• TABLE OF CONTENTS
HIDE
 Front Cover
 Table of Contents
 Common diseases
 Organisms reported on southern...
 Literature cited
 Back Cover














Group Title: Bulletin - University of Florida. Agricultural Experiment Stations ; no. 713
Title: Diseases of southern turfgrasses
CITATION THUMBNAILS PAGE IMAGE ZOOMABLE
Full Citation
STANDARD VIEW MARC VIEW
Permanent Link: http://ufdc.ufl.edu/UF00027369/00001
 Material Information
Title: Diseases of southern turfgrasses
Series Title: Bulletin University of Florida. Agricultural Experiment Station
Physical Description: 31 p. : ill. (some col.) ; 23 cm.
Language: English
Creator: Freeman, T. E ( Thomas Edward ), 1930-
Publisher: Agricultural Experiment Stations, Institute of Food and Agricultural Sciences, University of Florida
Place of Publication: Gainesville Fla
Publication Date: 1967
 Subjects
Subject: Turfgrasses -- Diseases and pests -- Florida   ( lcsh )
Genre: government publication (state, provincial, terriorial, dependent)   ( marcgt )
bibliography   ( marcgt )
non-fiction   ( marcgt )
 Notes
Bibliography: Bibliography: p. 30-31.
Statement of Responsibility: T.E. Freeman.
General Note: Cover title.
Funding: Bulletin (University of Florida. Agricultural Experiment Station)
 Record Information
Bibliographic ID: UF00027369
Volume ID: VID00001
Source Institution: University of Florida
Rights Management: All rights reserved by the source institution and holding location.
Resource Identifier: aleph - 000929304
oclc - 18363886
notis - AEP0084

Table of Contents
    Front Cover
        Page 1
    Table of Contents
        Page 2
    Common diseases
        Page 3
        Page 4
        Page 5
        Page 6
        Page 7
        Page 8
        Page 9
        Page 10
        Page 11
        Page 12
        Page 13
        Page 14
        Page 15
        Page 16
        Page 17
        Page 18
        Page 19
        Page 20
        Page 21
        Page 22
        Page 23
        Page 24
        Page 25
    Organisms reported on southern turfgrasses
        Page 26
        Page 27
        Page 28
        Page 29
    Literature cited
        Page 30
        Page 31
    Back Cover
        Page 32
Full Text


DISEASES OF SOUTHERN

TURFGRASSES


T. E. Freeman


agricultural Experiment Stations
institute of Food and Agricultural Sciences
university of Florida, Gainesville
.R. Beckenbach, Director


--~~--~~







CONTENTS


Page

I. Introduction .. ...- --- -------- 3


II. Common Diseases ........-
Rhizoctonia Brown Patch _-
Sclerotinia Dollar Spot -
Helminthosporium Diseases
Pythium Blight --------
Piricularia Leaf Spot ----
Rust Diseases ----
Mushroom Fairy Ring .--
Slime Molds -----
Seedling Blights --------
Curvularia Fading Out -
Cercospora Leaf Spot ----
Smut Diseases ----
Anthracnose ----
Mosaic ----------


S3
-- 4
------- 4
7
-- 9
12
15
---- 18
.....-- 19
21
-- 22
---- 23
23
---- 24
25
25


III. Organisms reported on Southern Turfgrasses ..
Cynodon dactylon (L.) Pers. (bermudagrass)
Eremochloa ophiuroides (Munro) Hack.
(centipedegrass) ------
Lolium multiflorum Lam. (ryegrass) ......
Paspalum notatum Fleugge (bahiagrass)
Stenotaphrum secundatum (Walt.) Kuntze
(St. Augustinegrass) ....-....--------
Zoysia spp. (zoysiagrass) -- ----


IV. Literature Cited


Cover picture. Sclerotinia dollar spot on bermudagrass. Note increased
incidence of disease in low fertility plot on right.






Diseases of Southern Turfgrasses


T. E. Freeman'

INTRODUCTION

A quality turf planting results from following a planned
management program designed to meet the needs of the par-
ticular grass being grown. Dealing with the diseases that affect
the various grasses is one facet of a properly executed main-
tenance program, because diseases occur frequently and, unless
controlled, cause considerable damage. Therefore, it is essential
that those interested in growing quality turf become acquainted
with the cause, factors affecting occurrence, symptoms, and con-
trol of the various diseases. This bulletin is designed to provide
such information for the diseases (excluding those caused by
nematodes) affecting the grasses used for turf in Florida as well
as in the rest of the southern United States. These grasses are:


SCIENTIFIC NAME
Cynodon dactylon (L.) Pers.
Eremochloa ophiuroides (Munro) Hack.
Stenotaphrum secundatum (Walt.) Kuntz
Paspalum notatum Fluegge
Zoysia spp.
Z. japonica Steud
Z. matrella (L) Merr.
Z. tenuifolia Willd.
Lolium multiflorum Lam.


COMMON NAME
bermudagrass
centipedegrass
St. Augustinegrass
bahiagrass
zoysiagrass



annual ryegrass


The last species, although not one of the permanent warm-
season grasses, is included because of its extensive use during
the winter months as a temporary overseeded grass.


COMMON DISEASES

More than one hundred diseases have been reported on the
various grasses used for turf in Florida and the South. Most of
these diseases are caused by fungi. In fact, representatives from
each of the five major groups of these organisims (Myxomycetes,
Phycomycetes, Ascomycetes, Basidiomycetes, and Fungi Imper-

SAssociate Plant Pathologist, Department of Plant Pathology, Florida Agri-
cultural Experiment Stations, University of Florida, Gainesville.







fecti) can be found affecting turfgrasses. Thus far, no bacterial
and only two minor viral diseases have been reported on these
plants. Fortunately, only a few pathogenic organisms occur
commonly and still fewer can be considered serious threats to
quality turf production. The fourteen diseases covered in detail
in this section constitute the commonly occurring ones. In Flor-
ida, the first seven of these are considered serious since they
account for the major portion of the annual disease damage to
turfgrasses. Any one of the remaining seven, however, may
cause considerable damage at any given time or location. The
common diseases of southern grasses, their cause, symptoms,
factors affecting occurrence, and control follow.

