United States 

Department of 

Agriculture

Forest 

Service

North Central

Research Station

Research Paper

NC-341

Long-Term Response of

Precommercially

Thinned Aspen Clones

to Hypoxylon Canker

M.E. Ostry, N.A. Anderson, D.J. Rugg, and K.T. Ward
North Central

Research Station 

USDA Forest Service

1992 Folwell Avenue

Saint Paul, Minnesota

55108

2004

www.ncrs.fs.fed.us
Increasing demand for quaking aspen (Populus

tremuloides Michx.) fiber has renewed interest in

precommercial and commercial thinning to

increase growth of individual trees and decrease

rotation intervals. After aspen stands are harvested or killed by fire, 10,000-100,000 suckers

ha-1 regenerate from root sprouts. Self-thinning

through intraspecific competition reduces this

to less than 1,000 stems ha-1 after 50 to 60

years. Precommercial thinning can shorten rotation length by accelerating early growth, while

commercial thinning can increase total stand

yield by capturing expected mortality from selfthinning.

Hypoxylon canker, caused by the fungus

Entoleuca mammata (Wahlenberg: Fr.) J.D.

Rogers & Y.-M. Ju, is a common disease killing

aspen throughout the Lake States. Some

research has suggested that stand density may

influence the incidence of Hypoxylon canker

(Anderson and Anderson 1968, Anderson and

Martin 1981, Bruck and Manion 1980, Capony

and Barnes 1974, Day and Strong 1959, Ostry

and Anderson 1998, Schreiner 1925). However,

other researchers have reached different conclusions (Anderson 1964, Pitt et al. 2001). The

potential effect of variation among aspen clones

on Hypoxylon canker prevalence was not examined in these previous studies. 

The objectives of this study were to determine

(i) the impact of Hypoxylon canker in a precommercially thinned stand of aspen and (ii)

the influence of aspen clone differences on the

effects of Hypoxylon canker. The hypotheses

tested were (i) Hypoxylon canker prevalence is

greater in thinned aspen relative to unthinned

aspen, and (ii) Hypoxylon canker-induced tree

mortality is greater in thinned aspen relative to

unthinned aspen. This study was a continuation

and reanalysis of the research described by

Anderson and Anderson (1968).

MATERIALS AND METHODS

Study Design

This study was conducted in a quaking aspen

stand regenerated after a clearcut in 1941 on

the Pike Bay Experimental Forest in the

Chippewa National Forest in Cass County,

Minnesota. The study site was level with sandy

loam soil and site index of 21-23 m. In 1951,

four 4-ha areas were delineated within the study

stand. Three treatments were applied: aspen

thinned with all other hardwoods removed

(THR); aspen not thinned with hardwoods

removed (HR); and aspen not thinned and

hardwoods left (control, C). For the THR treatment, two of the areas were thinned by hand to

an average density of 1,831 trees ha-1 and all

aspen with Hypoxylon stem cankers were

removed. In the HR and C treatment areas, the

aspen were not thinned and averaged 6,489

trees ha-1. The C treatment area contained 220

other hardwood trees ha-1, predominately black

ash (Fraxinus nigra Marsh.), bur oak (Quercus

macrocarpa Michx.), and American elm (Ulmus

americana L.). Ten permanently marked .04-ha

plots were systematically established in each of

the four areas, with adjustments to avoid natural openings, roads, and trails (fig. 1).

Additional details on the field design can be

found in Anderson and Anderson (1968).

Data Collection

In 1953, and in seven other years through

1998, all trees on each plot were examined for

the presence of Hypoxylon canker on the main

stem. These assessments were performed during

the dormant season with the aid of binoculars.

At each examination, tree diameter at breast

height (d.b.h.), number of Hypoxylon stem

cankers, and cause of tree mortality were

recorded. Since cankers on the lower half of

stems are more likely to be fatal to affected trees

than cankers higher on the stem (Day and

Strong 1959), canker height was recorded.

