United States 

Department of 

Agriculture

Forest Service

Pacific Southwest 

Research Station

General Technical Report 

PSW-GTR-236

December 2011

DEPAR TMENT OF AGRICULT URE

A Risk Assessment of 

Climate Change and the 

Impact of Forest Diseases 

on Forest Ecosystems in 

the Western United States 

and Canada

John T. Kliejunas
Author

John T. Kliejunas was a regional forest pathologist (retired), U.S. Department of 

Agriculture, Forest Service, Pacific Southwest Region, Vallejo, CA.

Cover photographs (clockwise from upper left): Armillaria root disease, by Michael 

Cruickshank, Natural Resources Canada; Dothistroma needle blight, by David 

Weaver, British Columbia Forest Service; yellow-cedar decline, by Paul Hennon, 

USDA Forest Service, Pacific Northwest Research Station; sudden oak death, by 

Marin Municipal Water District; white pine blister rust, by Detlev Vogler, USDA 

Forest Service, Pacific Southwest Research Station; dwarf mistletoe infection, by 

Paul Hennon, USDA Forest Service, Pacific Northwest Research Station.

The Forest Service of the U.S. Department of Agriculture is dedicated to the principle of 

multiple use management of the Nation’s forest resources for sustained yields of wood, 

water, forage, wildlife, and recreation. Through forestry research, cooperation with the 

States and private forest owners, and management of the National Forests and National 

Grasslands, it strives—as directed by Congress—to provide increasingly greater service 

to a growing Nation.

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Abstract

Kliejunas, John T. 2011. A risk assessment of climate change and the impact of 

forest diseases on forest ecosystems in the Western United States and Canada. 

Gen. Tech. Rep. PSW-GTR-236. Albany, CA: U.S. Department of Agriculture, 

Forest Service, Pacific Southwest Research Station. 70 p. 

This risk assessment projects the effects of eight forest diseases under two 

climate-change scenarios (warmer and drier, warmer and wetter). Examples are 

used to describe how various types of forest diseases may respond to environmental changes. Forest diseases discussed in this report include foliar diseases, 

Phytophthora diseases, stem rusts, canker diseases, dwarf mistletoes, root 

diseases, and yellow-cedar decline. The likelihood and consequences of increased 

damage to forests from each disease as a result of climate change are analyzed 

and assigned a risk value of high, moderate, or low. The risk value is based 

on available biological information and subjective judgment. Although results 

suggest that climate change will affect forest health, uncertainty arises regarding 

the degree of climate change that will occur; pathogen biology under changing 

climate; the effects of changing climate directly on the host; and the interactions 

between the pathogen, host, and climate.

Keywords: Climate change, forest pathogens, environmental risk assessment, 

foliar diseases, Phytophthora, Armillaria, stem rusts, canker diseases, dwarf 

mistletoe, root diseases, yellow-cedar decline.
Summary

This risk assessment projects the effects of eight forest diseases under two climatechange scenarios (warmer and drier, warmer and wetter). Examples are used 

to describe how various types of forest diseases may respond to environmental 

changes. The likelihood and consequences of increased damage to forests from 

each disease as a result of climate change are analyzed and assigned a risk value of 

high, moderate, or low. The risk value is based on available biological information 

and subjective judgment.

Foliar diseases. Because most foliar pathogens require moisture for sporulation, 

dissemination, and infection, decreases in precipitation generally will lessen the 

likelihood of disease damage. Some needle cast diseases caused by species of 

Davisomycella and Hypodermella also require moisture for sporulation, dispersal, 

and infection, but are more likely to infect trees that are stressed by drought. 

Phytophthora diseases. Increased precipitation during spring is likely to be associated with increased prevalence of Phytophthora ramorum in areas where it already 

occurs and expansion of the pathogen to new locations. Continued warming would 

increase areas suitable climatically for Phytophthora species, resulting in increased 

tree mortality if the pathogen is introduced to those areas. However, moisture must 

be sufficient for pathogen sporulation and infection. 

Stem rusts. The biology of stem rust pathogens on two-needled and three-needle 

pines in western North America—for example, western gall rust (Endocronartium 

harknessii), comandra rust (Cronartium comandrae), stalactiform rust (C. coleosporioides), and sweet fern rust (C. comptoniae)—is similar to white pine blister 

rust (C. ribicola). Infection and incidence of diseases caused by these fungi 

generally increase when conditions are cool and moist. Warmer conditions, 

whether wetter or drier, would be less favorable than cooler conditions.

Canker diseases. Most canker diseases are caused by facultative parasites such 

as Botryosphaeria, Sphaeropsis, Cytospora, and Biscogniauxia (Hypoxylon). We 

describe the risk potentials for Cytospora canker of alder, which can be extrapolated to other stress-related canker diseases. These fungi are more likely to cause 

damage to trees that are stressed by heat and drought. Not all canker diseases are 

associated with stressed hosts. The incidence of some canker pathogens, such as 

Thyronectria austro-americana on honeylocust (Gleditsia triacanthos L.) and 

Cryphonectria cubensis on Eucalyptus spp. L’Her., is associated with high rainfall, 

and their hosts display some resistance to drought stress.
Dwarf mistletoes. Warmer temperatures may enable range expansion of some 

dwarf mistletoes. An increased incidence of summer drought would increase 

mortality of infected trees.

Root diseases. A warmer climate will generally increase Armillaria incidence and 

impact as host stress increases. A drier climate would, in general, stress hosts more 

than a wetter climate, and thus increase host susceptibility to root diseases.

Yellow-cedar decline. Continued warming would likely increase mortality of 

yellow-cedar (Chamaecyparis nootkatensis (D. Don) Spach). The resulting economic and environmental loss rates are potentially high, but would depend on 

whether the trees are salvaged for value.

Although the results of this risk assessment suggest that climate change will 

affect forest health, the uncertainties associated with the risk potentials should be 

kept in mind. In this assessment, uncertainty arises regarding the degree of climate 

change that will occur; pathogen biology under changing climate; the effects of 

changing climate directly on the host; and the interactions between the pathogen, 

host, and climate. 

The information provided in this risk assessment is directed to decisionmakers 

and managers for strategic and management planning. This risk assessment also 

serves as the basis for subsequent products—such as fact sheets, press releases, 

presentations, or decision documents—for nontechnical audiences.
Contents

1 Introduction

1 Risk Assessment Process

5 Climate Change and Forest Pathogens

5 Climate Projections

7 Effects on Tree Diseases

8 Diseases Posing Risk of Increased Damage

9 Dothistroma Needle Blight

9 History and Current Status

10 Economic and Environmental Impacts

11 Disease Cycle

12 Environmental Drivers of Disease

13 Assessment and Analysis

15 Swiss Needle Cast

15 History and Current Status

16 Economic and Environmental Impacts

16 Disease Cycle

16 Environmental Drivers of Disease

17 Assessment and Analysis

18 Sudden Oak Death; Ramorum Blight

18 History and Current Status

20 Economic and Environmental Impacts

21 Disease Cycle

22 Environmental Drivers of Disease

23 Assessment and Analysis

25 White Pine Blister Rust

25 History and Current Status

25 Economic and Environmental Impacts

26 Disease Cycle

27 Environmental Drivers of Disease

29 Assessment and Analysis
30 Cytospora Canker of Alder

30 History and Current Status

30 Economic and Environmental Impacts

31 Disease Cycle

31 Environmental Drivers of Disease

32 Assessment and Analysis

33 Dwarf Mistletoes

33 History and Current Status

34 Economic and Environmental Impacts

34 Disease Cycle

34 Environmental Drivers of Disease

35 Assessment and Analysis

37 Armillaria Root Disease

37 History and Current Status

37 Economic and Environmental Impacts

39 Disease Cycle

40 Environmental Drivers of Disease

40 Assessment and Analysis

42 Yellow-Cedar Decline

42 History and Current Status

43 Economic and Environmental Impacts

44 Environmental Drivers of Disease

44 Assessment and Analysis

45 Summary and Conclusions

47 Acknowledgments

47 English Equivalents

48 Literature Cited

1

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Introduction

The objectives of this risk assessment are to estimate the likelihood that forest 

diseases will cause increased damage to forest ecosystems as a direct result of 

projected climate change by 2100, and to describe the potential economic and 

environmental consequences of that damage.

Risk Assessment Process

Risk analysis is a formal process that includes three successive steps: risk 

assessment, risk management, and risk communication (FAO and WHO 1995). 

A framework to guide risk assessments (NRC 1983) has been broadly adopted 

by national and international agencies. 

An ecological risk assessment is defined as a process that evaluates the 

likelihood and associated uncertainty that adverse ecological effects may occur 

or are occurring as a result of exposure to one or more stressors (EPA 1992). An 

ecological risk assessment organizes and analyzes data, information, assumptions, 

and uncertainties to evaluate the likelihood and consequences of adverse ecological 

effects. Basically, it is a process used to determine what can happen, what the 

likelihood of the occurrence is, what the consequences are, and how certain the 

knowledge is. The purpose of conducting an ecological risk assessment is to 

provide decisionmakers with scientific information and other factors they need to 

consider (e.g., social, legal, political, or economic) in selecting a course of action.

An ecological risk assessment includes three primary phases: problem formulation, analysis, and risk characterization. In the first phase, which also may be 

referred to as hazard identification, the problem (source of potential adverse effects) 

is stated and described and a plan for analysis is developed. Two activities are 

conducted during the analysis phase: characterization or assessment of the probability of exposure and characterization or assessment of ecological effects (i.e., consequences of exposure). During the risk characterization phase, ecological risks (risk 

potentials) are estimated, the level of uncertainty in the risk estimates is specified, 

and evidence supporting the risk estimates is cited.

In this ecological risk assessment, I estimate the likelihood that projected 

changes in climate by 2100 (the exposure) and associated responses of biotic and 

abiotic tree pathogens (the threats or hazards) will adversely affect forests. 

Problem formulation—

Recent literature reviews (Boland and others 2004, Desprez-Loustau and others 

2007, Dukes and others 2009, Kliejunas and others 2009, Klopfenstein and others 

2009a, Moore and Allard 2008, Sturrock 2007, Sturrock and others 2011, Woods 
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GENERAL TECHNICAL REPORT PSW-GTR-236

and others 2010) suggest that projected changes in climate will increase damage 

to forests from pathogens. 

A broad range of taxonomic groups and modes of infection of pathogens were 

considered for individual risk assessments. First, pathogens were classified by type 

of disease caused (e.g., foliar diseases, branch or bole diseases, root diseases). It was 

assumed that a risk assessment for one pathogen in a given class likely would be 

transferable to other pathogens in the class. Second, pathogens for which responses 

to weather or climate are documented in the research literature were identified. By 

necessity, risk assessments focus on those organisms for which biological information is available. Individual risk assessments were then conducted for two foliar 

pathogens (Dothistroma needle blight and Swiss needle cast), an aerial Phytophthora (sudden oak death/ramorum blight), a rust disease (white pine blister rust), 

a canker disease (Cytospora canker of alder), dwarf mistletoes, a root disease 

(Armillaria root disease), and an abiotic disease (yellow-cedar decline).

Analysis— 

In this climate change risk assessment, I analyzed the likelihood and consequences 

of increased damage to forests from each disease as a result of climate change.

The likelihood and the consequences of increased disease damage were 

assigned a risk value of high, moderate, or low. A risk value is based on available 

biological information and subjective judgment. The criteria used to determine 

risk values were based on those developed by the U.S. Department of Agriculture 

Forest Service’s Wood Import Pest Risk Assessment Mitigation and Evaluation 

Team (WIPRAMET) (Kliejunas and others 2003) and used by the U.S. Department of Agriculture Forest Service’s Exotic Forest Pest Information System for 

North America (ExFor) (Downing and O’Brien 2004). The criteria estimate the 

effects of climate change on host susceptibility to the pathogen and on the ability 

of the pathogen to reproduce, spread, and infect the host. Professional judgment is 

required to assign a risk value when information is unavailable or different sources 

of information conflict. Therefore, the likelihood and the consequences were each 

assigned a certainty category as described in Orr and others (1993). The certainty 

categories are a function of the information that is available and the confidence of 

the assessor in it. Certainty categories used in the risk assessment process are:

• Very certain

• Reasonably certain

• Moderately certain

• Reasonably uncertain

• Very uncertain
3

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Projected changes in climate vary by geographical region. In general, temperature is projected to increase. In different regions, and sometimes in different climate 

models for the same region, precipitation is projected to remain constant, decrease, 

or increase.

