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.

Several published polymerase chain reaction (PCR) primers to identify Pseudomonas syringae pv. actinidiae, the causal organism of bacterial canker of kiwifruit, were found not to be specific. Two new sets of PCR primers, PsaF1 ⁄ R2 and PsaF3 ⁄ R4, were designed to be complementary to a portion of the 16S-23S rDNA intertranscribed spacer (ITS) regions. These primers amplified a DNA fragment from strains of P. syringae pv. actinidiae, but not from 56 strains of bacteria from six genera and 17 species, except for a strain of the tea pathogen, P. syringae pv. theae. When tested against DNA extracted from a further 20 strains from Japan, Korea, Italy and the USA deposited in culture collections as P. syringae pv. actinidiae, all except six cultures produced the expected product of 280 bp with PsaF1 ⁄ R2 and 175 bp with PsaF3 ⁄ R4. Results of multilocus sequence analysis using five housekeeping genes (gyrB, acnB, rpoD, pgi and cts) showed that none of these six strains was phylogenetically similar to P. syringae pv. actinidiae. In contrast to the P. syringae pv. actinidiae type strain, these strains were positive in the determinative tests for ice nucleation and syringomycin production. It is suggested that these six strains were incorrectly identified as P. syringae pv. actinidiae. It was not possible to distinguish P. syringae pv. actinidiae from the phylogenetically similar P. syringae pv. theae using the ITS, gyrB, acnB, rpoD, pgi or cts gene regions to design PCR primers. Because P. syringae pv. theae is unlikely to be found on kiwifruit, primers PsaF1 ⁄ R2 and PsaF3 ⁄ R4 are recommended for screening bacteria isolated from kiwifruit tissue.

Avocado fruit can develop small, 1-5 mm diameter brown spots immediately after harvest. These symptoms are typically more severe among fruit harvested following rain. The incidence of the brown spots increased significantly when fruit were artificially imbibed with water, but not when immersed in water. Morphological examination with the light and electron microscope showed there was a change in lenticels that was caused by water uptake. In unaffected fruit, large intercellular spaces were observed in cells below the lenticels, but when the fruit had taken up water, these cells became turgid and filled these spaces. Swollen cells associated with lenticels were more distended than other cells in the mesocarp, because the expansion of mesocarp cells was limited by adjacent cells. Swollen cells in the lenticels became brown more rapidly than other cells, probably because their turgidity made them more susceptible than other cells. Cells close to the surface were also more susceptible to discoloration than internal fruit cells. They were not prone to compression from adjacent cells towards the surface and were consequently more distended than internal cells. At harvest, prior to coolstorage, no fungal mycelium or spores were observed associated with lenticel damage symptoms. Surface-sterilised samples of lenticel damaged tissue failed to yield a fungal pathogen. In coolstorage, however, these fruit developed slightly sunken dark brown patches with irregular margins, referred to as measles, about 10-50 mm diameter The fungi Colletotrichum acutatum and Phomopsis sp. were isolated from such tissue in greater quantities than adjacent green tissue. Imbibation had no effect on measles development, but fruit jostled in a plastic crate to simulate damage that occurs at harvest developed more severe measles than fruit that were not damaged. There was no evidence that lenticel damage lead to measles but both symptoms were worsened by jostling.

No abstract

Species of Colletotrichum, Botryosphaeria, and Phomopsis causing postharvest rots in avocado (Persea americana Miller) fruits are present in the living and dead branches and twigs of avocado trees, and in the living pedicels. They dominate the fungal population within the extra-cambial tissues but are less common within the xylem elements. There is no evidence that invasion of these tissues is pathogenic. With the possible exception of C. gloeosporioides they appear to be discontinuously present and are more properly termed phellophytes rather than endophytes. There was a higher incidence of stem-end rots than of body rots in untreated (control) 'Hass' avocados in New Zealand experiments and most of these stem-end rots were associated with B. parva and Phomopsis spp. A high proportion of stem-end infections appeared to be initiated during harvesting. Picking the fruit by snapping the pedicels instead of clipping, as in commercial practice, resulted in an unusually high level of stem-end rots caused by C. acutatum. Frequently sterilising the clippers used to harvest the fruits reduced the incidence of stem-end infections, in particular those caused by B. parva, indicating that contamination of the clippers is an important source of infection. It is suggested that this contamination is probably present as fragments of infected extracambial tissue.