L.21-G.Biology
Mycology
D.Ebtihal Muiz
Plant Diseases caused by fungi
While fungi do cause some diseases in animals, the diseases they
cause in plants are far more numerous, and some of these may also have
severe indirect effects on human health and well-being. At an
introductory level, we shall explore examples of significant plant
pathogens and examples of the different modes of attack employed by
plant fungal pathogens, how plants defend against fungi and how fungal
pathogens overcome the difficulty pose4 by having hosts that are largely
static.
1. Dutch Elm Disease
2. Late Blight of Potato
3. Rusts
4. Powdery Mildews
5. Interactions between Plants & Pathogens
6. Investigating Plant Pathogens
1. Dutch Elm Disease
Dutch elm disease first spread to Europe from
the USA in the 1920s, and is caused by the ascomycete Ophiostoma
ulmi.Lik most plant pathogens, its life cycle is complex; and particularly
so in the case of Ophiostoma ulmi as it
depends on a vector for spread, the elm bark beetle.
While the disease first came to prominence in the
1920s, the most severe outbreak has been since
1970, with over 20 million trees killed since that year in the UK. It is now
accepted that this outbreak was caused by new, more agressive strains of
the fungus which have been designated as a new species, Ophiostoma
novo-ulmi.
In brief, infection occurs when the fungus is carried into young twigs by
the Elm bark beetle. The infection then spreads by mycelial growth and
also through the host’s vascular system in the form of yeast. As the
infection spreads, toxins (such as the protein cerato-ulmin) and fungal
enzymes attack and digest the host tissue, and xylem vessels are blocked.
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Vascular browning caused
by Dutch Elm Disease © Gareth W. Griffith
Dutch elm disease is therefore an example of a vascular wilt disease.
As the infection proliferates, death of the tree will occur within a few
months. The scent of a dying, tree attracts more bark beetles which breed
in structures in the bark called breeding galleries. As the young beetles
emerge from the galleries, they are contaminated with the spores of the
fungus.
Controlling Dutch elm disease has proved difficult. Breeding resistant
varieties of trees takes decades. The other options are to spray with
fungicide or insecticide (or both) to control the fungus or the vector. With
trees the size of elms, this is particularly difficult to do with any measure
of success. This leaves only the possibility of drastic action, the cutting
down of infected trees, and this was not done early enough during the
epidemic to be effective.
2. Late Blight
Late blight of potatoes and related plants is caused by the Qomycete
fungus Phytophthora infestans, a member of the Peronosporales. As
discussed in the section on fungal taxonomy, Phytophthora is not a
“real” fungus but rather member of the Kingdom Stramenophila.
P. infestans was the first recognized plant pathogen; and to date ,it has
caused the most serious epidemics of plant disease. The worst occurred in
Ireland during the period 1845-1847. In an agriculturally based economy
dependerit potatoes as the main food crop, the consequences were far
reaching. The resulting potato famine led to the death of over a million
people and forced emigration of a million others. P. infestans first
reached Ireland via Europe, after infected potatoes were imported from
Mexico, which is believed to be ancestral home of the pathogen.
More recently, completely new populations of P. infestans have been
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detected in Britain, and in other European countries. These are thought to
have been introduced to Europe following the drought of 1976, which led
to the large-scale importation of potatoes. This r.mw population is
genetically much more diverse than the old one, and since it includes a
second mating type (only a single mating type having been present
formerly in Britain) there is the potential for that diversity to increase still
further, thereby allowing the pathogen to adapt more readily to
agricultural control methods.
The new population of P. infestans already contains strains that are
resistant to some of the front-line fungicides used to protect crops. In the
USA, also, new strains have been detected, including the genotype
designated US-8 which causes a highly aggressive, rapidly-spreading
infection and is also resistant to the commonly-used phenylamide
fungicides.
phytophthora infestans does, however, have a number of ‘weaknesses’ in
its life cycle. Infection occurs as a result of sporangia germinating on the
moist leaf surfaces of potato plants. Zoospores are released and they
infect the plant, germinating into hyphae which press into the plant. After
3-4 days, symptoms begin to appear on the plant, with necrotic lesions
spreading from the point of infection. After a week, new sporangia are
produced on the Ieaf surface, and these are released to infect new plants.
