Septoria and Stagonospora Diseases of Cereals - CIMMYT ...

Stagonospora nodorum releases a
wide range of cell wall degrading
enzymes including amylase, pectin
methyl esterase,
polygalacturonases, xylanases, and
cellulase in vitro and during
infection of wheat leaves (Baker,
1969; Lehtinen, 1993; Magro, 1984).
The information related to cell wall
degradation by enzymes agrees
with histological observations.
These enzymes may act in
conjunction with toxins. Enzyme
sensitivity may be related to
resistance and rate of fungal
colonization (Magro, 1984).
Like many necrotrophs,
Septoria and Stagonospora
pathogens produce phytotoxic
compounds in vitro. Cell
deterioration and death in advance
of hyphal growth into mesophyll
tissue (Bird and Ride, 1981) is
consistent with toxin production.
However, a definitive role for
toxins in the infection process and
their relation to host resistance has
not been established (Bethenod et
al, 1982; Bousquet et al, 1980; Essad
and Bousquet, 1981; King et al,
1983). Differences in host range
between wheat and barleyadapted
strains of S. nodorum may
be related to toxin production
(Bousquet and Kollmann, 1998).
Initiation of spore germination
and percentage of spores
germinated are not influenced by
host susceptibility (Bird and Ride,
1981; Morgan 1974; Straley, 1979;
Straley and Scharen, 1979; Baker
and Smith, 1978). Bird and Ride
(1981) reported that extension of
germ tubes on the leaf surface was
slower on resistant than on
susceptible cultivars. This
mechanism, expressed at least 48
hours after spore deposition,
indicates pre-penetration resistance
to elongation of germ tubes. There
were fewer successful penetrations
in resistant cultivars, and
penetration proceeded more slowly
on resistant cultivars (Baker and
Smith, 1978; Bird and Ride, 1981).
Lignification was proposed to
limit infection in both resistant and
susceptible cultivars, but other
factors slowed fungal development
in resistant lines. In susceptible
lines, faster growing hyphae may
escape lignification of host cells.
Four days after inoculation of
barley with a wheat biotype isolate
of S. nodorum, hyphae grew through
the cuticle and sometimes in outer
cellulose layers of epidermal cell
walls. Thick papillae were
deposited beneath the penetration
hyphae and the cells were not
penetrated (Keon and Hargreaves,
1984).
Infection by Septoria
tritici
Pycnidiospores of S. tritici
germinate in free water from both
ends of the spore or from
intercalary cells (Weber, 1922).
Spore germination does not begin
until about 12 hours after contact
with the leaf. Germ tubes grow
randomly over the leaf surface.
Weber (1922) observed only direct
penetration between epidermal
cells, but others concluded that
penetration through both open and
closed stomata is the primary
means of host penetration
(Benedict, 1971; Cohen and Eyal,
1993; Hilu and Bever, 1957). Kema
Stagonospora and Septoria Pathogens of Cereals: The Infection Process 43
et al. (1996) observed only stomatal
penetration. Hyphae growing
through stomata become
constricted to about 1 µm diameter,
then become wider after reaching
the substomatal cavity.
Hyphae grow parallel to the
leaf surface under epidermal cells,
then through the mesophyll to cells
of lower the epidermis, but not into
the epidermis. No haustoria are
formed and hyphal growth is
limited by sclerenchyma cells
around the vascular bundles,
except when hyphae are very
dense. Vascular bundles are not
invaded. Hyphae grow
intercellularly along cell walls
through the mesophyll, branching
at a septum or middle of a cell. No
macroscopic symptoms appear for
about 9 days except for an
occasional dead cell, but mesophyll
cells die rapidly after 11 days.
Pycnidia develop in substomatal
chambers. Hyphae seldom grow
into host cells (Hilu and Bever,
1957; Kema et al, 1996;
Weber, 1922).
Successful infection only occurs
after at least 20 hours of high
humidity. Only a few brown flecks
developed if leaves remained wet
for 5-10 hours after spore
deposition (Holmes and Colhoun,
1974) or up to 24 hours (Kema et
al., 1996). Host-parasite relations
are the same on resistant or
susceptible wheats. Spore
germination on the leaf surface is
the same regardless of
susceptibility. The number of
successful penetrations is about the
same, but hyphal growth is faster
in susceptible cultivars, resulting in
more lesions. Hyphae extend