Forest Service 

Northeastern Forest 

Experiment Station 

Research Paper NE-687 

Sapstreak Disease of 

Sugar Maple: Development 

Over Time and Space 

David R. Houston 
Abstract 

Sapstreak disease is a potentially serious problem of sugarbushes and forest 

stands. It is caused by the fungus Ceratocystis virescens, which invades sapwood of 

roots and bases of stems through wounds created during logging, saphauling, or 

other activities. This report describes the results of observations and experiments to 

learn more about the patterns of disease development and the factors that affect 

them, within individual trees and within representative forests and sugarbushes. 

The Author 

DAVID R. HOUSTON is a principal plant pathologist conducting research on 

dieback and decline diseases at the Center for Northeastern Forest Health 

Research, a laboratory of the USDA Forest Service's Northeastern Forest 

Experiment Station at Hamden, Connecticut. For the past 30 years Dr. Houston's 

research has focused on stress-initiated dieback and decline diseases of deciduous 

hardwoods, especially beech, maple, and oak. 

Manuscript received for publication 20 April 1993 

The use of trade, firm, or corporation names in this publication is for the information 

and convenience of the reader. Such use does not constitute an official 

endorsement or approval by the U.S. Department of Agriculture or the Forest 

Service of any product or service to the exclusion of others that may be suitable. 

Acknowledgments 

Thanks are given to the New York State Department of Environmental Conservation 

and to the South Central Connecticut Regional Water Authority (formerly New 

Haven Water Co.), who provided land and trees, to numerous maple syrup 

producers--especially Howard Lyndaker of Beaver Falls, New York, and to the late 

Ralph Mantle of Harrisville, New York, who let us prowl, probe, and poke through 

their sugarbushes for over a decade. Special thanks are given to Bruce Schneider 

and Terry Podolski of the New York State Department of Environmental 

Conservation and to Eileen Mahoney, Chris Fagan, and Gerald Walton, U.S. 

Department of Agriculture, Forest Service, Hamden, Connecticut. Without their 

valuable assistance in surveys and experiments, and in statistical analysis, these 

studies could not have been conducted. I also wish to thank Eileen Mahoney, 

Manfred Mielke, Margaret Miller-Weeks, Barbara Burns, Lewis Staats, Louise 

Tritton, and Sumner Williams for their reviews of the manuscript. 

USDA FOREST SERVICE 

5 RADNOR CORP CTR STE 200 

PO BOX 6775 

RADNOR PA 19087-8775 

June 1994 
Contents 

Introduction ..................................... 1 

Background ..................................... 1 

Disease development in sugarbushes and forests ................ 2 

Discussion and conclusions ............................ 16 

lmportanceofwounds .............................. 17 

Importance of root disease pathogens ...................... 17 

Influence of methods of sap collection ...................... 17 

Influence of infection court location ........................ 18 

Influence of season ................................ 18 
Introduction 

During the course of our research to clarify the stress factors 

and organisms associated with dieback and decline diseases 

of sugar maple, we encountered several instances in which 

declining trees in managed forest stands and sugarbushes in 

northern New York had not been subjected to stresses 

usually associated with these problems.' The subsequent 

discovery that a number of these trees were affected by 

sapstreak disease suggested that this disease might be 

causing more loss than previously recognized, and that 

management practices were involved. 

Background 

Sapstreak disease of sugar maple (Acer saccharurn Marsh) 

is a vascular xylem disease incited by Ceratocystis virescens 

(Davidson) C. Moreau (=C. coerulescens (Munch) Bakshi). 

See Smith (1 990) for a nomenclature history of the sapstreak 

fungus. The disease was first noticed in North Carolina about 

1935 (Hepting 1944), then in Michigan in 1959 (Kessler and 

Anderson 1960), Vermont in 1964 (Houston and Fisher 

l964), isc cons-in in 1971 (Kessler l972), and New York in 

1978 (Beil and Kessler 1979). In each of these cases, the Figure 1 .--A thin crown with leaves much smaller than normal, 

disease occurred in stands where activities such as logging, the first indication that a sugar maple tree may have 

road building, or sap hauling had injured the affected trees. sapstreak disease. 

lniuries apparently allow C. virescens to invade and then kill 

the xylem of the lower portions of stems and roots where it 

creates the distinctive "sapstreak" stain (Hepting 1944, 

Ohman and Kessler 1963, Kessler 1978, Houston 1985). The 

common occurrence of the fungus as a saprophyte on freshly 

cut bolts of sugar maple and other northern hardwood 

species (Shigo 1962) suggests that in managed stands 

inoculum is readily available. 

The external syndrome begins with leaves that are small and 

off-color (Fig. I), continues through progressive stages of 

crown dieback, and finally ends in tree death. These stages 

may ensue rapidly with trees dying in 1-2 years or the stages 

may stretch over several years. Kessler (1 972) reported that 

no symptomatic trees recover. 

Inside the tree, the diseased wood of roots and lower parts of 

stems exhibis a distinctive stain (Fig. 2). Freshly exposed, 

the stained wood is greenish yellow to yellow-tan with red 

flecks and the wood appears watersoaked. Often, in cross 

section, the stain columns appear to radiate outward and are 

bordered by a thin, dark-green margin. Soon after exposure, 

the stained wood darkens dramatically, and later still, fades 

to a light brown. 

'~hese trees were brought to our attention by New York State 

Department of Environmental Consewation (NYSDEC) 

personnel, who earlier had confirmed the presence of 

sapstreak disease in a sugarbush tree (Beil and Kessler Figure 2.--The unique stain of the sapwood, which occurs 

1 979). most often in roots and lower stems. 
The studies reported here were conducted to learn more 

about the patterns of disease development and the factors 

that affect them, within individual trees and within 

representative forests and sugarbushes. 

Disease Development in Sugarbushes and Forests 

Observations were made annually for up to 11 years in three 

stands in northern New York ~tate.~ These included a 

sugarbush in Diana, a forest stand near Barnes Corners 

logged in early summer 1981, and a second forest stand, 

also near Barnes Corners, thinned in 1980. While the 

majority of observations were made in these areas, 

numerous sapstreak diseased trees in other sugarbushes 

and forest stands in New York and Vermont were also 

examined, sometimes several times, and records were made 

of symptoms, locations, and disturbance histories. 

Pafterns in the sugarbush. The Diana sugarbush, a 65-acre 

portion of a mature, pure sugar maple stand, has been in 

operation for about 75 years. Sap is collected by buckets 

(2,000 taps) and hauled by tractor-drawn wagons. Summer 

activity includes felling of diseased or weakened trees and 

hauling the resulting wood to be stacked near the sugar 

house. The disease was observed first in the Diana stand in 

1978 and affected a single tree located close to the sugar 

house.' A survey the next year located four additional 

symptomatic trees. Isolations from stained buttress-root 

tissues yielded C. virescens. 

In 1980, six study plots, each containing at least one 

symptomatic sapstreak-diseased tree, were established to 

observe the progress of disease within the symptomatic 

trees, to observe for patterns of "spread" from diseased to 

*In each of these stands at least, one sapstreak-diseased tree 

had been detected previously by NYSDEC personnel. 

healthy trees, and to monitor the appearance of symptoms in 

infected but initially asymptomatic trees. A seventh plot was 

established in 1982. Plots varied in size and shape $nd 

contained 15 to 32 trees. The locations of all plot trees > 4.0 

in (10 cm) diameter at 4.5 ft (1.4 m) (d.b.h.), dead trees and 

stumps, and woods roads were mapped. The d.b.h., crown 

class, general crown condition, and the presence or effects of 

insects and disease agents were noted. The distances from 

each tree to haul roads, sapstreak-diseased trees and 

stumps; and the location, size, and probable cause of any 

visible root or buttress wounds were recorded. 

In 1979, it was determined that sapstreak-stained wood 

characteristically was very low in electrical resistance (ER), 

(s 50 K ohms and often as low as 5-1 0 K ohms), compared to 

healthy tissue (1 00-700 K ohms), and that tissues infected by 

sapstreak disease reliably could be identified by their ER 

measurements (Table 1) (Houston and Schneider 1 982).3 At 

the outset, and periodically thereafter, ER of buttress-root 

wood was measured for each plot tree to detect the presence 

of stained tissue in otherwise asymptomatic trees. 

Measurements were made in up to four roots, one each on 

opposite sides of the tree, or until diseased tissue was 

encountered (Table 2). 

