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Effects of Climate Change on Plant Pathogens
By: Usha Mina1 and Parimal
Sinha2
Introduction
Recent years have witnessed a
steady increase in National and International concern over the sustainability of
the global environment. Climate change has emerged as the most prominent of the
global environment issues. Global climate has changed ever since industrial
revolution and by now it is ascertained that major greenhouse gases especially
CO2 increased by 30%. Tropospheric ozone has increased two- to five-
folds since the last century. According to IPCC’s latest report, global mean
temperature would rise between 0.9 and 3.5°C by the year 2100. Speed of climate
change and the unpredictability of its characteristics are of great concern with
respect to the pathogens, insect pests and weeds that reduce crop yield. The
classic disease triangle recognizes the role of climate in plant diseases as no
virulent pathogen can induce disease on a highly susceptible host if climatic
conditions are not favorable. Climate influences all stages of host and pathogen
life cycles as well as development of disease. Disease severity over a period
can fluctuate according to climatic variation.
General impacts of climate
change on plants
Climate change will influence the
geographical distribution and growth of plant species around the world. The
magnitude of these impacts would vary depending upon the species involved and
their growth patterns, e.g. annual vs perennials, agricultural crop vs natural
vegetation, competition, migration, and recovery from disturbances. Therefore,
new combinations of species are likely to evolve. Evidences are now accumulated
which suggest that crop production would be affected differently depending on
latitude. Although increases in yields are expected at mid and high latitudes,
there may be decreases at lower latitudes where food requirements in future will
be highest. There are apprehensions that yield gains caused by increased CO2
could be offset partly or entirely by losses caused by phytophagous insects,
plant pathogens and weeds. It is, therefore, important to consider the effect of
biotic constraints on crop yields under climate change scenario.
Impact on plant - pathogen
systems
Most of the researches on how
climate change may affect plant diseases has concentrated on the effects of a
single atmospheric constituent or meteorological variables on the host,
pathogen, or the interaction of the two under controlled condition. However,
interactions are more complex in the real situation, where multiple
climatological and biological factors are varying simultaneously in a dynamic
environment. Climate change has the potential to modify host physiology and
resistance and to alter the stages and rates of development of the pathogen. The
most likely impacts would be shift in the geographical distribution of the host
and pathogen, change in the physiology of host-pathogen interactions and change
in crop losses. New disease complexes may arise and some diseases may cease to
be economically important if warming causes a poleward shift of agroclimatic
zones and host plant migrate into new regions. Pathogen would be following the
migrating hosts and may infect vegetation of natural plant communities not
previously exposed to the often more aggressive strains from agricultural crops.
Facultative parasites with broad host range may infect plants in their
proximity. 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 region. Change may occur in the type, amount, and
relative importance of pathogens and affect the spectrum of disease affecting
particular crop. Plants growing in marginal climate could experience chronic
stress that would predispose them to insect and disease out breaks. Warming and
other changes could also make plants more vulnerable to damage from pathogens
that are currently not important because of unfavourable climate. For example
Infection of Eucalyptus by Phytophthora cinnamomi is favored in wet soil
at temperature of 12 to 30°C, 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 due to climate change. As
under climate change plants may potentially be unable to migrate or adapt as
readily as environmental conditions change. But most pathogens have advantage
over plants because of their shorter generation time and in many cases the
ability to move readily through wind dispersal. Because of these
characteristics, rate of evolution will be highest among pathogens to reduce
sensitivity to climate change phenomenon.
Effects of various
components of climate change on fungal pathogens
Elevated CO2:
Both enhancement and reduction in disease severity under elevated CO2
has been reported. Elevated CO2 would increase canopy size and
density of plants, resulting in a greater biomass production and microclimates
may become more conducive for rusts, mildews, leaf spots and blights
development. Decomposition of plant litter is important for nutrient cycling and
in the saprophytic survival of many pathogens. Because of high C: N ratio of
litter as a consequence of plant growth under elevated CO2,
decomposition will be slower. Increased plant biomass, slower decomposition of
litter, and higher winter temperature could increase pathogen survival on
over-wintering crop residues and increase the amount of initial inoculation
available for subsequent infection.
