Blind seed disease

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ae

United States
Department of
Agriculture

Agricultural
Research
Service

Miscellaneous
Publication
Number 1567

November 2001

Blind Seed D

Historic, archived document

Do not assume content reflects current
scientific knowledge, policies, or practices.

United States
Department of
Agriculture

Agricultural
Research
Service

Miscellaneous
Publication
Number 1567

Blind Seed Disease

Stephen C. Alderman

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Alderman is a research plant pathologist, U.S. Department of
Agriculture, Agricultural Research Service, National
Forage Seed Production Research Center, Corvallis, OR.

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Abstract

Alderman, Stephen C. 2001. Blind Seed Disease.
United States Department of Agriculture, Agricultural
Research Service. Miscellaneous Publication No.
1567. 36 pp.

In blind seed disease, unfertilized or developing seed
of susceptible grasses are colonized by the fungus
Gloeotinia temulenta. Infection results in loss of seed
germination. About 56 species of grasses are suscep-
tible, including important forage and turf grasses such
as ryegrass and tall fescue. The disease occurs in all
areas of production of cool season grasses grown for
seed. Germination in infected seed samples has been
reported as low as | percent in New Zealand, 13
percent in the United States, and 50 percent in Great
Britain. Blind seed disease continues to periodically
plague growers in New Zealand, and a recent reap-
pearance of blind seed in the United States has re-
newed interest in the disease. This monograph pro-
vides a comprehensive review of our understanding of
G. temulenta and blind seed disease, including host
and geographical distribution, taxonomy, biology, and
control.

Keywords: Disease management, disease distribution,
Gloeotinia, grass seed, host range, seed production,
seed quality

This publication reports research involving pesticides.
It does not contain recommendations for their use nor
does it imply that uses discussed here have been
registered. All uses of pesticides must be registered by
appropriate state or Federal agencies or both before
they can be recommended.

Mention of trade names, commercial products, or
companies in this publication is solely for the purpose
of providing specific information and does not imply
recommendation or endorsement by the U.S. Depart-
ment of Agriculture over others not recommended.

While supplies last, single copies of this publication
can be obtained at no cost from USDA-ARS, National
Forage Seed Production Research Center, 3450 S.W.
Campus Way, Corvallis, OR 97331.

November 2001

Copies of this publication may be purchased from the
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Contents

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Introduction and Historical Overview

During the early 1920s, growers of perennial ryegrass
(Lolium perenne L.) seed in New Zealand were
troubled by poor germination of their seed crops. A
systematic inquiry initiated in 1923 associated re-
duced germination with humid conditions during seed
development (Foy 1927), but the cause was unknown.
By 1926, germination was as low as 19 percent, and in
the southern region of New Zealand 95 percent of the
seed lots tested had germination of 90 percent or less
(Foy 1927). Ungerminable seed had an abnormal
appearance characterized by opacity, roughness, and a
reddish caryopsis surface (Hyde 1932). These symp-
toms were difficult to see unless the lemma and palea,
which cover the caryopsis, were removed. The diffi-
culty in visual detection of the ungerminable (dis-
eased) seeds led Neill and Hyde (1939) to propose
“blind seed” as the common name of the disease.

By 1932, it was apparent that a conidia-producing
fungus was associated with affected seeds (Hyde
1932), but it was not until 1937 that pathogenicity of
the blind seed fungus (tentatively identified as a
Pullularia sp.) was established (Hyde 1937). How-
ever, another fungus, distinct from Pullularia, was
also found associated with infected seed. After careful
study, this second fungus, not Pullularia, was found to
cause blind seed disease (Muskett and Calvert 1940,
Wilson et al. 1940).

In 1942, after an investigation of the life history of the
blind seed fungus, Neill and Hyde (1942) determined
that a fungus called Phialea temulenta Prill. & Delacr.
was identical to the blind seed fungus on ryegrass in
New Zealand. P. temulenta was previously reported
on seed of rye (Secale cereale L.) in France in 189]
(Prillieux and Delacroix 1891, 1892b). In 1945,
Wilson et al. (1945) reviewed the taxonomic place-
ment of P. temulenta and erected a new genus,
Gloeotinia, to accommodate it. Thus the blind seed
fungus became Gloeotinia temulenta (Prill. & Delacr.)
M. Wilson, Noble, & E.G. Gray.

The effects of blind seed disease on the production of
grass seed can be tremendous. Germination in infected
seed samples has been as low as | percent in New
Zealand (Greenall 1943), 13 percent in the United
States (Hardison 1945), and 50 percent in Great
Britain (Noble and Gray 1945). Blind seed continues
to periodically plague growers in New Zealand (Skipp
and Hampton 1996), and its recent reappearance in the

United States (Alderman 1996) has renewed interest
in the disease here. This monograph provides a
comprehensive review of our understanding of G.
temulenta and blind seed disease, including host and
geographical distribution, taxonomy, biology, and
control.

Geographical Distribution and Host
Range

The blind seed fungus was first recorded on infected
seeds of rye (Secale cereale L.) in France in 1891
(Prillieux and Delacroix 1891, Neill and Hyde 1942).
Although first reported on rye, its subsequent occur-
rence on this crop is very rare. Blind seed disease is
primarily a problem of forage and turf grasses grown
for seed.

Blind seed disease was unknown in Great Britain until
after its discovery in New Zealand. However, the
connection between blind seed and low germination in
ryegrass (Lolium sp.) was suspected to be of long
standing in Great Britain, since low germination in
some years was well known (Calvert and Muskett
1944, 1945). Proof of the long-standing occurrence of
blind seed was established when conidia of G.
temulenta were found among stored seeds from a 1909
ryegrass crop grown in Ireland (Lafferty 1948). The
identification of blind seed disease in the United
States in 1944 established that the fungus was widely
distributed on ryegrass grown for seed, a distribution
likely established through the international grass seed
trade.

Blind seed has been reported from Australia, includ-
ing Tasmania, Victoria, and New South Wales (Neill
and Hyde 1939, Wade 1949, Anonymous 1955, Wade
1957, Anonymous 1962, McGee 1971a, Munro 1978):
Denmark (Noble 1939, Gemmell 1940, Lafferty 1948,
Kristensen and Jorgensen 1960); England, including
Kent, Sussex, Hereford, and the Isle of Man (Neill and
Hyde 1939, Gemmell 1940, Glasscock 1940); Ireland
(Gemmell 1940, Lafferty 1948); France (Prillieux and
Delacroix 1891, 1892a); The Netherlands (de Tempe
1950, 1966); New Zealand (Gorman 1939; Neill and
Hyde 1939; Blair 1947, 1948; Latch 1966; Hampton
and Scott 1980a); Northern Ireland (Neill and Hyde
1939; Gemmell 1940; Calvert and Muskett 1944,
1945); Scotland, including Ayrshire and the Shetland
Islands (Neill and Hyde 1939, Gemmell 1940, Noble
and Gray 1945, Dennis and Gray 1954); Sweden
(Neill and Hyde 1939); United States, including

Oregon (Fischer 1944, Hardison 1945, Alderman
1988): and Wales (Neill and Hyde 1939).

Worldwide, 56 host species have been reported as
susceptible to G. temulenta (table 1). Most hosts are in
the subfamily Pooideae, tribes Avenae and Poeae,
with heaviest infections reported in the genera
Agrostis, Festuca, Lolium, and Poa (Hardison 1962)
(table 2). Lolium perenne is widely recognized as
susceptible and has been identified as a host from all

countries reporting blind seed disease. In the Triticeae,

moderate to heavy infections were observed on
Psathyrostachys, Pseudoroegneria, and Secale
species. Grasses in the Bromeae appear less suscep-
tible, with little to no infection observed among
species of Bromus.

In the United States, blind seed disease was found on
species of Agrostis, Aira, Alopecurus, Bromus,
Cynosurus, Deschampsia, Danthonia, Festuca,
Glyceria, Hordeum, Holcus, Lolium, Phleum, and Poa
(table 1). Despite the susceptibility of many common
grasses in the United States, G. femulenta has been
reported only from Oregon. In New Zealand, blind
seed was reported on Agrostis, Cynosurus, Festuca,
Holcus, Lolium, Poa, and Secale cereale. In Northern
Ireland, blind seed was found on Agrostis, Cynosurus,
Festuca, Holcus, Lolium, and Poa. Additional host
reports include Calamagrostis from Germany,
Elytrigia from Norway, and Secale from France and
Germany.

Most of these U.S. hosts were reported in a compre-
hensive host range study by Hardison (1962) (tables |
and 2). However, there is one discrepancy in the U.S.
host range. Fischer (1944) reported G. remulenta on
Danthonia californica Boland (subfamily
Arundinoideae, tribe Danthoneae). Hardison (1962),
however, did not observe infection on D. californica
inoculated with G. fremulenta under natural or artificial
conditions. Additional studies are needed to determine
all grasses that are susceptible to G. femulenta and
their relative susceptibility.