3~lectrical resistance was measured with a Shigometer 

(Model 02-67, Osmose Wood Preserving Co. of America, 

Inc., Buffalo, New York) and twisted wire probe (Shigo and 

Shigo 1974). The method utilizes the fact that as wood 

becomes discolored, cations increase in concentration and 

electrical resistance decreases (Tattar et al. 1972). Holes 0.1 0 

in (2.4 mm) diameter were drilled to depths of 1 to 2 in 

(2.5-5.0 cm) in up to four buttress roots on opposite sides of 

the tree. The probe was inserted and resistance readings 

taken at 0.25 in (0.63 cm) intervals. 

Table 1.--Comparison of electrical resistance (K-ohms) of buttress-root tissues of a 

healthy tree and a tree with sapstreak disease 

Electrical resistance (K-Ohms) - July 1980 

De~th finches) into root wood 

Root .25 .50 .75 1.0 1.25 1.50 1.75 2.0 

Healthy 1 180 190 210 290 260 230 240 200 

Diseased: 1 21 34 18 27 22 46 21 

Symptoms in 

1980 2 15 18 23 17 13 13 9 11 

Alive in 1981 3 80 80 70 80 70 -. 

4 100 80 70 90 50 60 
Table 2.--Electrical resistance measurements taken in 2 successive years on 

different sides of diseased tree 68 reveals the progression of the disease 

Depth (inches) into root wood 

Time of Side .25 .50 75 1.0 1.25 1.50 1.75 2.0 

measurement of tree 

July 1980 N 24 45 35 110 80 35 - 

(Symptoms in W 500 500 450 380 300 500 500 - 

extreme top) S 450 250 180 170 250 190 380 200 

E 40 100 130 150 110 110 190 80 

July 1981 N 55 60 70 60 55 65 

(Symptoms W 100 175 45 40 40 38 40 - 

same as 1980) S 140 180 280 280 210 220 220 190 

E 20 12 12 8 7 6 5 4 

Annually through 1990, the condition of each plot tree was 

noted. When possible, photographs were taken of each 

diseased tree to provide a visual record of symptom 

progression. Each year the sugarbush, in general, was 

surveyed to detect any additional trees with crown symptoms. 

If such trees also possessed ER measurements and stain 

patterns characteristic of sapstreak disease, their locations in 

the stand were mapped and their conditions were followed 

annually until they died or were cut by the sugarbush owner, 

Results. Locations of the plots and diseased trees are shown 

in Figure 3. Over the course of this study, 19 trees in the 

study plots (Table 3) and 4 outside the plots developed foliar 

and crown symptoms or the characteristic stain of 

buttress-root wood and were confirmed as having sapstreak 

disease. Trees in all crown classes were affected and ranged 

in size from 7.0 to 43.6 in (18 to 11 1 cm) d.b.h. Most trees 

were located within 5 ft (1.5 m) of haul roads, although three 

were 10 ft (3.1 m) away. 

Although diseased trees often occurred and persisted as 

isolated individuals (Fig. 3: plots 1, 2, 4, 5), there were 

several cases where healthy trees relatively close to 

diseased trees became symptomatic (Fig. 3: plots 3, 6,7). 

For at least two of these cases (Figs. 4, 5), it is quite 

probable that other diseased trees had occurred earlier as 

descriptions provided by the sugarbush owner suggested 

strongly that many of the stumps present in these areas were 

of trees affected by sapstreak. 

Access roads and haul roads dissected the sugarbush, and 

depressions revealed the locations of many additional old 

roads no longer used. Most diseased trees possessed 

obvious and severe butt and root injuries attributable to 

equipment used in hauling sap or skidding logs. However, six 

trees bore no visible injury. Five of these were within 6 ft (1.8 

m) of a road; the sixth tree, located 10 ft (3.1 m) from a major 

access road, was determined later to be connected by root 

grafts to an asymptomatic diseased tree 0.5 ft (0.1 m) from 

the road (Fig. 6). The possibility of root-graft transmission 

Plot 3 

100 

- 

feet 

Figure 3.--Locations and years symptoms were first 

observed, of sapstreak-diseased trees (black dots), and 

stumps (circled dots), in and near study plots in a Diana, New 

York, sugarbush. Main access and sap hauling roads 

(dashed lines) lead to the sugarhouse adjacent to Plot 6. 
ble 3.4atterns of symptom expression in 19 sapstreak-diseased trees in a New York Sugarbush, 1979 to 1990 

Year Distance (ft) to: 

Plot Tree D.b.h. First Dead, Recovered Diseased Associateda 

no. no. (inches) symptoms cut (remission) Road tree root rots 

1 1 15.7 1979 1984 2.5 234 

2 32 17.6 1979 1981 3.5 23 

3 5 1 12.5 1984 4.0 

(ERA 980)~ 

7 120 26.3 1982 1985 10.0 7.0 123 

121 15.6 1988 3.0 

128 14.9 1983 1986 0.5 

(ER: 1 982) 

133 12.9 1983 4.0 1 .O 

(ER: 1 982) 

134 17.9 1983 1988 0.5 

IER:1982) 

al : Armillaria sp. 

2: Xylaria sp. 

3: Hypoxylon deustum 

4: Ganoderma applanatum 

b~lectrical resistance measurements in the given year 

were indicative of sapstreak. 

was explored later in a separate study (see inoculation trial 

5). Although roadways in this sugarbush were not excavated 

to determine if adjacent diseased trees had roots that 

extended beneath the road and had been wounded, we 

observed this to be the case in several forest stands 

elsewhere. Buttress-root injuries often were nearly closed 

over by callus by the time foliage symptoms first appeared. 

in this sugarbush some of the major access roads had been 

used earlier for skidding logs. In wet areas, especially on 

slopes, skidders caused deep ruts and injured and exposed 

roots. Plot 3 (Figs. 3,4), where sapstreak was severe, 

encompassed a road deeply rutted during the skidding. 

Sapstreak disease also was severe near the sugarhouse 

(Figs. 3,5: plot 6). Over the course of this study, nine trees in 

this plot developed symptoms. Although trees in the 

sugarhouse area suffered the most traffic-related injuries, 

other factors (including a possible buildup of the pathogen on 

wood from diseased trees stacked near the sugarhouse) also 

may have contributed to infection of nearby wounded trees. 

Patterns in forest stands. Disease development was followed 

in two forest stands on the Tug Hill Plateau near Barnes 

Corners, New York. The first of these (stand 1) was a red 

maple-sugar maple-ash stand (basal area: 120 $/acre; 25 

percent sugar maple), a portion of which had been harvested 

for sawlogs in early summer of 1981. The second (stand 2) 

was a sugar maple-beech stand (basal area: 131 fiacre; 80 

percent sugar maple) thinned during 1980. 

In stand 1, skid trails radiating from the log landing site were 

numerous and deep. A survey in 1984 disclosed 25 trees 

with crown symptoms, stain, and ER readings characteristic 

of sapstreak. Two additional trees developed crown 
Sapstreak tree 

suspect sylslreak stump 

Sapslreak slump 

Figure 4.--Study Plot 3 in the Diana, New York, sugarbush. 

The enlarged section of roadway (within dashed lines) was 

deeply rutted during logging in 1975-1 976. Dates represent 

years crown symptoms or electrical resistance (ER) 

measurements revealed sapstreak. "Suspect" stumps are of 

trees whose descriptions suggest disease. 

Plot 6 * Healthy tree 

0 Diseased tree 

O Stump 

Stump, sapstreak 

0 10 20 30 

feet I 

Figure 5.--Study Plot 6 in the Diana, New York, sugarbush. 

Numbered trees (larger solid circles) became diseased during 

the decade of observation (1 980-1 990). 

- U 0 

10 feet @ Sapstreak tree 

Stump 

Figure 6.--Study Plot 7 in the biana, New York, sugarbush. 

The diseased tree (large arrow), which first showed 

symptoms in 1982, had no discernible root or buttress 

wounds. Soil excavations revealed that its roots were grafted 

to the severely wounded and infected tree adjacent to the 

road (small arrow). 

symptoms by July 1985. All of these trees were adjacent to 

skid trails (Fig. 7) and all bore severe buttress or root 

wounds, or both. No diseased trees were found in 

nontrafficked portions of the stand. 

