TREES OVER TIME (PART 2): DISEASES

“I remember the time when my dad was ill and, as a remedy, my mum smeared butter all over his back. He went downhill quickly after that…”

Jokes involving disease-related scenarios are important when teaching this topic, for it can otherwise be dire and depressing. On the depressing side of things, I recall my training in forestry pests at Aberdeen where, week after week, we learnt about a new set of problems that, cumulatively, seemed to make it unlikely that one could ever grow a forestry crop in the UK. Since the early 1990s when I took that forestry degree, it feels like that list of tree-related pests has elongated exponentially – it’s hard to keep up – and dismal reading if you do!

A recent survey of Higher Education institutions in the UK found that very few of them were teaching plant pathology: given the high rate at which new plant pathogens come to damage our trees and gardens, this seems a major omission from UK degree courses and may indicate a lack of investment by private and public institutions in posts for plant pathologists. When I first started teaching the ‘pests and diseases’ module at Myerscough College, I incorporated an introduction into plant pathology, so students had at least ‘dipped their toes’ into this important discipline and might be enticed to study plant pathology in the future or base their research project on investigating a pest or disease. I have supervised quite a few good plant pathology studies as a consequence of taking this approach.

In this article, I have collated a few of my trees-over-time images that are related to diseases and how they have changed (or not) over a decade or so. There is a limitation to note here: if you wanted to time-lapse the foliage damage caused by a powdery mildew, for example, that damage occurs in just one growing season: taking my approach, where I am following up my own images of tree diseases from many years before, it is damage to the inner bark and woody parts of a tree that I can time-lapse, not in-season changes to temporary structures, such as deciduous leaves. Remembering that limitation, here are some collated images which I think tell a range of interesting ‘stories.’

A bleedin’ problem

If you wanted to study bleeding cankers (often caused by water moulds such as Phytophthora spp.), then the North West is where you want to be: on a very regular basis I get to see the death and decline of trees from these bleed-inducing diseases of the inner bark of trees and shrubs.

My time-lapse images show a range of outcomes, though. Very frequently, there is a relatively short period when a bleeding canker is active (one or two growing seasons) and then the problem abates. This tends to leave a patch of dead inner bark, the outer bark slowly sloughs off, and callousing occurs at the edges of such a wound (Fig.s 2 and 3). Even in quite extreme cases of stem damage by a water mould, if the tree is fairly young and growing conditions are not adverse, recovery is possible (Fig. 4). In other cases, the bleeding canker girdles the stem of the tree (“end game”) or opens such a large wound that secondary decay follows soon after – an effect I have seen en masse on a site near Caton, Lancashire, in a cohort of Italian alders affected by Phytophthora alni (Slater, 2018).

Figure 2: A bleeding canker at the first major branch junction in an Acer rubrum ‘Scanlon’. Note how the area of initial bleeding (in 2006) becomes an area of exposed sapwood of roughly the same shape and size in the later image (2018). Such an open wound, exposing dysfunctional sapwood, is a major court for secondary wood decay organisms.

Figure 3: A DEFRA officer inspecting a beech tree (Fagus sylvatica L.) with a bleeding canker at its base in 2007 at Myerscough College, Lancashire. Again, the lapse of eleven years shows that the area of damage was not greatly expanded in that time, but the wound remains open, not occluded.

Figure 4: Death of a large proportion of the inner bark at the base of a young honey locust (Gleditsia ‘Sunburst’), in a park in Knowsley, near Liverpool. On revisit, twelve years later, the tree has substantially recovered from the initial injury, producing callous and stem thickening either side of what was initially a large stem wound. Such a recovery in a young tree I have found to be quite common: mature trees generally fair much worse because the process of wound occlusion is so much slower (e.g. Figures 2 & 3).

As is often the case, dead and dying trees are quickly drawn to your attention when surveying –you may end up ignoring the trees that recover, as, often, no action is needed. Despite the major tree losses caused by bleeding cankers in the North West, some of my trees-over-time images show that trees can make a comeback when the bleeding abates. Very often, the disease advice available is downbeat: e.g. “Often a fatal disease.” Now, I’m a ‘glass half full’ sort of a person: how about rewording that disease advice so it is a bit more upbeat at times: e.g., “Sometimes the tree survives.” 

Cantankerous cankers

Another perennial feature caused by pathogens (which has fitted in with my method of revisiting trees a decade later) are cankers to the stems and branches of trees, often caused by fungi in the genus Neonectria (Strouts and Winter, 2000). At time of writing, I have only time-lapsed ten of these, and the outcomes are mixed: some of the cankers have grown in size (Fig.s 5 & 6), some have been in remission (Fig. 7) and some have pretty much stayed the same (Fig. 8). Given that these cankers are in different species of tree of different ages, situated in quite different growing conditions, all that can be concluded from this is that ‘prognosis’ can be difficult – a canker may grow, a canker may abate, or a canker may stay the same size. I have estimated that I would need about sixty of these time-lapsed cankers in just one species to be able to conclude anything science-based about their ‘typical’ progress – so that’s not likely to happen.

