untitled

beyond a treated area in a commercial glasshouse. The
area of diseased plants in each box was then assessed.
Treatment of the soil for 30 minutes at any temperat-
ure (61, 70 or 100°C) eliminated the resident Pythium
population. But after treatment at 100°C the soil
was sterile and highly conducive to the spread of
Rhizoctonia, which can grow rapidly through sterilized
soil. By contrast, soil treated at 61°C was free from any
disease. This was explained by the fact that Bacillusspp.,
which occur naturally as dormant spores in soil, can
not only survive pasteurization but also are triggered to
germinate at this temperature. These naturally occur-
ring biocontrol agents grow rapidly to fill the biological
“vacuum” and they produce several antifungal anti-
biotics that protect the newly sown crop.
The use of steam–air mixtures in glasshouse crops has
now been replaced by the use of Trichoderma spp. and
similar antagonists. But solar heating of soil (solariza-
tion) has become common practice for raising valuable
field cropsin many of the warmer parts of the world.
It is achieved by covering the soil with thin polyethy-
lene sheeting for a 20- to 30-day period. This creates
a “greenhouse effect,” raising the temperature at the
soil surface to 40°C or more, and often to 30°C or more
at even 50 cm soil depth. The spores of most soil-borne
pathogens can survive these temperatures in vitro,
but in moist, solar-heated soil the pathogens are pro-
gressively eliminated by the activities of competing
and antagonistic microorganisms that flourish at the
higher temperatures (Katan 1987).

Chemical control of fungi

Fungitoxic or fungicidal chemicals are often used to
control fungal growth, but a distinction must be made
between general toxicants and selectively toxic agents.

General toxicants

Fungitoxic chemicals play a major role in preventing
decay of a range of products including cosmetics,

starch-based materials, cotton fabrics, and structural

timbers. In each case the choice of preservative

depends on specific needs. For example, the preserv-

atives used in cosmetics and ointments must be non-

toxic, nonirritant, and compatible with the product

formulation. Often, low-molecular-weight alcohols

and esters of p-hydroxybenzoic acid (parabens) are used

in these cases. At the other extreme, marine timbers,

fence posts, and telegraph poles need to be treated with

persistent compounds that will protect against decay

and insect attack for several decades. The three most

commonly used wood preservatives are coal-tar cre-

osote, pentachlorophenol, and inorganic arsenicals

such as chromated copper arsenate. Timbers are often

pressure-treated with these compounds to ensure high

penetration and retention in the wood. Clearly, many

of these wood-treatment products pose potential health

hazards. Pentachlorophenol is a known carcinogen

that is absorbed by the lungs and skin, and it can

contain trace amounts of dioxin. Arsenic-based wood

treatments are widely known to be poisonous, and

the Environmental Protection Agency of the USA re-

cently announced (2003) that arsenic will be withdrawn

from use. The extreme toxicity of many of these wood

preservatives has spurred interest in the possible use of

biological control agents for wood protection. Among

the potential candidates are strains of Trichoderma

that frequently colonize the cut surfaces of logs and

that antagonize wood-decay fungi in laboratory tests

(Vanneste et al. 2002).

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

PRINCIPLES AND PRACTICE OF CONTROLLING FUNGAL GROWTH 341

(a) (b)

V

VV

V

VV

VV

VVV

V

Fig. 17.1(a,b) Diagram of the spread of disease
caused by Rhizoctoniafrom a pocket of surviving
inoculum.