Ascochyta clematidina Thüm. (1880)
Phoma clematidina is a fungal plant pathogen and the most common cause of the disease clematis wilt affecting large-flowered varieties of Clematis. Symptoms of infection include leaf spotting, wilting of leaves, stems or the whole plant and internal blackening of the stem, often at soil level. Infected plants growing in containers may also develop root rot.
The asexual stage (anamorph) of the fungus was first described by the German botanist and mycologist Felix von Thümen in 1880 as Ascochyta clematidina. Based on new scientific insights into the differences in spore formation between species, it was reclassified as Phoma clematidina by the Dutch mycologist Gerhard Boerema in 1978.
Genetic sequencing has suggested that Phoma clematidina is heterothallic which means that two compatible strains (mating types) of the fungus would need to come together under the right environmental conditions to produce a sexual stage (teleomorph). Both mating types of Phoma clematidina are known to occur in Europe, and yet no sexual stage (which is most likely to be a Didymella species) has ever been described.
Molecular phylogenetic analyses have revealed that some fungal isolates recovered from wild Clematis species, previously identified as Phoma clematidina, are in fact two closely related species of Phoma and Ascochyta with the sexual stages Didymella vitalbina and Didymella clematidis respectively. The latter fungus has been successfully used as a biological control agent of Clematis vitalba, which is seen as an invasive plant in New Zealand. Unlike Phoma clematidina, the two closely related Didymella species (and their anamorphs) have not been found on large-flowered Clematis varieties.
The previous misidentification of these species means that some literature, particularly that on the biological control of C. vitalba, referring to Phoma clematidina is actually describing work on Didymella clematidis and its Ascochyta anamorph.
The biology of Phoma clematidina is now reasonably well understood thanks to research into clematis wilt at the University of Canterbury in New Zealand  and the University of Derby and ADAS in the UK.
A full overview of its life cycle was first produced in 1999. Within a nursery or garden, the fungus is mainly spread through splash dispersal of its asexual spores (conidia) which are formed in bulbous fruiting bodies called pycnidia. Pycnidia can be formed on any infected part of the plant showing symptoms, including leaves, stems and roots. The pycnidia exude the spores in a sticky mass which is splash dispersed to other plants nearby during rain or irrigation. Contact, such as with pruning tools, may also spread the spores and, in addition, it is suspected that certain insect species may act as contact vectors. Movement of infected plant material forms an important method of spread to previously unaffected nurseries or gardens.
Unlike many other plant pathogens, Phoma clematidina is not a biotroph which means that it can infect plants but does not need them to survive. The fungus can live saprophytically on dead plant material or organic matter as well. In addition, it forms thick-walled resting spores (chlamydospores) which increase its survival in plant debris and soil during unfavourable conditions.
Many publications report Phoma clematidina to be a wound pathogen. However, although wounding may aid infection, scientific trials have shown that, in susceptible Clematis varieties, the fungus can cause extensive leaf spotting and wilt without any previous damage to plant tissues.
When spores of Phoma clematidina land on a leaf of a susceptible plant under the right environmental conditions (moisture, temperature 15 to 25 °C), they will germinate within 6 hours and infect leaf tissues directly or via leaf hairs (but never via stomata). Initial symptoms are small brown lesions which then rapidly spread, eventually killing the whole leaf. Unless the plant abcises the leaf in reaction to the infection, the fungus will spread via the leaf stalk to the node of the stem.
Infection may also occur directly into the stem. This is particularly common at or below soil level where the right amounts of moisture are more likely to persist. Once in the stem, Phoma clematidina destroys the internal tissues causing a distinctive, localised black discolouration. Such stem infections can be hugely destructive as they block the plant's vascular system and will lead to the wilting and death of all plant mass above the site of entry, no matter how substantial.
Relatively recently, it was discovered that Phoma clematidina can also infect the roots of Clematis and be a cause of black root rot. In practice, this has been found to be a particular issue in containerised plants.
Many gardening publications express a view on the susceptibility of different Clematis varieties and species to clematis wilt based on observations in practice, but very few comment on their susceptibility to disease caused by Phoma clematidina in particular compared with other causes of wilt.
Scientific trials have shown that large-flowered varieties are especially susceptible to disease caused by Phoma clematidina in line with their vulnerability to wilt observed in practice. It is believed that hybrids which have Clematis lanuginosa in their ancestry are most susceptible to wilt. Such hybrids include many cultivars in the early flowering, large-flowered group (such as C. 'Nelly Moser' and C. 'Elsa Späth') and, to a lesser extent, cultivars in the late flowering, large-flowered group (such as C. 'Jackmanii' and C. 'Perle d'Azur').
Clematis viticella and related varieties are also susceptible to infection with Phoma clematidina, yet are reported to wilt less often than large-flowered varieties, possibly because they are very vigorous and outgrow infections quite rapidly. Most other cultivated Clematis species and their varieties are largely resistant to both infection with Phoma clematidina and wilt in general.
