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Home , Armillaria, Armillaria mellea, Armillaria ostoyae, Armillaria root rot

February 2008 Forest Health Protection and State Forestry Organizations 11.1 WEB July 2010 Management Guide for By Susan K. Hagle US Forest Service Root Disease

Armillaria ostoyae (Romagnesi) Herink Topics Introduction 1 Hosts: Armillaria are the most Management overview 2 Primarily damaging and broadly distributed forest Ecology of Armillaria 4 Douglas- and pathogens in the world. ostoyae true A. ostoyae is the most pervasive killer of Patch dynamics 7 All may be Douglas-fir and grand fir in the northern damaged. Rockies. Resistance to Armillaria 8 root disease Mode I disease 9 A Disease of the Site Mode II disease 10 Armillaria root disease should Elsewhere in the northern and Mode II mortality rates 12 be considered a ―disease of the central Rockies, Armillaria is often Mode II site predictors 13 site‖. That is, established mycelia less damaging and more easily of this are essentially tolerated. is a Modes I and II thinning 14 permanent, so the best course to native pathogen with a broad host minimize losses is to manage tree range but is most common and Brush removal 15 species that will survive on damaging on Douglas-fir, grand fir Mode III disease 16 infested sites. In large areas of and subalpine fir. Mortality rates northern Idaho and western are highest on warm, moist Mode IV disease 17 Montana, this includes most of the habitats but large disease patches Armillaria and forest 17 potentially best timber-producing develop on dry sites and cold, high succession sites. -elevation sites as well. Armillaria 19 Other reading 20

Field Guide The Four Modes of Armillaria Root Disease

Management Guide Most patterns of Armillaria sapling , but secondary Index root disease can be identified as spread does not occur. By 20- one of four types. Management 30 years of age, root disease options vary according to the mode mortality has nearly ceased. of disease development. IV. Root lesions of limited extent, Key Points often accompanied by butt rot Know which type of I. Distinct, generally large, root probably resulting from Armillaria root disease disease patches with single or primary inoculum from dead you are managing. few host species. trees and stumps of a previous II. Multiple clones merge forming generation on the site. Little Manage for , , e s s e n t i a l l y c o n t i n u o u s mortalit y results until and cedar. coverage of sites. Grouped as a d v a n c i n g a g e o r Precommercial thinning well as dispersed mortality environmental stresses trigger may improve growth and occurs throughout the stand. A extension of root lesions. Small survival of pines and mosaic of brushy openings, groups of mortality result from larch. patches of dying trees, and limited secondary spread of the apparently unaffected trees disease. Impact is generally Avoid harvests that leave may cover large areas. low. susceptible species III. Primary spread of infection (usually Douglas-fir or from stumps of the previous true firs) as crop trees. generation results in clusters of mortality of seedling and

Pa ge 2 Back to menu Armillaria Root Disease 11.1 Management overview Armillaria mycelia can not be are more resistant to Armillaria practically eradicated from a site root disease than are true firs and See „About the Four Modes but damage can be kept at Douglas-fir over most of western of Armillaria Root Disease’ tolerable levels with appropriate . There are notable on page 9. management. Selecting the exceptions to this rule, depending management options best suited upon the mode of Armillaria root for each situation depends first on disease encountered and the understanding the mode of location. Precommercial thinning, Armillaria root disease. Other commercial thinning, and site options may also be considered, regeneration offer opportunities to depending on the mode of change species composition. Armillaria root disease to be managed. Tables 1 and 2 will help Inoculum reduction identify the mode of Armillaria Stumps can be removed by root disease in your forest. pushing out with a dozer (fig. 1), or pulling up using a grapple. Root- Root Disease Resistant Species raking removes root fragments The most widely used and from the soil. Push-over or pop-up successful approach to controlling logging, involves uprooting trees as Armillaria root disease damage is part of the harvest operation. Roth Figure 1. A 60-foot wide strip was destumped to control through the use of disease tolerant and others (2000) reported that spread of Armillaria root or resistant species that are from a destumping by push-out logging disease at the advancing local seed source and are well was only effective in reducing edge of the disease patch. adapted to the site (Table 2). mortality of the subsequent [Photo by Robert James] Pines, , , regenerated stand if accompanied western redcedar and hemlocks by hand-picking of root fragments.

Table 1. Diseases caused by Armillaria. (Exceptions are seen in all locations.)

Location Forest conditions Damage Management approach Mode I: Discrete root disease Mark the locations of centers before Eastern Montana Douglas-fir stands centers, often large and harvest; use resistant species; remove aggressive, but not common. inoculum in or around perimeter of center. Broad range of habitat Mode II: Present in most Highly significant losses usually requiring Western types with Douglas-fir stands. Diffuse mortality and species conversion. Important Montana, and true fir large and small root disease consideration in management plans. Northern Idaho components centers. Favor resistant species. Aggressive disease seen in lodgepole Mode I: Rare, discrete root Northern Idaho Lodgepole pine and associated subalpine fir. disease centers, can be large. Currently unmanaged. Southern Idaho Douglas-fir, subalpine Mode IV: Small groups and Minor impact overall, Significant decay or fir individual trees killed. defect from butt rot on some sites. Ponderosa pine, Mode III: Primary pathogen Usually minor impact. Favor resistant Southern Utah mature true firs, killing a few trees at a time species in disease pockets. Douglas-fir, grand fir, Mode IV: Broadly distributed; Remainder of Causes little direct mortality so it is rarely pines, spruce, mostly weak pathogen or Utah directly managed. subalpine fir saprophyte. Douglas-fir, grand fir Causes little direct mortality. Root disease Mode IV: Broadly distributed; pines, spruce, pockets closely associated with endemic Nevada mostly weak pathogen or subalpine fir, incense bark beetle populations. Rarely directly saprophyte. cedar managed. 11.1 Back to menu Armillaria Root Disease Pa ge 3

These procedures can Avoiding Hazardous sites. significantly reduce the food base Where root disease is limited to Chemical Control available to the fungus and delay discrete patches that occupy infection of susceptible crop trees. relatively small areas, these patches Chemical soil fumigants that On the other hand, direct may be excluded from timber destroy Armillaria in inoculum removal is temporary in management. Where root pathogens root fragments are effect (the fungus often re- are more generally distributed, useful in orchards infests), expensive and may avoid managing highly susceptible and vineyards. damage soil (Quesnel and Curran species on the most hazardous sites. Stumps are removed 2000) and other site amenities. It Moist grand fir, cedar and hemlock to remove most of has been used to good effect in habitat types are hazardous sites in the large inoculum high value plantations such as northern Idaho and western before fumigation. orchards and in ornamental Montana. Douglas-fir and true firs Chemicals can be plantings. may be especially poor risks on protectants, most of these sites. eradicants or curatives.

Table 2. Common disease expression by host and location.

Tree species Location Susceptibility Typical disease Douglas-fir Eastern Montana Highly susceptible at all Mode I. Relatively rare; distinct root ages disease patches Douglas-fir Idaho north of Salmon River and Highly susceptible at all Mode II. Diffuse and concentrated Montana west of the continental ages mortality involving entire stands and divide drainages. Often severe by age 40. Most stands affected. Subalpine fir Idaho north of Salmon River and Between Douglas-fir Mode II. Mortality often diffuse; also Montana west of the continental and grand fir in commonly large distinct disease patches. divide susceptibility Grand fir Idaho north of Salmon River and Highly susceptible at all Mode II. Diffuse and concentrated Montana west of the continental ages, though somewhat mortality over large areas. Large trees divide less so than Douglas-fir often develop butt rot while root disease progresses slowly. Pines, western Idaho, Montana, Utah and Highly resistant (with Mode III. Mortality common in saplings, larch Nevada rare exceptions) but rarely significant in mature trees. Western Idaho and Montana Moderately resistant Modes III and IV. Some mortality in redcedar saplings. Residuals of partial harvests often develop severe infections but are very slow to die. Engelmann Idaho, Montana, Utah and Moderately resistant Modes III, and IV. Mortality common spruce Nevada in saplings. Old trees may have butt rot. Engelmann Southern Utah Moderately resistant Mode IV. Mature stands on cool sites at spruce high elevations may develop patches. Grand fir Southern Utah Moderately resistant Mode IV. Mature stands on cool sites at high elevations may develop small patches. Douglas-fir Northwestern Montana (Eureka Moderately resistant Mode IV. Butt rot often develops in area) mature trees but mortality is uncommon. Incense cedar Nevada Moderately resistant Mode IV. Rare in young trees. Older trees may develop butt rot.