These sporangia represent the most delicate phase of the oomycete’s life
cycle. If the air temperature drifts outside the range of 16-21o0, or the
relative humidity drops below 75%, then spread is unlikely. If these
conditions are maintained for more than 48 hours, then a Beaumont
Period has occurred, and spread of the infection is highly likely. Weather
monitoring allows farmers to anticipate the spread of blight, and spray
potato crops at a point early enough to be effective. Detection of
sporangia in air samples taken near crops may allow forecasting to be
refined still further in the future.
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© J Day
3_Rusts
The pathogens mentioned earlier on this page are examples of
necrotrophic pathogens (although Phytophthora infestans exhibits an
initial biotrophic phase). Rusts, however (which belong to the
Basidomycete subphylum Uredinomycetes), are completely biotrophic
pathogens. They only parasitize their host plants, without killing them,
though they do cause some tissue damage.
Rust-infected plants may therefore appear quite healthy, apart from the
‘rusted’ appearance of the leaves due to the production of spores (usually
orange or yellow).
A field bean plant infected with n Agriculture, University of Readinç
University of Reading
Image courtesy LTSN Biosciern ImageBank
Rusts are obligate biotrophs, meaning that they cannot survive without
the presence of the host. The specificity of such fungi for their host is
extremely high, and they will only infect one or a small number of host
species. The small host range attacked by any given rust species means
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that it is essential for them not to kill off the host species, as happened
with Phytophthora infestans in Ireland in the 1840s. But biotrophs such
as rusts need to make loving as well, so they need to maximise their
opportunity to drain nutrients from the host plant without killing it. As
such, many rusts (and other biotrophs) have specialized structures called
haustoria (singular, haustorium) which act to maximise contact with the
host cells to allow good transfer of nutrients with excessively damaging
the host’s tissues.
4. Powdery Mildews
Powdery mildews (Erysiphales), members of the phylum
Ascomycota, are the most important pathogens of cereal crops in the UK,
and cause significant reductions in yield when they strike — up to a 20 %
loss as a result of the mildew continually drawing off the products of
photosynthesis that would otherwise go into producing grain. Again, as
with other biotrophs, the trend is for the development of a very narrow
host range; an example of this is Erysiphe graminis var. tritici and
Erysiphe graminis var. hordei, two varieties of the same species. The
former will only infect wheat, whereas the latter will only infect barley!
Barley infected with powdery mildew
© Gareth W. Griffith
Infection with powdery mildew occurs as conidia land on the leaf bf
a Host plant. The conidia germinate to form a hypha called a germ tube.
The end of the germ tube will form a swelling called an appressorium,
tightly attached to the host surface. From the appressorium, a narrow
hypha known as an infection peg is able to presses through the
host plant’s epidermis. The mildew can then grow in the spaces between
the plant cells and, like the rusts, it forms haustoria within the plant
cells to siphon off nutrients from the plant lissues. To complete the
disease cycle, hyphae appear on the surface, and conidia are
released into the air, allowing the infection to be spread between plants.
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5. Interactions between Plants and their Pathogens
While most of us are familiar with the rudiments of the human immune
system it is easy to forget that plants have evolved defences against their
pathogens in fact, plants have been waging a full-scale arms race against
their pathogens.
In humans, the skin forms the first line of defence against infection. In
plant this outer defence layer is the cuticle, a layer of waxy material
above the epidermis. This stops many would-be plant pathogens from
getting in on the act.
However, there is a weak spot in the plant’s defence. In order to exchange
carbon dioxide and oxygen for photosynthesis, plants have pores on their
leaf surface called stomata (singular, stoma). These pores are ideal backdoor entrances for fungal pathogens to get in (shown
on the right).
Top view (point to activate).
Side view (point activate).