Yield Loss and Economic Impact

In the production of grass seed, loss from blind seed
disease occurs through a reduction in germinable seed
since infected seeds are ungerminable. In addition,
seed lots with germination below certification limits,
or below seed contract standards, are of less value and

in some countries are unmarketable. Presence of G.
temulenta in import seed shipments may result in
rejection of the seed by some countries (Halfon-
Meiri 1978).

Australia. Blind seed was reported to cause few crop
failures, although in 1969, 2,400 out of 9,000 acres
could not be certified because of blind seed disease
(McGee 197 1a).

Denmark. A low level of blind seed was found in 6
percent of ryegrass samples exported from Denmark
to Ireland (Lafferty 1948). A low level of blind seed
was also found in 1957 (Kristensen and Jorgensen
1960).

England. In 1938 and 1939, germination as low as 50
percent was common in ryegrass (Noble and Gray
1945). In 1940, an average of 26 percent of ryegrass
seed from south England was infected (Gemmell
1940).

The Netherlands. In 1965, the level of infection with
the blind seed fungus ranged from 0 to 94 percent,
with an average infection rate of 19.2 percent (de
Tempe 1966).

Scotland. In 1938-1939, infection of ryegrass seed as
great as 50 percent was reported (Gemmell 1940,
Noble and Gray 1945). Average infection in samples
from Ayrshire was 26.4 percent (Gemmell 1940).

New Zealand. Between 1931 and 1934, cost of seed
lost to blind seed was estimated at £1,975-4,382
(Gorman 1939). In 1938, average germination of
ryegrass was 67—76 percent in Christchurch, Canter-
bury, and South Canterbury (Hyde 1938b). Greenall
(1943) reported germination of ryegrass as low as |
percent. Greenall also noted that the severity of blind
seed disease depended on environmental conditions,
and he expected that in South Otago one year in every
two or three would be accompanied by poor germina-
tion. During 1944-1946, 45—84 percent of samples
from the South Island had more than 20 percent blind
seed and 10—22 percent of samples had 70—100
percent diseased seed (Blair 1947). Stocks of seed
throughout New Zealand had germination below 40
percent—in some lots as low as 5 percent (Osborn
1947). In seed exported from New Zealand to Ireland,
26 percent of samples had a low level of blind seed
disease (Lafferty 1948).

Between 1948 and 1960, 70 percent of seed samples
tested positive for blind seed disease; the average was
12 percent (Hampton and Scott 1980a). Levels of
infection declined after 1960. During 1976-1978, 27
percent of samples tested positive, with a mean of 4
percent infected seed. The disease declined between
1964 and 1974 to the point that preharvest testing was
stopped (Scott 1974). Hampton and Scott (1980a)
related decreased levels of blind seed to the increased
use of nitrogen fertilizers. In 1980-1990, only low
levels of blind seed were detected (Skipp and Hamp-
ton 1996). In 1993, environmental conditions were
favorable for blind seed development, and 100 percent
of seed lots were infested, with a mean of 13.5 percent
infected seed (Skipp and Hampton 1996). Low levels
of blind seed infection returned in 1995 when condi-
tions were again less favorable for blind seed develop-
ment (Skipp and Hampton 1996).

Northern Ireland. By 1944, infection levels ranged
from 31 to 55 percent and were as high as 70 percent
in perennial ryegrass (Calvert and Muskett 1944).
During 1947-1948, 60-70 percent of samples had
trace to 60 percent infected seeds (Lafferty 1948).

United States. In the Willamette Valley of Oregon,
low germination in ryegrass was first noticed in 194]
(Hardison 1957). Blind seed disease was positively
identified in 1943 (Hardison 1948, 1949). By 1944,
the disease was found in 85 percent of certified
samples (Hardison 1945), and about one-quarter of the
seed crop could not be certified (Hardison 1948).

U.S. levels of infection with blind seed disease
declined during the late 1940s after the introduction of
field burning to control the disease (Hardison 1976,
1980). During the 1950s, blind seed increased as
growers explored alternatives to field burning. During
the 1960s, when field burning was again widely
practiced, blind seed occurrence returned to trace
levels. Low levels of the disease were detected during
1986-1989 (Alderman 1991a,b).

In 1991, the Oregon State legislature mandated an
incremental reduction in postharvest burning of grass
fields to a maximum of 16,000 hectares after 1997.
The area burned declined from about 80,000 hectares
in 1987 to about 28,000 in 1993 (Young et al. 1994).
In 1995, a high level of blind seed (20 percent infected
seeds) was found in several fields of tall fescue in
Oregon (Alderman 1996). However, surveys from
1995-1997 (Alderman 1999) indicate that blind seed
disease levels in most fields in Oregon remain low.

Symptoms

The seed is the only component of the host plant
infected by G. temulenta (Wilson et al. 1945). Infected
caryopses appear shriveled, rough on the surface, and
rusty brown or pinkish in color (Gemmell 1940,
Calvert and Muskett 1945, Hyde 1945, Noble and
Gray 1945, Wilson et al. 1945, Blair 1947). Conidia
accumulate on the seed surface in a spore secretion
(slime), which may be waxy and clear or pale pink in
color (Hyde 1938a) or may appear as a reddish-brown
crust (Calvert and Muskett 1945, Hyde 1945). Healthy
caryopses normally appear golden brown, plump, and
smooth (Calvert and Muskett 1945). However,
infected seeds covered by the lemma and palea are
difficult to discern from normal seeds (Gemmell 1940,
Neill and Hyde 1942, Hyde 1945).

A consequence of blind seed infection is reduced
germination, and the correlation between percentage
of infected seed and percentage germination in
ryegrass is well established (Hyde 1932; Gemmell
1940; Greenall 1943; Calvert and Muskett 1944,
1945; Hyde 1945; Lafferty 1948; Chestnutt 1958;
Hardison 1963; de Tempe 1966; Matthews 1980).
Germination of infected seed is rarely greater than 10
percent (Gemmell 1940, Lafferty 1948).

Causal Agent

The taxonomic placement of Gloeotinia is not clearly
established. Wilson et al. (1954) placed G. remulenta
within the family Sclerotiniaceae, based on its occur-
rence as a plant pathogen, presence of spermatia and
macroconidia, and formation of a fleshy cupulate
apothecium from a stroma. Although G. femulenta
shares many features of the Sclerotiniaceae, it devel-
ops only an interwoven mycelium within the infected
seed and does not form the true sclerotium that is
characteristic of the Sclerotiniaceae. Ellis (1956)
described Gloeotinia as structurally similar to
Symphyosirinia, a member of the family Leotiaceae.
Similar views were stated by Baral (1994) who
considered Gloeotinia and Symphyosirinia related and
members of the Leotiaceae, subfamily
Hymenoscyphoideae. In 1997, Holst-Jensen et al.
(1997) provided data from DNA analysis that
Gloeotinia was distinct from other fungi within the
Sclerotiniaceae. These studies support the concept that
Gloeotina should be considered a member of the
Leotiaceae, subfamily Hymenoscyphoideae.

Schumacher (1979) reported that a specimen de-
scribed on Bromus erectus by Quelet (1883) as

ee)

Phialea granigena was conspecific with G. temulenta
and therefore represented an older name of the fungus.
Alderman (1997) recognized G. temulenta and G.
granigena as separate species, based on host range
and morphological differences. Bromus erectus is not
believed to be a host for G. temulenta (Hardison 1962,
Alderman 1997). Little is known about G. granigena.
Additional studies concerning species identity and
their associated host range in the genus Gloeotinia are
needed. Unfortunately, specimens of Gloeotinia from
outside areas of commercial seed production are very
rare in nature.

Two other species of Gloeotinia from Germany have
been described: G. aschersoniana (P.C. Hennings and
T. Ploettner) H.O. Baral on Carex and G. juncorum (J.
Velenovsky) H.O. Baral on Juncus (Baral and
Krieglsteiner 1985). Nothing is known of the life
history of these species.

Synonymy

Teleomorph:

Gloeotinia temulenta Prill. & Delacr. (Wilson et al.
1954)

Phialea temulenta Prill. & Delacr. (Prillieux and
Delacroix 1892b)

Peziza (Phialea) temulenta Prill. & Delacr. (Prillieux
and Delacroix 1892a)

Ciboria (Stromatinia) temulenta Prill. & Delacr.
(Prillieux and Delacroix 1893)

Stromatinia temulenta Prill. & Delacr. (Prillieux
1897)

Sclerotinia secalincola Rehm (Rehm 1900)

Sclerotinia temulenta (Prill. and Delacr.) Rehm
(Hoéhnel 1903)

Stromatinia secalincola (Rehm) Boudier (Boudier
1907)

Phialea mucosa Gray (Gray 1942)

Gloeotinia granigena (Q.) Schumacher for hosts other
than Bromus (Alderman 1997)

Anamorph:
Endoconidium temulentum Prill. and Delacr. (Prillieux
and Delacroix 1891)

Technical Description

Stroma. Infection of the grass caryopsis results in the
mummification of the caryopsis, creating a substratal
stroma (Spooner 1987, Williams and Spooner 1991).
Hyphae, 3—4 um wide, ramify throughout the peri-
carp, teste, and endosperm and are not differentiated
into rind and medullary parenchyma (Gray 1942,

Wilson et al. 1945). A true sclerotium does not
develop, although the infected seed functions similarly
to a sclerotium as a means of survival through the
winter.

