Beech Bark Disease
From: Exotic Pests of Eastern Forests, Conference Proceedings - April 8-10, 1997, Nashville, TN, Edited by: Kerry O. Britton, USDA Forest Service & TN Exotic Pest Plant Council
In forests of North America the beech bark disease (BBD) complex affects
American beech, Fagus grandifolia Ehrh. BBD begins when bark
tissues, attacked by the exotic beech scale insect, Cryptococcus
fagisuga Lind. are rendered susceptible to killing attacks by fungi
of the genus Nectria (Ehrlich 1934). The principal fungus, N.
coccinea var. faginata Lohm. and Watson (Lohman and Watson 1943),
was probably introduced also, but the native pathogen, N. galligena Bres.,
also attacks and kills bark predisposed by C. fagisuga (Cotter 1974;
Houston 1994a; Mielke et al. 1982). The general framework for BBD's etiology:
Beech Trees + C. Fagisuga + Nectria Spp. = > BBD
indicates the chronology of events required for disease development,
and points out that although the effects of the insect are necessary, the
disease is expressed only after Nectria spp. attack and kill scale-altered
Following its accidental introduction to Nova Scotia around 1890 (Ehrlich
1934), the beech scale spread westward and southward through forests of
Canada and the United States. It now occurs throughout New England, New
York, much of New Jersey and Pennsylvania, and is present in northeastern
Ohio, northeastern West Virginia and northwestern Virginia (Fig.
1). Its recent discovery in the Great Smoky Mountain National Park along
the Tennessee-North Carolina border (Houston 1994a,b) has prompted considerable
|Figure 1. Known distribution of beech scale
(block areas) as of 1996, in relation to the range
of American beech (hatched areas).
|Figure 2. High tree mortality can occur when
forests are affected by teh causal complex for
the first time. Over 75% of the large beech in this
Vermont forest were dead or dying (bare and
gray crowns) in 1971.
Course of the disease and its effects: Generally, Nectria infections
and tree mortality (Fig. 2) occur 1 to 4 years after
heavy build-up of the insect on large trees (Fig. 3).
The area of current heavy mortality is termed the killing front; regions
where severe mortality occurred earlier comprise the aftermath zone (Shigo
1972). In aftermath forests the causal agents are established on small trees
of both root sprout and seedling origin that often develop after death or
harvest of their progenitors. Most of the new emerging trees and old survivors
become cankered and rendered highly defective by the scale-Nectria
complex (Fig. 4).
|Figure 3. Heavy infestations of beech
scale can cover tree boles with white wax.
|Figure 4a. Trees in aftermath forests
can become severely defective. Initially,
cankers are scattered and discrete (a);
|Figure 4b. ...with time cankers provide
habitat for scale and new cankers
develop and accumulate (b);
|Figure 4c. ...extreme defect
sometimes results (c).
Thus, in North America, where the introduced causal complex is still
advancing, there are two distinct phases of the disease. The first phase
encompasses the effects resulting from the invasions and epidemic buildups
of scale and pathogens (killing front); the second phase encompasses the
effects of the established causal complex on the survivors and the young,
small beech trees emerging in the aftermath of heavy tree mortality or salvage.
In phase one, scale populations build rapidly to high levels. Even though
heavy infestations can reduce growth, and, by killing cells in the outer
layers of the phellogen, cause bark fissuring, the insect alone rarely damages
the cambium (Lonsdale and Wainhouse 1987). Usually, however, infection of
bark by one or both Nectria pathogens soon follows infestation. Bark
exudation ("tarry spots"), which can result from many other causes
as well, is often the first sign that bark has been killed by Nectria.
Massive invasion by the pathogens of scale-infested trees usually ensues;
often, more than 50 percent of the beech trees > 10 inches in diameter
are killed, and many more are severely damaged. Such losses can be significant.
For example, as of 1977 the estimated loss in merchantable timber volume
attributed to BBD in Vermont had reached nearly 300 million board feet (including
trees dead, dying, or damaged beyond use) (Miller-Weeks 1983). Phase one
is now occurring in eastern Pennsylvania and northeastern West Virginia
and, no doubt, will occur soon in the recently affected stands in Ohio,
Virginia, North Carolina, and Tennessee.
