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Pseudomonas syringae pv. actinidiae (Psa) was identified as the causal agent of severe epidemics of bacterial canker on Actinidia chinensis (yellow kiwifruit) in central Italy occurring during 2008-9. A total of 101 strains were obtained from infected leaves, twigs, branches and trunks of cvs Hort16A, Jin Tao and CK3. Outbreaks were also found on A. deliciosa cv. Hayward. A representative set of 21 strains were compared with other Psa strains isolated from previous outbreaks in Japan and Italy as well as with P. s. pv. syringae strains obtained from A. chinensis and with strains of genomospecies 8. Repetitive-sequence PCR (rep-PCR) typing using BOX and ERIC primer sets revealed that all Psa strains obtained during 2008-9 showed the same fingerprinting profile. This profile, however, was different from those of strains previously isolated in Japan and Italy. Multilocus sequence typing (MLST) of gapA, gltA, gyrB and rpoD revealed a higher genetic variability among the strains than rep-PCR, with some of them showing the same sequence pattern although isolated from different areas, cultivars and years. None of the recently obtained strains possessed genes coding for phaseolotoxin or coronatine, and all had an effector protein, namely hopA1, differentiating them from the strains causing past outbreaks in Japan and Italy. All isolates were inhibited in vitro by copper-based compounds, antibiotics, geraniol, citronellol and by a chitin-based organic compound. The recent epidemics found in central Italy on yellow kiwifruit appear to have been caused by a different Psa population than those previously recorded in Japan, South Korea and Italy.
A recent re-emerging bacterial canker disease incited by Pseudomonas syringae pv. actinidiae (Psa) is causing severe economic losses to Actinidia chinensis and A. deliciosa cultivations in southern Europe, New Zealand, Chile and South Korea. Little is known about the genetic features of this pathovar. We generated genome-wide Illumina sequence data from two Psa strains causing outbreaks of bacterial canker on the A. deliciosa cv. Hayward in Japan (J-Psa, type-strain of the pathovar) and in Italy (I-Psa) in 1984 and 1992, respectively as well as from a Psa strain (I2-Psa) isolated at the beginning of the recent epidemic on A. chinensis cv. Hort16A in Italy. All strains were isolated from typical leaf spot symptoms. The phylogenetic relationships revealed that Psa is more closely related to P. s. pv. theae than to P. avellanae within genomospecies 8. Comparative genomic analyses revealed both relevant intrapathovar variations and putative pathovar-specific genomic regions in Psa. The genomic sequences of J-Psa and I-Psa were very similar. Conversely, the I2-Psa genome encodes four additional effector protein genes, lacks a 50 kb plasmid and the phaseolotoxin gene cluster, argK-tox but has acquired a 160 kb plasmid and putative prophage sequences. Several lines of evidence from the analysis of the genome sequences support the hypothesis that this strain did not evolve from the Psa population that caused the epidemics in 1984–1992 in Japan and Italy but rather is the product of a recent independent evolution of the pathovar actinidiae for infecting Actinidia spp. All Psa strains share the genetic potential for copper resistance, antibiotic detoxification, high affinity iron acquisition and detoxification of nitric oxide of plant origin. Similar to other sequenced phytopathogenic pseudomonads associated with woody plant species, the Psa strains isolated from leaves also display a set of genes involved in the catabolism of plant-derived aromatic compounds.
Angular, necrotic leaf spot, longitudinal cracks along the petiole, oozing and wilting of branches were observed during summer 2008 on Actinidia chinensis (yellow kiwifruit) cultivar Hort16A, cultivated in different orchards located the province of Latina (central Italy). Symptoms closely resembled those incited by Pseudomonas syringae pv. actinidiae on kiwifruit A. deliciosa. Isolates obtained from typical lesions were assessed by means of biochemical, pathogenicity and host range tests and compared with some Pseudomonas syringae pathovars by enterobacterial repetitive intergenic consensus (ERIC‐PCR) analysis. The isolates belong to Pseudomonas LOPAT group Ia, incited the death of pot‐cultivated A. chinensis cv. Hort 16A and A. deliciosa cv. Hayward plants in few days, but did not cause any symptoms to the other inoculated plant species. Upon ERIC‐PCR analysis, all the isolates showed similarity with P. syringae pv. actinidiae NCPPB 3739, type‐strain of the pathovar. This is the first report of this pathogen on A. chinensis in Italy and, as far as we currently know, in the world.
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