1

Long-Term Response of Precommercially

Thinned Aspen Clones to Hypoxylon

Canker

About the Authors:

M.E. Ostry, Research Plant

Pathologist; N.A. Anderson,

Research Plant Pathologist;

D.J. Rugg, Statistician; and

K.T. Ward, Forester; are all

with the North Central

Research Station, St. Paul,

MN.
2

Figure 1.—Plot (.04ha) locations in treatment areas and percentages of treeskilled by Hypoxyloncanker over the 47years on each plot.Each plot was in a single unique clone.
Volume was calculated using Schlaegel’s (1971)

aspen equation developed on plots in or near the

Pike Bay Experimental Forest. The equation generates cubic feet inside bark, which was converted to cubic meters.

Clone Delineation

In 1972 all live trees on each plot were mapped

and numbered. Also beginning at this time, phenological characteristics such as date of leaf flush

and leaf fall, fall coloration, bark color and texture, crown shape, and stem and branch form of

aspen on each plot were recorded to delineate

clone boundaries (Barnes 1969, Blake 1963). On

three different dates in May 1989, color-infrared

aerial photographs at a scale of 1:7920 were

taken to help delineate clones within the study

area using differences in the timing of leaf flush

and crown shape. Each plot was located on the

photographs and distinguishable clone boundaries were mapped.

Statistical Analyses

The suboptimal design of the study posed an

interesting problem. Our analyses ignore the

original breakdown of the thinned treatment into

two replicates, treating them instead as a single

large area. The technical validity of the analyses

rests on the assumption that the permanent plots

are spaced sufficiently far apart that the responses are independent. Responses of individual trees

on a plot are clearly correlated due to both spatial proximity and genetics, so they are treated as

subsamples.

We found that each plot was in a single unique

clone, so we were concerned that apparent differences in canker prevalence across treatments

might actually be due to the different clones in

those treatments. Statistically, this would manifest itself as greater than expected variation

across plots within a treatment. To address this

potential problem, we analyzed the data using a

categorical data method developed by Koehler

and Wilson (1986), as implemented in the program TableSim (Rugg 2003).

For categorical data, there is a certain variance

structure associated with a given response probability distribution. Under standard statistical

tests, different aspen clones in the same treatment group are expected to have the same base

response distribution and therefore the same

variance structure. If the null hypothesis of no

treatment differences is true, then clones in different treatment groups also have the same base

response distribution and therefore the same

variance structure. In such a case, the test statistic follows a standard chi-square distribution. If

the null hypothesis is false, then the response

distribution itself also has some variability (intertreatment variance). This extra variance inflates

the test statistic. If there is enough extra variability, one can conclude that there are significant differences among the treatments. 

If the treatment response varies by clone, the

variance in the data for each treatment is a combination of standard response distribution-based

variance (within clone) plus variance in the

response distribution itself (between clones within a treatment). Just like intertreatment variance

in the response distribution, this extra variability

inflates the computed test statistic. In such a

case, the test statistic may be large because of

interclone differences within treatments, treatment differences, or some combination of the

two. Clearly, inference about the existence of

treatment differences becomes suspect. 

While clones were our primary concern in

designing the analysis protocol, putative clone

effects are confounded with general plot effects.

The remainder of this section, as well as the

results section, will therefore refer to plot effects

rather than clone effects specifically.

The Koehler and Wilson (1986) method estimates the between plot variance within each

treatment and adjusts the test statistic so that it

again follows a standard chi-square distribution

when the null hypothesis of no treatment differences is true. Large values of the test statistic

once more reflect either chance events or differences among the treatments. The size of the

adjustment is related to the amount of extra,

3
interplot variance. One measure of the amount

of interplot variation is the statistic C(j) used by

the program TableSim (Rugg 2003). A C(j) value

of 1.00 indicates no interplot variation; higher

values indicate increasing interplot variation. In

this report, C(j) is referred to as the "variance

inflation factor" (VIF).

