Urediospores of U. viciae-fabae (broad bean rust) germinated well in the range 5-26 mC, with fastest germination at 20 mC. Exposure to 30 mC gave poor germination and damaged the spores. Infection of Vicia faba leaves depended on a moisture film. At 20 mC some infection occurred with only 4 h leaf wetness, but longer wet periods up to 24 h gave increased infection. At lower temperatures, the infection process was slower and final pustule numbers were smaller. Spore germination was delayed by daylight and by all artificial light sources that contained far-red (700-800 nm) wavelengths. The delay was increased at higher light intensities. When spores were subjected to alternating periods of light and darkness, it was found that 40 min of darkness was sufficient for the irreversible induction of germination at 20 mC.

A detailed study of conidial germination, germ-tube growth and the formation of infection structures in Phoma clematidina , the causal agent of clematis wilt, is described for two clematis varieties differing in disease resistance. On both the resistant and susceptible varieties, the fungus entered leaves and stems by direct penetration of the cuticle, often, but not always, following the formation of infection structures. More germ tubes per conidium were formed on the susceptible host, but these germ tubes were on average shorter than on the resistant host. Although germ tubes regularly entered the plant via trichomes, stomata were not found to be sites of entry. Following penetration of the cuticle of resistant plants, germ-tube growth was sometimes restricted to the subcuticular region, and halo formation occurred at the sites where penetration was attempted. Subcuticular growth and halo formation were not observed on susceptible plants. These observations may partly explain the resistance of small-flowered clematis varieties to P. clematidina .

Isolates of Phoma clematidina, the cause of clematis wilt, were recovered from diseased clematis plants throughout England and tested in vitro and in vivo for their sensitivity to benzimidazole fungicides. More than one third of 14 isolates tested on fungicide‐amended agar plates were found to be highly resistant to products containing carbendazim, benomyl or thiophanate‐methyl. On unamended agar, the growth and morphology of benzimidazole resistant and sensitive isolates of P. clematidina were clearly distinct; on attached clematis leaves not treated with fungicide, the resistant isolates were markedly less virulent than the sensitive ones. In a 3‐month trial on Clematis cv. Henryi, high volume sprays of a fungicide containing carbendazim reduced the incidence of leaf spotting caused by a benzimidazole sensitive isolate of P. clematidina by almost 80% but gave no significant reduction in disease caused by a resistant isolate. Fungicides found to be very effective against both benzimidazole sensitive and resistant isolates were products containing difenoconazole, azoxystrobin or kresoxim‐methyl. This is the first report of benzimidazole resistance in P. clematidina in the UK. Our findings indicate that growers should consider alternative fungicides and non‐chemical methods for the prevention and control of clematis wilt.

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