In PT4 the amount of S. subterranea DNA present in Russet Burbank potato roots increased in both fungicide treated and control treatment but the rate of increase was significantly less, over time, in the soil furrow mancozeb treatment (p < 0.001, Fig 4A, Table 2). Zoosporangial score was also reduced by mancozeb treatment, with the effect greater in the earlier assessments contributing to a significant reduction in AUDPC compared to the untreated control (p < 0.025, Fig 4B, Table 2). Similarly, root galling (pooled at 45 and 60 days) was significantly reduced by mancozeb treatment (p = 0.045, Fig 4C) while tuber disease incidence (Fig 4D) and severity (Fig 4E) showed non-significant reductions by the fungicide soil treatment.
Fig 4. The impact of mancozeb soil furrow treatment (7.5kg/ha) on root infection and disease in cultivar Russet Burbank in a pot trial (PT4—summer).
Multiple sequential assessments measured A- S. subterranea DNA concentration (pg/gm) in roots (n = 9); B- zoosporangia observation score (n = 3). Two assessments were made for C- root gall severity at 45 and 60 days (data pooled) after emergence (n = 3); and single assessments for D- mean tuber disease incidence and E- mean tuber disease severity at plant senescence (n = 3). Vertical bars are standard errors.
In PT5, where only the zoosporangial score was measured for a 25 day period, there were no significant differences seen between Desiree and Russet Burbank (p > 0.05) for each assessment and these data were pooled to provide a larger data set for subsequent analyses. All mancozeb treatments (3.25kg /ha,7.5kg/ha, 15.0 kg/ha) significantly reduced the zoosporangial score and slowed the rate of infection compared to the untreated control (p <0.001, Fig 5, Table 2).
Fig 5. The effect of different mancozeb soil furrow treatments (0, 3.25, 7.5 or 15.0 kg/ha) on mean zoosporangial score (0–4) in potato roots grown in a pot trial (PT5 –autumn/winter).
Data was pooled across the cvs. Desiree and Russet Burbank. Vertical bars are standard errors (n = 6).
Pre-plant soil inoculum levels were very low and seed inoculum levels very high in both field trials. Both trials produced high levels of S. subterranea root infection, root galling, and tuber disease in both cultivars. Exploratory analysis of the data indicated that there were no significant effects of cultivar on the disease outcomes assessed and thus data sets from Russet Burbank and Innovator were pooled to provide a larger data set.
The amount of S. subterranea DNA detected within roots increased with time over the five sequential assessment dates. The AUDPC analysis identified significant treatment differences in FT1 (p < 0.0001, Fig 6A, Table 2) but not in FT2 (p = 0.07, Fig 6B, Table 2). Essentially, the untreated control and mancozeb soil furrow treatments had significantly higher AUDPC’s than all other treatments in FT1, with analogous trends seen in FT2 indicating an increased rate of pathogen replication in these two treatments.
Fig 6. The effect of fungicide seed and soil treatments on the increase in pathogen content (pg S. subterranea DNA/gm) in potato roots.
Measurements were made 15–75 days after emergence (DAE) in two field trials (A—FT1, B—FT2). Data was pooled across the cultivars Russet Burbank and Innovator, vertical bars are standard errors (n = 9).
The soil treatment (fluazinam) and seed dips (formalin, fluazinam and mancozeb) consistently reduced (p < 0.05; 2–6 fold decrease, Fig 7A and 7B) mean zoosporangial score compared to the untreated control in both field trials. The mancozeb soil treatment produced a zoosporangial score equivalent (p > 0.05, Table 2) to the untreated control indicating that root infection developed more rapidly in these two treatments.
Fig 7. The effect of fungicide seed and soil treatments on root infection.
Measurements included mean potato root zoosporangia infection score (0–4) in FT1 (A) and FT2 (B) and root gall severity score (0–4) in FT1 (C) and FT2 (D). Data was pooled across the cultivars Russet Burbank and Innovator and two assessment dates, 45 and 60 days after emergence. Vertical bars are standard errors (n = 8).
Root galls were first observed at 45 days after plant emergence with consistent root galling observed across all treatments at 60 and 75 days after emergence (galling data was pooled across these last two assessment dates for Fig 7C and 7D). Consistent with the root infection data, similar trends were observed with the soil treatment (fluazinam) and seed dips (formalin, fluazinam and mancozeb) reducing (p < 0.05; 2–8 fold decrease) root gall score and root gall production rate (AUDPC, Table 2) compared to the untreated control. Once again, the mancozeb soil treatment and the untreated control produced similar (p > 0.05) levels of moderately high galling (root gall scores of 2.3–2.6).
The soil treatment (fluazinam) and seed dips (formalin, fluazinam and mancozeb) also significantly reduced mean tuber disease incidence and severity in both trials (FT1 and FT2). In FT1, both disease incidence (p = 0.01, Fig 8A) and disease severity (p = 0.003, Fig 8C) were significantly lower in the soil furrow treatment (fluazinam) and seed dip treatments (fluazinam, formalin and mancozeb) than the untreated control and mancozeb soil furrow treatment. The same trend was found in FT2 for both disease incidence (p = 0.001, Fig 8B) and severity (p = 0.003, Fig 8D).
Fig 8. The effect of fungicide seed and soil treatments on mean tuber disease.
Measurements included disease incidence in FT1 (A) and FT2 (B) and severity (0–6) in FT1 (C) and FT2 (D). Data was pooled across the cultivars Russet Burbank and Innovator. Vertical bars are the variation within the population (n = 8).
