Pseudomonas syringae pv. actinidiae
(bacterial canker of kiwifruit)

Bacterial canker of kiwifruit, caused by Pseudomonas syringae pv. actinidiae (Psa), is a serious threat to kiwifruit production worldwide. At least four related but genetically distinct lineages of Psa are currently known, and more are likely to exist. In 2008, a particularly virulent strain emerged in Italy and spread rapidly to all main global kiwifruit production areas. This strain is variously referred to as the pandemic strain, PsaV or Biovar 3. Different Actinidia species and cultivars show varying susceptibility to Psa, and breeding resistant or tolerant kiwifruit varieties is highly important to the industry.

Like all pathovars of Pseudomonas syringae, Psa is present in infected plant material. Transfer of nursery material is a major source of long distance spread, while agronomic techniques such as pruning can contribute to spread within and between orchards. The pathogen can be dispersed in aerosols and can be carried between trees and adjacent orchards in wind-driven rain.

Psa is listed on the EPPO Alert List.

Observations in Italy by Ballestra et al. (2008) suggested that damage is more severe on Actinidia chinensis (i.e. yellow cvs. Hort 16A, Jin Tao and Soreli) but recent observations indicate that A. deliciosa (green cultivars cv. Hayward, Summerkiwi, Tsechelidis and Greenlight) show an equivalent sensibility. However, progression of the disease is quicker in A. chinensis. In France, both yellow and green cultivars are attacked but, as in Italy, damage is more severe on yellow cultivars. Field observations in Italy and New Zealand indicate that male vines often show symptoms before female vines and are more severely affected (Balestra, pers. comm., 2011). On the basis of  field observations in Italy 'Tomuri' male vines appear to be less susceptible than 'Matua' male vines (Balestra, personal communication, 2011). P. syringae pv. actinidiae has been detected on A. arguta in France (Vanneste et al., 2014) and has also been isolated from wild A. kolomikta in Italy (Scortichini et al., 2012).

Actinidia is not a unique host for P. syringae pv. actinidiae. Liu et al. (2016) have reported Alternanthera philoxeroides, Setaria italica and Paulownia fortunei as interhosts in China.

Life-Cycle

In spring and early summer, P. syringae pv. actinidiae develops in expanding shoots and leaves. Small cankers develop on extending vines, and leaves develop angular leaf spots surrounded by chlorotic haloes. In winter and early spring, extending cankers form on trunks and branches (Serizawa et al., 1994).

Epidemiology

Serizawa et al. (1989) noted that the damage associated with P. syringae pv. actinidiae occurs in two phases. One phase occurs in autumn/winter and involves damage to the main vine structure and overwintering canes. The other phase occurs in spring and involves the new season's growth (leaves, flowers and canes). The bacterium infects the host through stomata, hydathodes, lenticels, trychomes, leaf scars or wounds, and can progress to the roots where it overwinters (Mazzaglia et al., 2010; Renzi et al., 2012).

P. syringae pv. actinidiae is most invasive at relatively low temperatures (10-20°C; optimum 15±3°C). The optimum temperature for growth of P. syringae pv. actinidiae on new canes is 12-18°C (Serizawa and Ichikawa, 1993b). Temperatures above 20°C are less favourable to the bacterium and Serizawa and Ichikawa (1993b) observed no symptoms on plants in Japan at temperatures above 25°C. However, in France, Italy and Portugal, symptoms have been observed at temperatures above 25°C (GM Balestra, personal communication, 2011).

Like many other bacterial plant diseases, strong winds and heavy rainfall favour the disease. Strong winds during rain may both injure the plants and disperse the bacterial exudate to the wounds and/or natural openings (Serizawa et al., 1989). Winter frost and late frost ('spring frost') as well as hail also favour the occurrence of the disease.

Damage caused by P. syringae pv. actinidiae was found to increase when high populations of Pseudomonas syringae pv. syringae or P. viridiflava, two other bacterial pathogens of Actinidia sp., were present on the plants (Mazzaglia et al., 2010).

Psa is reported to colonise various plant parts epiphytically. Stefani and Giovanardi (2011) demonstrated that populations were able to survive for 21 weeks on leaves. They also isolated Psa from flowers, where colonisation was observed to be more effective than on leaves. Psa has also been isolated from asymptomatic twigs collected from symptomatic and asymptomatic plants (Gallelli et al., 2011).

Incidence

There is currently no evidence that Psa infects seed, or is seed transmitted (Scortichini et al., 2012; EPPO, 2012b). Kiwifruit have small mature seeds which are extracted manually from mature and invariably healthy fruit. These factors reduce the likelihood of successful transmission or even association of pathogens such as Psa with seed (Hu et al., 1999). 

Seed Treatments

Not required. Seed from fruit for propagation obtained by aseptic excision will prevent transmission.

Isolates of P. syringae pv. actinidiae are very slow growing compared with other kiwifruit pathogens. P. syringae pv. actinidiae is negative in all API tests for utilization of raffinose, aesculin, xylose, arabitol, adonitol, mucate, protochatechuate and trigonelline, for production of acid from sucrose, and ice-nucleation capability. These tests discriminate P. syringae pv. actinidiae from all other known pathogens of P. syringae (Young et al., 1997). The Biolog reactions of P. syringae pv. actinidiae permit reliable identification of the pathogen (Koh, 1997).