Phoma clematidina has sporadically been reported from species of Clematis growing in the wild, including Clematis orientalis in Russia  and Clematis pubescens in Australia. Reported isolations from wild C. vitalba in Europe have proven to be Didymella vitalbina rather than Phoma clematidina.
- Boerema G.H. and Dorenbosch M.M.J. (1979) Mycologisch taxonomisch onderzoek. Verslagen en Mededelingen Plantenziektenkundige Dienst Wageningen 153 (Jaarboek 1978): 17-21.
- Woudenberg, J.H.C.; Aveskamp, M.M.; de Gruyter, J.; Spiers, A.G.; Crous, P.W. (2009). "Multiple Didymella teleomorphs are linked to the Phoma clematidina morphotype". Persoonia. 22: 56–62. doi:10.3767/003158509X427808.
- van de Graaf P. (1999) Biology and Control of Phoma clematidina, causal Agent of Clematis Wilt. PhD thesis, University of Derby, Derby, UK.
- "van de Graaf P. (1999) Biology and control of clematis wilt. Final project report. Horticultural Development Council, UK" (PDF).
- van de Graaf P., Joseph M.E., Chartier-Hollis J.M. and O’Neill T.M. (1998) Root infection of cultivated clematis by Phoma clematidina, causal agent of clematis wilt. In: Proceedings 7th International Congress of Plant Pathology, 1998. Edinburgh, UK: BSPP/ISPP, 3, 3·7·67
- Boerema, G.H.; Bollen, G.J. (1975). "Conidiogenesis and conidial septation as differentiating criteria between Phoma and Ascochyta". Persoonia. 8: 111–144.
- Woudenberg, Joyce H. C. (2011). "Analysis of the mating-type loci of co-occurring and phylogenetically related species of Ascochyta and Phoma". Molecular Plant Pathology. 13: 350–362. doi:10.1111/j.1364-3703.2011.00751.x.
- "Gourlay A.H., Wittenberg R., Hill R.L., Spiers A.G., and Fowler S.V. (2000) The biological control programme against Clematis vitalba in New Zealand. In: Spencer N.R. (ed), Proceedings of the 10th International Symposium on Biological Control of Weeds: 709–718. Montana State University, Bozeman, MT, USA" (PDF).
- Paynter, Quentin; Waipara, Nick; Peterson, Paul; Hona, Shane; Fowler, Simon; Gianotti, Alison; Wilkie, Paula (2006). "The impact of two introduced biocontrol agents, Phytomyza vitalbae and Phoma clematidina, on Clematis vitalba in New Zealand". Biological Control. 36: 350–357. doi:10.1016/j.biocontrol.2005.09.011.
- Smith G.R. (1987) Leaf Spot and Wilt of Clematis caused by Phoma clematidina (Thum.) Boerema. PhD thesis, University of Canterbury, Christchurch, New Zealand
- Smith, G.R.; Cole, A.L.J. (1991). "Phoma clematidina, causal agent of leafspot and wilt of Clematis in New Zealand". Australasian Plant Pathology. 20 (2): 67–72. doi:10.1071/app9910067.
- Smith, G.R.; Munro, M.H.G.; Fineran, B.A.; Cole, A.L.J. (1994). "Evidence for the involvement of ascochitine in phoma leafspot-wilt disease of Clematis". Physiological & Molecular Plant Pathology. 45 (5): 333–348. doi:10.1016/s0885-5765(05)80063-3.
- van de Graaf, P.; O'Neill, T.M.; Chartier-Hollis, J.M.; Joseph, M.E. (2001). "Susceptibility of clematis varieties and species to stem infection by Phoma clematidina as an indicator for resistance to wilt". European Journal of Plant Pathology. 107 (6): 607–614. doi:10.1023/A:1017902331872.
- van de Graaf, P.; Joseph, M.E.; Chartier-Hollis, J.M.; O'Neill, T.M. (2002). "Pre-penetration stages in infection of clematis by Phoma clematidina". Plant Pathology. 51: 331–337. doi:10.1046/j.1365-3059.2002.00727.x.
- van de Graaf, P. (2003). "Aspects of the Biology and Control of Benzimidazole Resistant Isolates of Phoma clematidina, cause of Leaf Spot and Wilt in Clematis". Journal of Phytopathology. 151: 442–450. doi:10.1046/j.1439-0434.2003.00748.x.
- RHS Clematis wilt
- Howells J. (1994) Vulnerability to clematis wilt in large flowered clematis. The Clematis, p. 51.
- Golzar, H.; Wang, C.; Willyams, D. (2011). "First report of Phoma clematidina the cause of leaf spot-wilt disease of Clematis pubescens in Australia". Australasian Plant Disease Notes. 6 (1): 87–90. doi:10.1007/s13314-011-0030-x.