Rhizoctonia potato

Rhizoctonia potato DEFAULT
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Image related to Potato (Solanum tuberosum)-Rhizoctonia Canker (Black Scurf)

Black masses (scurf) can be seen on the tuber surface.

Photo from OSU Extension Plant Pathology Slide Col

Image related to Potato (Solanum tuberosum)-Rhizoctonia Canker (Black Scurf)

Reddish-brown to brown lesions can be seen on stems, stolons, and roots.

Photo from OSU Extension Plant Pathology Slide Col

Image related to Potato (Solanum tuberosum)-Rhizoctonia Canker (Black Scurf)

Stem lesions are characteristic of Rhizoctonia canker.

Photo by Cynthia M. Ocamb, 1998.

By P. B. Hamm and C. M. Ocamb

CauseRhizoctonia solani, a fungus that is a common soil inhabitant and has a wide host range. Seed pieces can carry the fungus but soilborne inoculum can be equally as damaging.

Symptoms When sprouts are infected before emergence, they may be girdled and killed by reddish to dark brown girdling cankers found on the stems at or below ground. Stems seem to become more resistant to infection once they emerge. If plants are infected later in their development, they may have reddish-brown to brown lesions on stems, stolons, tubers, and roots. Aerial tubers may form on the stem if the fungus has girdled the stem below. Leaf curl, like that caused by the Potato leafroll virus, may occur. Tubers may have black bodies (scurf) on the surface and they are not easily removed. While the bodies do not affect the tuber's interior, enough of them on the surface of potatoes being grown for the fresh market will cause rejection.

Cultural control

  • Rotate out of potatoes, preferably for 3 years.
  • Shallow planting followed by gradual hilling-up speeds emergence and reduces damage.
  • Avoid over-irrigating early in the season. Cooling soil with irrigation slows emergence and favors the fungus.
  • If possible, avoid seed lots that contain sclerotia.
  • Warm seed before planting.
  • To encourage more rapid emergence, plant deep but cover with a shallow layer of soil.
  • The disease may be more severe when following sugar beets, alfalfa, or clover that was plowed down the spring of planting.
  • Delaying planting until soil temperatures warm and soil moisture is drier will reduce infection.

Chemical control

  • Elatus (Group 11 + 7) at 0.34 to 0.5 oz/1000 row feet applied in a 7-inches or less band either in-furrow at planting. Preharvest interval is 14 days. 12-hr reentry.
  • Evito 480 SC at 0.16 to 0.24 fl oz/1000 ft row. Do not apply within 7 days of harvest. 12-hr reentry.
  • Evolve Potato Seed Piece Treatment at 0.75 lb/100 lb seed pieces.
  • Headline at 0.4 to 0.8 fl oz/1000 row feet. Apply spray in-furrow at planting. 12-hr reentry.
  • Heads Up at 0.035 oz/34 fl oz water/220 to 582 lb seed pieces will stimulates pest suppression system of plants. Efficacy unknown. 12-hr reentry. O
  • Maxim MZ at 0.5 lb/100 lb seed pieces or Maxim 4FS at 0.08 to 0.16 oz/100 lb seed pieces. 12-hr reentry for Maxim 4FS; 24-hr reentry for Maxim MZ
  • Moncut 70DF at 0.75 to 1.0 lb/A in-furrow in at least 5 gal water/A. Rotation crop restrictions on label. 12-hr reentry.
  • OSO 5% SC (Group 19) at 3.75 to 13 fl oz/A on 7- to 14-day intervals. Can be applied the day of harvest. 4-hr reentry. O
  • Quadris Flowable at 0.4 to 0.8 fl oz/1000 row feet applied in a 7-inches or less band either in-furrow at planting or as a directed spray at cultivation. 4-hr reentry.
  • Quadris Ridomil Gold at 0.82 fl oz/1000 row feet applied in-furrow using 3 to 15 gal water/A. See label for reentry intervals.
  • Regalia (Group P5) at 1 to 2 quarts/A as an in-furrow treatment. 4-hr reentry. O