Temperature and moisture strongly affect pathogens and disease development 

by shaping survival, reproductive rate, and, in many cases, the probability of spread 

at a regional or larger scale. Two general scenarios of climate change were considered: warmer and drier, and warmer and wetter.

Likelihood of increased disease damage—

Five criteria were used to estimate likelihood (risk) of increased disease damage:

a. Suitability of conditions for pathogen survival, reproduction, spread, 

or host infection will increase as climate changes.

b. Changes in climate will stress the host and increase its susceptibility 

to the pathogen.

c. Pathogen is capable of substantial increases in population size (has a 

high reproductive potential).

d. Pathogen has a broad host range.

e. Control techniques are unknown, not feasible, or ineffective.

Criteria a and b are based on the direct effects of climate change on stages of 

the disease cycle (survival, reproduction, spread, infection) or on the effects of 

climate change on host stress. Factors considered included effect of milder winters 

on pathogen survival; effects of temperature and moisture (increase or decrease) 

on reproduction rates, infection, disease progress, and on subsequent success of 

pathogen; and effect on host stress. Criteria c, d, and e relate to the attributes of the 

disease or pathogen regardless of climate. For example, if the pathogen has a low 

reproductive potential or its host has a limited range, the likelihood of an increase 

in disease damage always will be low.

Using the above criteria, high, moderate, or low risk was assigned as follows:

High risk = Criteria a or b applies, and three or more of the remaining 

criteria a or b, c, d, and e apply.

Moderate risk = Criteria a or b applies, and two or fewer of the remaining 

criteria a or b, c, d, and e apply.

Low risk = Criteria a and b do not apply, and one or more of criteria c, d, 

and e apply.
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GENERAL TECHNICAL REPORT PSW-GTR-236

Consequences of increased disease damage—

Five criteria—based on the economic and environmental effects of increased 

disease, regardless of change in climate—were used to categorize the potential 

economic or environmental consequences of increased disease damage. 

a. Hosts of pathogen have substantial commercial value.

b. Pathogen directly causes host mortality or increases the probability that 

other organisms will kill the host.

c. Damage caused by pathogen decreases economic value of the host.

d. Pathogen causes substantial direct environmental effects, such as extensive 

ecological disruption or reduction in species richness over extensive areas.

e. Pathogen affects a host or hosts with limited natural distribution.

Risk was assigned as follows:

High risk = Three or more of the five criteria apply.

Moderate risk = Two of the five criteria apply.

Low risk = One or none of the five criteria apply.

Risk characterization (estimate of risk potential)—

The risk potential resulting from climate change was estimated as the likelihood 

of increased disease damage multiplied by the potential consequences of increased 

disease damage. The risk potential for each disease was estimated using a method 

developed by Orr and others (1993). The method has been used by WIPRAMET 

and quantified by ExFor by assigning integer values of 3, 2, and 1 to risk classes 

high, moderate, and low, respectively (table 1). 

Table 1—Classes and values of risk potential 

Likelihood of Consequences of

increased increased

disease damage disease damage Risk potential

High (3) High (3) Very high (9)

Medium (2) High (3) High (6)

Low (1) High (3) Medium (3)

High (3) Medium (2) High (6)

Medium (2) Medium (2) Medium (4)

Low (1) Medium (2) Low (2)

High (3) Low (1) Medium (3)

Medium (2) Low (1) Low (2)

Low (1) Low (1) Very low (1)
5

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Climate Change and Forest Pathogens

Climate Projections

Global—

Climate change often is projected at the global extent. The Intergovernmental Panel 

on Climate Change (IPCC) used several general circulation models and scenarios 

of greenhouse gas emissions to project global climate trends. Projected changes by 

2100 (IPCC 2007) include:

• An increase of 1 to 6 °C in the average global temperature.

▪ Increases in temperature will differ by season. Increases in winter will 

be greater than increases in summer.

▪ Changes in temperature will not be evenly distributed around the globe. 

Temperature will increase more in terrestrial areas than in oceans and 

more in high latitudes than in low latitudes. Increases in temperature 

are likely to exceed the global average in most of North America; all of 

Africa, Europe, and northern and central Asia; and most of Central and 

South America.

• An increase in global average annual precipitation, with changes varying 

from region to region. 

▪ Annual average precipitation will increase during winter over most of 

northern Europe, the Arctic, Canada, the northeastern United States, 

tropical and eastern Africa, the northern Pacific, Antarctica, northern 

Asia, and the Tibetan Plateau.

▪ Annual average precipitation will decrease during winter in most of the 

Mediterranean, northern Africa, the northern Sahara, Central America, 

the Southwestern United States, the southern Andes, and southwestern 

Australia.

▪ Summer precipitation will decrease over continental interiors owing to 

increases in evaporation.

• Extreme heat, heat waves, and heavy precipitation events will become 

more frequent.

If changes of the predicted magnitude occur, large portions of the Earth’s 

surface may experience climates not found at present, and some current climates 

may disappear (Williams and others 2007). The new combinations of temperature 

and moisture regimes will likely result in disruption of existing host-pathogen 

combinations and formation of new combinations.
6

GENERAL TECHNICAL REPORT PSW-GTR-236

Western United States and Canada—

All regional climate models project that temperatures will increase in the Western United States by 2100. Most models project increases in winter temperature, 

decreases in moisture, and more frequent droughts throughout the region (Karl and 

others 2009, USDA FS 2003). Precipitation may increase slightly in winter, but the 

duration of seasonal heat and drought is likely to increase (Karl and others 2009, 

USDA FS 2003). 

Regional projections for the Pacific Northwest (Mote and others 2003) 

suggest that temperature will increase from 0.5 to 2.5 °C by 2020, and from 1.5 

to 3.2 °C by 2040. Precipitation across the region is projected to increase except 

during summer. In British Columbia, snowmelt may occur earlier and more rapidly, 

with a reduction in summer streamflows (Hamann and Wang 2006). Winters in 

northern British Columbia likely will be warmer and wetter. Across the region, 

winters likely will be wetter, and the proportion of precipitation falling as rain 

rather than snow is projected to increase (Pojar 2010, Spittlehouse 2008). In the 

southern half of the province, summers likely will be progressively warmer and 

drier. In the northern half of the province, summers initially may be cooler but 

ultimately are likely to be warmer and wetter. 

Regional climate models all project that temperatures in California will 

increase substantially (Cayan and others 2006). Virtually all models project warming of at least a few degrees over the Sierra Nevada (Dettinger and others 2004). 

Projected increases in temperature by 2100 vary from 1.7 to 5.8 °C (Cayan and 

others 2006). 

Models differ considerably in their projections of precipitation for California 

(Dettinger and others 2004). There is no evidence that the Mediterranean pattern 

of precipitation will change. All of the models examined (Cayan and others 2006) 

indicate that the vast majority of precipitation will continue to fall during winter 

storms from the North Pacific. Summer precipitation is projected to change little, 

and decreases in some of the models (Cayan and others 2006).

Most climate models project that the Southwestern United States will be 

warmer and drier. There will be fewer frost days; warmer temperatures in winter 

and spring, increased demand for water by plants, animals, and people; an increased 

frequency of extreme weather events; warmer nights; and declines in snowpack 

(Archer and Predick 2008a, 2008b; Weiss and Overpeck 2005). 

Annual temperatures across the Colorado Plateau are projected to increase 

from 1.5 to 3.6 °C by 2050, and from 2.5 to 5.4 °C by 2100 (Garfin and others 2010). 

Summer temperatures are projected to increase more than winter temperatures 

(Ray and others 2008). Some models project an increase in annual mean 
7

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

precipitation, whereas others project a decrease of as much as 6 percent by 2100 

(Garfin and others 2010, Ray and others 2008).

Projected changes in temperature and precipitation in different subregions of the 

intermountain West (Great Basin and Columbia Plateau) will vary as a function of 

storm patterns and differences in topography (Chambers and Pellant 2008). Temperatures in the region are projected to increase 2 to 5 °C by 2100. Projected changes 

in precipitation are inconsistent, with average changes near zero. Any increases are 

likely to occur largely in winter with little change or decreases in summer. Water 

availability will depend on the magnitude of increases in temperature and its effects 

on snowpack and evapotranspiration. Snowpacks have declined across the Western 

United States since about 1950, especially in the intermountain West. Evapotranspiration is projected to increase regardless of whether precipitation increases. 

Effects on Tree Diseases

The literature on projected climate change and the potential effects on forest ecosystems and tree pathogens was recently summarized (Kliejunas and others 2009, 

Sturrock and others 2011). A synopsis is presented here.

The direction and magnitude of responses of tree diseases to climate change will 

differ. Changes will occur in the type, number, and relative importance of pathogens 

and diseases. Climate influences the survival and spread of pathogens as well as the 

susceptibility of their hosts. Climate change could alter stages and rates of development of the pathogen, modify host resistance, and lead to changes in the physiology 

of host–pathogen interactions. The most likely effects are changes in the geographical distribution of hosts and pathogens and changes in mortality of hosts, caused in 

part by changes in the efficacy of control strategies.

Although it is uncertain how specific forest pathogens will respond to climate 

change, some general inferences can be drawn:

The effects of climate change on individual plant diseases will depend on the 

ecosystem and climate conditions. 

• The distribution of pathogens and diseases, and their influence on the 

status and trend of forests, will change. The ranges of some diseases will 

expand, whereas the ranges of other diseases will shift. The influence of 

pathogens on the status and function of forests may change coincident with 

changes in species composition and climate. 

• Many pathogens currently are limited by winter temperature, and seasonal 

increases in temperature are expected to be greatest during winter. 

Therefore, both overwintering survival of pathogens and disease severity 

are likely to increase.
8

GENERAL TECHNICAL REPORT PSW-GTR-236

• Climate change will alter the epidemiology of plant diseases. Rapid 

climate change and unstable weather will make prediction of disease 

outbreaks more difficult.

• The rate at which pathogens evolve and overcome host resistance may 

increase.

• Because climate affects both host susceptibility to pathogens and pathogen 

reproduction and infection, the most substantial effect of climate change 

on plant diseases may be changes in interactions between biotic diseases 

and abiotic stressors.

• Climate change may facilitate invasion by new nonnative pathogens and 

thus new epidemics. 

Diseases Posing Risk of Increased Damage

Disease reflects the interaction of a susceptible host, a virulent pathogen, and 

conducive environmental conditions. Susceptibility and virulence are affected by 

environmental conditions, and an increase in either or both will result in increased 

incidence of disease 

Only a few observational or experimental studies or modeling efforts have 

documented pathogen responses to climate change. Responses will differ among 

pathogens and locations (Runion 2003, Sturrock 2007). Following are the descriptions of eight forest diseases that pose risks to forest ecosystems.
9

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Dothistroma Needle Blight

Causal agents—

Dothistroma septosporum (Dorog.) Morelet (teleomorph=Mycosphaerella pini 

Rostr. [Scirrhia pini A. Funk & A.K. Parker]); Dothistroma pini Hulbary 

(teleomorph unknown); Dothidiales, Dothidiaceae.

Hosts—

D. septosporum: over 80 species of Pinus, Pseudotsuga menziesii (Mirb.) Franco, 

Larix decidua Mill., 5 species of Picea; D. pini: Pinus nigra Arnold.

Distribution—

D. septosporum: worldwide; D. pini: north-central United States, Ukraine.

History and Current Status

Dothistroma needle blight (figs. 1, 2, and 

3), also referred to as red band needle 

blight because of the symptoms it causes 

on pine, is a conifer disease with a 

worldwide distribution (Bradshaw 2004, 

Gibson 1974) that causes substantial 

economic losses. Although first reported 

in Russia in 1911 (Doroguine 1911, 

Gibson 1974) and in the United States 

and elsewhere in Europe before 1920 

(Brown and Webber 2008), it was not 

considered a serious disease until the 

1950s (Bradshaw and others 2000). 

Most pines susceptible to infection are 

in stands less than 10 years old within 

plantations outside the natural range of 

the species. For example, the disease is 

absent from natural stands of radiata pine (Pinus radiata D. Don) in California 

but is present in stands planted north along the Pacific Coast, and in radiata pine 

plantations worldwide (Gibson 1972).

Dothistroma needle blight is primarily caused by D. septosporum. The 

teleomorph (sexual) state of the pathogen, Mycosphaerella pini (formerly 

Scirrhia pini), rarely has been observed. Recently, D. pini was found to cause 

Dothistroma needle blight in the north-central United States (Barnes and others 

2004) and the Ukraine (Groenewald and others 2007). To date, no teleomorph 

of D. pini has been identified.

Figure 1—Lodgepole pine killed by 

Dothistroma near Kispiox, British Columbia.