Opening up of stands by mortality or by salvage of diseased trees can
lead to the development of dense stands from root sprouts and seedlings
and has helped to create, over large areas, stands that are overly rich
to beech and impoverished in associated species. Development of these stands
ushers in phase two (Houston 1975). With time, the stems in these stands
gradually acquire spatial habitats for the beech scale. Infestation of these
habitats, which include bark figures and fissures, callused areas around
injuries and patches of protective lichens and mosses results in scattered,
isolated colonies. Bark beneath the colonies, altered by the insect's feeding
activity, may be attacked by Nectria spp. resulting in scattered, discreet
cankers. The callus that develops around each canker provides additional
refuges for scale. Aggregations of cankers develop over time, and trees
become increasingly defective, but rarely are they girdled and killed quickly
as were their progenitors in phase one.
Eventually, in long-affected stands, severely affected trees lose vigor,
grow slowly, and then die, out-lived by more vigorous, less severely diseased
and resistant beech trees and trees of other species. In any particular
forest the rate and pattern of this shift depend in large part on the relative
density and frequency of the beech component, on the distribution patterns
of resistant trees, and on management intervention. Thus, harvest operations,
even in badly diseased and slowly declining beech stands can initiate once
more, the formation of highly susceptible thicket stands.
Some Factors That Influence Disease Development
Stand composition and structure stand age and density,
tree size, and species composition affect disease severity, especially in
forests affected for the first time. Older stands with a high component
of large beech trees are most vulnerable, and in such stands tree mortality
can be very high (e.g., Valentine 1983). Large old trees with extensive
decay, conks, or large broken branches are most at risk and often die rapidly
as Nectria spp. becomes established (Mize and Lea 1979). One study
of forests in Massachusetts and New Hampshire showed that stands rich in
hemlock were especially vulnerable (Twery and Patterson 1984).
Environmental factors Once established in a forest stand,
scale populations tend to fluctuate at different rates and amplitudes related,
in part, to the temporal phase of the outbreak. I monitored the general
changes in annual populations of C. fagisuga on trees in plots from
Maine to West Virginia (D.R. Houston, unpublished data). In newly infested
stands, scale populations built up rapidly to high levels, whereas in long-affected
stands, established populations typically were maintained at lower levels
and exhibited less dramatic annual fluctuations (Fig. 5),
presumably in response to local climate change. Exceptionally cold winter
temperatures and heavy autumn rainfalls, both highly correlated with low
levels of BBD development, presumably adversely affected overwintering scale
populations and the establishment of new populations in late autumn, respectively
(Houston and Valentine 1988).
Figure 5. Annual population levels of C. fagisuga from 1979 to 1990 in the first decade of infestation (Inez, Pennsylvania) and in the sixth decade after initial infestation (Eddington, Maine). The infestation index was calculated as a weighted average of infestations scores for approximately 200 trees per plot. Trace populations were scored as 1, very heavy as 40 (Houston 1994a).
Predators and parasites no invertebrate parasites of C.
fagisuga are known. However, several predators are recognized of which
the twice-stabbed ladybird beetle Chilocorus stigma Say is the most common.
C. stigma is most abundant when scale populations are dense and,
although it responds numerically to high scale densities, its predatory
effectiveness is limited by its propensity to disperse, its failure to feed
on all life stages of scale, and, especially, by the high rate of scale
reproduction (Mayer and Allen 1983). Although scale populations on individual
trees can be markedly reduced when populations of coccinellids are high,
the overall effectiveness of these predators is limited.
Bark epiphytes some epiphytes growing on beech bark offer
favorable spatial habitats for C. fagisuga (Ehrlich 1934, Houston
et al. 1979). Colonies often develop initially beneath patches of moss and
lichen. However, not all epiphytes enhance infestations. For example, in
Nova Scotia, some stands on steep, south-facing slopes contain beech trees
that are remarkably free of disease compared to others in the general area.
These trees are heavily colonized by mosaics of crustose lichens, the predominant
species of which are rarely colonized by C. fagisuga (Houston 1983b).
Such preclusive lichens have thalli that are dense, smooth and epigenous
in contrast to the loosely compact, granular-surfaced hypogenous thalli
of readily colonized species.
Host resistance in affected stands, some trees remain
free of beech scale and disease (Fig. 6). Challenge trials
have shown them to be resistant to C. fagisuga (Houston 1982, 1983a).
Resistant trees occur in relatively low numbers (< 1.0 percent of the
beech stems) and many occur in groups (Houston 1983a). The occurrence of
resistant trees in groups is encouraging; groups of resistant trees are
easier to recognize than isolated individuals, and potentially are easier
to protect in forest management operations designed to discriminate against
diseased trees. Isozyme genetic studies have shown that resistant trees
in groups originate both from root sprouts (clones) and from seed (families)
(Houston and Houston 1986, 1990).
Isozyme patterns unique to resistant trees have not been found (Houston
and Houston 1994), and the control of resistance is probably multigenic.