Biological control

  • Amplitude at 3.2 to 4.8 fl oz/100 lb seed pieces, 6 to 8 fl oz per 1,000 ft row as an in-furrow treatment, or 3 to 4 quarts/A as a chemigation treatment on 14- to 21-day intervals. Preharvest interval is 0 days. 4-hr reentry. O
  • Double Nickel LC at 0.5 to 6 quarts/A on 3- to 10-day intervals. Can be applied the day of harvest. 4-hr reentry. O
  • Stargus at 6 to 8 fl oz per 1,000 ft row as an in-furrow treatment, 3 to 4 quarts/A as a soil drench on 10- to 14-day intervals, or 3 to 4 quarts/A as a chemigation drip treatment on 14- to 21-day intervals. Preharvest interval is 0 days. 4-hr reentry. O
Sours: https://pnwhandbooks.org/plantdisease/host-disease/potato-solanum-tuberosum-rhizoctonia-canker-black-scurf
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Bulletin #$2273, Rhizoctonia Disease on Potatoes (PDF)

Steven B. Johnson, crops specialist University of Maine Cooperative Extension. Simeon S. Leach, Ph.D., Research Plant Pathologist, USDA Agriculture Research Service

For information about UMaine Extension programs and resources, visit extension.umaine.edu.
Find more of our publications and books at extension.umaine.edu/publications/.


Rhizoctonia solani sclerotia on potato tubers.

Rhizoctonia disease of potato often referred to as black scurf, is caused by the fungus Rhizoctonia solani Kühn. The disease is found in most potato-producing areas of the world.

It was reported in Maine in 1913 by Morse and Shapovalo in the Maine Agricultural Station Bulletin #230, “The Rhizoctonia Disease of Potatoes.” This bulletin presents a very good explanation of the disease symptoms and control.

The importance of the Rhizoctonia disease complex of potatoes has long been debated. It is now considered a major cause of crop losses in Maine and potato-producing areas.

Life cycle

There are two phases of the disease: the stem and stolon phase and the tuber phase. The former usually occurs early in the growing season in the form of lesions or nipping off of the growing tips of sprouts, stems or stolons. This can occur throughout the growing season.

The second and most noticeable phase is the formation of sclerotia on tubers. Sclerotia are survival structures of the pathogen. These sclerotia are often referred to as black scurf and give rise to the name “the dirt that doesn’t wash off.” The accumulation of black sclerotia on tubers is initiated by the physiology of the plant. As the plant starts to die, the fungus begins forming sclerotia on tubers. The longer the potatoes remain in the soil after vine kill, the more sclerotia will be formed on the tubers.

The pathogen overwinters as sclerotia and mycelium on infected tubers, in plant residue, or in infested soils. High soil moisture, cool temperatures, high soil fertility and a neutral to acid soil (pH of 7 or less) favor development of the disease. A whitish mold can be formed on stems just above the soil line. This mold is the sexual stage of the fungus. Its role in the disease complex is not well known. When it is observed, stem lesions are often severe.

Nonemerged potato stems with Rhizoctonia lesions
Non-emerged potato stems with Rhizoctonia lesions.
Potato stem girdled by Rhizoctonia
Potato stem girdled by Rhizoctonia.


The symptoms of the disease are found on both above- and below-ground portions of the plant. Sprouts are often attacked before emergence. The growing tip may be killed or have reddish- to dark-brown cankers. Damage at this stage results in skips or delayed emergence and is expressed as poor and uneven stands.

Potato plants affected at this stage are characterized by a lack of vigor because much of their energy has been used to produce secondary or tertiary sprouts before a plant emerges. Sometimes, a heavily infested seed will not produce an above-ground plant. Instead, it will produce a stolon with several small tubers. This symptom is referred to as “no top” and can be confused with the same symptom caused by physiologically old seed that has been desprouted.

Stolons and roots, like sprouts, can be killed by the pathogen. The root system is reduced when this occurs. The number, shape, and size of tubers produced are also affected when the roots and stolons are attacked.

Early in the disease development, the stolons, roots, and stems have reddish-brown to brown lesions. As the stem lesions mature, they become cankers that are rough, brown and can have craters, cracks or both. If the cankers girdle the stem, they will interfere with the normal movement of water and carbohydrates within the plant. Often stunting or rosetting of the pant will develop. A leaf curl, which can be confused with symptoms of the Potato Leaf Roll Virus, has been reported in severely infected plants.

The interference of carbohydrate movement may also cause the formation of aerial tubers in the leaf axils of stems and the formation of many small, misshapen tubers. These affected plants are more erect and frequently are more difficult to kill with vine desiccants. This symptom can be observed after vine kill when individual plants are standing erect in an open field where most of the plants are dead.