Two perspectives were taken with tree survival

data. First, we examined the long-term fate of

trees over the entire 47-year experiment. Second,

we examined short-term changes from one sampling point to the next. For both perspectives,

the data were analyzed using the same categorical data methods described above for canker

prevalence data.

Tree diameter and height were analyzed using

ANOVA for the 1987 and 1998 sample points.

Treatments were compared using Fisher’s LSD.

The data consisted of the mean d.b.h. or height

on each plot, which removed plot effects on the

mean square error estimate. However, if all the

"best" growing plots happened to be in a particular treatment, that treatment would still appear

better even if it actually had no effect at all.

For each sample year from 1966 through 1998,

tree density within the treatments was compared

using pair-wise t-tests. The data were square root

transformed prior to analysis to make the distributions more normal. Because of severe variance

heterogeneity, in early years the treatments were

compared using the standard t-test for unequal

variances. The time trend over the entire study

was assessed by plotting average number of trees

per plot against year.

RESULTS

Canker Prevalence

Across the 47 years, the prevalence of

Hypoxylon canker (ratio of living infected trees

to total living trees) by treatment ranged from 2

to 13 percent (table 1). Of the eight sampling

years, only one showed a difference in canker

prevalence between THR and C plots (1956,

table 2), with C having the lower rate. All other

significant differences were between HR and

either C or THR. Removal of hardwoods consistently produced the lowest canker prevalence

over the first 15 years of growth after treatment,

but the C and HR treatments were indistinguishable from each other by the 20th year (1971).

No differences were found among the treatments

from the 36th year (1987) onward.

Early in the study (1953-1971), most Hypoxylon

cankers originated on the lower half of stems—

70 percent for C and HR plots, 76 percent for

THR plots. Later in the study (1972-1998),

cankers on the lower half of stems declined to 38

percent for C and HR plots, but only to 66 percent for THR plots. 

Tree Survival

Hypoxylon canker was clearly most damaging

during the early years. Of the trees dying from

Hypoxylon canker, over 60 percent died in the

first 20 years and over 90 percent died within 30

years after the regeneration clearcut. Analysis of

the 47-year tree survival rates and causes of mortality (table 3) showed differences among the

treatments in survival rate (P < 0.0001).

Cumulative over the 47 years, THR plots had a

much greater rate of tree survival, but of the

trees that did die in those plots, a larger proportion died from Hypoxylon canker than in the C

or HR plots. Tree mortality caused by Hypoxylon

canker among plots in the C, HR, and THR treatments ranged from 14 to 38 percent, 5 to 32

percent, and 19 to 64 percent, respectively, at the

end of the study in 1998 (fig. 1). When we compare the C and HR treatments (table 3), the HR

treatment was associated with less Hypoxylon

canker mortality (P = 0.052), but equal to C in

death from other causes (P = 0.70). Analysis of

the seven intersample measures of tree survival

showed that differences in mortality dissipated

over time; no differences were detected 45 years

after thinning (table 4). 

4
5

Table 1.—Prevalence of Hypoxylon stem cankers in thinned and unthinned quaking aspen trees per hectare

from 1953 to 1998 

Year Treatment1 Live Prevalence of VIF3

stems cankers2 (%)

1953 C 6,111 4 1.29

HR 7,247 2 2.20

THR 1,924 5 1.64

1956 C 4,658 9 3.93

HR 5,948 5 3.56

THR 1,897 13 1.50

1961 C 2,798 8 2.53

HR 4,367 2 3.90

THR 1,591 7 1.00

1966 C 1,571 7 2.22

HR 2,586 4 1.69

THR 1,326 8 1.54

1971 C 1,116 3 3.86

HR 1,709 2 2.30

THR 1,102 6 1.80

1987 C 568 8 1.04

HR 763 9 1.00

THR 573 10 1.14

1996 C 336 10 1.08

HR 467 7 1.00

THR 348 6 1.00

1998 C 314 6 1.59

HR 430 7 1.00

THR 331 6 1.00

1C = control; HR = aspen unthinned but hardwoods removed; THR = aspen thinned and hardwoods removed.

