Fungicides are
chemical compounds or biological organisms
used to kill or inhibit
fungi or
fungal spores . Fungi can cause serious damage
in
agriculture, resulting in critical
losses of
yield, quality and
profit. Fungicides are used both in
agriculture and to fight
fungal
infections in animals. Chemicals used to control
oomycetes, which are not fungi, are also referred
to as fungicides as oomycetes use the same mechanisms as fungi to
infect plants.
Fungicides can either be contact or systemic. A contact fungicide
kills fungi by direct contact; a systemic fungicide has to be
absorbed by the affected organism.
Most fungicides that can be bought retail are sold in a liquid
form. The most common active ingredient is
sulfur, present at 0.08% in weaker concentrates, and
as high as 0.5% for more potent fungicides. Fungicides in powdered
form are usually around 90% sulfur and are very toxic. Other active
ingredients in fungicides include
neem oil,
rosemary oil,
jojoba
oil, and the bacterium
Bacillus subtilis.
Fungicide
residues have been
found on food for human consumption, mostly from post-harvest
treatments. Some fungicides are dangerous to human
health, such as
vinclozolin, which has now been removed from
use.
Natural fungicides
Plants and other organisms have chemical defenses that give them an
advantage against microorganisms such as fungi. Some of these
compounds can be used as fungicides:
Whole live or dead organisms that are efficient at killing or
inhibiting fungi can sometimes be used as fungicides:
- The bacterium Bacillus
subtilis
- Kelp (powdered dried kelp is fed to cattle
to protect them from fungi in grass)
Resistance
Pathogens respond to the use of fungicides
by evolving
resistance. In the
field several mechanisms of resistance have been identified. The
evolution of fungicide resistance can be gradual or sudden. In
qualitative or discrete resistance a
mutation (normally to a single gene) produces a
race of a fungus with a high degree
of resistance. Such resistant varieties also tend to show
stability, persisting after the fungicide has been removed from the
market. For example
sugar beet leaf
blotch remains resistant to
azoles years after
they were no longer used for control of the disease. This is
because such mutations often have a high
selection pressure when the fungicide is
used, but there is low selection pressure to remove them in the
absence of the fungicide.
In instances where resistance occurs more gradually a shift in
sensitivity in the pathogen to the fungicide can be seen. Such
resistance is polygenic – an accumulation of many mutation in
different genes each having a small additive effect. This type of
resistance is known as quantitative or continuous resistance. In
this kind of resistance the pathogen population will revert back to
a sensitive state if the fungicide is no longer applied.
Little is known about how variations in fungicide treatment affect
the selection pressure to evolve resistance to that fungicide.
Evidence shows that the doses that provide the most control of the
disease also provide the largest selection pressure to acquire
resistance, and that lower doses decreased the selection
pressure.
In some cases when a pathogen evolves resistance to one fungicide
it automatically obtains resistance to others – a phenomenon known
as
cross resistance. These
additional fungicides are normally of the same chemical family or
have the same mode of action, or can be detoxified by the same
mechanism. Sometimes negative cross resistance occurs, where
resistance to one chemical class of fungicides leads to an increase
in sensitivity to a different chemical class of fungicides. This
has been seen with
carbendazim and
diethofencarb.
There are also recorded incidences of pathogens evolving multiple
drug resistance – resistance to two chemically different fungicides
by separate mutation events. For example
Botrytis cinerea is resistant to both
azoles and
dicarboximide
fungicides.
There are several routes by which pathogens can evolve fungicide
resistance. The most common mechanism appears to be alteration of
the target site, particular as a defence against single site of
action fungicides. For example
Black
Sigatoka, an economically important pathogen of banana, is
resistant to the
QoI fungicides, due to a single
nucleotide change resulting one
amino acid (glycine) being replaced by another
(alanine) in the target protein of the QoI fungicides,
cytochrome b. This presumably disrupts the
binding of the fungicide to the protein, rendering the fungicide
ineffective.
