Proceedings of Scotts Turfgrass Research Conference Volume 2 - Turfgrass Diseases October 1971 Proceedings of Scotts Turfgrass Research Conference Volume 2 - Turfgrass Diseases October 1971 EDITORS Philip M. Halisky Department of Plant Pathology Rutgers University, New Brunswick, New Jersey 08903 Richard T. Bangs William L. O. M. Scott & Sons Company Marysville, Ohio 43040 Schwaderer O. M. Scott & Sons Company • PUBLISHER Marysville, Ohio 43040 Proceedings of Scotts Turfgrass Research Conference Volume 2 — Turfgrass Diseases Copyright © 1971 by the O. M. Scott & Sons Company. Printed in the United States of America. Library of Congress Catalog Card Number; 75-180289 P R E F A CE This volume contains the proceedings of the second Scotts Turfgrass Research Conference. The sessions of this conference w e re devoted to turfgrass disease--their nature, impact and con- trol. Representatives f r om 31 states and Canada joined with the research staff of O. M. Scott & Sons Company at Marysville, Ohio, on June 16-17, 1969. Seven formal papers were presented; each followed by a question and answer period. special session was devoted to a general discussion of problems related to turfgrass pathology. In addition, a By far the largest number of turfgrass diseases are in- cited by members of an insidious horde of pathogenic fungi. How- ever, one of the papers presented here describes St. Augustine Decline, a new virus disease of lawngrass. Keeping turf healthy is a challenging, major responsibility. The contents of this volume bear testimony of the complexity and variability encountered among turfgrass pathogen. An evaluation of the biology and control of turfgrass diseases is both timely and worthwhile. We trust the information presented here will prove interesting and useful to all those concerned with growing high- quality, disease-free turf. Philip M. Halisky Richard T. Bangs William L. Schwaderer October 1971 Editors C O N T E N TS P r e f a ce Participants Environmental factors influencing turfgrass diseases JACK A LT M AN Mode of action of the disease organism R A Y M O ND J. LUKENS Diseases of warm-season turfgrasses T. E D W A RD F R E E M EN T u r f g r a ss diseases in western Canada JACK B. LE BEAU St. Augustine Decline (SAD) - -a new lawngrass disease R O B E RT W. T O L ER i ii v ii 1 13 31 43 55 Special discussion session on turfgrass disease problems . .. 69 Guttation fluid and root tip degeneration in turfgrasses R O B E RT M. ENDO Extracellular ribonuclease production by fungi B I LL B E R K E N K A MP 85 95 j P A R T I C I P A N TS JACK A L T M AN Department of Botany and Plant Pathology- Colorado State University- F o rt Collins, Colorado, 80521 DICK BANGS Government and Industry Relations O. M. Scott and Sons Company M a r y s v i l l e, Ohio, 43040 D A LE BENEDICT, Director Consumer Division O. M. Scott and Sons Company Marysville, Ohio, 43040 B I LL B E R K E N K A MP Research Branch Canada Department of Agriculture Lacombe, Alberta, Canada GEORGE H. BRIDGMON, Head Department of Plant Pathology and Horticulture University of Wyoming L a r a m i e, Wyoming, 82070 GUY E. BROWN Department of Plant Pathology Pennsylvania State University University Park, Pennsylvania, 16802 W I L L I AM F. C A M P B E LL Department of Plant Science Utah State University Logan, Utah, 84321 R O B E RT C. C A R L S T R OM Department of Botany and Microbiology Montana State University Bozeman, Montana, 59715 JAMES L. D A LE Department of Plant Pathology University of Arkansas Fayetteville, Arkansas, 72701 JOHN H. DUNN Department of Horticulture University of Missouri Columbia, Missouri, 65201 EDWARD S. E L L I O TT Division of Plant Sciences West Virginia University Morgantown, West Virginia, 26506 R O B E RT M. ENDO Department of Plant Pathology University of California Riverside, California, 92507 H A R RY S. FENWICK Department of Plant Sciences University of Idaho Moscow, Idaho, 83843 T. EDWARD F R E E M AN Department of Plant Pathology University of Florida Gainesville, Florida, 32601 JIM GABERT Bio-Chemical Research O. M. Scott and Sons Company M a r y s v i l l e, Ohio, 43040 M A R T IN B. HARRISON Cornell Nematology Laboratory State University Farmingdale, New York, 11735 GORDON E. HOLCOMB Department of Botany and Plant Pathology Louisiana State University Baton Rouge, Louisiana, 70803 N O EL JACKSON Department of Plant Pathology and Entomology University of Rhode Island Kingston, Rhode Island, 02881 JACK B. LEBEAU, Head Plant Pathology Section Canada Agriculture Research Station Lethbridge, Alberta, Canada L Y LE E. L I T T L E F I E LD Department of Plant and Soil Sciences University of Maine Orono, Maine, 04473 EDWARD H. L L O Y D, JR. Department of Plant Pathology North Dakota State University F a r g o, North Dakota, 58102 JOHN LONG, Director Bio-Chemical Research O. M. Scott and Sons Company Marysville, Ohio, 43040 RAYMOND J. LUKENS Connecticut Agricultural Experiment Station Post Office Box 1106 New Haven, Connecticut, 06504 JOHN E. M A X F I E LD Department of Plant, Water and Soil Sciences University of Nevada Reno, Nevada, 89503 L O R NE A. McFADDEN Department of Botany University of New Hampshire Durham, New Hampshire, 03 824 R O N A LD R. MUSE Department of Plant Pathology Ohio Agricultural Resource and Development Center Wooster, Ohio, 44691 R O B E RT E. P A R T Y KA Department of Plant Pathology Ohio State University Columbus, Ohio, 43210 N O R M AN E. P E L L E TT Department of Plant and Soil Sciences University of Vermont Burlington, Vermont, 05401 JOSEPH L. PETERSON Department of Plant Pathology Rutgers University N ew Brunswick, New Jersey, 08903 HOWARD E. REED Department of Agricultural Biology University of Tennessee Knoxville, Tennessee, 37901 M Y R ON SASSER Department of Plant Science University of Delaware Newark, Delaware, 19711 DONALD H. SCOTT Department of Botany and Plant Pathology Purdue University Lafayette, Indiana, 47 907 RAYMOND L. SELF Department of Plant Pathology Auburn University Mobile, Alabama, 36608 E M R OY L. SHANNON Department of Botany and Entomology N ew Mexico State University L as Cruces, New Mexico, 88001 JIM SIMMONS, Director Product Development O. M. Scott and Sons Company Marysville, Ohio, 43040 W I L L I AM S T O T T L E M Y ER Bio-Chemical Research O. M. Scott and Sons Company M a ry sville, Ohio, 43040 ROBERT W. T O L ER Department of Plant Sciences Texas A & M University College Station, Texas, 77843 D A L L AS F. WADSWORTH Department of Botany and Plant Pathology Oklahoma State University Stillwater, Oklahoma, 74074 JOHN L. WEIHING Department of Plant Pathology University of Nebraska Lincoln, Nebraska, 68503 A L B E RT S. WILLIAMS Department of Plant Pathology University of Kentucky Lexington, Kentucky, 40506 L A R RY WITTENBROOK Chemical Research O. M. Scott and Sons Company M a r y s v i l l e, Ohio, 43040 G A Y LE L. WORF Department of Plant Pathology University of Wisconsin Madison, Wisconsin, 53706 E N V I R O N M E N T AL FACTORS I N F L U E N C I NG TURFGRASS DISEASES Jack Altman Department of Botany and Plant Pathology Colorado State University Fort Collins, Colorado, 80521 Almost all turf-forming grasses are subject to seri- ous diseases, particularly when maintained under close clip- ping. A knowledge of the characteristics of these diseases, and of the best methods for their prevention and control is important in successful turf management (Musser, 19 50). Environmental factors that produce morbid conditions in growth and development of turf cause disorders referred to as physiogenic diseases. Such diseases are incited by envi- ronmental stress and include: extremes in soil moisture con- tent; unfavorable atmospheric and soil microclimate, and chemical or mechanical injuries. Environmental factors that produce physiogenic disease also create conditions that p r e- dispose host plants to pathogenic microorganisms. In all in- stances an interrelationship exists between the environment, the pathogen, the host and disease development. Environmental Conditions Favoring Fungus Diseases Climate and weather have a great influence on disease. Climate determines whether a pathogen can flourish or per- sist under normal conditions in a given locality. Micro-climate determines whether a host-pathogen relationship will de- velop into disease. A ll stages in the life cycle of a pathogen take place within fixed temperature ranges. Temperature appears to be the limiting factor in the behavior of some diseases. Humidity appropriate to the r e- quirements of a pathogen is necessary for all its active stages. Low humidity ordinarily retards or prevents the development of a pathogen. Few plant diseases are damaging under condi- tions of consistently low humidity. Within limits, an organism's need for moisture