| 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 posed 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. Like 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. Dutch elm disease is therefore
an example of a vascular wilt disease. |
Vascular browning caused
by Dutch Elm Disease
© Gareth W. Griffith |
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 Oomycete
fungus Phytophthora infestans, a member of the Peronosporales.
As discussed in the section on fungal
taxonomy, Phytophthora is not a “real”
fungus but rather a 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 dependent on 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
the emigration of a million others. P. infestans first
reached Ireland via Europe, after infected potatoes were imported
from Mexico, which is believed to be the ancestral home of the pathogen.
More recently,
completely new populations of P. infestans have been
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 new 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. |
An experimental potato crop
infected with late-blight
© J Day |
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 leaf surface, and these are released to infect new plants.
© J Day
|
These sporangia represent the most
delicate phase of the oomycete’s life cycle. If the air
temperature drifts outside the range of 16-21oC,
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. |
|
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
rust
Agriculture, University of Reading © University of Reading
Image courtesy LTSN
Bioscience 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 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
a living 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
without 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 of 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 tissues.
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. |
A haustorium of powdery mildew,
within the plant cell.
© Gareth W. Griffith |
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 plants, 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 back-door entrances for fungal pathogens to
get in (shown on the right). |
Top view (point to activate).
|
Side view (point to 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 on
the plants.
The next part of the plant’s defences against
fungi isn’t chemical, but 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. The 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
it 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 a 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 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
oxysporum 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. |
Vascular wilt in tomato.
© Gareth W. Griffith |
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 Japan’s 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 seedlings 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.
6. Investigating Plant Pathogens
Given the major economic impact of fungal plant
pathogens, it is often the case that they are better studied than
fungi which don’t do particular harm to plants or animals.
The science of plant pathology deals with several
major areas of research. First, there is the day to day work of
diagnosis of new outbreaks. This is important,
to allow the right treatment measures to be applied, and to notify
the authorities when an important outbreak occurs. Often diagnosis
is simply a case of an experienced plant pathologist taking a good
look at diseased plants, sometimes with the help of a microscope.
The next step is to isolate the plant pathogen on nutrient media
or on uninfected plants. However, sometimes it is necessary to use
advanced methods such as DNA testing or serology to identify the
fungus.
From this routine work it is possible to determine
the prevalence and importance of different fungal infections, allowing
plant pathologists to focus on the most important infections. Work
can then be directed to a number of directions. Epidemiology
focuses on how the disease spreads, and the life cycle of the fungus.
This can then be used to predict the spread of the disease, and
how to control it.
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Another key area of research is
the science of molecular plant pathology which
uses the tools of molecular
biology and biochemistry to investigate the pathogen’s
biology, and how plants and pathogens interact. |
Given a sound knowledge of the pathogen, its life
cycle, and how the plant responds to the pathology caused by the
pathogen, plant pathologists can begin to develop countermeasures
to control the infection. This can be as simple as which fungicides
to use, the development of new fungicides or measures to grow the
host crops in such a way that minimizes the spread of the disease.
In the longer term, the techniques of plant breeding and
genetics can be used to develop resistant crops. Traditionally,
this takes an exceedingly long time, but there are modern approaches
(including, but not restricted to, the controversial GM technology)
that can speed up the process.
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