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Maintain tree vigor Douglas-fir where Armillaria root Pay attention to Tree vigor plays a role in disease is often quite damaging, seed zones Armillaria resistance on sites or tree vigor, as the growth species where the fungus is not an efficiency of trees, was not a Severe root disease aggressive pathogen. In these factor in determining later is often seen in situations, the fungus may be infection and mortality. On planting stock that is secondary to predisposing events permanent plots monitored for at off-site, regardless such as insect attack, fire or least 10 years, Rosso and Hansen of the expected logging injury, or severe drought. (1998) found that the biggest and disease resistance of Where the pathogen is fastest growing trees were as the species. aggressive, tree vigor is probably likely to die from Armillaria as not an important factor. For the smallest and poorest trees. example, in young coastal Ecology of Armillaria in forest ecosystems Persistent and expanding others (2003) in the Blue mycelial clones Mountains of ranged Armillaria ostoyae is New clones result from from 20 to 965 hectares. This commonly found -infection of available included the largest genet infecting the same substrates. Survival rates of newly reported to date. It covers 2,200 trees and even the established mycelia are probably acres (965 hectares) and spans 3.5 same roots with other exceedingly low. This is evident miles (5.6 km). See the root pathogens. in the relative stability of clones ‗Armillaria ostoyae clones‘ on sites, which are often estimated sidebar on page 7. to be in excess of 1000 years of Established mycelia expand age (Shaw and Roth 1976, Smith outwardly, provided there is and others 1992, Ferguson and suitable substrate. (Read others 2003). An individual ‗Anatomy of a disease patch‘ on derived from a single mating of page 7.)Armillaria species are haploid (forming a diploid capable of forming specialized Genet ) is called a ‗genet‘. structures called rhizomorphs, which grow root-like through A genet is an soil. However, Armillaria ostoyae individual derived New genets originate from a produces few rhizomorphs from compatible single mating between two (Cruickshank and others 1997), pairing; a diploid haploid spores. The resulting relying, instead, on growth of mycelium spreads by mycelium. mycelium along and within tree vegetative growth of mycelium roots to facilitate spread. and rhizomorphs A single genet can . Expansion rates have been produce multiple estimated to be 0.7 to 1.3 m/yr clones (ramets) by Most recognizable mortality (2.3-4.3 ft./yr) in Douglas-fir fragmentation. patches are probably a single plantations in southern interior genet (Dettman & van der Kamp (Peet and others Fragmentation may 2001a). Genets vary greatly in 1996). result from loss of size, probably depending on site A similar spread rate (1 m/yr) substrate, or conditions and history. Dettman was reported for a young, replacement by and van der Kamp found most naturally regenerated ponderosa competing fungi in genets in southern interior British pine stand in Washington (Shaw portions of an area Columbia to be less than 2 and Roth 1976). occupied by a genet. hectares in size (2001b) and those In mature (110-yr old) Douglas- Isolation of portions in the central interior ranged from fir in central interior British of the genet results in less than one to more than 15 Columbia van der Kamp (1993) multiple clones that hectares (2001a). Several estimated the average spread rate are genetically remarkably large, and potentially of A. ostoyae to be 0.22 m/yr (0.7 identical. very old clones have been found. ft/yr), about a third that observed Those described by Ferguson and in young stands. 11.1 Back to menu Armillaria Root Disease Pa ge 5

Saprophytic and parasitic In young trees, terminal existence growth decline is often observed Armillaria ostoyae can survive for only one or two years before as a saprophyte on dead organic death. Much also depends on the matter such as old stumps and relative aggressiveness of the Rhizomorphs roots for several decades. pathogen and whether bark beetles Even small debris on a site may attack the weakened tree. Armillaria root disease has been called harbor significant amounts of the “shoestring root rot” fungus. Komroy and others (2005) Butt rot may develop because of the isolated Armillaria ostoyae from Under some conditions, the appearance of as much as a third of small (<2 fungus establishes infection in the rhizomorphs. These root- cm) woody fragments in the upper heartwood of the roots and in the like structures are used layers of soil. They also isolated lower stem (butt) of the tree. to seek out new A. ostoyae from a number of Generally the taproot falls victim substrates.* deciduous tree and shrub species at an early age and the pathogen including aspen, honeysuckle and travels from the decayed taproot Rhizomorphs are highly . Though not considered directly into the butt heartwood. differentiated aggregations of hyphae a primary parasite of these The fungus can produce a large surrounded by a dark species, the fungus is clearly cavity of decay in the heartwood cortex of protective capable of utilizing a wide variety of the stem, usually extending less cells. They grow from a of substrates to maintain itself on than three feet above the ground. tip that resembles the a site. Grand fir, cedars, hemlocks and meristem of a root. Hyphae of A. ostoyae spruces commonly develop this penetrate wood, causing a ‗white mode of disease which can persist Rhizomorphs facilitate rot‖ type of decay in which both for many decades without killing movement of the fungus cellulose and lignin are degraded. the tree. through soil and under The mycelium spreads from these bark. They grow from inoculum, usually roots woody substrates to the roots of Spores abundant but rarely or stumps of killed trees, live trees either through direct root successful to suitable substrates. contact with infected wood, or by Honey-colored rhizomorphs. may be produced at the base of Armillaria ostoyae Once established on a root of a infected trees during late summer produces relatively few live tree, the fungus invades and or early autumn. The role of spores rhizomorphs compared to kills the cambium of the root and from these mushrooms in disease many other species of the decays the dead root tissues. development is not well Armillaria. They have a The mycelium may eventually understood. dichotomous branching travel up the root to colonize the At times the fungus seems to pattern (Morrison 1989). root collar, and girdle the tree. invest tremendous energy in the Probably because of production of these sporophores. inoculum potential, Growth declines Hundreds of pounds of mushrooms rhizomorph-originated Decay and girdling are usually can be collected from a site at one infections are less slow processes that can be delayed time. Each is capable of successful than are for extended periods while the producing hundreds of thousands infections spread from fungus remains latent in non- of spores. And yet, no evidence of root contact with expanding lesions. Growth decline direct infection of living trees by inoculum (Robinson and of infected trees has been detected bas i di os pores ex i s t s . No Morrison 2001). for 30 years or more before death inoculations of live hosts using in mature Douglas-fir (Bloomberg have succeeded. *There is evidence rhizomorphs also provide and Morrison 1989). The longer Most likely, Armillaria spores water, nutrients and the period of decline before death, establish on woody debris initially. oxygen to the mycelium. the greater the cumulative growth The survival rate of even those loss. Smaller trees typically have spores that manage to land on a shorter detectable periods of suitable substrate are probably decline before death than larger exceedingly low. Thus, the great trees (Bloomberg and Morrison abundance of basidiospores may 1989). be necessary to ensure the occasional success.