varies with the temperature (Nat. Acad. Sci., 1968). Moisture The fungi that cause turfgrass diseases need liberal quantities of moisture to germinate spores and sclerotia, and to keep mycelial strands growing actively. The latter are very delicate and cannot withstand drying out. Satu- rated soils and high air humidity create ideal conditions for their rapid development. Poor drainage, heavy watering and excessive rains that keep soils waterlogged for long periods increase the chances of fungus infection. Humid air and heavy dews keep the foliage wet and also favor fungus growth. Pockets of stagnant air that occur where there is poor air drainage contribute to disease development. In this regard, landscape planning is important (Musser, 19 50). Excessive moisture produces lush grass and a more favorable m i c r o- climate for disease development. An added factor in water- logged soil is the inability of the grass to recover f r om in- jury because of low nutrient availability and shallow, r e- stricted root-system development. Soil Moisture Low soil moisture increases accumulation of toxic ions, such as manganese and boron, causing tissue damage. It can also cause stomatal closure by creating a water stress f r om the soil system through and including the plant system. High soil moisture leads to a lack of oxygen in soils. Over long periods, this soil moisture can make plants so succulent they become particularly sensitive to invasion by certain pathogens (Nat. Acad. Sci., 1968). Soil moisture af- fects both soil-borne and air-borne pathogens. High moisture can lead to root suffocation and injury through reduc- tion in oxygen content. Drying of soil is generally accom- panied by reduced pathogen activity, because most fungi go into resting stages as f r ee water disappears f r om the soil. Temperatures drop further and faster in a dry soil during the winter; therefore, winter kill is prevalent in dry winters. Temperature Excessive moisture alone will not cause fungus at- It must be accompanied by temperatures that are tacks. favorable for development of the disease-producing organisms. Like other plants, each fungus has an optimum temperature for growth. The brown patch organism, Rhizoctonia, grows best at the relatively high temperatures of midsummer. Snow mold, Fusarium nivale, represents the other extreme. It causes the most severe damage in the late winter and early spring when temperatures are close to the freezing point. Diseases, such as dollar spot and leaf spot, develop over a much wider temperature range than brown patch or snow mold, but they are apt to be more severe during cool, wet periods in the late spring and early fall. Soil Temperature Temperature affects the rate of moisture absorption. High soil temperature can induce disorders such as basal lesions, soil-cracking and root damage. The freezing of soil can directly kill the roots of many tropical and subtropical plants. Persistent and unseasonably low soil temperatures usually stunt plants. Soil temperature may affect disease either by its effect on the host or on the soil-borne pathogen. Cold soils affect mobility of nutrient elements and may cause temporary chlorosis. Therefore, soil temperature is closely connected with abiotic diseases. Soil Texture Soil structure can also affect disease development. Turf grown in heavy, compact and poorly-drained soils usu- ally shows greater losses f r om Pythium and Fusarium than does turf grown in well-drained soil (Altman, 19 66). Soil type may influence amounts of CO 2 in the soil, a change in the balance of microorganisms, lack of available nutrients or other factors. Light The diurnal light rhythm affects the periodicity of spore release, partly because of its direct effect and partly because of changes in temperature, humidity and air move- ment that accompany changes in light intensity at dawn and dusk. The shade microenvironment is also very important in disease development. Shade adversely alters the turf- grass microenvironment. It is the more favorable microenvironment of shaded conditions plus the lack of disease resistance that results in the severe disease problem. The microenvironment of shade which encourages disease activity includes: (1) High- er relative humidity; (2) extended dew periods; (3) reduced light intensities that produce a more succulent growth, and (4) low light intensities resulting in lowered respiration rates and, consequently, lower energy levels in the host which restricts cell wall development and maturation. Thus, thinner cuticles and underdeveloped cell walls are produced. The juvenescent state of the host is prolonged and physical mechanical barriers to pathogen penetration are reduced. Low light intensities do not affect stomatal opening. It seems reasonable to assume that 1,000 ft candles ( 10% of full sunlight) would be sufficient to open stomates since Zelitch ( 1961) has shown that only 250 ft candles of light in- tensity will achieve maximum stomatal opening in tobacco. Therefore, the shade microenvironment that affects the host, such as lower sugar transport under low light intensities, thinner cuticles and a more intense hydrosphere above and around the stomata, are more relevant in the disease syn- drome than stomatal opening. Helminthosporium vagans is favored by low light intensities. Lukens (19 68) r e f e rs to this pathogen as the low sugar disease pathogen since it is more severe when sugar levels in the host are curtailed. Soil pH No single characteristic of soil is more significant than its pH. Acidity is one reason for the thatching of turf, although not the sole cause (Musser, 1950). Grasses renew a large part of their root system each year. When soils are not too acid, the old roots slough off and decay due to indig- enous soil bacteria and fungi. Such decay tends to reduce thatch. However, in acid soils the dead roots, stems and leaves accumulate forming a thatch, due to lack of m i c r o- bial activity. This thatch impedes the penetration of air and water and is largely responsible for the formation of local- ized dry spots in turf. It also creates an excellent medium for pathogenic fungi. Helminthosporium thrives on dead organic matter (Altman, 19 65). The pH affects the number of earthworms, bacteria and fungi present in the soil. While fungi develop over a wide pH range, they are most prevalent under acid condi- tions (pH 4-5). Many of them are desirable and necessary because they are responsible for the initial decay of organ- ic matter, but certain groups are disease-producing. The dollar spot fungus and brown patch fungus, for example, are stimulated by excessive acidity and are checked when acid- ity is controlled by proper liming in certain areas of the country. Microbial competitors that keep the disease-producing fungi in check are more active when soil reaction is near neutral. Soil reactions below pH 6.0 tend to favor turf dis- ease fungi. It is often practicable to reduce the severity of disease outbreaks in such turf by light dressings of hydrated lime every 3 or 4 weeks during the time when disease is like- ly to occur. This practice is safe when soil reaction stays below pH 7.0, but will cause iron chlorosis and trace-element deficiencies when the reaction is pH 7.5 and above. Lime should not be used in the semi-arid sections. Thatch A heavy mat of spongy turf provides ideal conditions It always for the growth of disease-producing organisms. contains large amounts of dead leaves and stems which ab- sorb moisture readily and remain damp for long periods. This condition is favorable for the growth of fungi and in- creases the difficulty of obtaining good control with fungi- cides. Where turf is heavily thatched, it is often necessary to use excessive water to obtain adequate penetration with a fungicide. Normal fungicide treatments would be too dilute to be effective. To achieve effective disease control, heavier rates of chemicals are required, but these may discolor the turf. Winter Injury The most important types of winter injury to turf are desiccation (dehydration) and freezing-out. Desiccation is common in regions where there is limited rainfall and soil moisture is low during the winter months. It is aggravated by dry, cold winds. The dry soil and dry air draw so much moisture out of the dormant or semi-dormant grass plants that they shrivel and die. Injury of this type occurs on both greens and fairways and is most severe on knolls and other exposed areas that are blown f r ee of snow. The damaged grass first has a dull-brown color which may bleach to gray- ish-white by spring. The best method of avoiding winter in- jury by desiccation is to moisten the soil throughly to a depth of 5 to 6 inches late in the fall and again in winter if rain or snow fall are