Other trees, in areas where the stand was opened severely 

and where water tables were high, also exhibited crown 

dieback, but lacked the internal sapstreak stain. While some 

of these trees had basal injuries, most did not, and many 

were not situated adjacent to skid trails. A few of these trees 

died during the observation period, but many recovered as 

they adjusted to the changed stand environment. 

Twenty of the twenty-seven sapstreak diseased trees in this 

stand (1 0 in October 1984, 10 in May 1986) were felled and 

sawn into boards to determine the internal patterns of 

colonization (stain), the association of C. virescens with the 

stain, the persistence of C. virescens in air-dried lumber, and 

the appearance of diseased wood as it dried (Houston 1986). 

Six of the remaining seven diseased trees were dead by 

October 1985. All of these also were heavily colonized 

subcortically at their root collars by Armillaria sp. 

In stand 2, sapstreak-affected trees were scattered over the 

30-acre area (Fig. 8). Relatively few (1 2) symptomatic trees 

were discovered, and although they occurred on both upland 

and lower sites, five of them were concentrated in one lower 

and wetter area. Four diseased trees without obvious 

buttress or root wounds were residual members of sprout 

clumps. Stumps created when the sprout members were 

removed apparently served as infection courts; similar cases 

were found in two other New York stands where released, 

but otherwise unwounded, sprout members were affected by 

sapstreak disease. 
Sapstteak diseased 

trees 

15 

u 

50 feet 

Figure 7.--Locations of sapstreak-diseased trees in forest 

stand 1 near Barnes Corners, New York, a portion of which 

was logged in 1981. 

Patterns within individual sugarbush and forest trees. Within 

individual trees, the appearance of initial crown symptoms 

and the rate of their progression varied greatly (Table 3). 

Some trees with severe crown dieback, including some with 

but a few branches alive, survived for 5-6 years before they 

died, while others became symptomatic and succumbed 

rapidly, often within 2-3 years. Repeated measurements of 

ER on some individual trees revealed the progression of the 

disease. The pattern of development from July 1980 to July 

1981 within the root system of tree 68 is shown in Table 2. 

Several very severely affected trees were harvested by the 

owner before they died. Disease progression, as revealed 

externally by crown symptoms and internally by ER 

measurements or root dissections, was arrested, and 

recovery ensued in several symptomatic trees (two with z 40 

percent crown dieback). At least three trees in the 

sugarbush, and two in forest stand 2, with root-stain patterns 

and ER measurements characteristic of sapstreak disease 

never developed severe crown foliar symptoms during the 

course of the study. 

Usually, the first observed symptom of sapstreak was a 

distinctive "transparency" of the tree crown--a consequence 

- Tree with sapstreak 

@-Dead tree, 1990 

So - Tree with "stump" wound 

LOW. wet area ! ./' 

I 

Low, wet area I I 

I ! - 

100 m 

&id trail; -. '.! 1 

Road 1 

Figure 8.--Locations of sapstreak-diseased trees in a 30-acre 

portion of forest stand 2 near Barnes Corners, New York. The 

stand was thinned in 1980. 

of the presence of unusually small leaves, especially in upper 

branches, but sometimes over the entire crown (Fig. 1). 

Often, these small leaves were normal in color, shape, and 

number the first year, but became off-colored and sparse in 

subsequent years. Branch dieback often occurred where 

small leaves appeared the previous year, and this pattern of 

small leaves one year followed by death of supporting twigs 

and branches the next sometimes continued for several 

years until the tree died. Sometimes, however, symptom 

progression was arrested and resulted in trees with upper 

branch dieback or even major stagheading and lower 

branches fully foliated with leaves of normal size and color. 

While some of these trees apparently recovered with no 

further disease progression, others, after several years of 

apparent remission, again exhibited symptoms. 

External symptoms were related closely to development of 

internal stain. Stain columns were well established, 

especially in root tissues, by the time crown symptoms 

appeared. In many trees, especially those in remission of 

crown symptoms, stain columns appeared to be contained by 

newly formed rings of healthy sapwood. 

Associated organisms. In the sugarbushes and forest stands 

studied here, and in many others as well, trees dying of 

sapstreak disease also were almost always colonized at their 

roots or root collars by the root disease pathogens Armillaria 

sp., Xylaria sp., or, rarely, both (Table 3). This association 
was noted by Hepting (1 944). Although their actual role in the 

disease has nbt been demonstrated, it is likely that these 

fungi contribute significantly to the death of affected trees. 

Their consistent presence on dying trees and their apparent 

absence from severely affected but recovering trees 

suggests that their attack may determine which 

sapstreak-affected trees die or recover. 

Severely affected trees often were attacked, sometimes 

heavily, by one or two species of Ambrosia beetles. These 

attacks usually were concentrated, at least initially, near the 

buttress roots and lower bole. What role, if any, these insects 

or their fungal associates play in the disease is not known, 

but their appearance in later stages of disease development 

suggests that they probably are not vectors of C. virescens, 

but may hasten the demise of severely diseased trees. 

Patterns within artificially inoculated trees and saplings. The 

preceding observations revealed much about the patterns of 

occurrence of diseased trees and of the factors that 

contributed to them. A considerable amount was learned 

about the progression of the disease within symptomatic 

trees. Even so, many questions pertaining to stand 

management remained unanswered. Some of these 

questions were addressed in a series of inoculation trials that 

were conducted with saplings and trees to provide 

information needed for developing management guidelines. 

Speclcally, these studies attempted to determine: 

The nature and rate of symptom expression and disease 

development in saplings and trees beginning with the first 

infection, 

If trees are more susceptible or vulnerable to the disease at 

different seasons of the year, 

* If the common stress factor, defoliation, directly influences 

susceptibility or vulnerability to sapstreak, 

If the rate or extent of sapwood colonization is affected by 

the nature (orientation) of the wound, 

*If sapstreak disease can spread through root grafts, and 

If tapholes serve as infection courts for C. virescens. 

The nature of symptoms, the rate of disease development, 

and the relationship of season of infection and of defoliation 

stress to susceptibility and vulnerability were addressed in 

Trials, I, II, and Ill; the influence of wound orientation on 

disease development within individual trees in Trial IV; the 

spread of the pathogen through root grafts in Trial V; and the 

role of tapholes vs. buttress-root wounds as infection courts 

in Trial VI. 

TRIAL I (Symptom development, rate of disease 

development, season of inoculation vs. susceptibility and 

vulnerability) 

Materials and Methods. Two groups of saplings 2-4 in 

(5-1 0.2 cm) in diameter were used. The first group was 

growing in the understory near the edge of a stand of 

pole-size maple trees in southern Connecticut. This group of 

saplings was composed of single stems of seedling origin. 

The second group, growing about 50 ft (1 5 m) from the first, 

consisted of double stems of sprout origin that developed 

after a portion of the seedling grove was cut and thinned 

approximately 10 years earlier. The pole-size trees used in 

trial I were scattered within the stand and ranged in size from 

7.5 to 10.0 in (1 9.0-1 5.4 cm) in diameter and were of 

intermediate or codominate crown class. The stand 

containing the trees and saplings used in Trial I was 

defoliated severely by gypsy moth (Lymantria dispar) in the 

summer of 1981. Although not observed, it must be 

presumed that the maples used in these studies had been 

defoliated to some degree. 

lnoculum for these and subsequent trials was prepared by 

growing isolates of C, virescens obtained from sapstreak 

diseased trees on a sterile wheat grain medium for 10-1 4 

days.4 Groups of 10-20 saplings or sprouts were inoculated 

in November 1981 (1 O), May (20) and November (1 0) 1982 

and June 1983 (20) by forcing inoculum into a 0.375-in 

(0.95-cm)-diameter hole drilled horizontally nearly through 

the stem at 6 in (15 cm) above ground. Bark and drill bit were 

sterilized before drilling by scrubbing or dipping with 95 

percent ETOH. Drill holes, filled with inoculum or with sterile 

wheat grains for controls, were covered with masking tape. 

One member of each sprout clump was treated similarly. 

Fifteen pole-size trees were inoculated in May 1982 and 10 

more in June 1983 by forcing inoculum or sterile grain into 

two 0.375-in (0.95-cm)-diameter holes drilled 2 in (5.1 em) 

deep into buttress roots on opposite sides of the tree. 