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Fire because most of the inoculum Fire has been a historically resides deep in root systems. important factor in shaping forest Filip and Yang-Erve (1997) composition and structure in tested survival of Armillaria northern and central Rocky ostoyae in buried wood on sites Mountains. Based on the broadcast burned in fall and considerable age achieved by spring. In general, burning had no Armillaria clones, it is reasonable effect on inoculum survival to conclude that they typically although a reduction of viability survive forest fires. There is little was observed in inocula buried Figure 2. Fire probably has direct evidence of the effects of nearest the surface in the fall- little direct effect on Armillaria inoculum in roots fire on established Armillaria burning treatment. The burn that are more than an a few mycelia but abundant anecdotal treatments were not accomplished inches below the ground evidence suggests that the fungus according to plan, so it remains surface. is capable of surviving and unclear whether slash burning (Photo from USFS files) thriving in subsequent regenerated affects shallow inocula. stands. This is to be expected Primary vs. secondary spread Primary spread (Figure 3) Primary and secondary spread In inland western forests, root of disease is common in Douglas- disease of stands established after fir stands in inland forests; harvest or severe fires generally however in coastal forests of the results from infections spreading from Oregon to from primary inoculum (stumps or British Columbia, Douglas-fir buried woody material from the acts more like inland ponderosa previous stand). Inoculum pine. The disease may be severe potential slowly declines as the in young stands for a decade or roots of stumps and snags two after harvest but subsides deteriorate. Although the disease thereafter. Secondary spread of can be severe in the first few years the disease does not play a after stand establishment, mortality significant role. Figure 3. Primary spread of of resistant species, such as pines Similarly, while ponderosa infection from stump or snag and larch, generally declines after pine is relatively resistant to roots to trees following fire or two or three decades, often with secondary spread in most inland harvest. (Photo by John Schwandt) little lasting impact on stands. western forests, in some natural pine stands in central Washington Secondary spread (Figure 4) both primary and secondary Also in inland western forests, disease spread is common (Shaw root disease of Douglas-fir, grand and Roth 1976). On these sites, fir and, probably, western redcedar Douglas-fir is considered to be results from both primary and relatively resistant to root disease. secondary spread of the fungus. Secondary inoculum is produced on roots of Armillaria -killed trees. The fungus is capable of maintaining very large mycelia for Armillaria often becomes the at least several centuries by means primary pathogen in of secondary inoculum. regeneration after a fire or The ability of trees to wall off harvest, even though root infections and, eventually laminated or annosus root Figure 4. Secondary spread slough those infections, limits diseases were dominant in the from tree to tree may secondary spread of Armillaria. pre-harvest stand. continue throughout the life Secondary disease spread varies of the stand. (Photo by Susan Hagle) by location 11.1 Back to menu Armillaria Root Disease Pa ge 7

Waves of mortality and regeneration in root disease patches Wave patterns of mortality and The primary difference Armillaria clones regeneration are most clearly between the wave pattern in root are the largest observable on sites that have no disease infected stands on sites organisms known cutting history and large infection with no cutting history and that on to man. patches. At the margins of the sites that have been cut is that the disease patch, the slow advance of harvest sets the timing of the wave the fungus into the non-diseased by stimulating the regeneration Big portion of the stand produces the that will reach pole size at about The original “humongous initial wave of mortality (See the same time. fungus” is 38 acres ( 15 ‗Anatomy of a root disease patch‘ Primary spread from stumps hectares), 1500 to 10,000 years below). This is followed by a results in new infections in these old, weighs about 100 tons. It wave of regeneration in the young trees. As in the uncut stand, is A. gallica. Found living in canopy opening, then slow the young trees die a few at a time the upper peninsula of mortality of seedlings and until the survivors are large Michigan and was widely saplings. When the survivors of enough to provide a substantial covered in the press; even on this cohort of regeneration reaches food base for the fungus. At this a TV talk show (David roughly pole size, the food base point, secondary spread will Letterman). will be sufficient to fuel a second accelerate the rate of mortality. As (Smith and others 1992) wave of mortality in what is now trees die, they are replaced by the older portion of the disease abundant regeneration. Mortality patch. then slows until sufficiently large Bigger The result is a stand with root systems have been produced 1,500 acres (600 zones representing the temporal to fuel another wave of mortality. sequence of root disease Recognizable root disease patches hectares), A. ostoyae, development in the stand. These eventually re-emerge in cutover Southeast Washington zones form concentric rings from stands as groups of trees are killed (Shaw and Roth 1976) the center to the perimeter of the and openings are regenerated. disease-affected area . Biggest Anatomy of a root disease patch 2,400 acres (965

Trees from the original hectares) and estimated stand die at the margins to be at least 2,400 of the disease patch (A). years old, A. ostoyae, in A zone of open canopy, heavy fuel-loading and the Blue Mountains of new regeneration can eastern Oregon. been seen just inside the patch margin, where It stretches 3.5 miles recent mortality has expanded the patch area (5.6 km) wide and (yellow). covers an area larger

than 1,600 football fields. (Ferguson and others [Photo by James Byler] 2003)

In the older portions of the patch (shaded), some trees reach sufficient size to produce secondary inoculum. This leads to clusters of mortality (B) in older portions of the patch.

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Inoculum Potential Mechanisms of Resistance to Armillaria root disease Armillaria ostoyae occurs ―compartmentalize‖ a wound or Energy is required for throughout Europe and north infection (Tippet and Shigo 1981). Armillaria to overcome America and is primarily a This is a relatively rapid, generic, a tree‟s defenses. pathogen of conifers. It is also response of the tree to wounding When the fungus is known to attack and kill some or pathogenic infection. In effect, able to establish on a growing in association the cells near the infection site, large root mass, it has with conifers including that were present at the time of a large food base to (Morrison and others 1985) and infection, are fortified. The cell provide energy, which aspen (Pankuch and others 2003). walls become lignified and means it has a large Although all native forest conifers suberized. The cells also are made inoculum potential. in the Rocky Mountains are toxic to invading hyphae through considered susceptible, differences the deposition of secondary Low inoculum potential of are readily observed. The metabolites (phenolic compounds, rhizomorphs may render effectiveness of resistance mostly). Within months, trees will them less effective in mechanisms of conifers vary by produce an organized periderm to establishing infections host and pathogen species and by wall off the infection. than mycelium growing the age of trees. Referred to as necrophylactic directly from a more Bear in mind that there is a periderms, they consist of single substantial food base. world of difference between a or multiple phellem layers which pathogen simply being capable of wall off infected tissue. These infecting a host, and that pathogen periderms delay extension of the causing sufficient disease in that infection but they may be host to present a management eventually breached by hyphae. The main differences challenge. The main differences in host in host resistance resistance appear to be determined appear to be Primary Defense— Chemical by the frequency and longevity determined by the Root bark of conifers contains with which infections are frequency and phenolic compounds that are restricted by secondary periderms. longevity with which inhibitory to Armillaria ostoyae. Two important studies lesions are restricted La r c h h a s m u c h h i gh e r compared a relatively resistant by secondary concentrations of phenols in the species (western larch) to a highly periderms. root bark, compared to Douglas-fir susceptible species (Douglas-fir) or grand fir (Entry and others at three ages (Robinson and 1992). Ponderosa pine and western Morrison 2001, Robinson and white pine were intermediate. others 2004). At 6-11 years of age Secondary periderms may These chemical defenses probably both tree species were readily have several layers of prevent most infections. These infected, girdled and killed by phellem. The tree root authors also suggest that the Armillaria ostoyae. may have several relatively higher sugar content in Resistance was more effective successive necrophylactic Douglas-fir and grand fir bark in 18-19 year-olds of both species periderms that have been contributes to the success of the but differences between larch and produced as each pathogen. Douglas-fir were evident. previous periderm was Resin production in response N e c r o p h yl a c t i c p e r i d e r m breached. to infection of the cambium formation had delayed the presents at least a temporary advance of nearly half of the Most lesions are halted in physical barrier as well as infections in larch and only a the bark or cambium of biochemical. Time and energy are fourth of those in Douglas-fir roots. If prevented from required to digest resins in order (Robinson and Morrison 2001). expanding long enough, for hyphae to penetrate resin- At 25-27 years of age, the periderm-surrounded soaked tissues. necrophylactic periderms formed infections will eventually by larch roots were far more be sloughed (as the root Secondary Defense—Physical impervious to breaching (55% grows) and the root will Barriers intact) than those in Douglas-fir heal. As a secondary defense, a tree (none intact) (Robinson and others under attack will attempt to 2004). 11.1 Back to menu Armillaria Root Disease Pa ge 9