scarce. It is common practice in northern dry areas to place tree branches and brush on windswept greens, to collect and hold snow during the winter. In Colorado, particularly on the eastern slope of the In ad- Rockies, many golf courses are open for winter play. dition to winter watering of greens, the use of various acrylic turf colorants is increasing. These colorants are composed of polyvinyl acrylics containing a green dye. Treated greens are less prone to desiccation and disease. Less snow mold occurred on 50 greens in continuous play during 1967 and 1968 that had been treated with turf colorant and fungicide as com- pared to greens treated only with fungicide. Greens treated with the combination were less brittle and had better ball r e- tention qualities than non-treated greens. Non-treated aprons w e re infected with Fusarium snow mold in March and A p r il of each year. Winter injury of turf due to freezing-out, as distinct f r om desiccation, is caused primarily by poor surface or sub- surface drainage. It is often aggravated by the use of poorly adapted grasses and by management practices that weaken the turf and make it less tolerant to adverse conditions. Poor sur- face drainage causes water to collect in depressions. The f r o- zen soil prevents it f r om draining out, even when its physical condition is satisfactory. Acccumulations of snow and ice may produce the same result by damming back the water. The alter- nate freezing and thawing of such pools causes winter killing of the grass. A good program of turf maintenance during the growing season often prevents or reduces winter killing. The use of grasses that are cold hardy or adapted to the conditions under which they must be grown in an important factor. For example, when Kentucky bluegrass is destroyed, because of saturated soils on spring seepage or ponded areas, Colonial or creeping bentgrasses should be used. The bents are more tolerant of wet soils and will survive longer under such con- ditions. The various kinds of bents differ in cold tolerance. Some of the newer vegetative strains, such as Toronto and Old Orchard, are more resistant than other types. Seaside is very susceptible to freezing injury. Sound fall fertilization will help reduce winter injury provided nitrogen is not applied after mid-September. One pound of nitrogen per 1,000 sq ft will provide a tough grass that is less susceptible to winter damage. Reduced watering also helps to harden the turf and put it in good condition for winter; however, many turf areas will require late fall and winter watering, particularly in arid areas similar to east- ern Colorado. Summer Injury Turf is subject to many types of injury during the grow- It occurs as irregular areas of discolored turf on ing season that may be mistaken for disease attacks. These may be due to unfavorable weather and soil conditions or to inadequate maintenance. Scald is a common trouble of this kind. poorly drained soils or in depressions on greens during per- iods of excessive rainfall or when the grass is watered heav- ily in hot weather. Thorough aeration of the damaged areas to hasten drying and permit air to get down to the roots is a temporary remedy and may save some of the turf. The only permanent remedy is to provide adequate surface and subsurface drainage. The use of lateral stone drains 4-6 in. wide and 12-18 in. deep will help. Localized dry spots may develop on greens and fairways where the turf suffers f r om lack of moisture, even when i r r i- gated regularly. This condition may be caused by excessive compaction or because of thatch accumulation. Localized dry spots should be thoroughly aerated and lime and fertilizer added where needed to hasten organic matter decay. They should be watered regularly until normal soil moisture has been restored. In regions subject to high temperatures and hot dry winds, turf may be seriously injured because of wilting. This type of injury takes place when the grass roots cannot absorb moisture f r om the soil as fast as it is lost f r om the leaves. The first indications are the development of a dull, bluish-green color and severe footprinting on the turf. Wilted turf recovers very slowly, and in serious cases the leaves may shrivel and die. Injury can be avoided by frequent, light sprinkling ( s y r- inging) of turf, two to three times daily, to provide readily available moisture to reduce turf and soil temperatures. This type of watering cannot replace normal irrigation to r e- plenish the moisture supply throughout the root zone. Turf may lose its vigor and thin out because of t r e e- root competition. This competition can be eliminated by dit- ching between the putting green and trees that are sources of trouble, or by the periodic use of a deep running single- blade root cutter. Turf of low vigor, resulting f r om one or more factors that induce summer injuries, is usually predisposed to red thread and dollar spot. Rhizoctonia brown patch and Pythium grease spot also occur as high temperature diseases in the U. S. References Cited Altman, J. 1965. Nitrogen in relation to turf diseases. Golf Course Reptr. May issue, pp. 16-30. Altman, J. 19 66. Diseases of bluegrass with particular reference to Colorado. Colorado Agr. Expt. Sta. Tech. Bull. 9 3, 11pp. Lukens, R. J. 1968. Low sugar disease "melts-outM bluegrass. Turfgrass Times 3(5) : 1-3. Musser, H. B. 19 50. Turf management. McGraw-Hill Book Co., New York. 356 pp. National Academy of Sciences. 1968. Plant disease de- velopment and control. Publ. No. 159 6. 205 pp. Zelitch, I. 19 61. Biochemical control of stomatal open- ings in leaves. Proc. Natl. Acad. Sci. U. S. 47:1423. DISCUSSION PERIOD I was intrigued with your comments about Dr. Wadsworth: the Pythium blight outbreak on a golf course that was 11,000 feet high. Do you happen to recall what the average temper- atures were about this time, and whether or not this was on mature grass or newly-seeded grass? It was on newly-seeded Penncross. The tem- Dr. Altman: peratures during the day were between 50-60oF and at night around 32oF. Dr. Wadsworth: Would you normally expect this type of out- break with those temperatures in that area? Dr. Altman: No, not with Pythium blight. However, what is normal for disease in certain areas of the country is not nor- mal with regard to Colorado. Brown patch normally occurs in warm, moist periods, but I have noticed it on our grass in Colorado in late September and October when everything is dry. It may be that there is some selecting out of the Pyth- ium and Rhizoctonia strains that don!t react the way they normally do under much warmer temperatures and higher humidities. However, the humidity in this area was pretty high, and the soil was constantly moist. The soil was a silt loam that came out of a lake bottom. atures were unusual for Pythium development. I agree that the temper- Dr. Wadsworth: We've seen some Pythium outbreaks at rather low temperatures in the Oklahoma area but this has been after we have had periods of high humidity and warm temper- atures. Once the inoculum level was established, then all that was needed was a period of relatively high moisture for several days. I know that the weather was not warm prior to Dr. Altman: this Pythium occurrence. We are in the process of under- going a tremendous outbreak of Helminthosporium vagans and Fusarium roseum in Colorado. we had quite a bit of moisture and very cool temperatures. Grass began to go down rather rapidly toward the latter part of May. In the last two weeks we've been getting reports of disease from many areas of the eastern slope of Colorado. When cultured, almost all the samples are Fusarium roseum and it's one of the few times that I've noticed such a high In the early part of May In these instances, perhaps we incidence of only Fusarium, had the right moisture and temperature in early May to build up inoculum l e v e ls of Fusarium. T h e se conditions a re the same as those that occurred p r i or to the Pythium outbreak. M r. Benedict: You commented on the various f e r r o us sulfates used on M e r i on under high temperatures, causing the turf to turn black. What was the cause of that? How long did this last and what was the final result of this treatment? Dr. Altman: This black condition p e r s i s t ed f or w e ll over a month after application. A ll the leaf surfaces of the grass which had been treated, curled and seemed to be burned o^f; it just stood still. The grass r e c o v e r ed after s e v e r al w a t e r- ings but we w e re without any blades of grass in this area f or at least a month, and in some spots up to six weeks. Mr . B e n e d i c t: Do you expect any v a r i e t i al d i f f e r e n c es to this effect ? Dr. Altman: in this one instance. I don't know. It just