Annurev Phyto 37 1 399

P1: FHP/FGO P2: FHP/FGP/FGM QC: FHP/arun T1: FDX
June 29, 1999 14:33 Annual Reviews AR087-16
Annu. Rev. Phytopathol. 1999. 37:399426

Copyright
c 1999 by Annual Reviews. All rights reserved
CLIMATE CHANGE AND PLANT DISEASE

MANAGEMENT
?
Stella Melugin Coakley
Department of Botany and Plant Pathology, Oregon State University, Corvallis,
Oregon 97331; e-mail: coakleys@bcc.orst.edu
Annu. Rev. Phytopathol. 1999.37:399-426. Downloaded from www.annualreviews.org
Access provided by Ohio State University Library on 08/25/17. For personal use only.
Harald Scherm
Department of Plant Pathology, University of Georgia, Athens, Georgia 30602;
e-mail: scherm@uga.edu
Sukumar Chakraborty
CSIRO Tropical Agriculture, CRC for Tropical Plant Pathology, University of
Queensland, Queensland 4072 Australia; e-mail: sukumar.chakraborty@tag.csiro.au
Key Words climate variability, epidemiological models, global warming,

host-pathogen interactions, risk and impact assessment
Abstract Research on impacts of climate change on plant diseases has been lim-
ited, with most work concentrating on the effects of a single atmospheric constituent
or meteorological variable on the host, pathogen, or the interaction of the two un-
der controlled conditions. Results indicate that climate change could alter stages and
rates of development of the pathogen, modify host resistance, and result in changes
in the physiology of host-pathogen interactions. The most likely consequences are
shifts in the geographical distribution of host and pathogen and altered crop losses,
caused in part by changes in the efficacy of control strategies. Recent developments in
experimental and modeling techniques offer considerable promise for developing an
improved capability for climate change impact assessment and mitigation. Compared
with major technological, environmental, and socioeconomic changes affecting agri-
cultural production during the next century, climate change may be less important; it
will, however, add another layer of complexity and uncertainty onto a system that is
already exceedingly difficult to manage on a sustainable basis. Intensified research on
climate changerelated issues could result in improved understanding and management
of plant diseases in the face of current and future climate extremes.
INTRODUCTION
Global climate change is a major topic of discussion within both scientific and po-
litical forums. By mid-1998, evidence was mounting that 1998 would set a record
high for global mean temperature, with 1997 holding the current record. Combined
0066-4286/99/0901-0399$08.00 399
400 COAKLEY SCHERM CHAKRABORTY
ocean and land temperatures were 0.25 C warmer from January to May 1998 than
previously recorded (154). September 1998 was the hottest on record (104 years)
in the United States, with a mean of 20.6 C; the earlier record of 20.2 C was set in
1931 (11). Increasingly, scientists are convinced that human activity, primarily
in the form of increased emissions of carbon dioxide (CO2) and other greenhouse
gases (predominantly methane and nitrous oxide), is a major contributor to the
warming trend. Indeed, the Second Assessment Report of the Intergovernmental
Panel on Climate Change (IPCC), which was edited in 1995 (59), concluded that
?
(i) greenhouse gas concentrations have increased and will continue to do so given
their long life in the atmosphere; (ii) climate has changed over the past century in
response to increasing atmospheric CO2, with the global mean surface air temper-
ature increasing between 0.3 and 0.6 C; (iii) anthropogenic aerosols such as sulfur
dioxide tend to produce negative radiative forcing (i.e. a cooling trend) but are
relatively short-lived; and (iv) climate model simulations using future emission
scenarios of greenhouse gases and aerosols suggest an increase in global mean
temperature between 1 and 3.5 C by the year 2100 (67). Although the IPCC re-
port represents the broad consensus among many scientists from a wide range of
disciplines, alternative interpretations of the evidence presented in the report do
exist (61, 138).
The IPCC report was the basis for discussion at the Kyoto Conference in
December 1997 that led to a climate treaty ratified by more than 150 countries.
The United States signed the treaty in November 1998 but ratification by Congress
is not expected within the next two to three years. The Kyoto Protocol could result
in reductions in six greenhouse gases including CO2, methane, and nitrous oxide.
It calls for an average 5.2% reduction (from 1990 levels) of CO2 emissions by
38 industrialized nations by 2012, although increasing emissions from developing
countries could offset these reductions (85). Curbing of CO2 emissions is a very
charged political issue in the United States (73), in part because of the position
that any reduction in fossil fuel consumption would be damaging to the economy.
Nevertheless, scientists optimistically provide a road map and recommendations
of the technology necessary to achieve a reduction to below 1990 CO2 levels
(102, 115).
Is global warming an absolute? As recently as 1994, Time magazine carried
a feature article The Ice Age Cometh? (74), describing the January blizzard that
resulted in record low temperatures in dozens of cities in the United States. This
extreme expression of the weather is not inconsistent with the notion that cli-
mate change would lead to increased climate variability and more frequent or
more severe climatic extremes (39, 55, 92, 113, 162). Underlying all discussions
is the expectation that as climate changes, so does the human response to it. With
this in mind, there have been numerous attempts to predict the potential impacts of
climate change on human enterprises, including agriculture (1, 38, 101, 117, 118).
Despite the important role of plant pathogens in limiting agricultural production
and food supply (100), there has been limited research to assess the potential im-
pacts of climate change on plant diseases (22, 24, 26, 28). For example, a recent
CLIMATE CHANGE AND DISEASE MANAGEMENT 401
monograph entitled Climate Change and the Global Harvest: Potential Impacts
of the Greenhouse Effect on Agriculture (117) devoted only two pages (out of 324
total) to plant diseases. In contrast, potential impacts on infectious diseases of
humans have received considerably more attention, including a monograph pub-
lished by the World Health Organization (91) and a stand-alone chapter in the
1995 IPCC report (90). Suggestions in these publications that a warmer climate
will bring increases of human disease have been challenged as premature and
with little basis in fact, based on examination of historical patterns and the general
?
absence of research in this area (147). It is with this example that we enter into
a review of what appears probable, what may be possible, and what is unlikely in
terms of climate change and its impacts on plant diseases.

COMPONENTS OF CLIMATE CHANGE
Mahlman (84) commented on and updated the summary of IPCCs 1995 report.
He classified the relative certainty of change into several categories. Virtually
certain facts include that atmospheric concentrations of greenhouse gases would
continue to rise, largely caused by human activities such as burning of fossil fuel
and changes in land use. These gases, which may remain in the atmosphere from
a decade to centuries, act to heat the planet because of absorption and re-radiation
of infrared radiation. Changes in other radiatively active substances (e.g. sulfur
aerosols) and increased cloudiness caused by greater evaporation in a warmer
climate may offset some of the greenhouse effect. Another virtually certain fact
is that earths surface has warmed about 0.5 0.2 C during the past century. The
expected rate of increase is now at 0.1 C per decade (69).
Under virtually certain projections (99% likely to happen), Mahlman (84)
included the forecast that the stratosphere would continue to cool as CO2 levels
rise and that global mean concentrations of water vapor in the lower troposphere
would increase (approximately 6% per 1 C warming).
A very probable projection would have a greater than 90% chance of being
correct; under this category, Mahlman (84) predicted that a doubling of atmo-
spheric CO2 (from a current concentration of 360 ppm) would result in a warming
between 1.5 and 4.5 C. The rate of evaporation would increase in a warmer cli-
mate, which would lead to an increase in global precipitation of 2 0.5% per 1 C
warming. Higher latitudes in the Northern Hemisphere are expected to experience
above-average increases in both temperature and precipitation.
Mahlmans final category (probable projections, which have a greater than
two thirds chance of occurring) included the forecast that there would be decreases
in soil moisture because of increased temperatures, although this could be offset by
simultaneously increased precipitation. Further, changes in mean climate would
probably be accompanied by changes in the frequency and magnitude of climate
extremes; globally, this would include an increased probability of warm events
and decreased probability of cold events.
Hansen et al (49) proposed an easily understood climate index based on heating

degree days and frequency of precipitation to monitor climate change. For Asia
and western North America, the index indicates that climate change should be
evident already. Indeed, an increasing number of recent studies involving analyses
ranging from satellite temperature data (50) to borehole temperatures (108) is
lending support to the notion that climate change is occurring now. Mahlman (84)
concluded that it is virtually certain that human-caused greenhouse warming is
going to continue to unfold, slowly but inexorably, for a long time into the future.
?
What is much less certain is the magnitude of climate change and its impacts on
biological and ecological processes and on human enterprises.
IMPACTS ON CROPS
Climate change will influence the geographical distribution and growth of plant
species around the world. The magnitude of these impacts would vary depending
on the species involved and their growth patterns (e.g. annuals vs perennials;
agricultural crops vs natural vegetation). Natural vegetation would be affected
by factors such as competition, migration, and recovery from disturbances, and
therefore new combinations of species are likely to occur (41). In managed systems
(agriculture and forestry), any effects of climate change have important socio-
economic implications for the countries involved, hence considerable efforts have
been directed toward agricultural impact assessment (1, 38, 101, 117, 118). How
a particular agroecological region will fare under climate change will depend
largely on societys ability to use available knowledge, technology, and financial
resources.
Nicholls (98) analyzed historical trends in Australian wheat yields and estimated
that recent climate changes were responsible for as much as 30 to 50% of the
observed yield increase, with most of the variation explained by an increase in
minimum temperature. Goudriaan & Zadoks (44) summarized a large body of
evidence suggesting that elevated CO2 would result in increased photosynthesis
and water use efficiency. This would lead to yield increases in most crops in most
production conditions. Idso & Idso (60) reviewed hundreds of CO2 enrichment
studies done over ten years and reported that in most cases, there was evidence
of growth-enhancing effects. IPCCs 1995 report (112) predicted that a doubling
in CO2 could increase yields of several major crops by an average of 30%. In
contrast, recent data taken in field-scale experiments with elevated CO2 suggested
only an 8 to 12% wheat yield increase under optimal growing conditions (45).
Further, evidence is now accumulating that crop production would be affected
differentially depending on latitude. Although increases in yields are expected at
mid and high latitudes, there may be decreases at lower latitudes where food needs
are greatest (112, 117).
Any direct yield gains caused by increased CO2 or climate change could be off-
set partly or entirely by losses caused by phytophagous insects, plant pathogens,
and weeds. It is therefore important to consider these biotic constraints in stud-

