by Dr John Howells

First published in The Clematis, 1997. p42.

In addition to on-going research on clematis wilt in the UK there is activity in The Netherlands and New Zealand. These are reported below:


Two Dutch researchers have recently reviewed a new research effort on clematis wilt in The Netherlands.1 Their findings have significance for growers and clematarians in the UK. Their paper is summarised here. (My remarks on the relationship of the findings to the UK is in brackets.)

The extensive research work undertaken in the ‘60s and ‘70s in The Netherlands has been reported previously.2 At that time in the Netherlands it was thought that the responsible organism was Coniothyrium clematidis-rectae and Phoma clematidina to a lesser extent. The present research has shown that the situation is reversed. Phoma clematidina is more important. (This matches the situation in the UK where Phoma clematidina was found to be the responsible agent. It was also the operating fungus in the USA in 1915.3

A worrying situation led to the new research. It had become apparent in the nurseries that the well-tried fungicides benomyl (Benlate), carbendazim (Bavistin), and thiofanaat-methyl (Topsim M) so effective in the past cannot control the fungus now. This fact was tested in the laboratory. Fungi from 1975 stopped growing with low concentrations of the fungicide. But fungi from 1995 still grew even with high concentrations of fungicides. Thus the fungi have developed immunity to the fungicides and the fungicides are no longer of any value. (This situation already operates in the UK.)4

The Dutch researchers described the leaf spots produced by the fungus on leaves. They also gave much significance to the effect of water on the growth of the fungus. With the help of water the fungal spores germinate and move into the leaf and ultimately move down the leaf stalk to the stem. (It is not clear whether water as such is important as much as the humidity the water creates. Gloyer3 showed that humidity was a central factor in precipitating growth of the fungus.)

The authors advocate finding new fungicides but stress the importance of nursery hygiene. (Gloyer3 also emphasised the importance of this.) They point to the fact that the propagating process is ideal in its humidity and temperature for the growth of fungus in the seedlings. They stress the importance of eliminating dead stems and leaves from the propagating area. Propagating material must be carefully inspected to omit any infected cuttings. Equipment must be disinfected.

The research continues in order to find new effective fungicides. (As a short-term measure this is urgently necessary. But the fungus in the course of time will become immune to the next batch of fungicides. Now that we know that `stem rot’ almost exclusively affects the Early Large Flowered clematis, the group from vulnerable C. lanuginosa stock,5 the final solution is to bar the progeny of C. lanuginosa from the hybridising programme.)


The laboratory study summarised in The Clematis 1995, p95,6 takes us a step forward in our understanding of stem rot.

The study was based on the effect of ascochitine (isolated from Asochyta clematidina) on the leaves. It is important to stress that the study was based on the reaction of leaves alone. Ranking of five clematis in terms of least to most resistant to ascochitine on the leaves was as follows: `Huldine’ - `Lady Betty Balfour’ - `Ernest Markham’ - `Rouge Cardinal’ - C. montana

It would be wrong however to assume that the above would apply to plants in the field. The authors point out that `Huldine’, the least resistant, is generally regarded as wilt resistant in the field but susceptible to leaf damage. The authors explain "this is because plants display another defence mechanism in which the leaves senesce to prevent fungal infection of the node via the petiole". In `Huldine’ biochemical resistance to leaf damage is reduced "but the effective mechanism of leaf senescence operates to confer effective field resistance".

It may be relevant to comment that the susceptibility of a plant to stem rot may have more to do with deficiencies in stem protective mechanisms than in those of the plant leaves. But not excluded is the possibility that the readiness of a leaf to senesce may match the capacity of the stem in that clematis to employ its defence mechanisms. Further study is required.

The authors wisely conclude the "interpretation of laboratory results must be reconciled with observations of development of the disease in the whole plant".

1. Van Kuik and Brachter, E. Schimmelziekte B1J Clematis. Steekt opnieuw de Kop Op. 1997. De Boomkwekerij. 9. 16-17.
2. Howells, J. Clematis wilt. A Review of the Literature. 1993. The Plantsman. 15. 148-160.
3. Gloyer, W.O. Ascochyta clematidina. 1915. J.Agric.Res. 4. 331-342.
4. Van de Graaf, P. 1997. Personal communication.
5. Howells, J. The Genetic Background of Wilting Clematis. 1994. The Clematis. P62-67.
6. Smith, GR., Munro, MHG., Fineran, BA., Cole, ALJ. 1994. Evidence for the involvement of ascochitine in phoma leafspot-wilt disease of Clematis. Physiological and Molecular Plant Pathology 45, pp333-348.

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