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Calophoma clematidina
Scientific classification
Kingdom:
Fungi
Division:
Ascomycota
Class:
Dothideomycetes
Order:
Pleosporales
Family:
Didymellaceae
Genus:
Calophoma
Species:
C. clematidina
Binomial name
Calophoma clematidina
(Thüm.) Q. Chen & L. Cai (2015)[1]
Synonyms[2]

Ascochyta clematidina Thüm. (1880)
Phyllosticta clematis Brunaud (1889)
Phyllosticta clematis Ellis & Dearn. (1893)
Ascochyta indusiata Bres. & Hedwigia (1896)
Ascochyta davidiana Kabát & Bubák (1904)
Phoma clematidina Boerema (1978)

Calophoma 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.[3][4] Infected plants growing in containers may also develop root rot.[5]

Taxonomy[edit]

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,[6] it was reclassified as Phoma clematidina by the Dutch mycologist Gerhard Boerema in 1978.[7] More recently, multi-locus phylogenetic analyses led to the fungus being reclassified again as Calophoma clematidina.[1]

Genetic sequencing has suggested that Calophoma 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).[8] Both mating types of Calophoma 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.[2][8]

Molecular phylogenetic analyses have revealed that some fungal isolates recovered from wild Clematis species, previously identified as Calophoma/Phoma clematidina, are in fact two closely related species of Phoma and Ascochyta with sexual stages in Didymella.[2] Didymella clematidi has been successfully used as a biological control agent of Clematis vitalba, which is seen as an invasive plant in New Zealand.[9][10] Unlike Calophoma clematidina, the two closely related Didymella species (and their anamorphs) have not been found on large-flowered Clematis varieties.[2]

The previous misidentification of these species means that some literature referring to Calophoma clematidina or Phoma clematidina, particularly that on the biological control of C. vitalba,[9][10] is actually describing work on Didymella clematidis and its Ascochyta anamorph.[2]

The situation is further complicated by the existence of another Calophoma species known to infect Clematis: Calophoma clematidis-rectae (syn. Coniothyrium clematidis-rectae). This species is closely related to C. clematidina [1][2][11] and has in the past been implicated in cases of clematis wilt in the Netherlands.[12]

Biology[edit]

The biology of Calophoma clematidina is now reasonably well understood thanks to research into clematis wilt at the University of Canterbury in New Zealand [13][14][15] and the University of Derby and ADAS in the UK.[3][4][5][16][17][18]

A full overview of its life cycle was first produced in 1999.[3][4] 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.[3][4]

Unlike many other plant pathogens, Calophoma 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.[3][4]

Disease development[edit]

Many publications report Calophoma 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.[3][4]

When spores of Calophoma clematidina land on a leaf of a susceptible plant under the right environmental conditions (moisture, temperature 15 to 25 °C (59 to 77 °F)), they will germinate within 6 hours and infect leaf tissues directly or via leaf hairs (but never via stomata).[17] 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.[3][4][14]

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, Calophoma 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.[3][4][19]

Relatively recently, it was discovered that Calophoma 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.[3][4][5]

Host susceptibility[edit]

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 Calophoma clematidina in particular compared with other causes of wilt.

Scientific trials have shown that large-flowered varieties are especially susceptible to disease caused by Calophoma 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').[16][20]

Clematis viticella and related varieties are also susceptible to infection with Calophoma 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 Calophoma clematidina and wilt in general.[16]

Calophoma clematidina has sporadically been reported from species of Clematis growing in the wild, including Clematis orientalis in Russia [2] and Clematis pubescens in Australia.[21] Reported isolations from wild C. vitalba in Europe have proven to be an unnamed Didymella species rather than Calophoma clematidina.[2][22]

As biological control[edit]

This fungus has been reported as having been successfully used as a biological control agent of Clematis vitalba, which is seen as an invasive plant in New Zealand.[9] However, further genetic studies of the isolates used in those trials have revealed that the fungus released as biocontrol agent had been misidentified and was not Calophoma clematidina, which thus far has never been found on Clematis vitalba.[2][22]

Management[edit]

Benzimidazole fungicides are used.[23] Benzimidazole resistance has occurred.[23]

References[edit]

