Like all nematodes, PCN juveniles hatch from eggs. Unlike many other nematodes, this hatching is tightly regulated, occurring only in the presence of chemicals originating from the roots of a host plant. This signals to the otherwise dormant juveniles that a suitable host is nearby. After hatching, the juveniles use these same chemical signals to locate host roots. The juveniles enter the root and migrate through the host tissue, locating a feeding site. Using a probing, needle-like stylet (a hollow, spear-like mouthpart), the nematode begins modifying the host, restructuring plant cells to form a syncytium, a single feeding site made from merged plant cells. Up to this point, the nematodes are not sexually differentiated.

If feeding is successful, the nematodes will develop into females. Their muscles undergo atrophy and they remain at this single feeding site for the rest of their life. If feeding is unsuccessful, the juvenile develops into a male, exits the plant, and never feeds again. The females continue to feed from the syncytium, their bodies begin to swell, and eggs start to form within the body. The female diverts nutrients from the host to support egg production. For the host plant, this results in yellowing leaves, stunted growth and severely reduced tuber formation.

Eventually, the posterior end of the female nematode ruptures through the host root and becomes exposed to the surrounding soil. Males are then able to mate with the female, fertilising the eggs. As the female ages, her body begins to harden, forming a cyst that can contain ~500 eggs. The cysts detach from the roots and remain in the soil, where the next generation of juveniles enters a prolonged dormancy period, anticipating the absence of a suitable host crop until a future growing season. As in the previous generation, this dormancy is broken only when host-derived chemical signals are detected, and the lifecycle begins again. This lifecycle takes around 10–14 weeks and in cool climates typically only 1 generation is produced per growing season.

Why PCN is so hard to control

PCN management is extremely challenging as eggs can remain dormant in the soil for up to 20 years. Over their lifecycle, PCN are largely immobile. As with their initial introduction to Europe, almost all new infestations rely on the movement of dormant cysts into previously uninfected areas. Preventing the introduction of contaminated soil remains the most effective management strategy for controlling PCN. However, given their microscopic size, it is impossible to determine visually whether cysts are present on or around seed potatoes. In Europe, PCN are listed as A2 quarantine pests, and national plant protection organisations enforce strict phytosanitary measures (biosecurity rules covering plant health) to limit their spread.

There is an economic knock-on effect here. Under the UK’s Seed Potato Classification Scheme, land must test free of PCN before seed potatoes can be planted there, for certification or for a farmer’s own saved seed. Once a field tests positive, it is recorded as infested and removed from seed production; ware potatoes can still be grown there, but only under an approved control programme aimed at suppressing the pest. Because biosecurity measures slow spread rather than prevent it entirely, the area of infested land keeps growing: G. pallida-infested land in Scotland has been doubling roughly every 7 to 8 years, and recent estimates put PCN present on over a third of Scotland’s potato-growing land. For seed growers and landowners, this means a shrinking pool of land that still qualifies for seed production and can be rented out. It is therefore in everyone’s interest to manage PCN.

The most effective long-term control strategy is the use of naturally resistant potato varieties, which prevent successful nematode feeding and subsequent sexual development. The first major resistance gene, H1, was characterised phenotypically in 1952 using resources from the Commonwealth potato collection, still held by one of the CROPSAFE project partners (the James Hutton Institute, JHI).This resistance gene has been deployed commercially since 1966 and is present in over 40% of internationally important cultivars. There are now resistance genes available in commercial varieties against both major PCN species. However, resistance genes are often species- or pathotype-specific and do not always provide complete protection. In addition, not all resistant varieties are accessible to all growers due to breeding contracts and end-use requirements. There are, for instance, very few salad potato varieties that possess PCN resistance traits. Furthermore, resistance does not necessarily equate to tolerance, meaning that yield can still be severely affected under high PCN infestation pressure.

Where host resistance is not suitable or available, alternative management practices have relied on the use of chemical nematicides. The availability of these products varies greatly between countries. Currently available chemical nematicides target nematodes that have already hatched and are active in the soil, reducing infection pressure during the growing season and helping to protect crop yield. However, they cannot reach juveniles that are still within eggs. That egg reservoir stays viable in the soil, meaning cyst populations, and the risk they pose to future crops, are not significantly reduced by nematicide treatment alone.