Port-Orford Cedar Root Disease

Young trees killed by Port-Orford cedar root disease with symptomatic (chlorotic) trees nearby.

This is an unusual root disease in several ways:

  • It is non-native
  • It kills and rots the phloem and cambium, not the wood
  • It is very host-specific, infecting Port-Orford cedar.


Chamaecyparis lawsoniana (Port-Orford cedar or Lawson cypress) is the only important host in North America. It has a very limited natural distribution on the Oregon/California border. It is an attractive species with many cultivars used in planted landscapes. It is important also because the wood has many good qualities and is quite valuable. Elsewhere, C. obtusa and C. pisifera have been found infected (see next section).

In Japan, Chamaecyparis obtusa (hinoki falsecypress) is considered culturally significant, even sacred. Countless Shinto shrines and temples have been built using hinoki wood. Today there are few large forests of hinoki left. Chamaecyparis lawsoniana from North America is considered an acceptable substitute. It is used there to build and rebuild shrines, temples, and houses, as well as small novelty items.

Taxus brevifolia (Pacific yew) is significantly less susceptible, but infrequently can be infected and killed when growing among infected C. lawsoniana ​[1]​.

Pathogen and Distribution

The pathogen is Phytophthora lateralis. It is not in the Kingdom Fungi, as it was in days of yore, but is often put in Kingdom Chromista (Phylum Oomycota, Class Oomycetes, Order Peronosporales). Although people are quick to point out that it is not a “fungus”, I am not alone in considering the term to denote a life form rather than a taxonomic group. So I still call these things fungi.

The genus name means “plant destroyer”. That applies well to many pathogens in the genus, not least to this one.

The fungus first made its presence known to humans by killing Port-Orford cedar in northwestern USA. From the prior absence of such killing, the expansion of its distribution, and its destructiveness, it was pretty clear that it was introduced, but for many years it was unknown elsewhere. However, it has since been found in natural C. obtusa forests in Taiwan, where it infects roots as well as foliage ​[3, 9]​, but apparently causes little damage. Taiwan appears to be in its native range. It has been introduced to Europe, and attacks planted C. lawsoniana in the UK, France, and the Netherlands. In Scotland, it has also been found attacking C. pisifera (Sawara cypress, native to Japan) ​[6]​.

Several “lineages” have been identified around the world ​[2, 5]​. Most discoveries from Europe are in the same lineage as the North American samples, suggesting that those European introductions arose from North America. The American lineage likely evolved rapidly from one of the east Asian lineages after its introduction.


The host grows best along fens (peat-forming wetlands fed by groundwater) and in riparian zones (along streams). Near the coast, where conditions are wetter, it can grow more widely on upland sites. The pathogen thrives under such conditions, which enable the production and germination of zoosporangia, and facilitate swimming and infection by the zoospores.

Disease Cycle and Epidemiology

Port-Orford cedar root disease. This is an advance stage with necrosis going up the stem. Note the sharp border between dead and live phloem.

Phytophthora lateralis is a cortical root rotter. It kills feeder roots, then grows up to bigger roots, where it kills phloem and cambium. It can progress above the root collar and a short distance up the stem. Phloem and cambium turn from creamy white to cinnamon brown with a sharp line separating healthy and diseased tissues. Crowns fade through yellow to red to brown. Trees die quickly, in a few weeks for small trees and a few years for large trees.

In natural stands of C. lawsoniana, the fungus is soilborne and waterborne. It can move in running water and in soil contaminated with fungal spores that is transported on construction and logging machinery, vehicles, shoes, and livestock.

The disease can enter new areas when soil is carried in by vehicles, people, or animals. A study of 36 local introductions (in part of the tree’s range where it is restricted to riparian areas) suggested that 26 were spread by vehicles and the rest by foot traffic ​[4]​. Then, movement locally is clearly associated with drainages and downhill. Along streams, likelihood of infection increases with tree size and proximity to the stream. Larger trees present a larger target and those closest to the stream are most likely to be exposed to inoculum, primarily zoospores.

Chlamydospores. The pathogen survives periods unsuitable for growth as mycelium or as chlamydospores. Chlamydospores may survive up to 7 years in dead organic matter. They require a period of cold dormancy to germinate.

Oospores. Trione reported oospores produced, but only on certain media, including cedar foliage agar, at a certain concentration ​[8]​. He also showed that the fungus is homothallic, producing oospores on single-zoospore isolates. Others have had no success in observing gametangia or oospores ​[3]​. It does not appear that oospores are important epidemiologically, as chlamydospores are abundant and serve a similar function.

Sporangia and zoospores. Sporangia are produced abundantly, especially when nutrients are low. Although most remain attached to the sporangiophore, a small proportion are caducous (deciduous; see below). They are capable of germinating directly, producing hyphae, or producing zoospores ​[8]​. Direct germination is most common when there is no free water and temperature is above 20 C. Under cool, saturated conditions, zoospores are generally produced. To a tree, a sporangium is like a cluster bomb, producing dozens of independent propagules, each capable of infecting and killing the tree. Zoospores are short-lived and can swim only a few centimeters, but they can be carried farther in water. They readily attach to surfaces, round up, and germinate to produce hyphae.

In Phytophthora, features of the sporangium are generally associated with the means of dispersal and the type of disease caused ​[2]​. Phytophthora lateralis does not fit the usual pattern (see table). A small porportion of sporangia in this species is caducous (deciduous), which is associated with windborne dispersal and infection of aerial plant parts. Indeed, this has been observed in nurseries, in Taiwan, and in some cases in Europe ​[2, 9]​.