Other fungi have an enzyme called cutinase which seems to cut up the
cuticle so the fungi can get in — but this has proved difficult to prove!
So if our plant pathogen has got in, what can the plant do to stop it from
getting any further?
Well, the next lines of defence are molecules called phytoanticipins
These are ready-made and act in a general way against the fungi. If
someone were to ask you for an example of a phytoanticipin, then
saponin would be a good place to start. This is found in tomatoes, and is
toxic to most fungal pathogens as it mixes with the fats in fungal cell
membranes and causes the cells to leak, But fungi have a massive
biochemical toolkit, and some fungi have developed an enzyme that can
break down the saponin and as a result, they can grow the plants.
The next part of the plant’s defences against fungi isn’t chemical, but
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rather structural. Plant cell walls are characterized by being rigid, and full
of cellulose and other polysaccharides. When a plant is infected by a
fungus that grows as hyphae the cell wall can thicken dramatically to
form a papilla, which grows around the invading hyphae, preventing them
from going any further. However the fungi have enzymes capable of
breaking down the cellulose-based papillae, so plants often add lignin,
the brown wood polymer. This is difficult for most fungi to break down,
as many decomposer fungi know. Lignin is made of many phenolic
compounds, similar to the type we use as antiseptics and these tend to
saturate the area around the invading fungus, often killing it
However, this is only a stop-gap action, to allow the, plants to get the
next line of defence ready in time. The next step is to try to sacrifice the
infected cells with a massive amount of oxidation. While we think of
oxygen as being essential to life, on the molecular scale, oxygen atoms
with extra unpaired electrons (called radicals) can do much to damage
cells, particularly DNA. plants have the molecular machinery to take
oxygen from the atmosphere and use an electron carrier which will give
the oxygen a spare electron, making into highly reactive ion known as
superoxide. Quickly, the superoxide is converted into hydrogen
peroxide which, like phenolics, is used by humans as a disinfectant.
Hydrogen peroxide can then react with the proteins of the plant cell wall
to strengthen it: The production of hydrogen peroxide from superoxide is
found in animals too as a response to infection or damage to tissue.
Animals use hydrogen peroxide as a poison to kill invading bacteria.
However, the toxic hydrogen peroxide often seeps into the surrounding
tissue and causes inflammation and damage to the animals’ cells as well.
Plants use this phenomenon to their advantage, and the cells involved in
the. oxidative burst often die due to the toxic levels of hydrogen
peroxide. This forces the fungus to try and grow through the highly toxic
dead cells. Quite often, the fungus can’t. .
The oxidative burst mentioned above often activates metabolic
pathways. that produce molecules called phytoalexins. These molecules
often act in similar way to antibiotics, by inhibiting fungal enzymes and
blocking the synthesis of important molecules in the invading fungus.
Some phytoalexins however activate some of the host’s own enzymes,
such as chitinase, which breaks down the fungal cell wall. Some fungi
have got ahead of the game, and can break down the phytoalexins the
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plants have used to try and break the fungi themselves down!
The other side of the battle between plants and fungi is often quite
complex.
Vascular wilt pathogens such as Fusarium
oxysporurn and Ophiostoma ulmi disrupt the
plant’s delicate regulation of water by growing in the xylem vessels that
carry water up the plant, causing the plant to dehydrate and die.
Some fungi, like Ophiostoma ulmi, also use toxins to damage plants.
But perhaps the most interesting way a fungal pathogen causes disease in
plants is the. Foolish Seedling Disease caused by Giberella fungi. This
disease involves increased growth in the plant, and destroyed 40% of
Japans' rice crop in 1809. It was first isolated in 1908 by the Japanese
pathologist Hori, and subsequent studies identified a growth promoting
substance that they called a Giberellin. This is produced by the fungus,
and causes the seedling to grow beyond their means and die. Other work
then found giberellins produced by the plants themselves. Today,
giberellins are mainly recognized as plant hormones that regulate
growth, flowering, seed germination and so forth in a wide range of
plants.
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