Prepared by Laura Bostic
Class Project for PP 728, Soilborne Plant Pathogens, Fall 2012
Spongosporasubterranea is the causal agent of powdery scab on potato. Though this disease can reduce yield somewhat, the true economic effect is due to the unmarketable, scabbed appearance (Figure 1) as well as rejection of tubers as seed to prevent infestation of clean fields. Though the blemishes can be cut away with no effect to the rest of the tuber, the appearance reduces the marketability as fresh product and processing centers often reject them on the basis of needing to remove more skin to remove the infected portions. Beyond the effects of powdery scab itself, infected tubers are also more susceptible to other diseases, such as secondary storage diseases or as a vector of the mop-top virus (1,2,3,4).
Figure 1: Scabbed appearance on potato (Photo: Melodie Putnam, Oregon State University Plant Clinic)
Host range and distribution
Spongosporasubterranea can be found worldwide, wherever potatoes are consistently grown. Other than potato (Solanumtuberosum), few hosts have been reported. But it is assumed that solanaceous plants are susceptible including reports of tomato (Lycopersiconesculentum) and other Solanumsp. such as nightshade (S. demissum). Nasturtium sp. has also been reported as a host (1,2,3).
Spongosporasubterranea is an obligate biotroph and therefore requires a living host and cannot be cultured in vitro. Detection in the soil and on tubers is based on the presence of sporosori, the resting spores of the pathogen. These spores can be detected through bioassays, PCR, and antibody methods. Though the pathogen cannot be grown in culture, spore suspensions can be made for inoculation purposes. Infected tubers can be peeled and the skin dried and ground, then passed through a 53 µm sieve. The spores can be quantified using a hemocytometer (2,5).
Spongosporasubterranea is a protozoan-like organism of uncertain taxonomy in the family Plasmodiophoridae. It produces biflagellate zoospores which can result from zoosporangium or a resting spore produced in a spore ball or sporosori (Figure 2). Spore balls can be seen via a microscope in tissue where a lesion has already burst and has a white, powdery appearance (1,3).
Figure 2: Sporosori or spore balls of Spongosporasubterranea (Photo: Sandra Jensen, Cornell University, Bugwood.org)
The most notable symptom associated with Spongosporasubterranea is the blemish formed on the tuber. Initial infections begin with small, purple lesions, described as “pimple-like”. With time, the lesion will expand and eventually burst (Figure 3), exposing the white spore balls (Figure 4), lending the name “powdery scab”. Infected roots can also produce gall symptoms. With galling (Figure 5), reduced yield can also be observed, though this is not a major symptom (1,2,3,4).
Figure 3: Tuber exhibiting Powdery Scab (Spongosporasubterranea) lesions (Photos: Sandra Jensen, Cornell University, Bugwood.org)
Figure 4: A burst lesion exhibiting powdery spore balls (Photo: Melodie Putnam, Oregon State University Plant Clinic)
Figure 5: Powdery scab galls on roots and stolons of potato caused by S. subterranea (Photo: W.T. Cobb, apsnet.org)
Ecology and life cycle
The details of all parts of the life cycle of Spongosporasubterranea have not yet been fully proven, but the main aspects are known and assumptions based on other plasmodia have been applied to gain an understanding of the life cycle.
Starting with a biflagellate, uninucleate zoospore (n) there are two paths possible. The zoospore can directly infect the root, encyst, and form a uninucleate plasmodium which will multiply and develop into a multinucleate plasmodium, though all nuclei will remain identical (n). The plasmodium will develop into a thin-walled zoosporangium containing many new zoospores, all identical (n). Alternately, the zoospore (n) can fuse with another, differing zoospore (n) producing a zygote (2n). This zygote then infects the root, encysts, and creates a binucleate, single-celled plasmodium. The plasmodium will multiply and eventually undergo meiosis and form a spore ball or sporosori (2n), which contains the resting spores, each resting spore containing one zoospore with one nucleus.
Resting spores can persist in the soil for up to ten years. The cell walls contain three layers, aiding in the spore’s longevity. Zoospores swim through water films and therefore require free water in order to infect. After emergence, they swim to a host but only survive for about two hours. Infected seed tubers are a source of inoculum as well as infested soils where the organism persists for long periods of time. Symptomatic tubers will, therefore, not be accepted for seed (1,3).
The most effective method for disease control is to avoid the pathogen and use fields without infestations and prevent infestations through clean seed programs. Once the pathogen is present, resistant cultivars, pesticides, and cultural control may be necessary. Cultural control methods center around controlling the available water to prevent the zoospores from infecting; including irrigating appropriately, using appropriate soil types, and ensuring good drainage. Long rotations may reduce inoculum levels; however, due to the longevity of the sporosori in the soil, this may not be effective. Composting may also reduce inoculum, but since temperatures would need to be extremely high, some spores will still remain. Some chemical control has been shown with zinc oxide, fluazinam, mancozeb, and metam sodium (2,3,4).
Links to Other Sites
Spongospora Competence Center
Maine Extension- Powdery Scab of Potatoes
S. subterranea Taxonomy
1. Brierley J., Lees, A., and Wale, S. 2008. Powdery scab—strains and conducive conditions. Potato Council. Agricultural & Horticultural Review Board.
2. Fallooon, R. 2008. Control of powdery scab of potato: towards integrated disease management. Am. J. Pos. Res. 85:253-260.
3. Merz, U. 2008. Powder scab of potato—occurrence, life cycle, and epidemiology. Am. J. Pot. Res. 85:241-246.
4. Miller, J. 2001. Powdery scab workshop—summary notes. University of Idaho.
5. van de Graaf, P., Lees, A., and Wale, S. 2005. Effect of soil inoculum level and environmental factors on potato powdery scab caused bySpongospora subterranea. Plant Pathology 51: 22-28.