Sporodochia. In late winter or early spring, pinkish,
pulvinate, gelatinous sporodochia form either on the
surface of the pales or between the pales and caryopsis
(Neill and Hyde 1939, Gray 1942, Calvert and
Muskett 1945, Griffiths 1959b). They are 0.4-1 3
0.5—1.5 mm in size (Prillieux 1897, Neill and Hyde
1939, Gray 1942, Calvert and Muskett 1945).
Sporodochia consist of a core of closely septate,
branching hyphae (Neill and Hyde 1939, Griffiths
1959b) with the terminal cells of each branch bearing
1-4 microconidiophores (Gray 1942, Griffiths 1959b).

Microconidiophores and microconidia (spermatia).
Microconidiophores are 2—5 um in diameter and 5—9
um long, septate, guttulate, hyaline, and penicillate
(branched 2 or 3 times) (Neill and Hyde 1939, Gray
1942, Griffiths 1959b). Microconidia are first formed
by a constriction below the apex of the microconidi-
ophore. The rest bud off in succession inside a tube
formed by the terminal portion of the microconidi-
ophore (Prillieux and Delacroix 1892b; Neill and
Hyde 1939; Gray 1942; Wilson et al. 1945, 1954;
Griffiths 1959b).

Microconidia are unicellular, uninucleate, ovoid,
guttulate or biguttulate, hyaline, 1.8—3.0 3 2.3-6.0
um (Gray 1942, Calvert and Muskett 1945, Griffiths
1959b). In microconidial germination, a terminal germ
tube forms; or if a transverse septum forms, a terminal
or lateral germ tube will be produced (Griffiths
1959b).

Macroconidiophores and macroconidia.
Macroconidiophores are short barrel-shaped cells,

2—3 um wide and 5—15 um long, that arise laterally

on the hyphae (Neill and Hyde 1939, Griffiths 1959b).
Macroconidia are budded from the apex of the
macroconidiophores (Griffiths 1959b) (figure 1) and
arrange in clusters perpendicular to the hypha (Calvert
and Muskett 1945, Wilson et al. 1945). Up to 30
macroconidia develop per conidiophore (Wilson et al.
1945).

Macroconidia are smooth, unicellular, uninucleate,
hyaline, cylindrical to slightly cresentric with rounded
ends, and usually biguttulate (figure 2) (Gray 1942:
Calvert and Muskett 1945; Wilson et al. 1945, 1954;
Spooner 1987). They are 2.5—6 3 11-21 um in size.

Figure 1. Scanning electron micrograph of conidia of Gloeotinia temulenta being produced
on the surface of an infected seed. Arrow points to macroconidium.

Figure 2. Macroconidia of Gloeotinia temulenta.

The vegetative nucleus is 3—5 3 2 um and the nucleo-
lus may be as large as 2 um (Griffiths 1959b).

On the surface of the caryopsis, macroconidia are
embedded in a pinkish, slimy mass (Spooner 1987)
that dries to form a hard reddish-brown crust (Calvert
and Muskett 1945, Hyde 1945) (figures 3-5). When
germinating, macroconidia swell and produce one or
two germ tubes (Griffiths 1959b).

Apothecia. Apothecia are small, fleshy, and cup-
shaped. One to 7 (usually | to 3) apothecia emerge
from each infected seed (Prillieux 1897; Gray 1942;
Calvert and Muskett 1945; Wilson et al. 1945, 1954)
(figure 6). The stipe is smooth, velutinous under
magnification, externally white or gray, internally
pinkish brown, enlarging upward (Neill and Hyde
1939), and longitudinally furrowed (Spooner 1987).
The stipe varies from | to 10 mm in length and from
0.2 to 0.5 mm in diameter (Prillieux and Delacroix
1892b, Rehm 1900, Gray 1942, Calvert and Muskett
1945) and is composed of hyaline, parallel hyphae, 4—
6 um in diameter, occasionally intertwining and
seldom branched (Gray 1942, Calvert and Muskett
1945).

Apothecia emerge from the caryopsis and elongate
(figure 7). The disk of the apothecium is at first closed
(Gray 1942) but opens to cup-shaped and with age
becomes saucer-shaped and then flat (Gray 1942,
Calvert and Muskett 1945, Spooner 1987) (figures 8
and 9). The disc diameter ranges from 1.0 to 7.0 mm
(Prillieux and Delacroix 1892b, Rehm 1900, Neill and
Hyde 1939, Gray 1942, Calvert and Muskett 1945).
The disk color changes from light pinkish brown to
deep brown (Calvert and Muskett 1945), orange
brown (Spooner 1987), or pale pinkish cinnamon,
darkening to cinnamon when old (Neill and Hyde
1939, Gray 1942). The margin is smooth and entire
(Neill and Hyde 1939, Gray 1942, Calvert and
Muskett 1945, Spooner 1987) and is radially wrinkled
around the stipe apex (Spooner 1987).

Hymenium. The hymenium is 100-140 um deep
(Williams and Spooner 1991). The subhymenium
consists of intricately intertwined and coiled hyphae
2.5—3 um in diameter. The subhymenium blends into
the medullary excipulum, a 22—27 um deep layer
composed of fine, densely intertwining hyphae 2—5
um broad (Neill and Hyde 1939, Gray 1942, Williams
and Spooner 1991). The outermost layer (the ectal
excipulum) is 35—40 um thick and is composed of

6

parallel to somewhat interwoven hyphae 3.54.5 um
in diameter (Williams and Spooner 1991) (figure 10).

Asci. The asci are cylindrical and clavate, with 8
spores obliquely placed in a single row (uniseriate) in
the upper two-thirds of the ascus (Neill and Hyde
1939, Gray 1942, Calvert and Muskett 1945, Spooner
1987) (figure 11). Ascus size is variable but falls
within the range of 66-120 um long 3 3-8 um wide.
The ascus base tapers to about 2—5 um (Spooner 1987,
Williams and Spooner 1991). The apical cap is 1-3
um thick (Alderman 1997), and the apical plug does
not stain blue with 1odine (Prillieux and Delacroix
1892b, Neill and Hyde 1939, Gray 1942, Calvert and
Muskett 1945, Wilson et al. 1954, Spooner 1987).

Ascospores. Ascospores are hyaline, smooth, ellipti-
cal, fusoid to broadly fusoid, and usually biguttulate
(Neill and Hyde 1939, Gray 1942, Calvert and
Muskett 1945). One side is often flattened, or curved,
continuous, or rarely developing a central septum
(Spooner 1987, Williams and Spooner 1991). As-
cospore size is variable, 7-14 3 2.5-4.5 um. Germi-
nating ascospores swell to about 10 3 5 um (Neill and
Hyde 1939) (figure 12). The first germ tube is termi-
nal, followed by a second that is frequently lateral in
position and usually constricted at the point of origin.
They normally develop a central septum and two polar
hyphae, but often lack a septum and have a single
polar or lateral hypha (Neill and Hyde 1939, Calvert
and Muskett 1945)

Paraphyses. Paraphyses are fusiform, hyaline,
nonseptate (Neill and Hyde 1939, Gray 1942, Calvert
and Muskett 1945) or sparsely septate (Spooner 1987)
and 1.5—4 um wide (Neill and Hyde 1939, Gray
1942). Spooner (1987) described the paraphyses as
enlarging at the apex to 2.5—3.0 um, but others (Neill
and Hyde 1939, Gray 1942, Calvert and Muskett
1945) reported that the apex was not swollen. Para-
physes are as long as or slightly longer than the asci
(figure 13).

Growth on Media

On a nutrient medium such as potato dextrose agar, G.
temulenta grows slowly and produces a partly sub-
merged, branching, hyaline, septate mycelium (Neil
and Hyde 1939, Calvert and Muskett 1945). Sporula-
tion and slime production occur after 7 days (Calvert
and Muskett 1945, Wilson et al. 1945, Hair 1952) and
in culture appears reddish brown (Neill and Hyde
1939) or chocolate brown (Wilson et al. 1945). The

Figure 3. Seeds of Lolium multiflorum infected with Gloeotinia temulenta
(lemma and palea removed). Healthy seed is on left.

Figure 4. Seeds of Lolium multiflorum infected with Gloeotinia temulenta. Arrow
points to conidial slime.

Figure 5. Scanning electron micrograph of the surface of conidial slime of Gloeotinia temulenta.

Figure 6. Apothecia of Gloeotinia temulenta.

Figure 7. Scanning electron micrograph of the early stage of apothecium development of
Gloeotinia temulenta.

Figure 8. Scanning electron micrograph of developing apothecium of Gloeotinia temulenta.

9

Figure 10. Cross section of apothecium of Gloeotinia temulenta. Arrow points to
ectal excipulum.