Alex Woods, British Columbia Forest Service
10

GENERAL TECHNICAL REPORT PSW-GTR-236

Economic and Environmental Impacts

Damage is typically limited to reduced tree vigor and growth in response to 

defoliation (Bingham and others 1971, Patton 1997). Below about 40-percent 

crown infection, growth loss is proportional to the level of crown infection (Ades 

and others 1992, Bulman 1993, Van der Pas 1981). When crown infection exceeds 

40 percent, the incremental loss is more than 40 percent, and there is virtually no 

growth if crown infection exceeds 80 percent (Gadgil 1974). Mortality is rare but 

has occurred in stands with successive years of severe defoliation (Bradshaw 2004). 

Dothistroma needle blight has been a major constraint to the development 

of radiata pine plantations in New Zealand and Australia, Chile and other South 

American countries, and several African countries (Gibson 1972, 1974; Ivory 

1967). Crop failure has been extensive in New Zealand’s 400 000 ha of radiata pine 

(Marks and others 1989). Although mortality in New Zealand is rare, reduction 

in tree diameter and volume growth has caused losses on the order of $24 million 

per year (Bulman and others 2008). In Africa, the disease markedly reduced 

productivity of P. radiata plantations (Gibson and others 1964). In the United 

States, the disease has ruined ornamental and shelterbelt trees and plantations 

intended as sources of Christmas trees (Peterson 1966). 

Figure 2—Signs and symptoms of Dothistroma infection on needles of lodgepole pine.

David Weaver, British Columbia Forest Service
11

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Figure 3—Mature lodgepole pine stand in central British 

Columbia affected by Dothistroma needle blight.

Alex Woods, British Columbia Forest Service

In northwest British Columbia, outbreaks of the disease 

have occurred periodically on lodgepole pine (P. contorta

Douglas ex Louden var. latifolia Engelm. ex S. Watson) on 

some sites since the 1830s, with an increase in outbreak incidence and extent since the 1940s (Welsh and others 2009). In 

recent years, the impact of D. septosporum in British Columbia has increased dramatically (Woods 2003). An epidemic 

of D. septosporum was first detected in 1997 (Woods and 

others 2005). A survey of 41 000 ha in three forest districts 

from 2002 to 2004 detected the disease across 38 000 ha, 

with mortality occurring on 2700 ha. Even mature lodgepole 

pine trees were severely affected and dying (Worrall 2010). 

Lodgepole pine plantations between 15 and 20 years old had 

the most severe symptoms. Natural, mature stands of lodgepole pine also had substantial mortality (Woods 2003). 

Dothistroma needle blight historically was rare in Great 

Britain, but dramatic increases in disease levels were noted 

from the late 1990s onward on Corsican pine (Pinus nigra

ssp. laricio Maire) and occasionally on lodgepole pine 

(Archibald and Brown 2007, Brown and others 2003, Brown 

and Webber 2008). A 5-year moratorium on planting Corsican pine on public forests 

was implemented in 2007 (Brown and Webber 2008). The distribution and severity 

of the disease in France also increased in the late 1980s and early 1990s (Villebonne 

and Maugard 1999).

Disease Cycle

The disease cycle for both Dothistroma species is similar. Shortly after the death of 

needle tissue, the pathogen produces black fruiting bodies (stromata) that emerge 

through the dead epidermis. Conidial masses borne on the stromata typically begin 

to mature during the spring. Conidial production is largely dependent on sufficiently high temperature and duration of leaf wetness. Under optimal conditions, 

spores are released for up to 7 months (Karadzic 1989). Conidia may be released 

and cause infections at any point during the growing season when precipitation 

is falling (Peterson 1982) and temperatures are above 5 °C. Conidia are dispersed 

short distances by rain splash, and longer distances by wind-dispersed moisture 

droplets, mist, and low clouds (EPPO and CABI 1997). Ten hours or more of needle 

wetness is usually required for infection by D. septosporum (Bulman 1993, Gadgil 

1974). The sexual state of the pathogen is formed in a similar way, but consists of 

linear black ascomata that contain ascospores (Gibson 1972). 
12

GENERAL TECHNICAL REPORT PSW-GTR-236

Infection occurs on current-year or 1-year-old needles. Infection depends 

on several factors including the period of needle wetness, temperature, and the 

quantity of spores available for infection (Bulman 1993). Temperatures at which 

conidial germination and hyphal growth occur vary from a lower optimum of 15 °C 

(Gibson and others 1964) to an upper temperature threshold of 25 to 26 °C (Gibson 

and others 1964, Ivory 1972). Moisture is required for germination. The optimum 

temperature for successful establishment following germination is 12 to 18 °C when 

humidity is high (Brown and Webber 2008). Spores germinate and penetrate the 

needle through the stomata within 2 to 3 days (Bulman 2008).

Germinating spores produce a germ tube on which an appressorium (a swollen 

structure that adheres to the leaf surface and facilitates penetration) forms (Peterson 

and Walla 1978). From the appressorium, hyphae branch into intracellular and intercellular regions of the mesophyll layer of the needle tissue (Ivory 1972). In some 

hosts, distinct red bands (1 to 3 mm wide) appear around the needles within weeks 

of infection (Shain and Franich 1981). After 32 to 114 days, the host cells collapse 

and needle symptoms appear (Bradshaw 2004). The stromata generally mature and 

produce conidia a year or two after infection; in California and Oregon, the cycle 

may be completed in 1 year (Peterson 1982). 

Environmental Drivers of Disease

Two factors seem to have contributed to the current D. septosporum epidemic in 

northwest British Columbia. First, although lodgepole pine is native, the species 

has been planted extensively since the early 1980s, increasing host abundance. 

Second, summer precipitation increased in the late 1990s. Woods and others (2005) 

found a strong positive relationship between the frequency of warm rain events 

and disease severity. 

In Great Britain, springs are becoming earlier and warmer. Spring and summer precipitation has increased since the late 1990s compared with the previous 30 

years (Brown and Webber 2008). Severe disease episodes appear to be associated 

with higher than average rainfall at the time of infection (Archibald and Brown 

2007). 

Although the teleomorph of D. septosporum has not been reported in Great 

Britain, Groenewald and others (2007) found both mating types in collections from 

the region. The increased frequency of the disease in Great Britain may also reflect 

increased genotypic diversity and associated adaptation if the two mating types of 

D. septosporum are widespread and are reproducing sexually (Brown and Webber 

2008, Groenewald and others 2007). Also, the sexually produced ascospores are 

reported to be wind dispersed and therefore can move long distances (Gibson 1972).
13

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Assessment and Analysis

Likelihood of increased disease damage1—

Warmer, drier—Low (moderately certain) (Applicable criteria: c, d).

Warmer, wetter—Moderate (very certain) (Applicable criteria: a, c, d).

Fungi that cause foliar disease may be more responsive to climate change than 

most other organisms that cause forest disease because their ability to sporulate and 

infect is strongly associated with changes in temperature and precipitation (Gadgil 

1977, Hoff 1985, Peterson 1973).

The low level of disease detected in many regions with apparently suitable 

climate for the disease may reflect absence of hosts (Watt and others 2009). If the 

ranges of its hosts expand, the range of Dothistroma spp. could extend into Southeast China, Vietnam, Ireland, Western Australia, Venezuela, Guyana, Suriname, 

Panama, Turkey, Albania, and many countries bordering the Mediterranean Sea 

(Watt and others 2009).

Using slight variations of the CLIMEX (a model used to predict the effects of 

climate on species) parameter estimates used by Watt and others (2009), Venette2

found that climatic conditions that support Dothistroma are likely to persist in the 

Western United States through 2080, even if Dothistroma is assumed to be heatsensitive. The extent of climate conditions that support the pathogen may decrease 

by 2100 in eastern North America.3 The favorable effect of warming on Dothistroma blight may lessen if decreased summer rainfall accompanies the warming.

Consequences of increased disease damage—

Moderate (moderately certain) (Applicable criteria: a, c).

Hosts in plantations, such as radiata pine in the Southern Hemisphere and 

lodgepole pine in British Columbia, have substantial commercial value. The pathogen typically reduces growth, and also may cause mortality of lodgepole pine in 

British Columbia, decreasing the economic value of the trees. The environmental 

effects of the disease currently are minimal, but collateral effects could increase if 

chemicals are used more extensively to control the disease.

1 See pages 3 and 4 for definitions of the criteria used in the Assessment and Analysis 

section of each disease described.

2 Venette, R.C. 2010. Climate modeling for a risk assessment for climate change and forest 

pathogens in western North America. Unpublished progress report. On file with: USDA 

Forest Service, Pacific Southwest Research Station, Albany, CA 94710.

3 Venette, R.C. 2011. Personal communication. Research biologist, USDA Forest Service, 

Northern Research Station, 1561 Lindig Street, St. Paul, MN 55108.
14

GENERAL TECHNICAL REPORT PSW-GTR-236

Risk potential—

Warmer, drier—Low (2) (Likelihood of increased disease damage = low; 

consequences of increased disease damage = moderate).

Warmer, wetter—Moderate (4) (Likelihood of increased disease damage = 

moderate; consequences of increased disease damage = moderate). 

Increases in precipitation may be more important than increases in temperature for increasing the spread and impact of the disease. As demonstrated in portions of British Columbia, if wetter than normal conditions prevail and inoculum 

potential increases, the potential for significant host mortality, rather than only 

growth reduction, exists.
15

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Swiss Needle Cast 

Causal agent—

Phaeocryptopus gaeumannii (Rohde) Petrak; Pleosporales, Venturiaceae.

Hosts—

Douglas-fir.

Distribution—

Native range of Douglas-fir and most areas where Douglas-fir has been introduced, 

including much of North America, Europe, and New Zealand.

History and Current Status

Phaeocryptopus gaeumannii (fig. 4) is native to the Pacific 

Northwest. For decades, Swiss needle cast was not considered to reduce forest health. Boyce (1940) reported that P. 

gaeumannii was widespread in western North America, 

but was inconspicuous or scarce on native Douglas-fir. 

However, he recognized that the pathogen produced 

abundant fruiting bodies on 1- and 2-year-old needles of 

diseased trees in Europe and caused extensive defoliation. 

Accumulating evidence supports Boyce’s (1940) hypothesis 

that warm, humid summers with episodic rain are highly 

conducive to fungal growth and may allow the disease to 

reach epidemic levels, even in areas where it is native.

Since the early 1990s, a severe, unprecedented 

epidemic of Swiss needle cast has affected the coastal fog 

belt zone of Oregon, where Douglas-fir was not a dominant 

species in presettlement forests (Hansen and others 2000). 

Symptoms including chlorosis, premature needle loss, 

growth reduction, and abundant fruiting of the pathogen 

on 1- and 2-year-old needles are evident from Coquille 

and Bandon on the southern Oregon coast to Shelton, 

Washington, on Puget Sound; damage is concentrated in 

plantations near Tillamook, Oregon (Hansen and others 

2000). Douglas-fir plantations that are 10 to 30 years 

old, in which microclimate generally is moist, are most 

visibly affected, but the fungus is present on seedlings 

after their first growing season in the field, as well as in 

mature stands. Severely diseased plantations are usually 

Figure 4—Thin crown in a Douglas-fir infected with 

Phaeocryptopus gaeumannii along the Oregon Coast. 

Alan Kanaskie, Oregon Department of Forestry
16

GENERAL TECHNICAL REPORT PSW-GTR-236

located at lower elevations west of the Coast Ranges. They are often in areas with 

summer fog and on sites previously occupied by species of spruce and hemlock or 

by hardwoods.

Economic and Environmental Impacts

The pathogen occurs over about 500 000 ha of Douglas-fir in Oregon. Approximately 160 000 ha are severely affected with Swiss needle cast, and some landowners in these areas are converting their Douglas-fir plantations to spruce and 

hemlock (Hansen and others 2002).

The primary mechanism of damage appears to be the fruiting bodies produced 

in the stomatal apertures. The fruiting bodies occlude the stomates and reduce rates 

of carbon dioxide assimilation (Manter and others 2000).

Mean and maximum decreases in basal area growth in Oregon are 20 percent 

and 55 percent, respectively (Maguire and others 2002, Mainwaring and others 

2005). Douglas-fir radial growth was reduced by 85 percent at a severely diseased 

site (Black and others 2010). Vertical growth can decrease by about 25 percent. 

Decreases in growth can reduce the ability of planted Douglas-fir to compete with 

naturally seeded tree species (Maguire and others 2002). Decreases in growth have 

caused estimated losses of $200 million per year. Wood density and proportion of 

latewood to earlywood were higher in stands heavily infested (needle retention less 

than 2 years) with Swiss needle cast than in healthier stands (Johnson and others 

2005). 