Rhizoctonia Brown Patch

CAUSE: Rhizoctonia solani Kuhn (Perfect stage; Thanate-
phorus cucumeris [Frank] Donk.)
HOSTS: Cynodon dactylon (bermudagrass), Eremochloa
ophiuroides (centipedegrass), Lolium multiflorum
(ryegrass), Paspalum notatum (bahiagrass), Sten-
otaphrum secundatum (St. Augustinegrass), and
Zoysia spp. (zoysiagrass)
SYMPTOMS AND PATHOGEN MORPHOLOGY: This
prevalent and destructive disease kills the grass in a roughly
circular pattern that may range from a few inches up to several
feet in diameter (Fig. 1). When the disease is active, grass at
the outer edge of the affected area may appear dark and wilted
and exhibit profuse growth of the parasite on its surfaces.
Often healthy grass will persist or grow back into the interior
of the circle so that the diseased area has a "doughnut appear-
ance." In some instances, however, a circular pattern is not
discernable. In such cases, a rather large area of turf may be
thinned and eventually killed by the parasite. This type of dis-
ease manifestation is especially prevalent on St. Augustinegrass
growing in shady, moist locations.
If diseased grass is examined closely, a rotting of the leaf
sheath will be evident. This type of damage is especially notice-
able on coarser grasses such as St. Augustine. Because of this
rot, entire leaf fascicles can be pulled from the plant with little
effort. Where the grass is thinned over a large area, a root and
stem rot is usually evident. Centipedegrass is subject to aerial
attacks by Rhizoctonia in which only the leaf blades are affected.
In these aerial attacks, light tan lesions are evident on the leaves.







~5 -


Fig. 1.-Rhizoctonia brown patch on St. Augustinegrass.


These lesions may completely traverse the blade, causing death
of the distal portion.
Mycelium of the pathogen is often prominent on affected
leaf surfaces. The mycelium can be recognized under a micro-
scope as that of Rhizoctonia by its large size (5-151 in diam-
eter) and characteristic right angle branching with an accom-
panying constriction of the hypha at each branch (Fig. 2).
Sclerotia are variable in color, shape, and size but are- usually
brown to black, oval, and up to 2 mm in diameter. The perfect
stage (Thanatephorus cucumeris [Frank] Donk.) occurs in-
frequently on diseased plants.
OCCURRENCE: Rhizoctonia solani is a serious parasite of
all major grasses used for turf in the South. St. Augustinegrass
is very susceptible to attacks by this parasite, and rye and zoysia
grass are only slightly less susceptible. Bermuda, centipede,
and bahia are somewhat more resistant; nevertheless, plantings
of these grasses still are frequently damaged by brown patch.
Brown patch occurs during warm weather when sufficient
surface moisture is present for the pathogen to develop. The
sclerotia of R. solani germinate in the range of 64 to 68" F., and
parasitism of the grass begins when the temperature rises above
73" F. Pathogenic activity, which is most noticeable at 80" to
85" F., ceases as the temperature rises above 90" F. (7).2

2 Numbers in parentheses refer to Literature Cited.





















Fig. 2.-Mycelium of Rhizoctonia solani. Note right angle branching
with accompanying constriction of hyphae (arrow).

Soil fertility is another factor affecting the occurrence of
brown patch. Excess nitrogen fertilization enhances disease
severity, while low nitrogen lessens damage. On the other hand,
a low level of complete fertilization is more conducive to disease
development than a normal or even excess level (3, 5).

CONTROL: Since, at the present time, all of the warm-sea-
son grasses are subject to severe damage by R. solani, the choice
of which one to plant is not a prime factor of consideration for
disease control. Management of the grass, however, is import-
ant since certain practices can lessen disease severity and spread.
Foremost among these are watering and fertilization practices.
Watering should be regulated so that free moisture is present
on the plant for the shortest possible time. Removal of accumu-
lated water on plant parts by such practices as poling ( sweeping
the grass with a limber pole) and syringing is also an aid in
controlling the occurrence and spread of brown patch (21);
these practices are especially useful on golf greens that are
subject to frequent R. solani attacks. In the fertilization pro-
gram of a turf area, excessive use of a readily available nitrogen.
fertilizer should be avoided. The grass, however, should be
supplied with an adequate level of a balanced fertilizer.
Should brown patch occur-which it frequently does, regard-
less of the above precautions-then a fungicide must be used to
bring the disease under control. The inorganic mercury fungi-
cides were among the first to be used for brown patch control,
and they are still among the more effective that can be used.
They have the drawback, however, of being poisonous to humans
and corrosive to spray equipment. The organic mercury fungi-







cides also, as well as thiram and pentachloronitrobenzene (PC-
NB), will effectively control brown patch. All of these materials
should be used according to the manufacturers' directions. In
general, two applications spaced 10-14 days apart are sufficient
to bring a disease outbreak under control. During periods of
weather conducive to disease occurrence, however, it may be
necessary to make several applications on a 10-14 day schedule
if satisfactory control is to be maintained.

Sclerotinia Dollar Spot
CAUSE: Sclerotinia homoeocarpa F. T. Bennett.
HOSTS: Cynodon dactylon (bermudagrass), Eremochloa
ophiuroides (centipedegrass), Lolium multiflorum
(ryegrass), Paspalum notatum (bahiagrass),
Stenotaphrum secundatum (St. Augustinegrass),
and Zoysia spp. (zoysiagrass).

SYMPTOMS AND PATHOGEN MORPHOLOGY: On fine
textured and close-cut turf, the grass is killed in small patches
approximately the size of a silver dollar; hence, the common
name dollar spot. In severe cases, these small patches will coa-
lesce so that the affected turf has a mottled appearance (cover
picture). On coarse-textured grasses such as bahia and high-
cut turf, the grass may be killed in a larger, more diffuse pat-
tern. Under these conditions, dollar spot can be confused with
brown patch caused by R. solani. The two disorders are readily
distinguishable, however, by the characteristic leaf lesions
caused by the dollar spot fungus; these irregular lesions occur
on the blades of grass at the margin of the affected patch, are
light tan with a reddish-brown border, and usually radiate from
the edge of the leaf blade. If the grass that is being actively
parasitized is examined early in the day before the dew dries,
the cobweb-like mycelium of the pathogen can be seen growing
over the affected plants. During the early disease phases, af-
fected grass may be dark and wilted in appearance; however,
it will later turn a characteristic bleached straw color.
In culture, mycelium of S. homoecarpa is wooly in appear-
ance, white when young, but changing to cinnamon to reddish-
brown, occasionally tinged with yellow. Sclerotia are black and
parchment-like. Sporulating structures, both conidiophores and
ascophores, occasionally occur in culture but have not been ob-
served in nature (21). Hyphae of two distinct sizes are often
found intermixed, with the smaller hyphae predominating.