2 The canker prevalence rates are weighted using the variance inflation factor and therefore cannot be used to

compute the exact number of infected trees observed. 

3 VIF is the "variance inflation factor" and corresponds to C(j) in Rugg (2003); values greater than 1.00 indicate

increasing interplot variation. 
6

Table 2.—P-values1 of Hypoxylon stem canker prevalence analyses comparing thinned and unthinned aspen, adjusted and not

adjusted for plot effects 

Adjusted Not adjusted

Year Overall THR-C2 THR-HR C-HR Overall THR-C2 THR-HR C-HR

1953 0.002 0.26 0.0006 0.005 <<0.0001 0.17 <<0.0001 0.0002

1956 0.0001 0.032 < 0.0001 0.006 <<0.0001 0.0004 <<0.0001 <<0.0001

1961 0.0004 0.38 0.002 0.0003 <<0.0001 0.23 <<0.0001 <<0.0001

1966 0.004 0.54 0.0006 0.032 0.0001 0.37 <0.0001 0.0032

1971 0.032 0.23 0.018 0.65 0.0007 0.019 0.0003 0.43

1987 0.46 0.44

1996 0.40 0.37

1998 0.86 0.86

1 P-values are from the likelihood ratio tests (LR) provided by TableSim (Rugg 2003). When the overall test shows no differences, then

no multiple comparisons are performed. 

2 C = control; HR = aspen unthinned but hardwoods removed; THR = aspen thinned and hardwoods removed.

Table 3.—Fate of thinned and unthinned quaking aspen at the end of the study in 1998

Treatment1 Live2 Dead/canker3 Dead/other3 n4 VIF5

Percent Percent Percent

C 5 20 75 2,392 3.98

HR 6 14 80 2,886 3.94

THR 17 32 51 1,580 3.36

1 C = control; HR = aspen unthinned but hardwoods removed; THR = aspen thinned and hardwoods removed.

2 Live trees infected by E. mammata are included. 

3 The two categories of dead trees are cumulative over the 47 years of observation. "Other" refers primarily to trees dying from suppression. 

4 n is the sample size. 

5 VIF is the "variance inflation factor" and corresponds to C(j) in Rugg (2003); values greater than 1.00 indicate increasing interplot

variation. The percentages are weighted using the variance inflation factor and therefore cannot be used to compute the exact number

of trees observed in each category. 
7

Table 4.—Between sample estimates of tree survival and mortality rates by cause for thinned and unthinned quaking aspen from

1951 to 1998 

Cause of mortality

Years Trt1 Tree Hypoxylon Other2 Ratio3 VIF4 P(diff)5

survival canker

Percent Percent Percent

1951-56 C 74 5 21 19 1.07 0.0001

HR 80 4 16 20 3.33

THR 91 4 5 44 2.33

1956-61 C 63 10 27 27 2.84 0.0001

HR 76 6 18 25 8.31

THR 86 13 1 93 3.39

1961-66 C 59 9 32 22 2.55 0.0001

HR 59 4 36 10 3.64

THR 83 6 10 38 2.27

1966-71 C 75 7 19 27 3.64 0.0001

HR 68 4 28 13 3.64

THR 85 8 7 53 2.76

1971-87 C 50 1 49 2 1.00 0.0001

HR 44 2 54 4 1.12

THR 53 4 43 9 1.29

1987-96 C 60 1 39 – 1.68 0.29

HR 63 4 33 86 2.06

THR 65 4 31 – 2.42

1996-98 C 94 4 1 – 1.32 0.56

HR 92 3 5 586 1.34

THR 94 4 2 – 1.39

1 C = Control; HR = aspen unthinned but hardwoods removed; THR = aspen thinned and hardwoods removed.

2 Other mortality refers primarily to trees dying from suppression.

3 Ratio = (Hypoxylon mortality rate/(Hypoxylon mortality rate + Other mortality rate))*100.

4 VIF is the "variance inflation" factor and corresponds to C(j) in Rugg (2003); values greater than 1.00 indicate increasing interplot

variation. The rates are weighted using the variance inflation factor and therefore cannot be used to compute the exact number of trees

observed in each category. 