Disease Cycle

Black fruiting bodies (pseudothecia) are produced in early winter in lines on the 

lower surface of infected needles. The pseudothecia are often produced on green 

needles that are 1 year or older. Ascospore release usually occurs from March 

through June, but can continue into August. The airborne ascospores typically 

infect current-year needles. When adequate moisture is present, the spores germinate and the fungus penetrates the needle. These infections are often latent for 

several years, but when the disease is severe, symptoms and fungal fruiting may 

occur as early as the year after needle production. The fungus grows throughout the 

needle. Fruiting bodies form in the stomata in autumn and winter and mature the 

following spring. The proportion of infected needles may become substantial before 

defoliation occurs (Smith 1978).

Environmental Drivers of Disease

Increased severity of Swiss needle cast in the Oregon Coast Range reflects 

introduction of Douglas-fir, increases in winter temperatures, and increases in 
17

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

precipitation in the winter and spring (Stone and others 2008). Occurrence of 

the disease in the Pacific Northwest is positively correlated with degree-day 

accumulation during winter and leaf wetness hours from spring through autumn 

(warm winters and wet summers) (Manter and others 2005). Since 1970, winter 

temperatures increased by 0.2 to 0.4 °C and spring precipitation by 0.7 to 1.5 cm 

per decade (Stone and others 2008). 

In southern British Columbia, Hood (1982) observed a positive correlation 

between precipitation, particularly spring rainfall, and relative abundance of P. 

gaeumannii. In New Zealand, winter mean temperature explained approximately 

80 percent of the variation in severity of disease caused by P. gaeumannii (Stone 

and others 2007). Reductions in needle retention owing to P. gaeumannii infection 

were positively related to a projected increase in air temperature of 0.144 °C from 

2006 to 2090 (Watt and others 2010).

Assessment and Analysis

Likelihood of increased disease damage—

Warmer, drier—Low (reasonably certain) (Applicable criterion: c).

Warmer, wetter—Moderate (very certain) (Applicable criteria: a, c).

An increase of Swiss needle cast in the Oregon Coast Range is associated 

with long-term warming trends during the late winter and early spring (Black and 

others 2010). Winter temperature in the Pacific Northwest is projected to continue 

increasing by approximately 0.4 °C per decade through 2050 (Stone and others 

2008). A decrease in precipitation would likely decrease the probability of damage 

to Douglas-fir from P. gaeumannii.

Consequences of increased disease damage—

Moderate (reasonably uncertain) (Applicable criteria: a, c).

Douglas-fir has commercial value, but the pathogen attacks only that host and 

only causes significant damage in a limited area of the host’s range. The disease 

does not typically cause mortality or other direct environmental effects.

Risk potential—

Warmer, drier—Low (2) (Likelihood of increased disease damage = low; 

consequences of increased disease damage = moderate).

Warmer, wetter—Moderate (4) (Likelihood of increased disease damage = 

moderate; consequences of increased disease damage = moderate). 

Predicted warmer temperatures, along with sufficient moisture, will favor 

the pathogen and increase disease incidence on Douglas-fir.
18

GENERAL TECHNICAL REPORT PSW-GTR-236

Sudden Oak Death; Ramorum Blight

Pathogen—

Phytophthora ramorum Werres, de Cock & Man in’t Veld; 

Peronosporales, Pythiaceae.

Hosts—

More than 130 species of hardwoods, conifers, shrubs, herbaceous plants, and 

ferns in over 75 genera and at least 37 families.

Distribution—

United States: in native woodlands in Curry County, Oregon, and 14 coastal 

counties (Alameda, Contra Costa, Humboldt, Lake, Marin, Mendocino, Monterey, 

Napa, San Francisco, San Mateo, Santa Clara, Santa Cruz, Solano, and Sonoma) 

in California; detected and eradicated in nurseries (and residential plantings of 

infected nursery stock) in several states.

Canada: Nurseries in British Columbia and some related residential plantings 

(eradication efforts underway).

Europe: Detected and under official control in nurseries or gardens in Belgium, 

Czech Republic, Denmark, Estonia, Finland, France, Germany, Ireland, Italy, 

Latvia, Lithuania, Luxembourg, the Netherlands, Norway, Poland, Portugal, 

Slovenia, Spain (including Mallorca), Sweden, Switzerland, and the entire United 

Kingdom, including the Channel Islands; under eradication in forests in the United 

Kingdom and the Netherlands. 

History and Current Status

Phytophthora ramorum, the cause of sudden oak death (fig. 5) and ramorum 

blight, was first detected in 1993 in Germany and the Netherlands on ornamental 

rhododendrons (Rhododendron spp.) (Werres and others 2001). In June 2000, the 

pathogen was isolated from dying tanoak (Notholithocarpus densiflorus (Hook. & 

Arn.) Manos, C.H. Cannon & S. Oh) trees in California (Rizzo and others 2002). 

In December 2000, P. ramorum was recovered from rhododendrons with leaf 

symptoms in a Santa Cruz County, California, nursery surrounded by dying oaks 

(Garbelotto and Rizzo 2005). The pathogen was detected in July 2001 in a forest 

in Curry County, Oregon.

Following the first detection in a nursery in California in 2001, the pathogen 

was found in 20 nurseries in Oregon, Washington, and British Columbia. Dispersal 

of the pathogen in the nursery trade in North America and in Europe became 

a major concern. In 2004, P. ramorum was detected in two large nurseries in 
19

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Figure 5—Sudden oak death of tanoak on Mount Tamalpais, Marin County, California. 

Marin Municipal Water District

southern California and in one nursery each in Oregon and Washington. It was 

subsequently determined that these nurseries had shipped potentially infected 

plants to over 1,200 nurseries in 39 states (Frankel 2008). Phytophthora ramorum

continues to disperse via the nursery and ornamental trade in both North America 

and Europe.

Because P. ramorum was present in Germany and the Netherlands, surveillance for the pathogen began in England and Wales in July 2001 and subsequently 

in other European countries (Brasier and others 2006). In the United Kingdom, P. 

ramorum was first detected in a nursery in April 2002 on Viburnum tinus L. (Lane 

and others 2003). Phytophthora ramorum was subsequently found on southern red 

oak trees (Quercus falcata Michx.) in the United Kingdom, and on European beech 

(Fagus sylvatica L.) and American northern red oak (Q. rubra L.) in the Netherlands (Brasier and others 2004). As in the United States, the range of P. ramorum

in Europe is extensive and increasing. The pathogen affects a large number of plant 

genera and species in the ornamental nursery trade and in parks, gardens, and 

woodlands. The pathogen now has an extensive distribution but low incidence in 

the European Union’s nursery industry (Sansford and others 2009). Phytophthora 

ramorum is subject to official governmental control in the countries where it is 

known to occur (19 European Union member states plus Norway, Switzerland, 

the United States, and Canada). 
20

GENERAL TECHNICAL REPORT PSW-GTR-236

The geographic origin of P. ramorum is unknown. Before the mid-1990s, the 

species had not been reported in the United States or Europe. The European and 

North American populations are distinct and were transported independently from 

another, unknown, location. Populations of P. ramorum are clonal, consisting of 

three lineages, NA1, NA2, and EU1 (Grünwald and others 2008a, Ivors and others 

2006, Martin 2008).

Three different diseases are attributed to P. ramorum (Hansen and others 

2002). The first, known as sudden oak death in the United States and ramorum 

bleeding canker in Europe, is characterized by bleeding bark cankers on the bole, 

which can be lethal. The second disease, ramorum shoot dieback, results from 

foliar infection or infection of stems. The third, ramorum leaf blight, results from 

foliar infection. Thus, the diverse symptoms produced by P. ramorum depend on 

the host plant and host part affected. Individual plant species can display more than 

one disease type (e.g., leaf blight, shoot dieback, and bleeding cankers on tanoak. 

A comparison of symptoms of sudden oak death and ramorum blight (a combination of shoot dieback and leaf blight) published by Grünwald and others (2008b) is 

presented here in modified form in table 2.

Table 2—Comparison of symptoms of sudden oak death and ramorum blight, both caused by 

Phytophthora ramorum

Disease Symptoms Host categories Typical hosts Geography/environment

Sudden oak death Stem cankers; Forest and garden Coast live oak, tanoak, North American forests, 

bleeding cankers trees European beech, others European gardens

Ramorum blight Foliar and twig Ornamental trees California bay laurel, rhodo- North American nurseries

blight; tip and and woody shrubs; dendron, viburnum, pieris, and forests, European

shoot dieback; understory plants coast redwood (Sequoia nurseries, forest plantaleaf blight sempervirens (D. Don) tions and gardens 

Endl.), Japanese larch,

tanoak, others

Source: Modified from Grünwald and others 2008b.

Economic and Environmental Impacts

Many P. ramorum hosts are grown for their commercial, ecological, or social value. 

Tanoak, coast live oak (Q. agrifolia Nee), and black oak (Q. kelloggii Newberry) 

in the United States die relatively quickly after the onset of symptoms. Economic 

impacts in urban areas include reduction in property value and costs for removal 

of dead trees that may injure people or increase the probability of fire. Current 

economic impacts to the nursery and ornamental industry in the United States 

are estimated to be in the range of $100 to $300 million. Canada spent about $8.5 

million in one year on control. Current economic impacts in the European Union 

are estimated as minor to moderate (Sansford and others 2009). 
21

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

The current impact on nursery-grown ornamental species is thought to be 

moderate within the areas in which P. ramorum occurs in the European Union, 

United States, and Canada. Quarantine restrictions imposed on the horticultural 

industry have had substantial economic consequences. The costs of phytosanitary 

controls are considerable (Sansford and others 2009), but not quantified. 

In the United States, environmental impacts of P. ramorum have been greatest in coastal woodlands in California and southwestern Oregon. Mortality of 

tanoak and oaks are resulting in changes in forest composition, loss of habitat for 

animals, increases in soil erosion, and a substantial increase in fuel loads near 

heavily populated urban-woodland interfaces. In Europe, oak is a dominant native 

species in forest and savanna-woodland ecosystems. There are approximately 200 

million oak trees in the United Kingdom. Their loss could have a major impact on 

soil erosion, hydrology, and sedimentation in rivers. Other possible effects include 

loss of associated plants and animals and a reduction in tourism, cultural values, 

and local woodland-based economies (Sansford and others 2009, Sansford and 

Woodhall 2007).

Disease Cycle

The life cycle of P. ramorum is similar to that of other aerial Phytophthora species. The pathogen produces sporangia on the surfaces of infected leaves and twigs 

of foliar hosts that can be splash-dispersed to neighboring hosts or transported 

longer distances by wind and rain (Davidson and others 2005). Moderate temperatures (18 to 21 °C) accompanied by rain or overhead irrigation facilitate the spread 

of and infection by spores. Phytophthora ramorum is also spread downstream of 

infested areas in rivers and streams, and can be carried in soil or infected plants. 

On contact with a host, the sporangia germinate directly, by emergence of hyphae 

through the sporangial wall, or indirectly, by producing zoospores that encyst, 

penetrate the host, and initiate a new infection. Chlamydospores are readily 

produced in infected plant material and serve as resting structures in soil, allowing the pathogen to survive adverse conditions (Shishkoff 2007, Tooley and others 

2008). Moisture is essential for survival and sporulation, and the duration, frequency, and timing of winter rain events plays a key role in inoculum production. 

In California forests, P. ramorum epidemics are driven by presence of 

California bay laurel (Umbellularia californica (Hook. & Arn.) Nutt., on which P. 

ramorum sporulates prolifically (Davidson and others 2005). In southwest Oregon, 

tanoak is the key foliar host and inoculum producer (Rizzo and others 2005). In 

Europe, heavily infected wild Rhododendron ponticum L. in the understory is 

responsible for producing inoculum that infects neighboring trees (Brasier and 
22

GENERAL TECHNICAL REPORT PSW-GTR-236

others 2004). The pathogen also sporulates heavily on planted Japanese larch 

(Larix kaempferi (Lamb.) Carr) in England, Ireland, and Scotland (Webber and 

others 2010).