happened to be a ll M e r i on Dr. C a r l s t r o m: What w e re the symptoms of the Helmintho- sporium you a re seeing this y e a r? Dr. Altman: W e ' re getting some crown killing and also some long, purple lesions with dead centers. Also, f or the f i r st t i m e , w e ' re getting a tremendous amount of melting-out. Dr. C a r l s t r o m: Did you see any P l e o s p o ra in conjunction with Helminthosporium ? Dr. Altman: No. Dr. C a r l s t r o m: We saw this in Oregon two y e a rs ago. Dr. Altman: In culture we a re getting pure isolates of H e l- minthosporium. No p e r f e ct stage with the Fusarium, only Fusarium roseum and nothing else. You can find spores only on the t i l l e rs of the grass. Dr. C a r l s t r o m: A re you finding any Curvularia in conjun- ction with the Helminthosporium? Dr. Altman: No, this is one that I have been considering for a long time. Some researchers suggest that Curvularia may be an immature Helminthosporium which occasionally pro- duces a bent spore. I haven't seen any in our area. Dr. Carlstrom: What were the conditions conducive to Helminthosporium coming on? What were the weather con- ditions ? Dr. Altman: Temperatures between 60 and 80 degrees and high humidity promotes the disease. For the past 2 to 3 weeks our weather has been moist and cloudy with very little sunshine. Dr. Carlstrom: Was it following a dry period when you had the increasing moisture? Dr. Altman: Yes, we had probably a month-long dry period and then we had moisture. Dr. Weihing: You mentioned that you get Helminthosporium vagans in your isolations. Do you ever pick up Helmintho- sporium sativum? This is our common one and we rarely get H. vagans. Dr. Altman: Yes, we get H. sativum but I would say approxi- mately 80% of the turf samples are Helminthosporium vagans. Dr. Weihing: Do any of those samples come f r om the more eastern locations? Dr. Altman: They are coming f r om the Denver and Colorado Springs areas. I am interested in knowing whether you would be Dr. Worf: aware of a definitive study that concerns the breakdown of thatch and how this might be related to associated organisms, particularly bacteria and actinomycetes. Dr. Altman: I think they are important in the breakdown of the cellulose material. The bacteria can take over after the cellulose is broken down. You might build up some thatch, in the absence of fungi, particularly if you have a nitrogen-defi- cient turf. Furthermore, if you are using a fungicide for disease control, it's not only killing the pathogens, but also the fungal saprophytes. Here again, there is the possibility of a thatch build-up. I've been comparing clipping removal, versus no removal, of Merion in soil that was in agricultural production for the last 30 years. After five years, there was absolutely no difference in the thatch accumulation. The unique thing about this soil is its high microbial activity. I have tried the same thing on home lawns where excavated material has been used as soil, and for the first four or five years you do get a tremendous build-up of thatch. older lawns when turf is being replaced, this excavated soil becomes modified. and the thatch doesn't seem to accumulate quite as rapidly. But on farm soil, where I have about 8,000 sq ft of Merion, I have not been able to see any difference. It has a little more microbial activity In the In our observations, the removal of clippings has Dr. Worf: very little influence on the development of thatch. With respect to the thatch decomposition, would we be reason- ably safe in assuming that there is a broad spectrum of fungi involved in the initial breakdown process? Many of our fun- gicides are rather specific in the spectrum within which they work. Dr. Altman; Yes, there would be. For example, you would find Tricodermas that are not affected by some of the fun- gicides. Green and white Tricodermas, capable of breaking down this material, are present. Although I indicated that it's possible for the fungicide to restrict fungal activity, in- cluding saprophytic activity, I think there are ample numbers of fungi that are not inhibited and can continue to break down cellulose. MODE OF ACTION OF THE DISEASE ORGANISM Raymond J. Lukens Plant Pathologist Connecticut Agricultural Experiment Station New Haven, Connecticut, 06504 Recent contributions to the study of turf pathogens have been substantial. Four processes have been partly described: (a) a r r i v al of the pathogen at the site of infection, (b) penetra- tion of the grass, (c) growth in grass tissue, and (d) build-up of inoculum for an epidemic of disease. In addition to what is know, areas of little knowledge also will be emphasized. An understanding of the mechanisms by which pathogens cause diseases is necessary in order to devise more effective mea- sures f or control. A r r i v al of the Pathogen at Infection Site When disease breaks out in an area, the pathogen is us- ually not freshly introduced, but is already established. In a new lawn, the source of pathogen is infected soil, sod or seed. Once the disease breaks out, infected clippings can be distri- buted by foot, mower or other equipment to uninfected areas of turf. With rust diseases, the fungus is carried in the air. Turf is a unique crop, and its uniqueness makes it easy f or the pathogen to travel to the site of infection. The plants are arranged in a close compact carpet of thickness three- sixteenth of an inch in putting greens to two inches or more in lawns. The entire crop is wetted daily with dew because the vertical arrangement of leaves provides no canopy to prevent the formation of dew on other parts of the plant. Also, the v e r- tical fibrous structure of the carpet is conducive to formation of large amounts of dew. Air-borne Inoculum The common air-borne pathogens are those that cause rust and powdery mildew. Others whose spores may travel by air are the leaf spotting and blighting fungi- -Helminthospor- ium, Colletotrichum, Cercospora and Fusarium, Aeciospores of rust pathogens are carried long distances by air f r om the alternate host to leaves of grass. Urediospores produced on grass are air-borne also. Conidia of the powdery mildew path- ogens are carried by breezes or propelled by rotary mowers and settle on leaves of grass. Stripe smut disease produces a black cloud of chlamdospores which, when propelled by rot- ary mowers, drifts into the house and is a problem for home- owners. We have trapped conidia of Helminthosporium from air one foot above the turf. Because spores of Helminthosporium are large, compared with those of mildew and rust pathogens, the pathogen may travel short distances in the air down-wind f r om the disease site. Conidia of Fusarium nivale are blown by wind from the source of production to new infection centers (Couch, 1962). Spores are discharged into the air f r om infected turf when it is dry. Thus, transport of air-borne spores is r e- stricted to clear days f r om midmorning to early evening when the turf is f r ee f r om dew. Moisture on diseased leaves retain the spores and prevents them from becoming air-borne. We do not know if spores borne in moisture can become air-borne upon drying. If only spores that are formed without f r ee mois- ture become air-borne, spore production and transport will have to be accomplished during the same day. This information is critical in devising a proper schedule for applying f o l i a r - p r o- tecting fungicides. Hyphae of Fusarium, Sclerotinia, Helminthosporium, Pyth- ium, Rhizoctonia and Colletotrichum grow out f r om diseased tis- sue when the tissue is moist. During epidemics, it is common to find hyphae growing f r om leaf to leaf on dew covered grass. The extensions of hyphae into the air between leaves may be consid- ered a mode of air-borne inoculum over minute distances. Water-borne Inoculum Water contributes to the transport of inoculum in two ways: ( 1) spores, hyphae and sclerotia are carried to the host by flow and splashing rain drops; and (2) mycelium is encouraged to grow in water films, drops of dew and gutta- tion droplets on the host to uninfected sites. Water-borne inoculum is a major means of transport for turf pathogens. Spores of Helminthosporium, Colletotrichum, Cerco- spora and Fusarium may be splashed f r om the source to uninfected turf. The f o r ce of a rain drop, the distance of travel and the importance of inoculum traveling in splash- ing drops of water are not known. Such information may be important in choosing the size and speed of water droplets when irrigating turf. Fungi grow and move in a water environment on sod. Zoospores of Pythium aphanidermatum swim in films of water to uninfected turf to cause grease spot disease (Kraft and Endo, 19 66). Rhizoctonia solani grows saprophytically in