Tubers are affected in many ways by this pathogen. The main symptom observed is the black sclerotia on the surface, thus the name black scurf. These sclerotia are not easily removed. They do not affect the interior of the tuber. In severe cases, many small, misshapen tubers form in a tight cluster next to the stem.

Other tuber symptoms include necrosis in the stem end, russeting, cracking, knobbiness, infected lenticels, and malformed tubers. Both phases of this disease result in the reduction of marketable yield. Seed tubers infested with sclerotia and mycelium are major sources of inoculum for future crops.


Currently, there is no completely effective control of this disease, but there are practices that will reduce the severity of it. The causal organism lives in soil on organic matter and has a wide host range. To date, no variety has been found with immunity to the sprout nipping and stem lesion phase. Some varieties show varying degrees of resistance to the formation of sclerotia on tubers.

Plant certified seed free of sclerotia. If more than 20 sclerotia are visible on one side of washed tubers, consider using a different seed source. Tuber inoculum is more important than the soil inoculum as the primary cause of disease. Seed growers should plant only sclerotia-free seed.

Treat all seed! Even if sclerotia are not observed, the tubers could still be infested with mycelium of the pathogen. Large sclerotia are more difficult for seed treatment materials to penetrate. Poor control can be the result of large sclerotia on seed pieces. No seed treatment will compensate for poor seed.

Avoid planting in cold, wet soil because it reduces the rate of sprout growth and is optimum for the disease to occur. Cover seed with no more than two inches of soil to promote rapid emergence and less chance for infection of sprouts and stems. A level of resistance to Rhizoctonia infection is imparted to an emerging plant with light interception. Therefore, the faster a plant emerges, the less chance there is for infection to occur.

Practice good rotation and, at a minimum, avoid two consecutive seasons of potatoes on the same land. This reduces both the incidence and severity of the disease. Rhizoctonia does not compete exceptionally well with other microbes in the soil. Increasing the rate of crop residue decomposition and the amount of organic matter in the soil decreases the growth rate of Rhizoctonia.

Residue decomposition releases carbon dioxide, which reduces the competitive ability of Rhizoctonia. Since Rhizoctonia is not an effective cellulose decomposer, soil populations are greatly reduced by competing microflora and less disease is observed with good rotation. As soils become devoid of organic matter, Rhizoctonia becomes a competitor and flourishes. Planting potatoes in low organic matter soils with high Rhizoctonia populations encourages the growth of the pathogen and an increase in disease. Different soils and different crops incorporated into the soil have varying effects on Rhizoctonia growth and development.

Potatoes should be harvested as soon as the skin is set so minimal bruising will occur. The percent of tuber coverage with sclerotia increases as the interval between vine kill and harvest is lengthened. Vine removal or burning reduces the amount of fungus overwintering and thus the amount of inoculum available to infect future potato crops. Do not dump infested tubers on future potato fields. They can become sources of inoculum. Chisel plowing has been shown to reduce the incidence and severity of the disease.

Information in this publication is provided purely for educational purposes. No responsibility is assumed for any problems associated with the use of products or services mentioned. No endorsement of products or companies is intended, nor is criticism of unnamed products or companies implied.

© 2003, Reviewed 2020

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R. solani


R. solani

Scientific Name

Rhizoctonia solani
J.G. Kühn


Thanatephorus cucumeris
(A.B. Frank) Donk

Common Names and Diseases

Rhizoctonia damping-off, blight and rot, white blight, target spot, Rhizoctonia aerial blight, Rhizoctonia damping-off and fruit rot, target spot or sore shin of tobacco, Rhizoctonia brown patch, Rhizoctonia root rot, wirestem, Rice sheath blight

Author: Tatiana Sanchez, University of Florida

Reviewed by: Jeffrey Rollins, University of Florida

The type species for the genus Rhizoctonia was initially the species Rhizoctonia crocorum described by DeCandolle in 1815. It was later changed to R. solani by the International Code of Botanical Nomenclature (8). Rhizoctonia solani, described by Kuhn in 1858, is the most economically important species of the genus Rhizoctonia. Following the description of R. solani, a number of studies were conducted on this fungus and anastomosis groups (AGs) (sometimes also referred as intraspecific groups –ISGs), investigating the ability of different isolates to fuse together interchanging genetic material (7, 8). A total of 13 anastomosis groups had been described for this species (5). Many studies conducted from 1960 to the 1970’s, exemplified the wide geographical distribution of R. solani as well as its broad host range (8). The lack of distinctive morphological structures of this anamorph, combined with a lack of technology, lead to an incorrect description of numerous isolates that were all merged into the species complex R. solani.

