untitled

10 – 40% of oospores freshly harvested from culture

broth will germinate readily, and this value drops to

5% or less when the oospores are dried for storage, mak-

ing commercial production uneconomic. P. oligandrum

and other mycoparasitic Pythium spp. could only be

used as commercial biocontrol agents if methods can

be developed to ensure consistently high oospore ger-

mination. However, this does not preclude a natural

rolefor P. oligandrumas a biocontrol agent. There is

strong evidence that P. oligandrumhelps to suppress

disease caused by Pythium ultimumin the irrigated

cotton fields of California. It seems to do this by com-

peting with P. ultimumfor the crop residues at the end

of the growing season, preventing P. ultimumfrom using

these residues to build up its inoculum level in the soil

(Martin & Hancock 1986).

Competitive interactions on plants

Competition, as defined at the start of this chapter,

embraces all the types of interaction in which one

organism gains ascendency over another because it

arrives sooner, grows faster, uses the substrate more

efficiently, etc. Competition is probably the most

common type of interaction in natural environments,

but this is difficult to prove unless all other potential

mechanisms can be discounted. Here we consider a few

cases where the evidence for competition is strong.

Control of the take-all fungus by

Phialophora graminicola

As we saw in Chapter 9 (see Fig. 9.11), the take-all

fungus Gaeumannomyces graminisattacks the roots of

cereals and grasses by growing as dark runner hyphae

and invading the vascular tissues of the root. There

are three forms of this fungus, termed varieties. G.

graminisvar. triticiis a major pathogen of wheat and

barley roots; G. graminisvar. graminisis often non-

pathogenic; and G. graminisvar. avenaeattacks oat

crops and the fine turf grasses (Agrostisspp.) used on

golf-course greens, bowling greens, and other fine

playing surfaces (Fig. 12.16).

The take-all patch disease of fine turf grasses,

caused by G. graminis var. avenae, is rarely seen

because it occurs only in specific circumstances:

1 When the existing turf is heavily limed to correct for

over-acidity.

2 When new turf is established in sites that have

been chemically fumigated or fungicide-treated to

destroy pests and diseases.

3 When natural turf on golf course greens is removed

and replaced by new grass, laid on a bed of sand.

All three of these circumstances have one factor in

common – the natural, resident microbial antagonists,

which normally prevent take-all patch disease from

developing, are reduced or destroyed. For example,

over-acidity (case 1 above) is caused by the repeated

use of ammonium fertilizers, applied year after year,

to maintain the greenness of the turf. The ammonium

ion is absorbed by roots, and H+ions are released in

exchange, leading to a progressive lowering of the turf

pH. Eventually the turf pH is so low that the grass

no longer responds to added fertilizer. The turf is then

heavily limed to restore the pH to near-neutrality.

This leads to serious outbreaks of take-all patch dis-

ease (Fig. 12.16), initiated by air-borne ascospores of

FUNGAL INTERACTIONS 251

Fig. 12.16(a,b) Take-all patch disease of turf on a golf-course green, caused by G. graminisvar avenae. Note the poor
quality of the turf, where the fine turf grasses have been killed by the fungus and have been replaced by weeds and
course-leaved grasses.

(a) (b)