5 P(diff) is the overall probability of no differences among the treatments for mortality caused by Hypoxylon canker, using the likelihood ratio test generated by TableSim (Rugg 2003). 

6 In 1996 and 1998 there were no differences in mortality rate by treatment; therefore, the single value reported is pooled across treatments.
Plot Effects

In the analysis of Hypoxylon canker prevalence,

the VIF values in table 1 indicate strong plot

effects. When we compare P-values adjusted for

plot effects to P-values not adjusted (table 2), the

reduction in significance is often on the scale of

orders of magnitude. Nonetheless, the adjustment for plot effects produced only one qualitative change (1971 THR-C). The unadjusted Pvalues are generally either very small or very

large, so the qualitative conclusions do not

change much when plot effects are accounted

for. 

In the analysis of tree mortality caused by

Hypoxylon canker, the VIF values in tables 3 and

4 show strong plot effects, and the P-values are

generally very small or very large. Although we

do not present the raw analysis of mortality, the

parallels to the canker prevalence P-values make

it clear that plot effects substantially altered the

strength of the conclusions but rarely their qualitative outcome.

The likelihood ratio statistic (LR) used in the categorical data analysis of canker prevalence and

tree survival can be separated into additive

pieces. Therefore, we can compare the LR with

and without plot effects in the model to determine how much lack of fit is due to plot effects

and how much is due to treatment effects. The

LR calculation shows that plot effects accounted

for roughly half of the lack of fit in the first 20

years of the study for both canker prevalence

and tree survival (table 5). In later years, plot

effects continued to have strong impacts on survival, but only minor impacts on canker prevalence.

Tree Growth

In 1987 there were no differences among treatments in d.b.h. (P = 0.56) (table 6). Trees in the

HR plots had a greater average height than trees

in the THR (P = 0.05) or C (P = 0.002) plots;

trees in the THR and C plots did not differ in

height (P = 0.12). In 1998 trees in the HR plots

had a smaller average d.b.h. than trees in the

THR (P = 0.028) or C (P = 0.058) plots; trees in

the THR and C plots did not differ (P > 0.90)

(table 6). There were no differences in height (P

> 0.90).

Tree Density

Density declined in all treatments over the 47-

year growing period and approached similar levels across treatments (fig. 2). The t-tests showed

that THR and C plots did not differ in density

from 1966 onward (P = 0.11 in 1966, P > 0.50

thereafter). THR plots had lower density than HR

plots in all years except 1998 (P < 0.002 in

1966, 1971, and 1987; P = 0.023 in 1996; P =

0.057 in 1998). Similarly, C plots had lower density than HR plots in all years except 1998 (P <

0.001 in 1966 and 1971; P = 0.035 in 1987 and

1996; P = 0.079 in 1998).

8

Table 5.—Percentage reductions in likelihood ratio

(LR) test statistics from adjusting for plot effects in

the analyses of Hypoxylon stem canker prevalence

and tree survival; larger reductions mean that more

of the total variability in the response variable can

be attributed to plot, rather than treatment, effects

LR % reduction

Year Canker Tree

prevalence survival 

1953 48.4 48.3

1956 59.9 70.5

1961 69.0 61.0

1966 39.4 67.5

1971 53.6 12.4

1987 7.1 44.9

1996 5.3 25.5

1998 0.6 48.3
9

Figure 2.—Trend in

the average number

of quaking aspen per

hectare by treatment

from 1951 to 1998.

HR = aspen

unthinned but hardwoods removed; C =

Control; THR = aspen

thinned and hardwoods removed; n =

number of plots.