ies on crop yields under climate change. Unfortunately, nearly all previous cli-
mate changeyield studies were done under exclusion of insects, pathogens, or
weeds. For example, yield simulations using growth models have been com-
pleted for various crops in different agroecological zones (43, 113), but only
the models for rice have incorporated disease aspects in a mechanistic form
(7780).
?
IMPACTS ON PLANT PATHOSYSTEMS
The focus of this review is on how climate change manifested by elevated CO2,
increased temperature, and changes in precipitation may affect plant diseases and
their management. Considerable literature is available on the impacts of other as-
pects of global change, particularly air pollutants (26, 31, 82). For example, the
effects of ozone on plant metabolism, crop yield and productivity (54, 72), plant
health (87, 124, 156), host-pathogen interactions (53, 125), host defense mech-
anisms, and interactions with pathogenic and saprophytic organisms have been
extensively studied. Similarly, studies on the effects of increased UV-B on plants
(119, 153), pathogens (4, 71, 111), phyllosphere yeasts (46), and disease develop-
ment (2, 37, 47, 87, 104) are well represented in the literature.
Most research on how climate change influences plant diseases has concentrated
on the effects of a single atmospheric constituent or meteorological variable on the
host, pathogen, or the interaction of the two under controlled conditions (21, 2426,
28, 83, 87). Interactions are clearly more complex in the real world, however, where
multiple climatological and biological factors vary simultaneously in a dynamic
environment. Climate change has the potential to modify host physiology and
resistance and to alter stages and rates of development of the pathogen. The most
likely impacts would be shifts in the geographical distribution of host and pathogen,
changes in the physiology of host-pathogen interactions, and changes in crop
loss. Another important impact may be through changes in the efficacy of control
strategies.
Geographical Distribution of Host and Pathogen

New disease complexes may arise and some diseases may cease to be econom-
ically important if warming causes a poleward shift of agroclimatic zones and
host plants migrate into new regions. Pathogens would follow the migrating hosts
and may infect remnant vegetation of natural plant communities not previously
exposed to the often more aggressive strains from agricultural crops. Facultative
parasites with broad host ranges would mostly fall in this category, although obli-
gate parasites may also expand their host range to infect plants in their proximity
(35, 127). The mechanism of pathogen dispersal, suitability of the environment
for dispersal, survival between seasons, and any change in host physiology and
ecology in the new environment will largely determine how quickly pathogens
become established in a new region.
Changes may occur in the type, amount, and relative importance of pathogens
and affect the spectrum of diseases affecting a particular crop. This would be more
pronounced for pathogens with alternate hosts. For perennial species in plantation
and natural forests and orchards, plants may continue to be grown in existing
regions under marginal climatic conditions. The need for large tracts of suitable
land, infrastructure such as fruit- or timber-processing facilities, and the high
?
cost of establishing a new plantation could limit the mobility of perennial crops.
Plants growing in marginal climate could experience chronic stress that would
predispose them to insect and disease outbreaks. Warming and other changes could
also make plants more vulnerable to damage from pathogens that are currently not
important because of unfavorable climate. Infection of eucalypts by Phytophthora
cinnamomi is favored in wet soils at temperatures of 12 to 30 C (107), hence the
pathogen does not pose a serious threat to the susceptible Eucalyptus spp. grown in
southeastern Australia. This situation may change with an increase in temperature.
Similarly, poplar clones in northern Europe may experience increased damage from
the thermophilic rust, Melampsora alli-populina (76).
If the frost-line moves north in the Northern Hemisphere, higher winter tem-
peratures could be accompanied by increased survival of insects (109, 145). For
virus-vector aphids, this could lead to higher incidence of virus diseases, espe-
cially in those regions where the timing of virus arrival is linked to winter survival
and spring flight of aphids (51). Barley yellow dwarf potyvirus (BYDV) is an
example of a virus that causes more severe disease following mild winters. Since
BYDV is exclusively vectored by aphids, increased survival of pathogen reservoirs
could greatly increase the economic losses caused by infection. Similar increases
in viruses of potato and sugar beet have also been observed following warmer
winters (19, 51, 81, 150).
Physiology of Host-Pathogen Interactions

Elevated CO2
Increases in leaf area and duration, leaf thickness, branching, tillering, stem and
root length, and dry weight are well-known effects of increased CO2 on many
plants (13, 167). Based on a review of literature, Manning & von Tiedemann (87)
suggested that elevated CO2 would increase canopy size and density, resulting
in a greater biomass of high nutritional quality. When combined with increased
canopy humidity, this is likely to promote foliar diseases such as rusts, powdery
mildews, leaf spots, and blights.
The decomposition of plant litter is an important factor in nutrient cycling and
in the saprophytic survival of many pathogens. Increased C:N ratio of litter is
a consequence of plant growth under elevated CO2 (5). Evidence from pot and
field studies indicates that decomposition of high-CO2 litter occurs at a slower
rate. Increased plant biomass, slower decomposition of litter, and higher winter
temperature could increase pathogen survival on overwintering crop residues and

increase the amount of initial inoculum available to infect subsequent crops.
In recent studies on host-pathogen interactions in selected fungal pathosys-
tems, two important trends have emerged on the effects of elevated CO2. First,
the initial establishment of the pathogen may be delayed because of modifications
in pathogen aggressiveness and/or host susceptibility. Colletotrichum gloeospo-
rioides showed delayed or reduced conidial germination, germtube growth, and
appressorium production when inoculated onto susceptible Stylosanthes scabra
?
plants under increased CO2 (23). Similar effects in other pathosystems include a
reduction in the rate of primary penetration in Erysiphe graminis (barley powdery
mildew) (57) and a lengthening of the latent period in Maravalia cryptostegiae

(rubbervine rust) (S Chakraborty, MP Weinert & JR Brown, unpublished data).

In these examples, host resistance may have increased because of changes in
host morphology, physiology, nutrients, and water balance. A decrease in stom-
atal density (7, 13, 167) increases resistance to pathogens that penetrate through
stomates. In barley, although the thickness of epicuticular wax did not play a
role in resistance to E. graminis, plants in elevated CO2 were able to mobi-
lize assimilates into defense structures including the formation of papillae and
accumulation of silicon at sites of appressorial penetration (57, 58). High-CO2
wheat had an average 14% reduction in nitrogen concentration in its shoot tis-
sue (30) that was associated with decreased susceptibility to powdery mildew
(151).
The second important finding has been an increase in the fecundity of pathogens
under elevated CO2. Following penetration, established colonies of E. graminis
(57) and C. gloeosporioides grew faster under 2 CO2. Sporulation per unit area
of infected tissue was increased several-fold under elevated CO2 for C. gloeospo-
rioides (23) and for M. cryptostegiae (S Chakraborty, MP Weinert & JR Brown,
unpublished data).
There are few studies on how elevated CO2 may influence diseases other than
those caused by fungi. Malmstrom & Field (86) examined the effects of 2 CO2
on oats infected with BYDV. With virus infection, the oats showed a greater
biomass response to CO2 enrichment than did the healthy plants. Root biomass
increased more in the infected plants than in those not infected. It is possible,
therefore, that elevated CO2 could alter the epidemiology of BYDV by increasing
the virus reservoir due to improved winter survival of infected plants as the result
of increased root biomass and water use efficiency (86).
Elevated Temperature
Increases in temperature can modify host physiology and resistance. Considerable
information is available on heat-induced susceptibility and temperature-sensitive
genes (33, 42, 123). For example, a rise in temperature above 20 C can inacti-
vate temperature-sensitive resistance to stem rust in oat cultivars with Pg3 and
Pg4 genes (89). In contrast, lignification of cell walls increased in forage species
at higher temperatures (165) to enhance resistance to fungal pathogens (140).
Impacts would, therefore, depend on the nature of the host-pathogen interactions

and the mechanism of resistance.
Agricultural crops and plants in natural communities may harbor pathogens
as symptomless carriers (32, 66), and disease may develop if plants are stressed
in a warmer climate. Host stress is an especially important factor in decline of
various forest species. Climate extremes such as drought may increase invasion
by Armillaria spp. that are not normally very pathogenic (76, 114). High temper-
atures may increase the damage caused by diseases such as Scleroderris canker on
?
lodgepole pine (65, 76). Such projections, however, do not consider other factors
that can enhance the resilience of forest ecosystems to climate change, which led
Loehle (75) to conclude that there is a systematic bias toward alarmist predictions
in projections of tree health response to climate change.
Crop Loss
At elevated CO2, increased partitioning of assimilates to roots occurs consistently
in crops such as carrot, sugar beet, and radish. If more carbon is stored in roots,
losses from soilborne diseases of root crops may be reduced under climate change.
In contrast, for foliar diseases favored by high temperature and humidity, increases
in temperature and precipitation under climate change may result in increased
crop loss. The effects of enlarged plant canopies from elevated CO2 could further
increase crop losses from foliar pathogens (23, 87). Unfortunately, canopy char-
acteristics have not featured prominently in plant pathology research, despite their
influence on microclimate and pathogen dispersal (3). Recent developments in
three-dimensional modeling of plant architecture (virtual plants) offer new op-
portunities to integrate canopy architecture with microclimate effects and pathogen
dispersal (166).
Chakraborty et al (23) studied dispersal of and infection by C. gloeosporioides
under ambient weather conditions in the field on S. scabra plants that had been
raised under 1 or 2 CO2 in controlled environment chambers. Plants from
the two CO2 environments were exposed to naturally occurring inoculum in the
field on different dates, and conidial dispersal and infection were monitored. The
enlarged canopy of plants grown under elevated CO2 trapped more conidia that,
together with increased humidity in the denser canopy, led to more severe anthrac-
nose than on plants grown under 1 CO2 (Figure 1). In a separate experiment,
disease was reduced when plants were grown under elevated CO2 and inoculated
with C. gloeosporioides inside the controlled environment (23). The contrasting
results help to highlight dangers in extrapolating effects observed under controlled
environments to field situations.
It is difficult to arrive at realistic predictions of yield losses that may result
from a slow and gradual climate change by extrapolating findings from controlled
environment studies which generally considered only two contrasting CO2 levels.
Indeed, host and pathogen populations are apt to adapt to gradual changes in CO2
concentration. Long-term field studies utilizing free-air CO2 enrichment (FACE
technology) (136) or similar open-air facilities (99) offer the best approach to
?
Figure 1 Cumulative number of lesions (a) and disease severity expressed as per-
cent leaf area affected (b) caused by Colletotrichum gloeosporioides on susceptible
Stylosanthes scabra plants that had been raised under 1 or 2 CO2 in controlled
environment chambers before being exposed to naturally occurring inoculum in three
field plots for 48 h on five separate occasions. Data are means and standard errors
from five exposures with three plants from each field plot. Source: S Chakraborty, IB
Pangga, PM Room & D Yates (unpublished data).
studying disease development and crop losses caused by polycyclic pathogens.