Environmental Drivers of Disease

Temperatures for optimal growth of P. ramorum are between 18 and 22 °C 

(Werres and others 2001). Many species of Phytophthora germinate indirectly 

at temperatures below about 12 oC and directly at higher temperatures (Ribeiro 

1983). Maximum levels of zoospore germination occur at 100 percent humidity 

or water potentials of 1. Depending on the water potential, germination can occur 

between temperatures of 10 to 30 °C (Kessel and others 2007, Turner and Jennings 

2008). The prevalence of infection of California bay laurel leaves averaged 92 

percent at 18 °C, but only 50 percent at 12 °C and 37 percent at 30 °C (Garbelotto 

and others 2003). A minimum of 6 to 12 consecutive hours of free water is a 

prerequisite for the infection of California bay laurel leaves (Garbelotto and 

others 2003). Infection by zoospores tends to occur on plant parts where water 

accumulates, such as leaf tips. 

In California mixed-evergreen forests, sporulation and inoculum production 

is seasonal, largely dependent on rainfall events and temperature. Sporangial 

production in redwood/tanoak forests begins soon after the start of the rainy season 

(Maloney and others 2002). In California, P. ramorum is commonly recovered 

from rain traps from December into spring, peaking during warm rains in May 

(Davidson and others 2005). At one study site in a mixed-evergreen forest, detectable levels of P. ramorum inoculum were present primarily during the winter rainy 

season and were absent during the hot, dry summer (Davidson and others 2005). In 

contrast, P. ramorum inoculum (most likely dehiscent sporangia) in infested forests 

of southwest Oregon can be produced throughout the year whenever water is available (Hansen and others 2008).

Spore production differs yearly as well as seasonally. In California, relatively 

high levels of winter and spring rainfall extending into early summer are often 

followed by high levels of disease (Davidson and others 2005, Rizzo and others 

2005). Epidemic mortality of coast live oak occurred 1 to 2 years after high spring 

rainfall in the El Niño years of 1998 and 2005 (Davidson and others 2005, Rizzo 

and others 2005). In Oregon, Kanaskie and others (2008) attributed an unexpected 

expansion of the disease from sites where eradication efforts were being conducted 

to 2 consecutive years with an unusually wet spring and early summer. Hansen 

and others (2008) reported that rain in late May following a dry April triggered an 

infection event at two sites, resulting in dieback, subsequent sprouting of tanoak, 

and numerous new P. ramorum bole infections. 
23

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Assessment and Analysis

Likelihood of increased disease damage—

Warmer, drier—Low (moderately certain) (Applicable criteria: c, d, e).

Warmer, wetter—High (very certain) (Applicable criteria a, c, d, e).

Increased precipitation during spring is likely to be associated with increased 

prevalence of the pathogen in areas where it already occurs and expansion of the 

pathogen to new locations. Chlamydospores and zoospores of the pathogen can 

survive more than 30 days under moist conditions in the laboratory, but less than 

30 minutes when the relative humidity is less than 30 percent (Davidson and 

others 2002). 

Magarey and others (2008) used the North Carolina State University—Animal 

and Plant Health Inspection Service Plant Pest Forecasting System (NAPPFAST) to 

project P. ramorum infection across the conterminous United States as a function of 

temperature and moisture. Venette and Cohen (2006) used the CLIMEX model to 

identify areas of the United States where P. ramorum might occur. Venette (2009) 

also used the CLIMEX model to quantify the potential change in distribution of 

habitat and in habitat quality for P. ramorum on the basis of climate scenarios. 

The model suggested that high-quality habitat in the contiguous United States 

currently extends along the west coast from approximately Monterey, California, 

to the vicinity of Puget Sound, Washington. Large areas of habitat also occur in 

the Eastern United States. On the basis of projections from the Canadian General 

Circulation Model-1 (CGCM1), Venette projected that the extent of high-quality 

habitat will decrease substantially in the Eastern United States, but will increase in 

Washington, Oregon, and California. By 2050, habitat will extend from Los Angeles, California, to the Puget Sound area in Washington. Inland expansion of habitat 

by 2080 is projected to be modest. In the Eastern United States, small, isolated 

patches of high-quality habitat are projected to occur in far western North Carolina, 

the northeast quarter of West Virginia and from northern New Jersey to southern 

Massachusetts. The shift in distribution seems to result from changes in biological 

heat stress.

Consequences of increased disease damage—

High (reasonably uncertain) (Applicable criteria: a, b, c, d, e).

Numerous hosts of P. ramorum, including forest trees and ornamental plants, 

have substantial economic value. The Animal and Plant Health Inspection Service 

risk assessment for P. ramorum (Cave and others 2008) rated the environmental 

impact of the pathogen as high on the basis of its potential to disrupt native 

ecosystems and vegetation types within its current geographic range, the need 
24

GENERAL TECHNICAL REPORT PSW-GTR-236

for additional control programs, and the potential of the pathogen to directly 

or indirectly reduce probability of persistence of species listed as threatened or 

endangered under the federal Endangered Species Act (ESA 1973). Reasonable 

uncertainty reflects the difficulty in estimating environmental costs associated 

with use of herbicides to prevent, eradicate, or suppress the pathogen; effects on 

protected species; and effects on ecological processes such as water and nutrient 

cycling (Cave and others 2008).

Risk potential—

Warmer, drier—Moderate (3) (Likelihood of increased disease damage = 

low; consequences of increased disease damage = high).

Warmer, wetter—Very high (9) (Likelihood of increased disease damage = 

high; consequences of increased disease damage = high). 

Continued warming would increase areas suitable climatically for the pathogen, 

resulting in increased mortality if the pathogen is introduced to those areas. However, moisture must be sufficient for pathogen sporulation and infection. 
25

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

White Pine Blister Rust

Pathogen—

Cronartium ribicola J.C. Fischer in Rabenhorst.

Hosts—

In North America, eastern white pine (Pinus strobus L.), western white pine (P. 

monticola Douglas ex D. Don), sugar pine (P. lambertiana Douglas), southwestern 

white pine (P. strobiformis Engelm.), whitebark pine (P. albicaulis Douglas), 

limber pine (P. flexilis James), foxtail pine (P. balfouriana Grev. & Balf.), and 

Rocky Mountain bristlecone pine (P. aristata Engelm.).

Distribution—

North America, Europe, Asia.

History and Current Status

Cronartium ribicola was introduced from Asia into North America in the early 

1900s on seedlings of eastern white pine grown in Europe. The rust was introduced 

on numerous occasions into the Eastern United States, then on nursery stock into 

the Western United States (Bega 1978). 

White pine blister rust (fig. 6) now occurs in the northeastern and Western 

United States and in the Great Lakes region. It was introduced into British Columbia in 1910 and has spread from there throughout most white pine regions of 

Washington, Oregon, California, Idaho, Montana, Wyoming, and Colorado (Bega 

1978, Mielke 1943). All but one species of white pine (Great Basin bristlecone pine, 

Pinus longaeva D.K. Bailey) endemic to western Canada and the United States are 

currently infected.

Economic and Environmental Impacts

Blister rust infection of pines results in branch dieback, reproductive failure, and 

tree mortality. In North America, white pine blister rust has caused more damage 

and costs more to control than any other conifer disease (Bega 1978). The number 

of western white pine trees has decreased 90 percent in northern Idaho, where 

the species has been reduced to a minor component in stands it had historically 

dominated (Neuenschwander and others 1999). Since the 1920s, millions of dollars 

have been spent on the eradication of the alternate host, Ribes (currants and 

gooseberries). Thousands of white pine stands have been severely damaged. In the 

Western United States and Canada, mortality in some stands has been complete 

(Bega 1978). The size of populations of western white pine, sugar pine, whitebark 

pine, and several other species have declined substantially (Zeglan and others 2010).
26

GENERAL TECHNICAL REPORT PSW-GTR-236

The pathogen interacts with other stressors to induce mortality. The synergistic 

effects of C. ribicola, drought, increasing temperatures, and mountain pine beetle 

(Dendroctonus ponderosae) are considered the ultimate cause of the high mortality observed in many high-elevation populations of white pine (Gibson and others 

2008, Kegley and others 2004, Logan and Powell 2001, Tomback and Achuff 2010).

Disease Cycle

Cronartium ribicola is a heteroecious (requires at least two hosts to complete its 

life cycle), macrocyclic rust that produces five distinct spore stages during its life 

cycle. The pathogen alternates between five-needle pines and Ribes spp. (occasionally Pedicularis spp. and Castilleja spp.; McDonald and others 2006). Thin-walled 

basidiospores, produced on Ribes leaves, are wind-borne up to a few kilometers 

and infect through stomates of pine needles in autumn. The pathogen grows into 

and down the branch toward the main stem. It grows in the phloem and bark with 

no visible symptoms for at least 3 years before spores are produced. Spermatia are 

formed in the spring of the third or fourth year, followed a year later by the production of aeciospores in white blisters that break through the bark. Thick-walled 

aeciospores are wind-dispersed over distances up to about 480 km and are capable 

of infecting the telial host (Ribes spp.; occasionally Pedicularis and Castilleja). 

Figure 6—White pine blister rust on southwestern white pine in the Sacramento Mountains, 

New Mexico. 

Detlev Vogler, USDA Forest Service, Pacific Southwest Research Station
27

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Approximately 10 days after infection of leaves, urediospores develop and are 

produced on the leaves throughout the summer. Urediospores are able to reinfect 

Ribes spp., thus intensifying the disease. In autumn, teliospores and basidiospores 

are produced on Ribes spp., and the basidiospores transmit the disease back to pines 

to complete the life cycle.

Environmental Drivers of Disease

The environmental requirements for blister rust infection are well-documented 

(Bega 1960, Mielke 1943, Spaulding 1922, Van Arsdel 1954). Van Arsdel and others 

(2006) summarized the literature and their observations on the environmental 

conditions for growth, sporulation, germination, and infection. Although weather 

requirements for infection are complex, the disease apparently has no environmental limits wherever white pines and Ribes spp. cohabit (Kinloch 2003). Climate 

currently is not a limiting factor in white pine blister rust distribution in British 

Columbia (Campbell and Antos 2000). The pathosystem commonly displays a 

wave year phenomenon when especially favorable weather facilitates substantial 

increases in rust spread and intensification (Kinloch 2003, Peterson 1971).

Blister rust is considered a cool weather disease. In Wisconsin, rust distribution 

and average July temperatures were negatively correlated. Rust infection was more 

extensive where July temperatures averaged less than 21 °C. Where the average 

was higher, rust was usually confined to cool, moist microclimates (Van Arsdel 

and others 1961).

Inoculum production—

Aeciospores are usually produced in the spring at temperatures from 16 to 28 °C. 

They are released when the air is saturated (Van Arsdel and others 2006). The 

optimum temperature range for urediospore production is from 14 to 20 °C, with 

a night minimum of 2 °C (Van Arsdel and others 2006).

Telia seldom develop well when temperatures are high (Riker and others 

1947). In the sugar pine region of California and Oregon, rains from large-scale 

cyclonic warm fronts increase soil moisture and relative humidity near ground 

level. Teliospore production on Ribes begins a minimum of 2 weeks after aecial or 

uredial infection. The favorable range for teliospore formation is 1 to 20 °C, with 

an optimum at 16 °C. Temperatures greater than 20 °C or 0° for 12 hours at formation affect germination, but teliospores can recover from freezing (Van Arsdel and 

others 2006). Production is stimulated by cool temperatures, and inhibited by 3 

consecutive days above 28 °C, night minima above 20 °C, or daily maxima above 

35 °C (Van Arsdel and others 1956). 
28

GENERAL TECHNICAL REPORT PSW-GTR-236

Basidiospore production begins when viable teliospores are present and moisture is present as free water or relative humidity exceeds 97 percent. Germination 

is most successful at 100 percent relative humidity when teliospores are in contact 

with water (Van Arsdel and others 2006).

Inoculum dispersal—

Not only moisture and air temperature but air circulation affect the timing and 

pattern of rust spread (Van Arsdel 1965). Calm and clear nights cause radiant 

heat loss and down-slope flow of water-saturated air that controls patterns of local 

teliospore germination, basidiospore transport, and pine infection (Kimmey and 

Wagener 1961).

Establishment of infection—

Spore germination and infection of pine needles requires 48 hours with 100 percent 

relative humidity and temperatures not exceeding 20 °C.

The minimum time for Ribes infection by aeciospores is 7 to 8 days of 

temperatures of 5 to 24 °C for production, followed by 12 hours of saturated air 

for spore release, an additional 5 hours at 16 to 20 °C and greater than 97 percent 

relative humidity, and the presence of wet Ribes leaves for germination and 

penetration (Van Arsdel and others 2006). High foliar nitrogen concentrations 

increase susceptibility in pines and Ribes (McDonald and Dekker-Robertson 1998, 

Van Arsdel 1972), so association with nitrogen-fixing plants or artificial fertilization 

may increase Ribes susceptibility.