Table 6.—Diameter at breast height (d.b.h.), height and volume of quaking aspen by treatment in 1987 and 1998; the statistics were computed using plot means as the raw data

Year D.b.h. Height Yield Yield Plots

1987 (cm) (m) (m3/tree) (m3 ha-1)

2

Trt1 Mean S.E. Mean S.E. Mean S.E. Mean S.E. (n)

C 22.9 0.663 23.2 0.417 0.589 0.059 307.6 30.18 10

HR 22.2 0.572 25.1 0.243 0.580 0.034 408.1 15.80 10

THR 24.4 0.441 24.0 0.369 0.610 0.033 314.8 17.20 20

1998

C 29.3 0.915 23.9 0.434 0.742 0.056 199.0 18.88 10

HR 27.6 0.515 24.0 0.404 0.648 0.031 261.4 16.43 10

THR 30.1 0.615 24.0 0.343 0.762 0.043 240.1 20.20 20

1C = Control; HR = aspen unthinned but hardwoods removed; THR = aspen thinned and hardwoods removed.

2Yield reductions in 1998 were the result of windthrow throughout the study site in May 1996. 
DISCUSSION

Study Design

The study design is clearly not optimal by modern standards, and for some people, raises the

question of whether reliable inference can be

drawn from the observed data. In the context of

experimental designs similar to this one, the

problem is often referred to as one of pseudoreplication (Hurlbert 1984). As described by

Hurlbert (1984), pseudoreplication is primarily

an issue of testing hypotheses using variances

that are inappropriately small. Such variances

might arise from samples being dependent

instead of independent or from samples being

embedded in larger treatment areas that are more

uniform within a treatment than across treatments. There are at least four reasons to conclude that our analyses are not particularly subject to pseudoreplication effects. First, the measurement plots were spaced far enough apart for

an assumption of independence to be reasonable.

(Trees within plots, on the other hand, were

clearly dependent subsamples.) Second, there

were no obvious differences in terrain, soil,

weather regime, etc., across the large treatment

areas that would affect Hypoxylon canker incidence, tree mortality caused by Hypoxylon

canker, or aspen growth. Third, the removal of

substantive plot-to-plot variation by the KoehlerWilson analysis technique demonstrates the lack

of inappropriate uniformity of response within

treatment areas. Fourth, the undesirable effect of

pseudoreplication is to increase the frequency of

finding significant treatment differences when

none actually exist. Even if our assumptions

about processes and independence are so wrong

as to affect the analyses, our conclusions are

more about the lack of differences or the lessening of differences over time—the exact opposite

of what would be expected from pseudoreplication. 

Impact of Thinning (THR)

Resource competition among shade intolerant

aspen suckers results in significant self-thinning

among aspen (Bella 1975). Consequently, it is

not surprising that the proportion of trees dying

from Hypoxylon canker was higher in the THR

plots than in the C or HR plots because thinning

removed trees that most likely would have been

lost over time to self-thinning. This implies that

even if precommercial thinning had no effect on

tree mortality caused by Hypoxylon canker the

ratio of trees dying from Hypoxylon canker compared with trees dying from other causes would

always be higher in the THR plots. Therefore,

this often-reported ratio cannot, on its own,

answer whether precommercial thinning causes

disproportionate tree mortality caused by

Hypoxylon canker. 

The hypothesized damage caused by Hypoxylon

canker should result in effects on tree density or

dimensions. At the end of this study, the THR

and C treatments had very similar tree densities

(fig. 2); furthermore, the mean dimensions of

individual trees were also very similar (table 6).

Consequently, the study’s original hypothesis that

thinning would result in greater damage from

Hypoxylon canker was not borne out. Rather,

tree mortality from Hypoxylon canker appears to

be just one of a number of interchangeable biological agents that, together with intraspecific

competition (self-thinning), reduce quaking

aspen stand density over time. Given the lack of

stand differences in tree size in the THR and C

treatments at the end of this study, this interchangeability of mortality factors extends to

equivalent effects on stand health and productivity. Although these conclusions differ from some

studies and from analyses reported earlier in the

lifespan of this study, they are similar to the conclusions reported by Pitt et al. (2001). It is possible that short-term effects occur, but by the time

a stand matures and is ready for harvest, any

short-term effects are no longer discernible.

