerotia of the fungus.
Rhizoctonia 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 mycelium 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 will 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 is what 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 sclerotia/mycelium overwinter in plant debris, soil or host plants.
The young hyphae and fruiting basidia (rare) emerge and produce mycelia and rarely basidiospores.
The very rare production of the germinating basidiospores penetrate the stoma whereas the mycelia land on the plant surface and secrete the necessary enzymes onto the plant surface in order to initiate invasion of the host plant.
After the mycelia successfully invade the host, necrosis and sclerotia form in and around the infected tissue which then leads to the various symptoms associated with the disease such as soil rot, stem rot, damping off etc. and the process begins all over again