moisture on turf. Drops of guttated water at the ends of cut blades are important in brown patch disease (Rowell, 19 51). Wet turf is important for mycelium of Helmintho- sporium vagans to invade the crowns of bluegrass in spring (Couch, 1962). The requirement of soggy turf for snow mold diseases is indicative of the necessity of a water film for the pathogen to reach the grass. Refuse-borne Inoculum' The distribution of contaminated clippings and soil over turf by foot or implement occurs when sanitation procedures become lax. Both Pythium blight and melting-out diseases have appeared in streaks on putting green turf where small amounts of clippings have been allowed to dribble from the grass catcher or mower when golf course greens were groomed. Mowers may carry inoculum from one green to another. On several occasions, melting-out disease has been restricted to greens that were mowed with the same mower. P e n e t r a t i on of the G r a ss Fungi a re r e s t r i c t ed to p a r t i c u l ar s i t es of e n t ry and gain e n t r a n ce by c e r t a in p h y s i c al and c h e m i c al m e a n s. R o w- e ll ( 19 51) h as shown that R h i z o c t o n ia solani e n t e rs l e a v es of b e n t g r a ss through the cut ends when the g r a ss is clipped. U n d i p p ed g r a ss i n o c u l a t ed with hyphal f r a g m e n ts did not s u c- c u mb to d i s e a s e. Couch and B e d f o rd ( 1966) have r e p o r t ed that F u s a r i um r o s e um can invade t u rf g r a ss through the cut ends of l e a v e s. D i s e a se has been o b s e r v ed to p r o g r e ss f r om the cut end of b l u e g r a ss c h a m b er and dusted with s p o r es of C u r v u l a r ia spp. T he f a ct that wounds f r om mowing can s e r ve as s i t es of e n t ry f or path- ogens e m p h a s i z es the need f or s h a rp m o w e rs to avoid e n l a r g ed s h r e d d ed wounds of g r a ss l e a v es that w e re p l a c ed in a m o i st l e a v e s. l e a v es through the s t o m a ta (Couch, 1962; M o w e r, F u s a r i um n i v a l e, C o r t i c i um f u c i f o r me (the c a u se of r ed t h r e ad d i s e a s e ), H e l m i n t h o s p o r i um vagans and H. sativum can e n t e r g r a ss 1961). P r e s u m a b l y, m o st fungi c a p a b le of growing a p p r e s s o r ia can, by c h a n c e, p e n e t r a te the l e af by way of the s t o m a t a. the p r o c e s s, the hyphae f r om g e r m i n a t i ng conidia or m y c e l i um f o rm a pad or a p p r e s s o r i um which p r e s s es a g a i n st a s t o m a te and i n s e r ts a peg through the p o r e. Once i n s i de of the s t o ma - t al cavity, the fungus g r o ws hyphae of n o r m al width. A c t i v i ty of H e l m i n t h o s p o r i um is r e s t r i c t ed to the s t o m a t al cavity with only a few p a r e n c h y ma c e l ls being invaded ( M o w e r, 19 61). With H e l m i n t h o s p o r i u m, e n t ry into b l u e g r a ss through the s t o- m a ta is a m i n or m e c h a n i sm f or d i s e a se initiation. In D i r e ct p e n e t r a t i on of c u t i c le and e p i d e r m al l a y er of c e l ls with the aid of the a p p r e s s o r i um and i n f e c t i on peg is a c o m m on m e c h a n i sm of m a ny t u rf pathogens. Notably among t h e se a re H e l m i n t h o s p o r i u m, r u st fungi, E r y s i p he g r a m i n is and R h y n c h o s p o r i um s e c a l is (the c a u se of s c a l d ). In the p r o c e s s, a p p r e s o r ia f o r m ed at the t e r m i n a ls of g e rm tubes and hyphae, p r e ss a g a i n st the c u t i c le and i n s e r ts pegs through the waxy c u t i c le and e p i d e r m al c e l l s. With H e l m i n- t h o s p o r i u m, the pegs go b e t w e en the e p i d e r m al c e l l s, and with E r y s i p he g r a m i n is the peg p e n e t r a t es into the e p i d e r- mal cells (Mower, 1961; Couch, 1962). Zoospores of Pyth- ium aphanidermatum f o rm appressoria and penetrate roots of bentgrass by means of penetration pegs (Kraft et. al, 1967). The process of penetration requires moisture and nut- trients and may be aided by extracellular enzymes of the pathogen. Conidia of Erysiphe graminis require humidity approaching saturation but not f r ee water to germinate and make ingress. Nutrients f r om the host seem to be required because the presence of a grass leaf stimulates spore g e r- mination and appressorial formation. Humidity and f r ee moisture are required for the penetration process of most pathogens. With Helminthosporium vagans, the process takes place in 18 hours and f r ee moisture is required (Mower, 1961; Lukens, 1970). Nutrients f r om guttated water stimu- late spore germination and appressorial development of H. sorokinianum and Curvularia spp. (Endo and Amacher, 1964; Healy and Britton, 1968). The active ingredient in the guttated water is glutamine, a transient nutrient pro- duced by turf in large amounts following nitrogenous f e r t- ilization of the grass (Curtis, 1944). The amount of guttation water increases with increase in water content of the soil. Thus, both soil fertility and soil moisture can play a dir- ect role in the effectiveness of pathogenic fungi attacking turf grasses. The addition of glycine to spore suspensions of Helminthosporium vagans increases the number of leaf spots produced on inoculated bluegrass leaves. Most fungi c a r ry nutrients in spores and other dormant structures, however, a supplement of certain nitrogenous materials f r om the host may encourage these fungi to penetrate the host. Pathogens that macerate host tissue do so through act- ivity of extracellular enzymes which degrade the cement between cells of host tissue. Several pectinases and cellu- lases have been found in bentgrass blighted with Pythium ultimum (Moore, 1965). The appressorial peg may pene- trate, in part, by means of enzymic degradation of sub- stances between epidermal cells. Helminthosporium vagans produces pectinases in vitro in the absence of glucose (Patil, unpublished data). Glucose inhibits synthesis of the en- zymes and protects bluegrass against invasion by H. vagans Indeed, the chemical mechanism of host (Lukens, 19 68). penetration by turf pathogens needs more investigation. The knowledge may be useful in devising measures for the control of disease. Growth of Pathogen in Grass Tissue Growth of fungi in host tissue is accomplished by hyphae which grow into and between cells. The fungus in- vades by haustoria within the cell into which host nutrients permeate. The obligate parasites, Erysiphe graminis and Puccinia spp., grow haustoria without disturbing the deli- cate integrity of the host cell until the late stages of dis- ease (Couch, 1962). Ustilago striiformis grows systemi- cally within the grass plant without symptoms of disease. Hyphae of Rhizoctonia solani can ramble through leaf tissue of bentgrass with no outward symptoms until the water stress becomes acute and the entire leaf suddenly collapses. Rapidly wilted leaves turn black and cause the smoke ring typical of brown patch. Helminthosporium species which grow haustoria within host cells cause the collapse of the host protoplast shortly thereafter (Mower, 19 61). With Pythium, host cells collapse within an hour of penetration of the fungus (Kraft et al., 1967). Hypha of Helminthosporium grow inter cellular ly through palisade and mesophyll of the leaf to the vascular system. Along the way, parenchyma and sclerenchyma cells are invaded by haustoria of the fungus. The presence of the pathogen causes collapse of host cells within a day of invasion. However, little necrosis proceeds beyond the space occupied by the fungus. This suggests that if toxins are invol- ved in the death of the host cells, the toxins are not abundant- ly produced by the fungus and do not permeate beyond the im- mediate area of infection. On the other hand, with Victoria blight of oats, which is toxin-incited, yellowing extends to the terminals of leaves and stem f r om the point of infection (Luke and Wheeler, 1955). The mechanism of invasion of host tissue determines, in part, the size and appearance of the lesion. Pinpoint les- ions of Pythium on roots of bentgrass develop f r om the few cells that collapse immediately after invasion by the pathogen (Kraft, et al. 19 67). Necrotic spots of Helminthosporium and other leaf-spotting pathogens arise f r om the limited invasion of the pathogen (Mower, 19 61). Apparently, the leaf-spotting pathogens require moisture for further in- fection and the host cells that are collapsed lose water quickly and dry out. Pathogens that macerate tissue are able to extend the size of lesions because moisture is conserved in the macerated diseased tissue. Succulent growth of grass f r om high soil moisture Increase in and high nitrogen fertility is conducive to Rhizoctonia