Taxa belonging to the Rhizoctonia solani species complex have been rearranged and divided into three groups: 1) multinucleate Rhizoctonia with hyphae of approximately 6-10 µm in diameter with teleomorph in the genus Thanatephorus Donk; 2) binucleate Rhizoctonia with hyphae between 4-7 µm in diameter with teleomorphs in the genus Ceratobasidium Rogers; and 3) multinucleate Rhizoctonia with teleomorph in the genus Waitea Warcup & Talbot (7). This article will focus on R. solani (Thanatephorus cucumeris teleomorph) on potato causing black scurf and stem canker. Most of the R. solani isolates that infect potato belong primarily to the anatomosis group 3 (AG-3) although, there are also pathogenic isolates in other AGs for this crop. Isolates belonging to the AG-3, cause stem canker and black scurf on potato (5).

Symptoms can be observed on above and below ground plant parts. Symptoms observed above ground early in the season include necrosis at the tips of the sprouts (which may eventually cause the emerging plant to die) and sunken lesions on stolons, roots, and stems. Later in the season, sclerotia are produced in the tubers creating a sign called black scurf which is simply, sclerotized mycelium (5, 9). Stems with cankers can become girdled, resulting in stunted plants. Leaves of infected plants develop a purplish and chlorotic coloration. In severe infections, green tubers develop above the ground. Affected tubers are deformed and can produce sclerotia on the surface (9).

Rhizoctonia solani is a soil pathogen and thus is affected by soil conditions. Black scurf and stem canker are more severe in soils that are cool and moist. Development of these diseases is favored by soil temperatures between 16 to 23 °C, while soil temperatures above 25°C reduce the severity of canker (1). The disease also tends to be more severe on dry light soils.The sexual stage of this pathogen can be found in infected potato plants but is not clear the role of basidiospores in the epidemiology of stem canker and black scurf in potato (7). It is believed that R. solani sclerotia (i.e., resistant structures) are the structures responsible for long distance dispersal (2).

Life cycle of R. solani on potato: Production of asexual spores is not observed in R. solani (3). Sclerotia formed at the end of the cropping season, allow the fungus to overwinter. The fungus can also survive on infested tubers left on the ground, soil, and debris. During the spring, potato plants from any stage can become infected by mycelia of the pathogen that spread underground from plant to plant.

Rhizoctonia solani is a cosmopolitan fungus and infects a wide variety of plant families (4). Most of the isolates responsible for potato stem canker and black scurf are found ubiquitously and within the AG-3 (9).

Management of the disease should not rely solely on chemical control. It must be achieved through the combination of multiple management strategies:

  • Conduct a soil test prior to establishment of the crop to know nutrient content and soil pH. Low pH is not conducive for disease development.
  • Use disease-free soil. Avoid areas with history of potato production or history of potato scurf and stem canker.
  • Use certified potato seed and assure disease-free propagation material. If seed is not certified, it should be treated with antagonists or fungicides before planting.
  • Perform long rotations (i.e., 3 or more years) to produce a significant reduction on the inoculum of R. solani. Rotations with canola, barley, or sweet corn have been recommended in the literature for reduction of Rhizoctonia inoculum and enhancement in potato quality.
  • Separate tubers from crop residues after destruction of the stem to prevent an increase in black scurf.
  • Plant less susceptible cultivars. There are differences in susceptibilities among potato cultivars, however resistant cultivars have not been developed yet.
  • Consult your local extension specialist for legal and efficacious fungicide products available in your state. Remember, the label is the law and the product applicator is responsible for reading and following all chemical labeling.

Typical characteristics of this genus include brown pigmented hyphae and constrictions at the base of the branching hyphae, which are oriented at a right angle from the main hypha. The hyphae are broad and multinucleate, lack clamp connections, and are usually fast growing. Hyphae septa have dolipores with discontinuous parenthesomes. The hyphae are monilioid and sclerotia are produced in culture (3, 6). The lack of diagnostic morphological characters at the species level makes morphological differentiation among different species difficult. However, isolates can be classified by hyphal interaction, biochemical characteristics, pathogenicity and ultimately, by molecular techniques using genetic markers. Biological tests for pathogenicity are time consuming and require space. Molecular tests can be expensive but can provide a more accurate diagnosis. One of the most appropriate methods for diagnosis of Rhizoctonia to the species level is by ribosomal DNA internal transcribed spacer (ITS) sequence analysis (9).

