Type: Foliicolous Fungi; Description: Conidiomata pycnidial, solitary or in scattered groups, immersed, globose, pale brown; on small buff leaf spots with reddish margins, and on stems. Conidia ellipsoid, 0-septate, 4–7 × 2–3 μm, smooth, hyaline.

Distribution: Auckland.; 1st Record: Smith et al. (1987).

Significance: Under trial as a biocontrol agent against the invasive weed, Clematis vitalba. Shown by Smith & Cole (1991) to be the causal agent of leaf spot and wilt in large-flowered Clematis hybrids and leaf spot in small-flowered Clematis cultivars. It is considered to be a wound pathogen. On outdoor plants, stems are infected near the ground and are often girdled, causing wilt.; Host(s): Clematis vitalba, Clematis sp.

A field survey for plant pathogens of C. vitalba was carried out in Europe and North America in 1990. Pathogenic fungi were isolated from 57 collections of diseased C. vitalba leaves from nine countries. Only two species, Phoma clematidina (Thümen) Boerema and Colletotrichum gloeosporioides (Penz) Penz and Sacc., were pathogenic, each causing extensive leaf necrosis. A weakly pathogenic form of P. clematidina was already present in New Zealand. After host range testing a virulent strain of P. clematidina was introduced in 1996. Releases of P. clematidina have been made at 23 sites and establishment confirmed at 11 sites. Pathogens as potential biological control agents Spiers (1991) completed a survey of pathogens affecting old man’s beard in Continental Europe, England, and North America. He collected leaves of Clematis spp. that showed disease symptoms. The pathogens associated with those symptoms were isolated and identified. These included: Botrytis cinerea Pers. (anamorphic Sclertiniaceae), Ramularia sp., Septoria sp.(anamorphic Dothideaceae), Cercospora sp. (anamorphic Mycosphaerellaceae), Phoma clematidina (Thümen) Boerema (anamorphic Pleosporaceae), Colletotrichum actuatum Simmonds ex Simmonds , and Colletotrichum gloeosporioides (Penz) Penz and Sacc.(anamorphic Phyllachoraceae). All fungi were cultured and screened for aggressiveness towards C. vitalba leaves and 2 species were found to be pathogenic: P. clematidina and Colletotrichum gloeosporioides. The others were either not pathogenic (Ramularia sp., Septoria sp., Cercospora sp., Colletotrichum actuatum), or not host specific (B. cinerea). After extensive laboratory tests a single isolate of P. clematidina from C. ligusticifolia Torrey and Gray, that was collected in Washington State, USA, was selected for release in New Zealand (Spiers 1992). This pathogen was found to have caused severe defoliation of C. vitalba in parts of Europe (A.J.S., unpublished data). The new strain of P. clematidina was released in New Zealand in 1996. Colletotrichum gloeosporioides was also found to be pathogenic to New Zealand plants of C. vitalba, but was rejected as a potential biological control agent because it attacked some native Clematis species (Spiers 1994). Phoma clematidina (anamorphic Pleosporaceae) Phoma clematidina causes leaf and stem necrosis, girdling the stem in some cases and causing wilting, premature defoliation, and reduced vigour (Spiers 1995). Wilting induced by this pathogen has caused up to 50% loss amongst Clematis hybrids in some nurseries in Europe (Spiers 1992). Initial infection of leaves or stems in spring is caused by conidia released from pycnidia formed in lesions on overwintering leaves and dead stems. These conidia are dispersed by rain-splash (Spiers 1994). The severity of infection is governed by the amount of rainfall during spring and early summer. During collection trips (in Europe) this fungus was observed to cause severe defoliation of C. vitalba, sufficient to weaken the plant, but not kill it (Spiers 1998). Phoma clematidina infection can be assisted by wounding of the leaves and stems although this is not essential for infection to occur (Spiers 1992). The isolate recently released into New Zealand was specifically selected for its high pathogenicity and did not need wounding of the leaves or stems to facilitate infection, although wounding by an insect biological control agent should increase the damage to C. vitalba (Spiers 1994). Before host testing could start, an isolate of P. clematidina had to be identified that was pathogenic to expanding and fully expanded leaves of New Zealand collections of C. vitalba. This was done by placing leaves on capillary matting in plastic humidity chambers and atomizing on a spore suspension (Spiers 1994). To facilitate the spread of P. clematidina, conidia were washed from agar plates with distilled water and diluted to give 100,000 conidia/ml (Spiers 1994). This suspension was atomized onto both surfaces of detached, expanding, and fully expanded leaves of test plants. Phoma clematidina formed small lesions on petioles of Clematis paniculata J. G. Gmel., and C. quadribracteolata Colenso, and leaf spots on C. montana DC. (Spiers 1994). Necrotic spots were also formed on 3 weed Ranunculus species (Spiers 1994). Further tests were completed on endemic Clematis and Ranunculus species. Detached leaves, stems, and whole plants of 16 representatives of the genus Ranunculus and 16 endemic species of Clematis were tested. Minor spotting occurred on leaves of some plants but no pycnidia were formed on any species except C. vitalba. An application for release of the fungus was made in 1996 and approved. The new virulent strain of P. clematidina has now been released at 23 sites and has spread rapidly throughout the country. The fungus is well established at 11 sites and causing extensive leaf necrosis, leaf fall, and stem dieback at several of these.