Agriculture Reference
In-Depth Information
reddish-brown and are tapered to a fi ne point
(Color Plate 12c). Brownish lesions 1-3 mm
long are present on the root. The pathogen can
rot the root cortex, leaving a temporarily intact
stele, giving the roots a constricted or pinched
appearance at the site of infection (Paulitz
et al., 2002a). Seminal and crown root growth
is inhibited because of death of root tips.
Maturity is delayed and tiller formation is reduced
(Smiley and Wilkins 1993).
Rhizoctonia oryzae
can cause preemergence and postemergence
damping-off, but this is not common with
R.
solani
AG-8.
Rhizoctonia
primarily survives from year to
year in intact roots and crop debris.
Rhizoctonia
oryzae
can also survive as microsclerotia. Hyphae
of
Rhizoctonia
species are capable of spreading
long distances in soil from a food base (Garrett
1970; Bailey et al., 2000), moving through soil
pores and along the surfaces of soil particles. Most
of the inoculum is present in the top 10-20 cm of
soil (Neate 1987).
Rhizoctonia
is not uniformly or
randomly distributed in the fi eld but has an
aggregated spatial structure (Paulitz et al., 2003b).
Roots are infected by hyphae growing out from
crop debris or infected roots (Gill et al., 2002),
and infections of seedling roots causes more
damage to plants than infections of mature plant
roots.
Greenhouse studies have shown that
Rhizocto-
nia
spreads faster in sandy soil than in fi ner-
textured soil (Gill et al., 2000).
Rhizoctonia
in
Australia is associated with light-textured soils,
especially the sandy calcareous soils of South
Australia, but has also been found in red clays
and acid soils (MacNish and Neate 1996). In the
Pacifi c Northwest US, bare patch is more common
in sandy loam soils with low soil organic matter
than in silt loam soils.
Increased disease is associated with reduced-
tillage or no-till (Weller et al., 1986; Pumphrey
et al., 1987; Smiley and Wilkins 1993; Roget
et al., 1996), at least in the initial years of no-till
following conversion from conventional tillage
(Schroeder and Paulitz 2006). The mechanism
for this increase is unknown. Tillage may
disrupt hyphal networks (Gill et al., 2001a) or
shikimate pathway by this herbicide (Lévesque
and Rahe 1992).
RHIZOCTONIA ROOT ROT AND
BARE PATCH
Rhizoctonia root rot and bare patch of wheat
occur throughout the world (MacNish and Neate
1996; Mazzola et al., 1996a). The disease is caused
by a complex of
Rhizoctonia
species that infects
roots and seeds of wheat, barley, and other cereals,
resulting in aboveground stunting, pruning of
root tips, reduced tillering, and reduced yield.
Some groups of
Rhizoctonia
, including
R. solani
AG-8 and
R. oryzae
, have a wide host range
and will also infect broadleaf rotation crops
(Cook et al., 2002a; Paulitz 2002; Paulitz et al.,
2002a).
Symptoms and epidemiology
The main aboveground symptom of
Rhizoctonia
root rot is plant stunting. Plants can be stunted in
patches or individually. When in patches, called
bare patch, the classic symptom is expressed as
severe stunting of nearly all plants in roughly cir-
cular patches that can be small or up to many
meters in diameter. Patches are fi rst noticeable
about one month after planting spring wheat and
as late as early spring for winter wheat (Color
Plate 14b). Bare patch is associated with
R. solani
anastomosis group 8 (AG-8) and occurs most
commonly in areas with low rainfall and lighter-
textured soils such as sandy loam soils with low
organic matter. Roots of young seedlings are
pruned off, resulting in plants defi cient in nutri-
ents such as phosphorus, which can cause pur-
pling of the leaves in phosphorus-defi cient
soils—hence the name “purple patch” in some
regions.
Rhizoctonia
can also cause generalized
stunting and uneven plant heights without bare
patches, especially in areas of higher precipitation
with continuous annual cropping.
Rhizoctonia solani
AG-8 causes a characteristic
“spear tipping,” where the root tips appear