Figure 5: A large target canker on the stem of an ornamental cherry (Prunus sp.). Note, as is common, that the infection court was a dead branch stub, which can be seen at the centre of this canker. Over a period of ten years, this canker has grown in extent and minor secondary decay has set in.

Figure 6: A large canker on the stem of a mature ash (Fraxinus excelsior L.), which has expanded in size over the last ten years, killing some of the adjacent callous tissues.

Figure 7: Stem canker on a young beech (Fagus sylvatica L.) in a woodland setting. Again, youth and vigour are on the side of the tree in this competition between host and canker, resulting in this canker shrinking in size over the ten-year period shown.

 Figure 8: A large stem canker on a mature sycamore (Acer pseudoplatanus L.), growing adjacent to the sports fields at Myerscough College. Status quo for this canker – it has not discernibly grown or lessened in size over the last twelve years.

It was interesting to give a talk recently over in Ontario, Canada (providing training in natural bracing to thirty-three arborists) – and a few questions came from the audience about ‘treatment’ – e.g., “In this situation, what would you do about treating the tree?”, one attendee asked. In reply (and in jest) I said, “You’ve got to remember that I work in the UK – we mostly just leave the tree to get on with it.” It got a laugh at the time, but I have reflected since then that there are potentially effective treatments for cankers and other tree-related maladies and UK arboriculture should, perhaps, be more proactive and less fatalistic about some of these problems, particularly where there are other management options that are more effective than ‘hope’.

Knot of ash (caused by a bacterium – Pseudomonas syringae subsp. savastanoi pv. fraxini) is typically a minor problem to a small proportion of ash trees (Janse, 1982). I was pleased to capture this knotty tree over a long time-lapse period, where you can see that the diseased patches have become more sunken (and thus more dramatic in appearance) on the stem of this semi-mature ash tree (Fig. 9).

Figure 9: A severe case of knot of ash (Pseudomonas syringae subsp. savastanoi pv. fraxini) on the stem of a semi-mature ash (Fraxinus excelsior L.). Note that secondary thickening of the stem has caused the dead areas of the stem to become more sunken in appearance: few of the areas of infection have expanded much in size in this specimen.

Sadly, another consequence of visiting New York State and Ontario recently has been to see the fate of many thousands of ash trees killed by emerald ash borer (EAB). This also made me wonder about the optimistic articles I’ve recently read about finding ash trees that are resistant to ash dieback disease: with EAB spreading westward through Europe and with their ability to kill all mature ash trees in an area that they colonise, are we (analogously) merely rearranging deckchairs on a sinking ship? I argue that we need to find a Fraxinus that is resistant to ash dieback and also beetle-proof, or we are wasting our time and effort. It is very sad to think that we may be the last generation to see ash trees as a key component of our landscape. In this doomsday scenario for ash trees in the UK, diseases like knot of ash pale into insignificance.

Another bleedin’ problem

Some diseases attenuate over time (which is to say that if they initially start by being lethal to their hosts, at some point a weaker strain becomes more prevalent, as an obligate pathogen cannot survive without its host to live upon), but the degree to which they attenuate may result in them remaining a chronic (on-going, debilitating) health or structural problem.

From observation, Pseudomonas syringae pv. aesculi (horse chestnut bleeding canker, or what I like to call ‘HCBC’) is becoming a chronic problem in the UK. There are two dozen mature horse chestnuts on a stretch of the A6 near to Garstang, Lancashire that have on-going problems with HCBC – the wounds caused to the inner bark by this disease are often followed up by secondary decay organisms (typically Cerioporus, Coriolus, Ganoderma and Flammulina).

Again, the trees-over-time images show a mix of end-results, from initial bleeding opening up long strips of sapwood to the air (Fig. 10), to bleeding and wounding being occluded by secondary growth of the stem (Fig. 11). One study at Myerscough that I supervised found that damage from this disease regularly re-emerged in exactly the same locations on the tree stem, but with several years between instances of severe inner bark damage. Once it has colonised the inner bark of an Aesculus, it seems, HCBC tends to stick around. This can be seen in individual trees without dissection of their parts: branches dieback, shoots regrow, the tree’s health seems restored for a while, then branches dieback again (Fig. 12). That’s chronic.

Figure 10: From initial bleeding to a long strip-like open wound: a common outcome from initial infection of an Aesculus hippocastanum by horse chestnut bleeding canker.

Figure 11: From initial bleeding to wound occlusion: I do not know how common this outcome is from an initial infection of horse chestnut bleeding canker – but the pathogen is still likely to be present within the inner bark of this tree. There may be a ‘Round Two’ of this fight yet to come.

Figure 12: One of many debilitated horse chestnut trees in an avenue adjacent to the town of Garstang, Lancashire. This is a case of a chronic disease: HCBC has not abated – but HCBC has not proven fatal yet either. The pictured tree now has the fruiting body of a Ganoderma at its base, so its structural integrity is becoming compromised.