Survival—

Cronartium ribicola needs living host tissue to survive. Fires that remove soil 

organic layers kill Ribes in the seedbank, but fires of low to moderate intensity 

allow Ribes to regenerate (Arno 2000) from seed in lower levels of the soil profile 

and from living bases of surviving plants (Littlefield 1930, Miller 2000, Moss and 

Wellner 1953). Fire stimulates surviving seed to germinate (Lyon and Stickney 

1976). Seedling establishment is greatest in the first year after fire (Quick 1954). 

Ribes establishment can be particularly high where slash piles have been burned 

(Moss and Wellner 1953).
29

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Assessment and Analysis

Likelihood of increased disease damage—

Warmer, drier—Low (reasonably certain) (Applicable criteria: c, e).

Warmer, wetter—Low (moderately certain) (Applicable criteria: c, e).

Although increases in precipitation likely increase habitat quality for the pathogen, projected increases in temperature do not. Projected changes in climate to 2100 

would affect not only the rust disease but the distribution and status of white pine 

populations. The extent of habitat for whitebark pine (Warwell and others 2007) is 

likely to decrease substantially, with the species shifting to relatively cool locations 

at higher elevations and latitudes.

Some climate scenarios project decreases in summer precipitation in the Rocky 

Mountains but increases in the Southwestern United States (Bartlein and others 

1997, Kliejunas and others 2009). The probability of wave year occurrence of the 

disease decreases as temperatures increase and precipitation decreases (Kinloch 

2003), possibly resulting in less rust infection. The incidence of the disease may 

decrease in areas such as the southern Sierra Nevada if temperatures increase and 

precipitation decreases. Early season infection of pine is common in the coastal 

regions of British Columbia (Hunt 2005). In the southern Sierra Nevada, infection 

of white pine normally coincides with spring rains and summer thunderstorms 

(Kinloch and Dulitz 1990). A long and cool winter is required before Ribes break 

dormancy and become susceptible, telial hosts (Zambino 2010).

Consequences of increased disease damage—

High (reasonably certain) (Applicable criteria: a, b, c, d, e).

In general, an increase in incidence and severity of blister rust would increase 

economic loss of timber from western white pine and sugar pine, and have a substantial adverse effect on high-elevation white pines, some of which are narrowly 

distributed.

Risk potential—

Warmer, drier—Moderate (3) (Likelihood of increased disease damage = 

low; consequences of increased disease damage = high).

Warmer, wetter—Moderate (3) (Likelihood of increased disease damage = 

low; consequences of increased disease damage = high). 

A warmer climate, along with drier environmental conditions, would reduce 

rust sporulation and infection. Although wetter conditions would favor the pathogen, warmer temperatures would not.
30

GENERAL TECHNICAL REPORT PSW-GTR-236

Cytospora Canker of Alder

Causal agent—

Valsa melanodiscus G.H. Otth [anamorph = Cytospora umbrina (Bonord) Sacc.]; 

Diaporthales, Valsaceae.

Hosts—

Thinleaf alder (Alnus incana (L.) Moench ssp. tenuifolia (Nutt.) Breitung), Sitka 

alder (A. viridis (Chaix) DC. ssp. sinuata (Regel) A. Löve & D. Löve), green alder 

(A. viridis (Chaix) DC). 

Distribution—

Alaska, British Columbia, northern New Mexico, Colorado, southern Wyoming.

History and Current Status 

Cytospora spp. (anamorphs of Valsa spp.) are stem and branch canker pathogens of 

trees. The genus is distributed worldwide, infecting more than 70 species (Kepley 

and Jacobi 2000). Members of the genus are typically facultative parasites—usually 

saprobes, but capable of infecting trees and causing cankers when the hosts are 

stressed.

An alder canker disease associated with the fungal pathogen Valsa melanodiscus (anamorph = Cytospora umbrina) (Stanoz and others 2008) has caused damage 

to alders since the late 1980s in Colorado and nearby areas, and since about 2002 in 

Alaska (Trummer 2006, Worrall 2009). The pathogen kills vascular tissues; causes 

elongated, girdling stem cankers; and frequently causes stem dieback and mortality. Dieback and mortality of thinleaf alder within riparian areas is occurring in 

Colorado and adjacent areas and in south-central and interior Alaska. Sitka alder, 

and to a lesser degree green alder, are also affected in Alaska (USDA FS 2007). The 

pathogen is native and was first reported in Alaska in the 1930s (Trummer 2006).

Economic and Environmental Impacts 

Cytospora canker of thinleaf alder (fig. 7) is currently epidemic in the southern 

Rocky Mountains, Alaska, and other areas of western North America (Trummer 

2006, Worrall 2009). Of standing stems surveyed in Colorado and adjoining areas, 

37 percent were dead and 29 percent were diseased (Worrall 2009). Similar damage 

has been reported across thousands of acres in south-central and interior Alaska 

(Trummer 2006).

In Alaska, alder is a keystone early successional tree, and mortality may have 

adverse long-term ecological consequences (Rohrs-Richey 2008). In the Rocky 

Mountain region, thinleaf alder is often a dominant plant in high-elevation riparian 
31

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

areas. The alder stabilize soils, fix nitrogen, provide shelter for terrestrial animals, 

and shade streams, which improves fish habitat quality (Worrall 2009).

Disease Cycle

Conidia, produced in conidiomata in the spring and throughout the growing season, 

are transmitted by splashing or windblown rain. Infection sites include injured or 

dead host bark tissue; spores typically are unable to invade healthy bark. The spores 

germinate under moist conditions and penetrate the bark. Once established in the 

bark tissue, the fungus kills bark cells, girdles the branch or tree, and produces 

asexual or sexual fruiting structures. Cytospora fungi produce spores in tiny, black, 

pimple-like fruiting bodies, which break out through the bark. Ascomata (fruiting 

bodies of the sexual state) typically form in the summer and autumn. 

Environmental Drivers of Disease

Temperature-induced drought stress may increase host susceptibility and disease 

severity. In Colorado and adjacent areas, rapid canker growth and killing of 

branches and stems occurred from late June to late July, when temperatures were 

at the annual maximum and humidity was low (Worrall and others 2010). Canker 

Figure 7—Orange-red spore tendrils of Cytospora umbrina on thinleaf alder in the southern Rocky Mountains. 

James Worrall, USDA Forest Service, Forest Health Protection
32

GENERAL TECHNICAL REPORT PSW-GTR-236

growth ceased with the arrival of monsoonal precipitation despite the persistence of 

high maximum temperatures for several weeks. The increase in atmospheric moisture likely reduced transpiration and associated moisture stress. Projected increases 

in temperature will likely cause the Cytospora canker epidemic to continue and 

become more severe (Worrall and others 2010). 

Assessment and Analysis

Likelihood of increased disease damage—

Warmer, drier—High (moderately certain) (Applicable criteria: a, b, c, e).

Warmer, wetter—Moderate (reasonably uncertain) (Applicable criteria: a, c, e).

Warmer temperatures and drier conditions will stress the host, increasing its 

susceptibility to infection and to canker growth. Wetter conditions may reduce the 

host moisture stress, slowing or stopping canker growth. 

Consequences of increased disease damage—

Moderate (reasonably certain) (Applicable rating criteria: b, d).

Infection often results in host mortality. Although alder has limited economic 

value, it is a keystone species in riparian areas, and its loss from those areas would 

have substantial environmental consequences.

Risk potential—

Warmer, drier—High (6) (Likelihood of increased disease damage = high; 

consequences of increased pest damage = moderate).

Warmer, wetter—Moderate (4) (Likelihood of increased disease damage = 

moderate; consequences of increased disease damage = moderate).
33

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Dwarf Mistletoes

Causal agent—

Arceuthobium spp.; Santalales, Viscaceae.

Hosts—

The six genera of the Pinaceae (Abies, Larix, Picea, Pinus, Pseudotsuga, and 

Tsuga), Cupressaceae.

Distribution—

North America, Asia, Europe, parts of northern Africa.

History and Current Status 

Dwarf mistletoes (fig. 8) are parasitic flowering plants that infect conifers, producing characteristic aerial shoots that are leafless and yellow to orange or green to 

brown. Arceuthobium is defined by its bicolored, explosively dehiscent fruits. Many 

of the species are specific to individual commercially important conifer species 

in western North America (western Canada, Western United States, and Mexico) 

(Geils and others 2002).

The distribution of a dwarf mistletoe species is generally centered within the 

range of its principal host or hosts (Hawksworth and Weins 1996). Management 

Figure 8—A dead mature western hemlock tree with hemlock dwarf mistletoe infections created a 

canopy gap in a coastal Alaska forest. 

Paul Hennon, USDA Forest Service, Pacific Northwest Research Station
34

GENERAL TECHNICAL REPORT PSW-GTR-236

history explains the greatest proportion of variance in abundance of dwarf mistletoe 

in stands. Climate and topography also influence the current distribution of dwarf 

mistletoe (Hawksworth and Weins 1996). 

Economic and Environmental Impacts 

In the Western United States, Arceuthobium species cause an estimated loss of 

11.3 × 106

 m3 (3 × 109 board feet) per year via mortality and reduction in growth 

(Drummond 1982, Hawksworth and Wiens 1996). Annual mortality and growth 

loss caused by dwarf mistletoe ranges from 10 percent of the commercial harvest in 

the northern Rockies (Loomis and others 1985) to 50 percent in Arizona and New 

Mexico (Reich and others 1991). Infection results in reductions in tree growth, seed 

and cone production, and wood quality, and in increased tree mortality and host 

susceptibility to attacks from pathogens and insects (Giles and Hawksworth 2002, 

Hawksworth and Wiens 1970). In addition, Arceuthobium infection often results in 

formation of dense masses of branches (brooms) on the host that create fuel ladders 

into tree crowns (Hawksworth and Wiens 1970). 

Disease Cycle

Arceuthobium species are disseminated primarily by explosive seed. The berries 

ripen in the late summer or autumn and burst, shooting their sticky seeds as much 

as 15 m horizontally. The seeds adhere to needles, twigs, branches, and trunks and 

germinate the following spring. Host infection occurs when the rootlike structure 

(haustorium) from a germinated seed penetrates the bark. The haustorial system 

grows within the wood and provides the parasite with water and nutrients supplied 

by the host tree. The dwarf mistletoe plant continues to grow and spread in the host. 

Shoots of the obligate parasite form within 2 to 4 years, and fruits are produced in 

another 1 to 2 years (Scharpf 1978).

Environmental Drivers of Disease

Although dwarf mistletoes do not require specific environmental conditions after 

infection, environmental factors that stress the host affect the potential impact of 

the dwarf mistletoe. Dwarf mistletoes play a substantial role in mortality of trees 

that are stressed by drought or other factors. For example, the interactive effects 

of Arceuthobium and bark beetles are responsible for 40 to 60 percent of the pine 

mortality in southern California during years of average precipitation. Mortality is 

more frequent in the presence of other stress factors, such as drought, air pollution, 

or extremely high stand density (Schultz and Allison 1982, Schultz and Kliejunas 

1982). Wood and others (1979) attributed 90 percent of the mortality of Jeffrey pines 

(Pinus jeffreyi Balf.) at Laguna Mountain in southern California to the synergistic 

effects of California flatheaded borer (Melanophila californica), western dwarf 
35

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

mistletoe (A. campylopodum), and annosus root disease, caused by Heterobadision 

annosum. In the central Sierra Nevada, susceptibility of red fir (Abies magnifica

A. Murray) to infection by fir engraver (Scolytus ventralis) increases in response 

to severe drought, high tree density, annosus root disease, and dwarf mistletoe 

(Frankel and others 1988). Childs (1960) reported that death of conifer branches in 

the Pacific Northwest following an unusually hot summer in 1958 and an unusually 

dry summer in 1959 was extensive in trees stressed by dwarf mistletoe and other 

agents. Childs (1960) also suggested that the death of branches infected by dwarf 

mistletoe may reduce inoculum and thus reduce dwarf mistletoe spread.

Surveys during the 1976–1977 drought in California estimated that 12.3 million 

trees (equivalent to about 30 000 m3

 of wood) in diverse locations and forest types 

had died. Forest insects and pathogens explained 98 percent of the lost volume. Of 

this loss, 65 percent was attributed to a combination of dwarf mistletoe and root 

diseases that increased the susceptibility of the hosts to drought stress (Byler 1978, 

Craig 1979). Later surveys in California also indicated that trees infected with 

dwarf mistletoe were the first to die during drought (Byler 1978). Dwarf mistletoe 

increased the susceptibility of many stands to invasion by insects and have induced 

60 to 80 percent of all Jeffrey pine mortality in years of severe drought (Jenkinson 

1990). The occurrence and severity of effects of dwarf mistletoe on ponderosa 

pine in southwest Colorado were greatest in dry habitats (Merrill and others 1987). 

