Zebra chip disease is named after the dark stripes it forms inside afflicted potato tubers when cut and fried to make chips.

Zebra Chip of Potato is Caused by Liberibacter

Zebra chip disease is named after the dark stripes it forms inside afflicted potato tubers when cut and fried to make chips.

Zebra chip has caused millions of dollars in production and processing losses since its first reported U.S. occurrence in potato fields near McAllen and Pearsall, Texas, in 2000.

The disease, whose above-ground symptoms include necrosis and purplish, upward-curling leaves, among others, has since been reported in several other states (California, Nevada, Kansas, Nebraska, New Mexico, Colorado, Wyoming, Washington, Oregon, and Idaho), Mexico, parts of Central America, and New Zealand.

(Click to enlarge)

Potato Tubers affected by Zebra chip disease

The disease is caused by a bacterium, Candidatus Liberibacter solanacearum, while it is transmitted from plant to plant by potato psyllids, Bactericera cockerelli.

As of 2017 the potato psyllids responsible for the transfer of the zebrachip disease have been observed in Western Australia, but no Candidatus Liberibacter solanacearum has been detected so far.

In the Mediterranean, Liberibacter is present, but no psyllids seem to be present that effectively spread the bacterium to potatoes.

Scientific description of Zebra Chip of Potato (2020)

Based on Charkowski A., Sharma K., Parker M.L., Secor G.A., Elphinstone J. (2020) Bacterial Diseases of Potato. In: Campos H., Ortiz O. (eds) The Potato Crop. Springer, Cham

The authors of this content are Amy Charkowski, Kalpana Sharma, Monica L. Parker, Gary A. Secor, John Elphinstone

Taxonomy and Nomenclature

The genus 'Candidatus Liberibacter' is a gram-negative bacterium in the Rhizobeaceae family. At least seven Ca. Liberibacter species exist. Of these, 'Candidatus Liberibacter solanacearum' (Lso), which is a phloem-limited pathogen, is the only known potato-infecting species.

There are at least five Lso haplotypes, with haplotypes A and B causing disease on potato and the remaining three haplotypes infecting carrots and celery (Nelson et al. 2011; Teresani et al. 2014).

At 1.26 Mbp, the circular Lso genome is relatively small (Hong Lin et al. 2011) and there are relatively few genomic differences among Lso haplotypes (Wang et al. 2017a, b, c). Compared to related free-living bacteria, such as Agrobacterium, Lso has a low G + C content and lacks many genes involved in metabolism.

Host Range

Potato is the most economically important host of Lso haplotypes A and B, but Lso can also infect other solanaceous crops and weeds. All Ca. Liberibacter are spread by Bactericera species and Lso also infects its vector and can reduce vector fitness (Yao et al. 2016).

Although Lso is only spread in potato by B. cockerelli, but it can also be found in other Bactericera species, suggesting that vector feeding preferences limit the species of vectors important for zebra chip and not Lso-vector interactions (Borges et al. 2017).

Geographical Distribution

Potato psyllids are native to North and Central America, and it recently invaded New Zealand (Teulon et al. 2009). The bacterial pathogen has spread with its vector and can be found wherever potato psyllids are found. The highest disease incidence is typically found in the Southwestern United States, Mexico, and Central America.


Zebra chips symptoms are severe on both the foliage and the tubers. The upper parts of infected plants have leaf curling, chlorosis, shortened internodes, aerial tubers, and early necrosis and death (Buchman et al. 2012) (image below). The tubers appear to have glassy or brown streaks that darken when they are fried, giving the disease its name, zebra chip.

Tuber development slows or ceases in symptomatic plants, resulting in yield losses. Lso appears to reduce protease inhibitor levels in tubers, and as a result, tubers from infected plants have less protein (Kumar et al. 2015). Infected tubers either do not sprout or have only hair sprouts (Rashed et al. 2015).

If plants emerge from infected tubers, they die shortly after emergence. Storage temperature affects symptom development, with cooler storage (3 °C) resulting more tuber symptoms than warmer storage temperatures (6 or 9 °C) (Wallis et al. 2017).

Typical Lso symptoms on potato. Leaf curl symptoms on foliage (a); Necrotic specks in tuber (b); Blackened splotches on a fried chip (healthy on left, and diseased on right) (d) (Courtesy: Gary A. Secor, North Dakota State University)


Lso is transmitted solely by B. cockerelli, which feeds on phloem with its piercing-sucking mouthparts. The pathogen is transmitted in a persistent, propagative, and circulative fashion and it is also transmitted transovarially in the psyllid (Cicero et al. 2016; Hansen et al. 2008). A 2-week latent period occurs between psyllid acquisition of Lso and ability to transmit the pathogen (Sengoda et al. 2014).

In most regions in North America where the pathogen and vector are present, potatoes are infected late in the season. Surprisingly, Lso reduces the fitness of its insect vector, with haplotype B resulting in more insect mortality than haplotype A (Yao et al. 2016).

Once transmitted into a leaf, the pathogen does not cause symptoms for at least 3 weeks. It is also not evenly distributed in plants, which makes it difficult to detect prior to symptom development and this has hampered epidemiological studies.

Lso is not culturable, which also makes epidemiological studies more challenging and as a result, researchers rely mainly on PCR assays for pathogen detection (Ananthakrishnan et al. 2013; Secor et al. 2009).

Based on symptom development, Lso appears to be sensitive to temperatures above 32 °C and to thrive at 27–32 °C. Solanaceous weeds serve as important reservoirs for Lso and can provide a green bridge between potato crops (Thinakaran et al. 2015).

Infected tubers rarely sprout and when they do, they tend to develop hair sprouts. As a result, this disease is poorly transmitted through seed potatoes and insect transmission remains the most important mode of spread. For this reason, zebra chip is not currently regulated through seed potato certification in North America. It has, however, impacted export of potatoes from North America.

Pathogenicity Determinants and Resistance

Liberibacter pathogenicity determinants were recently thoroughly reviewed (Wang et al. 2017a, b, c). There are no resistant potato varieties, although timing and severity of symptoms differ among varieties (Lévy et al. 2015).

Tolerant lines still support Lso levels similar to those found in susceptible varieties, but the Lso has less impact on plant physiology and symptom development in tubers in tolerant lines (Rashidi et al. 2017; Wallis et al. 2015).

Recent results also suggest that psyllids are not able to transmit the pathogen with equal efficiency into all potato lines (Rashidi et al. 2017).

Significance and Economic Loss

Zebra chip has caused millions in losses in North America, and although seed tubers are not a major source of inoculum, it has affected the potato export market. The spread of this pathogen and its vector to New Zealand has also caused significant losses there.

In addition to losses in yield and quality, the high cost of vector management has added to financial losses caused by L. solanacearum.


Insecticides are the main management method used for control of zebra chip. Growers in North America monitor psyllids and determine when psyllids appear and the percentage of Lso-infected psyllids present.

They may spray insecticides a dozen or more times during the growing season to protect the potato crop, with imidocloprid and spirotetramat among the most commonly used (Guenthner et al. 2012).

Since the insects tend to be present on the underside of leaves, effectively covering the underside of the leaves is essential. These sprays are expensive and the potential for insecticide resistance and loss of natural enemies due to frequent sprays makes this approach unsustainable in the long term.
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