OCCURRENCE: Several factors condition the occurrence
and severity of dollar spot. Among these are the type of grass
grown and climatic and other environmental conditions includ-
ing soil moisture and fertility.
Bermuda, zoysia, and bahia grasses are most severely af-
fected by S. homoeocarpa, while St. Augustine and centipede
are damaged infrequently. Disease reaction varies within
grasses as well as between; i.e., the bermudagrass varieties Or-
mond, Uganda, and Tifway are more susceptible to dollar spot
than other improved varieties. Varietal variation in disease
reaction within other grass is not as pronounced as with ber-
mudagrass; however, it does exist.
Dollar spot is most prevalent during periods of mild weather
(60"-80" F.) such as occurs during the spring and fall months.
It can, however, occur throughout the summer when the tem-
perature is relatively warm (1, 11). These occurrences have
been related to the existence, in Florida at least, of high-tem-
perature-tolerant strains of the parasite. Bennett (2) has re-
ported differences in temperature tolerances between isolates
from the United States and England.
Low soil moisture has been reported to enhance dollar spot
severity and thus to account for the severe outbreaks that occur
during periods of low rainfall (5). Sufficient moisture from dew,
fog, and watering must be present during these periods for the
pathogen to develop. Another soil factor that affects dollar spot
severity is fertility (cover picture). Low levels of both nitrogen
and potash result in increased disease severity under field con-
ditions (12, 25). The nitrogen appears to be more important
since application of it alone will overcome the effect of low
potash. In fact, rather severe outbreaks of dollar spot on Tif-
lawn and Uganda bermudagrasses have been brought under
control through the use of a readily available nitrogen fertilizer
(25). The mechanism whereby nitrogen fertilization retards
disease development is not understood. Couch (4), however,
believes the beneficial effect is due entirely to rapid plant re-
covery during periods of lessened activity of the parasite. He
concluded this after greenhouse studies with bluegrass that
indicated nitrogen actually increased susceptibility to dollar spot.

CONTROL: The best control measure is to plant grasses or
grass varieties that are most resistant. If susceptible ones are
used, then judicious use of fertilizer is an aid in preventing and
overcoming outbreaks of dollar spot. At times, however, the
disease may reach such proportions that the use of a fungicide






becomes necessary. In the past, the fungicides containing cad-
mium have been extensively recommended for dollar spot control.
Others, however, such as the organic and inorganic mercury
fungicides as well as some of the newer turf fungicides such as
Daconil 2787 will provide a higher degree of control. Two appli-
cations may be necessary to bring the disease under adequate
control.



CAUSE: Helminthosporium cynodontis Margi., H. gigan-
teum Heald and Wolf, H. stenospilum Drechsl., H.
triseptatum Drechsl.
HOST: Cynodon dactylon (bermudagrass)
CAUSE: Helminthosporium rostratum Drechsl.
HOSTS: Cynodon dactylon (bermudagrass) and Stenota-
phrum secundatum (St. Augustinegrass)
CAUSE: Helminthosparium siccans Drechsl., H. sorkinian-
um Sacc. (H. sativum PBK)
HOST: Lolium multiflorum (ryegrass)

SY MPTOMS AND Fig. 3.-Helminthosporium disease
PATHOGEN MORPHOL- on bermudagrass.
OGY: Small, brown to pur-
ple lesions (1 to 4 mm in
length) occur on the leaf
blades (Fig. 3). These le-
sions tend to form streaks
in the case of H. siccans on
ryegrass and eyespots in
the case of H. giganteum
on bermudagrass. Other-
wise, the spots caused by
the various species of
Helminthosporium on the
grass are similar in appear-
ance. Leaf spots are usual-
ly more numerous near the
collar area of the leaf blade,
possibly because of accumu-
lation in this area of spores
washed from other portions







of the leaf. Severely affected leaves will turn reddish-brown,
then wither and die. In early, initial, stages a severely affected
turf area may have an overall purple cast. As the disease pro-
gresses, the grass is gradually thinned in areas that may involve
a major portion of the planting. This thinning is often quite
advanced before a disease is suspected and verified by the pres-
ence of leaf spots. Under severe disease conditions a sheath and
crown rot may be evident and the grass killed in patches.
Spores of the causal Helminthosporium can usually be found
on dead or dying leaves. They are colored, ranging from sub-
hyaline to dark olivaceous, smooth, multiseptate in one plane,
and are borne on definite conidiophores (Figs. 4 and 5). For a
complete description of the various Helminthosporium spp., the
reader is referred to Drechsler (8) and Sprague (26) ; and, for
identification, to the key prepared by Luttrell (22). The follow-
ing key, however, will serve for preliminary identification of the
species commonly occurring on southern turf grasses:

I. Spores sub-hyaline to pale or yellow-brown
A. Spores sub-hyaline, on bermudagrass H. cynodontis
B. Spores pale to yellow-brown
1. Spores up to 300, in length, cylindric H. giganteum
2. Spores less than 300, in length,
tapered towards the ends, on ryegrass H. siccans
II. Spores dark brown to olivaceous
A. Basal and distal septations darkened H. rostratum
B. Basal and distal septations not darkened
1. Spores regularly 2 to 3 septate H. triseptatum
2. Spores regularly more than 2 to 3 septate
a. Spores curved, convex wall thicker
than concave. H. stenospilum
b. Spores irregular, walls equally
thickened. H. sorkinianum

OCCURRENCE: Helminthosporium diseases are widespread
in occurrence and are of considerable importance on susceptible
grasses. They are most evident during periods of mild weather.
For example, studies have shown that the optimum temperature
for infection of bermudagrass by H. stenospilum is near 25'C,




























Fig. 4.-Spores of


Helminthosporium stenospilum from


bermudagrass.
bermudagrass.


Fig. 5.-Spores of Helminthosperium sorkinianum from ryegrass.

but some infection occurs over a wide range of temperatures
(20 to 35C). This may account for the fact that infected plant-
ings can be found at any time of the year that the grass is green.
Damage is especially severe, however, during the spring and
fall months when the grass is semi-dormant.







In extensive isolation and inoculation studies, Freeman (16)
found five species of Helminthosporium affecting bermudagrass
in Florida in the following descending order of occurrence: H.
cynodontis, H. triseptatum, H. stenospilum, H. rostratum, and
H. giganteum. The order of disease severity, however, did not
follow the same order as occurrence. The descending order of
disease severity was as follows: H. stenospilum, H. cynodontis,
H. giganteum, H. rostratum and H. triseptatum. However, the
difference in disease severity was negated to a certain extent by
the fact that simultaneous infection by more than one species
was frequently noted. In fact, in more than 50 per cent of the
samples studied, this condition occurred. Not only did infection
by different species occur on adjacent leaves but also on the same
leaf. Furthermore, it was not uncommon to find adjacent leaf
spots caused by different parasites.
Bermudagrass varieties exhibit varying degrees of suscepti-
bility to damage by Helminthosporium spp. (9, 17). In general
the improved varieties are more resistant, whereas common and
certain varieties of African origin are most susceptible.

CONTROL: Most of the bermudagrass varieties released in
recent years for use in the southeastern United States show a
degree of resistance to the commonly occurring species of Hel-
minthosporium. These more tolerant varieties should be used.
Helminthosporium diseases can be controlled through the
use of a turf fungicide. In general, the organic mercury com-
pounds have provided the best control. Other turf fungicides
such as Dyrene, thiram, and Acti-dione-thiram are also effective.
All of these materials will provide control, even though more
than one species of Helminthosporium may be attacking the
grass (5). Repeated fungicide applications may be necessary to
maintain adequate disease control.

