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CHAPTER 17: PRINCIPLES AND
PRACTICE OF CONTROLLING FUNGAL GROWTH
This
chapter deals with the major practical methods of
controlling fungi:
control
by management of environmental and
biological factors
biological and integrated control
chemical control of fungi
the principal cellular targets of
antifungal agents
the use of fungicides for plant disease
control
antifungal antibiotics used for plant
disease control
control of fungal infections of humans
SAMPLE
TEXT:
Control of human and crop
pathogens: the principle of selective toxicity
In contrast to general toxicants,
chemicals used to control fungi in the tissues of another
living organism must show selective toxicity. The
rest of this chapter will be devoted to this topic,
dealing first with the control of plant diseases and then
with the control of human mycoses. These areas are more
closely related than one might think, because the same
types of chemical are used to control both plant- and
human-pathogenic fungi. For example, the azole
fungicides (imidazoles and triazoles) were first
developed to control plant diseases, but in modified
forms they are now widely used to control human mycoses.
Similarly, the naturally occurring antifungal antibiotic griseofulvin
was first discovered as a ‘curling factor’ that
caused the germ-tubes of a plant-pathogenic fungus, Botrytis
allii, to grow in a distorted spiral fashion, but it
was developed commercially as an orally administered
antibiotic to control infections caused by the
dematophytic fungi. It acts by disrupting fungal
microtubules, and this explains its morphogenetic effect
because microtubules are involved in the delivery of
cellular components to the growing hyphal tip (Chapter
4).
The principal cellular targets
of antifungal agents
The main cellular targets
currently used to control plant or human diseases
are shown in Figure 17.2. At first sight it might seem
that there are a large number of cellular targets that
could be exploited for disease control. But in practice
the range is limited. Many of the compounds shown in Fig.
17.2 have a very restricted usage (shown as
“R”) and are used mainly in Japanese
agriculture. If we exclude these compounds then we are
left with just five main types of antifungal
target:
1) the cell membrane,
because fungi are unique in having ergosterol as
their characteristic membrane sterol;
2) the microtubules and microtubule-associated
proteins, which are disrupted by the antibiotic
griseofulvin, and by benzimidazole fungicides (which have
now been withdrawn);
3) mitochondrial
respiration, which is targeted by some plant
fungicides;
4) fungal cell wall components,
especially ß,1-3 glucans, for which a new group of
drugs, the echinocandins, has recently come into use
(2002);
5) various aspects of general
metabolism.
There is an urgent need to find new
chemicals (with novel modes of action) and new cellular
targets, to provide a greater range of options for
controlling fungal diseases.
| Table 17.2. Classification of
fungicides according to their main site or mode
of action |
| Site/mode of action |
Comments |
| Nucleic acid synthesis |
A few fungicides, including
the acylalanines that control diseases
caused by Oomycota; e.g. Phytophthora
infestans |
| Microtubules (mitosis
and cell division) |
A few fungicides, including
the benzimidazoles that act systemically |
| Respiration |
Many fungicides that block
steps in the mitochondrial electron transport
chain or that inhibit ATP synthesis |
| Amino acid and protein
synthesis |
A few fungicides and
antibiotics such as blasticidin-S and kasugamycin |
| Signal transduction |
A few fungicides that
affect G proteins in cellular signalling or MAP
protein kinase |
| Lipids and membrane
synthesis |
Several fungicides that
affect lipid peroxidation, phospholipid
biosynthesis or cell membrane permeability |
| Sterol biosynthesis |
Many important fungicides
that target different steps in the sterol
synthesis pathway |
| Glucan and cell wall
synthesis |
A few fungicides and
antibiotics (polyoxin, validamycin) |
| Melanin synthesis |
A few fungicides that block
melanin biosynthesis |
| Multi-site activity |
Several inorganic
fungicides (sulphur, copper) and protectant
(contact) fungicides that disrupt basic metabolic
processes |
| Induced host plant
defence |
A few compounds (e.g.
salicylic acid, chitosan) that activate
plant-defence mechanisms |
| Various; unknown mode of
action |
A few compounds, including
phosphorous acid and fosetyl-aluminium for
controlling Phytophthora root rot |
----------------------------------
| Table
17.3. Some antifungal antibiotics used for
control of plant or human mycoses |
| Antibiotic |
Produced by |
Fungi affected |
Site/mode of action |
| Griseofulvin |
Penicillium griseofulvum |
Many (not Oomycota) |
Fungal tubulins |
| Polyene macrolides |
Streptomyces spp. |
Many (not Oomycota) |
Cell membrane |
| Polyoxins |
Strep. cacaoi |
Many (not Oomycota) |
Chitin synthesis |
| Validamycin A |
Strep. hygroscopicus |
Some |
Morphogen |
| Blasticidin-S |
Strep. griseochromogenes |
Some |
Protein synthesis |
| Kasugamycin |
Strep. kasugaensis |
Some |
Protein synthesis |
| Streptomycin |
Strep. griseus |
Oomycota |
Calcium? |
| Pyrrolnitrin |
Pseudomonas spp. |
]* |
] ++ |
| Pyoluteorin |
Pseudomonasspp. |
]* |
] ++ |
| Gliotoxin |
Trichoderma virens |
]* |
] ++ |
| Gliovirin |
T. virens |
]* |
] ++ |
| Viridin |
T. virens |
]* |
] ++ |
| Viridiol |
T. virens |
]* |
] ++ |
| Heptelidic acid |
T. virens |
] * |
] ++ |
| Trichodermin |
Trichoderma spp. |
]* |
] ++ |
| 6-pentyl-a-pyrone |
Trichoderma spp. |
]* |
] ++ |
| Suzukacillin |
Trichoderma spp. |
]* |
] ++ |
| Alamethicine |
Trichoderma spp. |
]* |
] ++ |
| * = active against various plant
pathogens |
| ++ =
Implicated in biocontrol by nutrient-competition,
antibiosis, parasitism of other fungi, etc. |
------------------------------
Chapter 16 images. Click on
the thumbnails
|
Fig. 17.1
Fig. 17.5
Fig. 17.8
Fig. 17.13
|
Fig. 17.2
Fig. 17.9
Fig. 17.14
|
Fig. 17.3
Fig. 17.6
Fig. 17.10
Fig. 17.15
|
Fig. 17.4
Fig. 17.7
Fig. 17.11
Fig. 17.12
Fig. 17.16
|
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