Agriculture Reference
In-Depth Information
1968; Lucas et al., 1997). When absorbed by
roots, the ammonium ion reduces rhizosphere
pH and stimulates antagonistic components of
the root-surface microfl ora, such as fl uorescent
pseudomonads (Smiley 1978; Sarniguet et al.,
1992a,b).
Effi cient control of grass weeds and volunteer
cereals is important for eliminating additional
inoculum buildup (Ennaïfar et al., 2005;
Gutteridge et al., 2005) that may occur without
contributing to take-all decline, as reported for
blackgrass (
Alopecurus myosuroides
Hudsen),
barren brome [
Anisantha sterilis
(L.) Nevski], and
rye brome (
Bromus secalinus
L.) (Dulout et al.,
1997; Gutteridge et al., 2005).
Attempts have been made to develop a biologi-
cal method to control the disease based on various
hypotheses proposed to explain the phenomenon
of take-all decline (Lucas and Sarniguet 1998).
The most intensive work on this topic has involved
fl uorescent pseudomonads that produce antibi-
otic compounds (Weller et al., 2007). Due to often
inconsistent performance when these biocontrol
agents are applied to soil in an inundative biologi-
cal control, Cook (2007) stressed the importance
of managing the resident rhizobacteria with the
cropping system to achieve a conservation bio-
logical control.
sheath, and into the culm. Leaf striping often
does not occur on all leaves and tillers of affected
plants. Affected leaves senesce prematurely,
plants are typically stunted, and heads may ripen
prematurely to produce whiteheads (Color Plate
13a). As plants mature the culm of infected tillers
may darken at and below nodes. When seedlings
are heavily infected they may exhibit a mosaic-
like yellowing in late winter or early spring and
may die before stripes develop.
The pathogen is disseminated in infested seed
(Murray 2006), but most disease is caused by
infection of roots by soilborne conidia (Mathre
and Johnston 1975). The pathogen directly pen-
etrates adventitious (coronal) roots and lower
stems and moves into xylem vessels (Stiles and
Murray 1996; Douhan and Murray 2001). Conidia
produced in the xylem and those entering directly
through wounds are carried upward in the tran-
spiration stream and lodge and multiply at stem
nodes and in leaf veins. Occlusion of xylem vessels
by conidia impedes the transport of water and
nutrients (Wiese 1972).
The pathogen produces a chlorosis-inducing
toxin Graminin A and an exogenous polysaccha-
ride that are not required for pathogenicity and
virulence (Van Welt and Fullbright 1986). They
are important to development of disease symp-
toms (Kobayasi and Ui 1979; Creatura et al.,
1981; Rahman et al., 2001) and survival of the
pathogen in dead straw (Bruehl 1975; Wiese and
Ravenscroft 1978).
Foliar tissue infested during the parasitic phase
on living plants is returned to the soil during
harvest and tillage. The pathogen does not persist
in root tissue. In regions where summer rainfall
is common the fungus can survive for up to 3
years in infested residue but is mostly destroyed
within one year if the residue is buried by tillage.
In regions where most precipitation occurs during
the winter period the rate of straw decomposition
is slower and survival of the pathogen longer.
Acid soils favor saprophytic survival in straw and
production and survival of conidia (Murray and
Walter 1991).
Reduction in grain yield is correlated with
numbers of spores in soil (Martin et al., 1986;
CEPHALOSPORIUM STRIPE
Cephalosporium stripe is a vascular wilt caused
by a pathogen with a host range within the Poaceae
(Farr et al., 2007). Spring cereals are susceptible
but most economic damage occurs on winter
cereals (wheat, barley, oat, rye, and triticale)
in cool, temperate regions of North America,
Europe, Africa, and Japan.
Symptoms and epidemiology
One or more distinct longitudinal chlorotic stripes
appear in leaves during jointing (Color Plate 15a).
A dark brown leaf vein (Color Plate 15b) extends
from the base of each leaf stripe, through the leaf