Pythium Blight
CAUSE: Pythium aphanidermatum (Edson) Fitzpatrick
HOSTS: Cynodon dactylon (bermudagrass) and Lolium
multiflorum (ryegrass)
SYMPTOMS: Grass is rapidly killed in distinct spots that
tend to form streaks on sloping areas. These affected spots may
be several inches in diameter. In the early stages, affected grass
appears dark and water soaked. It will later collapse and appear
to be matted together. At this stage, the grass turns brown and
may exhibit a red tinge. When the disease is very active, myce-







lium of the pathogen grows profusely over affected plants so
that diseased areas have a cotton-like appearance. Because of
this latter symptom, the disease is often referred to as cottony
blight (Fig. 6).
Microscopic examination of killed plants will reveal the pres-
ence of oospores of P. aphanidermatum embedded in the dead
tissue (Fig. 7). These oospores are 17-19k in diameter. A ma-
ceration of diseased tissue can also be noted. Such a condition
is brought about by the action of cellulolytic and pectinolytic
enzymes produced by the pathogen (30). Mycelium of this para-
site is hyaline (white in mass), is 4-8, in diameter, and is asep-
tate.


Fig. 6.-Pythium blight on ryegrass. Note white mycelium growing in
the area of collapsed grass.

OCCURRENCE: Since the first report (29) of pythium
blight on ryegrass, it has been found to occur frequently in ephi-
phytotic proportions. For this and other reasons, cool-season
grasses such as bluegrass, bentgrass, and fescuegrass are often
considered as substitutes for ryegrass in overseeding programs.
Freeman and Horn (20), however, tested 15 varieties of these
three cool-season grasses and found that, from the standpoint
of avoiding pythium blight, nothing would be gained by substi-
tuting these grasses, since they were all subject to severe dam-
age by P. aphanidermatum. Only bluegrass was damaged less


























Fig. 7.-Oospores (arrow) of Pythium aphanidezratum embedded in
tissue of ryegrass.

than ryegrass, but the magnitude of difference was not enough
to be of practical value. They also found that of 28 varieties of
the various warm-season grasses tested, only bermudagrass was
susceptible to attack by P. aphanidermatum. Damage to this
warm-season grass was slight, however, in comparison to that
which occurred on the cool-season grasses.
Weather is an important factor in the occurrence of pythium
blight. An abundance of moisture is required; therefore, the
disease is most prevalent during rainy or foggy weather in low-
lying areas where air circulation is poor. Along with moisture,
warm temperatures are required for P. aphanidermatum to
cause damage. Freeman (13) has shown that disease activity is
negligible below 68 F. but increases with rising temperature
with maximum damage occurring at 90' to 95 F. In addition,
the fungus grows so rapidly that the temperature needs to re-
main in a conducive range for only a short period during suc-
cessive days. The length of this period is dependent on the tem-
perature, but may be as short as two hours for temperatures in
excess of 900. This accounts for the frequent damage by pythium
blight during relatively cool weather.
In cooler areas, pythium blight occurs most frequently on
seedling grass and is thus considered a seedling disorder. How-
ever, it has been shown that ryegrass up to 16 weeks of age is
only slightly less susceptible than seedling grass (15). There-
fore, limitation of the disease to the seedling stage of growth in
certain areas is probably due to the onset of cool weather rather


2131~
bt~J -~-~i
ur







than to an increase in resistance with aging of the plant. This
is further substantiated by the fact that pythium blight occurs
on ryegrass throughout the winter months in warmer regions
such as Florida.
In Florida, P. aphanidermatum is apparently widely dis-
tributed in the soils of golf courses. It was present in detectable
amounts (using ryegrass as an indicator) in 20 of 42 soil
samples taken from greens representing 17 different courses
located in various parts of the state. Eight of the 20 were con-
sidered heavily infested, while nine showed a medium degree of
infestation (17).

CONTROL: Pythium blight is difficult to control, partly be-
cause of the rapidity with which the disease spreads and causes
severe damage. Therefore, control measures must be timed pre-
cisely and should be conducted as a preventive program during
periods of weather favoring disease development. Spread of the
pathogen can often be reduced by curtailing mowing and water-
ing practices during periods of disease activity. In cooler re-
gions, severe damage can often be avoided, or at least reduced,
by delaying overseeding until the onset of cool weather.
Certain organic mercurial fungicides (Memmi and Panogen
Turf Spray) and the pythium specific fungicide Dexon have
been shown to provide the best degree of control of pythium
blight. Repeated applications at 7-8 day intervals may be re-
quired during periods of disease activity.

Piricularia Leaf Spot
CAUSE: Piricularia grisea (Cke.) Sacc.

HOSTS: Cynodon dactylon (bermudagrass), Eremochloa
ophiuroides (centipedegrass), Stenotaphrum se-
cundatum (St. Augustinegrass)

SYMPTOMS AND PATHOGEN MORPHOLOGY: This dis-
ease causes round to oblong leaf spots that are brown to ash
colored with purple to brown margins (Fig. 8). At times, the
spots are covered with fruiting structures of the parasite. Under
these conditions affected areas of the leaf have a gray, velvet
appearance; hence, the disease is commonly called gray leaf
spot. Severely affected leaf blades wither and turn brown. If
enough leaves are affected, the entire planting may have a
scorched appearance as if suffering from severe drought. Lesions
caused by the fungus also occur on the stems and spikes of af-







fected plants. Malca and Owen
(23) have reported detailed his-
tological studies concerning mi-
croscopic symptoms of P. grisea.
Spores of P. grisea are hya-
line, pyriform, and three-celled
when mature. A protruding hi-
lum occurs on the basal cell of
the spore (Fig. 9).

OCCURRENCE: Although P.
grisea occurs on other grasses,
it is primarily a parasite of St.
Augustinegrass. In fact, it is
omnipresent on this grass dur-
ing the warm, humid, summer
months. Not all plantings, how-
ever, are equally infected. Both
the type of grass grown and the
fertility level account for this
difference in disease occurrence.
The yellow-green or Roselawn
types of St. Augustinegrass
have an inherent degree of re-
Fig. 8.-Piricularia leaf spot on distance that is not present in
St. Augustinegrass.
the blue-green or Bitter Blue

types. In fact, strains of the former have been isolated which
are highly resistant to gray leaf spot; unfortunately, the ones
thus far found have not been desirable lawn types.
The severity of P. grisea infection on St. Augustinegrass is
enhanced by application of nitrogen fertilizer. Furthermore, the
magnitude of increased severity is related to the amount of
nitrogen applied. For example, in studies reported by Freeman
(18), varying the rate of nitrogen from 1 to 8 pounds per 1000
square feet resulted in a 65 to 125% increase in the number of
lesions per 100 leaves over that found in plots receiving no
nitrogen. This increase in disease occurrence can be noted only
on susceptible types, since the resistant yellow-green types are
not affected when grown under high levels of nitrogen fertili-
zation. The manner in which nitrogen affects disease severity
has not been completely elucidated; however, both the total nitro-
gen and free amino acid content of leaf tissue is correlated with
increased disease susceptibility resulting from nitrogen fertili-
zation (18).



























