In a survey of New Zealand vineyards at harvest 1985, isolates of Botrytis cinerea resistant to benzimidazole and to dicarboximide fungicides were common. The mean frequency of resistance in the major vine-growing districts ranged from 8 to 41% for benzimidazoles. and from 51 to 59% for dicarboximides. All benzimidazole-resistant isolates showed high levels of resistance (EC50 greater than 100 mg/l carbendazim based on radial growth response), and all dicarboximide-resistant isolates showed low levels of resistance. Two subgroups of dicarboximide-resistant isolates were recognized, distinguished in the first instance by their osmotic response. Low-level resistant isolates, which formed a dense margin on osmotically amended medium, exhibited an EC50 for mycelial growth on iprodione of c. 3-2 mg/l; ultra-low-level resistant isolates, which formed a fibrillose margin on osmotically amended medium identical to that of sensitive isolates, exhibited an EC50 of c. 1-B mg/l. In agar culture, radial growth rate, and conidial and sclerotial production of both subgroups were similar to those of sensitive isolates. Virulence (lesion size) and conidial production on grape berries were highest in sensitive isolates, intermediate in ultra-low-level dicarboximide-resistant isolates, and lowest in low-level dicarboximide-resistant isolates. Evidence is presented indicating that ultra-low-level dicarboximideresistant strains have progressively replaced low-level dicarboximide-resistant strains in the vineyard population. The presence of dicarboximide-resistant strains was linked with a partial loss of fungicide efficacy.

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.

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