Cameraria ohridella and Pseudomonas syringae var. aesculi – the compound impacts

In the UK, the introduced tree species horse chestnut (Aesculus hippocastanum) has been, over the centuries, a highly amenable tree. It has graced many important landscapes, features heavily as a mature population in many cities and their parks, and is a favourite amongst people of all ages for the conkers it drops and its stellar flowering display in spring. However, in recent times its amenity value in particular has been challenged, and namely by the various pests and pathogens obligated to the species: Cameraria ohridella (horse chestnut leaf miner), Guignardia aesculi (leaf blotch), and Pseudomonas syringae pv. aesculi (bleeding canker). Of course, such pests also impact upon the health of the tree. The repeated defoliations over successive years by the two leaf pests and pathogens, in addition to the bark lesions induced by Pseudomonas syringae pv. aesculi, will be progressively more taxing to the infected tree. Energy reserves may, therefore, eventually be entirely depleted, and the tree then ‘starves’ itself to death (if bark lesions haven’t girdled, and thus killed, the tree, by this point). At the same time, we must also remember that urban areas outside of parks may not be entirely suitable for the species (abiotic stressors), and therefore the trees may suffer as a result of human activity as well.

An example of horse chestnut foliage being attacked by the leaf miner. Source: The Wild Diary.

Because of this war of attrition the horse chestnut is suffering from, it is very much critical that we understand the drivers behind this evident multiple-pronged attack. In this case, we look at a study by Glynn Percival and Jonathan Banks, who investigated whether there is a relationship between Cameraria ohridella and Pseudomonas syringae pv. aesculi (Pae). Specifically, they sought to understand if the presence of the former heightened the severity of the latter, upon four year old horse chestnuts. Furthermore, they investigated whether secondary plant metabolites synthesised in response to Pae were impacted by a double-pronged attack courtesy of leaf miner. In order to ensure leaf blotch did not hamper the study, they treated all trees with a fungicide to prevent its manifestation.

In terms of what they found, it was identified that a combination of leaf miner and bleeding canker increased lesion sizes of Pae by 42%. Because the size of a lesion is one of the current recognised means of ascertaining pathogenicity of Pae, this is significant, as it suggests that if a horse chestnut suffers as a result of more than one biotic stressor, its health is quite likely going to suffer far more. By a similar token, where the two biotic agents were attacking the same host tree, leaf chlorophyll content and chlorophyll fluorescence were impacted slightly more significantly than when only leaf miner was present. For chlorophyll content, hosts only host to leaf miner had a loss of 86.1% of their content, and this increased marginally to 86.3% when bleeding canker was present too. Chlorophyll fluorescence was similarly impacted, with an adverse change of 72.4% and 75.2%, respectively. Both suggest the host trees are not photosynthesising in an efficient manner, and therefore cannot produce the carbohydrates required to defend themselves against such attacks – they will likely, in time, need to draw upon their energy reserves. Conversely, when only bleeding canker was present and leaf miner presence was controlled via insecticide application, chlorophyll content decreased and chlorophyll fluorescence was adversely impacted by only 12.3% (not significant – unsurprising as Pae is not principally a leaf pathogen) and 31.7% (significant), respectively. Leaf miner is, in this case, clearly has a massive impact.

Horse chestnut bleeding canker upon the main stem of an individual. Source: Beterebomen.

Looking now towards the synthesis of defensive enzymes against infection, it was found that in trees where only bleeding canker was present that such enzymes were at a level significantly higher than control trees in the areas surrounding lesions. Specifically, β-1,3-glucanase, which breaks down specific parts of the cell wall within fungal cells, was observed to increase by 57.7%, whilst peroxidase, a metabolite that increases lignin production in the host tree, increased in presence by 51.6%. Conversely, when the host tree was also being attacked by leaf miner, these metabolites were found in the locality of lesion sites at far reduced levels of 15.4% and 17.7%, respectively. Therefore, it can easily be recognised that these secondary metabolites, crucial to the effectiveness of the tree’s defensive response to attack, are markedly suppressed by leaf miner, and thus the tree will be in a far worse position to defend itself. Combined with reduced photosynthetic potential, one can really begin to recognise how, in the natural world, 1+1 may not necessarily equal two but instead five (basically, the compound impacts are synergistic, instead of additive). Furthermore, as photosynthesis is important in enabling a tree to create such secondary metabolites, horse chestnuts can, if they are impacted by leaf miner and bleeding canker (and bear in mind this is excluding leaf blotch, which is also common in the UK), suffer from a negative feedback cycle by where there is a continuous decline in tree health up until a point of human intervention (a spiral of decline, if you will).

Without question, it is also worth noting that this study was done on young trees grown under controlled conditions. Because young trees are usually more vigorous, if this study was to be done on old trees that were located out in the ‘real’ landscape, we could probably expect the effects to be jut as bad, if not worse.

Thus, next time you see a horse chestnut that is being battered by leaf miner and bleeding canker, don’t let anybody tell you it’s largely an amenity problem – it’s not! It’s a health problem, that may very well eventually kill the tree outright, or let another pest or pathogen come in and finish the job. Combined with leaf blotch and abiotic stressors common in urban locations (pruning, ground compaction, pollution, drought, and so on), urban horse chestnuts in particular may very well be suffering very significantly. If we don’t do something, we can very well expect for horse chestnuts to gradually decline in terms of mature populations, and I very much expect this isn’t something that anybody wants.

Source: Percival, G. & Banks, J. (2014) Studies of the interaction between horse chestnut leaf miner (Cameraria ohridella) and bacterial bleeding canker (Pseudomonas syringae pv. aesculi). Urban Forestry & Urban Greening. 13 (2). p403-409.

Cameraria ohridella and Pseudomonas syringae var. aesculi – the compound impacts

2 thoughts on “Cameraria ohridella and Pseudomonas syringae var. aesculi – the compound impacts

  1. […] Many studies undertaken by scientific researchers are – by a sort of default – quite limited, in terms of the study’s spatial scale. Whilst this is not necessarily a bad thing, when the point of the research is to use a specific area (such as a city) as a case study, it can limit the effectiveness of problems that occur across a very large geographical area. One such example would be Cameraria ohridella (horse-chestnut leaf miner) presence within the UK, where it is an invasive pest (having arrived in 2002) progressing across the UK that may aggressively defoliate Aesculus hippocastanum (horse chestnut) and thus cause serious tree health problems. […]


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