Runion et al (120) presented preliminary data on the effects of 2 CO2 on the
phyllosphere and rhizosphere microflora of cotton at the FACE-site in Arizona.
They found that soil infestation by Rhizoctonia solani tended to be greater under
elevated CO2 at one of their sampling dates; a laboratory bioassay of the soil,
however, showed no increased damping-off potential.
Regional Impact Assessment

There have been some efforts to estimate impacts of climate change on plant dis-
eases at regional or country levels. An assessment in New Zealand (110) concluded
that disease problems in the kiwifruit and pome fruit industries would probably
be amplified by increases in temperature and precipitation. Areas on the northern
island such as Hawkes Bay and Nelson are likely to experience increased levels of
Botrytis, Sclerotinia, blossom blight, and fire blight. In contrast, the impacts on the
vegetable industry should be minimal because this industry is mostly annual and
intensive in nature and management changes required to mitigate climate change

impacts may be made more easily.
In a review of potential impacts of climate change on Australia, plant pathol-
ogists developed qualitative impact assessments for important diseases of major
agricultural crops (22). For wheat, the analysis indicated that existing cultivars
would experience increased severity of stripe rust, Septoria tritici blotch, and
BYDV, but take-all would be reduced in warm and wet soils. It was further sug-
gested that increases in soil temperature may reduce Verticillium wilt in potato
?
and tomato but increase sugarcane root rot caused by Pachymetra chaunorhiza.
Increases in summer temperature and the frequency of precipitation would favor
apple powdery mildew but reduce peach leaf curl.

Carter et al (20) summarized results of five years work on the impacts of

climate change on agriculture in Finland. The assessment included pathogens
such as Phytophthora infestans and the root knot nematode, both of which were
predicted to increase because of additional pathogen generations in a warmer
climate. Another preliminary, country-wide assessment of impacts on important
plant diseases was presented by von Tiedemann (155) for Germany.
IMPACTS ON DISEASE MANAGEMENT
Because of the rudimentary knowledge about impacts of climate change on plant

pathosystems, it is impossible to predict implications for disease management
with any certainty. It is prudent to assume, however, that effects would occur
chiefly through influences on host resistance or chemical and biological control
agents. Particular attention is needed to identify cases where the efficacy of disease
management may be reduced under climate change.
Host Resistance
Cultivar resistance to pathogens may become more effective because of increased
static and dynamic defenses from changes in physiology, nutritional status, and
water availability (see Physiology of Host-Pathogen Interactions). Durability of
resistance may be threatened, however, if the number of infection cycles within
a growing season increases because of one or more of the following factors: in-
creased fecundity, more pathogen generations per season, or a more suitable mi-
croclimate for disease development. This may lead to more rapid evolution of
aggressive pathogen races. In a pilot study, Chakraborty et al (unpublished data)
monitored evolution of C. gloeosporioides on S. scabra under elevated CO2. A
susceptible cultivar was grown in a controlled environment under 1 or 2 CO2
and inoculated with three isolates of the pathogen. For each isolate, conidia col-
lected from infected host tissue were used to inoculate a second group of plants of
the same cultivar. Successive groups of plants were inoculated with conidia arising
from the previous infection cycle to simulate polycyclic disease development and
?
Figure 2 Disease severity (on a scale from 0 to 9) caused by Colletotrichum gloeospo-

rioides on susceptible Stylosanthes scabra plants under 2 CO2 over eight cycles of
infection. For each of the three isolates (indicated by different symbols and lines),
successive groups of plants were inoculated with conidia arising from the previous in-
fection cycle to simulate polycyclic disease development and pathogen evolution over
time. The regression lines for the three isolates were significantly different from zero
(P < 0.05). Source: S Chakraborty, PA Wilson & IB Pangga (unpublished data).
pathogen evolution over time. After each cycle, measurements were made on com-
ponents of pathogen aggressiveness, such as fecundity, lesion size, lesion number,
and disease severity. Preliminary results suggested a significant trend toward in-
creased disease severity (Figure 2); further, two of the three isolates showed a
gradual increase in fecundity under elevated CO2 after eight infection cycles.
Chemical Control
Climate change could affect the efficacy of crop protection chemicals in one of
two ways. First, changes in temperature and precipitation may alter the dynam-
ics of fungicide residues on the crop foliage. Globally, climate change models
project an increase in the frequency of intense rainfall events (39), which could
result in increased fungicide wash-off and reduced control. The interactions of
precipitation frequency, intensity, and fungicide dynamics are complex, and for
certain fungicides precipitation following application may result in enhanced dis-
ease control because of a redistribution of the active ingredient on the foliage (128).
Neuhaus et al (96) applied simulated rain to potato foliage at two intensities (6 and
30 mm h1) and found that the higher rate significantly reduced the fungicide
residue that could be measured with a chemical assay, but that there was no dif-
ference in disease between the two treatments when the leaves were challenged in
a bioassay with Phytophthora infestans.
Second, morphological or physiological changes in crop plants resulting from
growth under elevated CO2 could affect uptake, translocation, and metabolism
of systemic fungicides. For example, increased thickness of the epicuticular wax
?
layer on leaves (13, 167) could result in slower and/or reduced uptake by the host,
whereas increased canopy size could negatively affect spray coverage and lead to
a dilution of the active ingredient in the host tissue. Both factors would suggest
lowered control efficacy at higher concentrations of CO2. Conversely, increased

metabolic rates because of higher temperatures could result in faster uptake by and
greater toxicity to the target organism. In a pilot study with the herbicide chloro-
toluron, Edis et al (34) showed that a resistant biotype of the weed blackgrass
(Alopecurus myosuroides) became more sensitive to herbicide application when
grown under elevated CO2. The authors hypothesized that this was due to changes
in herbicide uptake and translocation because of altered stomatal physiology. De-
spite the potential for important interactions, no similar studies evaluating the
impacts of climate change variables on physiological aspects have been published
for fungicides.
Microbial Interactions
Climate change may alter the composition and dynamics of microbial communities
in aerial and soil environments sufficiently to influence the health of plant organs
(4, 46, 122). Changed microbial population in the phyllosphere and rhizosphere
may influence plant disease through natural and augmented biological control
agents. A direct effect of elevated CO2 is unlikely in the soil environment as
the microflora there is regularly exposed to levels 10 to 15 times higher than
atmospheric CO2.
Trees grown in soils of poor nutrient status, especially nitrogen, favor colo-
nization of roots by arbuscular mycorrhizal fungi (70). The relationship between
elevated CO2 and mycorrhizae is not well understood (139), and there are con-
flicting reports on how it may be influenced by the nutrient status of the plant and
soil. If a lower nitrogen status of plant tissue under increased CO2 results in more
mycorrhizal colonization, this could improve plant health through improved nutri-
ent uptake. Similar confusion exists on the potential role of vesicular-arbuscular
mycorrhizae and ectomycorrhizae in the suppression and biological control of
plant pathogens. Mycorrhizae can have positive, negative, or neutral effects on
plant disease, and their role is not well understood despite numerous studies on the
subject (105). Clearly, the influence of mycorrhizae on plant health under climate
change requires further research.
Changes in temperature may have highly nonlinear effects on tri-trophic interac-
tions of host, pathogen, and biocontrol agent. In wheat (152), a rise in temperature
from 17 to 22 C resulted in an increase in aphid (Sitobion avenae) reproduction

by 10%; at the same time, however, predatory activity by lady beetle (Coccinella
septempunctata) adults increased by 250%. Aphid damage was reduced further
because of earlier maturity of the crop. Similar data are not available for tri-trophic
interactions involving plant pathogens.
Quarantine and Exclusion
?
Management of climate change will put additional pressure on agencies responsi-
ble for exclusion as a plant disease control strategy (64). In some regions, certain
diseases of economic concern do not currently occur because the climate has
precluded the causal agents from becoming established. Use of Geographical In-
formation Systems and climate matching tools may assist quarantine agencies in
determining the threat posed by a given pathogen under current and future cli-
mates. This approach was used by Sansford & Baker (126) to assess the risk of
establishment of Karnal bunt in the cereal-growing regions of the European Union.
IMPACT MODELS
Most of what has been said about plant disease in relation to climate change is
based on qualitative, rule-based reasoning. This approach seems attractive because
of the substantial body of knowledge already available regarding the environmen-
tal requirements of plants and their pathogens (25, 28, 36). For example, it seems
plausible that increased air temperature would result in a poleward expansion of
the geographical range of pathogens and in more generations per year (109); that
elevated winter temperatures would increase survival and hence the amount of
initial inoculum in many pathosystems (28); and that greater continental dryness
during summer (6) would reduce risk of infection by pathogens that require leaf
wetness or saturated soils for infection. But will this really be what happens? The
answer will depend on complex interactions of atmospheric, climatic, and biolog-
ical factors with technological and socioeconomic changes that are exceedingly
difficult to predict (24). It would appear, therefore, that in all but the simplest
cases these interactions are not amenable to qualitative analyses. Hence, quanti-
tative (modeling) approaches, which allow one to investigate multiple scenarios
and interactions simultaneously, will become more important for impact assess-
ment (28). Guidelines for such model-based assessments are needed, and Sutherst
et al (146) and Teng & Yang (149) have given a framework. With few exceptions
(28, 146, 148), not enough attention has been given to modeling approaches and
the analytical tools needed for quantitative impact assessment in plant pathology.
Climate Matching
Climate matching involves the calculation of a match index to quantify the
similarity in climate between two or more locations. The match index is based on
variables such as monthly minimum and maximum temperatures, precipitation,