Some fungal pathosystems under
elevated CO2 revealed two important trends. First, delay in the
initial establishment of the pathogen because of modifications in pathogen
aggressiveness and/or host susceptibility. For example, reduction in the rate of
primary penetration of Eysiphe graminis on barley and a lengthening of
latent period in Maravalia cryptostegiae (rubervine rust) has been
observed under elevated CO2. Here, host resistance may have increased
because of change in host morphology, physiology, nutrients and water balance. A
decrease in stomatal density increases resistance to pathogens that penetrate
through stomata. Under elevated CO2 barley plants were able to
mobilize assimilates into defense structures including the formation of papillae
and accumulation of silicon at sites of appressorial penetration of Erysiphe
graminis.
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 soil-borne diseases of root crops may be reduced under climate change. In
contrast, for foliage 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.
The second important effect is an
increase in the fecundity of pathogens under elevated CO2. Following
penetration, established colonies of Erysiphe graminis grew faster and
sporulation per unit area of infected tissue was increased several-fold under
elevated CO2. It has been also observed that under elevated
CO2 out of the 10 biotrophic pathogens studied, disease severity
was enhanced in six and reduced in four and out of 15 necrotrophic pathogens,
disease severity increased in nine, reduced in four and remained unchanged in
the other two.
Elevated temperature: Increases in temperature can modify
host physiology and resistance. Both temperature and the length of exposure are
important in determining the effect of climate change on disease severity. Even
if the temperature change may be well within the limits of current climatic
variability, a modest warming can cause a significant increase in
cumulative-temperature above a critical temperature threshold to affect crop
physiology and resistance to a disease. Temperature change might lead to
appearance of different races of the pathogens hitherto not active but might
cause sudden epidemic. Change in temperature will directly influence infection,
reproduction, dispersal, and survival between seasons and other critical stages
in the life cycle of a pathogen.
At higher
temperature, lignification of cell walls increased in forage species and
enhanced resistance to fungal pathogens. Impact would, therefore, depend on the
nature of the host- pathogen interactions and mechanism of resistance. A rise
in temperature above 20°C can inactivate temperature sensitive resistance to
stem rust in oat cultivars. Increase in temperature with sufficient soil
moisture may increase evapo-transpiration resulting in humid microclimate in
crop canopy and may lead to incidence of diseases favoured under warm and humid
conditions. Some of the soil-borne diseases may increase at the rise of soil
temperature. If climate change causes a gradual shift of cropping regions,
pathogens will follow their host. Analysis of long-term data of wheat and rice
diseases in China has shown trends of an increase in minimum temperatures in
association with the abundance of rice blast or wheat scab. In most locations,
temperature changes had significant effects on disease development. However,
these effects varied between different agro-ecological zones. In cool
sub-tropical zones such as Japan and northern China, elevation of ambient
temperature resulted in greater risk of blast epidemics. Situations in the humid
tropics and warm humid subtropics were opposite to those in cool areas. A lower
temperature resulted in greater risk of blast epidemics.
Elevated levels of atmospheric pollutants (ozone and nitrous oxide):
Most air pollutants
indirectly influence diseases through their effect on host. Ozone induces
reactions similar to those normally elicited by viral and other pathogens. Of
the 49 bacteria and fungal pathogens examined, exposure to elevated ozone
concentration enhanced disease in 25, did not affect 10 and reduced 14.
Pollutant concentrations, which inhibit pathogen development, also injure the
host. Similarly, infection by plant pathogens can alter ozone sensitivity of
plants. Exposure to 5-10 ppm ozone for a few hours can cause visible injury to
sensitive crops like barley, tomato, onion, potato, soybean, tobacco, and wheat.
Plants
appear to be less sensitive to nitrous oxide, however, higher concentrations can
cause water-soaked lesions, which soon turn brown. Ozone and nitrous oxide
injury on plants in turn may add new problem to pathologists in diagnosis.
Current climate change scenarios predict a further increase of tropospheric
ozone, which is well known to inhibit plant photosynthesis and growth process.
Ozone can also predispose plants to enhanced biotic attack, as proposed in
particular for necrotrophic fungi, root rot fungi and black beetles. However, at
present it does not seem possible to predict whether increased ambient ozone
will lead to higher or lower disease likelihood in particular plant-pathogen
system. Several root pathogens show a preference for stressed trees, although
the direct role of ozone is not always evident. Onions injured by ozone exposure
were more susceptible to Botrytis cinerea, but not to B.
squamosa. Increased onion yields and reduced dieback when filters removed
ambient ozone has been also observed in some experimental studies.
Acid
rain: Most
studies on the effect of acid rain were done with simulated acid rain since it
is not easy to establish experiments under field conditions. In first year of
experiment no effect of acid rain has been observed on any of four pathosystems:
alfalfa leaf spot, peanut leaf spot (PLS), potato late blight (PLB), and soybean
brown spot. In the second year, PLS severity decreased with increasing acidity
and the dose response was linear; PLB severity showed a curvilinear response to
acid rain.
