Pseudomonas syringae pv. actinidiae, the causal agent of bacterial canker of kiwifruit, was detected for the first time in New Zealand in November 2010. Only in Bay of Plenty, one of the four regions where this pathogen had been detected, did symptoms evolve beyond leaf spots, resulting in cane die-back, wilting of canes, and canker, sometimes leading to death of the vine. Molecular analysis (cts haplotype and BOX-polymerase chain reaction [PCR] electrophoretic pattern) of strains isolated from different regions of New Zealand revealed that two biovars could be distinguished. They have been called biovar 3 and biovar 4 to differentiate them from strains from Japan (biovar 1) or Korea (biovar 2), which have a different cts haplotype or a different BOX-PCR pattern. Biovars 3 and 4 displayed different degrees of virulence, as measured by their ability to cause leaf spots on young, potted kiwifruit plants. Biovar 3, which has also been present in Italy since 2008 and in France, was found in the Bay of Plenty, where cane diebacks were observed. In contrast, no symptoms other than leaf spots have been observed in orchards where strains of biovar 4 have been isolated. We report the distribution and the disease progression of biovars 3 and 4 in New Zealand.

Pseudomonas syringae pv. actinidiae, the causal agent of canker in kiwifruit (Actinidia spp.) vines, was first detected in Japan in 1984, followed by detections in Korea and Italy in the early 1990s. Isolates causing more severe disease symptoms have recently been detected in several countries with a wide global distribution, including Italy, New Zealand, and China. In order to characterize P. syringae pv. actinidiae populations globally, a representative set of 40 isolates from New Zealand, Italy, Japan, South Korea, Australia, and Chile were selected for extensive genetic analysis. Multilocus sequence analysis (MLSA) of housekeeping, type III effector and phytotoxin genes was used to elucidate the phylogenetic relationships between P. syringae pv. actinidiae isolates worldwide. Four additional isolates, including one from China, for which shotgun sequence of the whole genome was available, were included in phylogenetic analyses. It is shown that at least four P. syringae pv. actinidiae MLSA groups are present globally, and that marker sets with differing evolutionary trajectories (conserved housekeeping and rapidly evolving effector genes) readily differentiate all four groups. The MLSA group designated here as Psa3 is the strain causing secondary symptoms such as formation of cankers, production of exudates, and cane and shoot dieback on some kiwifruit orchards in Italy and New Zealand. It is shown that isolates from Chile also belong to this MLSA group. MLSA group Psa4, detected in isolates collected in New Zealand and Australia, has not been previously described. P. syringae pv. actinidiae has an extensive global distribution yet the isolates causing widespread losses to the kiwifruit industry can all be traced to a single MLSA group, Psa3.

Leaves from gold kiwifruit plants, Actinidia chinensis, with dark brown angular spots and flowers that were brown and wilted, first yielded non-fluorescent bacterial colonies following isolation. These bacterial colonies were identified by diagnostic polymerase chain reaction (PCR) as Pseudomonas syringae pv. actinidiae. These samples were obtained from the Te Puke region of New Zealand. All isolates were Gram negative and were levan positive, oxidase negative, potato soft rot negative, arginine dehydrolase negative and tobacco hypersensitivity positive (LOPAT 1a). Sequences of the gyrB and the rpoD genes of these isolates were 100% homologous to sequences of P.s. pv. actinidiae deposited in GenBank including the type strain. Koch's postulates were proven by pathogenicity tests on kiwifruit seedlings.

A rapid and sensitive method has been developed for the specific detection of Erwinia amylovora (Burr.) Winslow et al. using the polymerase chain reaction (PCR). The method involves amplification of a 187 bp DNA fragment, probably of chromosomal origin. All 69 cultures of E. amylovora in an international collection from 10 host species in five countries were successfully identified using the primers. In contrast, discrete PCR products were not amplified from 29 other Erwinia species or from 20 other species of plant pathogenic and saprophytic bacteria. A detectable 187 bp product was consistently amplified from reactions containing † Corresponding author. H00034

A PCR‐based method was developed for the specific detection of Xanthomonas campestris pv. phaseoli var. fuscans from plant material. Primers Xf1 and Xf2, based on a sequence conserved amplified region (SCAR) derived from RAPD PCR analysis of X. c. pv. phaseoli var. fuscans, amplified a DNA fragment of 450 bp from all such isolates. In contrast, no amplification product was obtained from any X. c. pv. phaseoli isolates, or from any other DNAs tested. As few as 10 cells of X. c. pv. phaseoli var. fuscans (equivalent to about 100 fg DNA) could be detected in vitro. In planta, following an initial inoculation of as little as one cell, an amplification product was generated after only 2 d of incubation, allowing highly sensitive detection 10 d before disease symptoms were observed. Moreover, the failure to amplify DNA from X. c. pv. phaseoli isolates shows that these primers provide a rapid, improved method to differentiate these two varieties using PCR.