Impact of Hardwood Removal (HR)

The HR treatment had the greatest number of

living trees throughout the study, producing a

clear yield advantage at the end of the 47 years

10
of observation. It also had the lowest prevalence

of Hypoxylon canker through the 1966 observation period. This may have been the result of

earlier natural lower stem branch pruning resulting from shading and thus the presence of fewer

potential infection sites (Anderson and Martin

1981, Ostry and Anderson 1979, Ostry and

Anderson 1998) than on trees in the THR and C

treatments. 

Aspen Clone Effects

Apart from treatment effects, the impact of plot

variability on canker prevalence and cankerinduced tree mortality was quite striking. The

apparent effect of thinning on canker prevalence

was much less when plot effects were included

in the analysis. Recall that each plot was in a single unique clone. We are not aware of any

research showing differences in the incidence or

severity of Hypoxylon canker on a set of common clones on multiple sites. Experimental evidence has, however, demonstrated varying levels

of resistance to Hypoxylon canker among common sets of aspen clones when challenged with

the pathogen in field and greenhouse tests

(Bucciarelli et al. 1998, 1999; Enebak et al. 1997,

1999). This leads us to believe that the high

interplot variability in canker prevalence and

canker-induced mortality (table 5) was primarily

due to clonal differences in canker resistance

rather than to site differences. The biological reasons for the observed decrease in clone effects on

canker prevalence after 1971 (tables 1, 5) are

unknown; however, the portion of plot variability in tree survival of diseased trees continued to

be large. This may be explained by the ability of

resistant clones to inactivate cankers by producing callus barriers (Ostry and Anderson 1998).

Given their magnitude, these clone effects should

be taken into account in future studies. The

definitive test of the effects of thinning aspen on

the prevalence of Hypoxylon canker would be to

evaluate the same clones across the various treatments to eliminate the confounding genetic

effects on disease susceptibility. 

LITERATURE CITED

Anderson, G.W.; Anderson, R.L. 1968.

Relationship between density of quaking aspen and incidence

of Hypoxylon canker. Forest Science. 14: 107-112.

Anderson, G.W.; Martin, M.P. 1981.

Factors related to incidence of Hypoxylon cankers in aspen

and survival of cankered trees. Forest Science. 27: 461-476.

Anderson, R.L. 1964.

Hypoxylon canker impact on aspen. Phytopathology. 54: 253-

257.

Barnes, B.V. 1969.

Natural variation and delineation of clones of Populus tremuloides and P. grandidentata in northern lower Michigan. Silvae

Genetica. 18: 130-142.

Bella, I.E. 1975.

Growth density relations in young aspen sucker stands. Info.

Rep. NOR-X-124. Edmonton, AB: Canadian Forestry Service,

Northern Forest Research Center. 12 p.

Blake, G.M. 1963.

Clone identification and delineation in the aspens. 107 p. St.

Paul, MN: University of Minnesota. Ph.D. thesis. 

Bruck, R.I.; Manion, P.D. 1980.

Interacting environmental factors associated with the incidence of Hypoxylon canker on trembling aspen. Canadian

Journal of Forest Research. 10: 17-24.

Bucciarelli, B.; Jung, H.G.; Ostry, M.E.;

Anderson, N.A.; Vance, C.P. 1998.

Wound response characteristics as related to phenylpropanoid

enzyme activity and lignin deposition in resistant and susceptible Populus tremuloides inoculated with Entoleuca mammata

(Hypoxylon mammatum). Canadian Journal of Botany. 76:

1282-1289.

Bucciarelli, B.; Ostry, M.E.; Fulcher, R.G.;

Anderson, N.A.; Vance, C.P. 1999. 

Histochemical and microspectrophotometric analyses of early

wound responses of resistant and susceptible Populus tremuloides inoculated with Entoleuca mammata (Hypoxylon mammatum). Canadian Journal of Botany. 77: 548-555.

