Powdery scab is a disease of potato tubers. It is caused by the cercozoan Spongospora subterranea f. sp. subterranea and is widespread in potato growing countries. Symptoms of powdery scab include small lesions in the early stages of the disease, progressing to raised pustules containing a powdery mass. These can eventually rupture within the tuber periderm. The powdery pustules contain resting spores that release anisokont zoospores (asexual spore with two unequal length flagella) to infect the root hairs of potatoes or tomatoes. Powdery scab is a cosmetic defect on tubers, which can result in the rejection of these potatoes. Potatoes which have been infected can be peeled to remove the infected skin and the remaining inside of the potato can be cooked and eaten.
Disease cycle
In general, not a lot is known about the life cycle of Spongospora subterranea f.sp subterranea (Sss). Most of the currently-proposed life cycle is based on that of Plasmodiophora brassicae, a closely related and better-studied protozoan. It has been proposed, due to this similarity, that there are two distinct stages that Sss can exist as; the asexual and sexual stages.
Asexual Stage: A zoospore infects root tissue and becomes a uninucleate plasmodium. This plasmodium undergoes mitotic nuclear division (creates many nuclei within a single cell) and turns into a multinucleate plasmodium. Then, the multinucleate plasmodium forms zoosporangium, which eventually release more zoospores. This process can happen relatively quickly and can act as an important source of secondary inoculum within a field.
Sexual Stage: This stage follows a similar pattern to the asexual stage, but with a few exceptions. It is hypothesized that two zoospores fuse together to form a dikaryotic zoospore (with two separate haploid nuclei, n+n) and then infect the roots. Once the infection occurs, the dikaryotic zoospore develops into a binucleate plasmodium (one pair on nuclei, n+n). Similar to the asexual stage, this plasmodium will also replicate its nucleus to create a multinucleate plasmodium (many pairs of nuclei, n+n). The second main different between stages occurs here. The pairs of nuclei (n+n) will fuse by karyogamy, and the plasmodium will quickly divide into numerous resting spores within a sporosori (spore sack, alternatively called cystosori). These resting spores have three-layered walls and are extremely resistant to the environment, allowing them to persist in the soil for longer than 10 years.
As a reminder, most of the life cycle is still unclear. However, the presence of zoospores, plasmodia, zoosporangia, and resting spores have been observed in the field and lab. The ploidy levels and karyogamy events are only theorized and have yet to be proven.
Environment
Spongospora subterranea pathogenesis is most effective in cool, damp environments, such as northern Britain, the Columbia Basin of south-central Washington, and north-central Oregon. The environmental condition is particularly critical during the release of infective agents (zoospores) into the soil-environment . Upon release from resting spores, zoospores require moisture to swim towards the host tuber or roots. One study, found powdery scab was significantly more common on plants grown in constant dampness compared to plants grown with varying moisture levels. In this same study it was concluded that disease risk was related more to the environment, or moisture level, than the level of inoculum present. Inoculum may be present but not able to disperse due to environmental conditions, and therefore does not reach host tissue to infect. Other environmental factors that affect Spongospora subterranea infection are directly related to agronomic practices. Increased use of fertilizers containing nitrate or ammonium nitrogen increase the incidence and severity of powdery scab. It is thought that the fertilization increases root growth, and thus provides more tissue for infection and disease cycling to occur. Also, reduced cellulose within the cell walls caused by excess nitrogen may increase susceptibility of host to infection. It is apparent that the environment can directly affect both the host susceptibility and the dispersal of the pathogen ultimately setting the pace for the disease cycle.