and evaporation. Software packages for climate matching include BIOCLIM (18),
CLIMEX (143), HABITAT (158), and WORLD (9). These packages often come
with additional useful features such as internal algorithms for generating climate
surfaces through interpolation between stations. Climate matching may be used
for climate change impact assessment by identifying those locations on the globe
with a current climate that is most similar to the predicted future climate at the
location of interest. An analysis of the plant disease problems at the matching
?
locations, for example based on disease distribution maps (161), would allow
predictions to be made about future disease risk at the location of interest.
Booth et al (10) used climate matching to identify regions suitable for Cylin-
drocladium leaf blight on Eucalyptus spp. in Southeast Asia and around the world.
They first established a simple rule for presence or absence of the disease based
on long-term means of temperature and precipitation. This rule was then imple-
mented in a climate matching program to identify high-risk regions in Africa,
Australia, Latin America, and Southeast Asia under current climate. Further, two
climate change scenarios were run for locations in Southeast Asia. The results sug-
gested an increase in disease risk in northern Vietnam, southern Laos, and eastern
Thailand. These predictions are consistent with limited field observations indi-
cating that severe disease can occur in these regions during years with extreme
weather.
Possible effects of climate change on Phytophthora cinnamomi, a soilborne
oomycete with an extremely wide host range, were considered by Brasier (15)
and Brasier & Scott (16). This pathogen requires warm, wet soils and is hence
limited primarily to tropical and subtropical regions (76, 88, 107). More recently,
P. cinnamomi has been associated with oak declines in southern and Mediterranean
Europe. It was hypothesized (14) that this may be an early indication of climate
warming as the pathogen may have become more active because of higher soil tem-
peratures and/or increased host susceptibility caused by stress (e.g. more frequent
winter droughts in the region). For a more formal impact assessment, Brasier &
Scott (16) used the CLIMEX climate matching program (143) to map regions in
Europe favorable or unfavorable for this pathogen under present and future cli-
mate scenarios. The climate change simulations suggested that the pathogen could
extend its range further north, although it appeared unlikely that it could become
established in those regions where winter temperatures are low such as central and
eastern Europe (15). It was further hypothesized that the pathogens host range
could increase if spread occurs into regions where it is currently absent.
Empirical Models
Four diseases of two major crops in China, wheat and rice, were examined by
regression analysis to determine how they have varied through time and whether
this may relate to recent increases in mean and minimum temperatures (169). Rice
blast and wheat scab have increased sharply since the 1970s. The wheat acreage
infected with powdery mildew has become more extensive, whereas stripe rust
has decreased steadily (169). This may be related to the increased spring and
early summer temperatures and would be consistent with the changes in stripe rust
observed in the Pacific Northwest associated with climate variability (27).
Boag et al (8) used data from soil samples collected during the European Plant-
Parasitic Nematode Survey to assess the possible impacts of climate warming on
the geographical range of virus-vector nematodes. Initial analyses of nematode
presence-absence data suggested a close association between mean July soil tem-
?
perature and nematode distribution. Based on this result, the authors predicted that
climate change could result in increased nematode and virus problems in northern
Europe; they estimated that a 1 C warming would allow the species in study to mi-
grate northward by 160 to 200 km (95). Although nematodes migrate very slowly,
humans are credited with efficiently disseminating them. Hence, nematode spread
into new regions could put a wide range of crops at risk; additionally, introduction
of new crops into a region could also expose them to infestation by nematode
species already present. Changes in precipitation, which were not considered in
these analyses, could influence nematode distribution on a large scale, although
previous findings had suggested that soil moisture would not affect nematode
distribution in most agricultural soils in northern Europe (8, 95).
In a similar study, Jahn et al (62) utilized long-term plant disease monitor-
ing records collected by the State Plant Protection Service in the former German
Democratic Republic (GDR) to develop empirical climate-disease models for 15
individual host-pathogen combinations. These models were then used with vari-
ous climate change scenarios to predict possible changes in infestation levels in
a future climate. Calculations with the most realistic scenario (a temperature in-
crease of 1 C combined with a decrease in precipitation of 30%) indicated that
leaf rusts of wheat and barley and powdery mildew of sugar beet could increase
substantially, reaching levels between two and five times as high as under the cur-
rent climate. Infestation levels on small grains by powdery mildews would remain
virtually unchanged, whereas those caused by foot rots and leaf blotch diseases
would decrease. Most notable was a decrease in potato late blight to a mere 16%
of its current level. The authors cautioned against over-interpreting their results,
which were based on calculations with data from only 1 of 14 regions in the former
GDR.
Population Models
A very different conclusion regarding the importance of potato late blight under
climate change was reached by Kaukoranta (68). This author developed degree-
day models for the emergence of potatoes and the date of late blight outbreaks
in Finland. The two models were coupled and extended by including leaf area
expansion of the crop as a function of thermal time; calculating radiation inter-
ception as a function of leaf area; transforming the intercepted radiation to tuber
dry matter; and simulating the effects of late blight on tuber dry matter through a
reduction in green leaf area, assuming that disease reduced leaf area to zero within
14 days after the predicted outbreak. Model parameters were obtained and model
validation was done using data from a three-year field and greenhouse study. The
combined model was then used with various temperature change scenarios to pre-
dict possible changes in potato yield and yield losses caused by late blight in a
warmer climate. The results suggested that tuber yield could increase by 2 t ha1
per 1 C warming in the absence of late blight. This potential yield gain was al-
most completely offset when late blight was considered, chiefly because late blight
?
outbreaks occurred 4 to 7 days earlier and the period during which the crop was
susceptible was lengthened by 10 to 20 days per 1 C warming. This study did not
consider possible yield-enhancing effects of elevated CO2, nor did it incorporate

the effects of changes in precipitation on late blight.
Simulation Models
Simulation models have been used extensively to predict yields of various crops
in different agroecological zones under climate change (43, 113). Biotic yield-
reducing factors such as insects, pathogens, and weeds have, however, been largely
ignored in these simulations (148). Because of this shortcoming, the development
of linked disease-crop models is an important objective within the overall goal
of developing a predictive capability for agricultural impact assessment and mit-
igation (130, 146, 148). For at least one key crop, rice, preliminary analyses con-
sidering the combined effects on yield of increased temperature, elevated UV-B
radiation, and rice blast disease (Pyricularia grisea) have been done using a cou-
pled simulation model (7780). The model consisted of a physiological rice growth
model and a leaf blast epidemic simulator, linked via the quantitative effects of
leaf blast on photosynthesis and biomass production (78). Climate change was im-
posed by increasing mean temperature in fixed increments and by either including
or omitting effects of UV-B on the host and pathogen (77). The results suggested
that elevated UV-B could result in direct yield losses of 10%. Impacts of increased
temperature varied by agroecological zone, with an increase in blast and associ-
ated yield losses in cool, subtropical rice production regions (e.g. Japan) and a
decrease in humid tropics and subtropical regions (e.g. the Philippines). The au-
thors cautioned that the results must be considered preliminary as the simulations
did not include neck and panicle blast, two other important symptom types caused
by P. grisea. Further, increased CO2 was not considered, nor were changes in
precipitation as preliminary analyses had indicated that the combined model was
insensitive to changes in rainfall (77).
Modeling for Impact Assessment: Prospects and Limitations

What does the future hold for the use of models for climate change impact
assessment in plant pathology? On the one hand, several new and exciting de-
velopments offer considerable prospect for modeling; examples include the emer-
gence of object-oriented programming and increasing interest in the development
of integrated impact assessment models. Object-oriented programming is an ap-

proach to model-building that is highly modular and generic, hence allowing model
development by non-modelers and avoiding the substantial costs associated with
developing and maintaining computer code for conventional simulation models
(141, 144). Integrated assessment models include multiple drivers of global change
(e.g. land-use changes in addition to climate changes) and multiple effects (e.g.
biological and socioeconomic outcomes), with the goal of providing comprehen-
sive advice on impacts and mitigation to policymakers and stakeholders (146).
?
A proposed integrated case study of impacts of global change on vector-borne
diseases of crops, livestock, and humans was outlined by Sutherst et al (142).
On the other hand, numerous challenges remain regarding the use of models for
climate change impact assessment. For example, no studies using state-of-the-art

climate change scenarios [e.g. those predicted by various General Circulation Mod-
els (GCMs)] have been published in plant pathology. Instead, authors have relied
on simplified sensitivity analyses that assumed fixed changes in mean temperature
or precipitation, regardless of time of year or geographical location. There is now
increasing evidence that the most important effects of climate change will be felt
not through changes in mean climate, but through increased climate variability
and more frequent or more severe climatic extremes (39, 55, 92, 113, 162). These
effects must be considered in future impact assessments by plant pathologists
(131). This could be accomplished through a better understanding of the effects
of natural, medium-range climate variability (such as that caused by El Nino and
similar climate cycles) on plant pathosystems, as discussed below.
The preoccupation with temperature in many climate change impact assess-
ments is unfortunate as it overlooks the fact that changes in precipitation have
more pronounced effects on the development of many plant diseases, particularly
those caused by fungi. Unfortunately, precipitation, which is temporally and spa-
tially discontinuous, is still difficult to simulate with current GCMs (6, 137). Most
GCMs predict increases in precipitation on a global scale (6) that could result in
a more favorable environment for plant pathogenic fungi. This could be offset by
other factors, e.g. greater dryness during summer because of increased evapora-
tion (6) and possible reductions in dew deposition because of increased cloudiness
and higher night-time temperatures. Recent developments in statistical downscal-
ing algorithms offer progress to the goal of making precipitation predictions with
sufficient temporal and spatial resolution to be useful in epidemiological models
(56, 121, 163, 164).
The magnitude of climate change in a high-CO2 world is still uncertain. De-
pending on the GCMs used and their underlying assumptions, these uncertainties
result in a wide range of possible scenarios for the future. Kacholia & Reck (63),
who compared 108 climate projections published between 1980 and 1995, re-
ported that predicted global mean air temperature changes under 2 CO2 ranged
from +0.16 to +8.7 C. As stated above, uncertainties in precipitation scenarios
are even greater. Uncertainty in model inputs can compromise the reliability of
the outputs of impact assessment models because of error propagation. Hence, the
development of methods to quantify uncertainty is a critical issue in climate change