  1. ^ a b c Chen, Q.; Jiang, J.R.; Zhang, G.Z.; Cai, L.; Crous, P.W. (2015). "Resolving the Phoma enigma". Studies in Mycology. 82: 137–217. doi:10.1016/j.simyco.2015.10.003. PMC 4774273. PMID 26955202.
  2. ^ a b c d e f g h i 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. PMC 2789541. PMID 20198138.
  3. ^ a b c d e f g h i van de Graaf P. (1999). Biology and Control of Phoma clematidina, causal Agent of Clematis Wilt. PhD thesis, University of Derby, Derby, UK.
  4. ^ a b c d e f g h i van de Graaf, P. (1999). "Biology and control of clematis wilt" (PDF) (Final project report). Horticultural Development Council, UK. Archived from the original (PDF) on 2016-03-04.
  5. ^ a b c van de Graaf, P.; Joseph, M.E.; Chartier-Hollis, J.M.; O’Neill, T.M. (1998). Root infection of cultivated clematis by Phoma clematidina, causal agent of clematis wilt. Proceedings 7th International Congress of Plant Pathology. Edinburgh, UK: British Society for Plant Pathology/International Society for Plant Pathology. Archived from the original on 2016-03-04. 3, 3·7·67.
  6. ^ Boerema, G.H.; Bollen, G.J. (1975). "Conidiogenesis and conidial septation as differentiating criteria between Phoma and Ascochyta". Persoonia. 8: 111–144.
  7. ^ Boerema G.H. and Dorenbosch M.M.J. (1979). "Mycologisch taxonomisch onderzoek". Verslagen en Mededelingen Plantenziektenkundige Dienst Wageningen 153 (Jaarboek 1978): 17-21.
  8. ^ a b Woudenberg, J.H.C. (2011). "Analysis of the mating-type loci of co-occurring and phylogenetically related species of Ascochyta and Phoma". Molecular Plant Pathology. 13 (4): 350–362. doi:10.1111/j.1364-3703.2011.00751.x. PMC 6638728. PMID 22014305.
  9. ^ a b c Gourlay, A. H.; Wittenberg, R.; Hill, R. L.; Spiers, A. G.; Fowler, S. V. (4–14 July 1999). Spencer, Neal R. (ed.). The Biological Control Programme against Clematis vitalba in New Zealand (PDF). X International Symposium on Biological Control of Weeds. Montana State University Bozeman, Montana, USA (published 2000). pp. 799–806. CiteSeerX 10.1.1.589.6666. S2CID 82909885. bugwoodcloud.org/ibiocontrol/proceedings/pdf/10_709-718.pdf.
  10. ^ a b 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 (3): 350–357. doi:10.1016/j.biocontrol.2005.09.011. S2CID 55137731.
  11. ^ Aveskamp, M.M.; de Gruyter, J.; Woudenberg, J.H.C.; Verkley, G.J.M.; Crous, P.W. (2010). "Highlights of the Didymellaceae: A polyphasic approach to characterise Phoma and related pleosporalean genera". Studies in Mycology. 65: 1–60. doi:10.3114/sim.2010.65.01. PMC 2836210. PMID 20502538.
  12. ^ Blok I. (1965). "Verwelkingsziekte in clematis". Jaarboek Proefstation voor de Boomkwekerij te Boskoop 1964: 82-87.
  13. ^ Smith G.R. (1987). Leaf Spot and Wilt of Clematis caused by Phoma clematidina (Thum.) Boerema. PhD thesis, University of Canterbury, Christchurch, New Zealand
  14. ^ a b 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. S2CID 44476448.
  15. ^ 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.
  16. ^ a b c 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. S2CID 20130388.
  17. ^ a b 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 (3): 331–337. doi:10.1046/j.1365-3059.2002.00727.x.
  18. ^ 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 (7–8): 442–450. doi:10.1046/j.1439-0434.2003.00748.x.
  19. ^ RHS Clematis wilt
  20. ^ Howells J. (1994). "Vulnerability to clematis wilt in large flowered clematis". The Clematis, p. 51.
  21. ^ 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.
  22. ^ a b Johnston, P.R.; Park, D.; Ho, W.W.H.; Alexander, B.J.R. (2017). "Genetic validation of historical plant pathology records – a case study based on the fungal genus "Phoma" from the ICMP culture collection". Plant Pathology. 66 (9): 1424–1431. doi:10.1111/ppa.12728.
  23. ^ a b FRAC (Fungicide Resistance Action Committee (May 2020). "List of First Confirmed Cases of Plant Pathogenic Organisms Resistant to Disease Control Agents" (PDF).
source: https://en.wikipedia.org/wiki/Phoma_clematidina

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