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Spread of Armillaria spp. In the bark of Eucalyptus obliqua and
... In Victoria, colonization by A. luteobubalina can extend to a height of 7 m in the ®brous bark of E. obliqua L'Herit. (Marks et al., 1976). In Western Australia, the author has also observed A. luteobubalina spreading to similar heights under the bark of mature karri trees in virgin stands. ...
The incidence of Armillaria root disease was recorded during routine measurement of a silvicultural experiment designed to test the effect of thinning and nitrogen fertilizer application on the growth of karri regenerated after clearfelling. The experiment was established in 1984, when the stand was 12-year-old. Ten years after thinning, the level of disease increased significantly with increased thinning intensity, and disease accounted for 51% of the mortality in the plots thinned to 200 stems/ha. Fifteen years after thinning, the level of infection had increased in all treatments but was still significantly lower in the unthinned treatment. In the thinned treatments, 54–63% of the trees ranked in the largest 200 stems/ha were infected, and 50–100% of the mortality within these trees was attributed to Armillaria luteobubalina. In the unthinned treatment, no mortality within the dominant trees was associated with disease. Ten years after thinning and fertilizer treatments, it could not be determined whether fertilizer application had had any effect on the level of disease. Whole tree thinning, which results in stump and root removal, is discussed as a viable management option in high-quality karri regrowth stands infested with A. luteobubalina.
... Not all of these species are pathogenic. In eucalypt forests, ARD will normally express itself in the latter stages of the disease with the presence of inverted V-shaped scars or callused lesions at the base of trees, dead and brownstained bark extending up the stem, mycelial fans under the bark and wet stringy white-rotted wood at the root collar, and the production of basidiomes at the base of infected trees in the autumn (Marks et al. 1976;Kile 1981;Robinson 2003). ...
Intensive survey based on aboveground symptoms of Armillaria root disease underestimated true levels of disease by at least 20% and sometimes by up to 40% in high-quality karri regrowth stands. The results challenge the reliability of surveys based on aboveground disease symptoms. While most disease was established within the subdominant stratum, a very high proportion (30-60%) of the dominant trees were also infected. Within the study areas 15 distinct genotypes of Armillaria luteobubalina were identified. Individual genotypes existed as clones, with 2-3 clones per hectare. These factors need to be considered in stand management planning and yield predictions. A broader study, including lower-quality sites, is needed to determine whether these findings apply to all types of karri regrowth.
... The symptoms of Armillaria attack and mode of spread in Eucalyptus obliqua and E. globulus subsp. bicostata have been described (Marks et al. 1976). Exudation of kino through stem and root rot bark occurs on some diseased trees (Edgar, Kile, and Armillaria luteobubalina is only one of a Almond 1976). ...
Species of the woody root rot fungus Armillaria are indigenous in cool temperate rain forest, mixed forest, and wet and dry sclerophyll eucalypt forests in Australia. Four species have been described or identified from southeastern Australia: A. luteobubalina Watling and Kile, A. fumosa Kile and Watling, A. hinnulea Kile and Watling, and A. novae-zelandiae (Stevenson) Boesewinkel. The latter species was first described from New Zealand, and A. hinnulea also occurs in that country. Armillaria novae-zelandiae and A. hinnulea occur in wet forests (rain forest, mixed forest, and wet sclerophyll communities), while A. luteobubalina and A. fumosa are found mainly in dry sclerophyll forests. Armillaria luteobubalina is so far the only species known to behave as a primary pathogen in native forests. While the fungus has an extensive geographical distribution in southeastern Australia, damage is most severe in selectively logged forests in the central highlands of Victoria, where it is estimated that approximately 3-5% of the forest area is moderately to severely affect~. The fungus kills all species of eucalypts and a wide range of the under- story trees and shrubs present in the forests. Most infections occur in small (0.1-1.0 ha), well-defined patches, but larger (up to 20-30 ha), more diffuse infections also occur. Evidence of primary pathogenicity includes (a) constant association of the fungus with disease; (b) the pattern of disease development within stands (the fungus spreads by root contact from infected food bases); (c) correlation between root infection and symptom development in large trees; (d) evidence of host resistance to infection; and (e) pathogenicity in pot and field trials. There is no evidence that climatic stress or other pests or pathogens initiate disease. Within the forest, the fungus has a discontinuous distribution. Studies of genotypes of the fungus (identified by analyses of mating alleles, since Armillaria sp. are bifactorial heterothallic, or intraspecific antagonism), suggest that A. luteobubalina consists of a community of genetically distinct mycelia. Individual genotypes may contract, expand, or coalesce, depending on circumstance. The development and status of the community depends on the two processes of new basidiospore infection and local spread by vegetative growth through root systems. Similar patterns of genotype distribution and clonal development were evident in logged and unlogged forest. It is concluded that root rot caused by the fungus is endemic in these forests but that logging has aggravated the disease.
An undescribed but native species of Armillaria is a secondary pathogen in declining stands of Eucalyptus obliqua and Eucalyptus regnans in southern Tasmania. The fungus is almost ubiquitous in healthy and diseased forest and occurred epiphytically or parasitically in local lesions on the roots of 74 % of eucalypts partially excavated in 15 forest stands, 25–75 years of age. The fungus infected 85 % of logging stumps and 64 % of fire killed trees. Although the fungus only infected the sapwood of the eucalypts, it survived in infected stumps for at least 70 years. Rhizomorphs initiated most infections but did not grow freely through the soil. Pathogenicity tests confirmed that the Armillaria is a weak pathogen.
Trees up to 25 m tall died suddenly at the edges of a steadily extending patch of dead and dying trees in a fast-growing plantation of Eucalyptus regnans F. Muell. near Traralgon, Victoria. Measurements of tree height and stem diameter made during the 12 years since the plantation was established indicate that, prior to their death, trees at the margins of the extending patch grew as rapidly as unaffected neighbours. During May 1973 and May 1974, Armillaria luteobubalina Watling & Kile sp.nov. fruited prolifically on dead and infected trees. Few rhizomorphs have been found so that spread of infection seems to have been mainly by mycelial growth within root systems and at root contacts. Infection has spread from inoculum in a single stump of Acacia melanoxylon R. Br. at an average annual rate of 2.5 m. Untreated stumps of healthy 10-year-old trees felled in unaffected parts of the plantation during the fruiting season of 1973 have not become infected. In pathogenicity tests with an isolate from the cap of a fruiting body, E. regnans seedlings have suddenly wilted and died following penetration of the tap root-root collar zone and subsequent girdling of the stem. It is concluded that the deaths at Traralgon are due to primary attack by A. luteobubalina.
Infection by A. mellea in Britain occurs by means of rhizomorphs; the transfer of mycelium at root contacts is probably not important as a means of spread. Following the initial phase of rhizomorph penetration, established infection in the cambium is preceded by ectotrophic spread of mycelium in the bark scales.
Field investigation confirmed reports in the literature that in susceptible conifers the greatest number of deaths generally occurs approximately 6–8 years after planting. However, attacks can also occur in much older crops and the reasons for this are discussed.
Inoculation experiments showed that suppressed trees and those experiencing conditions of reduced light intensity are more susceptible to infection than dominant trees and trees in full light. Species susceptibility in a variety of soils was studied by inoculation of trees 20–30 cm tall. Of the conifers tested Pseudotsuga menziesii and Abies grandis were more resistant than Picea abies, P. sitchensis, Larix kaempferi and Pinus sylvestris. Quercus robur and Fagus sylvatica were more resistant than all the conifers except A. grandis . Soil type influenced disease development and the proportion of trees infected was higher in an acidic sand soil than in an alkaline clay soil.
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