Phytophthora cinnamomi

Robin, C., Smith, I., and Hansen, E.M. 2012. Phythophthora cinnamomi. Forest Phytophthoras 2(1). doi: 10.5399/osu/fp.2.1.3041

Phytophthora cinnamomi


P. cinnamomi Rands (1922) was first described in Sumatra in 1922 as the cause of stripe canker on the cinnamon tree, and the islands of SE Asia are still considered the likely evolutionary home of this most important Phytophthora pathogen of woody plants, including forest trees. It was spread worldwide, starting in the era of plant exploration and sailing ships. It is now widespread and continues to be destructive in forests of Australia, Mediterranean countries, and the SE United States, but is only recently appreciated as a danger to forests in western North America. P. cinnamomi has the broadest host range of any Phytophthora species.


Hyphal swellings or thin-walled chlamydospores. These are usually formed readily in water in greater abundance than sporangia, but may be slow to form and are sparse in agar.

Colony morphology on V8 agar is distinctive (medium-dense, wooly, uniform, filling the space between lid and agar surface); hyphae are tough. Ovoid non-papillate sporangia form in water but are usually rather sparse. Sporangia often appear almost semi-papillate due to slight apical thickening. Sporangia (average 57 μm by 33 μm) are broadly ellipsoid or ovoid, and persistent. They are formed on simple, unbranched or lax sympodial sporangiophores, and exhibit internal proliferation.

Hyphal swellings or thin-walled chlamydospores are usually formed readily in water in greater abundance than sporangia, but may be slow to form and are sparse in agar. Hyphal swellings are globose and often in botryose clusters. P. cinnamomi is heterothallic, with oogonia not seen in single culture. Typically only one mating type is found in a region.

Ovoid non-papillate sporangia in water. Sporangia will often appear almost semi-papillate due to slight apical thickening not seen here. Sporangia are usually rather sparse.


P. cinnamomi is in phylogenetic clade 7 with P. cambivora, with which it shares many features.

Phylogenetic tree from

(Blair et al 2008).


The temperature optimum for hyphal growth is between 24° and 28°C, although some growth occurs between 5°C and about 32–34°C. Growth at 20°C on V8 or corn meal agar averages 5 or 6 mm/d, and is slower, 2 or 3 mm/d, on potato dextrose agar.

Colony morphology at 14 days on potato dextrose agar (left) and V8 agar (right).

Distinguishing characteristics for identification

Colony morphology on V8 agar is distinctive (medium-dense, wooly, uniform, filling the space between lid and agar surface), and hyphae are tough. In water sporangia are usually rare, but botryose hyphal swellings are common. These characters are usually sufficient for identification. Although described as non-papillate, a slight apical thickening may give sporangia a scarcely semi-papillate appearance.

The searchable web-based database is useful for rapid identification of Phytophthora species based on sequencing of the ITS or Cox spacer regions, followed by BLAST searching the database. The database includes only sequences that are associated with published Phytophthora species descriptions or classic Phytophthora phylogenetics references.

Disease History

P. cinnamomi was first described in Sumatra in 1922 as the cause of stripe canker on the cinnamon tree, and the islands of SE Asia are still considered to be the likely geographic origin of the species. This is currently the most important Phytophthora pathogen of forest trees, but is also destructive in woody ornamentals, especially rhododendrons and other Ericaceae, and orchard crops including avocado. It was spread worldwide, starting in the era of plant exploration and sailing ships. It is now widespread and continues to be destructive in forests of Australia, Mediterranean countries, Mexico and the SE United States, and is of increasing concern in forests and wildlands of western North America. The host range of P. cinnamomi includes more than 1,000 species (Erwin and Ribeiro, 1996).

Impacts in the Forest

Although P. cinnamomi causes disease in many forests and native plant communities worldwide, the largest disease impact is in Australia where it has caused extensive destruction of native forests and heathlands in areas subject to a Mediterranean type climate (Weste and Marks 1987; Zentmeyer 1980). In southern Western Australia, one of the most biological diverse plant communities globally, more than 40% of the native plant species are susceptible to Phytophthora dieback (Shearer et al. 2004), including jarrah (Eucalyptus marginata), banksias, and grass trees. Similar disease of monocalyptus eucalypts and healthland species are recorded in southeastern Australia (Weste and Marks 1987). This soil-dwelling pathogen causes lethal root and collar rot, preventing uptake of water and nutrients. In Australia, advancing fronts of disease reflected the introduction of the pathogen to susceptible ecosystems. The pathogen spreads slowly through root-to-root contact and more rapidly with water movement. Human activities that move soil, such as road construction, mining, vehicular traffic, and the planting of infested nursery stock exacerbate pathogen spread. Disease management includes restrictions on soil and water movement, and preventive treatment of hosts with phosphite (Dunstan and Hardy 2005). Eucalypt dieback affected sites in Victoria have successfully been regenerated with susceptible eucalypts using a high sowing rate to aid in selection for resistance (Department of Sustainability and Environment 2008).