Decay over time

Personally, I don’t categorise wood decay in general as a ‘disease’ – it’s a process of the breaking down of wood and the wood could consist entirely of dead tissues. Many of the issues around decay in standing trees are ones that relate to substantial decay occurring earlier than it should in the tree’s lifecycle: what I term ‘early-onset decay’. This frequently occurs in our urban trees, where the rough treatment frequently meted out to them (mechanical wounding, harsh pruning, physiological stresses) causes internal decay to be initiated in relatively young trees. Another cause of early decay in trees can be from wood decay organisms that are also capable of killing living tissues in trees. The capacity of various commonly-occurring wood decay fungi to also act as pathogens has not been fully explored through scientific research but a few, such as honey fungus (Armillaria spp.), are known to kill live tissues as well as to rot away dysfunctional wood.

Many of the urban trees I have tried to time-lapse over ten or more years with substantial decay evident in them in the original photograph – perhaps unsurprisingly – are no longer in-situ. Felled or failed, they have gone. When I’m lucky and the tree (or the stump) is still there, it is perennial woody brackets that are the easiest to time lapse (Fig. 13).

Figure 13: A cascade of fungal brackets of the species Ganoderma australe, situated in the cleft of a late mature beech tree. The development of these brackets over ten years was accompanied by the failure of the main stem of this tree, leaving only a two-metre-high stump.

Decay modelling in standing trees remains a poorly explored area: it would be very beneficial to more reliably be able to predict the progress of root and basal decay, for instance. Old models of decay are insufficient to do that prediction for us, so we should look to remodel how decay acts within trees. One interesting aspect of revisiting trees with decay is that sometimes the fungal brackets have died, rather than the tree (Fig. 14). I think this effect is highly under-reported: and, no, the death of perennial brackets does not mean the decay has been ‘compartmentalised’: my working model for wood decay is based more on principles of ‘momentum’ and ‘attrition’. To keep fruiting, a fungus needs to achieve a target amount of wood decay (by volume): if that volume is not available to the fungal mycelium within one season, fruiting will not occur. This is easy to observe in very hollow veteran trees with shell-like trunks: you can see that wood decay is present on the inner surface of the remaining thin part of the wood, but, very often, no fruiting bodies of macro-fungi are present, as the resource is too meagre to support the demands of fructification.

Figure 14: Ganoderma brackets growing within a cleft at the base of a stem of a maidenhair tree (Ginkgo biloba L.) at Holker Hall, Cumbria. Although a few more annual layers have been added to these brackets since the initial image, the fruiting bodies have now blackened and died. In contrast, the tree clearly has good crown density and vigour. Judging by its condition, this tree, exhibiting only minor stem decay, may have a long life ahead of it, despite the early-onset decay it has suffered (I am going to guess, from a basal wound probably inflicted by grass cutting equipment, given its setting). When I put this image up on LinkedIn, several arborists suggested that the tree should be cut down: I prefer a much stronger evidence-base than that shown by this image before condemning a healthy tree.

Many of my attempts to time lapse trees have confirmed common industry experience of wood decay: look for a beech with Meripilus at its base, and, twelve years later, the tree’s failed or been felled, for example. Where the trees are hosts to decay fungi reported to be slow to act on living trees, such as Fistulina hepatica or Inonotus dryadeus, then the trees are often still standing there on my revisit (Fig. 15).

Figure 15: The fruiting bodies of Inonotus dryadeus on a mature oak (Quercus robur L.) in the deer park at Levens Hall, Cumbria. These fruiting bodies are annual, but old, darkened and dried brackets often persist for a year or more to lie at the base of an affected tree. Here, twelve years on, it is clear that fructification has occurred at least twice in exactly the same place at the base of the tree’s stem. View the tree’s canopy and form, and one can see no sign of dysfunction. It is common collated experience that decay by I. dryadeus upon oak can be slow and may not result in tree failure, and this trees-over-time image supports that collective knowledge.

Conclusions

Many of these trees-over-time images make great stories and are proving to be valuable teaching resources, especially for those studying with us at Myerscough. I freely admit that, although I have a mental picture of what I envisage will have happened to a tree before I revisit it, quite often something unexpected has happened – or there are details and differences I had not anticipated. It’s turning out to be a good learning exercise for me, as an arboricultural lecturer and an arboriculturist, as much as it is for our students.

I am pleased to have the privilege to share a few of these images with you here, in this article. I hope to provide a ‘Part Three’ soon, with some trees-over-time images that illustrate structural faults and failures. 

With best wishes, Duncan.

THIS ARTICLE FIRST APPEARED IN THE SPRING EDITION OF THE ARB MAGAZINE 2019, AS PUBLISHED BY THE ARBORICULTURAL ASSOCIATION.

References

Janse J D (1982) The bacterial disease of ash (Fraxinus excelsior) caused by Pseudomonas syringae subsp. savastanoi pv. fraxini III: Pathogenesis; Forest Pathology 12, 218-231.

Slater D (2018) The association between natural braces and the development of bark-included junctions in trees; Arboricultural Journal 40 (1), 16-38.

Strouts R G and Winter T G (2000) Diagnosis of ill-health in trees; London: TSO.