- The disease
- Control measures
- Susceptible species
- How it spreads
- Long term prospects
- Report a sighting
Sweet chestnut blight is a plant disease caused by the ascomycete fungus Cryphonectria parasitica. This pathogen has caused severe epidemics resulting in death and dieback of American sweet chestnut (Castanea dentata) in North America and European sweet chestnut (C. sativa) in continental Europe after its identification in North America in the early 20th century, and in Europe (in Italy) in 1938.
C. parasitica infection is usually fatal to European and North American sweet chestnut trees. It devastated sweet chestnut forests in the eastern USA during the first half of the 20th century, killing an estimated 3.5 billion trees after it was accidentally introduced there from Asia. Although losses have not been on the same scale in Europe, it has spread steadily throughout much of Europe, and tree losses have been regionally significant. Sweet chestnuts are grown commercially in Europe and the UK for the timber and nut markets, so in addition to environmental and biodiversity impacts, it can have an economic impact.
Chestnut blight is not known to be currently present in the UK. However, C. parasitica was identified in November 2011 as the cause of dieback in European sweet chestnut in Warwickshire, central England. Approximately 300 trees had been planted for nut production in 2007, and infection become apparent in about half of the plants. A second outbreak was later found on a smaller site containing about 30 trees on a site in East Sussex which had been planted for nut production with trees from the same source as the Warwickshire trees. A following trace-forward exercise identified that a small number of infected trees were delivered to seven other locations in England. All the trees traced were destroyed. It had never previously been found in Britain, but is now widespread in continental Europe.
The disease was confirmed again near Maidstone, Kent, in 2016 in a single sweet chestnut tree which had been planted in 2009. The owner noticed symptoms and reported it to us with Tree Alert. The tree was destroyed with the owner's co-operation, and a survey was conducted of sweet chestnut and oak trees within 5km (3.2 miles). No further cases were found. However, we do appeal to sweet chestnut owners and managers to continue to be vigilant for the disease, regularly inspecting their trees and reporting suspicious symptoms to us, preferably with Tree Alert.
All symptoms on infected trees occur above the ground. C. parasitica attacks the bark of European sweet chestnut and enters through fissures or wounds. On grafted trees, infections are most frequently found in the region of the graft, where callusing occurs. In coppices or orchards, infections are often located at the base of the stem (collars or insertion points), although bark death does not spread into the root system.
The fungus can spread so rapidly in infected bark that stems or branches are soon girdled and the dead bark becomes visible as a sunken canker. Above the girdling canker, leaves wilt and turn brown, but remain hanging on the tree. Below the canker, branches have healthy foliage and, after a short time, new shoots are produced below the area of dead bark. It is common to find many cankers on a single tree.
On young, smooth-barked branches the cankered bark can be a bright brown, in contrast to the greenish colour of normal bark. On older stem infections, the discoloration or sunken nature of the infected bark is much less obvious. When the bark is killed rapidly the stem is girdled without any callus formation. However, sometimes the disease’s progress is slower, and new layers of bark form under the affected areas so that swelling and subsequent cracking of the outer bark occurs.
Masses of yellow-orange to reddish-brown pustules, the size of a pin-head, develop on infected bark. These fruit bodies erupt through lenticels and exude long, orange-yellow tendrils of spores in moist weather.
Another characteristic symptom is the formation of pale-brown mycelial fans in the inner bark, although these can only be revealed by cutting away the outer bark.
Some of the symptoms caused by C. parasitica, such as crown dieback, can be confused with other diseases caused by other pathogens, including Phytophthora species, e.g. Phytophthora cinnamomi or P. cambivora (commonly associated with ‘ink disease’, named after a blue-black stain found around damaged roots). These pathogens are already present on a range of host plants in the UK, and have been known for many decades to cause disease on sweet chestnut. Other diseases that cause dieback and cankers on sweet chestnut are forms of Amphiporthe castanea (formerly Cryptodiaporthe castanea), Diplodina castaneae and Ramorum disease (Phytophthora ramorum).
We served notice on the owners of the affected trees to uproot all sweet chestnut plants and burn them on site. Surveys of 3-kilometre (2011) and 5km (2016) radii around the infected sites and into surrounding woodland were carried out to determine the extent of any symptomatic chestnut. No further evidence of infection was found.
APHA (the Animal & Plant Health Agency) was fully involved in the investigations and represented on the disease incident management teams. It contacted other recipients of plants from the same sources, as well as liaising with the European Commission and the French authorities. (The 2011 trees had been sourced from a French nursery.) The 2011 findings were used to inform decisions about where we carry out our annual survey of sweet chestnut for the UK’s Protected Zone status. The UK's EU protections were strengthened in response to the 2011 findings, including a requirement that plants must originate from pest-free areas (areas free of C. parasitica).
Information from the 2011 outbreaks, and from woodland surveys, were used to update and publish our contingency plan for new disease outbreaks.