Elevated ultraviolet B:
There is considerable
information on the effects of increased UV-B on crops and natural vegetation and
on the growth and life cycle of pathogenic organisms such as fungi. Studies
indicate that the UV-B component of solar radiation plays a natural regulation
on plant diseases. Stimulatory effect of near-UV light on reproduction of many
fungi, and spore production in Leptosphaerulina trifoli peaks at 287 nm
are reported. Fungi differ in their sensitivity to UV-B. Some strains of
Septoria tritici are more sensitive to UV-B than others and S. nodorum,
as a species, is more sensitive than S. tritici. UV-B radiation can
modify the relative composition of phylloplane organisms, such as pink and white
yeast. Continued exposure to enhanced UV-B radiation lowers the level of
antifungal compounds in foliar parts. UV-B has been shown to reduce tolerance of
rice to blast (Pyricularia grisea) and although higher UV-B reduced plant
biomass and leaf area; there was no increase in blast severity. There are some
evidences that sunlight can influence pathogen by causing accumulation of
phytoalexins or protective pigments in plant tissues. Therefore, UV-B may affect
plant diseases directly via the pathogen or indirectly via the host.
Effects of climate change
on viral pathogens
Most of
the climate change studies have been conducted on diseases caused by fungal
pathogens. Viral diseases mostly have been ignored. Only few studies have
reported the response of plants infected with viral diseases to various climate
change components. It has been observed that oats infected with Barley yellow
dwarf virus (BYDV) showed greater biomass accumulation to CO2
enrichment than the healthy plant. Tobacco plants grown at increased CO2
concentrations showed a markedly decreased spread of virus. It appears that CO2
rise in the air may have some positive effects, which may likely offset the
negative effects of virus infection. However, generalization is difficult
without much information from different virus-host infections.
Average
temperature increase of 0.7°C over the last hundred years and average of 6.3 °C
predicted by the year 2100 will dramatically affect both mobile (fauna) and
immobile (flora) organisms, resulting in both altered and novel forms of
interactions between plants, pathogens and their vectors. Most plant viruses are
transmitted by vectors and majority by insects. Particularly aphids are expected
to react strongly to environmental changes because of their short generation
time, low developmental threshold temperatures and ability to survive mild
winters without winter storms. An increase in the number of insect vectors will
inevitably lead to a higher risk for viral infection of plants. The aphid
transmissible complex of barley yellow dwarf viruses in cereals and potato virus
Y in potato are amenable to show potential effects on the prevalence of
infection because of climate change. In mild winters, high intensity of aphid
movement during spring and a high frequency of PVY-infected potatoes have been
reported. The severity of viral diseases is determined in large part by the
amount of inoculums and the time of infection. The amount of virus inoculum is
influenced by winter survival of its hosts. For some viruses, higher
temperatures also cause more severe symptoms development. Aphids are expected to
have increased survival with milder winter temperatures, and higher spring and
summer temperatures will increase their development and reproductive rates and
lead to more severe disease. Milder winters are also expected to increase
survival of alternate weed hosts of viruses. Increases in frequency and
intensity of summer storms with high winds, rain, and hail will increase
wounding of plants and result in increased transmission of viruses by mechanical
means. Therefore, with predicted changes in climate, viral diseases of plants
are expected to increase in importance. Potentially of greater importance will
be the effects of diseases caused by newly, introduced viruses that, because of
the changed climate, will be able to persist. A warmer climate might also allow
viruses that are present in greenhouses, such as Pepino mosaic virus
(PepMV), to establish infection in the field. The main effect of temperature in
temperate regions is to influence winter survival of vectors. Natural spread of
vectors, pests and diseases is accelerated towards the North, as former climate
barriers are no longer effective. This results in more severe outbreaks of
plant-disease vectors like aphids, white flies, thrips or beetles, an extension
of the period of disease infection further into the growing season and also
introduction and establishment of new vector species. The described effects on
vectors can have severe negative effects on food production or result in an
increased use of plant protection products to control the vectors.
