Arboriculture & Urban Forestry 33(2): March 2007 127 the canker margins, where a reddish brown fluid exudes from the bark (Hinds 1981; Sinclair and Lyon 2005). Cryptosphae- ria canker is widespread throughout the range of aspen, par- ticular in the western United States (Hinds 1981). Although Cryptosphaeria canker is not the most common canker dis- ease of poplar, it does have a high mortality rate because it frequently infects younger trees, which are more easily girdled. Juzwik et al. (1978) surveyed trees in Colorado and attributed one-fourth of tree mortality to Cryptosphaeria canker. Ceratocystis fimbriata causes cankers on poplar with symptoms of bleeding cankers. For the fungus to infect the tree, a wound is required (Manion and French 1967). The fungus is carried to fresh wounds by various insect vectors, most commonly nitidulid beetles (Hinds 1972b). The elliptic canker develops as a depression in the bark around the wound. Often the face of the canker becomes covered with amber-colored sap exuding from the margins, and rusty brown fluid can also bleed from the margins (Hinds 1972a; Sinclair and Lyon 2005). Growth halts after the first dormant season, but fruiting bodies develop on the canker and under- neath the bark after two growing seasons and cankers are apparent for several more growing seasons (Manion and French 1967). Cankers developed when Wood and French (1963) inoculated C. fimbriata into wounds on the main stem. This disease is known throughout the range of aspen but is more common when site conditions are poor (Manion and French 1967; Hinds 1972a). STONE FRUIT (PRUNUS) Bacterial cankers caused by Pseudomonas syringae are light tan with a water-soaked appearance, a sour odor, and gum- mosis (Hepting 1971; Weaver 1978). Both the sapwood and cambium show signs of necrosis (Klement et al. 1984). Many important fruit trees, including members of the genera Prunus and Pyrus, are hosts (Hepting 1971). Girdling by the cankers on the branches decreases productivity and may kill the tree. The bacterium relies on cold temperatures to cause symp- toms. It reduces the sugar content of the tree and has ice- nucleating proteins to promote frost damage and susceptibil- ity. When temperatures dip low enough, the bacterium is able to promote the formation of frost, causing the symptoms to appear (Klement et al. 1984). Therefore, plants can have high concentrations of bacteria but be asymptomatic (Cameron 1970). Because of this, treatment is difficult. Cameron (1970) showed that the bacterium was found far from symptomatic tissue. Consequently, removal of infected branches may not be effective. Bactericide sprays may be effective if infection is not yet systemic, but this is difficult to determine (Cameron 1970). Pruning wounds infected by Phytophthora syringae can lead to oozing cankers in almond. Bostock and Doster (1984) used isolates collected from cankers to inoculate pruning wounds; cankers similar to the naturally infected trees devel- oped (Bostock and Doster 1984). Wounds are necessary for P. syringae to infect the tree. The treatment of wounds with fungicides, or the avoiding of wounding during the cooler months, when the pathogen is active, may prevent this disease (Ogawa and English 1991). OAK (QUERCUS) Phytophthora ramorum, although first identified as the cause of blight on rhododendron and viburnum in Europe, is now rapidly gaining notoriety as the cause of sudden oak death in California and Oregon. P. ramorum is pathogenic on a wide range of plants. Oak species infected include Q. kelloggii, Q. parvula, Q. agrifolia, and Q. chrysolepsis in California and Q. cerris, Q. falcata, Q. ilex, and Q. rubra in Europe (Hen- ricot and Prior 2004). Inoculation experiments conducted on detached logs indicate the host range may actually be much broader (UK PRA 2003). Bleeding cankers develop as brown–black patches of bark seep dark red sap. This is com- bined with severe wilt and dieback of the crown and eventual death of the tree (Rizzo et al. 2002). Rizzo et al. (2002) inoculated mature trees with mycelial plugs placed into holes made with a cork borer. The bark was then replaced, and cankers developed on all inoculated trees within 6 months. Because of the recent discovery of this pathogen and the diseases it causes, disease management strategies are still being developed. In Europe and in Oregon, efforts have fo- cused on eradication, whereas in some areas of California, the pathogen is considered well established, necessitating man- agement toward quarantine efforts (Henricot and Prior 2004). Once an area has become infected, management strategies depend on the intended scale of the treatment. Single trees on the interface of the urban and wildland are often highly val- ued by homeowners. Phosphite fungicides are available for trunk injection and can be also be applied with a surfactant as a bark drench. On the national level, control is focused on restricting interstate movement of potentially infected plants. Treatment on the forest landscape level is the most difficult given the broad host range of the pathogen and because little is known of its biology and ecology (Rizzo et al. 2005). Surveys in California for P. ramorum have revealed P. nemorosa is also associated with bleeding cankers on tanoak and coast live oak (Hansen et al. 2003). P. nemorosa occurs sporadically and does not seem to spread as rapidly or cause as much mortality as P. ramorum (Rizzo et al. 2005). Miller (1941) identified bleeding cankers on coast live oak in California, isolated P. cactorum, and inoculated healthy oaks to produce identical symptoms: thin light brown to thick reddish exudates from bark fissures dry to form black tar-like areas on the surface of the bark. Howard (1942) documented the same disease in the Northeast. Mircetich et al. (1977) performed inoculations with P. cactorum, P. cinnamomi, and ©2007 International Society of Arboriculture
March 2007
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