10

Figure 11. Cross section of apothecium of Gloeotinia temulenta. Arrow points to ascus.

Figure 12. Germinating ascospores of Gloeotinia temulenta.

germ tube.

Arrow points to

Figure 13. Surface of hymenium of Gloeotinia temulenta. Arrow points to paraphysis.

2

addition of 1-percent peptone to PDA or malt agar
increases spore mucilage production (Calvert and
Muskett 1945). However, some cultures are predomi-
nantly mycelial while others are conidial (Wilson et
al. 1945).

In culture, macroconidia are produced from short
conidiophores formed at intervals perpendicular to the
hypha (Calvert and Muskett 1945, Wilson et al. 1945).
Conidia from culture may be larger (Wilson et al.
1945) or appear less regular than those from seed
(Calvert and Muskett 1945). Growth is slow at 5 °C,
optimal at about 20 °C, less at 27 °C, and restricted at
30 °C (Neill and Hyde 1939, Alderman 1992). Radial
growth slows with decreasing water potential through
~9.0 to —1.0 MPa (Alderman 1992).

Sporodochia develop in culture at 5 °C to room
temperature after about 1-3 months (Calvert and
Muskett 1945). Growth characteristics on various
media were described by Neill and Hyde (1939) and
Calvert and Muskett (1945).

Similar-Looking Fungi

Calvert and Muskett (1945) collected other
discomycetes associated with ryegrass and detritus
that are similar to G. temulenta but differ in morphol-
ogy in culture and do not produce spores. Unfortu-
nately, neither species identification nor technical
descriptions of these other fungi were recorded.

Neill and Hyde (1939) found a fungus on Lolium that
is similar to G. temulenta. They defined it as Lolium
fungus number 2. Unfortunately, the taxonomic
description and species identity of this fungus was not
established either.

Biology and Epidemiology
Overwintering and Production of Apothecia

The general life cycle of G. temulenta is illustrated in
figure 14. The overwintering, or survival, unit of G.
temulenta is the infected seed. Infected seeds reach the
soil by shattering, by seed loss during harvest opera-
tions, by planting of diseased seeds, and by natural
seed dispersal in harvested areas (Hardison 1945).
Infected, ungerminable seeds resist attack by bacteria
and molds and do not decay as they overwinter (Neill
and Hyde 1939; Calvert and Muskett 1944, 1945).

At or near the soil surface, G. temulenta continues to
develop within the seed. Moist soil conditions with
temperatures near 2 °C for about 8 weeks are required

to induce the sexual (apothecial) stage of G. temulenta
(Griffiths 1958). The precise biochemical changes that
occur or metabolic pathways affected during this
conditioning have not been determined.

In spring or early summer, at or prior to flowering of
perennial ryegrass, apothecia emerge from the over-
wintering infected seeds (Calvert and Muskett 1945,
Wilson et al. 1945). Usually one to three, but as many
as seven, apothecia can emerge from a single infected
seed (Gray 1942, Calvert and Muskett 1945). Not all
infected seeds will yield apothecia. In fact, only 5-30
percent of ungerminated seed produce apothecia
(Calvert and Muskett 1945, Griffiths 1958).

Production and Release of Ascospores
(Primary Inoculum) and Primary Infection

Large numbers of ascospores are ejected from each
apothecium in response to slight changes in relative
humidity (Calvert and Muskett 1945). In New
Zealand, spore release occurs between early Novem-
ber and middle December, with peak numbers coin-
ciding with flowering in perennial ryegrass (Neill and
Armstrong 1955). Most spores are airborne between
10:00 a.m. and 2:00 p.m. (Johnston et al. 1965).

Ascospores that land on flowers, including the stigma,
ovary, or styles, will germinate and infect the host.
However, seeds can be infected up to the time they
reach their maximum size (Hyde 1937).

Secondary Infection

Within about 7 days (Hyde 1937, 1945; Wilson et al.
1945) to 16-17 days (Calvert and Muskett 1945) after
inoculation, the conidial stage is manifest—a pinkish
slime in which conidia are embedded. These spores
are relatively short-lived, about 1 month (Cunningham
1941, Neill and Hyde 1942). However, a few conidia
may survive as long as 4-6 months if stored under
cool, dry conditions (Calvert and Muskett 1945).

Disease Development and Spread

Wet seasons, especially during anthesis in the grasses,
are clearly supportive of blind seed infection (Foy
1927; Gorman 1940; Osborn 1947; Blair 1947, 1948;
Lithgow and Cottier 1953; Chestnutt 1958; de Tempe
1966; Grant 1985). Based on field surveys in New
Zealand, Lithgow and Cottier (1953) found that
districts which produced ryegrass seed with high
germination (low blind seed disease) had less than
half the rain days during flowering than districts
producing seed with low germination. Hardison

ascospores
infect flowers conidia 1
2-7 SY
conidia reinfect W
flowers or

developing seeds

ascospores released

from apothecia

apothecia emerge from
infected seeds in spring oe

a -> Ga

infected seeds

Figure 14. General life cycle of Gloeotinia temulenta.

14

(1957) concluded that blind seed in Oregon was not
present in inflorescences formed in fields after the
regular harvest because postharvest conditions in
Oregon are typically dry with little precipitation.

Large numbers of apothecia can appear during wet
weather. Blair (1948) counted 20 apothecia per square
foot and observed subsequent severe disease develop-
ment during a wet season in New Zealand. Under the
dry conditions of 1947, no apothecia were found, and
subsequent disease development did not occur.
Hardison (1963) estimated that under favorable
conditions in Oregon, 100 pounds of severely infected
seed dispersed per acre would be expected to yield
10-50 apothecia per square foot.

Wet seasons, combined with low temperatures, extend
the period of apothecial production and spore release.
However, not all apothecia are produced at the same
time. Some apothecia develop early, others late.
Under cool (13 °C), wet conditions, apothecia can be
produced over a 2-month time frame (Wright 1956).
The expected lifespan of an individual apothecium 1s
about 8—14 days, although they shrivel within a few
hours in a dry atmosphere (Neill and Hyde 1939).

Temperatures of 10-16 °C and high humidity are
considered ideal for blind seed development (Anony-
mous 1948, Alderman 1992). Infection does not occur
under very warm (30 °C) temperatures (Alderman
19972),

Calvert and Muskett (1944, 1945) were the first to
suggest that blind seed disease could spread from
infested areas to noninfested areas, based on observa-
tions of commercial fields and field plots planted with
pathogen-free seed. Additional sources of infection
include seed for pastures (Hardison 1945), hedgerows
with susceptible grasses, and waste ground (Calvert
and Muskett 1945). Direct observations of spore
movement were made by Neill and Armstrong (1955),
who trapped spores of G. temulenta 18 m high and at
ground level 1.6 km from the nearest infected field.

The highest rate of infection occurs while florets are
open. The potential for infection reduces greatly
after flowering (Calvert and Muskett 1944, 1945;
Blair 1947). Corkill (1952) reported 90 percent
infected seed when florets were open during inocula-
tion, compared with 33 percent when florets were
closed. Cool, moist weather conditions aid dispersal,

prolong the period of pollination (Calvert and Muskett
1945), and extend the period of greatest susceptibility
of the plant.

Flowering in a ryegrass spike begins at the top and
progresses downward over about 10 days (Noble and
Gray 1945). Production of conidia begins within 6
days of infection and increases for about 16 days
(Alderman 1992). Consequently, infection of upper
florets by windborne ascospores may result in the
spread of subsequently produced conidia to lower
florets (Noble and Gray 1945) under rainy conditions.
Rain dissolves the slime in which conidia are embed-
ded and provides a vehicle for their secondary spread
(Neill and Hyde 1939, Calvert and Muskett 1945,
Hyde 1945).

Calvert and Muskett (1945) speculated that insects
may be involved with transmission of the condidial
slime. However, no observations or data on associa-
tion of Gloeotinia with insects or their ability to vector
G. temulenta has been published.

Infections occurring at flowering or prior to en-
dosperm formation resulted in seeds that are thin and
light in weight (Neill and Hyde 1939, Hyde 1945).
These infected seeds may not be capable of supporting
apothecial production (Wilson et al. 1945), although
they may support development of macroconidia (Hyde
1945). Abundant production of macroconidia during
early flowering or seed development provides inocu-
lum for secondary spread and subsequent disease
development.

Seeds infected during the early to middle stages of
development are approximately normal size and
weight (Neill and Hyde 1939, Hyde 1945, Wilson et
al. 1945), and a large quantity of spores are produced
(Hyde 1945). Seeds infected late in development may
be capable of germination (Wilson et al. 1940, Calvert
and Muskett 1945, Hyde 1945, de Tempe 1950).
Fewer spores are produced from late infections than
from early ones (Hyde 1945).

The potential for rapid increase in blind seed severity
was emphasized by Hardison (1948, 1957), who
noticed a rapid increase in disease over a |- to 3-year
period. De Tempe (1966) noted that seed with a 6.3
percent infection rate produced a crop with 26.7
percent seed infection.