TRIAL I1 (season of inoculation vs. susceptibility and 

vulnerability) 

* Materials and Methods. Beginning 1 July 1983, groups of 10 

saplings each, growing in the understory of a second stand, 

were inoculated as above at intervals of approximately 2 

weeks (1 July through 18 October 1983; 5 March through 3 

July 1984) or of 4 weeks (10 November 1983 through 5 

March 1 984). 

For both trials, all inoculated plants were examined for 

symptom expression and disease development at least once 

each growing season through 1990. ER measurements were 

made in buttress roots or lower stems of all trees with 

symptoms. Stems and buttress roots of all trees, and of 

representative saplings and sprouts that died, were dissected 

to determine the internal patterns of disease. Isolations were 

attempted from the tissues of all the pole-size trees that died. 

For saplings and sprouts, however, re-isolation attempts 

were made only for those that died shortly after inoculation. 

In saplings and sprouts that died more than a year after being 

4l 00 gm wheat grain in a 250-ml Erhlenmeyer flask 

moistened with enough water to equal the volume of wheat; 

flasks were plugged with cotton and autoclaved at 15 psi for 

25 minutes. 
inoculated, sapstreak-killed tissues usually were too decayed 

to support the pathogen. 

Results. In Trial I the rates of disease development, 

expressed as onset of foliar and crown symptoms and the 

occurrence of mortality, varied markedly with tree size 

(saplings and sprouts vs. pole-size trees), season, and year 

of inoculation. Moreover, the nature of symptoms between 

trees of the same inoculation series also was remarkably 

varied. 

Nine of twenty saplings and 7 of 20 sprouts inoculated in May 

1982, died within 1 year, and of these, six of each group 

exhibited complete wilt and death within 2 months. 

Proportionately fewer saplings or sprouts inoculated at other 

times during this trial developed symptoms and died (Fig. 9). 

In contrast, none of the 15 pole-size trees inoculated in May 

1982, developed symptoms before leaf drop in 1982. 

However, by 18 months, six of these trees had developed 

crown symptoms and died. One of these trees did not leaf 

out in 1983, one flushed and then died suddenly in June, and 

another, which flushed normally, became increasingly 

chlorotic, then brown, and died in August. Two more of these 

trees had died by 1990. 

Only 2 of 60 non-inoculated mem.bers of sprout clumps died 

even though they shared a common, and sometimes 

infected, root system. And, in contrast to the single-stem 

saplings, which continued to die through 1990, mortality 

among sprouts occurred only during the first 4 years after 

inoculation (Fig. 9). 

Dissection of saplings and trees that died or possessed 

severe symptoms revealed extensive invasion of rocits and 

often of stems by C. virescens. In most trees, vascular 

staining was present in, and the fungus was recovered from, 

xylem tissues in upper portions of stems often to 30-45 ft 

(1 0-1 5 m) above ground. As in naturally infected trees, dead 

or dfing inoculated saplings and trees were attacked 

severely by Armillaria or Xylaria, or both. Also, as in naturally 

infected trees, inoculated trees and saplings dying of 

sapstreak frequently were infested, sometimes heavily, by 

one or more species of Ambrosia beetles. Attacks were 

concentrated primarily at the bases of the trees near, and 

especially below, the points of inoculation. Occasionally, 

however, these attacks occurred higher up the stems into 

streaks of sapstreak-killed xylem tissue that were close to the 

cambium. 

In Trial II mortality patterns of saplings inoculated at different 

times during the season (July 1983 to July 1984) suggest 

that trees may be more susceptible or vulnerable to infection 

and disease development at particular times of the year 

(Figs. 10, 11). 

r\ 100 

tR - 90 -- 

0 Trees 1990 a 

8 80 -- 

O -- Saplings 1990 

Sprouts 1987 

60 -- 

% Controls 

a Trees inoculated May 1982 

and June 1983 only 

No eontrols died 

NOV. 81 MAY 82 NOV. 82 JUNE 83 

INOCULATION DATES 

Figure 9.--Percent of saplings, sapling sprouts, or pole-size trees that died in 1987 and 1990 following 

inoculation on four different dates. Ratios indicate number died of number inoculated. 

8 
Mortality was highest (from 5 to 8 of 10) among each of the 

four sapling groups inoculated from early July through 

midAugust 1983, was lowest (from 0 to 3 of 10) among the 

four groups inoculated from late August 1983 through early 

April 1984, and then increased (with two exceptions) to from 

4 to 5 of 10 in groups of trees inoculated from mid-April to 

early July 1984 (Fig. 10). The somewhat lower death rate 

among trees inoculated during 1984 compared to 1983 may 

reflect, at least in part, the 1-year shorter observation period 

given this group. When the 200 saplings were sorted into five 

groups of seasonal inoculation times, mortality patterns 

ranged from a low of 2.5 percent (1 of 40) in winter months to 

a high of 52.5 percent (21 of 40) in the summer (Fig. 11). 

TRIAL Ill (Defoliation stress vs. susceptibility and 

vulnerability). The high mortality rate among trial I saplings 

and trees inoculated in May 1981 (Fig. 9), the first and 

second growing season after they had been defoliated 

severely by gypsy moths, prompted a trial to determine if 

defoliation stress before or after inoculation with C. virescens 

increased sapling and tree susceptibility or vulnerability. 

Materials and Methods. Eighty saplings, 2-3 in (5-7.6 

diameter, growing in a more open portion of the same 

utilized in Trial II, were inoculated with wheat grain ino 

as described in Trial 1; 40 on 15 May 1985, and 40 on 2 

April 1986. Half of both groups were defoliated completely by 

hand on 14 June 1985 (a time chosen to reflect the period of 

peak defoliation activity by the gypsy moth). 

Results. The mortality of the trees in each of the four groups 

of 20 saplings through 1991 is shown in Figure 12. By August 

1990, more of the saplings inoculated in May 1985 had died 

(1 6=40 percent) than those inoculated a year later (6=15 

percent). No additional tr'ees succumbed in 1991. Defoliation 

had no effect on mortality rates for the trees inoculated in 

1985--equal numbers of trees died in each category. For 

those trees inoculated in 1986, however, only one of the 

Mortality by end of 

INOCULATION DATES 

Figure 10.--The pattern of annual mortality within 20 groups of 10 saplings, each inoculated 

at biweekly or monthly intervals from July 1983 to July 1984. 
I I Years after inoculation 

- Nov-Feb Mar-April May-June July-mid Aug Late Aug-Oct 

INOCULATION PERIODS 

Figure 11 .--The pattern of cumulative mortality, by years after inoculation, among five 

groups of 40 saplings inoculated at five different seasonal periods. 

Inoculated 15 May, 1985 0 no defoliation 

Inoculated 15 May, 1985 

defoliated 14 June, 1985 

Inoculated 28 April, 1986 

no deFoliatim 

Inoculated 28 April, 1986 

defolialed l4 June, 1985 

DATES OBSERVED 

Figure 12.--Percent mortality over time, within two groups of 20 defoliated, and two groups 

of 20 nondefoliated saplings inoculated with C. virescens. 
defoliated trees died compared to five of the nondefoliated 

series. Apparently, defoliation has no direct effect on 

resistance to C. virescens. 

TRIAL IV (Wound orientation vs, pattern of disease 

development within individual trees). In a number of earlier 

studies, dissection of sapstreak-diseased trees revealed that 

the patterns and extent of sapstreak discoloration within 

individual trees varied considerably (Houston 1991, 1986, 

1985). The extent of discoloration and decay within living 

trees following wounding is known to be related, in part, to 

the ability of trees to compartmentalize wounded tissues. 

One factor that influences this ability is the orientation of the 

wound relative to natural barriers within the tree, especially 

those created by annual rings and vascular rays (Shigo 1977, 

1979). A small study was conducted to determine whether 

orientation of infection courts affects the pattern and extent of 

sapstreak development within individual trees. 

* Materials and Methods. In July 1988, 10 trees,, 4-6.7 in 

(1 0-1 7 cm) d.b.h., were inoculated with C. virescens. Wheat 

grain inoculum was introduced into increment borer holes. 

One hole made at 4.5 ft (1.4 m) was oriented radially, through 

the pith center and thus intersected relatively few vascular 

ray boundaries. The second hole, made at 3.25 ft (1.0 m) and 

oriented tangentially to the pith, intersected and thus 

disrupted nearly all of the vascular rays on one side of the 

tree. 