Morphological identification

P. syringae pv. actinidiae should be isolated for morphlogical identification. For symptomatic samples, non-selective growth media: PPGA (Takikawa et al., 1989), KB (King et al., 1954) and NSA (Crosse, 1959), and semi-selective media produced by modifying KB and NSA media (by adding boric acid 1.5 g/l, cycloheximide 200 mg/l and cephalexin 80 mg/l) can be used (GM Balestra, personal communication, 2011; Gallelli et al., 2011a). Populations can be characterized using phenotypic characteristics as described by Takikawa et al. (1989) and Vanneste et al. (2011).

Molecular tests

PCR primer sets have been developed for the detection of P. syringae pv. actinidiae (Sawada et al., 1997; Koh and Nou, 2002); however, these were not specific to P. syringae pv. actinidiae. Rees-George et al. (2010) have developed specific primers PsaF1/PsaR2. These primers do not allow P. syringae pv. actinidiae to be distinguished from P. syringae pv. theae, but this pest has only ever been isolated from tea plants (Scortichini et al., 2002). However, these primers are able to detect Pseudomonas syringae pv. actinidifoliorum which affects kiwifruit plants causing minor damage in New Zealand (Vanneste et al., 2013), France (Cunty et al., 2014) and Spain (Abeillera et al., 2015).

Several diagnostic methods have been developed to specifically detect P. syringae pv. actinidiae: a duplex PCR assay (Gallelli et al., 2011b) able to specifically detect all Psa biovars and distinguish them from P. syringae pv. theae and  Pseudomonas syringae pv. actinidifoliorum. A multiplex PCR assay has recently been developed to quickly indicate the origin and virulence of P. syringae pv. actinidiae strains, as well as test a large number of samples collected during surveillance and prevention activities (Balestra et al., 2013). An end-point PCR and a quantitative real-time PCR, able to detect strains belonging to the more aggressive biovar (3) were developed by Gallelli et al. (2014). A nested PCR to specifically detect the pathogen from bleeding sap (Biondi et al., 2013), a real-time PCR assay, able to detect strains of biovar 3 (Andersen et al., 2018) and a LAMP-PCR (Ruinelli et al., 2017) have also been developed. Some inter-laboratory studies have provided a comparison of several diagnostic methods suggesting the use of the most reliable methods for screening of symptomatic and asymptomatic samples during monitoring assays and for the specific identification of the bacterium (Loreti et al., 2014; Loreti et al., 2018).

P. syringae pv. actinidiae is one of several related pathogens that attack kiwifruit. There is a need to discriminate P. syringae pv. actinidiae from Pseudomonas viridiflava, Pseudomonas syringae pv. syringae, P. syringae pv. actinidifoliorum and the distinct Pseudomonas sp. of the genomovar savastanoi, pathogenic to kiwifruit, reported by Young et al. (1997). All these pathogens produce similar, if not identical, chlorotic, angular leaf lesions and infections of floral buds and flowers, but only P. syringae pv. actinidiae commonly causes the exudation of translucent gum from floral buds and the undersurfaces of leaves. Only P. syringae pv. actinidiae and P. syringae pv. syringae produce gumming, invasive, necrotic lesions which develop along canes and trunks to produce extensive cankers. The translucent gum becomes rusty brown when it is exuded from larger cankers.

Due to the variable regulations around (de)registration of pesticides, your national list of registered pesticides or relevant authority should be consulted to determine which products are legally allowed for use in your country when considering chemical control. Pesticides should always be used in a lawful manner, consistent with the product's label.

Cultural Control

In countries and regions where P. syringae pv. actinidiae is not present, new plantings should be produced from nursery material from disease-free sources. In countries and regions where P. syringae pv. actinidiae is present, prophylactic measures should be implemented in orchards to prevent its spread/infection, e.g. disinfection of pruning tools between cuts or at the time of harvest, avoidance of cutting and re-growth of plants already compromised at trunk level and eliminating them completely, including the root apparatus; and avoiding grafting on plants cut after infection.

Chemical Control

Although some symptoms of the disease, such as leaf spots, may be reduced by antibacterial spray applications (Serizawa et al., 1989) economic and reliable control of the disease and prevention of vine canker is difficult. Cupric compounds are able to protect/prevent and reduce many of the risks of infection/re-infection by P. syringae pv. actinidiae if sprayed at the right concentration and the right time.

Biological Control

A natural antagonist (Bacillus amyloliquefaciens subsp. plantarum strain D747) has recently (2012) been successfully registered in the EU for use as a preventive control strategy against P. syringae pv. actinidiae.

08/01/18 Review of Diagnosis section by:

Stefania Loreti, Consiglio per la ricerca in agricoltura e l'analisi dell'economia agraria, Centro di ricerca Difesa e Certificazione, Sede di Roma, Rome, Italy.

20/12/16 Reviewed by:

Jocelyn A Berry, Policy and Risk Directorate, Ministry for Primary Industries, Wellington, New Zealand.