brown patch and Helminthosporium blights. disease by succulent growth may be caused, in part, by an increase in infectivity of the pathogen. The cuticle and walls of cells are thinner so that barriers to host infest- ion are weak. The pathogen can grow more rapidly in the enriched secretions of leaves of highly fertile turf. The production of simple carbohydrates from photosynthesis in succulent tissue is less than that f r om hardy tissue. The pathogens utilizing extracellular enzymes growing through host tissue are not hindered by sugars in synthes- izing these enzymes. Melting-out disease of Kentucky blue- grass is a low sugar disease (Lukens, 1970). The area of foot-rot infection in turf is proportional to the percent of solar radiation shaded from turf (Fig. 1). The reduction in sugar content was consistent with the reduction in solar radiation. A short cutting height increases melting-out (Halisky et al., 19 66). Leaves f r om turf of low cut contain less reducing sugar than leaves of turf of higher cut. M o r e- over, an analysis of data f r om disease and sugar content of leaves of five bluegrass varieties at two cutting heights gives a correlation coefficient of 0.96 (Fig. 2). An applica- tion of glucose to Kentucky bluegrass turf reduced the rate of disease development for about a month (Lukens, 1968). Hence, by altering the sugar content of grass leaves with shade, cutting height, variety and sugar spray, disease in- creased inversely with the content of sugar in the host. Glucose sprayed to turf caused a delayed increase in disease. Apparently, the pathogen had grown saprophyti- cally on the sugar in sod; Inoculum f r om this sugar-induced growth was sufficient to overcome the resistance of the turf conveyed by an increase in sugar content in the host. A Fig. 1. Fig. 1. Effect of shade on the incidence of infection of Kentucky bluegrass turf by Helminthospor- ium vagans after four weeks of treatment in May (Lukens, 19 68). Fig. 2. Fig. 2. Effect of leaf sugar on melting-out by Helminthospor ium vagans. Variety of bluegrass: P= Park; K = Kentucky; N= New- port; W = Windsor; and M = M e r- ion. Cutting height: 1 and 2 in. respectively. The curve is the regression line of leaf sugar on disease, b = 160**. (Lukens, 19 70). sugar which conveys resistance to the host but does not serve as a carbon source for the pathogen is needed to ef- fectively control this disease. Build-up of Inoculum Large amounts of inoculum are required to sustain an epidemic of disease. The inoculum is produced by the pathogen from mycelium in diseased tissue of the host or in refuse in the sod. The build-up of inoculum in turf oc- curs f r om several cycles of disease; each cycle requires about three days. In the disease process, mycelium builds up in lesions of a certain size. With powdery mildews, in- fection is superficial and the mycelial mat or stroma is pro- duced externally on the leaf. Conidiophores grow out f r om the stroma and, shortly thereafter, conidia are produced. Pustules of uridiospores of rust are born superficially on leaves of bluegrass. With Helminthosporium, the stroma is produced in the diseased tissue and conidiophores are borne on the outer surface of the host. With stripe smut, the fungus grows systemically f r om crown to leaves in which it produces a mass of black chlamydospores. The leaf ruptures and the spores are exposed to air currents. Various pathogens that are able to live as saprophy- tes can produce inoculum on decayed clippings and organic matter in sod. Inoculum f r om overwintering material may be sexual spores, asexual spores, sclerotia or merely hyp- hal fragments. Certain of these inocula are also produced during the growing season. Hyphal filaments of Helminthos- porium, Pythium, Fusarium and Rhizoctonia growing f r om refuse to the host in moist sod are an important source of inoculum for disease. The amounts of hyphal inoculum f r om these sources is dependent upon moisture, tempera- ture and the nutrition of the refuse. Sporulation in fungi accompanies a change in growth of the fungus f r om filamentous to a budding type. In sexual reproduction, other habits of the pathogen enter the picture. With change in growth habit there occur changes in metabol- ism and, in turf, changes in response of the fungus to envir- onment. Helminthosporium vagans grows mycelium at its maximum rate of 25° C. (Horsfall, 19 30) and sporulates at 15° C. (Lukens, 1968). Hence, spore inoculum is produced by H. vagans most abundantly in cool weather and pathogen- esis advances at a faster rate in moderate weather. These opposing effects of temperature may explain, in part, the lack of a clear relationship between temperature and melt- ing-out disease (Bean and Wilcoxon, 19 64). Conclusion Mechanisms of fungal attacks on turf grasses have been described. The fungus, in the form of hyphae, scler- otia and spores, arrive at sites of new infections by air, water or debris. It infects a grass plant through cut ends of leaves through stomata, or directly through the cuticle. The fungus grows special structures — the appresorium and peg, for infecting grass. The development and func- tions of these structures require moisture, nutrients and possibly extracellular enzymes. Hyphae of the pathogen grow between cells of grass tissue and small branches of the hyphae penetrate into host cells. Haustoria, cells for absorbing nutrients f r om the host protoplasm, are produced inside of host cells by the fungus. Host cells tolerate haus- toria of obligate parasites, but they collapse when infected by haustoria and hypha of other pathogens. Fungi may kill host cells some distance away f r om the invading hypha by excreting substances that are toxic to the host. Soon after establishment in the grass plant, the fungus grows a mat of mycelium f r om which more inoculum in the f o rm of hypha, sclerotia and spores are produced. Usually, epidemics of disease break out following several rapid cycles of dispersal penetration, infection and inoculium production of the path- ogen. References Cited Bean, G. A. and R. D. Wilcoxon. 1964. Pathogenicity of three species of Helminthosporium on roots of bluegrass. Phytopathology 54:1084-1085. Couch, H. B. 1962. Diseases of Turfgrasses. Reinhold Publishing Corp. New York. 289 pp. Couch, H. B. and E. R. Bedford. 1966. Fusarium blight of turfgrasses. Phytopathology 56:781-786. Curtis, Li. C. 1944. The exudation of glutamine f r om lawn grass. Plant Physiol. 19:1-5. Endo, R. M. and R. H. Amacher. 1964. Influence of gutta - tion fluid on infection structures of Helminthosporium sorokinianum. Phytopathology 54:1327-1334. Halisky, P. M., C. R. Funk, and R. E. Engel. 1966. Melt- ing-out of Kentucky bluegrass varieties by Helmin- thosporium vagans as influenced by turf management practices. Plant Disease Rept. 50:703-706. Healy, M. J. and M. P. Britton. 1968. Infection and devel- opment of Helminthosporium sorokinianum in Agrostis palustris. Phytopathology 58:273-276. Horsfall, J. G. 1930. A study of meadow-crop diseases in New York. Memoir 130. Cornell Univer. Ag. Exp. Sta. 1930. 139 pp. K r a f t, J. M. and R. M. Endo. 1966. Zoospore infection of bentgrass roots by Pythium aphanidermatum. Phyto- pathology 56:149 (Abstr.) Kraft, J. M. and R. M. Endo, and D. C. Erwin. 1967. Infec- tion of primary roots of bentgrass by zoospores of Pythium aphanide rmatum. Phytopathology 57:86-90. Luke, H. H. and H. E. Wheeler. 1955. Toxin production by Helminthosporium victoriae. Phytopathology 45:453-458. Lukens, R. J. 1968. Low light intensity promotes melting- out of bluegrass. Phytopathology 58:1058 (Abstr.) Lukens, R. J. 1970. Melting-out of Kentucky bluegrass, a low sugar disease. Phytopathology 60:1276-1278. Moore, L. D. 1965. Pectic and cellulolytic enzyme activ- ity with Pythium ultimum blighted Highland bentgrass. Phytopathology 55:1069 (Abstr.) M o w e r, R. G. 1961. Histological studies of suscept-path- ogen relationships of Helminthosporium sativum, Helminthosporium vagans, and Curvularia lunata on leaves of Merion and common Kentucky bluegrass (Poa pratensis), Ph. D. Thesis, Cornell Univ., Ithaca, New York. 150 p. Rowell, J. B. 1951. Observations on the pathogenicity of Rhizoctonia spiani on bentgrasses. Plant Disease Reporter 35:240-242. DISCUSSION PERIOD I was interested in your correlation with low Dr. Endo: sugar content in relation to Helminthosporium. thinking of an alternative hypothesis. I have inoculated leaves of Kentucky bluegrass at different ages with Hel- minthosporium and found a difference in behavior of the g e rm tubes on senescence leaves, the g e rm tubes grow directly to the stomata. cells are thoroughly ramified with mycelium. On v e ry young leaves the g e rm tubes are v e ry long, f ew appres- oria are