*Corresponding author Bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa) is one of the most destructive diseases affecting kiwifruit (Actinidia spp.) worldwide (Scortichini et al., 2012; Vanneste, 2017). Since the pathogen was first described in Japan (Takikawa et al., 1989), severe epidemics have occurred in many kiwifruit-producing countries (Ferrante and Scortichini, 2009; Koh et al., 1994). Psa populations are classified into several biovars that differ in virulence, geographic distribution, and epidemic potential (Chapman et al., 2012; McCann et al., 2017). Among these, Psa biovar 3 (Psa3) has been associated with recent global epidemics in yellow-fleshed kiwifruit production systems and is considered a lineage with high epidemic potential (Ferrante and Scortichini, 2010; Vanneste, 2017). Similar outbreaks associated with highly susceptible yellow-fleshed cultivars have also been reported in Korea (Koh et al., 2010).
Kiwifruit cultivation in Korea began in the late 1970s and expanded mainly in southern regions including Jeonnam, Gyeongnam, and Jeju provinces (Fig. 1) (Koh, 1995). For nearly three decades, commercial production relied predominantly on the green-fleshed cultivar Actinidia deliciosa ‘Hayward’. During this period, bacterial canker outbreaks were sporadic and were primarily associated with Psa biovar 2 (Kim et al., 2017; Ko et al., 2002).
Fig. 1.
Major cultivation areas of kiwifruit in Korea. Red circles indicate the relative cultivation acreage of kiwifruit in major production regions based on aggregated orchard records. This map provides a geographic overview of kiwifruit production in Korea, where bacterial canker has been repeatedly reported.
A major transition in cultivar composition occurred in the mid-2000s following the introduction and rapid expansion of yellow-fleshed A. chinensis cultivars driven by market demand. Because kiwifruit is a perennial crop, large-scale changes in cultivar composition may influence pathogen population dynamics over extended periods. However, the relationship between host cultivar transitions and pathogen lineage prevalence has received limited attention.
To examine possible relationships between cultivar composition and pathogen populations, national records of kiwifruit cultivar acreage were compiled from the National Institute of Horticultural and Herbal Science and Zespri Korea. These records summarized annual planting areas of major cultivars grown in Korea from 2003 to 2022 (Table 1). Temporal changes in Psa lineage prevalence were assessed using diagnostic records from regional plant disease diagnostic centers located in major kiwifruit-producing regions. Infected plant samples submitted from commercial orchards were confirmed by bacterial isolation and polymerase chain reaction-based identification of Psa biovars according to previously described methods (Kim et al., 2016a, 2016b).
Table 1.
Cultivation acreages (ha) of major kiwifruit cultivars in Korea during 2003-2022
Cultivar responses to infection were also examined using greenhouse inoculation assays and field observations. In greenhouse tests, leaves of potted plants were wound-inoculated with bacterial suspensions (approximately 108 CFU ml-1) of two representative Psa3 strains (SYS1 and ITK3). Symptom development was evaluated 7 days after inoculation on multiple plants per cultivar. Disease expression under natural infection conditions was additionally assessed in commercial orchards by observing symptoms on leaves, canes, and trunks of multiple trees per cultivar.
Long-term cultivation records indicate that commercial kiwifruit production in Korea was almost exclusively based on ‘Hayward’ until the early 2000s. Beginning in the mid-2000s, yellow-fleshed A. chinensis cultivars such as ‘Hort16A’ were introduced and rapidly expanded, followed later by the cultivar ‘Zesy002’ and several domestically developed cultivars (Table 1). After severe bacterial canker outbreaks affecting highly susceptible cultivars, the acreage of these cultivars declined and relatively tolerant cultivars, including tetraploid selections, were gradually adopted.
Temporal changes in Psa lineage prevalence are summarized in Fig. 2. During the period when kiwifruit production was dominated by ‘Hayward’, bacterial canker outbreaks were relatively sporadic and were mainly associated with the endemic lineage Psa biovar 2. Following the expansion of diploid yellow-fleshed A. chinensis cultivars in the early 2000s, the detection frequency of Psa biovar 3 increased markedly and eventually replaced Psa biovar 2 as the dominant lineage in Korea. These changes in pathogen lineage prevalence occurred concurrently with major transitions in host cultivar composition (Fig. 3).
Fig. 2.
Temporal changes in the prevalence of Pseudomonas syringae pv. actinidiae (Psa) biovars in Korea during 2003-2022. Values represent the proportion (%) of surveyed kiwifruit orchards in which each biovar was detected annually based on diagnostic records from regional plant disease diagnostic centers. Psa biovar 2 (Psa2) predominated during periods when kiwifruit production was dominated by the cultivar ‘Hayward’, whereas Psa biovar 3 (Psa3) became prevalent following the expansion of yellow-fleshed Actinidia chinensis cultivars, illustrating a strong temporal association between host cultivar transitions and pathogen lineage prevalence.
Fig. 3.
Changes in cultivation acreages (ha) of the yellow-fleshed kiwifruit cultivars ‘Hort16A’ and ‘Zesy002’ in Korea during 2004-2022. These cultivars represent major yellow-fleshed Actinidia chinensis selections associated with periods of increased bacterial canker incidence and are shown to illustrate long-term transitions in host cultivar composition.
Clear cultivar-dependent differences in disease expression were observed in both greenhouse inoculation assays and field observations. Diploid yellow-fleshed cultivars generally exhibited severe foliar symptoms following inoculation with Psa3, whereas tetraploid cultivars showed reduced symptom development. The hexaploid cultivar ‘Hayward’ developed leaf lesions but showed comparatively limited disease severity in woody tissues under field conditions (Tables 2, 3, Supplementary Fig. 1).
Table 2.
Degree of leaf symptoms on seedlings of major kiwifruit cultivars grown in pots 7 days after artificial wound inoculation with two strains of Psa3 under greenhouse conditions
Table 3.
Symptom expression on major kiwifruit cultivars in farmers’ orchards naturally infected with Psa3
Although direct causal relationships cannot be inferred from observational data, the strong temporal association between cultivar transitions and pathogen lineage replacement suggests that host cultivar composition may influence pathogen population structure at the production-system scale. Similar host-associated patterns have been reported in other kiwifruit-producing countries where epidemics on yellow-fleshed cultivars coincided with the emergence and spread of highly epidemic Psa lineages (Ferrante and Scortichini, 2010; Vanneste, 2017). Rather than reflecting direct competition among pathogen lineages, such changes are more plausibly explained by differences in host susceptibility that influence pathogen multiplication, inoculum production, and transmission opportunities. These interpretations are consistent with previous studies highlighting the importance of host resistance, defense responses, and cultivar characteristics in the management of bacterial canker in kiwifruit (Reglinski et al., 2013; Tahir et al., 2019, 2020; Wang et al., 2022).
The Korean kiwifruit production system therefore provides a well-documented example in which long-term transitions in host cultivar composition were accompanied by clear shifts in pathogen lineage prevalence. These findings highlight the importance of considering host cultivar deployment together with pathogen monitoring when developing sustainable management strategies for bacterial canker in perennial fruit crops.
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