1. ANDERSON, N. A. 1982. The genetics and pathology of Rhizoctonia-solani. Annual Review of Phytopathology, 20, 329-347.

2. DAS, S., SHAH, F. A., BUTLER, R. C., FALLOON, R. E., STEWART, A., RAIKAR, S. & PITMAN, A. R. 2013. Genetic variability and pathogenicity of Rhizoctonia solani associated with black scurf of potato in New Zealand. Plant Pathology, n/a-n/a.

3. GARCIA, V. G., ONCO, M. A. P. & SUSAN, V. R. 2006. Review. Biology and systematics of the form genus Rhizoctonia. Spanish Journal of Agricultural Research, 4, 55-79.

4. FARR, D.F., & ROSSMAN, A.Y. Fungal Databases, Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved April 2, 2014, from http://nt.ars-grin.gov/fungaldatabases

5. LEHTONEN, M. J., AHVENNIEMI, P., WILSON, P. S., GERMAN-KINNARI, M. & VALKONEN, J. P. T. 2008. Biological diversity of Rhizoctonia solani (AG-3) in a northern potato-cultivation environment in Finland. Plant Pathology, 57, 141-151.

6. OBERWINKLER, F., RIESS, K., BAUER, R., KIRSCHNER, R. & GARNICA, S. 2013. Taxonomic re-evaluation of the Ceratobasidium-Rhizoctonia complex and Rhizoctonia butinii, a new species attacking spruce. Mycological Progress, 12, 763-776.

7. OGOSHI, A. 1987. Ecology and pathogenicity of anastomosis and intraspecific groups of Rhizoctonia-solani KUHN. Annual Review of Phytopathology, 25, 125-143.

8. SNEH B, J.-H. S., NEATE S, DIJST G 1996. Rhizoctonia Species: Taxonomy, Molecular Biology, Ecology, Pathology and Disease Control, Dordrecht, Netherlands, Kluwer Academic.

9. TSROR, L. 2010. Biology, Epidemiology and Management of Rhizoctonia solani on Potato. Journal of Phytopathology, 158, 649-658.

Sours: https://wiki.bugwood.org/Rhizoctonia_solani_(Black_scurf_and_stem_canker_in_potato)
Potato Diseases: Rhizoctonia solani

Cornell University

Rhizoctonia solani isa fungus that attacks tubers, underground stems, and stolons of potato plants. Although it probably occurs wherever potatoes are grown, it causes economically significant damage only in cool, wet soils. In temperate production areas, losses from R.solani are sporadic and occur only when weather is cold and wet in the weeks following planting. In northern areas, where growers often must plant in cold soils, Rhizoctonia is a more consistent problem. Poor stands, stunted plants, reduced tuber number and size, and misshapen tubers are characteristic of the Rhizoctonia disease.

Symptoms and Signs

The phase of the disease called black scurf is common on tubers produced commercially and in home gardens. The irregular, black to brown hard masses on the surface of the tuber are sclerotia, or resting bodies, of the fungus (Figure 1). Although these structures adhere tightly to the tuber skin, they are superficial and do not cause damage, even in storage. They do perpetuate the disease and inhibit the establishment of a plant from the tuber if it is used as seed.

Black scurf is the most noticeable sign of Rhizoctonia. But the most damaging phase of the disease occurs underground and often goes unnoticed. The fungus attacks underground sprouts (Figure 2) before they emerge from the soil. Stolons that grow later in the season can also be attacked (Figure  3). The damage varies. The fungal lesion, or canker, can be limited to a superficial brown area that has no discernible effect on plant growth. Severe lesions are large and sunken, as well as necrotic. They interfere with the normal functioning of stems and stolons in translocating starch from leaves to storage in tubers. If the fungal lesion expands quickly, relative to the growth of the plant, the stolon or stem can be girdled and killed.

Rhizoctonia figures 1 through 6

Damage is most severe at cold temperatures, when emergence and growth of stems and stolons from the tuber are slow relative to the growth of the pathogen. Wet soils also contribute to damage because they warm up more slowly than dry soils and excessive soil moisture slows plant development and favors fungal growth. If Rhizoctonia damage is severe and lesions partially or completely girdle the shoots, sprouts may be stunted or not emerge above the soil. Stolon cankers reduce tuber numbers and size and are identical to shoot cankers in appearance.