Diagrammatic representation of the sporangium of Phytophthora lateralis.
Sporangial features generally associated with two types of disease caused by Phytophthora spp.; those of P. lateralis are underlined.
 PedicelPapillaCaducityDispersalTypical type of disease
Soilborne propagulesNo preformed pedicelNon-papillateNon-caducous (persistent)Sporangium produces zoospores in placeCortical root rot, basal cankers
Windborne propagulesPreformed pedicelPapillate to semi-papillateCaducous (deciduous) (1-5%)Sporangium is wind-dispersed, can germinate directly (like conidium) or produce zoosporesInfection of foliage and other plant parts

Impacts and Management

Cleaning soil potentially contaminated with Phytophthora lateralis from a log truck before entering the forest.
Cleaning potentially contaminated soil from shoes before entering the forest.

The disease appeared in a nursery near Seattle in 1923, got into ornamental plantings, and eventually reached the native range in 1952. It is widespread in that range, but still most of the area is uninfested ​[1]​. Additional movement is a constant danger.

Impacts of this disease have been great. It has caused severe losses to the ornamental cedar industry, estimated at up to 1 million dollars annually. Port-Orford cedar is extremely valuable, and timber losses have been estimated at 250 million to nearly 1 billion dollars. Ecosystem effects are also considerable.

Mortality of trees has been high in areas infected ten years or more. High-risk sites may experience 90% mortality.

Detailed management recommendations can be found in the FIDL ​[1]​. Briefly:

  • Sort sites into two categories
    • High Risk: Wet/riparian sites that are below infested areas or below likely sites for introduction, especially roads.
      • Consider removal of cedar along roads to prevent introduction. Keep these areas free of cedar.
    • Low Risk: Every place else.
      • Focus management of Port-Orford cedar here.
  • Exclusion
    • Wash vehicles, equipment, and footwear before entering disease-free areas.
    • Through seasonal or permanent road closures, where practical, entry into uninfested areas should be restricted.
  • Spacing. During commercial or precommercial thinning in high-risk sites, create spacing to prevent disease spread between trees or groups of trees.
  • Resistance. Selection of resistant stock, development of seed orchards, and outplanting trials of resistant stock have been fairly successful ​[7]​. Resistant stock should be planted on low-risk sites.
  • Eradication. If hosts are absent for some years, the fungus will eventually die out. The time required is uncertain, but may be as little as four to as many as 10 years.


  1. 1.
    Betlejewski F, Goheen DJ, Angwin PA, Sniezko RA. 2011. Port-Orford-Cedar Root Disease.  Forest Insect & Disease Leaflet 131. Portland, Oregon, USA: USDA Forest Service, Pacific Northwest Region (R6) <https://www.fs.usda.gov/Internet/FSE_DOCUMENTS/stelprdb5346825.pdf>.
  2. 2.
    Brasier CM, Franceschini S, Vettraino AM, Hansen EM, Green S, Robin C, Webber JF, Vannini A. 2012. Four phenotypically and phylogenetically distinct lineages in Phytophthora lateralis. Fungal Biology, pp. 1232–1249 <10.1016/j.funbio.2012.10.002>.
  3. 3.
    Brasier CM, Vettraino AM, Chang TT, Vannini A. 2010. Phytophthora lateralis discovered in an old growth Chamaecyparis forest in Taiwan. Plant Pathology 59(4):595–603 <10.1111/j.1365-3059.2010.02278.x>.
  4. 4.
    Jules ES, Kauffman MJ, Ritts WD, Carroll AL. 2002. Spread of an invasive pathogen over a variable landscape: a nonnative root rot on Port Orford cedar. Ecology 83(11):3167–3181 <10.1890/0012-9658(2002)083[3167:SOAIPO]2.0.CO;2>.
  5. 5.
    Robin C, Brasier C, Reeser P, Sutton W, Vannini A, Vettraino AM, Hansen E. 2015. Pathogenicity of Phytophthora lateralis lineages on different selections of Chamaecyparis lawsoniana. Plant Disease 99(8):1133–1139 <10.1094/PDIS-07-14-0720-RE>.
  6. 6.
    Schlenzig A, Campbell R, Eden R. 2014. First report of Phytophthora lateralis on Chamaecyparis pisifera. New Disease Reports 29:15 <10.5197/j.2044-0588.2014.029.015>.
  7. 7.
    Sniezko RA, Hamlin J, Hansen EM. 2012. Operational program to develop Phytophthora lateralis-resistant populations of Port-Orford-cedar (Chamaecyparis lawsoniana). In: Proceedings of the 4th International Workshop on Genetics of Host-Parasite Interactions in Forestry: Disease and insect resistance in forest trees. Gen. Tech. Rep. PSW-GTR-240, eds Sniezko RA, Yanchuk AD, Kliejunas JT, Palmieri KM, Alexander JM, Frankel SJ, pp. 65–79. Albany, California, USA: USDA Forest Service, Pacific Southwest Research Station <https://www.fs.usda.gov/treesearch/pubs/44026>.
  8. 8.
    Trione EJ. 1957. The physiology and pathology of Phytophthora lateralis on native Chamaecyparis lawsoniana. Ph.D. thesis. Oregon State College <https://search.library.oregonstate.edu/permalink/f/kgr9kh/CP71164807800001451>.
  9. 9.
    Webber JF, Vettraino AM, Chang TT, Bellgard SE, Brasier CM, Vannini A. 2012. Isolation of Phytophthora lateralis from Chamaecyparis foliage in Taiwan. Forest Pathology 42(2):136–143 <10.1111/j.1439-0329.2011.00729.x>.