ECOS 40(4): Undergraduate runner up: The crash of ash

Ash trees across the UK are dying following the relentless spread of the ‘ash dieback’ fungus, Hymenoscyphus fraxineus. It is crucial to understand the mechanisms behind dieback dispersal to secure the future of ash in Britain.

Global trade, travel and migration have facilitated the dispersal of many species, including pests and pathogens, to new areas. Associated invasions of non-native species represent the third most important threat to biodiversity (1). One major pathogen newly invading UK and European woodland is the fungus Hymenoscyphus fraxineus, causing ash dieback.

In the UK, ash dieback was first confirmed in 2012 in nursery stock imported from the Netherlands to Norfolk. Symptoms of the disease are easily identifiable. They include leaf dieback and small white fungal fruiting bodies found on the woodland floor.

A study was carried out in South Norfolk over the summer of 2018 to investigate the disease’s spread through three young woodlands and three ancient woodlands. The approach was designed to test how woodland age, location of trees, their diameter at breast height (DBH) and height influence infestations. The results can inform the future management of woodlands to minimise disease spread and conserve ash in British woodlands.

Methodology and data analysis

Ash trees were surveyed in 3 ancient and 3 young woodlands. Marked footpaths were walked located in ~N-S and E-W directions. Up to 25 trees were identified in each woodland along the paths in four categories: trees in the canopy or sub-canopy layers and being alive (carrying leaves) or dead. If specimen numbers falling into any category exceeded 25 on the transect walks, then 25 trees were chosen randomly, with all tree locations marked using a Global Positioning System (GPS) device.

Trees were given an infection score using the following system:

0 – no signs of symptoms

1 – minor damage (<10% loss of leaves, early stages of lesions on stem)

2 – significant damage (10-50% loss of leaves, lesions on stem, dead branches and twigs)

3 – severe damage (>50% loss of leaves, many stem lesions, dead branches and twigs)

4 – dead

Tree DBH was measured with a tape measure and tree height recorded using the tangent method with a clinometer. Only trees >1.3m were measured. In total, 292 trees were assessed, 135 located in the ancient woodlands and 157 in the young woodlands. Approximately 12% of all trees were dead, whilst 2.5% of ash trees showed no signs of disease.

Tree locations showed no correlation with infection scores. Disease patterns were spatially more heterogeneous in younger woodlands, with dead trees found neighbouring trees with little sign of infection (Figs 1 and 2), suggesting other factors influence the extent of infection. The extent and severity of disease appeared to be closely related to tree size, with both DBH and tree height significantly negatively correlated with tree size and therefore age (Fig. 3). Overall, 80% of dead trees were in the juvenile size category (DBH <0.1m), whereas no juvenile trees were found to be completely healthy. Similarly, no dominant trees (DBH of 0.3m to 0.6m), were found to be dead, but accounted for more than 60% of trees scored 0. This data highlights how DBH is related to disease severity; larger trees being more tolerant to infection, while smaller trees show higher mortality rates.

Figure 1: Rogerson’s Wood (exemplifying tree DBH and ash dieback distribution in young woodland) – tree colour indicates infection scores and size indicates tree DBH
Figure 2: Lower Wood ( exemplifying tree DBH and ash dieback distribution in young woodland) – tree colour indicates infection scores and size indicates tree DBH
Figure 3: Percentage of tree sizes in each infection category. Juvenile: DBH<0.1m, Intermediate: DBH 0.1-0.3m, Dominant: DBH>0.3m.

How does ash dieback spread?

The lack of spatial pattern in disease occurrence is clearly exemplified by Rogerson’s Wood (Fig. 1), where a healthy tree stands within a few metres from a severely infected and a dead tree; and, to a lesser degree, in Lower Wood, where trees scoring 1 and 3 are often encountered in close vicinity (Fig. 2). Aggregate groups of infected trees exist, too, for example on the eastern boundary of Lower Wood. This boundary lies perpendicular to arable farmland, where tree roots are more prone to disturbance, potentially increasing infection rates and associated crown dieback. Small-scale variations in environmental conditions could be responsible for the overall lack of spatial pattern, with localised high moisture levels and temperatures believed to be particularly conducive to pathogen fruiting body growth.