Resistant and susceptible trees differ in their bark chemistry. Bark of
Figure 6. A few trees are resistant
to beech scale and remain free of
disease (center) in contrast to their
resistant beech has significantly lower concentrations of some amino acids
and total amino nitrogen than does uninfested bark of susceptible trees
Options available to reduce the effects of BBD are determined by the
temporal phase of the disease, stand structure and composition, and the
harvesting and silvicultural systems available (Mielke et al. 1986, Ostrofsky
and Houston 1989). There are two major management situations or problems
posed by the disease. The first is how to deal with forests that are about
to become, or that have recently been, infested for the first time, and
where heavy beech mortality can be expected within a few years. The second
problem is how to handle aftermath stands where dense, disease susceptible,
and defective stands have developed. In brief, managing recently-infested
stands entails a) reducing the proportion of beech, b) discriminating
against large, overmature trees with roughened bark and signs of decay,
c) removing heavily infested trees, and d) removing advance beech regeneration
with herbicides where overstory beech is heavily infested (Mielke et al.
In killing front and aftermath forests, Mielke et al. (1986) propose
that a) dead or declining trees with heavy beech scale populations be removed,
and b) susceptible advance regeneration and understory beech be treated
with herbicides. They recommend leaving beech with little or no scale or
Nectria infection. Ostrofsky and Houston (1989) suggest using harvesting
systems that by minimizing injuries to beech root systems, should reduce
development of root sprouts from roots of susceptible trees.
It is clear that close surveillance of stand conditions and scale populations
is important during all stages of disease development. In early stages of
an outbreak, scale-free trees may not be resistant but merely "escapes."
But, as the outbreak ensues, large trees that remain free of scale, or only
very lightly infested, are good candidates for retention in the stand. Infested
trees do vary in their levels of resistance to scale and possibly to Nectria.
As a consequence, diseased trees persisting in aftermath forests may differ
in how seriously they are damaged, e.g., on some trees what appear to be
severe bark injuries, actually may be restricted to the outer bark leaving
the cambium and wood unaffected (Burns and Houston 1987).
Increasing the relative number of resistant trees seems to be the most
promising approach for reducing the impact of this disease in the long run.
The results of trials to determine how various harvesting regimes affect
the initiation, development, and survival of root sprouts are being analyzed.
In addition, studies to determine ways to clone selected resistant genotypes
have been conducted. Tissue-culture techniques which use sprouts from root
segments and forced buds of mature resistant trees, have brought several
genotypes through to rooting (Barker et al. 1995). Still needed are trials
to develop ways to grow the tissue culture plantlets in soil and introduce
them into the forest.
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of American beech with resistance to beech bark disease. Phytopathology
Burns, B.S.; Houston, D.R. 1987. Managing beech bark disease. Nor.
J. Appl. For. 4:28-33.
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organisms. Durham, NH: University of New Hampshire. 138 p. M.S. thesis.
Ehrlich, J. 1934. The beech bark disease, a Nectria disease
of Fagus following Cryptococcus fagi (Baer.). Can. J.
Houston, D.B.; Houston, D.R. 1994. Variation in American beech (Fagus
grandifolia, Ehrh.): Isozyme analysis of genetic structure in selected
stands. Silvae Genetica 43:277-284.
Houston, D.R. 1975. Beech bark disease: The aftermath forests are structured
for a new outbreak. J. For. 73:660-663.
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the beech scale, Cryptococcus fagisuga (Lindinger). Broomall,
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Fig. 1. Known distribution of
beech scale (block areas) as of 1996, in relation to the range of American
beech (hatched areas).
Fig. 2. High tree mortality
can occur when forests are affected by the causal complex for the first
time. Over 75% of the large beech in this Vermont forest were dead or dying
(bare and gray crowns) in 1971.
Fig. 3. Heavy infestations
of beech scale can cover tree boles with white wax.
Fig. 4. Trees in aftermath
forests can become severely defective. Initially, cankers are scattered
and discrete (a);
...with time cankers provide habitat for scale and new cankers develop
and accumulate (b);
...extreme defect sometimes results (c).
Fig. 5. Annual population levels
of C. fagisuga from 1979 to 1990 in the first decade of infestation
(Inez, Pennsylvania) and in the sixth decade after initial infestation (Eddington,
Maine). The infestation index was calculated as a weighted average of infestation
scores for approximately 200 trees per plot. Trace populations were scored
as 1, very heavy as 40 (Houston 1994a).
Fig. 6. A few trees are resistant
to beech scale and remain free of disease (center) in contrast to their