Five of the ten trees were harvested after 1 year (7 June 

1989), and five after 2 years (25 July 1990). Stems were 

sectioned at 4- or 8-in (10 or 20 cm) intervals from ground 

line through each of the inoculation wounds and above until 

stain columns disappeared. Photographs made of the ends of 

sections were used to characterize the cross-sectional 

patterns and linear extent of stain associated with each 

inoculation wound. The heights of the stain columns were 

rounded to the nearest 2 in (5 cm). 

Results. None of the inoculated trees developed foliar 

symptoms before they were harvested. The extent and crosssectional patterns of the stain columns resulting from 

invasion by C. virescens varied considerably between trees 

(Table 4). Columns associated with the tangentially oriented 

wounds generally were greater, both in cross section and in 

linear extent than those associated with radially oriented 

wounds. In a few trees, these differences were striking (trees 

5, 6); while in some, (trees 3, 4, 10) the columns were limited 

in development regardless of wound orientation. 

The dramatically greater colonization in this study of wounds 

that disrupted more of the tree's pre-established 

compartment barriers suggests that the type of wounds 

created in logging or sap hauling can influence disease 

incidence and severity in a major way. 

TRIAL V (Root graft transmission of C. virescens). As 

mentioned previously, a few of the sapstreak-diseased trees 

observed did not possess the usually obvious root or lower 

stem wound infection courts. Observations in permanent 

plots (Figs. 6,7) suggested that some of these trees may 

have become infected when the fungus moved into their 

roots across root grafts with adjacent diseased trees. An 

experiment was conducted to determine if root-graft 

transmission does occur and if so, whether it is an important 

consideration in management of this disease. A preliminary 

report has been published (Houston 1991). 

Materials and Methods. In 1987, 4 0 pairs of healthy 

pole-size sugar maples growing in forest stand 1 near Barnes 

Corners, New York, were selected for the study. Members of 

each pair were growing in close proximity (6 to 10 ft, 1.8 to 

3.1 m) and, as revealed by careful excavation, were 

connected by presumably functional root grafts. Electrical 

resistance (ER) measurements were made (Shigometer with 

twisted wire probe) in the roots on both sides of the graft as 

well as in the major buttress roots of the trees to assure that 

they were healthy at the time of inoculation. In July 1987, one 

tree of each of five pairs of trees was inoculated with C. 

virescens. Inoculated roots included the grafted root and all 

major buttress roots. The second group of five pairs was 

treated similarly in July 1988. 

A conidial isolate of C. virescens selected for its tolerance to 

2 pprn MBC (benomyl), obtained originally from diseased 

tissue (tree 1, plot 1, Fig. 3), was used. Use of this marked 

isolate made it possible to determine later whether infection 

and colonization had resulted from our inoculations or from 

natural "wild" inoculum. lnoculum consisted of 2-week-old 

cultures grown on and mixed thoroughly with a wheat grain 

substrate. 

Bark surfaces were scrubbed briefly with water to remove dirt 

and then with 95 percent ETOH (ethyl alcohol). When dry, 

0.25-in (036cm)-diameter drill holes 2 in (5.1 cm) deep were 

made and filled with inoculum. Drill holes were covered with 

masking tape. Sketches were made of the excavated roots 

and inoculation points before roots were covered with soil 

and loose litter (Fig. 13). 

In June 1990, the root systems of both trees in each pair 

were re-excavated, then dissected to determine the extent of 

infection and colonization. Root samples were taken for 

re-isolation of the pathogen where ER measurements or stain 

patterns, or both, suggested that the fungus had moved 

across the grafts. When stain columns extended above 

stump height, trees were felled and dissected to determine 

the height of the stain columns. 

*Results. Results are presented in Table 5 and Figure 13. 

Eight of the ten inoculated trees of each pair were infected 

(determined by crown symptoms, ER measurements, 

characteristic stain, and re-isolation, or both (Table 5)). In 

three of these cases, C. virescens moved across the root 

grafts to the uninoculated member of the pair (Table 5, Fig. 

13) (determined by crown symptoms, ER measurements, 

stain patterns, and re-isolation and growth of the marked 

isolate on malt agar amended with 2 ppm benomyl). Grafts 

between three of the remaining infected and uninoculated 

pairs were found to be nonfunctional. 
Table 4.--Comparison of the pattern and extent of colonization by C. virescens of stem tissues, 

wounded radially or tangentially 

Height of stain above 

Tree D.b.h. Date Radial Tangential 

No. (cm) harvested wound (cm) wound (cm) staina 

1 11.2 6/89 65 85 + + + (both somewhat 

limited) 

2 9.9 6/89 55 55 + + + + 

3 10.2 6/89 35 35 + + (both quite limited) 

4 10.3 6/89 35 45 + + (both quite limited) 

5 12.8 6/89 35 85 +++++ 

Average (1 year) 45 61 

6 15.5 7/90 95 105 +++++ 

7 17.2 7/90 ? ? ++++ 

8 14.5 7/90 70 90 ++++ 

9 10.5 7/90 50 85 +++ 

10 11.6 7/90 25 25 + (both strongly limited) 

Average (2 years) 60 76 

aThe relative amount of cross-sectional areas discolored: tangential wound site vs. radial wound site: + indicates 

discolored area around tangential wound; + + + indicates approximately three times greater than around radial wound. 

Not inoculated 

View from above 1 Inoculated 

July. 1987 I 

- Side view 

-0.5 0 0.5 1 .O 1.5 2.0 2.5 

DISTANCE (METERS) 

Figure 13.--A representative diagram of two sugar maple root 

systems showing location of potential root grafts between the 

systems, the points of inoculation on one of the tree's roots, 

and the pattern of discoloration caused by C. virescens 

following its introduction. 

in others was extensive with stain columns extending several 

m in length. In two of the three tree pairs in which graft 

transmission occurred, infections within the inoculated trees 

were less extensive than within the trees to which they 

spread (Fig. 13). The variable response by individual trees to 

inoculations made on the same day in the same way, and 

with the same inoculum, supports results of others (Shigo et 

al. 1977) that the ability of trees to compartmentalize injuries 

and infection by fungi is under strong genetic regulation. 

The results of this experiment showed that root grafts 

between trees growing in close proximity can serve as 

conduits for the sapstreak pathogen. However, the relatively 

low occurrence of transmission in this study, together with 

the low incidence of diseased pairs and of nonwounded 

diseased trees in nature, suggest that infection through root 

grafts is much less important than direct infection through 

wounds above ground. 

TRIAL VI (Tapholes vs. buttress wounds as infection courts 

for C. virescens). The relatively high incidence of sapstreak 

in some sugarbushes prompted a study to determine if 

tapholes serve as infection courts and if so, how important 

are they compared to other wounds inflicted during sap 

hauling or other activities. A preliminary report has been 

published (Houston 1992). 

Materials and Methods. In 1984,34 groups of 10 

intermediate-codominant sugar maples, 6-8 in (15-20 cm) 

d.b.h. growing in a 15-acre stand near Barnes Corners, New 

York, were wounded and inoculated as follows: 

Dissections revealed that disease development within the Treatment 1 (One open taphole and one taphole with a metal 

inoculated trees varied greatly (Table 5). Thus, infection did spout): At one of two dates (1 4 March, 17 April), two 711 6-in 

not occur at all in two trees; colonization was strongly (0.43-cm)-diameter tapholes, 2.0 in (5.0 cm) deep, were 

restricted and extended only a few cm in others; colonization made on opposite sides of the trees. One taphole (chosen at 
Table 5.--Infection success, rates (extents) of colonization, and movement across root grafts in trees 

inoculated with C. virescens 

ER (K-Ohms) Infec- Cross- Height 

Year tion over of stain 

Pair Tree inoc. 1988 1 989 1990 (+,-I (+,-I (cm) Remarks 

1 Inoc. 1987 

N-lnoc. 

2 I 1987 

NI 

dead 

15-50 

27-1 90 

40-1 00 

60-1 90 

90-1 40 

16-30 

40-50 

20-30 

70-200 

10-70 

990-1 70 

6-1 8 

150-250 

6-1 08 

1 30-1 40 

83-250 

176-235 

186-300 

Crown symptoms - 

l988,l989,l99O 

Crown symptoms - 1988 

No symptoms 1989, 

1 990 

No infection 

No symptoms - 1988 

Symptoms on 1,1989, 

and on both in 1990 

lnfection did not move 

into graft root 

Nonfunctional graft 

lnfection reached graft 

but no cross-over 

lnfection well contained 

lnfection well contained 

No infection 

random) was left open; a standard metal spout was inserted 

in the other. Both tapholes subsequently were inoculated by 

atomizing into them 2 rnl of a conidial suspension of C. 

virescens containing 150,000 to 600,000 spores per ml Controls consisted of trees with non-inoculated tapholes. Groups 

of 10 trees each were inoculated once, either when tapped or 

at weekly intervals thereafter, until 31 May (Table 6). 