Poor stands may be mistaken for seed tuber decay, caused by Fusarium species or soft rot bacteria, unless the plants are excavated and examined. Rhizoctonia does not cause seed decay; its damage is limited to sprouts and stolons. Poor stands and stunted plants can also be caused by blackleg, a bacterial disease that initiates from the seed tuber and progresses up the stems, causing a wet, sometimes slimy, rot. In contrast, Rhizoctonia lesions are always dry and usually sunken.

Late season damage to plants is a direct result of cankers on stolons and stems causing problems with starch translocation. Tubers forming on diseased stolons may be deformed. If stolons and underground stems are severely infected with Rhizoctonia canker, they cannot carry the starch produced in the leaves to the developing tubers. In this case, small, green tubers, called aerial tubers, may form on the stem above the soil (Figure  4). Formation of aerial tubers may indicate that the plant has no tubers of marketable quality below ground.

At the end of the growing season, the fungus produces its sexual state, Thanetephorus cucumeris, on stems just above the soil line. It appears as a superficial delicate white mat which is easily removed (Figures 5 and 6). The fungus does not damage the tissue beneath this mycelium.

R. solani is a specialized pathogen. Only a subset of the isolates of this fungal species can cause cankers on potato. Isolates are grouped by the ability of their hyphae to fuse; isolates that can fuse, or anastomose, are in the same anastomosis group (AG). Isolates that are pathogens of potato are in AG-3. Rarely, isolates in other AG groups can form sclerotia on tubers and mycelial mats on stems. Though not damaging to potato, other AGs of R. solani cause diseases on sugar beet, beans, crucifers, and rice. In the absence of host plants, R. solani can exist by deriving its nutrients as a soil saprophyte from organic debris.

The Disease Cycle

The disease cycle is very straightforward. Inoculum usually is introduced into fields on potato seed tubers, although it may be introduced via contaminated soil. Sclerotia in soil or on seed tubers germinate, and the resulting mycelium colonizes plant surfaces where nutrients are available. Seed inoculum is particularly effective in causing stolon damage because it is so close to developing sprouts. The fungus penetrates young, susceptible tissue, causing cankers that slow or stop the expansion of the infected stem or stolon. Cankers can sever the stolon or shoot from the plant or kill the growing point (fig. 2). The plant’s resistance to stolon infection increases after emergence, eventually limiting expansion of lesions. Sclerotia form on tubers and in soil, providing inoculum for other growing seasons.

Disease Management

Getting potato plants to emerge quickly in the spring is key to minimizing damage to shoot and stolon cankers because plants are more susceptible before emergence. Planting seed tubers in warm soil and covering them with as little soil as possible will speed the emergence of the shoots and increase resistance to canker infection. Plant fields with coarse-textured soils first because they are less likely to become waterlogged and will warm up faster.

Crop rotation reduces inoculum that can cause cankers because those R. solani isolates are specific to potato. Sclerotia are relatively resistant to degradation in the soil, however, and may survive for several years in the absence of potato. The fungus can also exist as a saprophyte in soil by colonizing organic debris. The longevity of the population is determined by the initial density of sclerotia at the start of the rotation period, the soil conditions, and the amount of microbial activity in the soil. Planting sclerotia-free seed is an excellent management strategy. Fungicide treatments applied to tubers may help suppress tuber-borne inoculum but are not a replacement for clean seed.  For labeled seed treatments see current Cornell Integrated Crop and Pest Management Guidelines for Commercial Vegetable Production.

Black scurf, or sclerotia, can be minimized by harvesting soon after vines are killed. Sclerotia begin to form on tubers as vines senesce and become larger and more numerous over time. Therefore, harvesting tubers as soon as possible after skin set reduces tuber scurf significantly. Sclerotia do not form and grow in storage, and there is no increase in tuber storage rot.

More information/prepared by:

Originally created by Rosemary Loria, Roseann Leiner, and Donald Carting for Vegetable MD Online.  Updated April 2021 by:

Margaret Tuttle McGrath
Associate Professor
Long Island Horticultural Research and Extension Center (LIHREC)
Plant Pathology and Plant-Microbe Biology Section
School of Integrative Plant Science
College of Agriculture and Life Sciences
Cornell University
[email protected]

Sours: https://www.vegetables.cornell.edu/pest-management/disease-factsheets/rhizoctonia-canker-and-black-scurf-of-potato/

Potato rhizoctonia


Here, Harper Adams potato expert Dr Matthew Back offers an in-depth look at the epidemiology and control of this damaging pathogen to maximise output and produce a bright and clean skin finish.