Histopathology

Detailed infection studies were conducted by Wilson
et al. (1945) and Neill and Hyde (1939). Infections
occurred at the base of the stigma in ovaries within |
week of fertilization (Wilson et al. 1945). Hyphae
invaded the inner epidermis, nucellus, and embryo
sac. Within 9 days, conidia were produced between
inner epidermis and outer integument and appeared on
the surface. The endosperm and embryo filled with
hyphae. The resulting grains were as long as healthy
seeds but thinner. Hyphae invaded the embryo and
endosperm when infections occurred after the embryo
was differentiated into scutellum, plumule, radicle,

and endosperm.

Neill and Hyde (1939) observed greater ramification
and degradation of endosperm and embryonic tissues
than Wilson et al. (1945), who observed extensive
invasion of both embryonic and endosperm tissues.
Wilson et al. (1945) observed hyphal penetration
through the epithelial and aleurone layers, while Neill
and Hyde (1939) reported that G. temulenta did not
appear to penetrate cells of the aleurone layer. Sys-
temic infections beyond the seed were not observed
(Cunningham 1940, 1941; Neill and Hyde 1942;
Wilson et al. 1945).

Fungal Genetics and Physiology

G. temulenta is heterothallic—it requires genetic
exchange between two different mating types for
sexual reproduction and subsequent production of
apothecia (Griffiths 1958). G. temulenta has two
mating types that are identical in all morphological
features. Within each apothecium half of the as-
cospores are of each mating type, arbitrarily called “a”
and “b.” Apothecia will develop only after mating
types a and b come into contact with one another and
undergo fusion.

Conidia produced following infection from an
ascopore of one mating type will produce only conidia
of that mating type. Genetic exchange between types
can occur through transfer of macroconidia from one
infected seed to another or through transfer of micro-
conidia, which can develop on the seed in spring after
the seed has overwintered. A conjugation tube—a
device to exchange genetic information—can form
between pairs of macroconidia even before either
conidium germinates (Wilson et al. 1945). As ex-

16

pected from the heterothallic requirement of G.
temulenta, relatively few infected seeds produce
apothecia.

The vegetative hyphae are uninucleate. Chromosome
number in G. temulenta 1s n=15, and mitotic chromo-
somes range in size from 0.25 to 1.0 um. (Griffiths
1959b). In the microconidiophores the nucleolus is
lacking, RNA is low, and the level of RNA depends
on the level in the subtending cells (Griffiths 1959a).
Microconidia have not been observed to germinate
and produce a vegetative mycelium but can serve a
sexual function (Griffiths 1958).

Little is known about variability in virulence of G.
temulenta. Sproule and Faulkner (1974) reported
variation in aggressiveness among strains of G.
temulenta. Wright and Sproule (1969) reported that
disease ranking of clones was the same when mixed
blind seed isolates from The Netherlands or the
British Isles were used.

Little is known about the physiology of G. temulenta.
A cold conditioning period of about 8 weeks is
required to induce the apothecial phase. The metabolic
pathways or mechanism associated with the induction
have not been investigated.

Toxicity

Prillieux and Delacroix (1892a) and Prillieux (1897)
described toxic properties associated with infection of
rye by the asexual stage of the blind seed fungus,
Endoconidium temulentum (anamorph of G.
temulenta). Consumption of bread made from the
flour induced dizzyness, faintness, vertigo, and an
intensive stuporous state lasting for several days.
Dogs, pigs, and poultry that consumed the bread
became depressed, numb, and refused to eat or drink
for 24 hours. The symptoms in humans and animals
differed from those produced after ingestion of ergot
(Claviceps purpurea) or darnal (Lolium temulentum)
(Prillieux and Delacroix 1892a, Prillieux 1897). This
is the only known report of toxicity from seed infected
with G. temulenta.

Cunningham (1958) conducted trials in which sheep
were fed seed infected with G. temulenta. No abnor-
mal symptoms or effects were observed.

Disease Management

The survival propagule of G. temulenta is the infected
seed. Control measures center around removing as
many infected seeds as possible from the field during
harvest and avoiding introduction of infected seed by
using disease-free or treated seed. Maintaining a
healthy stand through good fertilization practices also
contributes to control of blind seed. An integrated
approach to blind seed control should consider disease

resistance, field location, seed source, seed treatments,

planting, time of closing, fertilization, stand density,
fungicide sprays, methods of harvest, postharvest
residue management (straw residue removal,
postharvest plowing, crop rotation, field burning), and
postharvest seed cleaning.

Disease Resistance

The search for resistance to blind seed began shortly
after discovery of the disease. Early investigations in
New Zealand compared indigenous grasses to com-
mercial grasses (Hyde 1932, Calvert and Muskett
1944, Corkill and Rose 1945, Blair 1947). Differences
in susceptibility were attributed to timing of flowering
and favorability of climatic conditions during flower-
ing (Gorman 1939, Gemmell 1940, Calvert and
Muskett 1945, Corkill 1952, Wright 1956).

Early attempts at breeding ryegrass for resistance to
G. temulenta were confounded by high variability and
inconsistent results (Corkill 1952). Corkill and Rose
(1945) examined progeny of crosses of resistant and
susceptible ryegrass plants and concluded that resis-
tance or susceptibility to the disease was inherited.
Sproule and Faulkner (1974) reported that resistance
was quantitative and repeatable across environmental
conditions and fungal strains. Wright (1967) con-
cluded that more than one gene was involved in
resistance. Wright and Faulkner (1982) used a back-
cross program to introduce resistance to G. temulenta
into S24 perennial ryegrass. Cultivars Calan and
Logan were found to have significantly greater
resistance than $24. Unfortunately, little resistance is
believed to be present in most cultivars of perennial
ryegrass and tall fescue now grown commercially for
seed.

Field Location

Locating fields away from infested fields to avoid the
introduction of inoculum from nearby sources is
recommended (Blair 1947, 1948, 1952; Hardison
1949; Lithgow and Cottier 1953). To prevent estab-

lishment and persistence of infected seed, grazed areas
not kept for seed should be topped when seed heads
appear (Blair 1948). Surrounding fields with crops
such as cereals or root or forage crops may provide a
barrier to movement of spores into a field (Blair
1947), although long-distance (more than | km)
airborne movement of ascospores can occur (Neill and
Armstrong 1955).

Seed Source

Since infected seed is the source of inoculum, planting
disease-free seed is recommended (Calvert and
Muskett 1944; Blair 1947, 1948; Hardison 1949).
Osborn (1947) and Blair (1948) suggested that in New
Zealand supplies of disease-free seed could be ob-
tained in dry years when little disease develops.

Prillieux (1897) reported that in France the disease
was scarce on rye (Secale cereale L.), but recom-
mended that, where the disease is present, seed from
regions free of contamination be used for planting.

Seed Treatments

G. temulenta has limited survival in seed stored dry.
Seed stored for 18 (Blair 1947), 21 (Calvert and
Muskett 1945), or 20-22 months before spring
planting (Hardison 1949, 1957) and 24 months before
fall planting (Hardison 1949, 1957; Wade 1955) is
considered safe to plant.

Calvert and Muskett (1944, 1945) controlled blind
seed with a hot water treatment that included either a
4-hour pretreatment with tepid water, then 15 minutes
at 50 °C, or no preimmersion treatment and 30 min-
utes at 50 °C. The treatments provided full control
with little or no reduction in seed germination. After
hot water treatment, infected seeds decayed in the soil
(Calvert and Muskett 1944). Untreated infected seeds
resisted decay. De Tempe (1966) reported complete
blind seed control with no effect on germination when
seed was treated with water at 45—46 °C for 2-200
hours. Gorman (1940), however, reported lack of
adequate control from hot water treatments.

Numerous fungicides have been evaluated for their
efficacy as seed treatments for blind seed disease.
Although Hair (1952) reported some success, most of
the early research indicated that chemicals applied as
seed protectants were not effective against blind seed
disease (Gorman 1940; Calvert and Muskett 1944,
1945; Blair 1947; de Tempe 1966; Hardison 1975).

—~

However, modern systemic fungicides such as
benomyl have proven effective as a seed treatment
(Hardison 1970, 1972; McGee 1971b). In New
Zealand, seed treatment with fungicides has proven
effective and is recommended for control of blind
seed disease (Rolston and Falloon 1998).

Planting

Calvert and Muskett (1944) reported that seed samples
from fields sown with a high level of blind seed did
not on average show a higher rate of infection than
seed from fields sown with disease-free seed. Simi-
larly, de Tempe (1966) found no association between
severity of blind-seed-infected seed at planting and
subsequent level of infection at harvest. However, the
effect of infected seed introduced at the time of
planting depends on the method of planting and
planting depth. Hardison (1957) observed that maxi-
mum production of apothecia occurred when fields
too small for drill planting were planted by broadcast-
ing seed over the soil surface. When seeds are planted
more than one-half inch deep, apothecia have diffi-
culty reaching the soil surface (Hardison 1949, 1957).
Good preparation of the seed bed facilitates planting
at the proper depth and good coverage of seed
(Hardison 1949, 1963).