Fig. 9.-Spores of Piricularia grisea from St. Augustinegrass.

The damage caused by P. grisea is especially evident on newly
sprigged, rapidly growing grass. In tests conducted at the
University of Florida (14), controlling the disease during the
first 10 weeks after sprigging increased coverage by more than
35 % over that in areas where the disease was not controlled.


Fig. 10.-Rust disease on Zoysiagrass. Note orange pustules on leaf
surface.







Climatic conditions, especially temperature and humidity,
affect the occurrence of gray leaf spot. Abundant moisture and
warm temperatures are required for the fungus to actively para-
sitize susceptible grass (23).

CONTROL: Since nitrogen fertilization increases severity
of gray leaf spot, this nutrient should be used as sparingly as
possible to achieve the desired turf appearance. In addition, as
with brown patch, watering should be timed so that the grass
is wet for the shortest possible time. Such procedures will aid
in reducing disease severity; but, for complete control, fungi-
cidal treatments are usually required. Most available turf fun-
gicides will adequately control gray leaf spot; however, repeated
applications at 10 to 14 day intervals may be necessary during
rainy periods.

Rust Diseases
CAUSE: Puccina coronata Cda.
HOST: Lolium multiflorum (ryegrass)
CAUSE: Puccinia cynodontis Desm.
HOST: Cynodon dactylon (bermudagrass)
CAUSE: Puccinia stenotaphri Cumm.
HOST: Stenotaphrum secundatum (St. Augustinegrass)
CAUSE: Puccinia zoysiae Diet.
HOST: Zoysia spp. (zoysiagrass)

SYMPTOMS AND PATHOGEN MORPHOLOGY: These
four rust diseases have similar symptoms on the various grasses.
Affected turf will appear unthrifty and begin to thin. In severe
cases, the grass turns chlorotic as if suffering from a nutrient
deficiency. If diseased plants are examined closely, orange-
colored, linear pustules 1 to 2 mm in length will be evident on the
leaf blades (Fig. 10). Under ideal disease conditions, pustules
may be so numerous that the entire planting may have an orange
cast; and if a severely affected blade of grass is pulled through
the fingers, an orange deposit will be left on them. As the pus-
tules age, they turn a brown to black color.
Urediospores of these four rusts are one-celled, thick-walled,
and round to oblong in shape. They are echinulate in all species
except P. cynodontis. Those of P. cynodontis and P. stenotaphri







are cinnamon-brown while those of the other two species are
hyaline to yellow. Teliospores are two-celled and chestnut-brown
in color (6) (Fig. 11).


Fig. 11.-Spores of Puccinia zoysia from Zoysiagrass. Teliospores (t)
and urediospores (u).

OCCURENCE: Rust diseases occur most frequently during
mild to warm, humid weather. Ryegrass and zoysiagrass are
more severely damaged by rust than are St. Augustinegrass and
bermudagrass. Difference in severity also occurs within the
various zoysiagrasses. Freeman (19) reported that Zoysia ja-
ponica, especially the variety Meyer and the Emerald variety
(hybrid between Z. japonica and Z. tenuifolia), are more severe-
ly affected than Z. tenuifolia and Z. matrella. Certain varieties
of ryegrass also show resistance to rust infection.

CONTROL: When available, rust resistant or tolerant va-
rieties of grass should be grown. Rust diseases can be controlled
by the use of fungicides such as sulfur and zineb.

Mushroom Fairy Ring
CAUSE: Fleshy fungi such as Agaricus campestris L. ex
Fr., Chlorophyllum Molybdities (Meyer ex Fr.)
Moss, and Marasimus oreades (Bolt. ex Fr.) Fr.

HOSTS: All commonly cultivated turf grasses.







SYMPTOMS: Usually the first noticeable symptom of a fairy
ring is a circular or semi-circular band of stimulated grass. This
band of grass is only a few inches in width (6 to 12), but the
circular area may be several feet in diameter. The stimulation
of the grass is due to the availability of nutrients resulting from
the decomposition, by the fungus, of organic complexes in the
soil. Grass inside the vigorous area is usually in a state of de-
cline. This decline is thought to result from either: 1, parasitic
action by the fungus; 2, depletion of the nutrients; 3, lack of
moisture due to the impervious mat formed by the fungal my-
celium; 4, a toxic agent produced by the fungus; or 5, a com-
bination of two or more of the preceding (5, 21). The most
characteristic symptom associated with fairy ring is the presence
of mushrooms, which are the fruiting bodies of the causal fun-
gus, in the zone of stimulated grass (Fig. 12).



















Fig. 12.-Mushroom fairy ring on St. Augustinegrass. Note stimulation
of the grass in area of mushrooms.

OCCURRENCE: Fairy rings are most noticeable during the
warm months of the year. The fruiting bodies (mushrooms) of
the causal fungus appear during periods when moisture is
abundant. The fungus can be active, however, without the pres-
ence of mushrooms. Unlike the other turf disorders, the type of
grass grown has little, if any, influence upon the occurrence of
a fairy ring. In addition, once a fairy ring becomes established,
it will persist and increase in diameter each year if left un-
disturbed.







CONTROL: Fairy rings are difficult to control with fungi-
cides, and attempts to do so often meet with only partial success.
The method most commonly used consists of placing a concen-
trated fungicide solution (2 to 3 times normal rate) into holes
punched 4 to 6 inches deep in, and adjacent to, the zone of stim-
ulated grass. Some success has also been obtained by drenching
a fungicide, again 2 or 3 times normal rate, into the soil after
aerifying the area to be treated. The fungicide must be thor-
oughly washed into the soil by irrigating with at least 1 inch of
water. The cadmium and mercurial fungicides used in this man-
ner have provided the highest degree of control (5, 21). How-
ever, because of the increased strength of the fungicidal mixture,
some temporary injury to the grass may occur.
Positive control of fairy rings can be accomplished by either
removing and replacing the soil in the affected area or by fumi-
gation with materials such as formaldehyde and methyl bromide.
These methods are expensive, and, unless the ring is very small,
their use can be justified only on high-maintenance turf areas
such as putting greens.
The declining grass within a fairy ring often will respond to
an increased watering and fertilization program. This method
of overcoming the effects of the fungus is often adequate for
low-maintenance turf areas.


Fig. 13.-Slime mold (Physarum) on St. Augustinegrass.