11
Capony, J.A.; Barnes, B.V. 1974.

Clonal variation in the incidence of Hypoxylon canker on trembling aspen. Canadian Journal of Botany. 52: 1475-1481.

Day, M.W.; Strong, F.C. 1959.

A study of Hypoxylon canker on aspen. Michigan State

University. Agriccultural Experiment Station. Quarterly Bulletin.

41: 870-877.

Enebak, S.A.; Ostry, M.E.; Anderson, N.A.

1999.

Inoculation methods for selecting Populus tremuloides resistant to Hypoxylon canker. Canadian Journal of Forest Research.

29: 1192-1196.

Enebak, S.A.; Bucciarelli, B.; Ostry, M.E.; Li,

B. 1997.

Histological analyses of the host response of two aspen genotypes to wounding and inoculation with Hypoxylon mammatum. European Journal of Forest Pathology. 27: 337-345.

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Pseudoreplication and the design of ecological field experiments. Ecological Monographs. 54: 187-211.

Koehler, K.J.; Wilson, J.R. 1986.

Chi-square tests for comparing vectors of proportions for several cluster samples. Communications in Statistics: Part A.

Theory and Methods. 15: 2977-2990.

Ostry, M.E.; Anderson, G.W. 1979. Hypoxylon

canker incidence on pruned and unpruned aspen. Canadian

Journal of Forest Research. 9: 290-291.

Ostry, M.E.; Anderson, N.A. 1998.

Interactions of insects, woodpeckers, and Hypoxylon canker on

aspen. Res. Pap. NC-331. St. Paul, MN: U.S. Department of

Agriculture, Forest Service, North Central Research Station.

15 p.

Pitt, D.; Weingartner, D.; Greifenhagen, S.

2001. 

Precommercial thinning of trembling aspen in northern

Ontario: Part 2- Interactions with Hypoxylon canker. Forestry

Chronicle. 77: 902-910.

Rugg, D.J. 2003.

TableSim — A program for analysis of small sample categorical data. Gen. Tech. Rep. NC-232. St. Paul, MN: U.S.

Department of Agriculture, Forest Service, North Central

Research Station. 27 p.

Schlaegel, B.E. 1971.

Growth and yield of quaking aspen in north-central Minnesota.

Res. Pap. NC-58. St. Paul, MN: U.S. Department of

Agriculture, Forest Service, North Central Forest Experiment

Station. 11 p.

Schreiner, E.J. 1925.

Preliminary survey of Hypoxylon poplar canker in Oxford

County, Maine. Mycologia. 17: 218-220.

12
Ostry, M.E.; Anderson, N.A.; Rugg, D.J.; Ward, K.T. 

2004. Long-term response of precommercially thinned aspen clones to 

Hypoxylon canker. Res. Pap. NC-341. St. Paul, MN: U.S. Department of 

Agriculture, Forest Service, North Central Research Station. 12 p.

Reports response of precommercially thinned quaking aspen to Hypoxylon

canker across 47 years in northern Minnesota. Compares canker prevalence, tree

mortality, tree density, height, diameter, and volume among two thinned treatments (aspen thinned, other hardwoods removed; aspen not thinned, other

hardwoods removed) and a control (aspen not thinned, other hardwoods not

removed).

KEY WORDS: Populus tremuloides, Entoleuca mammata, Hypoxylon mammatum,

stem disease.

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MISSION STATEMENT

We believe the good life has its roots in clean air, sparkling water, rich soil, healthy economies and 

a diverse living landscape. Maintaining the good life for generations to come begins with everyday

choices about natural resources. The North Central Research Station provides the knowledge and

the tools to help people make informed choices. That’s how the science we do enhances the 

quality of people’s lives.

For further information contact:

Or visit our web site:

www.ncrs.fs.fed.us

North Central 

Research Station

USDA Forest Service

1992 Folwell Ave.

St. Paul, MN 55108