Pythium-induced
root rot is a common crop disease. When the organism kills newly emerged or emerging seedlings it is known as
damping off, and is a very common problem in fields and greenhouses.[SUP]
[1][/SUP] This disease complex usually involves other pathogens such as
Phytophthora and
Rhizoctonia.
Phytophthora is sometimes referred to as a
fungal-like organism but it is classified under a different kingdom altogether:
Chromalveolata (formerly
Stramenopila and previously
Chromista). This is a good example of
convergent evolution:
Phytophthora is morphologically very similar to true fungi yet its evolutionary history is quite distinct. In contrast to fungi, chromalveolatas are more closely related to plants than animals. Whereas fungal cell walls are made primarily of
chitin, chromalveolata cell walls are constructed mostly of
cellulose. Ploidy levels are different between these two groups; Phytophthora have
diploid (paired) chromosomes in the vegetative (growing, non-reproductive) stage of life, Fungi are almost always
haploid in this state. Biochemical pathways also differ, notably the highly conserved
Lysine synthesis path.
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,[SUP]
[2][/SUP] bare patch of
cereals,[SUP]
[3][/SUP]
root rot of
sugar beet,[SUP]
[4][/SUP] belly rot of
cucumber,[SUP]
[5][/SUP] sheath
blight of
rice,[SUP]
[6][/SUP] 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.[SUP]
[7][/SUP]
Rhizoctonia solani causing crown rot infection on Beta vulgaris L, common beet
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.[SUP]
[8][/SUP]
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.
Symptoms on common beans, Rhizoctonia damping-off, blight, and rot
[h=2]Disease cycle[
edit][/h]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 innoculum 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- 1)the sclerotia/mycelium overwinter in plant debris, soil or host plants. 2)The young hyphae and fruiting basidia(rare) emerge and produce mycelium and rarely basidiospores. 3)The very rare production of the germinating basidiospore penetrate the stoma whereas the mycelium land on the plant surface and secrete the necessary enzymes onto the plant surface in order to initiate invasion of the host plant. 4)After they mycelium 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.[SUP]
[9][/SUP]
[h=2]Environment[
edit][/h]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 and thus most farmers do not become aware of the diseased crop until harvest. A combination of environmental factors have 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.[SUP]
[10][/SUP] The pathogen is dispersed as sclerotia, and these sclerotia can travel by means of wind, water or soil movement between host plants.
Trichoderma harzianum is a
fungus that is also used as a
fungicide. It is used for
foliar application, seed treatment and soil treatment for suppression of various disease causing fungal pathogens
Trichoderma koningii is a pathogen and antagonist of fungi and also has a negative effect on certain nematodes. It is being used as a biological fungicide.
Trichoderma viride is a
fungus and a bio
fungicide. It is used for
seed and
soil treatment for suppression of various diseases caused by
fungal pathogens. It is also a pathogen in its own right, causing green mould rot of
onion.
Information from wiki-