CAUSE: Primarily Physarum cinereum (Batsch) Pers. and
Fuligo septica (L) Weber.
HOST: All commonly cultivated turf grasses.

SYMPTOMS: In the case of Physarum cinereum, grass blades
are covered with the small, crust-like, light to dark-gray fruiting
bodies of the fungus (Fig. 13). From a distance, the grass ap-
pears to be covered with soot. In the case of Fuligo septica, the
fruiting body is tan to orange and in the form of a glob that
may be up to an inch in diameter. Since these slime molds do
not actively parasitize the grass, they can be readily wiped from
the leaf blades. In addition, the grass tissue under the area on
which they occur will be found to be healthy. They may, how-
ever, damage the grass by exerting a shading effect.

OCCURRENCE: Slime molds occur commonly during warm,
moist weather. Although several species are found on turf-
grasses, the two listed are the most common, with P. cinereum
being the one most frequently encountered. This fungus often
becomes so abundant that large turf areas are affected. Under
such conditions it may be a nuisance because of the abundance
of dark spores that rub off on shoes and clothing.
CONTROL: The fruiting structures can be removed from the
grass blades by brushing with a broom or washing with a gar-
den hose. No other control measures are required.

Seedling Blights
CAUSE: Primarily Pythium spp. and Rhizoctonia spp.
HOSTS: Cynodon dactylon (bermudagrass), Eremochloa
ophiuroides (centipedegrass), Lolium multiflorum
(ryegrass), Paspalum notatum (bahiagrass)
SYMPTOMS: Seedling blights kill the young plants either
before or just after emergence, resulting in a reduced stand.
Post-emergence attacks cause the seedling to collapse and die
soon after emergence.
OCCURRENCE: As the name implies, seedling blights are
a problem on grasses established from seed and are of no con-
cern in vegetative propagation. They are especially damaging
during periods of adverse conditions, such as cool, wet weather.
Improper planting, such as covering the seed too deeply, also
increases seedling blight.






CONTROL: The incidence of seedling death due to attack by
fungi can be reduced in several ways. First, only top quality
seed should be used. Stronger seedlings that are better able to
resist attack are produced by such seed, while old or low quality
seed produce weak seedlings. Pre-emergence damage can be re-
duced by using seed treated with a fungicide such as thiram.
Another method is to drench the area immediately after seeding
with a fungicide such as thiram or one of the organic mercurials.
With either of the above methods, use only fumigated top dress-
ing material. A final method of reducing damage, should the
seedlings begin to die after emergence, is to treat with a fungi-
cide in the regular manner.

Curvularia Fading Out
CAUSE: Curvularia spp.
HOST: All commonly cultivated grasses.

SYMPTOMS AND PATHOGEN MORPHOLOGY: Grass
generally declines and becomes thin and unsightly. Curvularia
can be identified by the dark, multiseptate, curved spores that
occur on the dead leaves. In many cases, only a few curved
spores can be found; however, the center cell in the spore is
usually larger and darker than the others, and this character-
istic distinguishes Curvularia when straight spores predominate
(Fig. 14). Sporulation by Curvularia on dead leaves is often so
abundant that the leaves have a darkened appearance.

OCCURRENCE: Curvularia spp. can be isolated from most
dead and dying warm-season grasses. However, it is difficult
to show that they are the primary cause of the condition ex-
hibited by the grass. They appear to be weak parasites that
invade grass that has been weakened by some other factor such
as another disease, improper cultural conditions and practices,
insect pests, or nematodes.

CONTROL: Most available turf fungicides will control Cur-
vularia spp. However, correction of the primary cause of the
weakened grass is often the better control procedure.

Cercospora Leaf Spot
CAUSE: Cercospora fusimaculans Atk.
HOST: Stenotaphrum secundatum (St. Augustinegrass)








I


VO q


U.


Fig. 14-Spores of Curvularia sp. from bermudagrass. Note curved
nature of some spores and the enlarged middle cell.
SYMPTOMS AND PATHOGEN MORPHOLOGY: Brown
to purple oblong spots that are 1-3 by 0.5-1 mm in size are pres-
ent on the leaf sheath and blades. Young spots are uniformly
colored, but tend to develop a tan center as the disease develops.
Severely affected leaves become chlorotic and eventually die,
leading to the gross symptoms of an overall thin turf. Because
of the similar symptoms, this disease is often confused with
piricularia leaf spot (10).
During moist weather, sporulation of the pathogen may be
so abundant that the spots have a whitish sheen. Spores of C.
fusimaculans are cylindric, hyaline, 2-7 septate, and 33-60/ X
1. 8-31 in size.
OCCURRENCE: This disease occasionally occurs in damag-
ing proportions on St. Augustinegrass. The yellow-green types
are more frequently damaged than the blue-green ones. Warm,
humid weather favors disease development.
CONTROL: Should control of this disease become necessary,
available turf fungicides will provide adequate control.

Smut Diseases
CAUSE: Ustilago affinis Ell. and Ev.
HOST: Stenotaphrum secundatum (St. Augustinegrass)


u







CAUSE: Ustilago cynodontis P. Henn.
HOST: Cynodon dactylon (bermudagrass)

SYMPTOMS AND PATHOGEN MORPHOLOGY: Smut
galls replace the seed in the spike. The infloresence is often dis-
torted. Spores of both fungi are olivaceous and round to oblong.

OCCURRENCE: These diseases are found infrequently in
Florida, but occur with regularity in other areas. When they do
occur, damage is negligible from the standpoint of turf alone.
Seed production, however, is drastically reduced.

CONTROL: Usually not necessary on grass maintained for
turf purposes.

Anthracnose
CAUSE: Colletotrichum graminicola (Ces.) G. W. Wilson

HOSTS: Cynodon dactylon (bermudagrass), Eremochloa
ophiuroides (centipedegrass), Lolium multiflorum
(ryegrass), Paspalum notatum (bahiagrass)

SYMPTOMS AND PATHOGEN MORPHOLOGY: Scab-like
lesions occur on the various plant parts, and in these lesions can
be found fruiting structures of the parasite. These structures
are cushion-like and have prominent black spines setaee) that
can be seen with the aid of a magnifying lens. The conidia are
hyaline, non-septate, spindle-shaped with a tendency to be fal-
cate, and contain two or more prominent oil globules.

OCCURRENCE: Anthracnose occurs during periods of ex-
treme moisture and warm temperatures. It is most damaging
on weakened grass affected by factors such as other pests, low
fertility, etc. The disease is found more frequently on centipede
than on the other warm-season grasses.

CONTROL: Available turf fungicides will provide control;
however, it is usually not necessary on healthy, vigorous grass.

Mosaic
CAUSE: Sugarcane mosaic virus.