Fields with heavy soils or poor drainage may be more
favorable for blind seed development because they
provide the prolonged moist conditions that are
favorable for production of ascospores. Good soil
drainage provides conditions that are less favorable
for apothecial production (Hardison 1949, 1963).

Infected seed must undergo a cool, moist period for
about 8 weeks to induce the reproductive (apothecial)
phase of the pathogen. Wright (1956) found that when
seed was planted in spring, apothecial production did
not occur; the requirement for cold conditioning was
not met. Similar results were reported by Fischer
(1944), who detected no apothecia when seed was
planted in spring but found 75.6 apothecia per square
meter in fall-planted seed.

Planting a susceptible first-year companion crop such
as L. temlentum is not recommended because of its
potential to increase inoculum if seed becomes
infected (Hardison 1949, 1957, 1963).

Time of Closing (Grazing)

Crops in New Zealand that are closed to grazing very
early or very late in the season may yield a crop that

18

escapes peak ascospore dispersal (Blair 1947). Early
closing was recommended in New Zealand by
Gorman (1940), Lithgow and Cottier (1953), and
Lynch (1952).

Nitrogen Fertilization

Numerous studies indicate a reduction in blind seed in
response to manure or nitrogen fertilization.

Chestnutt (1958) and Rutherford (1956) reported a
significant reduction in blind seed in manured plots,
compared with unmanured plots of perennial ryegrass.
Lynch (1952) and Lithgow and Cottier (1953) ob-
served that nitrogen improved yield and germination,
although the effect of nitrogen on blind seed was
uncertain. In a paired-plot experiment, Stewart (1963)
found blind seed levels decreased in plots treated with
nitrogen compared with untreated plots.

Hampton and Scott (1980a) established that a decline
in blind seed between 1960 and 1980 in New Zealand
correlated with the increased use of nitrogen fertilizer.
In field trials, they demonstrated that as nitrogen rate
increased, the rate of blind seed infection decreased, a
result also reported by Hampton (1987) and de Filippi
et al. (1996).

Under laboratory conditions, Hampton and Scott
(1980a) observed that urea directly suppressed apo-
thecial formation. However, in field plots, Hampton
and Scott (1981) found no significant differences in
number of apothecia among field plots treated with
various levels of urea, although a reduction in blind
seed infection was observed in urea treatments. They
concluded that nitrogen fertilization altered the
physiology of the plant, enhancing resistance to G.
temulenta (Hampton and Scott 1980b).

In subsequent studies de Filippi et al. (1996) examined
the level of blind seed in adjacent irrigated and
nonirrigated field plots to which various rates of urea
had been applied. In irrigated field plots, nitrogen
application significantly reduced blind seed disease,
but this did not occur in nonirrigated plots. As the
inoculum source was external to the trial, they con-
cluded that plants which are able to utilize available
nitrogen develop a greater capacity to resist blind
seed. The mechanisms associated with this resistance
need to be determined.

Hampton (1987) reported there was no advantage to a
split application of nitrogen (fall, spring) and recom-
mended that all nitrogen be applied in spring. Blind

seed levels in the study were lowest when all of the
spring nitrogen was applied at spikelet initiation.

In addition to increasing resistance, nitrogen applica-
tions can also increase lodging or increase stand
density, providing a physical barrier to restrict spore
movement up through the canopy (Gorman 1940,
Noble and Gray 1945, Blair 1947).

Stand Density

Movement of ascospores upward through ryegrass
stands is believed to be reduced in a dense canopy, in
stands that lodge, or where clover is planted with the
ryegrass (Gorman 1940, Noble and Gray 1945, Blair
1947). Hampton (1987) reported that as lodging
increased, blind seed disease decreased.

Lynch (1952) and Lithgow and Cottier (1953) found
no evidence that germination was related to crop
density or the extent of bottom growth, although they
noticed improved germination in crops that lodged or
those with increased percentages of grass in the sward.
Wilson et al. (1945) observed that a ryegrass crop
which remains standing until harvest was more likely
to become infected by G. femulenta than a dense,
heavily lodged crop. Noble and Gray (1945) found
that acidic soils could contribute to poor stands of
ryegrass and recommended replacement of ammo-
nium sulfate with nitro chalk.

Fungicide Sprays

Under field conditions, fungicides applied as foliar or
inflorescence sprays were not demonstrated effective
in blind seed control by Corkill and Rose (1945), Hair
(1952), or Hardison (1970). However, recent research
from the Foundation for Arable Research (Rolston and
Falloon 1998) has established that fungicides such as
tebuconazole or carbendizim are effective for blind
seed control in New Zealand.

Sprays applied as soil drenches or to the soil surface
have been shown effective in reducing the number of
apothecia. McGee (1971b) observed that benomyl
applied at 2.8 and 5.6 kg/ha reduced apothecia 80 and
90 percent, respectively. Hardison (1970) eliminated
apothecia during April and May with a single applica-
tion of benomyl (4.5 kg/ha) applied the previous
November, December, or January. Hardison (1972,
1975) lists other fungicides effective against G.
temulenta under greenhouse conditions.

Harvest

Since the primary source of inoculum is the infected
seed, early harvest to avoid excessive seed shatter is
recommended. Osborn (1947) suggested early harvest
under dry conditions as a source of disease-free seed,
since late season disease could develop with a change
in the weather to wet conditions. In Oregon, there is a
narrow window of time in which swathing can occur
to avoid seed shatter and obtain optimum seed yields.

Removal of lightweight or infected seeds during
harvest reduces inoculum left in the field. Hardison
(1949, 1957, 1963) recommends adjusting combines
to retain lightweight seeds for removal from fields.

Straw Residue Removal

Since dry soil conditions are unfavorable for apoth-
ecial development and spore release, Hardison (1949)
recommended removing the straw after harvest to
allow the soil surface to dry more rapidly in spring. In
Oregon, residue is commonly baled and removed from
the field. In some cases the straw is finely chopped
with specialized flails. Residues that are not suffi-
ciently chopped decompose slowly and can interfere
with crop growth or development and may leave the
soil wet for prolonged periods (Young et al. 1992).

Postharvest Plowing

Plowing infested fields reduces the area of infestation
by burying much of the inoculum source—the in-
fected seeds (Hardison 1963). Hardison (1949)
recommended plowing in Oregon before May 15 to
prevent emergence of apothecia near the time of
flowering in ryegrass. The effectiveness of plowing in
control of blind seed in Oregon was demonstrated by
Hardison (1949, 1957, 1963).

Crop Rotation

Blair (1947) reported that less infection occurred in
stands following 3-4 years of arable crops, suggesting
that rotation with crops not susceptible to blind seed
may provide a means to reduce inoculum within a
field.

Field Burning

The effectiveness of field burning in control of blind
seed was established by Hardison (1949, 1980).
Excellent control of blind seed 1s achieved with
postharvest field burning. For optimal control, the
entire dry-straw residue should be open burned.
Burning by propane flaming after residue removal

(baling) is not as effective as open burning, since
propane does not achieve the temperatures of open-
grass burning (Johnston et al. 1996).

Seed Cleaning

Recleaning of seed lots is not very effective in reduc-
ing the level of blind seed (de Tempe 1966). Hampton
et al. (1995) reported that cleaning to a higher seed
weight by removing infected seeds improved germina-
tion for some seed lots with a high level of infection;
but in lots with a low level of blind seed, cleaning
simply removed small but viable seed. A relationship
between seed weight and germination could not be
established.

Since infected seed are present in screenings, destroy-
ing the screenings destroys the inoculum. Destruction
of screenings infested with blind seed was advocated

by Hardison (1949).

Methods for Detection and Assessment
Postharvest Disease Detection and Assessment

Early methods of blind seed detection involved the
direct observation of seed. Gemmell (1940) detected
infection by looking for small pinkish spots on
dehusked seed under a binocular microscope illumi-
nated by direct light on a white background. At
Lincoln College in New Zealand, the usual procedure
was to place 100 paled seeds under magnification and
examine them for infection (Blair 1947), although
removing the lemma or palea to examine the caryopsis
can be tedious. Sproule and Wright (1966) developed
a manually operated apparatus to facilitate the re-
moval of lemma and palea.

Infected seeds generally appear more opaque than
healthy seeds. A diaphanoscope was used to differen-
tiate infected and healthy seeds based on opacity
(Noble 1939, Glasscock 1940, Hyde 1945, Muskett
1948). However, opaque seeds can also occur if the
seed is weathered before threshing, in which case
opacity increases due to pigmentation (Gemmell 1940,
Calvert and Muskett 1945, Muskett 1948).

For estimation of total infection, Hyde (1945), Blair
(1947), and Matthews (1980) believed that direct
observations were not as reliable as placing seed in
water and looking for spores under the microscope. A
magnification of 1003 is suitable for examination for
conidia of G. temulenta (Calvert and Muskett 1945).
The lemma and palea may be removed (Calvert and

20

Muskett 1945, Hyde 1945, Sproule and Wright 1966)
or left intact (Kolk and Rennie 1978). Kolk and
Rennie (1978) soaked seed for 4 hours; Matthews
(1980) soaked seed for at least 2 hours.