Larch periderms also were more r o o t c o l l a r , r e a c t m o r e often replaced if breaching did aggressively and are more occur. These studies suggest that successful at containing infections. resistance develops in larch somewhere between 8 and 15 Timing is everything years of age but much later in Young trees have small root Douglas-fir, probably closer to 35 systems that provide little years. inoculum pot enti al when Most of the lesions on older overcome by the pathogen (figure trees are contained in the bark or 5). Therefore, the earl y outer portions of the root near susceptibility of larch and pines infected cambium (Robinson and probably contributes little to Morrison 2001). If prevented from secondary spread of Armillaria expanding long enough, these root disease. The converse is also infections will eventually be true; as older, larger trees are sloughed and the root healed. If killed the mass of each root system the pathogen manages to girdle the contributes significantly to the root cambium, the distal portions inoculum potential of the of roots are killed and decayed by pathogen. As inoculum potential Figure 5. Although susceptible the pathogen (Shaw 1980). At increases, secondary spread of the at a young age, the surviving some point the inoculum potential disease also increases. Therefore, will become resistant before they developed by the fungus on these the delayed resistance of Douglas- are large enough to killed roots may become sufficient fir probably contributes greatly to contribute significantly to to allow it to breach the periderm. the increases in inoculum potential inoculum potential on this The host is often seen to lay down and to the secondary spread site. With little potential for secondary spread, Armillaria repeated periderms following each observed in Douglas-fir forests. root disease will decline. breaching. Larger roots, nearer the This may hold for true firs as well. [Photo by James Byler] About the Four Modes of Armillaria root disease MODE I — DISTINCT ROOT DISEASE PATCHES The etiology (pattern of development) of Armillaria root disease mode I is best understood. This disease mode is typified by more or less round patches of root disease-killed trees (figure 6). They are ringed with newly dead and dying trees and usually have advanced regeneration in their centers, where young trees have taken advantage of the disease- caused opening. These disease patches increase in radius at a rate of about 0.2–1.3 m (0.7-4 feet ) per year. As susceptible trees at the margin are encountered, the pathogen infects, girdles and kills these trees and then uses the root system to spread to adjacent live trees. In the interior of the disease patch, Figure 6. These three root disease patches in a Douglas-fir forest in eastern Montana form distinct fairy-ring patterns when observed from a distance. susceptible trees regenerate and Discrete patches with clearly defined edges are typical of Mode I Armillaria grow in the opening. They are in root disease. [Photo by Ralph Williams] turn killed as their roots encounter inoculum in the decaying roots of the previous generation.

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Root disease patches in eastern These patches probably Montana represent single successful genets Managing Root disease patches east of established hundreds or thousands Mode I the Continental divide in Montana of years ago. They survive on one appear to fit this etiology very generation of trees after another as Resistant species well. Armillaria is nearly always wildfires sweep through on long If there are resistant tree the only disease of consequence in intervals to restart stands on the species that are suited these patches. They are typically site. Douglas-fir generally occurs and economically feasible seen in Douglas-fir stands of as single-species stands in this to grow on the infected uniform age, and density. The situation. site, this is usually the disease patches are strikingly most effective and uniform in shape (round or oval) Disease patches on dry sites efficient means of and profile. The profile (figures 6 Dry site types, such as those reducing damage. & 7) shows the largest advanced with Douglas-fir habitat types regeneration in the center of the (Dry Biozone in British Avoid infected sites patch. The size and age of Columbia) generally have a lower This may be an option for regenerated trees declines toward incidence and smaller extent this type because the the margins of the patch where an Armillaria genets than do moist infected area may be increasing number of still-standing sites (Byler and others 1992, fairly limited and distinct. dead trees are seen. In the margins, Morrison and others 2000). They The fungus is likely to recently dead, red trees are commonly form distinct patches continue to expand at the mingled with thin-crowned dying in a forest typifying Mode I root margins of the disease trees and those showing little or no disease. patch if susceptible trees apparent decline. are present. Lodgepole pine and subalpine fir in northern Idaho Reduce inoculum Large, apparently single-genet Stump removal, Armillaria disease patches are especially around the uncommonly seen in lodgepole perimeter of the disease pine stands and mixtures of patch may contain the lodgepole pine and subalpine fir in fungus. Removal within northern Idaho. Here, as in the the disease patch can be Douglas-fir stands of eastern expected to reduce but Montana, the fungus aggressively not eliminate the disease. Figure 7. Mode I Armillaria root disease eats away at the margins of the patches have a distinct margin. The disease patch while infecting the interior of the patch has successively trees that regenerate in the older, older regeneration nearer the center of central portions of the disease the patch. [Photo by Ralph Williams] patch.

MODE II — PATCH AND DIFFUSE MORTALTIY Mode II Armillaria root primary spread from killed trees disease is by far the most common and stumps following disturbance mode in Idaho and western such as stand-replacement fires 66% of acres in northern Idaho and Montana. The disease probably has and regeneration harvests western Montana a similar etiology to Mode I but establish the pathogen in the have significant root there may be many more clones, subsequent generation of trees on disease impacts. perhaps larger individuals and, the site. sometimes, more variety of both Secondary spread from roots Most is due to Mode host and root pathogen species of infected trees to adjacent trees II Armillaria alone or involved. The profile of a diseased results in mortality beyond the in combination with stand is much more complicated reach of infected stump roots and Annosus root disease than that of Mode I, but the maintains the fungus long after the or laminated root rot. development of the disease may stumps have rotted away. not be. As in Mode I disease, 11.1 Back to menu Armillaria Root Disease Pa ge 11 W EB A wave-like pattern of mortality of Armillaria merge they produce is evident but made more difficult extensive disease patches (figure to observe as patch boundaries 8). Studies of naturally occurring Managing merge. Armillaria colonies have shown Mode II Mode II Armillaria is most minimal overlap of individual typical of root disease in Idaho clones of the species indicating Resistant species and western Montana. Douglas-fir that they are capable of excluding is typically the most-damaged other individuals of the same For Mode II Armillaria host with grand fir, white fir and species (Smith and others 1992, root disease, conversion subalpine fir als o ver y Ferguson and others 2003). to disease resistant susceptible. As individual clones species is usually the only practical method to control damage.

Increasing proportions of less-susceptible species to 60% may greatly reduce damage to susceptible trees by interfering with root transfer of the fungus on site.

Species diversity can be enhanced with Armillaria ostoyae resistant hardwoods such as birch or mountain maple. Figure 8. Dispersed and concentrated groups of mortality and irregular clusters of regeneration mark this hillside on the Nez Perce forest in Idaho with a long history of Mode II Armillaria root disease. The boundaries of patches are indistinct with The presence of many continuous root disease symptoms extending for several miles in all directions in this overlapping clones, and forest type. [photo by Susan Hagle] nearly continuous distribution over large Dettman and van der Kamp (comparable to grand fir habitat areas limits the (2001) studied the distribution of types in Idaho and Montana). application of inoculum Armillaria ostoyae in moist Thirty two percent were infected reduction and forests (Interior Cedar-Hemlock) on wet (cedar and hemlock habitat hazardous site of southern interior British types) if there were dead trees avoidance. Columbia (presumably similar to present. Even where no dead trees that across the border in northern were present, 25% on moist and Partial harvests that Idaho). They found 88% of the 15% on wet types were infected. leave a large forested area to be infested, with As stands age, these infection rates composition of genets less than 2 hectares (5 increase steadily. By comparison, susceptible species may acres) in size. The genets were only 10% of trees on dry sites produce the undesirable uniformly pathogenic and were found to be infected even outcome of loosing probably mostly very old and with mortality present. On dry most of the remaining stable. sites, in southern interior British trees within a few Root infection is common, Columbia, Idaho and Montana, years. even in young trees. Morrison and Armillaria root disease tends to fit others (2000) estimated that about the Mode I pattern. Genets are 38% of 13-24 year old trees were fewer leaving most of the forest infected on moist sites in southern uninfected (Byler and others 1992, interior British Columbia Morrison and others 2000).