HOST: Stenotaphrum secundatum (St. Augustinegrass)







SYMPTOMS: Young leaves turn chlorotic soon after emer-
gence. Upon close examination, a mosaic pattern of dark green
tissues can be noted even though the leaf has an overall yellow
appearance.

OCCURRENCE: Todd (27) first reported the natural occur-
rence of this disease on St. Augustinegrass in Florida in 1964.
Little is known concerning the disease on this grass, but it ap-
pears to be most prevalent on the Roselawn types. It is not
presently a serious disease, but has the potential of being very
destructive. It is the only virus disease thus far noted on one of
the major, warm-season turf grasses.

CONTROL: The Bitter Blue types of St. Augustinegrass
should be used since they seem to exhibit a degree of resistance
to the disease.


ORGANISMS REPORTED ON SOUTHERN
TURFGRASSES

In addition to the parasites covered in the previous section,
many other organisms have been found on the various southern
turfgrasses. A check list of these organisms (excluding nema-
todes) is presented in this section. It has been compiled from
sources such as the books by Sprague (26) and Couch (5),
Index of Plant Diseases in the United States (28), reports in
periodicals such as Phytopathology, Plant Disease Reporter, and
Review of Applied Mycology, and the author's personal findings
as well as those recorded in the Florida Agricultural Experi-
ment Station Herbarium. Due to the diversity of literature,
however, it is impossible to be positive that the list is all in-
clusive. The validity of some of the names used may be open to
conjecture in light of more current mycological literature;
nevertheless, they are listed as reported. In some cases synony-
mous names and the names of the perfect and imperfect stages
are included in parenthesis. In using such a list it should be
kept in mind that in a few cases the role of the organism as a
primary parasite may be questionable, because in some instan-
ces organisms have been reported on various plant parts (in
some cases after death) without subsequent proof that they
were responsible for the disease condition exhibited.
The southern grasses and the organisms that have been
found occurring on them are as follows.







Cynodon dactylon (L.) Pers. (bermudagrass)


Apiospora montagnei Sacc.
Ascochyta graminea (Sacc.)
Sprague and A. G. Johnson
(Diplodina graminea Sacc.)
Cercospora seminalis Ell. and
Ev.
Claviceps sp.
Colletotrichum graminicola
(Ces.) Wils.
Coniosporium rhizophilum
(Preuss) Sace.
Corticium fuciforme (Berk.)
Wakef.
Corticium sasakii (Shirai) T.
Matsu (Rhizoctonia grisea
[Stevenson] Matz)
Curvularia sp.
Dimerosporium erysipheoides
Ell. and Ev.
Diplodina graminea Sacc. (As-
cochyta graminea [Sacc.]
Sprague and A. S. Johnson)
Ephelis mexicana Fr.
Erysiphe graminis DC.
Fusarium nivale (Fr.) Ces.
Gloeosporium bolleyi Sprague
Helminthosporium cynodontis
Marig.
Helminthosporium giganteum
Heald and Wolf
Helminthosporium rostratum
Drechsl.
Helminthosporium spiciferum
(Bain) Nicot
Helminthosporium stenos-
pilum Drechsl.
Helminthosporium trisep-
tatum Drechsl.
Helminthosporium sp.
Leptostromella cynodontis
Sacc.


Marasimus graminis Murrill
Macrophoma sp.
Papularia arundinis (Fr.)
Cda.
Phymatotrichum omnivorum
(Shear) Duggar
Phyllachora cynodontis
(Sacc.) Niessl.
Physoderma graminis (Bus.)
Fisher
Physarum cinereum (Batsch.)
Pers.
Piricularia grisea (Cke.) Sace.
Puccinia cynodontis Lacroix
ex Desm.
Puccinia graminis Pers.
Pyrenochaeta terrestris (Han-
sen) Gorenz, Walker, and
Larson
Pythium aphanidermatum,
(Edson) Fitzpatrick
Pythium debaryanum Hesse
Pythium ultimum Trow.
Pythium sp.
Rhizoctonia grisea (Steven-
son) Matz
Rhizoctonia solani Kuhn
(Thanatephorus cucumeris
[Frank] Donk.)
Sclerospora farloweii Griff.
Sclerotinia homoeocarpa F. T.
Bennett
Sclerotium portoricense F. L.
Stevens
Sclerotium rolfsii Sacc.
Septoria cynodontis Fckl.
Sorosporium syntherismae
(Pk.) Farl.
Striga asiatica (L.) Kuntze
Ustilago cynodontis P. Henn.







Eremochloa ophiuroides (Munro) Hack.
(centipedegrass)


Colletotrichum graminicola
(Ces.) Wils.
Curvularia sp.
Piricularia grisea (Cke.) Sacc.
Rhizoctonia solani Kuhn
(Thanatephorus cucumeris
[Frank] Donk.)


Sclerotinia homoeocarpa F. T.
Bennett
Stachybotrys sp.
Striga asiatica (L.) Kuntze
Stictis helicatricha Ell. and
Ev.


Lolium multiflorum Lam. (ryegrass)


Ascochyta desmazierii Cav.
Cladosporium graminum Pers.
ex Lk.
Claviceps purpurea (Fr.) Tul.
Colletotrichum graminicola
(Ces.) G. W. Wils.
Curvularia sp.
Fusarium acuminatum Ell.
and Ev.
Fusarium culmorum (W. G.
Sm.) Sacc.
Helminthosporium sativum
Pam, King and Bakke (H.
sorkinianum Sacc.)
Helminthosporium siccans
Drechsl.
Helminthosporium vagans
Drechsl.
Heterosporium sp.
Leptosphaeria sp.
Mosaic virus
Ophiobolus graminis Sacc.
Ovularia hordei (Cav.)
Sprague
Phialea temulenta Prill. and
Del.


Phytophthora sp.
Pseudomonas coronafaciens
(Elliot) F. L. Stevens
Physarum cinereum (Batsch)
Pers.
Puccinia coronata Cda.
Puccinia graminis Pers.
Puccinia montanensis Ell.
Pythium aphanidermatum
(Edson) Fitzpatrick
Pythium ultimum Trow.
Rhizoctonia solani Kuhn
(Thanatephorus cucumeris
[Frank] Donk.)
Rhynchosporium orthsporum
Caldwell
Rhynchosporium secalis
(Oud.) J. J. Davis
Sclerotinia homoeocarpa F. T.
Bennett
Scolecotrichum graminis Fckl.
Septoria loligena Sprague
Septoria tritici var. lolicola
Sprague and A. G. Johnson
Titaea sp.
Typhula sp.
Ustilago sp.







Paspalum notatum Fleugge (bahiagrass)


Claviceps paspali F. L. Stevens
and J. G. Hall
Colletotrichum sp.
Curvularia sp.
Fusarium heterosporium Nees.
Helminthosporium victoria
Meehan and Murphy
Helminthosporium sp.
Myriogenospora paspali Atk.