Wilson and Tkacz (1992) reported that severe drought, dense stands, and presence 

of pinyon dwarf mistletoe (A. divaricatum) were associated with infection of pinyon 

pine (Pinus edulis Engelm.) in northern Arizona by pinyon ips (Ips confusus). 

Millar and others (2005) suggested that an increase in limber pine mortality in the 

central Sierra Nevada from 1993 to 1998 may have been a response to multiple 

stressors, including low precipitation, high minimum temperatures, and infection 

by dwarf mistletoe (A. cyanocarpum) and bark beetles.

Assessment and Analysis

Likelihood of increased disease damage—

Warmer, drier—Moderate (moderately certain) (Applicable criteria: a, b).

Warmer, wetter—Moderate (reasonably certain) (Applicable criterion: a). 

Increases in temperature will increase dwarf mistletoe survival and host infection. Decreases in precipitation will likely increase host stress, increasing damage 

from the pathogen. However, extremely dry conditions may result in host mortality, 

resulting in a decrease in survival and infection of dwarf mistletoe.

As climate changes, the distribution of dwarf mistletoes is expected to follow 

the shift in distribution of their hosts. Because cold temperatures limit the ranges 
36

GENERAL TECHNICAL REPORT PSW-GTR-236

of many dwarf mistletoes, increases in temperature likely will result in range extensions. Southwestern dwarf mistletoe (A. vaginatum ssp. cryptopodum) does not occur 

throughout the entire range of ponderosa pine; distinct northern and upper and lower 

elevational limits exist (Mark and Hawksworth 1976). The northern and upper elevational limits appear to be related to cold temperatures. Surveys of occurrence, slope 

association, and severity of infection of several dwarf mistletoe species in Colorado 

revealed elevational zones specific to each host-parasite interaction (Williams 1971). 

For example, A. vaginatum was absent below 1860 m. Below 2130 m, ponderosa 

pine is vigorous and may be resistant, with temperature possibly being important. 

Dwarf mistletoe (A. americanum) on lodgepole pine occurs at the lower but not at 

the upper elevational limits of its host (Hawksworth 1956). The growing season at 

higher elevations may not be long enough for the fruit of the mistletoe to mature 

before autumn frosts occur. Although ponderosa pine in the Black Hills is susceptible to dwarf mistletoe infection, dwarf mistletoe is absent from the Black Hills and 

Bearlodge Mountains, apparently because early onset of the cold season kills young 

embryos of an essentially tropical mistletoe (Alexander 1987). Bloomberg (1987) 

suggested that differences in incidence and severity of hemlock dwarf mistletoe 

(A. tsugense) among geographic areas (low in Alaska, moderate to high in British 

Columbia, and moderate in Washington and Oregon) reflect the effects of climate on 

seed production and spread, stand composition and growth rate, and local adaptations of dwarf mistletoe. Lodgepole pine dwarf mistletoe is a pathogen of jack pine 

(Pinus banksiana Lamb.) in western Canada, but is absent from jack pine forests in 

colder, more northern areas (Brandt and others 2004). The distribution of the pathogen may expand if temperatures in Canada’s northern interior continue to increase, 

with a decrease in the frequency of extremely cold periods during the winter, similar 

to weather over the last several decades.

Consequences of increased disease damage—

High (very certain) (Applicable criteria: a, b, c).

Dwarf mistletoes attack hosts with substantial commercial value, cause tree 

mortality or predispose their hosts to other disease agents, and reduce host growth.

Risk potential—

Warmer, drier—High (6) (Likelihood of increased disease damage = moderate; 

consequences of increased pest damage = high).

Warmer, wetter—High (6) (Likelihood of increased disease damage = moderate; 

consequences of increased disease damage = high).

Warmer temperatures may enable range expansion of some dwarf mistletoes. An 

increased incidence of summer drought would increase mortality of infected trees.
37

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Figure 9—Armillaria root disease killing Douglas-fir in clumps near 

Salmon Arm, British Columbia. 

Michael Cruickshank, Natural Resources Canada, Canadian Forest Service

Armillaria Root Disease

Pathogen—

Armillaria spp.; primarily Armillaria solidipes Peck (Armillaria ostoyae

(Romagnesi) Herink); Agaricales, Marasmiaceae.

Hosts—

Many conifer species, occasionally hardwoods.

Distribution—

Nine species of Armillaria are known from North America. Of those, Armillaria 

solidipes causes the greatest damage to conifers in the Western United States 

and Canada. 

History and Current Status

Armillaria species cause root rot in forests 

worldwide (Kile and others 1991). Some Armillaria species are primary pathogens and attack 

healthy trees in western forests, whereas other 

species act as secondary agents, infecting after 

hosts have been stressed by agents such as 

drought, other diseases, insects, or reductions 

in habitat quality. Thus, the ecological roles of 

Armillaria species include primary pathogen, 

secondary invader, and saprotroph. In western 

North America, A. solidipes (A. ostoyae) causes 

disease in conifers (figs. 9 and 10) (Wargo and 

Shaw 1985). The species is widespread and 

infects a wide range of hosts (Kile and others 

1991).

Economic and 

Environmental Impacts

Several species of Armillaria cause root disease 

in forest trees, resulting in mortality or reduced 

growth (Shaw and Kile 1991). In many temperate coniferous forests, A. solidipes causes tree 

mortality throughout a stand’s life (Kile and 

others 1991), ranging from extensive within a 

disease center to diffuse throughout a stand. In 

young stands, mortality can reach 2 percent per 
38

GENERAL TECHNICAL REPORT PSW-GTR-236

Figure 10—Armillaria mushrooms growing near a tree stump near Valemount, British Columbia. 

Typically Armillaria feeds on root systems or colonizes stumps left after harvesting, and then 

spreads to adjacent trees. 

Michael Cruickshank, Natural Resources Canada, Canadian Forest Service
39

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

year (Filip and Goheen 1995, Livingston 1990, Morrison and Pellow 1994, Singh 

and Richardson 1973, Whitney 1988), and cumulative mortality can reach 15 to 20 

percent when the stand is 20 years old (Morrison and Pellow 1994, Whitney 1988). 

Infection can substantially decrease growth in some hosts, especially Douglas-fir 

and true fir (Abies spp.) (Kile and others 1991). Up to 40 percent loss of volume over 

4 to 8 years in 18-year-old Douglas-fir, frequently in the absence of aboveground 

symptoms, has been reported in British Columbia (Cruickshank 2000, Morrison 

and others 2000). Armillaria root disease caused by A. solidipes is responsible for 

losses in timber volume of 2 to 3 million m3

 per year in Canada’s Pacific Northwest 

(Morrison and Mallett 1996). Tree mortality and subsequent windthrow owing to 

Armillaria decay may be substantial hazards in recreational and urban areas. 

Disease Cycle

In general, Armillaria decays wood in the roots, lower boles, and stumps of either 

dead or living trees. Under favorable environmental conditions, the fungus in 

the infected root—or in the case of the more saprophytic species, in the infested 

wood—produces mushrooms, the source of the reproductive basidiospores. The 

mushrooms are produced in clusters of various sizes at the base of dead or dying 

trees and stumps. These basidiospores are discharged and are carried by air currents to wounds in uninfected trees. The importance of basidiospores in dissemination and infection differs among species (Kile 1986, Smith and others 1992). Local 

spread from a host tree or stump to an uninfected live tree occurs either by root 

contact or by rhizomorphs (rootlike fungal structures) that grow through the soil to 

susceptible tree roots and establish new infections. Most pathogenic species produce limited rhizomorphs and spread primarily through root-to-root contact. Once 

contact has been made, the fungus spreads along the root system of the uninfected 

tree, penetrating its bark and entering into the cambium. The fungus continues to 

spread along the root until it reaches the root collar, where it spreads to the other 

primary roots. Death of the host occurs when the tree is girdled at the root collar, 

bark beetles attack, or windthrow occurs. Armillaria typically causes a white to 

yellowish stringy rot. Armillaria commonly survives as a saprophyte on dead roots 

and stumps for 20 to 30 years. 

Symptoms of infection in the crown, such as crown thinning, reduced height 

growth, and distress cone crop, are often unnoticed or similar to other root diseases. 

Diagnostic signs of Armillaria include white mycelial fans under the bark, black 

rhizomorphs penetrating root surfaces, and honey-colored mushrooms near the base 

of the tree in autumn. 
40

GENERAL TECHNICAL REPORT PSW-GTR-236

Environmental Drivers of Disease

Armillaria root disease is often associated with stressed trees (Wargo and Harrington 1991). Stand disturbances such as drought, temperature extremes, and 

soil compaction reduce host resistance to Armillaria (Goheen and Otrosina 1998). 

Armillaria itself makes trees more susceptible to bark beetle attack.

Lack of precipitation decreases trees’ resistance to Armillaria infection. In 

general, losses attributed to Armillaria root disease are most severe in Mediterranean or continental interior regions (Kile and others 1991). Armillaria occurs 

most frequently and is most severe in the dry forests of eastern Washington. 

Whitney (1984) found that conifers were more heavily infected on dry than on wet 

sites. Morrison and others (2000) found that the percentage of trees showing 

aboveground symptoms in a dry region was twice that in moist and wet regions. 

McDonald and others (1987) reported that Armillaria species were absent from 

areas that were relatively warm and dry and cold and wet in national forests of 

the northern Rocky Mountains. 

Although mortality from A. solidipes is greater in inland than in coastal 

forests (Goheen and Otrosina 1998), the pathogen is widespread in both regions 

(Hadfield and others 1986, Morrison 1981). On coastal sites in British Columbia, 

A. solidipes was prevalent on sites with slightly dry soils, and occurred at low 

frequency on sites with moist soils. On interior sites, the frequency of A. solidipes

was lowest on sites with dry soil (Cruickshank and others 1997). In moist northtemperate and boreal coniferous forests, A. solidipes causes lethal primary root 

disease and reduces timber yield (Kile and others 1991). In British Columbia, 

tree mortality and growth losses attributed to A. solidipes were severe throughout 

the moist southern interior. In addition, Williams and Marsden (1982) found that 

disease incidence in Idaho was greatest on wet sites with low water retention and 

on dry sites with high water retention. 

Assessment and Analysis

Likelihood of increased disease damage—

Warmer, drier—High (very certain) (Applicable criteria: a, b, d, e).

Warmer, wetter—Moderate (moderately certain) (Applicable criteria: a, d, e).

The incidence of Armillaria root disease is likely to increase as temperatures 

increase and precipitation decreases (Shaw and Kile 1991, U.S. Office of Technology Assessment 1993), especially when hosts are stressed by moisture deficiency. 
41

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Such increases not only will decrease tree growth and increase direct mortality, but 

may increase the incidence or severity of insect outbreaks on stressed trees (Battles 

and others 2006). Klopfenstein and others (2009a) projected that the area that can 

support Douglas-fir in the interior Northwestern United States will decrease in the 

decade 2060, and suggested that stressed Douglas-fir will be more susceptible to 

Armillaria root disease.

Armillaria sinapina, typically regarded as a weak pathogen of diverse hosts 

(Morrison and others 1985), is projected to cause more disease as incidence of 

stressed hosts increases (Klopfenstein and others 2009b). In the Pacific Northwest, 

where the mean annual temperature currently is below the optimum (25 °C) 

for Armillaria growth, increases in temperature are likely to result in increased 

prevalence and rate of spread of root disease (IPCC 2001).

Consequences of increased disease damage—

High (reasonably certain) (Applicable criteria: a, b, c). 

As precipitation decreases, increased growth reduction and mortality losses in 

British Columbia could increase.4

 Increased growth loss and mortality would likely 

increase as sites become drier elsewhere as well.

Risk potential—

Warmer, drier—Very high (9) (Likelihood of increased disease damage = high; 

consequences of increased disease damage = high).

Warmer, wetter—High (6) (Likelihood of increased disease damage = moderate; 

consequences of increased disease damage = high).

A warmer climate will generally increase Armillaria incidence and impact as 

host stress increases. A drier climate would, in general, stress hosts more than a 

wetter climate, and thus increase host susceptibility.

4 Cruickshank, M.G.; Morrison, D.J. 2003. Armillaria mortality and growth loss estimates 

for interior Douglas-fir in the Interior Cedar-Hemlock ecosystem. Unpublished report. 