Dieback of Jarrah, Western Australia (left). Red oak with embedded lesions in France (right)

P. cinnamomi is listed In Australia as a key threat under the Environment Protection and Biodiversity Conservation Act 1999. This requires the Australian Government to prepare and implement a threat abatement plan to mitigate the harm caused by P. cinnamomi to Australian species and ecological communities.

P. cinnamomi was introduced during the 18th century in Europe where it caused chestnut ink disease (Crandall 1950). However because P. cambivora also is responsible for the same disease it is difficult to infer the exact time of introduction of P. cinnamomi in Europe. However, the disease rapidly spread in France and in all chestnut growing areas (Vettraino et al. 2005). It is one of the main reasons for abandonment of several chestnut orchards. More recently, P. cinnamomi was reported, mainly in France, as the agent responsible of ink disease of red oak (Quercus rubra, Robin et al. 1992a, b, c), and as the primary factor of root infection resulting in oak decline and mortality in Spain, Portugal and France (Brasier 1993, Robin et al. 1998, 2001; Gallego et al. 1999).

In the Americas, reports of forest and wildland damage from P. cinnamomi are increasing from western Mexico (Tainter et al. 2000) and from southern (Garbelotto et al. 2006) and central California, including both coastal and Sierra foothills counties. In particular situations it is destructive, causing expanding mortality centers in oak, manzanita, and mixed hardwood stands in California. Isolations from the Pacific Northwest are infrequent (Middleton and Baxter, 1955), but perhaps increasing as well. It has been considered to be too dry in the summer, and too cold in the winter for P. cinnamomi to spread in many western forests (Roth and Kuhlman, 1966), despite the susceptibility of many forest plants, and frequent introduction from horticultural settings. With changing climates, P. cinnamomi is expected to expand its sphere of destruction, particularly in Europe and North America.

Forest and Wildland Hosts and Symptoms

P. cinnamomi has the broadest host range of any Phytophthora species. It is especially associated with root diseases of eucalyptus, oaks and chestnuts, pines, and members of the Ericaceae (the heath family,) as well as diverse agricultural crops. Symptoms range from fine root mortality leading to gradual tree decline, to enlarging basal cankers, often with bleeding spots, and tree mortality. The table below includes just a few examples.

Host Latin Name Host Common Name Symptoms Habitat Region
Abies procera Noble fir Canker, Root rot Christmas Trees USA - Oregon
Abies spp. Frasier fir Root rot Christmas trees USA - Southeast
Agathis australis Kauri Canker, Root rot Forest New Zealand
Arbutus menziesii Madrone Canker Forest USA - Pacific Northwest
Banksia spp. Banksia Collapse Wildland Australia - Western
Castanea dentata American chestnut Canker, Root rot Forest, Ornamental Nursery, Plantations USA - Southeast
Castanea sativa European chestnut Canker, Root rot Forest, Ornamental Nursery, Plantations Europe
Eucalyptus marginata Jarrah Canker, Root rot Forest Australia - Western
Metrosideros polymorpha Ohia Decline Forest USA - Hawaii
Pinus echinata Shortleaf pine Decline Forest USA - Southeast
Protea spp. Protea Root rot Wildland South Africa
Quercus agrifolia Coast live oak, Oak Decline Forest USA - California
Quercus alba Oak, White oak Decline Forest USA - Ohio
Quercus engelmannii Engelmann Oak, Oak Decline Forest USA - California
Quercus glaucoides Lacey Oak, Oak Forest Mexico
Quercus peduncularis Oak Forest Mexico
Quercus rubra Oak, Red oaks Canker, Root rot Forest France, Mexico, USA
Quercus salicifolia Oak, Willow-leaved oak Forest Mexico
Quercus suber Cork oak, Oak Canker, Root rot Agricultural setting, Forest tree nurseries, Plantations France, Portugal, Spain
Xanthorrhoea spp. Grass tree Decline Wildland Australia - Victoria, Australia - Western

Educational and Management Materials


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