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In mixed forests of the Armillaria ostoyae. HOW FAST Blue Mountains in northeast In unthinned stands, mortality DO THEY DIE? O r e g o n , F e r g u s o n a n d rates of ponderosa and lodgepole others(2003) measured genets pines, western redcedar and ranging from 20 to 965 hectares western hemlock averaged 1.5% (49-2,385 acres) in size. They to 10% per decade. Likewise, estimated the age of genets to mortality rates for coastal range from 1,900 to 8,650 years. Douglas-fir were less than five Although similar in most ways to percent per decade. Young Armillaria root disease in northern western larch averaged 18% Idaho, in these stands true fir mortality in one study (Morrison species appear to be more and others 1988). The rate of susceptible to the disease than mortality of larch declined Douglas-fir. throughout the 14-yr monitoring period. Grand fir was variable, Expected mortality rates in Mode ranging from 10 to 30% per II disease decade. Douglas-fir mortality Douglas-fir 17 to 23 Mortality rates vary by stand averages ranged from nearly 20% years of age took an average of one to age, species composition and site to a little more than 30% per three years to die quality. In the northern Rocky decade in the various studies. after basal resinosus Mountains, Douglas-fir and grand Little is known about mortality was detected. fir mortality rates are considerably rates of subalpine fir but they higher than those of pines, appear to fall between those of (Morrison and Pellow western larch, western redcedar Douglas-fir and grand fir. 1974) and western hemlock (figure 9). In general mortality rates of (Photo by Susan Hagle) From nine studies that have pines, coastal Douglas-fir and employed permanent plots to western larch declined with age monitor root disease mortality of and thinning. The opposite was Sources of data for forest trees, results are remarkably the case for inland Douglas-fir and graph: consistent. The primary causes of grand fir. Mortality rates ranged mortality on plots in the northern from 13%/decade in 5-19 yr old Byler, Marsden and Rockies were usually a Douglas-fir (Morrison and others Hagle 2006, Root dis- combination of Armillaria ostoyae 1988) to 30%/decade at 100 yrs of ease-caused tree mortal- ity in northern Idaho and Phellinus weirii (fir type). age (Byler and others, in stands: 22 year monitor- Elsewhere, it was almost entirely preparation). ing results and implica- tions. (In preparation)

Hagle, Marsden and Wel- Figure 9. Root disease mortality rates of trees at least 20 yrs old. born, 2006. Indicators and patterns of conifer mortality caused by root disease. (In prepara- tion). The range (bar) and average (*) mortality rates Hagle, 2005. Root dis- by species. ease and associated bark beetle mortality estima- tion for intermountain west risk map. Summary of results from 758 per- manent plots in northern Idaho and western Mon- tana, monitored 8-18 years. In-house report.

Morrison and others 1988 Morrison and Pellow 1994 11.1 Back to menu Armillaria Root Disease Pa ge 13

Site Predictors of Mode II trees survive, have been reported to Armillaria root disease occupy 5.1% of the Coeur d‘Alene Figure 10. Percent of plots Site factors such as moisture Forest (Williams and Marsden with root disease by habitat and temperature show promise as 1982). This agrees well with a later type series Lolo National Forest (Source: Byler and indicators of disease-proneness. assessment of root disease on the others 1990) Coeur d‘Alene Basin Forest in Disease incidence which 5.8% of stands had severe Incidence of Armillaria root root disease, defined as having 75% disease is highest on hemlock, or greater loss of canopy to root grand fir and cedar habitat types. disease (Hagle and others 1994). On the Lolo National Forest, Byler Approximately one third of the and others (1990) reported a high Coeur d‘Alene Basin Forest has of 80-88% of stands with root Douglas or grand fir cover type. disease (mountain and western Williams and Marsden (1982) hemlock habitat types) to a low of reported finding most of the disease only 13% (ponderosa pine habitat patches on grand fir or western type). Half of the stands on grand hemlock habitat types. Hagle and fir habitat types had root disease. others found severe disease most A third or fewer were afflicted on common on grand fir, western other habitat types (figure 10). hemlock or moist subalpine fir Figure 11. Mortality rates by Species composition interacts habitat types. Mortality rates of habitat type series and initial significantly with habitat type to Douglas-fir and grand fir are highest plot root disease severity. influence root disease prevalence. at a relatively younger age on highly (Percent of trees/10 years) In this case, many stands on cedar productive sites such as western habitat types were dominated by redcedar and western and mountain western redcedar and grand fir hemlock habitat types (Hagle and with few live Douglas-fir others, in preparation). remaining whereas Douglas-fir Visually estimated root disease was a primary component on severity (Hagle 1992) is a measure grand fir, Douglas-fir and western of cumulative root disease impact in hemlock habitat types. Species a stand. Recent analysis of composition alone was not a good permanent plot data from north predictor of root disease because Idaho found the root disease severity of the strong influence of habitat assigned at the time of plot type. establishment was the best predictor Surveys of Douglas-fir stands of mortality in the subsequent 20 on moist cedar-hemlock in years. Figure 12 illustrates this southern interior British Columbia relationship (Hagle and others, in found root disease on 88% of preparation). hectares (Dettman and van der Kamp 2001b). An assessment of the Coeur d‘Alene Basin National Forest (figure 11) uncovered root disease in 98% of stands with Douglas-fir and grand fir cover types, across all habitat types, but the highest severity classes were most common on grand fir and cedar/hemlock habitat type groups (Hagle and others 1994).

Disease severity is highest on grand fir and moist subalpine fir habitat types with Douglas-fir, grand fir or subalpine fir forest types. The most severe condition, Figure 12. Mortality rates (all tree species) root disease patches in which few from permanent plots in Idaho and Montana.

Pa ge 14 Back to menu Armillaria Root Disease 11.1 Thinning in Modes I and II Armillaria root disease Commercial thinning Comparing It is fairly safe to say that harvest, compared to the first 15 commercially thinned Armillaria-afflicted stands will not years. Also, in the Byler study, and unthinned stands respond favorably to commercial Douglas-fir timber volume thinning if susceptible species are decreased at both 15 and 22-year Figure 13. Root disease left. Mortality rates vary greatly by remeasurements post-treatment mortality; trees location and through time. By the (figure 14). However, grand fir Mature Douglas-fir and time stands reach commercial size volume increased in the first 15 grand fir many have high mortality rates. If years following thinning then Percent change; stems/10yrs mortality rates in a stand are declined rapidly. Grand fir already high, increases in mortality appeared to respond positively to after thinning tend to be small or sanitation thinning for at least the none. However, where mortality short term, leading the authors to rates were initially moderate or suggest that grand fir may be an low, increases can be dramatic acceptable leave tree choice when following thinning. a regeneration harvest is to follow Most reports are from within 10-15 years. retrospective studies comparing H a g l e a n d o t h e r s thinned stands to uncut stands. For (unpublished) found the grand fir example, comparing selectively decline to begin sooner, between 8 harvested stands to uncut stands, and 10 years after thinning with a Morrison and others (2001) net loss of 67% in 20 years in the observed a trend in infection and thinned stands compared to 22%

Figure 14. Root disease mortality rates, subsequent to loss in the unthinned stands mortality; volume harvest, that was associated with (figures 13 & 14). Douglas-fir site quality. Rates were low on dry mortality rates were slightly Mature Douglas-fir, grand sites, moderate on wet sites, and higher if measured as proportion fir and western larch high on moist sites. All site types of stems, or not significantly Percent change; volume/10yr had slightly higher mortality rates different, if measured as if stands were selectively harvested proportion of volume following compared with the uncut stands. thinning. In both Byler and Hagle Differences were statistically studies, the largest and most significant in two out of four vigorous-appearing trees were comparisons. retained during the thinning. Byler and others demonstrated Thinning did not improve survival differences in response between of remaining Douglas-fir or grand Douglas-fir and grand fir where fir. laminated root rot and Armillaria Morrison and others (2001) root disease were both primary found that, on moist sites, as much causes of mortality (unpublished as 90% of live, codominant trees report). The permanent plots, in in undisturbed stands had northern Idaho, were monitored for Armillaria root lesions. Root 22 years after commercial systems remain alive for a time sanitation thinning (with unthinned after the tree is severed, during Data sources: controls). Mortality rates (percent this time they can prevent (a) Hagle and others (in preparation) 213 of trees) for Douglas-fir remained colonization by saprophytic fungi permanent plots fairly consistent between the two but the Armillaria lesions are able monitored 20 years. time intervals regardless of to expand (Shaw 1980). During (b) Byler and others (in whether stands were thinned or this time the stumps may become preparation) 12 permanent plots not, and regardless of the time extensivel y colonized by monitored 22 years. following thinning (Figure 13). pathogenic fungi. This increase in Both studies located on the Grand fir, however, had a low inoculum potential allows the Idaho Panhandle National initial rate of mortality after pathogen to spread from roots of Forest in northern Idaho. thinning. This rate nearly doubled stumps to residual trees and post- between 15 and 22 years after harvest regenerated trees. 11.1 Back to menu Armillaria Root Disease Pa ge 15 WEB

