3.7.2S
SAPSTAIN FUNGI IN PINE AND THE EFFECT OF TIMBER AGEING AND DEATH

NJ STRONG1, JF WEBBER2 and RA EATON1

1School of Biological Sciences, University of Portsmouth, King Henry Building, King Henryl Street, Portmouth. P01 2DY, UK; 2Forest Research, Alice Holt Lodge, Farnham, Surrey, GUIO 4LH, UK

Background and objectives
Fungal defacement of sawn pine lumber and logs by sapstain and mould fungi remains a major problem, causing significant economic losses although the damage is largely cosmetic. It has been estimated that the global market for sapstain control treatment is more than 50 million US$ annually. However, little is known about the factors that influence the susceptibility of pine to sapstain and whether changes occur in lumber as it undergoes aging and cell death after harvesting which change it's susceptibility to sapstain fungi. To gain insight into this issue, a trial was initiated to study the growth of three species of sapstain fungi in pine logs incubated under controlled conditions, which had first been naturally aged or killed by autoclaving or irradiation.

Materials and methods
Logs of Scots pine (Pinus sylvestris) about 0.5 m in length were cut from a commercial crop during a thinning exercise; the exposed cut ends were immediately painted with a bitumous sealant to reduce moisture loss. Some of these logs were inoculated after autoclaving or gamma irradiation when freshly felled (time zero) or when nine weeks old. In addition, untreated logs were inoculated at time zero, then three, six or nine weeks later. The fungi comprised two isolates each of Leptographium wingfleldii, Ophiostoma piceae and Sphaeropsis sapinea; these were inoculated into logs which were incubated at 20C. After two weeks, the bark was removed from the logs and any lesions visible on the sapwood measured and recorded photographically.

Results and conclusions
The three species showed markedly different growth characteristics in the sapwood of the logs after two weeks incubation. O. piceae had the poorest growth, but this improved slightly in the logs that had been aged. The two isolates of L. wingfiedii differed in colonising ability, but both showed the greatest growth in time zero and three week old logs, but then a decline in growth in logs that had been aged for longer. S. sapinea was the most vigorous coloniser, but showed a more or less steady decline in colonising ability when inoculated into logs that had been aged for increasing lengths of time. However, the growth of all the fungi was most extensive in the freshly felled (time zero) logs which had been killed by autoclaving or irradiation. In both the treated and untreated logs, three regions could be defined around the lesions produced by the sapstain fungi: healthy tissue, stained tissue and a pale, dry-looking zone between them. These regions were characterised using light and scanning electron microscopy.

The results suggest that the physiological state of host tissues (in this case pine logs) can have a marked effect on the colonising ability of sapstain fungi and ultimately affect the degree of discolouration and defacement that may occur. The ability of the host material to resist fungal invasion may also depend on whether cell death occurs through gradual senescence during aging, as opposed to rapidly killed irradiated or autoclaved material. The pathogenic/saprotrophic abilities of the inoculated fungi are discussed in this context and related to changes that may occur in lumber as it ages.

ICPP98 Paper Number 3.7.2S
3.7.2S
EASTERN FILBERT BLIGHT: LIVING WITH AN INTRODUCED PATHOGEN ON AN INTRODUCED HOST

KB JOHNSON

Dept. of Botany and Plant Pathology, Oregon State University, Corvallis, OR 97331, USA

Background and objectives
European hazelnut, Corylus avellana L., is produced commercially on 12,000 ha in western Oregon, which represents 98% of production in North America. Eastern filbert blight, caused by the pyrenomycete Anisogramma anomala (Peck) E. Miller (Diaporthales) was first observed in Oregon in 1986. A. anomala is an endemic parasite of the American hazel, C. americana, in eastern North America, and had not been reported west of the Rocky Mountains until 1970 when it was found in a European hazelnut orchard in southwest Washington state. On European hazelnut, cankers can expand perennially along branches at rates of up to 1 m per year. Canker expansion results in canopy dieback and death of trees in 5 to 12 yr if diseased limbs are not removed. Most Oregon orchards in the vicinity of the initial detections have been destroyed by the disease, and currently, 30-40% of Oregon orchards are infested with the pathogen. Over the last 10 years, an intensive research and extension effort has been conducted to reduce the potential impact of eastern filbert blight on Oregon's hazelnut industry.

Results and conclusions
A. anomala gains entry into a hazelnut tree through infection of immature tissues near the apical meristem of growing shoots. Thus, hazelnut trees are susceptible to infection by A. anomala only after vegetative buds have initiated active growth in spring (budbreak). Initially, the fungus produces a vesicle-like structure within young epidermal cells, and then grows along a branch via the cambium and the outermost layer of xylem. Canker formation does not begin until late spring of the year after infection. Under Oregon conditions, ascospores are released from late autumn to rnid-spring with most spores (70-90%) being released during periods when the host is not susceptible to infection. A. anomala is obligate and apparently biotrophic as it does not survive saprophytically in dead hazelnut branches nor grow readily in culture.

Orchardists have implemented the use of regular scouting, fungicides, therapeutic pruning, and other methods of sanitation to slow the eastern filbert blight epidemic. In research plots, complete protection from infection has been obtained with three to five applications of chlorothalonil during March and April, but these sprays are expensive and do not provide 100% control when applied in commercial orchards. Host resistance to eastern filbert blight is the most promising approach to control. Quantitative resistance appears to exist in two major forms that govern how readily a shoot becomes infected and how rapidly cankers expand once the pathogen becomes established. The degree of quantitative resistance in some European hazelnut cultivars (e.g. 'Tonda di Giffoni') is on par with that of some selections of American hazel. These cultivars, however, lack one or more of the horticultural characteristics needed for commercial production. A complete resistance to eastern filbert blight also has been found, which is conferred by a single, dominant gene. The European hazelnut cultivar in which this resistance was first observed has many undesirable characteristics; therefore, the resistance gene is being transferred with a modified backcross procedure to more acceptable selections. Roughly 10,000 seedlings from the first and second backcross generations are in the field.

References
1. Johnson KB, Pinkerton JN, Mehienbacher, SA, Stone JK, and Pscheidt JW, 1996. Plant Disease 80, 1308-1316.