The number of seeds considered to provide an accu-
rate estimate of rate of infection was reported as 100
(Calvert and Muskett 1945, Blair 1947, de Tempe
1966), 200 (Hyde 1945, Matthews 1980), or 500
(Muskett 1948). Matthews (1980) referred to the
soaking and examination of seed as the “soaking test.”
Matthews also performed a “droplet test,” in which
100 seeds were individually soaked in drops of water
on microscope slides for at least 4 hours. The drops
were examined at 1003 and classified subjectively as
having light, moderate, or heavy spore concentration.
However, Matthews did not find a significant correla-
tion between the droplet test and ungerminated seed.

Rose (1945) correlated conidial numbers removed
through soaking samples of 100 seeds with germina-
tion rate, but high variability in the number of conidia
prevented accurate prediction of germination.
Hardison (1957) mixed 18 ml of seeds and 18 ml of
water in 250-ml flasks, soaked the seeds for 20
minutes, then counted conidia in a 0.0063-mm*
hemacytometer chamber. The number of conidia per
0.0063 mm? corresponded to five infection classes
ranging from trace to heavy. One to three conidia per
0.0063 mm? corresponded to a trace infection level,
and more than 30 conidia corresponded to a heavy
infection. Alderman (1999) used a similar seed-
washing procedure and established a linear relation-
ship between the number of conidia washed from a
standardized seed sample and the percentage of
infected seed.

Matthews (1980) described a detection method based
on production of apothecia. In this test, 200 seeds
were scattered over moist perlite in 14-cm-diameter
petri dishes. The dishes were placed in plastic bags
and stored at 5 °C for 12 weeks. Normal germinated
seeds were removed. Dishes were transferred to 20 °C
under a 12 hour light/12 hour dark cycle for a further
4—5 weeks. Seeds with apothecia were recorded. This
procedure estimates the potential inoculum from seed,
but since many infected seeds do not produce apoth-
ecia, the total number of infected seeds is greatly
underestimated.

The number of seeds infected with viable G.
remulenta can be assessed by isolating the pathogen

on nutrient media. In this test, the palea are removed
from the seeds, the caryoposis is surface sterilized and
bisected, and the halves are plated on malt-extract
agar (Neill and Hyde 1942, Calvert and Muskett 1945,
Muskett 1948).

Preharvest Testing

Preharvest testing of blind seed was common during
the 1940s in New Zealand (Scott 1974) to determine
if the ryegrass seed crop should be harvested. Greenall
(1943) sampled seed heads 2 weeks before harvest and
found good correlation between the percentage of seed
not infected (healthy seed) and germination of ma-
chine-dressed seed. However, samples should be taken
within | week of cutting (Hyde 1942, 1945; Lithgow
and Cottier 1953; Munro 1978; Alderman 1988,
1991b). Infection can occur up to the time of cutting,
so samples collected too early could underestimate
postharvest infection levels.

The number of seed heads believed to be representa-

tive of the area was reported as 50 (Wade 1949), 300
(Hyde 1945, Osborn 1947), or 400-500 (Lithgow and
Cottier 1953; Alderman 1988, 1991b).

Outlook

The past decade has seen considerable changes in the
management of grass seed as growers moved away
from open-field burning of postharvest residue.

Current management practices generally include
baling and removing straw residue followed by flail
chopping any remaining residue. In some cases,
specialized flail choppers are used on the full straw
load. Some growers practice no-till planting. It is not
clear what long-term effect these practices will have
on development of blind seed disease. Weather’s role
is significant. Several consecutive years of wet
weather during flowering could be highly favorable
for disease development.

Surveys of blind seed disease conducted over the past
decade have established the presence of a low level in
Oregon. The recent appearance of a high level of blind
seed in some fields of tall fescue indicates the poten-
tial for development of the disease. The greatest risk
will come from residue management practices that
leave large numbers of seeds in the field. Practices
such as field cleaning or late harvesting in which
considerable seed shatter occurs will only encourage
the disease under favorable conditions.

Although significant yield losses are possible, it is
important to keep in mind that there can be a signifi-
cant drop in seed value at relatively low levels of
infection. Germination rates below 90 percent can
significantly reduce the value of the crop. Thus, the
presence of only 5 to 10 percent blind seed can hurt
profits.

Table 1. Geographical and host distribution of Gloeotinia temulenta

Agropyron cristatum (L.) Gaertn.: United States (Hardison 1962)

Agrostis canina L.: Northern Ireland (Calvert and Muskett 1944), United States (Hardison 1962)

Agrostis capillaris L. [= A. tenuis Sibth.]: United States (Hardison 1962, Alderman 1991a,b)

Agrostis exarata Trin. [= A. exarata Trin. var. monolepsis (Torr.) Hitche.]: United States (Fischer 1944)

Agrostis gigantea Roth: New Zealand (Blair 1947)

Agrostis stolonifera L. [= A. alba L.; = A. palustris Huds.]: New Zealand (Blair 1947), Northern Ireland (Calvert
and Muskett 1944), United States (Hardison 1962, Alderman 199 1a,b)

Aira caryophyllea L.: United States (Fischer 1944)

Alopecurus geniculatus L.: United States (Fischer 1944)

Alopecurus pratensis L.: United States (Hardison 1962)

Arrhenatherum elatius (L.) Beauv. ex J. and C. Presl: United States (Hardison 1962)

Bromus carinatus Hook. and Arn.: United States (Hardison 1962)

Bromus inermis Leyss.: United States (Hardison 1962)

Bromus racemosus L.: United States (Fischer 1944)

Bromus rubens L.: United States (Hardison 1962)

Calamagrostis bolanderi Thurber in S. Watson [= Calamagrostis varia Bol. ex. Thurber]: Germany (Schmid-
Heckel 1988)

Cynosurus cristatus L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944)

Cynosurus echinatus L.: United States (Fischer 1944)

Dactylis glomerata L.: United States (Hardison 1962)

Danthonia californica Boland: United States (Fischer 1944)

Deschampsia cespitosa (L.) P. Beauv.: United States (Fischer 1944, Hardison 1962)

Elymus elymoides (Raf.) Swezey [= Sitanion hystrix (Nutt.) J.G. Sm.]: United States (Hardison 1962)

Elymus glaucus Buckley: United States (Hardison 1962)

Elymus lanceolatus (Scribn. and J.G. Sm.) Gould [= Agropyron dasystachyum (Hook.) Scribn.]:
United States (Hardison 1962)

Elymus repens (L.) Gould [= Agropyron repens (L.) Beauv.; = Elytrigia repens (L.) Nevski]: Norway
(Schumacher 1979), United States (Hardison 1962)

Elymus trachycaulus (Link) Gould ex Shinners [= Agropyron trachycaulum (Link) Malte]: United
States (Hardison 1962)

Festuca idahoensis Elmer: United States (Hardison 1962)

Festuca nigrescens Lam. [= F. rubra L. var. commutata Gaud.; = F. fallax auct. non Thuill.; = F.
rubra L. subsp. fallax auct. non (Thuill.) Nyman |: New Zealand (Neill and Hyde 1942, Blair
1947), United States (Hardison 1962, Alderman 199 1a,b)

Festuca ovina L.: Northern Ireland (Calvert and Muskett 1944), United States (Hardison 1962)

Festuca rubra L.: United States (Hardison 1962)

Festuca trachyphylla (Hackel) Krajina [= F. ovina var. duriuscula (L.) Koch]: United States (Hardison 1962)

Glyceria borealis (Nash) Batsch.: United States (Fischer 1944)

Holcus lanatus L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944), United States
(Fischer 1944, Hardison 1962)

Hordeum marinum Hudson subsp. gussoneanum (Parl.) Thell. [= H. hystrix Roth]: United States
(Fischer 1944)

Hordeum murinum L. subsp. leporinum (Link) Arcang. [= Hordeum leporinum Link]: United States
(Hardison 1962)

Hordeum vulgare L.: United States (Hardison 1962)

Lolium arundinaceum (Schreber) Darbysh. [= Festuca arundinacea Schreb.; = F. elatior L.]: New
Zealand (Neill and Hyde 1942, Blair 1947), United States (Hardison 1962; Alderman
1988, 1991a,b)

Lolium giganteum (L.) Darbysh. [= Festuca gigantea (L.) Vill.]: United States (Hardison 1962)

Table 1. Geographical and host distribution of Gloeotinia temulenta Continued

Lolium multiflorum Lam.: Denmark (Lafferty 1948), Ireland (Lafferty 1948), Scotland (Noble and Gray 1945),
New Zealand (Hyde 1938b, Lafferty 1948, Latch 1966), Northern Ireland (Calvert and Muskett 1944,
1945), United States (Hardison1962)