impact assessment. In a pilot study, Scherm (129) used fuzzy numbers to express
uncertainties in climate projections in a generic pest risk model. Fuzzy numbers
are uncertain numbers for which there is a range of possible values and some val-
ues are more possible than others. Three climate scenarios were considered in
simulations with two hypothetical pest species: present climate; crisp climate
change; and fuzzy climate change. Under the crisp climate change scenario, tem-
perature and precipitation changes were expressed using the best estimates of the
?
1995 IPCC report (67). Under the fuzzy scenario, climate changes were expressed
as triangular fuzzy numbers, utilizing the lowest and highest predictions in addition
to the best estimates. Simulations with the crisp climate change scenario suggested
only minor changes in environmental favorability for the two species compared
with the current climate. When simulations were conducted with the fuzzy climate
change scenario, important changes in environmental favorability emerged. In
some regions, the possibility of considerably increased winter precipitation led to
Figure 3 Uncertainties in simulated values of environmental favorability at two loca-

tions (a and b) in Southern Europe for a hypothetical pest species under climate change
when projected temperature and precipitation changes were modeled with fuzzy num-
bers. The ecoclimatic index describes the relative favorability of the locations for the
pest; it is scaled between 0 (highly unfavorable environment) and 1.0 (highly favorable
environment). The certainty associated with a given value of the ecoclimatic index is
expressed by the belief attached to it. Source: H Scherm (unpublished data).
greater environmental favorability. The simulations further showed that this result
harbored considerable uncertainty, with a very broad range of possible outcomes
(Figure 3). Fuzzy logic could provide a simple but formal means of expressing
uncertainty that could be used across different levels of model complexity.
CLIMATE VARIABILITY AS ANALOGUE

FOR CLIMATE CHANGE
?
Climate cycles such as the El NinoSouthern Oscillation (ENSO) are major mech-
anisms of interannual atmospheric variability (17, 106). Indeed, the ENSO is con-
sidered second only to the seasonal cycle in its impacts on climate variability
(103). It has been suggested, therefore, that ENSO-related climate extremes could
serve as an analogue for assessing possible impacts of long-term climate change
(103, 168). This approach seems particularly appropriate as ENSO events may
become more frequent in a high-CO2 climate (134).
Numerous studies in veterinary and medical epidemiology have established re-
lationships between ENSO and outbreaks of infectious disease (12, 29, 48, 97, 103,
159). There is a conspicuous lack of published work on plant disease in relation
to ENSO. In an early paper, Zhao & Yao (170) reported that the occurrence of
El Nino coincided with increased wheat scab and that observation of sea surface
temperature (a proxy for the strength of El Nino) could be used to predict the disease
along the median and lower reaches of the Yangtze River in China. More recently,
Scherm & Yang (132, 133) established similar associations between ENSO events
and other climate cycles (teleconnection patterns) with rust diseases of wheat in
various production regions.
Mitigation measures developed in response to natural climate extremes such
as ENSO may be useful in adapting to long-term climate change (93, 94, 116).
Hence, promotion of research on climate analogues in relation to plant disease
constitutes a true no-regrets approach; it would result in concrete benefits to
society regardless of the magnitude of climate change.
CONCLUSIONS
Climate change can have positive, negative, or neutral impact on individual patho-
systems because of the specific nature of the interactions of host and pathogen.
As a result, it has been difficult to decipher rules of thumb that may be used for
specific impact assessment. Three factors are largely responsible for this apparent
lack of general principles. First is a serious lack of knowledge of the effects of
some important factors such as CO2. The role of pathogens in the response of
plants to increased CO2 has not been well studied, hence its effect on disease is not
currently considered in crop simulation models. Second, there is only rudimen-
tary information on the interactions of individual factors that collectively influence
plant disease in a changing climate. For example, recent studies showed that the
impacts of ozone in the field cannot be estimated without considering the pre-
disposing effects of fungal infections and the compensating effects derived from
elevated CO2 (156). Third, impacts on plant disease have largely been consid-
ered in small-scale experiments. Given that climate change operates at a global
scale, a lack of understanding of epidemic processes at relevant environmental and
spatial scales has hampered progress. The uncertainties associated with climate
change projections and the difficulty in extracting epidemiologically meaningful
?
environmental variables such as surface wetness from GCMs have contributed
to this.
From a disease management viewpoint, information is generally required for

a specific disease at a field scale; hence, data on potential impacts of climate

change need to be assessed and evaluated at a detailed level to capture important
mechanisms and dynamics that drive epidemics. In the absence of climate change
considerations, existing site-specific knowledge of individual pathosystems, often
incorporating environmental variables at the microclimate level, serves well to
understand and manage disease. When climate change considerations are included,
deficiencies arise because of a lack of detailed knowledge of epidemiology and
the relevant meteorological variables needed to predict epidemics at this spatial
scale. Ideally, the necessary epidemiological data would be gathered from long-
term field studies in facilities where more than one climate change variable can be
examined (99, 136). As for meteorological data, statistical downscaling of GCM
output offers interesting opportunities for developing climate change predictions
for small-scale spatial units such as a farm (56, 121, 135, 163, 164).
Information is also required by planners and policymakers at a much broader
spatial scale such as a region, state, or country. Climate matching and similar
models are not based on mechanisms or dynamics that drive epidemics; neverthe-
less, these approaches are useful as first pass analyses and to develop integrated
assessment models that incorporate socioeconomic aspects (146). If measures of
uncertainty are included (129), output from GCMs is well suited for impact as-
sessment at these coarse levels of resolution. Data on pathosystems would have
to be acquired and synthesized at this scale to include both on- and off-farm ef-
fects of disease and other production constraints for a realistic appraisal of crop
loss.
Apart from the technical difficulties listed above, the most significant limitation
to climate change impact assessment is our inability to predict how technological
and socioeconomic forces will interact with atmospheric, climatic, and biological
factors to shape the agriculture of the twenty-first century. Technological progress
over the next 50 years will doubtless revolutionize crop production and animal hus-
bandry. Hence, even in the absence of climate change it would be a daunting task
to predict future agricultural production potential. For example, how will land-use
patterns change in response to market demands, technology, and accelerated popu-
lation growth? To what degree will transgenic technology be able to alleviate crop
stresses caused by drought, nutrient limitations, and pests? Will crop protection
chemicals still be available to control insects, diseases, and weeds? Compared

with these changes, the prospect of climate change seems a minor concern indeed.
Nevertheless, climate change and climate variability add another layer of complex-
ity and uncertainty onto a system that is already exceedingly difficult to manage.
Better understanding of how these forces interact with biological yield constraints
such as plant pathogens will therefore contribute appreciably to the development
of sustainable agricultural systems.
?
Visit the Annual Reviews home page at http://www.AnnualReviews.org
LITERATURE CITED
1. Adams RM, Fleming RA, Chang CC, Mc- dorus in Europe. Nematologica 37:312
Carl BA, Rosenzweig C. 1995. A reassess- 23
ment of the economic effects of global 9. Booth TH. 1990. Mapping regions climat-
climate change on US agriculture. Clim. ically suitable for particular tree species at
Change 30:14767 the global scale. For. Ecol. Manage. 36:47
2. Asthana A, McCloud ES, Berenbaum MR, 60
Tuveson RW. 1993. Phototoxicity of Citrus 10. Booth TH, Jovanovic T, Old KM, Dudzin-
jambhiri to fungi under enhanced UV-B ra- ski MJ. 1999. Using climatic mapping pro-
diation: role of furanocoumarins. J. Chem. grams to identify high risk areas for Cylin-
Ecol. 19:281330 drocladium quinqueseptatum leaf blight on
3. Aust HJ, von Hoyningen-Huene J. 1986. eucalypts in mainland South East Asia and
Microclimate in relation to epidemics of around the world. Environ. Pollut. In press
powdery mildew. Annu. Rev. Phytopathol. 11. Borenstein S. 1998. Torrid September one
24:491510 for the record book. The Oregonian, Oct.
4. Ayres PG, Gunasekera TS, Rasanayagam 7, pp. A1, A13
MS, Paul ND. 1996. Effects of UV-B 12. Bouma MJ, van der Kaay HJ. 1996. The El
radiation (280320 nm) on foliar sapro- Nino Southern Oscillation and the historic
trophs and pathogens. See Ref. 40, pp. 32 malaria epidemics on the Indian subconti-
50 nent and Sri Lanka: an early warning sys-
5. Ball AS. 1997. Microbial decomposition at tem for future epidemics? Trop. Med. Int.
elevated CO2 levelseffect of litter qual- Health 1:8696
ity. Glob. Change Biol. 3:37986 13. Bowes G. 1993. Facing the inevitable:
6. Barron EJ. 1995. Climate models: How re- plants and increasing atmospheric CO2.
liable are their predictions? Consequences Annu. Rev. Plant Physiol. Plant Mol. Biol.
1(3):1727 44:30932
7. Bettarini I, Vaccari FP, Miglietta F. 1998. 14. Brasier CM. 1992. Oak tree mortality in
Elevated CO2 concentrations and stom- Iberia. Nature 360:539
atal densityobservations from 17 plant 15. Brasier CM. 1996. Phytophthora cin-
species growing in a CO2 spring in central namomi and oak decline in southern Eu-
Italy. Glob. Change Biol. 4:1722 rope: environmental constraints including
8. Boag B, Crawford JW, Neilson R. 1991. climate change. Ann. Sci. For. 53:34758
The effect of potential climatic changes on 16. Brasier CM, Scott JK. 1994. European oak
the geographical distribution of the plant- declines and global warming: a theoretical
parasitic nematodes Xiphinema and Longi- assessment with special reference to the
activity of Phytophthora cinnamomi. analyzing meteorological and rust data.

