plant will suffer no significant damage. But if the host
response is slow the fungus can progressively colonize
the vessels, causing rapid wilting and plant death
(Figs. 14.15, 14.16).
The interesting feature of vascular wilt fungi is that
they remain confined to the nonliving xylem vessels
until the plant is heavily diseased, and only then do
they invade the living parenchyma cells, producing
thick-walled resting structures which eventually return
to the soil when the tissues decompose.
Vascular wilt fungi
The three main fungi that cause vascular wilt diseases
are Fusarium oxysporum, Verticillium albo-atrum, and
V. dahliae. Of these, F. oxysporumis the most import-
ant because it consists of more than 80 strains that
show specific pathogenicity to particular crop species
(Armstrong & Armstrong 1981). These strains are
termed “special forms” (formae speciales), abbreviated
to ff. ssp (plural) or f. sp (singular). For example,
the vascular wilt pathogen of bananas is termedF.
oxysporumf. sp. cubense, and the vascular wilt pathogen
of tomato is F. oxysporumf. sp.lycopersici. All these
strains look identical, and all survive by producing
chlamydospores (spores derived from individual
hyphal compartments by accumulating nutrients and
developing a thick, resistant cell wall). These spores
can survive in soil for many years, but probably also
germinate and maintain their population by growing
in a saprotrophic mode in the rhizosphere. Verticillium
albo-atrum and V. dahliaealso cause serious wilt diseases,
such as verticillium wilt of hops and many other
plants. However, they seem to be less host-specific
than F. oxysporum, because strains isolated from one
host will often infect several other unrelated hosts in
artificial inoculations.Pathogenicity determinantsThe typical symptoms of vascular wilt diseases usually
include the progressive yellowing and death of leaves,
accompanied by early collapse of the petioles (leaf
stalks) so that the leaves hang down – a feature termed
epinasty. These symptoms strongly suggest a role of
toxins in the disease syndrome. Fusaric acidwas
one of the first potential toxins to be identified. It is
known to be produced by F. oxysporumin laboratory
culture. It has also been detected in diseased plants, and
when applied to plant protoplasts in vitroit increases
their permeability to ions. However, there is still
doubt about the role of fusaric acid in vivobecause
its concentrations in xylem fluid are often low. A
more convincing role has been established for a toxin
termed cerato-ulmin, produced by Ophiostoma ulmi(the
cause of Dutch elm disease). When the bases of cut elm
shoots are immersed in solutions of cerato-ulmin they
develop the typical leaf symptoms of Dutch elm dis-
ease. Cerato-ulmin is a hydrophobin (see Chapter 5),
and hydrophobin molecules spontaneously assemble
into water-repellent layers at an air–water interface.
Therefore they could have a significant role in restrict-
ing water flow in xylem vessels.Role of environmental factorsEnvironmental factors play a major role in vascular wilt
diseases. Early evidence of this was found in the major
banana plantations of Central America, where soils could
be categorized as either “long-life” or “short-life.” In
long-life soils, banana plantations could remain pro-
ductive for many years, with little evidence of disease,
whereas short-life soils became nonproductive within
a few years of establishing the crop. Chemical analyses
revealed a general correlation between the different
types of clay mineral and the life of banana plantations.
Long-life soils tend to have a higher proportion of
montmorillonite clays, as opposed to the kaolinite294 CHAPTER 14
Fig. 14.14Diagrammatic representation of pathogen
spread and occlusion of the xylem vessels in vascular wilt
diseases. Spores or yeast-like cells are carried upwards in
the water flow and become trapped on the perforated
vessel end walls. They germinate, grow through the pores,
and produce further cells that are carried upwards to the
next vessel end wall, and so on. (Based on Beckman &
Talboys 1981.)