Precommercial thinning in modes I and II

Even small stumps, from the long-term losses but the money precommercial thinning have spend thinning may prove to be been found to be colonized by poorly spent if few of the residual Armillaria spp. Cruickshank and trees reach maturity. others (1997) reported finding up to 77% Armillaria infection in If less susceptible species are precommercial thinning stumps in favored in thinning and the British Columbia. Infection rates resultant stand has an improved were highest on interior cedar/ species composition, thinning hemlock sites, where rates ranged can be an excellent investment. from 28 to 77% and averaged 51%. Inland Douglas-fir sites Western larch and lodgepole averaged about one third. Lowest pine are particularly sensitive to Figure 15. Precommercial rates were in the coastal forests lateral competition (crowding). thinning and weeding, (average 12-22%). Thinning may be required to removed mostly Douglas-fir and grand fir while retaining About half of the individual maintain these species even where mostly western larch. These stump root infections lead directly root disease mortality rates are released larch can be to infection of Douglas-fir crop expected to be fairly high among expected to become trees; again the rates were a little competing Douglas-fir and grand increasingly resistant to higher in the interior cedar/ fir. Large root pathogen biomass Armillaria root disease. hemlock type. These sites develop may be maintained by dying Mode II disease so these early Douglas-fir and grand fir. infections have the potential to Armillaria attacks on larch and lead to considerable long term pines may be more frequent under impacts. Resulting mortality has t h e s e c o n d i t i o n s , w i t h not, as yet, been monitored. subsequently higher rates of Although little can be said, as mortality and lower rates of yet, about mortality rates of growth in these species as well. Douglas-fir, grand fir or subalpine Also a factor, is the delay fir after thinning, we have fairly between crown closure and the reliable data suggesting that highest rates of root disease resistant species improve growth mortality. It may take decades a n d s u r v i v a l f o l l o w i n g after crown closure before precommercial thinning. sufficient root disease mortality In stands or portions of stands has occurred to open the canopy. with low root pathogen incidence, In many cases, the easing of precommercial thinning may crowding occurs too late to benefit provide satisfactory results. The intolerant species; larch and increase in growth of the residual lodgepole pine, in particular. stand may offset subsequent The infection rates detected in mortality enough to justify the young, unthinned stands that have thinning investment. However, few above-ground symptoms careful examination of the suggests that new infections candidate stand is in order resulting from thinning may not because even a moderate rate of greatly alter the impact on stands. infection may not be obvious in As stated earlier, Morrison and young stands. Young trees die and others (2000) found 32-38% of loose their foliage quickly. Close saplings to have root infections on inspection of small openings in moist and wet sites in interior young stands may reveal more British Columbia. Mortality rates mortality than is otherwise were low in these stands at this a p p a r e n t . P r e c o m m e r c i a l age but could be expected to thinning, especially in sapling- increase as the infections spread size trees may not greatly increase across the tree root systems.

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To the extent that thinning mortality rates of resistant species increases growth, it probably also following thinning (Filip and increases infection rates as the others 1989). However, species larger root systems contact more with inferior resistance, such as inoculum. In trees of resistant Douglas-fir and grand fir have species with good growth, this higher mortality rates among the increase in contact with inoculum faster-growing trees. is presumably offset by the ability Precommercial thinning in of the tree to contain and mixed-species stands is discussed eventually shed infections. This is in more detail under Mode III— demonstrated through lower Disease of young trees.

Brush removal improves conifer growth and may increase Armillaria root disease Removal of shrubs others 2005). Although the birch and trees (by cutting) to release thinning significantly improved young conifers is a common residual tree growth, Douglas-fir practice in the intermountain and lodgepole pine mortality due west, especially on private timber to Armillaria root disease also land. Early seral hardwood shrubs increased with increasing and trees often grow rapidly in hardwood thinning intensity. In the first decades after disturbance. general, a 1.5 to several times In many cases, hardwood trees increase in Douglas-fir mortality and shrubs endure long-term rates were measured following where root disease prevents hardwood thinning compared to conifer canopy closure or unthinned stands. The increased produces openings by killing mortality of lodgepole pine was trees. temporary, lasting only 3 years Several recent studies in the after thinning (Simard and others Brushing can increase interior cedar-Hemlock and 2005). mortality rates Interior Douglas-fir forest types Increased growth of crop tree of southern interior British roots probably accounts for at There is mounting Columbia have reveal ed least some of the mortality evidence that increased significant increases in Armillaria increase. Larger root systems growth following brush ostoyae activity following cutting cutting may lead to contact inoculum more readily. several fold increases in of competing hardwood trees. Also, although birch is considered crop tree mortality rates. Paper birch, in particular were tolerant to Armillaria, severed removed by various means to root systems may have been release young Douglas-fir utilized by the fungus to increase (Baleshta and others 2005, inoculum potential. Simard and others 2005) and lodgepole pine (Simard and 11.1 Back to menu Armillaria Root Disease Pa ge 17

MODE III — DISEASE OF YOUNG TREES Managing Armillaria root disease stands. Mode III commonly develops in young Figure 15. Mortality after pines, and western larch precommercial thinning Tolerate losses regenerated on harvested sites. Percent change; stems/10yrs Damage from primary Young spruces, cedars and inoculum is short-term hemlocks are sometimes killed as and usually not well. Primary spread of the significant in at the final pathogen occurs from large harvest. stumps of the previous generation. Young trees are infected and Reduce inoculum killed as their roots contact Stump removal can infected stumps. significantly reduce Two or three decades later, as primary inoculum on sites the inoculum dies out or recedes and prevent most into the interior of the old stumps, damage from this the mortality rate of young trees inoculum source. The declines. Secondary spread is economics of stump minimal, probably due to Thinning is generally intended removal depends on increasing resistance of the young to improve growth of crop trees anticipated damage from pines, larch, spruces, hemlock and by reducing inter-tree competition primary inoculum and redcedar to Armillaria. Therefore, and, in some cases, to alter species potential damage to the these species should be favored composition. Douglas-fir stands in site. over inland Douglas-fir and grand Western Cascades realized no fir in silvicultural treatments. significant differences in growth Match planting stock In young stands with extensive or mortality Filip and Goheen to the site root disease mortality, thinning (1995) following precommercial Resistance does not hold should be delayed, but lightly t h i n n i n g . I n c o n t r a s t , up if the planting stock is affected stands can be thinned. precommercial thinning may have not appropriate for the Mortality due to mode III been an effective method of site. Check seed zones Armillaria root disease declines increasing both growth and and potential vegetation after about 15 to 20 years and is survival of ponderosa pine stands or habitat types. minimal after 25-30 years of age. with Armillaria root disease (Filip There is usually little lasting effect and others 1989). Precommercially thin from this early mortality. The In another study in the Thin favoring resistant small canopy openings are usually Cascades (Rosso and Hansen species, and to maintain insignificant in a mature stand. 1998) Armillaria root disease in growth of resistant trees. In contrast to inland Douglas- Douglas-fir was described as more fir which nearly always exhibits consistent with Mode II behavior mode I or mode II disease, coastal in that mortality continues well Douglas-fir generally follows the beyond the first two to three mode III pattern. Little damage is decades. Here, a positive increase seen after the first two or three in growth was measured following decades after stand establishment. precommercial thinning but incidence of Armillaria root Disease Types I Precommercial thinning in Mode disease was also higher in thinned or II in Douglas- III Armillaria root disease stands compared to unthinned fir and true firs Among tree species exhibiting controls. The most significant may occur on the mode III disease, response to finding in this study was that tree same site with precommercial thinning varies vigor was not a factor in root type III in other significantly. Therefore, species disease. Vigorous and non- tree species if a composition is an important factor vigorous Douglas-fir were equally variety of tree in realizing benefits from likely to be killed by Armillaria species are precommercial thinning in root disease. present. Armillaria ostoyae- affected