What is R. solani?

It is a pathogen belonging to a large group of fungi known as the basidiomycetes, which also include cereal diseases such as the smuts, bunts and rusts.

It has an extremely large host range and causes economically important diseases in countless arable crops around the world, including cereals, oilseed rape, pulses, sugar beet and potatoes.

Is all R. solani the same?

The pathogen species is made up of a number of sub-groups, known as anastomosis groups (AG). The AG often dictates which host or hosts it favours and, in some cases, even the symptoms caused.

In the field, belonging to the same AG means hyphae – the branches of a growing fungus – from each organism are able to fuse together, share resources and help the pathogen thrive.

Some AGs are more damaging to potatoes than others. For example, AG 2-1, AG 3 and AG 5 are important for potatoes in the UK. AG 8 has been detected in soil, but not on daughter tubers.

There is variation in symptoms, depending on the AG group or groups present. AG 3 is the most common and causes typical stem and stolon canker and black scurf on tubers later in the season.

AG 2.1 causes mainly stem and stolon canker, with less black scurf. AG 8 only affects roots and might not be picked up by agronomists.

What is its lifecycle?

The pathogen is one of the great survivors amongst plant diseases. It is a saprophyte, so can rest on decaying organic matter, which allows it to survive on senesced crop and other debris through the winter.

In addition, sclerotia – resting structures in the form of a compact mass of mycelium – are formed at the end of the growing season and remain in the soil for a period of time until a suitable host is found. Additional sources of inoculum for following crops include infected seed, volunteer potatoes or groundkeepers and a number of weed hosts.

Research suggests survival in the soil decreases over an 18-month period, but with such a vast host range, combined with seed transmission and infected volunteers, its proliferation is very difficult to supress during a cropping rotation.

As a soil-borne disease, R. solani is affected by soil conditions. Symptoms tend to be more common and severe in cool, moist soils at temperatures of 16C-23C. When soil temperature is above 25C, stem canker reduces in severity. The disease can also be more severe on dry, light soils or where pH is neutral to acid (£ 7).

It is very common in all UK soils, although it does have a greater preference for soils where there are pores or cracks, as mycelium can grow and infect hosts more readily.

The most important part of the R. solani lifecycle is this asexual phase. It does have a sexual phase where basidiospores are produced, but its importance and impact in potato production is not well understood.

When and how does initial infection occur?

Whether R. solani is present in the soil or introduced on seed tubers with black scurf or less visible mycelium on the surface, initial infections take place shortly after planting.

The fungus is stimulated by carbohydrates produced by the plant as it grows. These same secretions guide hyphae to the surface of the shoots, stolons or stems, where they aggregate to form a structure known as an infection cushion.

This secretes toxins and a series of cell wall-degrading enzymes which soften the plant tissue. The combination of pressure from the cushion and the cell wall-degrading enzymes allow the fungus to invade, macerate and kill the surrounding tissue. As R. solani is a saprophyte, is survives on dead material and aims to kill as much of the plant as possible.

What are the symptoms?

There are two phases to the disease in potatoes. The first is the stem and stolon phase, which is typically seen when infection occurs soon after planting. Symptoms include stolon pruning, where lesions develop on tips of stolons within the soil, or lesions on stems known as stem canker.

This can cause uneven emergence and growth and as plants have fewer primary stolons, there is an increase in very small and very large tubers, so less marketable yield in the size brackets packers and processors are looking for. Optimal timing of inputs such as herbicides, fungicides and desiccants becomes more difficult.

A further consequence of stolon infection at tuber initiation is a hard, necrotic patch at the rose end of the tuber. As the tuber bulks up, this is stretched and creates an unsightly scab, which resembles an elephant’s hide.

In the worst cases, deep cracks can develop as soft tissue grows around the scarring, forming jigsaw-like necrotic pieces that can sometimes run down the length of the tuber.

The final evidence of R. solani infection can be seen towards the end of the season in the form of black scurf. It forms as black sclerotia on the surface of the tuber as the crop begins to senesce and can be scratched off easily with a fingernail.

Potatoes free of black scurf may still be infected with R. solani, because hyphae barely visible to the naked eye can be growing across the surface. These thin black lines can be picked up by using a x10 hand lens.

How damaging is R. solani?

As a rule of thumb, yield loss is often cited as being about 30%. However, where poor size distribution and skin blemishes are rife, rejections or downgrading of marketable yield can make losses much worse.