Treatment 2 (Closed tapholes--plastic spouts with tubing): 

Tapholes were made in six groups of 10 trees as described 

above and plastic spouts fitted with 12-in (30cm) lengths of 

plastic tubing were installed in both tapholes. The tubing was 

clipped back onto the spout to form a loop. Sap-filled loops 

sewed to maintain a closed system characteristic of tubing 

systems. Tapholes were inoculated as above immediately 

after spouts were removed on 2 or 31 May (Table 7). 

Controls were tapped but not inoculated. 

Treatment 3 (Buttress root injuries): On different groups of 10 

trees each, two buttress roots, one each on opposite sides of 

the tree, were injured at approximately weekly intervals 

(Table 8) by bruising them with a heavy mallet. On one bruise 

the bark was removed; on the other the bark was broken and 

loosened but not removed. Approximately 2 ml of the 

previously described spore suspension were atomized onto 

the wounds immediately after they were made. Control trees 

were injured but not inoculated. 

Table 6.--Schedule of wounding and Inoculation, and 

resulting infection for trees inoculated with 2 ml conidlal 

suspension into one taphole with metal spout and one 

open taphole 

Treatment 1 

Number trees Number 

Date tapped 

(1 984) 

1 4 March 

Date inoculated 

(1 984) 

14 March 

19 March 

26 March 

9 April 

2 May 

31 May 

Controls 

harvested 

(1 989-90) 

5 

5 

5 

5 

5 

5 

5 

tapholes 

infected 

0 

0 

0 

0 

0 

0 

0 

17 April 17 April 5 0 

23 April 5 1 

2 May 5 0 

31 May 5 0 

Controls 5 0 
Table 7.--Schedule of wounding and inoculation and 

resulting infection for trees inoculated wlth 2 mi conidial 

suspension in each of two tapholes with plastic spouts 

and tubing 

Treatment 2 

Number trees Number 

Date tapped Date inoculated harvested tapholes 

(1 984) (1 984) (1 989-90) infected 

14 March 2 May 5 0 

31 May 5 0 

Controls 5 0 

17 April 2 May 5 0 

31 May 5 0 

Controls 5 0 

Treatment 4 (Root injuries): One group of 10 trees was 

treated on 31 May by atomizing a spore suspension onto ax 

cuts made on an excavated root approximately 2 ft (0.6 m) 

from the tree. The root was then covered with forest floor 

litter. Control trees similarly were injured but not inoculated. 

Treatments 5 and 6 (to check on the pathogenicity of the 

inoculum isolate used (Table 9)): In treatment 5 groups of 10 

trees each were inoculated on 14 March, 17 April, or 31 May 

by forcing wheat-grain inoculum into two 0.25-in-diameter 

holes drilled 2 in deep into buttress roots on opposite sides of 

the tree. Holes were covered with masking tape. In treatment 

6, one group of 10 trees was inoculated on 31 May by filling 

the drill holes with the conidial suspension used to inoculate 

tapholes and buttress bruises. 

Annually, from 1985 through 1989, each tree was observed 

for presence of foliar symptoms or other evidence of infection 

(poor wound closure, exudation from wounds, canker 

development near wounds). 

In June 1989 or July 1990, 5 of the 10 trees within each 

treatment group were randomly selected and examined for 

the presence of sapstreak. Trees in treatments 1 and 2 were 

felled and cross sectioned through the tapholes and at 20.0- 

in (0.5-m) intervals above and below the tapholes to observe 

radial patterns of discoloration. Sections were split 

longitudinally to trace the linear extent of the discolored 

Table 8.--Schedule of wounding and inoculation and 

resulting infection for trees inoculated with 2 ml conidial 

suspension into two buttress-root bruises - - 

~reatment 3- 

Date wounded Number t rees 

and inoculated harvested Number 

(1 984) (1 989-90) trees infected 

14 March 5 0 

19 March 5 0 

26 March 6 0 

9 April 5 0 

2 May 5 3a 

31 May 5 4a 

8 June 5 0 

15 June 6 1 a 

Controls 

14 March 6 0 

31 May 5 0 

a~ive ofeight infected trees were infected through both 

wounds. 

DResults. No trees developed foliar symptoms characteristic 

of sapstreak during the 5-year observation period. Closure of 

both inoculated and non-inoculated tapholes proceeded at an 

apparently normal rate, although it was more rapid for 

tapholes without spouts. Some of the basal injuries exhibited 

cambial dieback, and on some trees sprouts developed near 

the inoculated injuries. 

Incidence: Very few tapholes (3 of 146 examined) showed 

evidence of infection by C. virescens (Tables 6,7). None of 

the trees in treatment 1 tapped on 14 March and inoculated 

then or later through open tapholes or metal spouts 

developed sapstreak. Controls also were not infected. Two 

trees in the series tapped on 17 April had stain patterns that, 

while limited, were suggestive of sapstreak (Figure 14). One 

of these had been inoculated on 23 April, the other was the 

open taphole of a non-inoculated control tree. Similarly, in 

treatment 2 none of the trees tapped on 14 March and 

inoculated later when the spouts and tubing were removed, 

nor their non-inoculated controls, developed sapstreak. 

However, one of the trees tapped on 17 April and inoculated 

on 31 May had discoloration about one taphole suggestive of 

sapstreak (Fig. 15). The tangential orientation of this taphole 

may account in part for the stain patterns (Trial IV). 

column associated with each taphole. Column lengths were 

measured to the nearest cm. Photographs were taken of the Incidence of sapstreak infection in trees inoculated through 

discoloration present in all dissected trees, Inoculated roots buttress-root bruises (treatment 3) was considerably higher 

were excavated and dissected to determine presence and than through tapholes (Table 8). And infection was influenced 

extent of infection. strongly by treatment date. While no infection occurred in 

trees wounded and inoculated on 14, 19,26 March, or 9 

April, three of five, four of five, and one of five trees wounded 

Trees in treatments 3, 5, and 6 were felled, cut through the and inoculated on 5 and 31 May and 15 June, respectively, 

buttress-root bruises or drill holes to expose the were infected. Of these eight infected trees, five were 

cross-sectional infection patterns, and dissected to reveal the infected through both bruise wounds. None of the wounded, 

upward linear extent of infection. non-inoculated trees was diseased. Infection ranged from 
Figure 1 4.--"Breakoutv pattern of stain around taphole wound 

"w", suggestive of sapstreak (cross section cut through the 

taphole); and the associated column of discoloration (radial 

section split through the discolored column). 

Figure 15.--A rare instance in which sapstreak disease 

occurred when the fungus was placed in the taphole (arrow); 

the fungus was contained by the tree and discolored columns 

were limited. The apparent ability of the fungus to spread 

from taphole "Em probably is attributable to the tangential 

orientation of the taphole, which cut across normally effective 

ray boundaries. 

being strongly limited in some trees (Fig. 16) to extensive in 

others (Fig. 17). However, even in trees where extensive 

infection in roots had occurred, upward spread into stems 

was restricted to a few centimeters. 

Two of the five trees inoculated through ax cuts into the roots 

(treatment 4) developed stain columns characteristic of 

sapstreak disease. Both were strongly limited and had 

spread only a few cm from the inoculated wound. None of the 

controls had stains suggestive of the disease. 

Rates of infection in the trees inoculated through drill holes in 

their buttress roots (treatments 5 and 6) were high (Table 9), 

especially in trees inoculated in late May. Of the examined 

trees wounded and inoculated with wheat grain inoculum on 

14 March, 17 April, or 31 May, one of five, two of five, and 

four of five, respectively, were infected. Infection occurred 

through both wounds on six of these seven trees. Of the five 

trees examined whose drill hole wounds had been inoculated 

with conidial suspensions on 31 May, four were infected, 

three through both wounds. As in trees infected through 

bruised bark, the extent of colonization ranged from slight to 

severe. 

Figure 16.--In this tree, both developing columns of 

discoloration are limited strongly by compartmentalization. 