Phyllachora conispora Atk.
Rhizoctonia solani Kuhn
(Thanatephorus cucumeris
[Frank] Donk.)
Sclerotinia homoeocarpa F. T.
Bennett
Stagnospora sp.
Striga asiatica (L.) Kuntze


Stenotaphrum secotndatum (Walt.) Kuntze
(St. Augustinegrass)


Ascochyta graminicola Sacc.
Cercospora fusimaculans Atk.
Curvularia sp.
Helminthosporium ravenelii
Curt. and Berk.
Helminthosporium rostratum
Drechsl.
Helminthosporium sp.
Himantia stellifera J. R.
Johnson
Meliola stenotaphri F. L.
Stevens
Nigrospora sphaerica (Sacc.)
Mason
Piricularia grisea (Cke.) Sacc.


Puccinia stenotaphri Cumm.
Physarum cinereum (Batsch.)
Pers.
Rhizoctonia oryzae Ryker and
Gooch
Rhizoctonia solani Kuhn
(Thanatephorus cucumeris
[Frank] Donk.)
Sclerotinia homoeocarpa F. T.
Bennett
Sugarcane mosaic virus
Uromyces ignoblis (Syd.)
Arth.
Ustilago affinis Ell. and Ev.


Zoysia spp. (zoysiagrass)


Claviceps yanagawensis
Togashi
Curvularia lunata (Wakker)
Boed.
Helminthosporium sp.
Puccinia zoysiae Diet.


Rhizoctonia solani Kuhn
(Thanatephorus cucumeris
[Frank] Donk.)
Sclerotinia homoeocarpa F. T.
Bennett







LITERATURE CITED

1. Bain, D. C. 1962. Sclerotinia blight of bahia and coastal bermuda
grasses. Plant Dis. Reptr. 46: 55-56.
2. Bennett, F. T. 1937. Dollarspot disease of turf and its caussl organism,
Sclerotinia homoeocarpa N. sp. Ann. Appl. Biol. 24: 236-257.
3. Bloom, J. R., and H. B. Couch. 1960. Influence of environment on dis-
eases of turfgrasses. I. Effect of nutrition, pH, and soil moisture on
Rhizoctonia brown patch. Phytopathology 50: 532-535.
4. Couch, H. B., and J. R. Bloom. 1960. Influence of environment on dis-
eases of turfgrasses. II. Effect of nutrition, pH, and soil moisture on
Sclerotinia dollarspot. Phytopathology 50: 761-763.
5. Couch, H. B. 1962. Diseases of turfgrasses. Reinhold Publishing Corp.,
New York. 289 pp.
6. Cummins, G. B. 1956. Host index and morphological characterization of
the grass rusts of the world. Plant Dis. Reptr. Suppl. 237.
7. Dickinson, L. 1930. The effect of air temperature on the pathogenicity
of Rhizoctonia solani parasitizing grasses on putting-green turf. Phy-
topathology 20: 597-608.
8. Drechsler, C. 1923. Some graminicolus species of Helminthosporium: I.
J. Agric. Res. 24: 641-740.
9. Freeman, T. E. 1957. A new Helminthosporium disease of bermuda-
grass. Plant Dis. Reptr. 41: 389-391.
10. Freeman, T. E. 1959. A leaf spot of St. Augustinegrass caused by
Cercospora fusimaculans. Phytopathology 49: 160-161.
11. Freeman, T. E. 1959. Florida isolates of dollarspot fungus stand hot
weather. Fla. Agric. Exp. Sta. Res. Rept. 4(3): 3.
12. Freeman, T. E. 1960. Control dollarspot by fertilization. Fla. Agric.
Exp. Sta. Res. Rept. 5(4): 17.
13. Freeman, T. E. 1960. Effects of temperature on cottony blight of
ryegrass. Phytopath. 50: 570. (Abstr.)
14. Freeman, T. E. 1962. Gray leafspot on St. Augustinegrass. Fla. Agric.
Exp. Sta. Res. Rept. 7(2): 8-9.
15. Freeman, T. E. 1963. Age of ryegrass in relation to damage by
Pythium aphanidermatum. Plant Dis. Reptr. 47: 844.
16. Freeman, T. E. 1964. Helminthosporium diseases of bermudagrass.
Golf Course Reptr. 32(5): 24-26.
17. Freeman, T. E. 1964. Turf disease research. Proc. Univ. Fla. Turf
Management Conf. 12: 142-145.
18. Freeman, T. E. 1964. Influence of nitrogen on severity of Piricularia
grisea infection of St. Augustinegrass. Phytopathology 54: 1187-1189.
19. Freeman, T. E. 1965. Rust of Zoysia spp. in Florida. Plant Dis. Reptr.
49: 382.
20. Freeman, T. E., and G. C. Horn. 1963. Reaction of turfgrasses to at-
tack by Pythium aphanidermatum (Edson) Fitzpatrick. Plant Dis.
Reptr. 47: 425-427.
21. Howard, F. L., J. B. Rowell, and H. L. Keil. 1951. Fungus diseases of
turf grasses. Rhode Island Exp. Sta. Bul. 308.
22. Luttrell, E. S. 1951. A key to species of Helminthosporium reported on
grasses in the United States. Plant Dis. Reptr. Suppl. 201.
23. Malca, I. M., and J. H. Owen. 1957. The gray leaf spot disease of
St. Augustinegrass. Plant Dis. Reptr. 41: 871-875.
24. Monteith, John Jr., and A. S. Dahl. 1932. Turf diseases and their
control. Bul. U. S. Golf Assoc. Green Section 12: 87-187.







25. Pritchett, W. L., and G. C. Horn. 1963. Research on turf fertilization.
Proc. Univ. Fla. Turf Management Conf. 11: 159-163.
26. Sprague, R. 1950. Diseases of cereals and grasses in North America.
Ronald Press, New York. 538 pp.
27. Todd, E. H. 1964. Sugarcane mosaic on St. Augustinegrass in Florida.
Plant Dis. Reptr. 48: 442.
28. U. S. Department of Agric. 1960. Index of plant diseases in the United
States. Agric. Handbook 165. U. S. Government Printing Office,
Washington, D. C. 529 pp.
29. Wells, H. D., and B. P. Robinson. 1954. Cottony blight of ryegrass
caused by Pythium aphanidermatum. Phytopathology 44: 509-510.
(Abstr.)
30. Winstead, N. N., and C. L. McCombs. 1961. Pectinolytic and cellu-
lolytic enzyme production by Pythium aphanidermatum. Phytopath-
ology 51: 207-273.















>'

r
I 1 !




University of Florida Home Page
© 2004 - 2010 University of Florida George A. Smathers Libraries.
All rights reserved.

Acceptable Use, Copyright, and Disclaimer Statement
Last updated October 10, 2010 - - mvs