Ash dieback affects all tree size and age classes, but progresses through each category at different rates, with more rapid mortality rates in younger trees. Here, the pathogen is able to penetrate through the cambium faster compared to older trees, whilst larger energy resources and vigour of older trees potentially allow them to withstand infection for longer. Tall trees are generally less prone to infection too, since pathogen spores produced in the leaf litter have to travel further to infect their leaves. Since ash in ancient woodlands are up to three times higher, their populations are overall healthier than ash in young woodland. Importantly, the young ash measured here were <20 years old. It is hence very possible that these trees became infected in their initial stages of growth, when the pathogen first took hold in the UK. Despite classified as an ancient woodland, Lower Wood critically experiences frequent coppicing, and coppice regrowth is known to display similar infection rates to young stands, with some regrowth succumbing to ash dieback in one season (2).

Whilst age and size clearly influence the speed of mortality, the variation in susceptibility is fundamentally determined by the tree’s specific genotype, which likely explains trees of very different infection scores in close vicinity to each other. Phenological traits such as fast leaf senescence has been found to influence susceptibility because as the disease entrance pathway is through leaves, trees with this particular trait exhibit a smaller time frame for the tree to become diseased, and thus are generally healthier. Fortunately, the importance of genetics provides hope for the maintenance of this species through artificial selection.

Future management of ash in the UK

With genotypes holding a potentially pivotal role in the disease, artificial selection is hailed as a method to maintain a healthy presence of ash in the UK. Genetic manipulation has been carried out following the devastation caused by Dutch Elm disease, where hybrid populations were created and show good levels of tolerance and resistance to the pathogen (3). Therefore, the hybridisation of F. excelsior with other ash species, although costly and time consuming, may provide a method of achieving tolerance to the pathogen and controlling the extent of the disease.

However, with the disease showing preference to the infection of smaller trees, management could be to remove ash that show traits most susceptible to infection, i.e. young, short and thin trees. This could limit the spread of the disease, as only those with the highest natural tolerance would be left in the landscape, creating populations with reduced susceptibility. However, the maintenance of deadwood is said to represent a new opportunity for wildlife, with it providing new habitats for fungi and insects.

An alternative approach is to leave the woodlands to natural processes and stop all forms of current management. From this method, it is hoped that a dense understorey would form, acting as a physical barrier to fungal spores, reducing the likelihood of the pathogen entering through the leaves above this barrier. Nonetheless, this technique is likely hampered by high prevailing numbers of deer in many UK woodlands, as grazing on the understorey will reduce the efficiency of this hypothesized barrier.

Given the current lack of knowledge and varying success from these forms of management, a diversity of management techniques is recommended. Climate change is likely to complicate the success of these methods further, as it is unknown how it will impact the spread and distribution of both pathogen and host. Despite this uncertainty, it is evident that the loss of ash in UK woodlands is inevitable, with few trees in this research showing current levels of good resistance. Action on the protection of ash must be immediate, and I hope that this research has shed more light on the mechanisms of ash dieback and how this can inform management.

References

[1] Maxwell, S.L., R.A. Fuller, T.M. Brooks, J.E.M. Watson (2016) ‘Biodiversity: The ravages of guns, nets and bulldozers’ Nature, Vol.536, 7615, pp. 143-145.

[2] Edwards, A. and A. Downie (2016) ‘Ash Dieback Disease: A plague on our ashes’ (WWW) https://microbiologysociety.org/blog/ash-dieback-disease-a-plague-on-our-ashes.html, accessed 12/1/19.

[3] Skovsgaard, J.P, G.J. Wilhelm, I.M. Thomsen, B. Metzler, T. Kirisits, L. Havrdova, R. Enderle, D. Dobrowolska, M. Clearly, J. Clark (2017) ‘Silvicultural strategies for Fraxinus excelsior in response to dieback caused by Hymenoscyphus fraxineus, Forestry: An International Journal of Forest Research, Vol. 90, 4, pp. 455-472.

Cite:

Ward, Nicola “ECOS 40(4): Undergraduate runner up: The crash of ash” ECOS vol. 40(4), 2019, British Association of Nature Conservationists, www.ecos.org.uk/the-crash-of-ash/.

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