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Precommercial thinning in generally less than 0.5%/year but dense lodgepole pine stands in ranged as high as 1.5%/yr on a few Managing Alberta, British Columbia, did not plots. From this it is reasonable to Mode IV change mortality rates during 11 conclude that precommercial years after thinning compared to thinning is probably of benefit to Maintain tree vigor unthinned controls, but did species that normally develop Mode Initial infection is improve growth (Blenis 2000). III Armillaria root disease. probably not Post-thinning mortality rates were preventable because the fungus can establish small lesions and maintain quiescent infections for MODE IV — WEAK OR SECONDARY ROOT AND BUTT DECAY prolonged periods on healthy trees. Armillaria root disease is typically conditions such as drought, fire or Therefore the goal of manifest in aging or stressed trees. logging injuries, fir engraver strip preventing the Root lesions probably establish attacks, budworm defoliation, etc. development of severe from primary spread early in the Some infections spread enough to root disease is process of stand establishment contribute to tree mortality. Killed accomplished by following harvest or fire. Lesions roots may provide sufficient scheduling harvest to progress little, perhaps even inoculum to support secondary avoid tree senescence; become quiescent for some time. spread of the fungus to adjacent live proper timing of Lesions may begin to expand as trees. Small groups of mortality may thinning to help trees trees become less efficient through result. The overall stand impact is resist drought affects; aging or as a result of stressful minor. and prevention of bark beetle and defoliator outbreaks. Armillaria root disease and forest succession

The status of Douglas-fir, at least in limiting Douglas-fir in these forests the white pine type, has as far back as at least the 1940‘s. undoubtedly changed greatly in the Analysis of results from the above past 80-100 years. Early in the 20th plots led Haig and others to century, Douglas-fir was not conclude, generally a major stand component; “Douglas-fir fails to keep up sufficiently certainly not like it is now. For rapid height growth to maintain its “Douglas-fir is a example, based on 400 permanent position in the dominant canopy and is short-lived species plots established in the white pine not sufficiently tolerant to thrive in an on the better white type in northern Idaho and western intermediate position. Its susceptibility to pine sites; root- Montana between 1909 and 1927 , attack by fungi, particularly the root rot fungus (), removes rotting fungi often Davis (1942) described the average individuals from the stand at a cause heavy mature stand as having only 15% comparatively early age. – according to mortality beginning larch and Douglas-fir (combined) . consistent records from permanent in the sixth or He reported 22% grand fir, 49% sample plots on the better white pine sites seventh decade of white pine and 14% western this weeding-out process may begin as redcedar in the stands. early as 40 years.” [Haig and others life.” Watt, 1960 1941] Armillaria root disease was recognized as an important factor in 11.1 Back to menu Armillaria Root Disease Pa ge 19

Watt, 1960 also observed the when they would average about Succession temporary nature of Douglas-fir age 82. However, only 9% of mediated by root importance in stands but noted the these stands met this expectation. disease on a relatively longer tenure of grand Most of the sample stands western redcedar fir. Based also on permanent plot were dominated by cedar in 1975, site results, Watt stated, most of the Douglas-fir had Time period: 43 years already died out. Many other “At 75 years (oldest age class), stands had become low density A mixed stand of 45-yr grand fir was still hanging in and old Douglas-fir and increasing its proportion of the grand fir or Douglas-fir stands stands. ” with severe root disease. They had grand fir had understory less than 20,000 board foot of grand fir and western Larch in these stands grew volume per acre; very low redcedar in 1962. The well in young age classes on the stocking for 80 year old stands on owner of this forest better sites but, in the absence of these productive sites. projected culmination of thinning, declined in the sixth or the stands and expected In most of these stands, harvest of mature seventh decades because of lateral Armillaria root disease is still Douglas-fir at age 90 (in competition. active in what Douglas-fir remains 2007). Today, the A recent study in forests of on the site, and has become Douglas-fir can be seen northern Idaho and Montana increasingly active in the grand fir on the forest floor under further examined effects of root component. The Douglas-fir a 40-60 year-old stand disease on forest succession wasn‘t harvested; there was no of western redcedar and (Hagle and others 2000). evidence of tree cutting in the grand fir. Composition and structure sample. This represents a natural [Photos by Susan Hagle] changes were analyzed for 25,670 course of succession on cedar acres of western redcedar habitat habitat types where root diseases type over a 40-year period. from are an important feature of most 1935 to 1975. This was a good sites. time to look at forest change in the Root disease was the primary Northern Rockies. Early seral tree driver of succession in 83% of species (pines and western larch) these acres. Douglas-fir beetle was were still abundant in 1935 also active on 14% of acres. although white pine blister rust Between the two, they directed (Cronartium ribicola) had succession on 86% of acres. Only recently invaded many white pine those stands with no detectable forests, and fire control was just root disease activity followed the beginning to be effective. expected successional pathway by Stands that were well-stocked, retaining Douglas-fir forest type pole size (6-14 inch average while growing to large tree and diameter at breast height) well-stocked stand structures. Douglas-fir on western redcedar The pervasive influence of site types (habitat types) averaged root disease in northern Rocky 42 years of age in 1935. They Mountain forests is easily were actually mostly mixed overlooked because change species stands with Douglas-fir happens slowly. It is also less making up the majority of the obvious, in many cases, because the stand volume. Regional yield mortality and brushy openings are tables would project these to be so consistently present as to appear larger diameter, well-stocked unremarkable to the untrained eye. Douglas-fir stands 40 years later,

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Identity Crisis Averted Originally recognized for it‘s which has lead to better common and edible mushroom, understanding of Armillaria Armillaria species have been species ecologies (Wargo and known since the early 1700‘s Shaw 1985). By the late 1970‘s, (Watling et al 1991). Armillaria the species Armillaria mellea was mellea was, until relatively recognized as an amalgam of at recently, the name assigned several least 10 distinct ―biological of these pathogens of trees species‖. Among these, Armillaria throughout much of the northern ostoyae emerged as the primary hemisphere. conifer pathogen in western North Mating reaction studies in American forests (Morrison and Finland starting in the early 1970‘s others 1985, McDonald and others contributed to unraveling the 1987). Armillaria species confusion Other Reading Baleshta, K. E., S. W. Simard, R. D. Guy, C. P. Chanway. 2005. Reducing paper birch density increases Douglas-fir growth rate and Armillaria root disease incidence in southern interior British Columbia. Forest Ecol. and Man. 208: 1-13. Blenis, P. V. 2000. Post spacing mortality of lodgepole pine from Armillaria root disease. The Forestry Chronicle 76(5): 753-757. Bloomberg, W. J. and D. J. Morrison. 1989. relationship of growth reduction in Douglas-fir to infection by Armillaria root disease in southeastern British Columbia. Phytopathology 79: 482-487. Byler, J. W. ; M. A. Marsden; S. K. Hagle. 1992. The probability of root disease on the Lolo national Forest, Montana. Can. J. For. Res. 20: 987-994. Cruickshank, M. G., D. J. Morrison, and Z. K. Punja. 1997. Incidence of Armillaria species in precommercial thinning stumps and spread of Armillaria ostoyae to adjacent Douglas-fir trees. Can J. For. Res. 27: 481-490. Dettman, J. R. and B. J. van der Kamp 2001a. The population structure of Armillaria ostoyae and Armillaria sinapina in the central interior of British Columbia. Can. J. Bot. 79: 600-611. Dettman, J. R. and B. J. van der Kamp 2001b. The population structure of Armillaria ostoyae in the southern interior of British Columbia. Can. J. Bot. 79: 612-620. Entry, J. A., N. E. Martin, R. G. Kelsey and K. Cromack Jr. 1992. Chemical constituents in root bark of five species of western conifer saplings and infection by Armillaria ostoyae. Phytopathology 82: 393-397. Filip, G. M., D. H. Goheen. 1995. Precommercial thinning in Pseudotsuga, , and Abies stands effected by Armillaria root disease: 10-year results. Can. J. For. Res. 25: 817-823. Filip, G. M., D. H. Goheen, D. W. Johnson, J. H. Thompson. 1989. Precommercial thinning in a ponderosa pine stand affected by Armillaria root disease: 20 years of growth and mortality in central Oregon. West. J. Appl. For. 4(2): 58-59. Filip, G. M. and L. Yang-Erve. 1997. Effects of prescribed burning on the viability of Armillaria ostoyae in mixed-conifer forest soils in the Blue Mountains of Oregon. Northwest Sci. 71(2): 137-144.. Ferguson, B. A., T. A. Dreisbach, C. G. Parks, G. M. Filip and C. L. Scmitt. 2003. Coarse-scale population structure of pathogenic Armillaria species in a mixed-conifer forest in the Blue Mountains of northeast Oregon. Can. J. For. Res. 33: 612-623. 11.1 Back to menu Armillaria Root Disease Pa ge 21

