- The disease
- Control measures
- Susceptible species
- How it spreads
- Long term prospects
- Report a sighting
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 Europe in the 1930s. It was first identified 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 nut market, so in addition to the environmental and biodiversity impact, it can have an economic impact as well.
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 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. It had never previously been found in Britain, although it has been present in southern continental Europe since the 1930s, and can now be found in much of the continent.
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 with such rapidity 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 disease 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, less common diseases that cause diebacks and cankers on sweet chestnut are forms of Amphiporthe castanea (formerly Cryptodiaporthe castanea) and Diplodina castaneae.
We served notice on the owners of the affected trees to uproot all sweet chestnut plants and burn them on the affected sites. Surveys of a 3-kilometre radius around the infected sites and into surrounding woodland were carried out to determine the extent of any symptomatic chestnut. All field staff and individuals working for the owners of the sites adopted biosecurity measures to prevent further spread of this harmful organism.
Fera (now Apha) was fully involved in the investigation and represented on the disease outbreak management team. It contacted other recipients of plants for planting from the same source, as well as liaising with the European Commission and the French authorities. The findings were used to inform decisions about where we carry out our annual survey of sweet chestnut for the UK’s Protected Zone status. We also considered whether any changes to the EU requirements were needed in response to these findings.
We followed our disease outbreak contingency plan, and a strategy for our longer-term response to this disease is being developed. Findings from woodland surveys and follow-up investigations of other sites planted with the same material will be used to determine the longer-term strategy. The devolved administrations in Scotland, Wales and Northern Ireland were alerted so that they could consider equivalent surveys.
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 number 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 round timber and isolated bark into countries with protected-zone status is not permitted unless the timber or bark has been passported and is accompanied by an official statement to show that 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 Platanus (Plane), Quercus (Oak), and Fraxinus (Ash) - came into effect on 17 January 2013.
C. parasitica is a serious pathogen mainly of American and European sweet chestnuts, although the latter may 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), as well as Holm oak (Q. ilex) and others. However, the cankers tend to be superficial infections of the bark that 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.
The first record of the disease in Europe was made in Italy in 1938. 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 Ireland, Sweden and the Greek islands of Crete and Lesvos. These countries (other than Greece) currently 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 outbreaks in England were on two sites that 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 all 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 in 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 the insect vectors. 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.
In North America, the accidental introduction of C. parasitica on infected plants caused the almost complete destruction of American sweet chestnut in the eastern USA. It has also caused serious damage in orchards and forests in Europe.
However, 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) that 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.