Pest Risk Assessment (Fera) - measures to protect the UK from further entry.
C. parasitica is treated as a European Union (EU) quarantine organism, which means that movements of planting material must be free from it, with plant passports issued to provide an assurance of compliance with requirements and to ensure traceability of the material.
A small umber of European countries, including the United Kingdom, are also Protected Zones for C. parasitica, listed in the EU’s Plant Health Directive. Movements into such zones require compliance with additional requirements, accompanied by specific plant passports eligible for the zones in question.
In the case of C. parasitica, movement of plants intended for planting (including seed), and round timber and isolated bark, into countries with protected-zone status is not permitted unless the plants, timber or bark have been passported and are accompanied by an official statement to show that they either originate in a pest-free area, or (in the case of timber and bark) it has been kiln dried, or that the bark has been fumigated.
Requirements for statutory pre-notification of imports of Castanea (Sweet chestnut), as well as Plane (Platanus), Oak (Quercus), and Ash (Fraxinus), came into effect on 17 January 2013.
C. parasitica is a serious pathogen mainly of American and European sweet chestnuts, although the latter might be slightly less susceptible than the American chestnut. The main types at risk in the UK are European sweet chestnut, which is grown for nut production, and introduced plantings of American sweet chestnut.
The familiar horse chestnut ‘conker tree’ (Aesculus hippocastanum) is unrelated to Castanea and is not affected, and nor is chestnut oak (Quercus prinus).
Other oak species can be infected, including Britain’s native sessile and, less often, pedunculate oaks (Quercus petraea and Q. robur respectively), as well as Holm oak (Q. ilex) and others. However, the cankers tend to be superficial bark infections which rarely cause the death of branches, sprouts or whole trees. The European Plant Protection Organisation (EPPO) also lists Castanopsis, Acer, Rhus typhina and Carya ovata as host species.
It originated in eastern Asia, where the disease occurs on indigenous Castanea species, causing little damage. Asian chestnuts have adapted and become tolerant to infection as a result of their long co-evolution with C. parasitica.
The susceptibility of American chestnut soon became apparent after the first discovery of chestnut blight in New York in 1904. Within 40-50 years the disease had spread over the entire native range of the chestnut, from Maine in the north to Georgia in the south, and west to Ohio and Tennessee, devastating much of the estimated 4 billion American chestnut population.
It is now widespread in Europe, with the exception of some countries with EU Protected Zone (PZ) status. Annual PZ surveys have been carried out in sweet chestnut woodland in Britain since 1993 without the disease being detected.
Some European countries and regions remain free of the disease, including the Czech Republic, Ireland, Sweden and the Greek islands of Crete and Lesvos. These countries (other than Greece) have EU Protected Zone status for the pathogen.
European countries and regions where it has been confirmed.
At present it is not possible to confirm how the pathogen entered the UK. It has the potential to be moved on infected timber and on infected plants for planting. The outbreak sites in England were planted with material supplied from the same nursery in France, although the source of the infection might never be proven.
Long-distance spread of C. parasitica occurs through international trade, with infected plants, wood or bark acting as pathways. Once bark has been colonised, the mycelium of the pathogen is reported to survive in this tissue for up to 10 months, even if it has been air dried. There is also a small risk of transmission by fruits or seeds.
Locally, the spores of C. parasitica are spread by wind and rain, but might also occasionally be transmitted by other agents such as insects and birds. Entry into suitable tissue for infection might be aided by wounds produced by insect vectors, including the Oriental chestnut gall wasp, which was found in South-East England in 2015. It is also reported that the pathogen can exist as a saprotroph (i.e. it lives and feeds on dead organic matter) on broad-leaved trees beyond its parasitic host range, allowing it to persist even when infected chestnut trees have been removed.
There is evidence that the pathogen can weaken in virulence in Europe, allowing infected sweet chestnut plants to recover. This weakening or attenuation in virulence is due to a phenomenon known as hypovirulence.
Hypovirulence results when C. parasitica is infected by a naturally occurring virus (dsRNA hypovirus CHV1) which limits the ability of the pathogen to grow in chestnut bark, or to produce spores. Hypovirulence is used as a form of biological control in many European countries affected by chestnut blight disease. It involves the application of hypovirulent strains of C. parasitica to trees affected with virulent, growing cankers. The treatment converts the virulent pathogen to a less aggressive form through the action of CHV1, and this allows the trees to recover from infection. There are now chestnut sites in Europe where the disease was introduced more than 30 years ago and where the CHV1 is well established, so the blight severity is low.
However, the success of hypovirulence depends on having populations of C. parasitica with only a limited genetic diversity. Populations with high levels of genetic variation pose a significant obstacle to the spread of the hypovirus, and limit its effectiveness. This appears to be the main reason why hypovirulence has only had a limited impact in the USA, where C. parasitica populations are much more genetically variable.
If you think you have spotted the disease, please check the symptoms section before reporting it.