Phytophthora cinnamomi is a destructive and widespread soil-borne pathogen that infects woody plant hosts. P. cinnamomi spreads both by chlamydospores as well as water-propelled zoospores. The presence of the oomycete is only determinable by soil or root laboratory analysis, although its effects upon the vegetation it destroys are readily evident (Parks and Wildlife, 2004). Infection often results in the death of the plant, with earlier symptoms including wilting, yellowing and retention of dried foliage and darkening of young feeder roots and occasionally the larger roots. The plant is unable to adequately absorb enough water from the soil because its roots are damaged and consequently may die (Botanic Gardens Trust, UNDATED). P. cinnamomi causes water deficiency symptoms which can result in tree death, following a slow or abrupt decline. Primary symptoms caused by this pathogen in temperate oaks (Quercus rubra and Q. robur) include fine root lesions which may extend into larger roots, collar and trunks causing bleeding cankers, but no water deficiency has been described (Moreau & Moreau, 1952; Robin et al. 1992; Robin et al. 2001). Bergot et al. (2004) observe that, \"The initial lesions at root or collar level develop upwards in the trunk and the disease expression is typically a bleeding trunk canker, therefore named 'ink disease'. Since P. cinnamomi essentially develops in inner cortical tissues and not in the wood, oaks keep track of past infections in the form of necroses at the cambium level (scars)\".

Robin et al. (2001) state that, \"Waterlogging increased the severity of Phytophthora cinnamomi induced diseases in the field (Fagg et al. 1986). Under controlled experiments, when waterlogging was imposed at or after the time of inoculation, lengths of lesions caused by P. cinnamomi significantly increased (Davison & Tay, 1987). Moreover, waterlogging and associated hypoxia had a direct effect on P. cinnamomi by reducing mycelial growth and sporangium production (Davison & Tay, 1986). It is likely that in the field, the combination of heavy rainfalls leading to occasional waterlogging, and summer droughts, may act sequentially and predispose oaks to decline when infected by P. cinnamomi.\"

Bergot et al. (2004) states that, \"Disease development was shown to be strongly hampered by cold winters (Robin et al. 1992b; Marçais et al. 1996), in agreement with the known sensitivity of P. cinnamomi to frost (Benson, 1982). The hypothesis that lethal frost effects on the pathogen could be a major factor limiting disease range in oaks was put forward by Delatour (1986).\"

The Australian Department of Conservation and Land Management (2003) states that, \"When conditions are warm and moist the mycelial threads (or hyphae) that form the body of the oomycete in the soil or host-plant tissue vegetatively produce micrscopic spore sacks called sporangia and thick-walled chlamydospores. Mycelium of different mating types may grow together to produce thick walled sexual spores called oospores. Zoospores have flagellae, which allow them to swim very short distances (25-35mm) in standing water or in films of water in soil pores. They can also be carried along in moving water over large distances. Zoospores are short-lived and fragile, but are produced in large numbers and probably are the cause of most new infections. As they move through the soil zoospores are attracted to the tips of plant roots, where they lodge, encyst, and germinate to produce germ tubes which penetrate roots. Mycelium then grow within the roots of susceptible plants and may grow from plant to plant via root contact points. This root to root growth is the main cause of spread of a P. cinnamomi infestation upslope. Chlamydospores are much larger spores that are tough and long-lived (within dead plants and the soil). They are produced within plant roots in response to drying conditions, and are the resistant, 'resting' phase of the oomycete. They may be transported in root fragments or soil and then germinate to cause a new infection when they encounter warm, moist conditions. Germinated chlamydospores may produce sporangia, more chlamydospores, or mycelium which directly infect roots. After infection, the mycelium grows through the root tissue causing cell breakdown and 'rotting' of the tissue. The pathogen extends into the major roots of susceptible species and may girdle the base of the trunk. Plant death occurs because transport of water from the roots is prevented. Various environmental factors control the rate of growth of mycelium within the root. For instance, there is little growth when the water content of the plant tissue is below 80%. In very susceptible species, such as banksia, death may occur in weeks, while in moderately susceptible species such as jarrah the tree may not die till a year or more after infection. Moderately susceptible and resistant species have the ability to 'wall off' the infection to prevent further spread of the mycelium, with varying degrees of success.\"

Phytophthora cinnamomi requires moist soil conditions and warm temperatures to be active, but damage caused by the disease most often occurs in summer when plants are drought stressed (Botanic Gardens Trust, Undated). Menge (1998) states that, \"Soil with poor drainage, high clay content, high water tables, hard pans, clay pans or where water pools after irrigation or rainfall, have historically been associated with sites where P. cinnamomi infection is severe.