EPPO Bull. 24:22132 Phytopathology 78:54350
17. BurroughsWJ.1992.Weather Cycles: Real 28. Coakley SM, Scherm H. 1996. Plant dis-
or Imaginary? Cambridge: Cambridge ease in a changing global environment.
Univ. Press Asp. Appl. Biol. 45:22738
18. Busby JR. 1991. BIOCLIMa bioclimate 29. Colwell RR. 1996. Global climate and in-
analysis and prediction system. Plant Prot. fectious disease: the cholera paradigm.
Q. 6:89 Science 274:202531
?
19. Carter N, Harrington R. 1991. Factors in- 30. Cotrufo MF, Inescon P, Scott A. 1998. El-
fluencing aphid population dynamics and evated CO2 reduces the nitrogen concen-
behavior and the consequences for virus tration of plant tissues. Glob. Change Biol.
spread. In Advances in Disease Vector Re- 4:4354

search, ed. KF Harris, 7:1951. New York: 31. Darley EF, Middleton JT. 1966. Problems
Springer of air pollution in plant pathology. Annu.
20. Carter TR, Nurro M, Torkko S. 1996. Rev. Phytopathol. 4:10318
Global climate change and agriculture in 32. Dinoor A. 1974. Role of wild and culti-
the North. Agric. Food Sci. Finl. 5:223385 vated plants in the epidemiology of plant
21. Chakraborty S. 1997. How will plant diseases in Israel. Annu. Rev. Phytopathol.
diseases impact on pasture production 12:41336
under climate change: a case study of Sty- 33. Dyck PL, Johnson R. 1983. Temperature
losanthes anthracnose. Proc. Int. Grass- sensitivity of genes for resistance in wheat
lands Conf., 18th, Calgary, Canada, pp. to Puccinia recondita. Can. J. Plant Pathol.
95, 96 (Abstr.) 5:22934
22. Chakraborty S, Murray GM, Magarey PA, 34. Edis D, Hull MR, Cobb AH, Sanders-
Yonow T, OBrien RG, et al. 1998. Po- Mills GE. 1996. A study of herbicide ac-
tential impact of climate change on plant tion and resistance at elevated levels of
diseases of economic significance to Aus- carbon dioxide. Asp. Appl. Biol. 45:205
tralia. Aust. Plant Pathol. 27:1535 10
23. Chakraborty S, Pangga IB, Lupton J, Hart 35. Eshed N, Dinoor A. 1981. Genetics of
L, Room PM, Yates D. 1999. Production pathogenicity in Puccinia coronata: the
and dispersal of Colletotrichum gloeospo- host range among grasses. Phytopathology
rioides spores on Stylosanthes scabra 71:15663
under elevated CO2. Environ. Pollut. In 36. Farrow RA. 1991. Implications of poten-
press tial global warming on agricultural pests in
24. Chakraborty S, von Tiedemann A, Teng Australia. EPPO Bull. 21:68396
PS. 1999. Climate change and air pollution: 37. Finckh MR, Chavez AQ, Dai Q, Teng PS.
potential impact on plant diseases. Environ. 1995. Effects of enhanced UV-B radiation
Pollut. In press on the growth of rice and its susceptibility
25. Coakley SM. 1988. Variation in climate and to rice blast under glasshouse conditions.
prediction of disease in plants. Annu. Rev. Agric. Ecosyst. Environ. 52:22333
Phytopathol. 26:16381 38. Fischer G, Frohberg K, Parry ML, Rosen-
26. Coakley SM. 1995. Biospheric change: zweig C. 1996. The potential effects of cli-
Will it matter in plant pathology? Can. J. mate change on world food production and
Plant Pathol. 17:14753 security. In Global Climate Change and
27. Coakley SM, Line RF, McDaniel LR. 1988. Agricultural Production, ed. F Bazzaz, W
Predicting stripe rust severity on win- Sombroek, pp. 199235. Chichester, UK:
ter wheat using an improved method for Wiley
39. Fowler AM, Hennessy KJ. 1995. Poten- 1998. A common-sense climate index: Is
tial impacts of global warming on the climate changing noticeably? Proc. Natl.
frequency and magnitude of heavy preci- Acad. Sci. USA 95:411320
pitation. Nat. Hazards 11:283303 50. Hansen JE, Sato M, Ruedy R, Lacis A,
40. Frankland JC, Magan N, Gadd GM, eds. Glascoe J. 1998. Global climate data and
1996. Fungi and Environmental Change. models: a reconciliation. Science 281:930
Cambridge: Cambridge Univ. Press 32
41. GCTE-LUCC. 1998. The Earths Chang- 51. Harrington R, Bale JS, Tatchell GM. 1995.
?
ing Land. GCTE-LUCC Open Science Con- Aphids in a changing climate. See Ref. 52,
ference on Global Change. Barcelona: pp. 12555
Inst. Cartogr. Catalunya 52. Harrington R, Stork NE, eds. 1995. Insects
42. Gerechter-Amitai ZK, Sharp EL, Rein- in a Changing Environment. London: Aca-
hold M. 1984. Temperature-sensitive genes demic
for resistance to Puccinia striiformis 53. Heagle AS. 1982. Interactions between air
in Triticum dicoccoides. Euphytica 33: pollutants and parasitic plant diseases. In
66572 Effects of Gaseous Air Pollution in Agricul-
43. Goudriaan J. 1996. Predicting crop yields ture and Horticulture, ed. MH Unsworth,
under global change. See Ref. 157, pp. DP Ormrod, pp. 33348. London: Butter-
26074 worth
44. Goudriaan J, Zadoks JC. 1995. Global cli- 54. Heagle AS. 1989. Ozone and crop yield.
mate change: modelling the potential re- Annu. Rev. Phytopathol. 27:397423
sponses of agro-ecosystems with special 55. Hennessy KJ, Pittock AB. 1995. Green-
reference to crop protection. Environ. Pol- house warming and threshold temperature
lut. 87:21524 events in Victoria, Australia. Int. J. Clima-
45. Gregory PJ, Ingram JSI, Campbell B, tol. 15:591612
Goudriaan J, Hunt T, et al. 1999. Man- 56. Hewitson BC, Crane RG. 1996. Cli-
aged production systems. In Implications mate downscalingtechniques and appli-
of Global Change for Natural and Man- cations. Clim. Res. 7:8595
aged Ecosystems: A Synthesis of GCTE 57. Hibberd JM, Whitbread R, Farrar JF. 1996.
and Related Research, ed. BH Walker, Effect of elevated concentrations of CO2
WL Steffen, J Canadell, JSI Ingram. Cam- on infection of barley by Erysiphe grami-
bridge: Cambridge Univ. Press. In press nis. Physiol. Mol. Plant Pathol. 48:3753
46. Gunasekera TS, Paul ND, Ayres PG. 58. Hibberd JM, Whitbread R, Farrar JF. 1996.
1997. Responses of phylloplane yeasts to Effect of 700 mol mol1 CO2 and infec-
UV-B (290320 nm) radiation: interspe- tion with powdery mildew on the growth
cific differences in sensitivity. Mycol. Res. and carbon partitioning of barley. New Phy-
101:77985 tol. 134:30915
47. Gunasekera TS, Paul ND, Ayres PG. 1997. 59. Houghton JT, Meira Filho LG, Callander
The effects of ultraviolet-B (UV-B: 290 BA, Harris N, Kattenberg A, et al, eds.
320 nm) radiation on blister blight disease 1996. Climate Change 1995. The Science of
of tea (Camellia sinensis). Plant Pathol. Climate Change. Cambridge: Cambridge
46:17985 Univ. Press
48. Hales S, Weinstein P, Woodward A. 1996. 60. Idso KE, Idso SB. 1994. Plant response to
Dengue fever epidemics in the South Pa- atmospheric CO2 enrichment in the face of
cific: driven by El Nino Southern Oscilla- environmental constraints: a review of the
tion? Lancet 348:166465 past 10 years research. Agric. For. Mete-
49. Hansen J, Sato M, Glascoe J, Ruedy R. orol. 69:153203
61. Idso SB. 1998. CO2induced global warm- 75. Loehle C. 1996. Forest response to climate
ing: a skeptics view of potential climate change: Do simulations predict unrealistic
change. Clim. Res. 10:6982 dieback? J. For. 94(9):1315
62. Jahn M, Kluge E, Enzian S. 1996. Influence 76. Lonsdale D, Gibbs JN. 1996. Effects of cli-
of climate diversity on fungal diseases of mate change on fungal diseases of trees.
field cropsevaluation of long-term mon- See Ref. 40, pp. 119
itoring data. Asp. Appl. Biol. 45:24752 77. Luo Y, TeBeest DO, Teng PS, Fabellar
63. Kacholia K, Reck RA. 1997. Comparison NG. 1995. Simulation studies on risk anal-
?
of global climate change simulations for ysis of rice leaf blast epidemics associated
2 CO2induced warming. Clim. Change with global climate change in several Asian
35:5369 countries. J. Biogeogr. 22:67378
64. Kahn RP. 1991. Exclusion as a plant disease 78. Luo Y, Teng PS, Fabellar NG, TeBeest DO.
control strategy. Annu. Rev. Phytopathol. 1997. A rice-leaf blast combined model
29:21946 for simulation of epidemics and yield loss.
65. Karlman M, Hansson P, Witzell J. 1994. Agric. Syst. 53:2739
Scleroderris canker on lodgepole pine 79. Luo Y, Teng PS, Fabellar NG, TeBeest DO.
introduced in northern Sweden. Can. J. 1998. Risk analysis of yield losses caused
For. Res. 24:194859 by rice leaf blast associated with temper-
66. Katan J. 1971. Symptomless carriers of ature changes above and below for five
the tomato Fusarium wilt pathogen. Phy- Asian countries. Agric. Ecosyst. Environ.
topathology 61:121317 68:197205
67. Kattenberg A, Giorgi F, Grassl H, Meehl 80. Luo Y, Teng PS, Fabellar NG, TeBeest DO.
GA, Mitchell JFB, et al. 1996. Climate 1998. The effects of global temperature
modelsprojections of future climate. See change on rice leaf blast epidemics: a sim-
Ref. 59, pp. 285357 ulation study in three agroecological zones.
68. Kaukoranta T. 1996. Impact of global Agric. Ecosyst. Environ. 68:18796
warming on potato late blight: risk, yield 81. Mackerron D, Boag B, Duncan JM, Harri-
loss and control. Agric. Food Sci. Finl. 5: son JG, Woodford JAT. 1993. The prospect
31127 of climate change and its implications for
69. Kerr R. 1998. Among global thermometers, crop pests and diseases. In Plant Health
warming still wins out. Science 281:1948 and the European Single Market, ed. D
49 Ebbels, pp. 18193. Farnham: Br. Crop
70. Klironomos JN, Rillig MC, Allen MF, Zak Prot. Counc.
DR, Kubiske M, et al. 1997. Soil fungal- 82. Madden LV, Campbell CL. 1987. Poten-
arthropod responses to Populus tremu- tial effects of air pollutants on epidemics
loides grown under enriched atmospheric of plant diseases. Agric. Ecosyst. Environ.
CO2 under field conditions. Glob. Change 18:25162
Biol. 3:47378 83. Magan N, Baxter ES. 1996. Effect of in-
71. Krupa SV. 1997. Air Pollution, People, and creased CO2 concentration and tempera-
Plants. St. Paul: APS Press ture on the phyllosphere mycoflora of win-
72. Laurence JA, Weinstein LH. 1981. Ef- ter wheat flag leaves during ripening. Ann.
fects of air pollutants on plant productivity. Appl. Biol. 129:18995
Annu. Rev. Phytopathol. 19:25771 84. Mahlman JD. 1997. Uncertainties in pro-
73. Lawler A. 1998. Global change fights off a jections of human-caused climate warm-
chill. Science 280:168284 ing. Science 278:141617
74. Lemonick M. 1994. The ice age cometh? 85. Malakoff D. 1997. Thirty Kyotos needed to
Time 143(5):7981 control warming. Science 278:2048
86. Malmstrom CM, Field CB. 1997. Virus- schlagen auf die biologische Wirkung
induced differences in the response of oat von Fungiziden zur Phytophthora-Bekam-
plants to elevated carbon dioxide. Plant pfung. Nachrichtenbl. Pflanzenschutz DDR
Cell Environ. 20:17888 28:14953
87. Manning WJ, von Tiedemann A. 1995. Cli- 97. Nicholls N. 1993. El Nino-Southern Os-
mate change: potential effects of increased cillation and vector-borne disease. Lancet
atmospheric carbon dioxide (CO2), ozone 342:128485
(O3), and ultraviolet-B (UV-B) radiation 98. Nicholls N. 1997. Increased Australian
?
on plant diseases. Environ. Pollut. 88:219 wheat yield due to recent climate trends.
45 Nature 387:48485
88. Marcais B, Dupuis F, Desprez-Loustau 99. Norby RJ, Edwards NT, Riggs JS, Ab-
ML. 1996. Modeling the influence of win- ner CH, Wullschleger SD, Gunderson
ter frosts on the development of the stem CA. 1997. Temperature-controlled open-
canker of red oak, caused by Phytophthora top chambers for global change research.
cinnamomi. Ann. Sci. For. 53:36982 Glob. Change Biol. 3:25967
89. Martens JW, McKenzie RIH, Green GJ. 100. Oerke EC, Dehne HW, Schonbeck F, Weber
1967. Thermal stability of stem rust resis- A. 1994. Crop Production and Crop Pro-
tance in oat seedlings. Can. J. Bot. 45:451 tection: Estimated Losses in Major Food
58 and Cash Crops. Amsterdam: Elsevier
90. McMichael AJ, Ando M, Carcavello R, 101. Parry M. 1992. The potential effect of cli-
Epstein P, Haines A, et al. 1996. Human mate changes on agriculture and land use.
population health. See Ref. 160, pp. 561 Adv. Ecol. Res. 22:6391
84 102. Parson EA, Keith DW. 1998. Fossil fuels
91. McMichael AJ, Haines A, Sloof R, Ko- without CO2 emissions. Science 282:1053
vats S. 1996. Climate Change and Human 54
Health. Geneva: WHO 103. Patz JA, Epstein PR, Burke TA, Balbus JM.
92. Mearns LO, Rosenzweig C, Goldberg R. 1996. Global climate change and emerging
1997. Mean and variance change in climate infectious diseases. JAMA 275:21723
scenarios: methods, agricultural applica- 104. Paul ND. 1999. Stratospheric ozone deple-
tions, and measures of uncertainty. Clim. tion, UV-B radiation and crop disease. En-
Change 35:36796 viron. Pollut. In press
93. Meinke H, Stone RC, Hammer GL. 1996. 105. Pfleger FL, Linderman RG, eds. 1994. My-
SOI phases and climatic risk to peanut pro- corrhizae and Plant Health. St. Paul: APS
duction: a case study for northern Aus- Press
tralia. Int. J. Climatol. 16:78389 106. Philander G. 1989. El Nino and La Nina.
94. Mjelde JW, Thompson TN, Hons FM, Am. Sci. 77:45159
Cothren JT, Coffman CG. 1997. Us- 107. Podger FD, Mummery DC, Palzer CR,
ing Southern Oscillation information for Brown MJ. 1990. Bioclimatic analysis of
determining corn and sorghum profit- the distribution of damage to native plants
maximizing input levels in east-central in Tasmania by Phytophthora cinnamomi.
Texas. J. Prod. Agric. 10:16875 Aust. J. Ecol. 15:28189
95. Neilson R, Boag B. 1996. The predicted 108. Pollack HN, Huang S, Shen PY. 1998.
impact of possible climatic change on Climate change record in subsurface tem-
virus-vector nematodes in Great Britain. peratures: a global perspective. Science
Eur. J. Plant Pathol. 102:19399 282:27981
96. Neuhaus W, Stachewicz H, Dunsing M. 109. Porter JH, Parry ML, Carter TR. 1991.
1974. Uber den Einfluss von Nieder- The potential effects of climatic change on
agricultural insect pests. Agric. For. Me- 121. Russo JM, Zack JW. 1997. Downscaling
teorol. 57:22140 GCM output with a mesoscale model. J.
110. Prestidge RA, Pottinger RP, eds. 1990. Environ. Manage. 49:1929
The Impact of Climate Change on Pests, 122. Sadowsky MJ, Schortemeyer M. 1997.
Diseases, Weeds and Beneficial Organ- Soil microbial responses to increased con-
isms Present in New Zealand Agricul- centrations of atmospheric CO2. Glob.
tural and Horticultural Systems. Hamil- Change Biol. 3:21724
ton: MAF Technol. 123. Sanden GE, Moore LD. 1978. Effect
?
111. Rasanayagam MS, Paul ND, Royle DJ, of heat-induced susceptibility to tobacco
Ayres PG. 1995. Variation in responses black shank on protein content and on
of spores of Septoria tritici and S. nodo- activity of peroxidases. Phytopathology
rum to UV-B irradiation in vitro. Mycol. 68:116467