Lolium perenne L.: Australia (Anonymous 1955, 1962; Wade 1957; McGee 1971a; Munro 1978), Denmark
(Gemmell 1940, Lafferty 1948, Kristensen and Jorgensen 1960), England (Neill and Hyde
1939, Gemmell 1940, Glasscock 1940), Ireland (Gemmell 1940, Lafferty 1948), Netherlands (de
Tempe 1950, 1966), New Zealand (Gorman 1939; Hyde 1942; Blair 1947, 1948; Lafferty 1948;
Hampton and Scott 1980a; Neill and Hyde 1939, 1942), Northern Ireland (Neill and Hyde 1939,
Calvert and Muskett 1944), Scotland (Neill and Hyde 1939, Gemmell 1940, Noble and Gray 1945,
Dennis and Gray 1954), Sweden (Neill and Hyde 1939), United States (Fischer 1944; Hardison
1962; Alderman 1988, 1991a,b) and Wales (Neill and Hyde 1939)

Lolium pratense (Hudson) Darbysh. [= Festuca pratensis Huds.]: Northern Ireland (Calvert and
Muskett 1944), New Zealand (Neill and Hyde 1942)

Lolium temulentum L.: New Zealand (Neill and Hyde 1942), United States (Fischer 1944, Hardison 1962)

Lolium temulentum L. subsp. remotum (Schrank) A. and D. Love [= Lolium remotum Schrank]:

United States (Hardison 1962)

Phleum pratense L.: United States (Fischer 1944, Hardison 1962)

Poa ampla Merr.: United States (Hardison 1962)

Poa arachnifera Torrey in Marcy.: United States (Hardison 1962)

Poa compressa L.: United States (Hardison 1962)

Poa nemoralis L.: United States (Hardison 1962)

Poa pratensis L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944), United States
(Hardison 1962, Alderman 1991a,b)

Poa secunda J. Pres subsp. juncifolia (Scribner) Soreng [= P. juncifolia Scribn.; = Poa nevadensis
Vasey ex Scribn.]: United States (Hardison 1962)

Poa trivialis L.: New Zealand (Blair 1947), Northern Ireland (Calvert and Muskett 1944), United States (Hardison
1962)

Psathyrostachys juncea (Fisch.) Nevski [= Elymus junceus Fisch.]: United States (Hardison 1962)

Pseudoroegneria spicata (Pursh) A. Love [= Agropyron inerme (Scribn. and J.G. Sm.) Rydb.; =A.
spicatum (Pursh) Scribn. and J.G. Sm.]: United States (Hardison 1962)

Secale cereale L.: France (Prillieux and Delacroix 1891), Germany (Rehm 1900), New Zealand (Neill and Hyde
1942), United States (Hardison 1962)

Thinopyrum intermedium (Host) Barkworth and D.R. Dewey [= Agropyron intermedium (Host) P.
Beauv.; = A. trichophorum (Link) Richt.; = Elytrigia intermedia (Host) Nevski]: United States
(Hardison 1962)

Vulpia myuros (L.) C.C. Gmelin [= Festuca myuros L.]: United States (Fischer 1944, Hardison 1962)

Table 2. Relative susceptibility of grass species to Gloeotinia temulenta

Relative
Subfamily Tribe Species Infection
Arundinoideae Danthoneae Danthonia californica Boland none
Pooideae Aveneae Agrostis canina L. none to light
Agrostis capillaris L. [= A. tenuis Sibth. none to heavy
Agrostis stolonifera L. [= A. alba L.: =A. none to moderate
palustris Huds. ]
Aira caryophyllea L. var. capillaris (Host) none
Mutel [= Aira elegans Willd. ex. Gaudin]
Alopecurus aequalis Sobol. none
Alopecurus arundinaceus Poir. in Lam. none
Alopecurus pratensis L. none to light
Anthoxanthum odoratum L. none
Arrhenatherum elatius (L.) Beauv. ex J. none to trace
and C. Pres]
Avena fatua L. none
Avena sativa L. none
Deschampsia cespitosa (L.) P. Beauv. none to trace
Holcus lanatus L. none to light
Phalaris aquatica L. {= Phalaris tuberosa L.] none
Phalaris arundinacea L. none
Phleum pratense L. none to light
Trisetum flavescens (L.) Beauv. none
Trisetum spicatum (L.) Richter none
Poeae Cynosurus cristatus L. none

Dactylis glomerata L.

Festuca idahoensis Elmer

Festuca ovina L.

Festuca rubra L.

Festuca rubra subsp. fallax Thuill [= F.
rubra L. var. commutata Gaud. |

Festuca trachyphylla (Hackel) Krajina
(= F.ovina var. duriuscula (L.) Koch)

Lolium arundinaceum (Schreber) Darbysh.
(= Festuca arundinacea Schreb.;
= F. elatior L.)

Lolium giganteum (L.) Darbysh.
[= Festuca gigantea (L.) Vill.]

Lolium multiflorum Lam.

Lolium perenne L.

Lolium pratense (Hudson) Darbysh.
[= Festuca pratensis Huds.)

Lolium temulentum L.

Lolium temulentum L. subsp. remotum
(Schrank) A. and D. Love (= Lolium
remotum Schrank)

none to trace
none to heavy
none to heavy
none to moderate
none to trace

light

light to heavy

none to heavy

heavy
heavy
light

heavy
heavy

Table 2. Relative susceptibility of grass species to Gloeotinia temulenta Continued

Relative
Subfamily Tribe Species Infection
Poa ampla Merr. trace to heavy
Poa arachnifera Torrey in Marcy none to heavy
Poa compressa L. heavy
Poa nemoralis L. heavy
Poa palustris L. none
Poa pratensis L. none to heavy
Poa secunda J. Presl |= P. canbyi (Scribn.) trace to heavy
Howell]
Poa secunda J. Presl subsp. juncifolia light to heavy
(Scribner) Soreng [= P. juncifolia Scribn.;
= P. nevadensis Vasey ex Scribn.]
Poa trivialis L. none to heavy
Vulpia myuros (L.) C.C. Gmelin light to heavy
[= Festuca myuros L.]|
Triticoideae Bromeae Bromus arvensis L. none
Bromus carinatus Hook. and Arn. none to trace
Bromus catharticus Vahl none
Bromus commutatus Schrad. none
Bromus erectus Huds. none
Bromus hordaeceus L. {= B. mollis L.} none
Bromus inermis Leyss. none to trace
Bromus madritensis L. none
Bromus marginatus Nees in Steud. none
Bromus polyanthus Scribn. in Shear none
Bromus rigidus Roth none
Bromus rubens L. none to trace
Bromus secalinus L. none
Bromus squarosus L. none
Bromus tectorum L. none
Triticeae Aegilops cylindrica Host none
Agropyron fragile (Roth) Candargy [= A. none
sibiricum (Willd.) P. Beauv.; = A. fragile
(Roth) Candargy subsp. sibiricum (Willd.)
Melderis]
Agropyron cristatum (L.) Gaertn. trace
Elymus canadensis L. none
Elymus caninus (L.) L. [= Agropyron none
caninum (L.) Beauv. ]
Elymus elymoides (Raf.) Swezey |= Sitanion trace
hystrix (Nutt.) J.G. Sm.]
Elymus glaucus Buckley light
Elymus lanceolatus (Scribn. and J.G. Sm.) trace to light

Gould [= Agropyron dasystachyum
(Hook.) Scribn. |

Table 2. Relative susceptibility of grass species to Gloeotinia temulenta Continued

Relative
Subfamily Tribe Species Infection
Elymus repens (L.) Gould [= Agropyron trace
repens (L.) Beauv.; = Elytrigia repens
(L.) Nevski]
Elymus sibiricus L. none
Elymus trachycaulus (Link) Gould ex trace

Shinners [= Agropyron trachycaulum
(Link) Malte]
Elymus trachycaulus (Link) Gould ex none
Shinners subsp. subsecundus (Link)
A. and D. Léve[= Agropyron
subsecundum (Link) A.S. Hitchce. |

Hordeum brachyantherum Nevski none
Hordeum bulbosum L. none
Hordeum marinum Hudson subsp. none
gussoneanum (Parl.) Thell. [= H. hystrix
Roth]
Hordeum murinum L. subsp. leporinum none to trace
(Link) Arcang. [= Hordeum leporinum
Link]
Hordeum vulgare L. none to trace
Leymus triticoides (Buckley) Pilg. none
[= Elymus tritcoides Buckley |
Pascopyrum smithti (Rydb.) A. Love none
[= Agropyron smithiti Rydb.]
Psathyrostachys juncea (Fisch.) Nevski none to heavy
[= Elymus junceus Fisch. |
Pseudoroegneria spicata (Pursh) A. Love trace to moderate

[= Agropyron inerme (Scribn. and

J.G. Sm.) Rydb.; = Agropyron spicatum

(Pursh) Scribn. and J.G. Sm.]
Secale cereale L. none to heavy
Thinopyrum intermedium (Host) Barkworth trace

and D.R. Dewey [= Agropyron inter-

medium (Host) P. Beauy.; = A. trich-

ophorum (Link) Richt.;= Elytrigia inter-

media (Host) Nevsk1]
Triticum aestivum L. none

Source: Based on data from Hardison (1962).

26

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