formed, penetration is r a r e, and colonization is usually limited to a single epidermal cell. I was In 24 hours the epidermal F i r st of all, the g e rm tubes react differently according to the age of the leaf; penetration is different and colonization varies. When plants a re shaded, senescence and cell m e m- brane permeability may be increased, favoring the exuda- tion of inorganic and organic compounds. whether the leaching of nutrients f r om the shaded plants could have influenced Helminthosporium. Also, the behavior of proteins in senescent leaves might be different and, there- f o r e, the host defense mechanisms might also be affected. I was wondering In your work with the guttated nutrients, would Dr. Lukens; you say that different age leaves f r om the same plant have different characteristics, and that nutrients exuded to the surface vary? Guttation has a great bearing on disease. In reference to our shade work, the grass in 70% and 90% shade grew so fast in height that I complained to the f a rm manager, who had always taken good care of my turf, that he wasn't mowing the grass faithfully. A f t er all, he never let the grass get six inches high. Friday, when the turf was just mowed, and when I returned the next Monday, the grass in 90% shade had grown 6 to 8 inches. Turf in the open sun g r ew less than one-fourth of an inch. The turf was not neglected. Shading had caused etiolated and v e ry succulent growth with little indication of senescence. I went to get samples one Of course, shading does change the protein structure. Dr. M. Zucker at our laboratory, working on proteins of tobacco and potatoes, found perhaps 9 0% of the protein in the leaf contained in the chloroplast. Since shading reduces chloro- phyll formation, we are altering the chemical composition of the plant. I don't deny that. However, we found a good relat- ionship between leaf sugar and disease. This relationship may just be an outward expression of something more subtle. At least it is a hypothesis that works. it to some kind of mechanism. I'm trying to relate Dr. Altman: With regards to shade and Dr. Endo's comment on senescence, I think the shade grasses have a thinner cuti-\ cle and, also, inside the substomathal chamber there is a thinner cuticle lining. The barrier to entrance by the appres- soral peg is reduced in shade so you may not have to have a variation in senescence. this increased elongated type of growth, rather than senescence, and more of a juvenile stage. Maturity and hardening off pro- cesses are not as well-developed under shade as they are in full light. This may be part of your story. What I wanted to ask you about was glucose. more glucose at the hypocotyl area are more susceptible to Rhizoctonia. hypocotyl interface. What is the relationship of this to your suggesting glucose as a means of control of disease? I'm talking about broad leaf plants near the soil- I'm inclined to think that you get I found that those plants that exude Dr. Lukens: Glucose can reduce infection f r om Helminthospor- ium, but glucose outside of the plant appears to stimulate the pathogen to grow saprophytically. The high level of inoculum produced may overcome any effect one may induce in the plant by the sugar supplement. week for eight weeks to calculate the increments of increase in disease per day. During the first few weeks the disease was reduced proportionally by the long concentration of the sugar in the spray. But after four weeks the whole thing fell apart. The organism grew saprophytically on sugar and this upset the whole balance. Subsequently, disease was increased by the sugar supplement. I rated the disease f r om week to Dr. Altman: Under the shade microenvironment, in the sphere that surrounds the stoma, there's usually a higher oxygen content. Could this be involved in getting more direct or mechanical penetration? In Infections of the stomates were pretty much lim- Dr. Lukens; I'm relying mostly on Dr. Mower's work. his thesis he studied H. vagans and H. sativum. I think roughly 80% of the infections in common Kentucky blue- grass were by direct penetrations and about 20% through stomata. ited to the area around the stomatal cavity. With Merion bluegrass, most of the infections were through stomatal cavity; very few through the direct penetration of the cuti- cle. I didn't emphasize this in trying to explain the r e s i s- tance of Merion to the disease. It's probably one means, among many, which makes Merion fairly resistant to the Helminthosporium melting-out disease. Apparently, the disease also is related to the nature of plant growth. Sugar may be one reason; thin cuticle may be another. They all play a part. Dr. Pellett: Most of the discussion during the last few min- utes has been centered around the physiological and anatomi- cal relationships of the host. effect of the quality of radiation has on the development of these organisms in shade versus full light and at various elevational differences. I'm wondering what the direct Dr. Lukens: Helminthosporium vagans is one of the fungi studied by Dr. C. M. Leach at Oregon State when he exam- ined the influence of light on sporulating habits of fungi. We have done some work with two fungi. Liglit both increases and decreases asexual sporulation. The response depends upon the stage of sporulation being irradiated. Light of the near UV range causes hypha to grow conidiophores through inducing the synthesis of a sporogenic substance. Conidio- phores, the stalks on which spores are borne are wider and have thicker walls than hypha. Light of visible wave lengths may prevent conidiophores f r om growing spores and the de- gree of photo-inhibition depends upon temperature. A l t e r- naria solani sporulates in the dark only at 25°C and in the light or dark at 15°C. Helminthosporium vagans does not require a dark period. It requires a cool temperature to produce a spore. Sporulation decreases with departure f r om 15°C. So various components of the environment affect fun- gus sporulation. I raised the question in the paper of inoculum release f r om a dry surface. If wind-blown spores are the main vehicle for spread of the fungus, spores on a wet surface will float off and would no longer be capable of becoming air-borne. This raises other questions that may relate to disease. donft know how much inoculum of turf fungi is wind-borne. If appreciable, a mere manipulation of the environment can effectively control disease. I Mr. Stottlemyer: What do you think this sugar is doing? What is the mechanism? It was originally I suggested one mechanism. Dr. Lukens: suggested by my colleague, Dr. Patel, who is now with the University of Hawaii. His idea is that these low sugar path- ogens require extra cellular enzymes at pinpoint spots were the infection peg penetrates through the cuticle and through the cells. The enzymes may degrade pectin between cells and cellulose in the cell wall. These low-sugar pathogens, in vitro, will not produce pectinase in the presence of glu- cose or any simple sugar. Mr. Stottlemyer: be able to inhibit this enzyme. If you make a sugar analog, you should Dr. Lukens: This is what I was to examine this year. I made two criteria for the search of that carbon source. One, that the sugar had been reported to not serve as a carbon source for some plant pathogen. And two, that it's cheaper than a dollar or so a pound. I came up with about 6 or 7 and I planned to use them on my grass. Unfortun- ately, the turf was infested with so many weeds that I de- cided to delay this experiment until next year. Since I mea- sure disease by visual estimates of the percent area brown f r om foot rot, a thoroughly uniform surface is required to grade disease accurately. Scotts Plus-2 to get rid of the weeds. Instead of experimenting, I used Mr. Stottlemyer: Did you run any spectra in the shade to determine which wave lengths were coming through? Dr. Lukens: No, but this can be readily accomplished. I assume it's just light scattering and light absorption of a general nature with little selective removal of a particular wave length. Dr. Worf: F r om time to time we make the observation of a severe Helminthosporium leaf spot. On other occasions we see quite a bit of foot rot. Also, in some seasons we have the diseases and other seasons the diseases are almost ab- sent. We have generalized that this is being influenced by the environment to a great extent. But in light of your sugar hypothesis, I wonder if there might also be some changes in sugar levels within the individual tissues of the plant. P a r- ticularly, let!s say, in the crown.area or in the root area at a certain stage of physical development of the plant. be influencing what we are seeing. It might Dr. Lukens: I was measuring foot rot, and infection