New Disease Reports (2005) 11, 8.

Foliar infection of sweet chestnut (Castanea sativa) by Phytophthora ramorum in the UK

S. Denman 1*, S.A. Kirk 1, C.M. Brasier 1, K.J.D. Hughes 2, R. Griffin 2, E. Hobdon 2 and J.F. Webber 1

*sandra.denman@forestry.gsi.gov.uk

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Accepted: 25 Feb 2005

Phytophthora ramorum is the cause of oak mortality in mixed-hardwood forests of central coastal California and south-western Oregon, but also causes a number of distinct disease symptoms on a wide range of hosts (Hansen et al., 2005). Bleeding cankers on stems, often leading to death of mature trees, shoot tip dieback (ramorum dieback) and foliar necrosis (ramorum leaf blight) are the main disease forms; the latter two types occurring on understorey shrubs and ornamental species. Inoculum is produced on infected shoots and leaves of foliar hosts but not on bole cankers. Foliar hosts are therefore critical in initiating and maintaining epidemics of tree mortality resulting from lethal bark cankers. Ramorum dieback and leaf blight have been found in Europe; Rhododendron being the main host but others including Camelia, Kalmia, Pieris and Viburnum are also affected (http://www.rapra.csl.gov.uk).

The discovery of infected rhododendrons and trees in the UK prompted more detailed surveys in areas with similar climate to areas of infection in California and Oregon. In November 2003 leaves on epicormic shoots of mature sweet chestnut trees (Castanea sativa) at a site in Cornwall, showed blackening and watersoaking. Lesions began at leaf margins or tips and around spine-tipped teeth on the edge of leaves. Phytophthora ramorum was isolated from the dead-live junction of leaf tissue. Morphological studies, ITS sequencing (GenBank Acc. No. AY924252), and other physiological and genetic analyses showed that isolates were of the A1 sexual compatibility type and fitted into the European population.

When detached sweet chestnut leaves were dipped for 10 s in zoospore suspensions (4x105 spores per mL) and incubated at 20°C, lesions similar to those seen in the field developed within 6 days. In separate tests, necrosis also developed on inoculated young leaves on intact seedlings, but was slower on older leaves. The pathogen was re-isolated fulfilling Koch's postulates.

This is the first report of P. ramorum on the foliage of a native European tree species. At least twelve infected sweet chestnut trees have now been found in the UK. Laboratory tests show that the pathogen sporulates on leaves of sweet chestnuts but the role this host would play in the development of an epidemic is unknown. However, it is not expected to be highly significant because infections are restricted to leaves on epicormic shoots and juvenile leaves, and leaves are deciduous.

Figure1+
Figure 1: (left): Sweet chestnut foliage necrosis caused by P. ramorum; Foliage on epicormic shoots arising from the tree trunk of a mature sweet chestnut tree.
Figure 1: (left): Sweet chestnut foliage necrosis caused by P. ramorum; Foliage on epicormic shoots arising from the tree trunk of a mature sweet chestnut tree.
Figure2+
Figure 2: (above): Sweet chestnut leaf from an epicormic shoot, leaf showing necrosis caused by P. ramorum; Note the necrosis moving down the mid-rib vein.
Figure 2: (above): Sweet chestnut leaf from an epicormic shoot, leaf showing necrosis caused by P. ramorum; Note the necrosis moving down the mid-rib vein.

References

  1. Hansen EM, Parke JL, Sutton W, 2005. Susceptibility of Oregon forest trees and shrubs to Phytophthora ramorum: A comparison of artificial inoculation and natural infection. Plant Disease 89, 63-70.

This report was formally published in Plant Pathology

©2005 The Authors