How potato psyllids spread bacteria that cause zebra chip disease

Jenn Hoskins
9th January, 2026

How potato psyllids spread bacteria that cause zebra chip disease

A sequential transmission assay (a) revealed that potato psyllid (Bactericera cockerelli) nymphs transmit 'Candidatus Liberibacter solanacearum' haplotype B significantly earlier than haplotype A, indicating a shorter latency period and greater transmission efficiency for LsoB (b).

Image adapted from: Oh et al. / CC BY (Source)

Key Findings

  • In Texas potato psyllids, haplotype B of Candidatus Liberibacter solanacearum (LsoB) accumulates more quickly in nymphs than haplotype A (LsoA)
  • LsoB is transmitted to tomato plants earlier than LsoA by potato psyllid nymphs, indicating a shorter time between infection and spread
  • Nymph guts show different gene activity changes depending on whether they are infected with LsoA or LsoB, potentially explaining the differing transmission rates
‘Candidatus Liberibacter solanacearum’ (Lso) is a bacterium that causes significant disease in crops like potatoes, tomatoes, and other members of the nightshade family (Solanaceae). The pathogen resides within the plant’s phloem – the tissue responsible for transporting nutrients – making it difficult to detect and control[1]. In the United States, two main genetic types, called haplotypes A and B, are spread by the potato psyllid, Bactericera cockerelli. Understanding how these haplotypes behave is critical for developing effective disease management strategies. The problem of “zebra chip” disease, caused by Lso, has been a concern for potato growers for decades, first appearing in Mexico in 1994 and spreading to other regions[2]. Early observations of symptoms – necrotic flecking and streaking in potato tubers, reduced yields, and early plant senescence – were linked to the presence of B. cockerelli[2]. Researchers initially hypothesized a bacterium-like organism was the cause, with psyllids acting as vectors[2]. Later, PCR-based testing confirmed the presence of Candidatus Liberibacter solanacearum in affected plants[2]. A recent study conducted by researchers at Texas A&M University investigated the differences in how B. cockerelli nymphs – the immature form of the psyllid – acquire and transmit Lso haplotypes A and B. Previous work by the same team had already established that adults and nymphs handle the pathogen differently, prompting a deeper look into nymphal dynamics. The study focused on quantifying the amount of each haplotype accumulated within the nymphs’ bodies after exposure to infected plants for varying durations (1, 3, 5, and 7 days). They then assessed how efficiently the nymphs transmitted each haplotype to healthy tomato plants through sequential inoculation. Quantitative PCR revealed that nymphs accumulated higher levels of LsoB compared to LsoA after just three days of exposure. Critically, LsoB was also transmitted to new plants earlier than LsoA, indicating a shorter period between infection of the psyllid and its ability to spread the disease. To understand why LsoB is transmitted more efficiently, the researchers examined changes in gene activity within the nymphs’ guts following exposure to each haplotype. They used a technique called RNA-seq to measure which genes were turned on or off at 1 and 5 days post-acquisition. The results showed a greater overall change in gene activity at 5 days, suggesting a more substantial response to the pathogen over time. Importantly, the response was different depending on the haplotype. Exposure to LsoA primarily affected genes involved in protein translation – the process of building proteins – as well as genes related to ER stress (a response to cellular disruption) and cell cycle regulation. In contrast, LsoB exposure triggered changes in genes involved in autophagy (a cellular self-cleaning process), apoptosis (programmed cell death), and immune pathways. These differences in gene regulation likely explain why LsoB is acquired and transmitted more readily by the psyllids. These findings build upon earlier research showing the association between Candidatus Liberibacter solanacearum and disease in various solanaceous crops, including husk tomato[3]. That study, conducted in Mexico, identified haplotype B in both plants and B. cockerelli psyllids, reinforcing its importance as a pathogen and vector. Furthermore, research into other host plants, like carrots, has revealed a diversity of Lso haplotypes and even novel haplotypes[4]. The Texas A&M University study adds to this understanding by demonstrating that even within a single vector species, the pathogen’s genetic makeup can influence its transmission efficiency. The identification of haplotype-specific gene regulation in B. cockerelli nymphs provides valuable insights into the mechanisms driving disease spread. This knowledge could inform the development of targeted control strategies, such as breeding potato varieties with enhanced resistance or identifying specific genes in the psyllid that could be targeted by insecticides.

AgricultureBiotechPlant Science

References

Main Study

1) Accumulation and transmission dynamics of ‘Candidatus liberibacter solanacearum’ haplotypes A and B by potato psyllid nymphs: bioassay and transcriptomic insights

Published 6th January, 2026

https://doi.org/10.1007/s11033-025-11417-y

Related Studies

2) A New 'Candidatus Liberibacter' Species in Solanum tuberosum in New Zealand.

https://doi.org/10.1094/PDIS-92-10-1474A

3) Conventional and qPCR reveals the presence of 'Candidatus Liberibacter solanacearum' haplotypes A, and B in Physalis philadelphica plant, seed, and Βactericera cockerelli psyllids, with the assignment of a new haplotype H in Convolvulaceae.

https://doi.org/10.1007/s10482-019-01362-9

4) Genetic Variation of 'Candidatus Liberibacter solanacearum' Haplotype C and Identification of a Novel Haplotype from Trioza urticae and Stinging Nettle.

https://doi.org/10.1094/PHYTO-12-17-0410-R


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