Upregulation of target genes can also render the fungicide
ineffective. This is seen in DMI resistant strains of
Venturia inaequalis.
Resistance to fungicides can also be developed by efficient
efflux of the fungicide out of
the cell.
Septoria tritici
has developed multiple drug resistance using this mechanism. The
pathogen had 5
ABC type
transporters with overlapping
substrate specificities that
together work to effectively pump toxic chemicals out of the
cell.
In addition to the mechanisms outlined above, fungi may also
develop
metabolic pathways that
circumvent the target protein, or acquire
enzymes that enable metabolism of the fungicide to a
harmless substance.
Fungicide resistance management
The fungicide resistance action committee (FRAC) has several
recommended practices to try to avoid the development of fungicide
resistance, especially in at-risk fungicides including
Strobilurins such as
azoxystrobin.
Products should not be used in isolation but rather as mixture, or
alternate sprays, with another fungicide with a different mechanism
of action. The likelihood of the pathogen developing resistance is
greatly decreased by the fact that any resistant isolates to one
fungicide will hopefully be killed by the other – in other words
two mutations would be required rather than just one. The
effectiveness of this technique can be demonstrated by
Metalaxyl, a
phenylamide fungicide.
When used as the sole
product in Ireland
to control
potato blight (Phytophthora
infestans) resistance developed within one growing
season. However in countries like the UK
where it was only ever marketed as a mixture
resistance problems developed more slowly .
Fungicides should only be applied when absolutely necessary,
especially if they are in an at-risk group. Lowering the amount of
fungicide in the environment lowers the selection pressure for
resistance to develop.
Manufacturers’
doses should always be followed.
These doses are normally designed to give the right balance between
controlling the disease and limiting the risk of resistance
development. Higher doses increase the selection pressure for
single site mutations that confer resistance, as all strains but
those that carry the mutation will be eliminated, and thus the
resistant strain will propagate. Lower doses greatly increase the
risk of polygenic resistance, as strains that are slightly less
sensitive to the fungicide may survive.
It is also recommended that where possible fungicides are only used
in a protective manner, rather than to try to cure already infected
crops. Far fewer fungicides have curative/eradicative ability than
protectant. Thus fungicide preparations advertised as having
curative action may only have one active chemical; a single
fungicide acting in isolation increases the risk of fungicide
resistance.
It is better to use an
integrative pest management
approach to disease control, rather than relying on fungicides
alone. This involves the use of resistant varieties and hygienic
practises, such as the removal of potato discard piles and stubble
on which the pathogen can overwinter, greatly reducing the titre of
the pathogen and thus the risk of fungicide resistance
development.
See also
References
- Latijnhouwers M, de Wit PJ, Govers F. Oomycetes and fungi:
similar weaponry to attack plants. Trends in Microbiology
Volume 11 462-469
- Pesticide Chemistry and Bioscience edited by G.T Brooks and T.R
Roberts. 1999. Published by the Royal Society of Chemistry
- Hrelia et al. 1996 - The genetic and non-genetic
toxicity of the fungicide Vinclozolin. Mutagenesis Volume 11
445-453
- Metcalfe, R.J. et al. (2000) The effect of dose and
mobility on the strength of selection for DMI (sterol demethylation
inhibitors) fungicide resistance in inoculated field experiments.
Plant Pathology 49: 546-557
- Sierotzki, Helge (2000) Mode of resistance to respiration
inhibitors at the cytochrome bc1 enzyme complex of Mycosphaerella
fijiensis field isolates Pest Management Science
56:833-841
- Schnabel, G., and Jones, A. L. 2001. The 14a-demethylase
(CYP51A1) gene is overexpressed in V. inaequalis strains
resistant to myclobutanil. Phytopathology
91:102-110.
- Zwiers, L. H. et al. (2003) ABC transporters of the
wheat pathogen Mycosphaerella graminicola function as protectants
against biotic and xenobiotic toxic compounds Molecular
Genetics and Genomics 269:499-507
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