On file with: Canadian Forest Service, Pacific Forestry Centre, 506 West Burnside Road, 

Victoria, BC V8Z 1M5.
42

GENERAL TECHNICAL REPORT PSW-GTR-236

Yellow-Cedar Decline

Pathogen—

Abiotic.

Host—

Yellow-cedar (Callitropsis [Chamaecyparis] nootkatensis (D. Don) Florin. 

Distribution—

Southeastern Alaska, northern coastal British Columbia.

History and Current Status

Studies of stand age suggest yellow-cedar decline (fig. 11) began in southeast 

Alaska around 1880, at the end of several centuries with relatively cool temperatures (Hennon and others 1990a). Yellow-cedar decline was first reported in 1909 

(Sheldon 1912). Aerial photographs indicate that, by 1920, large stands of cedar 

were dead. By the 1970s and 1980s, yellow-cedar mortality was so high that pathologists thought a biotic pathogen was infecting the trees (Hennon and others 1990b). 

However, no biotic factor appears to be the cause (Hennon and others 1990b).

Yellow-cedar decline is most severe on trees at elevations lower than 300 m in 

southeast Alaska and British Columbia. Wet soils, an open canopy, and low elevations appear to be associated with decline (Hennon and others 1990a). The decline 

Figure 11—Dead Alaska yellow-cedar near Slocum Inlet, Alaska.

Paul Hennon, USDA Forest Service, Pacific Northwest Research Station
43

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

is believed to result from thaw-freeze damage to roots. As spring temperatures 

increase and the depth of the snowpack, which insulates roots, decreases, roots 

deharden prematurely and are susceptible to injury and death following spring 

freezes (Hennon and others 2006, Klinka and others 2000, Schaberg and others 

2008). 

The initial symptom of yellow-cedar decline is death of fine roots. Trees that 

lose rootlets fade, have thin or off-color crowns, and develop necrotic lesions on 

large roots. Infested stands may have numerous standing dead trees, some that 

died recently and others that died as much as 100 years ago (Hennon and Shaw 

1997). Snags may remain standing for many years because yellow-cedar heartwood 

decomposes slowly (Barton 1976). As the number of standing dead trees increases, 

more than 70 percent of the basal area of yellow-cedar may be dead (Hennon and 

others 2005). 

Decline of yellow-cedar has occurred on 200 000 ha of temperate rain forests 

across southeastern Alaska (Beier and others 2008, Snyder 2005) and northern 

coastal British Columbia (Hennon and others 2005). In Alaska, concentrated mortality occurs in a wide band from western Chichagof and the Baranof Islands to the 

Ketchikan area. Ground surveys show that in this band, 65 percent of the basal area 

of yellow-cedar is dead (USDA FS 1999). The distribution of decline parallels milder 

winter temperature isoclines in the region (Hennon and Shaw 1994). The total area 

affected by yellow-cedar decline has been increasing quite gradually (less than 1 m 

per year). Most stands contain dead trees; dying cedars with yellow, red, or thinning 

crowns; healthy cedars; and other tree species (USDA FS 1999).

Economic and Environmental Impacts

The economic value of dead yellow-cedar is high, but the trees often are not harvested. Accordingly, economic impacts appear to be minimal. Yellow-cedar decline 

alters stand structure by increasing the number of snags and alters stand composition 

as other trees replace the yellow-cedar. Over time, stands are dominated by other 

conifer species (USDA FS 1999). Growth of trees that co-occur with yellow-cedar 

may increase if competition with yellow-cedar decreases. Growth of other species of 

trees also may decrease, and mortality increase, on sites with poor drainage. Stands 

in which yellow-cedar decline has been present for the past century increasingly 

are dominated by western hemlock (Tsuga heterophylla (Raf.) Sarg.) and mountain 

hemlock (Tsuga mertensiana (Bong.) Carr). Accumulation of understory biomass of 

shrubs also is increasing considerably in some of these stands (USDA FS 1999).

The presence of yellow-cedar decline in southeast Alaska was associated with 

a 3.8-fold increase in the frequency of landslides compared to unaffected slopes 

because soil was prone to erosion (Johnson and Wilcock 2002).
44

GENERAL TECHNICAL REPORT PSW-GTR-236

Environmental Drivers of Disease

Yellow-cedar decline is caused by a reduction in depth of spring snowpack at lower 

elevations. Snow acts like a blanket on the ground, maintaining the soil and fine 

cedar rootlets at a consistent temperature. The trees continue to thrive at higher 

elevations where deep snowpack minimizes the probability that roots will freeze 

during the early spring.

Assessment and Analysis

Because yellow-cedar decline is caused by abiotic factors, criteria related to biology, such as reproduction, spread, infection, and reproductive potential, are not 

applicable. Assessment was based on the remaining criteria. 

Likelihood of increased disease damage—

Warmer, drier—Moderate (reasonably certain) (Applicable criteria: b, e).

Warmer, wetter—Low (reasonably certain) (Applicable criterion: e).

If temperature continues to increase and precipitation and depth of snowpack 

continues to decline, yellow-cedar decline may expand to higher elevations. This 

type of expansion has been observed at a few sites in southeast Alaska (Beier 2006, 

Beier and others 2008). If snowfall increases, the roots may be protected, and hosts 

will be less stressed despite increases in temperature; therefore, criterion b would 

not apply.

Consequences of increased disease damage—

High (moderately certain) (Applicable criteria: a, b, d, e).

Lower elevation forests may undergo changes in tree species composition. 

The economic value of dead yellow-cedar is high, but few trees currently are 

salvaged. Trees will persist at higher elevations where temperatures are relatively 

low and snow cover protects roots from freezing. Yellow-cedar has a limited 

natural distribution.

Risk potential—

Warmer, drier—High (6) (Likelihood of increased disease damage = moderate; 

consequences of increased disease damage = high).

Warmer, wetter—Moderate (3) (Likelihood of increased disease damage = low; 

consequences of increased pest damage = high). 

Continued warming would likely increase mortality of yellow-cedar. The 

resulting economic and environmental loss rates are potentially high, but would 

depend on whether the trees are salvaged for value.
45

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

Table 4—Risk potentials for selected diseases given projected increases in temperature and 

precipitation 

by 2100 

Likelihood of increased Consequences of increased 

Disease disease damage disease damage Risk potential

Dothistroma needle blight Moderate (2) Moderate (2) Moderate (4)

Swiss needle cast Moderate (2) Moderate (2) Moderate (4)

Sudden oak death/ramorum blight High(3) High (3) Very high (3)

White pine blister rust Low (1) High (3) Moderate (3)

Cytospora canker of alder Moderate (2) Moderate (2) Moderate (4)

Dwarf mistletoes Moderate (2) High (3) High (6)

Armillaria root disease Moderate (2) High (3) High (6)

Yellow-cedar decline Low (1) High (3) Moderate (3)

Table 3—Risk potentials for selected diseases given projected increases in temperature and 

decreases in precipitation by 2100

Likelihood of increased Consequences of increased 

Disease disease damage disease damage Risk potential

Dothistroma needle blight Low (1) Moderate (2) Low (2)

Swiss needle cast Low (1) Moderate (2) Low (2)

Sudden oak death/ramorum blight Low (1) High (3) Moderate (3)

White pine blister rust Low (1) High (3) Moderate (3)

Cytospora canker of alder High (3) Moderate (2) High (6)

Dwarf mistletoes Moderate (2) High (3) High (6)

Armillaria root disease High (3) High (3) Very high (9)

Yellow-cedar decline Moderate (2) High (3) High (6)

Summary and Conclusions

This risk assessment of climate change projected the effects of eight forest diseases 

under two climate-change scenarios (tables 3 and 4).

Because most foliar pathogens, including P. ramorum, require moisture for 

sporulation, dissemination, and infection, decreases in precipitation generally will 

decrease the likelihood of disease damage. Some needle cast diseases caused by 

species of Davisomycella and Hypodermella also require moisture for sporulation, 

dispersal, and infection, but are more likely to infect trees that are stressed by 

drought (Worrall and Sullivan 2002). 

The biology of stem rust pathogens on two-needled and three-needle pines 

in western North America—for example, western gall rust (Endocronartium 

harknessii), comandra rust (Cronartium comandrae), stalactiform rust (C. 

coleosporioides), and sweet fern rust (C. comptoniae)—is similar to C. ribicola. 

Infection and incidence of diseases caused by these fungi generally increases 
46

GENERAL TECHNICAL REPORT PSW-GTR-236

when conditions are cool and moist. The risk potential of these rusts likely is 

similar to that of white pine blister rust. Warmer conditions, whether wetter or 

drier, would be less favorable than cooler conditions.

The risk potentials for Cytospora canker of alder could be extrapolated to 

other stress-related canker diseases. Most canker diseases are caused by facultative parasites such as Botryosphaeria, Sphaeropsis, Cytospora, and Biscogniauxia

(Hypoxylon) (Desprez-Loustau and others 2006). These fungi are more likely to 

cause damage to trees that are stressed by heat and drought (Lonsdale and Gibbs 

2002; Schoeneweiss 1975, 1981). Not all canker diseases are associated with 

stressed hosts. The incidence of some canker pathogens, such as Thyronectria 

austro-americana on honeylocust (Gleditsia triacanthos L.) and Cryphonectria 

cubensis on Eucalyptus spp., is associated with high rainfall, and their hosts display 

some resistance to drought stress (Desprez-Loustau and others 2006).

The root pathogen Armillaria is more successful when hosts are stressed by 

drought. A root disease similar to Armillaria, Heterobasidion root disease, may also 

have a higher risk potential as temperature increases and precipitation decreases. 

In North America, Heterobadision irregulare and H. occidentale—formerly the 

intersterility groups P and S, respectively, of H. annosum (Otrosina and Garbelotto 

2010)—cause substantial wood decay (Goheen and Otrosina 1998). Host stress, in 

particular soil moisture stress (Towers and Stambaugh 1968), increases host susceptibility to Heterobadision. Infection and damage in coniferous forests is lowest 

when temperatures are low and precipitation is high (Shaw 1988). In the southeastern United States, Heterobasidion root disease is more prevalent in sandy, dry soils 

than in heavier soils with poor drainage or high water tables (Froelich and others 

1966, Kuhlman and others 1976).

The criteria used here to determine likelihood of increased disease damage are 

not entirely appropriate for a strictly abiotic disease such as yellow-cedar decline. 

The criteria for consequences of increased damage apply, but the criteria for 

likelihood of increase damage include two (a and c) relating to pathogen biology 

that do not. 

Although the results of this risk assessment suggest that climate change will 

affect forest health, the uncertainties associated with the risk potentials should be 

kept in mind. In this assessment, uncertainty arises regarding the degree of climate 

change that will occur, pathogen biology under changing climate; the effects of 

changing climate directly on the host, and the interactions between the pathogen, 

host, and climate. 
47

A Risk Assessment of Climate Change and the Impact of Forest Diseases on Forest Ecosystems in the Western U.S. and Canada

The information provided in this risk assessment should be useful to decisionmakers and managers for strategic and management planning, the second step in a 

risk analysis. This risk assessment also serves as the basis for subsequent communication instruments or products for audiences in addition to technical users. The 

communication of the risk assessment, the third step in a risk analysis, can have 

different written and oral forms to meet the needs of the intended audiences (e.g., 

risk managers, the public). 

Acknowledgments

This risk assessment is the result of the “Climate Change and Western Forest Diseases” project sponsored by the USDA FS Western Wildland Environmental Threat 

Assessment Center (WWETAC) and the Pacific Southwest Research Station (PSW). 

The project builds on a June 2007 workshop on climate change and forest insects 

and diseases held by WWETAC (Beukema and others 2007) in October 2007 that 

was sponsored by the USDA FS, WWETAC, and PSW in cooperation with the 2007 

Western International Forest Disease Work Conference, and a literature review of 

climate change and forest diseases in western North America (Kliejunas and others 

2009). The author appreciates the reviews and assistance of Susan Frankel, USDA 

FS, PSW; Jeff Hicke, USDA FS WWETAC; James Worrall, USDA FS, Forest 

Health Protection, Rocky Mountain Region; and Erica Fleishman, University of 

California, Santa Barbara. 

English Equivalents

When you know: Multiply by: To find:

Millimeters (mm) 0.0394 Inches

Centimeters (cm) 0.394 Inches

Kilometers (km) 0.621 Miles

Meters (m) 3.28 Feet

Hectares (ha) 2.47 Acres (ac)

Cubic meters (cm3

) 35.314 Cubic feet (ft3)

Degrees Celsius (°C) 1.8 and add 32 Degrees Fahrenheit
48

GENERAL TECHNICAL REPORT PSW-GTR-236

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