Res. 99:137177 124. Sandermann H Jr. 1996. Ozone and plant
112. Reilly J, Baethgen W, Chege FE, van de health. Annu. Rev. Phytopathol. 34: 347
Geijn SC, Erda L, et al. 1996. Agricul- 66
ture in a changing climate: impacts and 125. Sandermann H Jr. 1999. Ozone and bi-
adaptation. See Ref. 160, pp. 42767 otic disease interactions. Proc. Int. Congr.
113. Riha SJ, Wilks DS, Simoens P. 1996. Im- Plant Pathol., 7th, Edinburgh, Scotland,
pact of temperature and precipitation vari- 1:4.2.2 (Abstr.)
ability on crop model predictions. Clim. 126. Sansford CE, Baker RHA. 1998. The ap-
Change 32:293311 plication of scientific principles to pest
114. Rishbeth J. 1991. Armillaria in an an- risk analysis with special reference to
cient broadleaved woodland. Eur. J. For. Karnal bunt. Proc. Int. Congr. Plant
Pathol. 21:23949 Pathol., 7th, Edinburgh, Scotland, 1:
115. Romm J, Levine M, Brown M, Petersen 4.6.2S (Abstr.)
E. 1998. A road map for U.S. carbon re- 127. Savile DBO, Urban Z. 1982. Evolution
ductions. Science 279:66970 and ecology of Puccinia graminis. Pres-
116. Rosenzweig C. 1994. Maize suffers a sea lia 54:97104
change. Nature 370:17576 128. Schepers HTAM. 1996. Effect of rain
117. Rosenzweig C, Hillel D. 1998. Climate on the efficacy of fungicide deposits on
Change and the Global Harvest: Po- potato against Phytophthora infestans.
tential Impacts of the Greenhouse Effect Potato Res. 39:54150
on Agriculture. New York: Oxford Univ. 129. Scherm H. 1999. Simulating uncertainty
Press in climate-pest models with fuzzy num-
118. Rosenzweig C, Parry ML. 1994. Potential bers. Environ. Pollut. In press
impact of climate change on world food 130. Scherm H, Sutherst RW, Harrington R, In-
supply. Nature 367:13338 gram JSI. 1999. Global networking for as-
119. Runeckles VC, Krupa SV. 1994. The sessing impacts of global change on plant
impact of UV-B radiation and ozone pests. Environ. Pollut. In press
on terrestrial vegetation. Environ. Pollut. 131. Scherm H, van Bruggen AHC. 1994.
83:191213 Global warming and nonlinear growth:
120. Runion GB, Curl EA, Rogers HH, Back- How important are changes in average
man PA, Rodriguez-Kabana R, et al. temperature? Phytopathology 84:1380
1994. Effects of free-air CO2 enrichment 84
on microbial populations in the rhizo- 132. Scherm H, Yang XB. 1995. Interannual
sphere and phyllosphere of cotton. Agric. variations in wheat rust development in
For. Meteorol. 70:11730 China and the United States in relation
to the El Nino/Southern Oscillation. Phy- 5762. Brisbane: Univ. Queensland