Figure 17.--The discoloration pattern in this tree indicates that 

C. virescens rapidly invaded the sapwood following infection 

through bark bruises. 
Table 9Achedule of wounding and inoculation and 

resulting Infectlon for trees inoculated with wheat grain 

lnoculum (treatment 5) or conidial suspension (treatment 

6) in two, 0.25-in-diameter holes drilled 2 in deep into 

buttress roots 

Treatment 5 

Date wounded Number trees 

and inoculated harvested Number trees 

(1 984) (1 989-90) infected 

14 March 5 1 

17 April 5 2 

31 May 5 4 

Treatment 6 

occur that were related to treatment and to the date of 

tapping: 

*The mean length of discoloration columns about open or 

metal-spout tapholes (n=30) (treatment 1) was significantly 

longer (P=0.009) than that about closed, plastic-spout 

tapholes (treatment 2). 

Within treatment 1, the mean length of the discoloration 

columns about open tapholes (n=59) was significantly greater 

(P=0.013) than that about tapholes with a metal spout. 

Columns of discoloration about tapholes made on 14 March 

were longer than about those made on 4 April. This was 

significant for treatment 1 tapholes (P=0.02, n=30) but not for 

treatment 2 tapholes (n=61). 

The lengths of the discoloration columns (not related to 

sapstreak infection) associated with tapholes (treatments 1 

and 2) were analyzed statistically to determine if there were 

differences between inoculated and non-inoculated tapholes 

attributable to wound date, treatment, or inoculation date. 

Results are presented in Table 10. Columns of discoloration 

associated with inoculated tapholes were no longer than 

those of the controls. However, significant differences did 

Thus, the mean discoloration lengths reflect gradients of 

taphole "openness" and time. The more open the taphole, 

and the longer it existed before resumption of physiological 

activity, the longer the columns were. 

Discussion and Conclusions 

Several significant relationships were revealed or suggested 

by the series of observations and experiments reported here. 

While a number of these confirm earlier reports, others 

Table 10.-Comparison of lengths of discoloration In treatments 1 and 2a (A), the 

influence of tapping date (B,C,D) and of open vs, metal spout (E) 

Tapholes Average 

(no.) column length 

(cm) SD P 

A. All treatment 1 30 67.23 17.86 

vs . 0.009 * 

All treatment 2 40 50.62 12.83 

B. All treatment 1 +2: 

14 March 60 62.30 18.24 0.098 

17 April 64 55.48 13.03 

C. Treatment 1 only: 

14 March 30 72.1 7 18.58 0.020 * 

17 April 30 57.73 13.01 

D. Treatment 2 only: 

14 March 32 50.81 12.98 0.83 

17 April 32 53.37 13.11 

E. Treatment 1 only: 

Open 59 34.02 10.99 0.01 3 * 

Metal 61 29.30 9.21 

'~reatment 1 : Metal spouts and open tapholes; 

Treatment 2: plastic spouts with tubing. 

* indicates statistical significance at > 99 percent probability level. 

*indicates statistical significance at > 95 percent probability level. 
extend our understanding of disease expression and of 

factors affecting disease incidence and severity. 

Importance of Wounds 

Sapstreak disease rarely occurs in nonwounded trees. Only 

a few cases were encountered while observing disease 

occurrence in many sugarbushes and forests, and when 

such trees were excavated they were found to be connected 

by functional root grafts to diseased trees that had been 

wounded. Our studies (trial V) showed that root-graft 

transmission between closely adjacent trees can occur. But 

the low level of its occurrence in our studies, and the 

relatively few times adjacent trees were observed to become 

diseased in the field, suggest that this means of disease 

spread probably is not very common. 

The nearly universal association of wounds and sapstreak 

disease is pivotal to the development of control guidelines. 

The understanding gained in these studies, that the suitability 

of wounds as infection courts depends on their type, their 

location on the tree, and possibly the season in which they 

are inflicted, provides added information for development of 

management guidelines. 

The general levels of "natural" disease incidence, especially 

of trees with initial symptoms, observed in these studies was 

very low. Repeated observations reyealed that for some 

sugarbushes, the disease is occurring continuously--with a 

few new trees becoming symptomatic every year or so. In 

contrast, in forest stands the majority of "new" trees often 

appears within a relatively short time span. This pattern of 

occurrence probably reflects thednfrequent but severe 

wound-inflicting disturbances related to logging activities, and 

contrasts the less severe, but annual traffic-related 

disturbances in some sugarbushes. In forest stands, 

sapstreak diseased trees usually exhibit initial symptoms 3-6 

years after the injury-causing event. While the period over 

which diseased trees die is frequently more protracted in 

forest stands, the trees that are going to die will have done so 

within 6-8 years after having become infected. 

Which infected trees die and which do not is probably related 

to 1) the capacity of the tree to compartmentalize injuries and 

limit the spread of infection, 2) the condition of the tree and 

its position in the stand, and 3) the presence or absence of 

pathogens capable of attacking and killing weakened root 

systems. Our studies and observations suggest that each of 

these factors is involved. Inoculation Trials IV, V, and V1 

clearly showed that trees of approximately the same age, 

size, and vigor, inoculated with equal amounts of the same 

isolate at the same time and by the same method, varied 

greatly in their ability to resist or limit the spread of the 

pathogen. Indeed, some inoculated trees remained free of 

infections altogether. Patterns of colonization, revealed 

through dissection, showed that trees usually recovered if 

extensive spread and distribution of the fungus, particularly 

through the root system, had not occurred within the first year 

or so after inoculation. 

Importance of Root Disease Pathogens 

Most naturally and artificially inoculated trees and saplings 

with root systems well colonized by C. virescens died within 1 

to 3 years after symptoms appeared. The nearly universal 

presence of Armillaria sp. and Xylaria sp. (or both) fruiting 

bodies, mycelial fans, rhizomorphs or decay on trees that 

died, and the absence of these organisms from 

sapstreak-infected trees that recovered suggests that their 

attack is a major mortality-determining factor. These root 

fungi are ubiquitous inhabitants of long-established northern 

hardwood forest stands. Successful invasion (at least for 

some Armillaria sp.) is governed by stress factors or events 

that, by altering tree physiology, reduce resistance (Wargo 

and Shaw 1985). The debilitating effect caused by extensive 

internal colonization of roots by C. virescens undoubtedly is a 

significant stress. Other stresses, including defoliation and 

drought, also weaken and predispose roots to infection. 

These factors, together with forest practices such as thinning, 

ensure a relatively continuous supply of pathogen food bases. 

The fact that significant mortality occurred soon after 

inoculation with C. virescens of saplings and pole-size trees 

that had been severely defoliated earlier by gypsy moths 

probably reflects the influence of defoliation, both as a 

predisposing factor to these root pathogens and as a factor 

contributing to the buildup of their inoculum. That defoliation 

per se does not affect susceptibility to C. virescens was 

shown by Trial Ill. The saplings in this stand had not been 

defoliated earlier and, by consequences of its more recent 

origin, this stand did not harbor a significant load of root 

disease inoculum. 

Conversely, some trees with severe sapstreak root infections 

also recovered. These were saplings and trees whose 

position in the stand was favorable for growth and that also 

may have escaped attack by root pathogens. 

The opportunity to grow rapidly--to produce the energy 

required to establish barriers that restrict infection--is 

dependent in large part on the amount of sunlight received. 

Saplings in the more open stands, for example, Trial Ill and 

the sapling-sprouts of Trial I, were able to limit infection and 

subsequent mortality compared to those saplings in Trials I 

and I1 growing nearby in denser shade. The sprouts also 

probably benefited from having an energy-producing, 

non-inoculated sprout member. And, as discussed earlier, in 

addition to a: better light regime, the saplings in Trial Ill and 

the sprouts in Trial I also probably benefited from a 

somewhat lower root-pathogen inoculum potential 

characteristic of young forest stands established on recently 

abandoned open land. 

Influence of Sap Collection Methods 

Very low incidences of sapstreak were observed in 

sugarbushes employing tubing collection systems compared 

to bushes where sap is collected in buckets. Whether the 

abundant buttress root and root injuries found in many 

"bucket" sugarbushes were the result of saphauling or of 

traffic at other times of the year is not certain. When the 

disease did occur in tubing system sugarbushes, it was on 
injured trees near sugarhouses, along logging skid trails, and 

in areas where cattle had trampled root systems. 