Hagle, S. K. 1992. Rating for root disease severity. In: Frankel, S., comp. Proceedings, 40th annual western international forest disease work conference; 1992 July 13 - 17; Durango CO, San Francisco, CA: USDA Forest Service, Pacific Southwest Region: 80-86. Hagle, S. K.; Byler, J. W. 1994. Root diseases and natural disease regimes in a forest of western U.S.A. In: Johansson, Martin; Jan Stenlid, eds. Proceedings of the eighth international conference on root and butt rots, 1993 August 9-16; Wik, Sweden and Haikko, Finland, Uppsala, Sweden: Swedish University of Agricultural Sciences [S-750 07]: 606-617. Hagle, S., J. Byler, S. Jeheber-Matthews, R. Barth, J. Stock, B. Hansen, and C. Hubbard. 1994. Root disease in the Coeur d’Alene River Basin: An assessment. In: Proceedings of Interior Cedar-Hemlock-White pine forests: Ecology and Management, March 2-4, 1993, Spokane, WA; Dep. Nat. Res. Sci., Wash. St. Univ., Pullman 335-344. Hagle, S.K. and R. Schmitz. 1993. Managing root disease and bark beetles. Pp. 209-228. In: Schowalter, T. D. and G. M. Filip, eds., Beetle Pathogen interactions in conifer forests. Academic Press Ltd, London. ISBN 0-12-628970-0. Hagle, S. K. and C. G. Shaw, III. 1991. Avoiding and reducing losses from Armillaria root disease. In: Shaw, C. G., III and G. A. Kile, eds., Agriculture Handbook No 691, Washington D. C.: USDA Forest Service. 157-172. Hagle, S. K., K. E. Gibson, S. Tunnock. 2003. Field guide to diseases and insect pests of northern and central Rocky Mountain conifers. U.S.D.A. Forest Service, Northern and Intermountain Regions, Rept. No. R1-03-08. 197 pp. Haig, I. T.; K. P. Davis; R. H. Weidman. 1941. Natural regeneration in the western white pine type. USDA Tech. Bull. 767. Washington, DC: 99 p. James, R. L.; C. A. Stewart; R. E. Williams. 1984. Estimating root disease losses in northern Rocky Mountain national forests. Can. J. For. Res. 14: 652-665. Komroy, K. W., R. A. Blanchette and D. F. Grigal. 2005. Armillaria species on small woody plants, small woody debris and root fragments in red pine stands. Can. J. For. Res. 35: 1487-1495. McDonald, G. I.; N. E. Martin; A. E. Harvey. 1987. Occurrence of Armillaria spp. in forests of the Northern Rocky Mountains. Research Paper INT-381. Ogden, UT: USDA Forest Service, Intermountain Research Station. 7 p. Morrison, D. J. 1989. Pathogenicity of Armillaria species is related to rhizomorph growth habit. In: Morrison, D. J., ed. Proceedings of the 7th international conference on root and butt rots; 1988 August 9-16; Vernon and Victoria, BC, Victoria BC: International Union for Forestry Research Organizations: 584-589. Morrison, D. J.; D. Chu; A. L. S. Johnson. 1985. Species of Armillaria in British Columbia. Can. J. Plant Path. 7: 242-246. Morrison, D. J. and K. Mallett. 1996. Silvicultural management of Armillaria root disease in western Canadian forests. Can. J. plant. Pathol. 18: 194-199. Morrison D. J. and Pellow. 1994. Development of Armillaria root disease in a 25-year-old Douglas-fir plantation. In: Proceedings of the 8th international conference on root and butt rots, August 1993, Wik, Sweden and Haikko, Finland. M. Johansson and J. Stenlid, Eds., Swedish University of Agricultural Sciences, Uppsala. 560-571. Morrison, D. J., K. W. Pellow, A.F.L. Nemec, D. J. Norris, P. Semenoff. 2001. Effects of selective cutting on the epidemiology of Armillaria root disease in the southern interior of British Columbia. Can. J. For. Res. 31: 59-70.

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Morrison, D. J., K. W. Pellow, D. J. Norris, A.F. L. Nemec. 2000. Visible versus actual incidence of Armillaria root disease in juvenile coniferous stands in the southern interior of British Columbia. Morrison, D. J., G. W. Wallis and L. c. Weir. 1988. control of Armillaria and Phellinus root diseases: 20-year results from the Skimikin stump removal experiment. Canadian Forestry Service, Pacific Forestry Centre. Report BC-X-302. 16 p. Pankuch, J. M., P. V. Blenis, V. J. Lieffers, and K. I. Mallet. 2003. Fungal Forest Health colonization of aspen root following mechanical site preparation. Can. J. Protection and For. Res. 33(12) 2372-2379. State Forestry Peet, F.G., D.J. Morrison, K.W. Pellow. 1996. Rate of spread of Armillaria Organizations ostoyae in Douglas-fir plantations in the southern interior of British Columbia. Can. J. For. Res. 26(148-151). Assistance on State And Private Lands Quesnel, H. J. and M. P. Curran. 2000. Shelterwood harvesting in root- disease infected stands— post-harvest soil disturbance and compaction. Montana: (406) 542-4300 For. Ecol. and Manag. 133:89-113.

Idaho: (208) 769-1525 Robinson, R. M. and D. J. Morrison 2001 Lesion formation and host response to infection by Armillaria ostoyae in root of western larch and Utah: (801) 538-5530 Douglas-fir. For. Path. 31 (2001) 371-385.

Nevada: (775) 684-2500 Robinson, R. M., D. J. Morrison, G. D. Jensen. 2004. Necrophylactic periderm formation in the roots of western larch and Douglas-fir Wyoming: (307) 777- infected with Armillaria ostoyae. II. The response to the pathogen. For. 5659 Path. 34:119-129.

Assistance on Rosso, P. and E. Hansen. 1998. Tree vigour and the susceptibility of Federal Lands Douglas-fir to Armillaria root disease. Eur. J. For. Path. 28:43-52.

US Forest Service Region Roth, L. F., C. G. Shaw, III, L. Rolph. 2000. Inoculum reduction measures One to control Armillaria root disease in a severely infected stand of Missoula: (406) 329-3605 Ponderosa pine in south central Washington: 20 year results. Coeur d’Alene: (208) 765- 7342 Simard, Hagerman, S. M., Sachs, D. L., Heineman, J. L., Mather, W. J.2005. Conifer growth, Armillaria ostoyae root disease, and plant diversity US Forest Service Region responses to broadleaf competition reduction in mixed forests of Four Southern Interior British Columbia. Can. J. For. Res. 35: 843-859. Ogden: (801) 476-9720 Boise (208) 373-4227 Shaw, C. G. III., 1980. Characteristics of Armillaria mellea on pine root systems in expanding centers of root rot. Northwest Sci. 54(2): 137-145. Shaw, C. G., III, and Roth, L. F. 1976. Persistence and distribution of a clone of Armillaria mellea in a ponderosa pine forest. Phytopathology 66:1210-1213. Smith, M. L., J. N. Bruhn and J. B. Anderson. 1992 The fungus Armillaria bulbosa is among the largest and oldest living organisms. Nature 356: 428-431. Tippett, J. T. and A. L Shigo. 1981. Barriers to decay in conifer roots. Eur. J. For. Pathol. 11: 51-59. 11.1 Back to menu Armillaria Root Disease Pa ge 23

van der Kamp, B. J. 1993. Rate of spread of Armillaria ostoyae in the central interior of British Columbia. Can. J. For. Res. 23: 1239-1241. van der Kamp, B. J. 1995. The spatial distribution of Armillaria root disease in an uneven-aged, spatially clumped Douglas-fir stand. Can. J. For. Res. 25: 1008- 1016 Wargo, P. M., Shaw, C. G., III. 1985. : the puzzle is being solved. Plant Disease 69: 826-832. Watt, R. F. 1960. Second -growth western white pine stands. Tech. Bull. No. 1226. Washington DC: USDA Forest Service: 60 p. Williams, R. E.; C. D. Leaphart. 1978. A system using aerial photography to estimate area of root disease centers in forests. Can. J. For. Res. 8(2): 214-219. Williams, R.E., and M.A. Marsden. 1982. Modeling probability of root disease center occurrence in northern Idaho forests. Can. J. For. Res. 12: 876-882.

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