Agriculture Reference
In-Depth Information
Plate 13a) form if plants are water-stressed late in
the season.
The main source of inoculum is the conidia,
which are large and strongly pigmented and can
survive for several years in soil (Wildermuth and
McNamara 1991).
Bipolaris
sorokiniana
can be
seedborne (Couture and Sutton 1980), but seed
transmission is unlikely to occur from common
root rot-infected plants unless spot blotch is also
present.
Incidence of infection is related to the density
of conidia in soil (Tinline et al., 1988). Spore
density, and disease incidence and severity, are
higher in cultivated soils than in no-tillage systems
where seed is directly drilled into residue of a
previous crop (Reis and Abrao 1983; Mathieson
et al., 1990; Wildermuth et al., 1997). This may
be related to dispersion of spores within the soil
during cultivation. A high proportion of spore
production from wheat residues is from crowns
(Duczek 1990), and removal of residue by burning
has been shown to reduce the severity of common
root rot (Wildermuth et al., 1997).
High spore populations and disease severity
occur under continuous wheat (Wildermuth and
McNamara 1991; Conner et al., 1996). Continu-
ous wheat also increases the average aggressive-
ness of fi eld populations towards wheat (El-Nashaar
and Stack 1989). Wheat and barley (
Hordeum
vulgare
L.) are among the most susceptible
hosts, with oat (
Avena sativa
L.) being less sus-
ceptible while legumes are generally resistant
(Wildermuth and McNamara 1987). Spore popu-
lations decline under fallow or nonhosts, such as
oilseeds or legumes, compared with cereals
(Wildermuth and McNamara 1991).
The effect of nutrients on common root rot is
equivocal. Most attention has been paid to chlo-
ride, which reduces disease severity in some
experiments but has no consistent effect in others
(Windels et al., 1992; Tinline et al., 1993). Low
nitrogen levels possibly reduce disease severity, so
that severity in continuous wheat with no added
nitrogen is less than in wheat-legume sequences,
despite the rotation effect (Dalal et al., 2004;
Fernandez and Zentner 2005). This is probably
due to an interaction between high nitrogen levels
and water use (Dalal et al., 2004).
Incidences of common root rot and Fusarium
crown rot are often inversely related when both
diseases are present. Severity of common root rot
declined as incidence of Fusarium crown rot
increased in a long-term trial (Wildermuth et al.,
1997). This may represent competition between
the pathogens, because
B
.
sorokiniana
is a poor
competitor with
Fusarium
species in plant tissue
(Tinline 1977). However,
B
.
sorokiniana
is
strongly antagonized by the crown rot
Fusarium
species in culture, and symptoms of the two
diseases are similar. It is therefore possible that
B
.
sorokiniana
is diffi cult to detect by isolation or
symptoms in the presence of
Fusarium
species.
Because of possible interactions, reports of
common root rot when it co-occurs with
Fusarium crown rot must be interpreted with
caution.
Causal organism
Bipolaris sorokiniana
(Sacc.) Shoemaker [teleo-
morph =
Cochliobolus sativus
(S. Ito and Kurib)
Drechsler ex Dastur] has a worldwide distribu-
tion and a wide host range among small grain
cereals and grasses (Kumar et al., 2002). This
pathogen is widely reported in older literature as
Helminthosporium
sativum
Pammel, C.M. King &
Bakke. The sexual state is readily produced in the
laboratory (Singleton et al., 1992) but has not
been reported in the fi eld.
Some evidence exists for host specialization
within the species. Isolates from barley are
more virulent to barley roots than to wheat roots,
and vice versa (Conner and Atkinson 1989).
Wheat isolates vary greatly in their virulence on
wheat leaves (Duveiller and Garcia Altamirano
2000) but no clear evidence for races has been
found.
Bipolaris
sorokiniana
produces several sesqui-
terpenoid toxins, the most important of which is
prehelminthosporol (Kumar et al., 2002). Isolates
with low prehelminthosporol production in
culture tend to have reduced virulence on barley
roots (Apoga et al., 2002), but evidence for a
major role of toxins in pathogenesis is not
available.
