Swiss Needle Cast
The host is Douglas-fir, Pseudotsuga menziesii. In most areas, younger trees, especially in dense stands (think Christmas tree plantations), are attacked more than older, open-grown trees. However, in coastal Oregon, where a huge, sustained epidemic is underway, even large, open trees are attacked.
The pathogen is Phaeocryptopus gäumannii. Black pseudothecia that are about 0.1 mm or a bit smaller form in stomates in lines on the lower surface of infected leaves and shoot airborne ascospores. The pseudothecia may appear on green needles that are one year or more old.
Areas where Swiss needle cast is severe tend to be moist. The fact that younger trees in dense stands, such as Christmas tree plantations, tend to be most heavily attacked may be related, at least in part, to the moist microclimate of such stands. In Oregon, a severe, unprecedented epidemic has continued since the early 1990's in the coastal fog belt, where Douglas-fir was not a dominant species in presettlement forests.
Pseudothecia are produced in early winter. Ascospore release is concentrated in March through June, but can continue into August. Ascospores generally infect current-year needles. In the typical form of the disease, these infections are often nonsymptomatic (or latent) for several years. In the more severe form of the disease, symptoms and fruiting of the fungus may occur as early as the year after needle production.
Inoculum is often produced on green needles. Substantial proportions of infected needles can build up before much defoliation occurs.
Symptoms typically appear one to three years after infection (which occurs in the year of needle production). The oldest infected needles show symptoms first. Needles first become yellow-green, chlorotic, then mottled or entirely brown, then dehisce. Trees have thin crowns. In the typical form of the disease, symptoms are more severe in the lower and inner foliage. Trees may eventually suffer reduction in height and diameter growth.
A sign of the pathogen, important diagnostic, is the presence of lines of pseudothecia on the undersides of needles in stomata.
The disease occurs in most areas where the host has been introduced, including much of North America, Europe, and New Zealand. On the Oregon coast near Tillamook, a huge, severe epidemic began in the 1990's. It covers about 50,000 ha and follows the coastal fog belt inland up to about 20 km. See "Other issues" below for more information.
Commercial thinning seems to make the "new" form of the disease worse. Pathologists are recommending a shift away from Douglas-fir where feasible, thinning early and favoring other species, and interplanting with other species. Most land managers are following this recommendation in the epidemic areas of coastal Oregon.
The fungicide Bravo has been tested using two aerial applications per year. After a lag of a few years, substantial decrease in infection and increase in growth is observed. This benefit is observed even several years after terminating treatment. However, it seems unlikely that Bravo will be used in practice because of potential environmental impacts. Work is underway to dertermine if sulfur is similarly effective.
Although Swiss needle cast is thought to be native to the Pacific Northwest of North America, it was first reported in 1925 from Switzerland (thus the name) presumably imported there on seedlings used to establish plantations (®). It was quickly found in Germany, Austria and the British Isles. It was first reported in the U.S. in 1938 but was present at least by 1929. In 1940 it was widespread in New England. It has since been found in the central United States and New Zealand.
In 1940, Boyce considered it to be widespread but harmless in the Pacific Northwest, where Douglas-fir is native, and more damaging in other areas where Douglas-fir has been planted (®). However, since about 1990 observers have noticed increased severity and damage from the disease (®). It is attacking younger foliage than before and trees of all sizes. Prior to 1990, the disease was typically worse in lower and inner crowns, but now symptoms are worst in the upper crown and on south slopes. In coastal plantations it has caused as much as 50% volume growth loss beginning in 1990 and up to 25% height growth loss beginning in 1992 (®). Healthy Douglas-fir in coastal areas usually has 4 years of needle retention; diseased areas have retention as low as 1.1 (1 year and 0.1 of the previous year). Even mature trees can be severely diseased and significant mortality is occurring due to the disease in mature stands.
Surveys suggest that incidence of the disease has not changed much in the last five years. Occurrence is correlated with degree day accumulation during winter and leaf wetness hours during spring to fall (warm winters and wet summers).
Many hypotheses have been proposed to explain the rapid increase in severity of this disease: new strain of the pathogen, pollution, change in tree nutrition, change in genetics of Douglas-fir through management, planting of Douglas-fir in a spruce-hemlock zone, and forest management practices. The pathogen has much greater genetic diversity in the Pacific Northwest than in eastern U.S., New Zealand, and Europe, consistent with the pathogen being native to the Pacific Northwest, with its host. Epidemic areas, where the disease has become more severe, have more diversity than non-epidemic areas. Two lineages are found in the area, possibly at the level of species, but it does not appear that the new epidemic is due to a more virulent population or species. Instead, it seems likely that planting of Douglas-fir in the coastal spruce-hemlock zone, where it was not a major component in pre-settlement forests, is an important factor. The disease may have determined the native forest type in that coastal zone under presettlement conditions. Another important factor is weather, especially warm winters, which have been associated historically with increases in disease severity. The most severe disease in the current epidemic also occurs in areas with warm winter temperatures.
The primary mechanism of damage, surprisingly, appears to be the production of fruitbodies in the stomatal apertures, occluding the stomates and interfering with gas exchange.
Data suggest that the pathogen is more closely related to the Dothideales than with the Venturiales where it is traditionally classified.