topathology 85:97076 145. Sutherst RW, Maywald GF, Skarratt DB.
133. Scherm H, Yang XB. 1998. Atmospheric 1995. Predicting insect distributions in a
teleconnection patterns associated with changed climate. See Ref. 52, pp. 59
wheat stripe rust disease in north China. 91
Int. J. Biometeorol. 42:2833 146. Sutherst RW, Yonow T, Chakraborty S,
134. Scripps Institute of Oceanography. 1992. ODonnell C, White N. 1996. A generic
Simulated Global Warming and Model approach to defining impacts of climate
?
ENSO Cycles. La Jolla: Scripps Inst. change on pests, weeds and diseases in
Oceanogr. Australasia. In Greenhouse, Coping with
135. Seem RC, Magarey RD, Zack JW, Russo Climate Change, ed. WJ Bouma, GI Pear-
JM. 1999. Weather forecasts at the whole man, MR Manning, pp. 281307. Mel-
plant level: implications for estimating bourne: CSIRO
disease risk with global climate models. 147. Taubes G. 1997. Apocalypse not. Science
Environ. Pollut. In press 278:10046
136. Senft D. 1995. FACE-ing the future. 148. Teng PS, Heong KL, Kropff MJ, Nutter
Agric. Res. 43(4):46 FW, Sutherst RW. 1996. Linked pest-crop
137. Shuttleworth WJ. 1996. The challenges models under global change. See Ref.
of developing a changing world. Eos 157, pp. 291316
77(36):347 149. Teng PS, Yang XB. 1993. Biological im-
138. Singer SF. 1996. Climate change and con- pact and risk assessment in plant pathol-
sensus. Science 271:58182 ogy. Annu. Rev. Phytopathol. 31:495
139. Staddon PL, Fitter AH. 1998. Does ele- 521
vated atmospheric carbon dioxide affect 150. Thomas T. 1989. Sugar beet in the green-
arbuscular mycorrhizas? TREE 13:455 housea global warming warning. Br.
58 Sugar 57:2426
140. Strange RN. 1993. Plant Disease Con- 151. Thompson GB, Brown JKM, Woodward
trol: Towards Environmentally Accept- FI. 1993. The effects of host carbon diox-
able Methods. London: Chapman & Hall ide, nitrogen and water supply on the
141. Sutherst RW. 1998. Implications of global infection of wheat by powdery mildew
change and climate variability for vector- and aphids. Plant Cell Environ. 16:687
borne diseases: generic approaches to 94
impact assessments. Int. J. Parasitol. 28: 152. Triltsch H, Freier B, Rossberg D. 1996.
93545 TemperaturSchlusselfaktor fur Nutz-
142. Sutherst RW, Ingram JSI, Scherm H. lingsleistungen im Winterweizen? Mitt.
1998. Global change and vector-borne Biol. Bundesanst. Land Forstwirtsch.
diseases. Parasitol. Today 14:29799 321:447 (Abstr.)
143. Sutherst RW, Maywald GF. 1985. A com- 153. Vakalounakis DJ, Christias C. 1981.
puterised system for matching climates in Sporulation in Alternaria cichorii is con-
ecology. Agric. Ecosyst. Environ. 13:281 trolled by a blue and near ultraviolet re-
99 versible photoreaction. Can. J. Bot. 59:
144. Sutherst RW, Maywald GF. 1998. 62628
DYMEX modelling workshops: a na- 154. Vogel G, Lawler A. 1998. Hot year,
tional, collaborative approach to pest risk but cool response in Congress. Science
analysis and IPM in Australia. In Pest 280:1684
ManagementFuture Challenges, ed. 155. von Tiedemann A. 1996. Globaler Wan-
MP Zalucki, RAI Drew, GG White, 2: del von Atmosphare und Klimawelche
Folgen ergeben sich fur den Pflanzen- logical variables using general circulation
schutz? Nachrichtenbl. Dtsch. Pflanzen- model output. J. Hydrol. 205:119
schutzdienstes 48:7379 164. Wilby RL, Wigley TML. 1997. Down-
156. von Tiedemann A, Firsching KH. 1999. scaling general circulation model output:
Interactive effects of elevated ozone and a review of methods and limitations. Prog.
carbon dioxide on growth and yield of leaf Phys. Geogr. 21:53048
rust-infected vs. non-infected wheat. En- 165. Wilson JR, Deinum B, Engels FM. 1991.
viron. Pollut. In press Temperature effects on anatomy and di-
?
157. Walker B, Steffen W, eds. 1996. Global gestibility of leaf and stem of tropical and
Change and Terrestrial Ecosystems. temperate forage species. Neth. J. Agric.
Cambridge: Cambridge Univ. Press Sci. 39:3148
158. Walker PA, Cocks KD. 1991. HABITAT: 166. Wilson PA, Chakraborty S. 1998. The vir-
a procedure for modelling a disjoint en- tual plant: a new tool for the study and
vironmental envelope for a plant or ani- management of plant diseases. Crop Prot.
mal species. Glob. Ecol. Biogeogr. Lett. 17:23139
1:10818 167. Wolfe DW. 1995. Physiological and
159. Ward MP, Johnson SJ. 1996. Bluetongue growth responses to atmospheric carbon
virus and the Southern Oscillation Index: dioxide concentration. In Handbook of
evidence of an association. Prev. Vet. Med. Plant and Crop Physiology, ed. M Pes-
28:5768 sarakli, pp. 22342. New York: Dekker
160. Watson RT, Zinyowera MC, Moss RH, 168. Yang XB, Scherm H. 1997. El Nino and
eds. 1996. Climate Change 1995. Im- infectious disease. Science 279:739
pacts, Adaptations and Mitigation of 169. Yang XB, Sun P, Hu B-H. 1998. Decadal
Change: Scientific-Technical Analyses. change of plant diseases as affected by
Cambridge: Cambridge Univ. Press climate in Chinese agroecosystems. Proc.
161. Weltzien HC. 1972. Geophytopathology. Int. Congr. Plant Pathol., 7th, Edinburgh,
Annu. Rev. Phytopathol. 10:27798 Scotland, 3:4.2.1 (Abstr.)
162. Wigley TML. 1985. Impact of extreme 170. Zhao S, Yao C. 1989. On the sea tem-
events. Nature 316:1067 perature prediction models of the prevail-
163. Wilby RL, Hassan H, Hanaki K. 1998. ing level of wheat scab. Acta Phytopathol.
Statistical downscaling of hydrometeoro- Sin. 19:22934

Annurev Phyto 37 1 399

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Annurev Phyto 37 1 399

Uploaded by

Copyright:

Available Formats

P1: FHP/FGO P2: FHP/FGP/FGM QC: FHP/arun T1: FDX

June 29, 1999 14:33 Annual Reviews AR087-16

Annu. Rev. Phytopathol. 1999. 37:399426

CLIMATE CHANGE AND PLANT DISEASE

Key Words climate variability, epidemiological models, global warming,

400 COAKLEY SCHERM CHAKRABORTY

CLIMATE CHANGE AND DISEASE MANAGEMENT 401

terms of climate change and its impacts on plant diseases.

COMPONENTS OF CLIMATE CHANGE

402 COAKLEY SCHERM CHAKRABORTY

Hansen et al (49) proposed an easily understood climate index based on heating

CLIMATE CHANGE AND DISEASE MANAGEMENT 403

and weeds. It is therefore important to consider these biotic constraints in stud-

Geographical Distribution of Host and Pathogen

404 COAKLEY SCHERM CHAKRABORTY

Physiology of Host-Pathogen Interactions

CLIMATE CHANGE AND DISEASE MANAGEMENT 405

temperature could increase pathogen survival on overwintering crop residues and

mildew) (57) and a lengthening of the latent period in Maravalia cryptostegiae

(rubbervine rust) (S Chakraborty, MP Weinert & JR Brown, unpublished data).

406 COAKLEY SCHERM CHAKRABORTY

Impacts would, therefore, depend on the nature of the host-pathogen interactions

in projections of tree health response to climate change.

CLIMATE CHANGE AND DISEASE MANAGEMENT 407

studying disease development and crop losses caused by polycyclic pathogens.

Regional Impact Assessment

408 COAKLEY SCHERM CHAKRABORTY

intensive in nature and management changes required to mitigate climate change

apple powdery mildew but reduce peach leaf curl.

Carter et al (20) summarized results of five years work on the impacts of

IMPACTS ON DISEASE MANAGEMENT

Because of the rudimentary knowledge about impacts of climate change on plant

CLIMATE CHANGE AND DISEASE MANAGEMENT 409

Figure 2 Disease severity (on a scale from 0 to 9) caused by Colletotrichum gloeospo-

410 COAKLEY SCHERM CHAKRABORTY

lowered control efficacy at higher concentrations of CO2. Conversely, increased

CLIMATE CHANGE AND DISEASE MANAGEMENT 411

from 17 to 22 C resulted in an increase in aphid (Sitobion avenae) reproduction

Quarantine and Exclusion

412 COAKLEY SCHERM CHAKRABORTY

variables such as monthly minimum and maximum temperatures, precipitation,

CLIMATE CHANGE AND DISEASE MANAGEMENT 413

414 COAKLEY SCHERM CHAKRABORTY

consider possible yield-enhancing effects of elevated CO2, nor did it incorporate

the effects of changes in precipitation on late blight.

Modeling for Impact Assessment: Prospects and Limitations

CLIMATE CHANGE AND DISEASE MANAGEMENT 415

of integrated impact assessment models. Object-oriented programming is an ap-

climate change impact assessment. For example, no studies using state-of-the-art

416 COAKLEY SCHERM CHAKRABORTY

development of methods to quantify uncertainty is a critical issue in climate change

Figure 3 Uncertainties in simulated values of environmental favorability at two loca-

CLIMATE CHANGE AND DISEASE MANAGEMENT 417

CLIMATE VARIABILITY AS ANALOGUE

418 COAKLEY SCHERM CHAKRABORTY

From a disease management viewpoint, information is generally required for

a specific disease at a field scale; hence, data on potential impacts of climate

CLIMATE CHANGE AND DISEASE MANAGEMENT 419

chemicals still be available to control insects, diseases, and weeds? Compared

420 COAKLEY SCHERM CHAKRABORTY

activity of Phytophthora cinnamomi. analyzing meteorological and rust data.

spread. In Advances in Disease Vector Re- 4:4354

CLIMATE CHANGE AND DISEASE MANAGEMENT 421