Abstract |
- Root rot of ponderosa pine caused by Armillaria mellea was
studied in a pine forest that had been under management for 30 years
in Klickitat County, Washington. Information sources included
disease survey, detailed observation and description of specific
disease situations, and examination of roots in situ and removed.
Roughly circular infection centers in stands of sapling and pole-sized
pines appear to arise regularly from stumps of harvested old-growth
trees, some of which have contained viable A. mellea for
over 30 years.
Distinctive concentric zones caused by the disease mark the
infection centers. These zones differ in above-ground appearance,
in degree of root decomposition, and in level of infection. Location
of a specific zone depends on the interval since cutting of the old-growth
tree, while zone width depends on tree sizes in the young stand. Distribution of root material in the interior zones is
influenced most strongly by rooting characteristics of the former
old-growth trees, and by activity of A. mellea and other decay agents
over time, while in the young growth pines of the intermediate
zones, time since lethal attack by A. mellea and tree size most
influence root condition.
Extensive examination of the outer zones disclosed that, in
stands containing trees from 3 to 6 inches in diameter, infected root
material extended into the healthy-appearing pines 11 ft beyond the
outermost dead tree of the infection center, while in stands with
trees up to 16 inches in diameter the extent reached 18 ft. A highly
significant linear regression with good correlation was found between:
1) the extent of infected root material beyond the outermost dead
tree; and 2) mean tree size of the affected stand. Infected root segments
from beyond the outermost dead tree, within the region where
infected and healthy roots intermingle, produced rhizomorphs, the
assumed infection structures, when incubated in bags of moist quartz
sand.
The expansion rate of infection centers was calculated to be
2. 9 ft (0.88 m) /year.
Cross plating techniques indicated that the 1500 acre study
area was occupied by a single strain of A. mellea, suggesting that
spores are unimportant to the field disease cycle. Current loss to disease in the 1500 acre tract is 35 cu ft per
acre per yr, three times the loss in 1957. From 1957 to 1971, the
proportion of the area in which disease was detectable remained
constant. The increased loss resulted from death of fewer, but larger,
trees in 1971.
In inoculation tests on ponderosa pine seedlings, A.
mellea isolates from old-growth pine stumps and from young pine trees
were pathogenic, while isolates from living hardwoods were weakly
or nonpathogenic.
Reliable methods are described for isolating A. mellea from
infected tissues and of testing the capacity of naturally infected root
materials to produce rhizomorphs.
The abundance of A. mellea over a three year interval following
five root removal treatments increased in missed root residues.
Resinous lesions were commonly found at the site of A. mellea
attack. Rarely does mycelium spread proximally along a living
root from one of these lesions, but growth frequently occurs from
the lesion toward the root tip following, or concurrent with death of
the extremity. Girdling resinous lesions on lateral roots show little
effect on tree vigor, while such lesions high on the tap root kill the
tree. Soon after tree death, mycelial fans spread under the bark
throughout the root system. To obtain insight on how the resinous lesions retard the fungus,
tests were conducted on the effects of resin on growth of A. mellea
in culture. Autoclaved resin, acetone extracts of resin, water
extracts of resin, and non-sterilized resin all stimulated, rather than
restricted, growth over non-resin containing media. Removal of
phenols from the water extract of resin with polyvinylpyrrolidone
destroyed the growth stimulating effect of the resin. Propylene
oxide was effective for sterilization of granulated resin.
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