Effects
of climate change on bacterial pathogens
Milder and shorter winters are
expected to have little effect on soil-borne bacterial pathogens, however,
survival of host or debris-borne and vector-borne primary inoculum is expected
to increase. Soil-borne, bacterial plant pathogens, such as Agrobacterium
tumefaciens, may build up their populations in host plants and could be
released into the soil where they can survive as primary inoculum in the next
season. Host or debris-borne bacteria survive on and in host tissues. On
perennial hosts, bacteria, such as Erwinia amylovora on apple, overwinter
on infected host tissue, and primary inoculum is spread from host to host in the
next season. On annual hosts, bacteria such as Pseudomonas syringae pv.
phaseolicola may survive in host debris in soil or on the soil surface.
Vector-borne bacterial pathogens, such as Erwinia stewartii, survive in
insect vectors, and these vectors act as the source of primary inoculum in the
next season.
Bacterial
pathogens, such as Pseudomonas syringae pv. tomato and
Xanthomonas campestris pv. vesicatoria, arise from infected seed and
possibly also survive in debris, soil, and weeds. Bacteria are spread to their
host plants mainly by water, usually in the form of rain splash, and insects. In
humid, wet conditions, infected plant tissues can exude masses of bacteria that
are spread from host to host by rain splash and insects. Therefore, the warmer
drier summers expected with climate change should limit bacterial diseases.
However, bacteria often enter hosts through wounds and the expected increase in
frequency and intensity of summer storms with high winds, rain, and hail will
increase wounding of plants and provide moisture for the spread of bacteria.
Effects
of climate change on nematodes
Majority
of plant-pathogenic nematodes spend part of their lives in soil, and therefore,
soil is the source of primary inoculum. Life cycle of a nematode can be
completed within 2–4 weeks under optimum environmental conditions. Temperature
is the most important factor, and development is slower with cooler soil
temperatures. Warmer soil temperatures are expected to accelerate nematode
development, perhaps resulting in additional generations per season, and drier
temperatures are expected to increase symptoms of water stress in plants
infected with nematodes such as the soybean cyst nematode. Overwintering of
nematodes is not expected to be significantly affected by changes in climate,
although for some, such as the soybean cyst nematode, egg viability may be
reduced in mild winters.
Effects
of climate change on disease development due to abiotic stresses
Diseases
can also result from indirect effects, where plants have their defenses weakened
by an abiotic factor and are predisposed to infection by plant pathogens.
Several important plant diseases are initiated by abiotic stresses, including
forest decline diseases, which are an example of a disease complex caused by a
combination of plant predisposition and a repetitive sequence of plant stresses
that weaken a plant to become susceptible to weak pathogens that then can often
infect and kill the plant These weak pathogens, called saprogens, are often
ubiquitous inhabitants of soil and decaying plant material and, normally, they
do not cause disease in healthy, unstressed plants. However, under conditions of
environmental stress, plants can become susceptible to these saprogens and their
opportunistic infections. One of the more prevalent examples of these saprogens
is the girdling fungi of the genus Armillaria. As climate changes, new
combinations of host–stress–saprogens will be encountered and might give rise to
new types of decline diseases, particularly in tree species. In temperate
climates, plants that are stressed by biotic or abiotic factors during a growing
season are often predisposed to freezing damage during the subsequent winter.
Plant diseases associated with interactions of biotic and abiotic stresses, or
disease complexes, are a unique and important area of consideration for
assessing the influence of climate change on plant diseases. In particular,
forest declines are an example of plant diseases that result from a combination
of interacting biotic and abiotic factors. Such diseases are characterized by a
variety of disease symptoms and signs, are typically scattered in a random
pattern throughout a population within a region, and are often host-specific,
although more than one tree species in a region may have its own specific
decline symptoms. Decline diseases are one example where a strong association
between climate change and disease incidence and (or) severity has already been
established in several forest species. Facts of extensive forest declines have
been documented in Europe and North America in ash, birch, balsam fir and maple,
and a strong relationship was evident between climate warming in the Northern
Hemisphere and the onset of crown dieback in 1925, 1937, and 1981 on selected
species of northern hardwoods in eastern Canada.
Impact of
climate change on disease management
New
dimensions of climate change may add extra uncertainty in management strategies
for diseases caused by different pathogens. Delayed planting to avoid a pathogen
may become less reliable. There may be problems with applications of bio-control
agents in the field because of the vulnerability of bio-control agent
populations to environmental variations and environmental extremes If
appropriate temperature and moisture are not consistently available, bio-control
agent populations may reach densities that are too small to have important
effects, and may not recover as rapidly as pathogen populations when congenial
conditions reoccur.
1Division of Environmental Sciences, Indian
Agricultural Research Institute, New Delhi – 110012
2Division of Plant Pathology, Indian
Agricultural Research Institute, New Delhi – 110012 |