Can you test for it?

Seed tuber infection not visible to the naked eye can be tested using real-time PCR assay extraction of the pathogen’s DNA and is considered a very reliable way of assessing the need for seed treatments.

More recently, a test for detection and quantification of soil inoculum has been developed in the UK and Australia using the same method and can help potato growers develop more robust management strategies.

Commercial testing services for presence of  diseases like R. solani on seed tubers are available at FERA and NIAB CUF in England and SASA in Scotland.

How is R. solani managed?

1. Source clean seed

Good seed health is important in minimising disease risk. Sourcing clean, certified seed is advised, and seed samples should be washed and inspected for signs of visible black scurf. Microscopic fungal growth that isn’t visible to the naked eye can also be present, so laboratory testing can help detect seed infection and help guide seed treatment requirements.

2. Know field history

Rhizoctonia is a sporadic disease and risk is difficult to assess, but field history can help. Consider the frequency of potato growing on a particular field and whether potato cyst nematode (PCN) is present. Where soils have been subject to intense potato production, risk from both R. solani and PCN is likely to be high. Soil testing can help quantify this risk.

PCN damage on potato roots leads to a greater loss of the carbohydrates that stimulate and guide R. solani hyphae to the surface of plant tissue, increasing infection risk. Where possible, minimise the impact of PCN on any potato crop with integrated control, including longer rotations, PCN-resistant varieties and nematicides. This should also help reduce the impact of R. solani.

3. Manage volunteers

Allowing potato volunteers to flourish through an arable rotation helps many soil-borne pests and pathogens to survive until the next crop is planted, including R. solani.

Ensure potato harvesters are set up to minimise tuber losses at harvest. An application of growth regulator/sprout suppressant maleic hydrazide can help minimise volunteer establishment. Any growing volunteers should be controlled with herbicides in all crops or stubbles through the year to reduce disease inoculum in the soil.

4. Variety choice

Varietal susceptibility to black scurf caused by R. solani varies and is linked to how long potatoes are in the ground, which is determined by speed of skin set. In high-risk situations and where growing for fresh markets, choose a less susceptible variety with rapid skin set.

Where this is not possible due to market requirements, carefully manage nitrogen applications and ensure rapid haulm destruction to speed up skin set. Also consider an early harvest to minimise build-up of black scurf on tubers.

5. Plant into warm, moist seed-beds

As slow crop emergence can increase the risk of R. solani infection, consider delaying planting where it could be a problem. If forced to plant in cold and wet conditions, place seed at a shallower planting depth to reduce the risk of compaction under ridges, prevent rooting issues and speed up emergence.

6. Consider chemical treatment

Where R. solani risk has been identified, chemical treatments may be required to minimise problems such as black scurf, particularly when growing for the packing market where skin blemish tolerance is low.

Whilst black scurf is not as important in processing crops, R. solani can cause deep necrosis on tubers in the form of netted scab and may affect tuber size distribution due to stolon cankers, so fungicide treatment may still be justified.

In addition, some processors now require a good skin finish for skin-on convenience products, which are becoming more popular with consumers.

The available fungicides negate stem and stolon canker and treatments are applied to seed tubers as a liquid at grading or a powder at planting. Accurate and even application of these seed treatments is essential for suppressing seed-borne sclerotia and mycelium of R. solani.

Liquid in-furrow fungicides at planting can also help reduce disease severity.

Matthew Back is a reader and researcher at Harper Adams University, specialising in potatoes. He supervises several PhD projects looking at the biology and management techniques of plant parasitic nematodes. He also speaks regularly to the potato industry and at academic conferences.

Choose RhiNo for flexible seed tuber protection

The availability of liquid and powder formulations of fungicide RhiNo (flutolanil) gives growers the flexibility of two different application methods at different timings for effective control of R. solani, says manufacturer Certis.

Liquid formulation RhiNo allows for the treatment of seed tubers using application equipment above a roller table or conveyor as seed is being graded, while powder product RhiNo DS is applied at planting via a specialist applicator fitted to the potato planter.

Both formulations are systemic and provide protection of stems and stolons during growth and guard against soil-borne infection, protecting total and marketable yield.

Flutolanil also has some curative effect on seed-borne R. solani and is active against all anastomosis groups. There is an added benefit of a reduction in silver scurf.


Sours: https://www.certiseurope.co.uk/
Control Rhizoctonia in Potatoes with Elatus


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