A study (Moreira & Martins, 2005) undertaken during 1995-98, surveyed cork and holm oak stands in four different regions of Portugal (Trás-os-Montes, Alentejo, Ribatejo and Algarve) for the presence of P. cinnamomi. Tree decline severity, sudden death and site characteristics were assessed in varied conditions. Analysis of the survey results indicated: that 56% of surveyed flora were infected with the pathogen; the flora belonged mainly to the following families Ericaceae, Cistaceae and Leguminosae; recovery of the pathogen was more frequent in shallow soils; soils with low fertility and low mineral nutrient levels, particularly phosphorus, seemed to favour infection and sites facing south showed higher occurrence of P. cinnamomi, which was also more frequent in slopes and valleys than on hilltops.

Botanic Gardens Trust (Undated) states that, \"Small swimming zoospores are released which attach to and infect roots, normally behind the root tip. All spores and structures of P. cinnamomi are microscopic and cannot be seen with the naked eye. There is no way of visually telling if the pathogen is present in the soil. P. cinnamomi grows through the root destroying the tissue which is then unable to absorb water and nutrients. Further zoospores are produced in sporangia, particularly when the soil is moist and warm, and are released into the soil. Consequently zoospore numbers can build up quite rapidly. Zoospores move in water and may infect neighbouring plants especially those down slope from a site of infection. These spores are easily transported in storm water, drainage water, contaminated soil and on tools, footwear and vehicles. A further two spore types may be produced, a chlamydospore and an oospore, which are survival structures produced when conditions become unfavourable such as when a food source is exhausted or in periods of low temperature or drought. These spores are capable of surviving for extended periods of time, and when conditions become favourable they germinate and renew the life cycle. This allows P. cinnamomi to survive in dead plant tissue for a number of years.\"

The food source of Phytophthora cinnamomi is the root and basal stem tissue of living plants (Department of Primary Industries, Water and Environment, 2004).

Phytophthora cinnamomi is one among the most destructive species of Phytophthora associated to the decline of forestry, ornamental and fruit species, as well as of some 900 other woody perennial plant species (Ferraris et al. 2004). Commercial enterprises such as agricultural projects and related plant industries are negatively impacted by the impact of the P. cinnamomi infection. In Italy P. cinnamomi infections are being reported with increasing frequency: first on chestnut coppices and Rhododendron spp. in plant nurseries and more recently on chestnuts (causing ink disease) and Chamaecyparis in nurseries and on avocado, oak, walnut and highbush blueberry (Vaccinium corymbosum) in nurseries and the field. The ability of P. cinnamomi to infect oaks has led to speculation that P. cinnamomi is involved in the severe decline of oaks in the general Mediterranean region (Robin et al. 2001). The pathogen also causes significant damage on the African continent and is highlighted as the most damaging disease in South African avocado orchards, where is causes root rot and heavily reduces crop yields (Bezuidenhout et al. 1987). \r\n

Just as concerning is the impact that P. cinnamomi may have on native species. According to Rudman (Undated) 181 plant species have so far been recorded as hosts for P. cinnamomi in Tasmania, Australia. At least 39 of Tasmania's threatened plant species are susceptible to P. cinnamomi and it is possible that native species may be rapidly killed and unable to regenerate in infected areas. As is the case in other areas there is considerable variation in response to infection by P. cinnamomi amongst host species, some showing resistance and some extreme susceptibility.

P. cinnamomi is causing and has the potential to cause significant ecological damage in native North American biomes from California to the Appalachian mountains, impacting on ecosystems as diverse at the Sierra Nevada desert and the Appalachian forests. A scientific study of the recent mortality of Ione manzanita- a rare, endemic, evergreen shrub restricted to Ione formation soils in the foothills of the Sierra Nevada, California, (Arctostaphylos myrtifolia) found that the cause of mortality was due to the P. cinnamomi pathogen. The pathogen which causes wilting, foliage desiccation and root necrosis in native plants is believed to have a significant impact on the conservation of the already threatened A. myrtifolia (Swiecki and Bernhardt 2003). P. cinnamomi is also impacting native Californian species in the woodlands around Lake Hodges, where 27% of coast live oaks (Quercus agrifolia), show disease symptoms and are suspected to be infected with the pathogen (Garbelotto, Hüberli and Shaw 2006). All natural oak woodlands in the western United States are potentially at risk of ecological damage from the pathogen and studies such as the one by Garbelotto, Hüberli and Shaw (2006) may contribute to an understanding disease factors (susceptibility, present of other pests) and may ultimately help to minimise the spread of the disease. In eastern North America, in the Appalachian forests, chestnut forests are struggling to regenerate, a situation partly attributable to the impact of P. cinnamomi. While chestnut blight disease has historically been linked to chestnut mortality, among the chief obstacles facing chestnut restoration are the oomycete pathogens of the genus Phytophthora. Recent plantings of chestnut seedlings in Appalachian forests have experienced high mortality attributable through standard diagnostic practices to Phytophthora, principally P. cinnamomi (Rhoades et al. 2003).

Drenth et al. 2006 describe the development and \r\nvalidation of a DNA-based diagnostic assay that can detect and identify 27 different Phytophthora species.
For details on preventative measures, chemical, physical, biological control options, please see management information.