Our studies examining the suitability of tapholes as infection 

courts (Trial VI) confirmed these observations. Tapholes, 

regardless of their nature, were poor infection courts 

compared to buttress-root bruises. Interestingly, however, the 

lengths of the discoloration columns (associated with all 

tapholes) were greater about open (metal) than about closed 

(plastic with tubing) spouts--and tapholes made early in the 

season had longer discoloration columns than those made 

later. The greater amount of discoloration associated with 

metal spouts used in bucket collection systems is perhaps 

another factor in favor of tubing systems. 

Influence of Infection Courts Location 

Injuries associated with sapstreak were almost always close 

to the ground. Even though stem tissues were infected 

following their inoculation with large amounts of a 

grain-based inoculum (Trial IV), and invasion of upper stems 

from infections originating in the roots or stem bases is 

common (Trial I), no cases were observed that suggested 

infection had occurred through broken branches or other 

wounds of upper crowns or stems. Tapholes inoculated with 

conidial suspensions very rarely became infected and when 

they did, the infections were strongly limited (Trial VI). In a 

number of cases, stump surfaces created when one member 

of a sprout clump was removed in early summer thinning 

operations appeared to be the avenue of infection for the 

residual stem. Such near-the-ground wounds comprise 

especially suitable infection courts for C. virescens. 

Influence of Season 

Late spring to midsummer appears to be a critical period for 

sapstreak disease. The results of several studies indicated 

that sugar maples are most susceptible to infection during 

this time (Trials I, It, and VI). Mortality was highest in trees 

inoculated in late spring through mid-August. Late spring and 

early summer is the periocl of greatest susceptibility of other 

tree species to similar vascular pathogens, including elms 

(Dutch elm disease) and oaks (oak wilt). Not only are trees 

inherently more susceptible at this time, this also is the 

period when heavy equipment used in the forest can create 

excessive rutting and cause damage to roots and massive 

injuries to bark and wood of lower stems. And, finally, 

temperatures and moisture conditions during this period 

usually are very favorable for rapid growth and sporulation of 

C. virescens and for growth of the associated root pathogens 

as well. 
Literature. Cited 

Beil, J. A.; Kessler, Jr., K. J. 1979. Sapstreak disease of 

sugar maple found in New York State. Plant Disease 

Reporter. 63: 436. 

Hepting, G. H. 1944. Sapstreak, a new killing disease of 

sugar maple. Phytopathology. 34: 1069-1 076. 

Houston, D. R. 1985. Sapstreak of sugar maple: How 

serious is it? Maple Syrup Digest. 25(2): 24-27. 

Houston, D. R. 1986. Sapstreak of sugar maple: 

appearance of lumber from diseased trees and 

longevity of Ceratocystis coerulescens in air-dried 

lumber. Phytopathology. 76: 653. Abstract. 

Houston, D. R. 1991. Spread of the sugar maple sapstreak 

disease pathogen, Ceratocystis coerulescens, via root 

grafts between Acer saccharum. Phytopathology. 81 : 

122. Abstract. 

Houston, D. R. 1992. Importance of buttress root and 

taphole wounds as infection courts for the sugar maple 

(Acer saccharum) sapstreak pathogen, Ceratocystis 

coerulescens. Phytopathology. 82: 244. Abstract. 

Houston, D. R.; Fisher, K. D. 1964. sapstreak of sugar 

maple found in the northeast. Plant Disease Reporter. 

48: 788. 

Houston, D. R.; Schneider, B. 1982. Sapstreak disease of 

sugar maple in N.Y. sugarbushes. Phytopathology. 72: 

262. Abstract. 

Kessler, K., Jr. 1972. Sapstreak disease of sugar maple 

found in Wisconsin for the first time. Res. Note NC-140. 

St. Paul, MN: US. Department of Agriculture, Forest 

Service, North Central Forest Experiment Station. 2 p. 

Kessler, K. J., Jr. 1978. How to control sapstreak disease 

of sugar maple. Information leaflet. St. Paul, MN: U.S. 

Department of Agriculture, Forest Service, North Central 

Forest Experiment Station. 5 p. 

Kessler, K., Jr.; Anderson, R. L. 1960. Ceratocystls 

coerulescens on sugar maple in the Lake States. Plant 

Disease Reporter. 44: 348-350. 

Ohrnan, J. H.; Kessler, Jr., K. J. 1963. Current status of the 

sapstreak disease of sugar maple in the Lake States. 

Res. Note LS-10. St. Paul, MN: U.S. Department of 

Agriculture, Forest Service, Lake States Forest Experiment 

Station. 4 p. 

Shigo, A. L. 1962. Observations on the succession of 

fungi on hardwood pulpwood bolts. Plant Disease 

Reporter. 46: 379-380. 

Shigo, A. L. 1977. Compartmentalization of decay in trees. 

Agric. Inf. Bull. No. 405. Washington, DC: U.S. Department 

of Agriculture, Forest Service. 73 p. 

Shigo, A. L. 1979. Tree decay: an expanded concept. 

Agric. Inf. Bull. No. 419. Washington, DC: U.S. Department 

of Agriculture, Forest Service. 73 p. 

Shigo, A. L.; Shigo, A. 1974. Detection of discoloration and 

decay in living trees and utility poles. Res. Pap. NE294. Upper Darby, PA: U.S. Department of Agriculture, 

Forest Service, Northeastern Forest Experiment Station. 

11 p. 

Shigo, A. L.; Shortle, W. C.; Garrett, P. W. 1977. Genetic 

control suggested in compartmentalization of 

discolored wood associated with tree wounds. Forest 

Science. 23: 179-1 82. 

Smith, K. T. 1990. Sapstreak disease and biodeterioration 

of sugar maple. Biodeterioration Research. 3: 303-310. 

Tattar, T. A.; Shigo, A. L.; Chase, T. 1972. Relationship 

between the degree of resistance to pulsed electric 

current in wood in progressive stages of discoloration 

and decay in living trees. Canadian Journal of Forest 

Research. 2: 236-243. 

Wargo, P. M.; Shaw Ill, C. G. 1 985. Armillaria root rot. The 

puzzle is being solved. Plant Disease. 69: 826-832. 

Q Printed on Recyt?kd Paper 

a u. s. GOVERNMENT PRINTING OFFICE: I 9 94 - 5 50- I I 2 / 800 I 5 

19 
Houston, David R. 1993. Sapstreak disease of sugar maple: development 

over time and space. Res. Pap. NE-687. Radnor, PA: U.S. Department of 

Agriculture, Forest Service, Northeastern Forest Experiment Station. 19 p. 

Sapstreak disease is a potentially serious problem of sugarbushes and forest 

stands. It is caused by the fungus Ceratocystis virescens, which invades 

sapwood of roots and bases of stems through wounds created during logging, 

saphauling, or other activities. This publication describes the results of 

observations and experiments to learn more about the patterns of disease 

development and the factors that affect them, within individual trees and 

within representative forests and sugarbushes. 

Keywords: Ceratocystis virescens, root and buttress root wounds, vascular 

disease, sugarbush, root grafts 
Headquarters of the Northeastern Forest Experiment Station is In Radnor, Pennsylvanla. Field laboratories are maintained at: 

Amherst, Massachusetts, In cooperatlon with the University of Massachusetts 

Burllngton, Vermont, In cooperatlon with the University of Vermont 

Delaware, Ohlo 

Durham, New Hampshire, In cooperation wlth the University of New Hampshlre 

Hamden, Connecticut, in cooperation with Yale Unhrerslty 

Morgantown, West Vlrglnla, in cooperatlon with West Virginia University 

Orono, Maine, in cooperatlon with the University of Maine 

Parsons, West Vlrglnia 

Princeton, West Vlrglnla 

Syracuse, New York, In cooperatlon with the State Unhrersity of New York, Coilege of Environmental Sclences and Forestry at Syracuse Universlty 

University Park, Pennsylvania, in cooperation with The Pennsylvania State University 

Warren, Pennsylvania 

The United States Department of Agriculture (USDA) Forest Service is a diverse 

organization committed to equal opportunity in employment and program delivery. 

USDA prohibits discrimination on the basis of race, color, national origin, sex, religion, age, disability, political affiliation, and familial status. Persons believing that they 

have been discriminated against should contact the Secretary, U.S. Department of 

Agriculture, Washington, D.C. 20250, or call 202-720-7327 (voice), or 202-720-1 127 

m. 

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