Pseudomonas syringae pv. actinidiae: Ecology, Infection Dynamics and Disease Epidemiology

Abstract

Since 2008, the kiwifruit industry has been devastated by a pandemic outbreak of Pseudomonas syringae pv. actinidiae (Psa), the causal agent of bacterial canker. This disease has become the most significant limiting factor in kiwifruit production. Psa colonizes different organs of the host plant, causing a specific symptomatology on each of them. In addition, the systemic invasion of the plant may quickly lead to plant death. Despite the massive risk that this disease poses to the kiwifruit industry, studies focusing on Psa ecology have been sporadic, and a comprehensive description of the disease epidemiology is still missing. Optimal environmental conditions for infection, dispersal and survival in the environment, or the mechanisms of penetration and colonization of host tissues have not been fully elucidated yet. The present work aims to provide a synthesis of the current knowledge, and a deeper understanding of the epidemiology of kiwifruit bacterial canker based on new experimental data. The pathogen may survive in the environment or overwinter in dormant tissues and be dispersed by wind or rain. Psa was observed in association with several plant structures (stomata, trichomes, lenticels) and wounds, which could represent entry points for apoplast infection. Environmental conditions also affect the bacterial colonization, with lower optimum values of temperature and humidity for epiphytic than for endophytic growth, and disease incidence requiring a combination of mild temperature and leaf wetness. By providing information on Psa ecology, these data sets may contribute to plan efficient control strategies for kiwifruit bacterial canker. Keywords Actinidia chinensis Planch. var. chinensis. Actinidia chinensis var. deliciosa (A.Chev.). Temperature. Relative humidity. Confocal laser scanning microscopy (CLSM). Overwintering

WITHDRAWN: Genotype-Dependent Recruitment of the Strawberry Holobiome

“…Interestingly, several strawberry pathogens were found among the core fungal OTUs, namely Plectosphaerella cucumerina (fruit, root and collar rot), Botrytis caroliniana (gray mold) and Alternaria alternata (black leaf spot) ( Table S2). The colonisation of plant organs by a pathogen is not su cient, per se, to result in a successful infection causing disease symptoms 33 . This observation con rms that abiotic (e.g.…”

Genetic Diversity of Pseudomonas syringae pv. actinidiae: Seasonal and Spatial Population Dynamics

“…actinidiae (Psa), has been affecting kiwifruit orchards worldwide for the past decade. The severity of the disease and lack of control led to a pandemic causing significant losses in production, risking the economic viability of the sector [ 1 , 2 , 3 , 4 ].…”

“…Nowadays, the mechanisms of penetration and colonization of Psa are better understood, and beside the susceptibility of the host, are modulated by biotic and abiotic conditions [ 4 , 24 , 25 ]. Indeed, temperature and humidity contribute decisively to the severity and dispersal of the disease [ 4 , 8 ]. Host plant colonization can occur throughout the year; nevertheless, bacterial growth is favoured in certain seasons, while temperatures between 12 °C and 18 °C and high humidity foster Psa multiplication, growth is reduced above 25 °C and below 10 °C [ 26 , 27 ].…”

“…For a successful infection cycle, Psa strains need to surpass host plant defences, making a transition from the epiphytic phase to the endophytic phase to cause disease [ 25 ]. Indeed, Psa can enter the host plant through natural surface structures or wounds, like stomata, trichomes, lenticels, and fruit abscission scars or fresh cuts, and endophytically migrate from the leaves to shoots and canes via apoplast [ 4 , 24 , 30 ]. Once inside the host’s tissues, Psa can migrate systemically to different organs preferentially through xylematic vessels [ 4 ].…”

“…Indeed, Psa can enter the host plant through natural surface structures or wounds, like stomata, trichomes, lenticels, and fruit abscission scars or fresh cuts, and endophytically migrate from the leaves to shoots and canes via apoplast [ 4 , 24 , 30 ]. Once inside the host’s tissues, Psa can migrate systemically to different organs preferentially through xylematic vessels [ 4 ]. Endophytic colonization occurs only after Psa epiphytic population exceeds the infection threshold that varies according to plant susceptibility [ 4 ].…”