Swiss Needle Cast

Hosts

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.

Pathogen

The pathogen is Nothophaeocryptopus gäumannii. For some time it was placed in the genus Phaeocryptopus, which it closely resembles morphologically, but phylogenetic studies showed it to be in a different order (Capnodiales: Mycosphaerellace) from the type species of Phaeocryptopus (Dothideales: Dothioraceae) ​[7, 8]​. The new genus name means “false Phaeocryptopus”. Black pseudothecia that are about 0.1 mm or a bit smaller form in stomata arranged in lines on the lower surface of infected leaves. They shoot airborne ascospores. Pseudothecia may appear on green needles that are one year or more old.

Environment

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. It is associated in part with an increase in winter temperatures and wet spring and summer ​[5]​. It appears that warmer winters allow the fungus to colonize needles more rapidly, while a wet spring is conducive to spore dispersal and infection.

The increased preponderance of Douglas-fir in coastal Oregon is also thought to be a factor ​[5]​. Before active forest management of coastal forests, Douglas-fir was not a dominant species, but shared forests with ample populations of Picea sitchensis (Sitka spruce), Tsuga heterophylla (western hemlock), and Alnus rubra (red alder). These forests have been replaced with Douglas-fir plantations over wide areas, increasing potential disease severity.

Disease Cycle

Pseudothecia production begins in early winter. Ascospore release is concentrated in the period of needle emergence and expansion, but can continue for a month or so after. In coastal Oregon, needle emergence and expansion occur May-June, depending on elevation. 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

Symptoms typically appear one to three years after infection. 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.

An important diagnostic sign of the pathogen is lines of pseudothecia in stomata on the undersides of needles.

Distribution

The disease is thought to be native in the native range of Douglas-fir, the Pacific Northwest of North America. It now occurs in most areas where the host has been introduced, including much of North America. It was discovered in Switzerland in 1925 ​[1]​ and has since moved throughout Europe. It was found in New Zealand in 1959 ​[3]​.

In the native range, it never caused much damage before about 1990. But on the Oregon coast near Tillamook, a huge, severe epidemic began in the 1990’s ​[2]​. 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.

Management

In New Zealand, the disease is estimated to reduce volume growth by 32% ​[3]​. In coastal Oregon volume growth loss is estimated at 23% ​[6]​ to as much as 50% beginning in 1990 and up to 25% height growth loss beginning in 1992 ​[4]​. Mortality is relatively rare, but where trees are grown for lumber production, these are huge losses.

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.

Other Issues

Although Swiss needle cast is thought to be native to the Pacific Northwest of North America, it was first found in 1925 in Switzerland (thus the name) presumably imported there on seedlings used to establish plantations ​[1]​. 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 ​[1]​. 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 ​[1]​. However, since about 1990 observers have noticed increased severity and damage from the disease ​[2]​. 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. 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 presettlement 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 stomata and interfering with gas exchange. Needles are shed when approximately 25% of stomata become urns for pseudothecia ​[5]​.

Links

  1. 1.
    Boyce JS. 1940. A needle-cast of Douglas-fir associated with Adelopus gaumanni. Phytopathology 30(8):649–659.
  2. 2.
    Hansen EM, Stone JK, Capitano BR, Rosso P, Sutton W, Winton L, Kanaskie A, McWilliams MG. 2000. Incidence and impact of Swiss needle cast in forest plantations of Douglas-fir in coastal Oregon. Plant Disease 84(7):773–778 <10.1094/PDIS.2000.84.7.773>.
  3. 3.
    Kimberley MO, Hood IA, Knowles RL. 2011. Impact of Swiss needle-cast on growth of Douglas-fir. Phytopathology 101(5):583–593 <10.1094/PHYTO-05-10-0129>.
  4. 4.
    Maguire DA, Kanaskie A, Voelker W, Johnson R, Johnson G. 2002. Growth of young Douglas-fir plantations across a gradient in Swiss needle cast severity. Western Journal of Applied Forestry 17(2):86–95 <https://academic.oup.com/wjaf/article/17/2/86/4741314>.
  5. 5.
    Mulvey RL, Shaw DC, Filip GM, Chastagner GA. 2013. Swiss Needle Cast. Forest Insect and Disease Leaflet 181, FS/R6/RO/FIDL#181-13/001. USDA Forest Service, Pacific Northwest Region (R6), Portland, Oregon, USA <https://www.fs.usda.gov/Internet/FSE_DOCUMENTS/stelprdb5426973.pdf>.
  6. 6.
    Ritóková G, Shaw D, Filip G, Kanaskie A, Browning J, Norlander D. 2016. Swiss needle cast in western Oregon Douglas-fir plantations: 20‐Year monitoring results. Forests 7(8):1–11 <10.3390/f7080155>.
  7. 7.
    Videira SIR, Groenewald JZ, Nakashima C, Braun U, Barreto RW, de Wit PJGM, Crous PW. 2017. Mycosphaerellaceae – Chaos or clarity? Studies in Mycology 87:257–421 <10.1016/j.simyco.2017.09.003>.
  8. 8.
    Winton LM, Stone JK, Hansen EM, Shoemaker RA. 2007. The systematic position of Phaeocryptopus gaeumannii. Mycologia 99(2):240–252 <10.1080/15572536.2007.11832584>.