of crowns, and analyzing leaf sugar, which I should probably relate to the leaf-spotting stage. But we feel, with this disease, that the permanent damage is due to foot rot, and spores may or may not be the inoculum. We found foot rot infections immediately when the grass greened up in the spring. Leaf spotting, which is indicative of spore production, followed shortly. We believe that the mycelum or the hyphae penetrates directly f r om the thatch into the crown with little spore involvement. To say which is more prevalent would be merely an academic ques- tion, since mycelum and spores are both produced in the sod when the grass starts growing in the spring. sugars formed in the leaf by photosynthesis migrate to other parts of plants where they are needed. I assume that Dr. Worf: Does the sugar content vary in the crown tissue f r om one stage of plant development to another? Let's say at the time of the year when flowering and fruiting is taking place. Is there a reduction in the sugar content at that time which would make the crown area more susceptible? Dr. Lukens: During flowering, the sugar moves from leaves to flowers. Thus, sugar level of leaves and possibly the crowns will go down. A ll of our analyses were done on leaf tissue. I didn't vary the sugar by flowering. Sugar levels were varied by choice of variety, height of cut, shading and concentration of sugar in the spray. DISEASES OF W A RM SEASON TURFGRASSES T. Edward Freeman P r o f e s s or of Plant Pathology University of Florida Gainesville, Florida, 32601 The grasses and their disease problems in Florida and the southern part of the United States may not differ widely f r om other areas of the country, but I think they are a little unique in many respects. Warm-Season Turfgrasses F i r st of all, the primary grass we grow for the home lawns is St. Augustine (Stenotaphrum secundatum). This is especially true in the peninsula part of Florida and along the coastal region of other southern states, including Texas. This grass has salt and shade tolerance and, hence, is well- adapted to our area. F or those of you who are used to bluegrasses and bentgrasses, St. Augustine is rather coarse with leaf blades up to one-half inch in width. Bermudagrass (Cynodon dactylon) is our principal grass for fine turf areas and golf courses, including the tees, fairways and putting surfaces. Another popular grass is centipedegrass (Eremo- chloa .ophiuroides), also a rather coarse grass. in the northern parts of Florida and along the southern por- tions of other southern states. It is popular Bahiagrass (Paspalum notatum) is popular also. This is a v e ry coarse, tall-growing grass that was first used as a pasture grass and still is one of the dominant pasture gras ses in Florida. It grows well and, due to a deep root system is drought-tolerant. A few years ago, people thought that thi grass did not have any problems. About that time, chinch bugs were wiping out our St. Augustinegrass and many peo- ple converted to bahiagrass. Due to its rapid growth, they soon became slaves to this grass and many ended up with what looked like a pasture for a lawn. Nevertheless, it is still a very popular lawn grass. Japanese lawn grass (Zoysia spp.) is not extensively grown in Florida. We tried zoysia a few years ago and most people are converting back to other grasses. Zoysia seems to have too many problems in Florida. During the winter when our bermudagrasses go dormant and turn brown, we overseed with annual ryegrass ( Lolium multiflorum). W e ' re beginning to use some bents and other grasses, but primar- ily we use ryegrass for over seeding purposes in the winter. Turfgrass Diseases As far as the diseases are concerned, we have seven important fungus diseases that occur on grasses in Florida (Freeman, 1967). Brown patch (Rhizoctonia solani) is pro- bably our most important problem. This disease affects all of our grasses, but St. Augustine and centipede seem to be more affected than some of the others. Dollar spot (Sclerotinia homoeocarpa) is of primary importance on our bermuda, bahia and zoysiagrasses. We are also troubled with the various Helminthosporium diseases. On bermuda- grasses, we isolate six such species: cynodontis, steno- spilum, rostratum, triseptatum, spiciferum and giganteum. In bahiagrass, we find H. micropus, which we have recently identified as a pathogen on this grass. The primary spec- ies affecting ryegrass are H. sativum and H. siccans. Another important disease, Pythium blight, usually occurs during the winter in Florida on overseeded grasses. This is somewhat unusual because the common pathogen is P. aphanidermatum, which is a warm season Pythium. In fact, some of our work a few years ago established the optimum temperature for disease development somewhere around 9 5°F. This disease occurs because of a unique situation in Florida during the winter. The weather may be rather cool, but temperatures can go up into the 80's in the southern part of the state during the day. This disease kills the grass very rapidly. We have found that, once inoculum potential is built up, the temperature needs to rise into a con- ducive range for only a few hours during the day (on several suscessive days) for the grass to become damaged. T h e r e- fore, we can have disease damage f r om Pythium even dur- ing periods that most people in Florida would consider cool. We almost lost the confidence of people in industry when we reported Pythium blight as a warm-weather disease in Florida. This didn't make sense because people were seeing it during the winter months. ber of diseases during the winter in Florida. Incidentally, we see quite a num- We consider brown patch a winter disease in south- ern Florida. It occurs predomiantly f r om about November through March and April. The summer temperatures seem to be too hot for brown patch, and we see very little of it in Florida during the hotter months. Gray leaf spot, or blast disease of St. Augustinegrass (caused by Piricularia grisea) is another disease which is of concern. The causal fungus is a very close relative of the Piricularia that occurs on rice. It attacks many other grasses but is of prime importance only on St. Augustine. During the summer months, practi- cally no plantings of St. Augustine can be found f r ee of this particular disease. It does not kill the grass but it causes plantings to look rather ragged in many instances. The fun- gus attacks young, vigorously-growing grass more severely than it does more mature grass. Consequently, it is of prime interest to the sod industry since they are concerned with rapid coverage by the grass plants. We have rust diseases in Florida, although they are not of prime importance. Occasionally they occur in damaging proportions, but not with any degree of regular- ity. We have rust on bermudagrass (caused by Puccinia cynodontis), St. Augustinegrass (caused by P. stenotaphri), zcysiagrass (caused by P. zoysiae) and ryegrass (caused by P. coronata). On ryegrass, rust usually does not occur un- til spring. Rust on Zoysia appeared in Florida a couple of years ago and was so severe that the grass appeared orange. It was the most devasting rust outbreak that I had ever seen. However, if you would ask me to find rust today on zoysia in Florida, I would be hard pressed. Since that initial outbreak, the disease has almost disappeared. donft think it can thrive in our warm temperatures. to do some temperature relationship studies a year ago, but couldn't get enough spores for inoculation purposes. I I wanted Another problem in Florida is nematode diseases. Bermudagrasses, centipede and zoysiagrasses are the three most severely affected by nematodes. Sting and lance nema- todes appear to be the most damaging to these grasses. It has become a common practice to use nematicides on golf courses in Florida. Practically all golf courses use them on their greens and tees and many of the richer courses are beginning to use nematicides on their fairways. You can get a very dramatic response f r om their use. Nitrogen Studies We have sandy soils that are very low in nutrients. Nitrogen, especially, is leached f r om these sandy soils very readily and is lost. Therefore, we find that fertilization with soluble forms of nitrogen is necessary on nearly a two week-cycle in bermudagrass. With less soluble forms, the interval may be a little longer. Nevertheless, most golf courses use f r om 25-50 lbs of nitrogen per 1,000 sq ft yearly on greens and tees. We have been concerned with the effect of nitrogen fertilization on disease development. Based on observations of fertility plots, in coopera- tion with Dr. G. C. Horn, we have found that high rates of soluble nitrogen increase the incidence of brown patch in St. Augustine and centipedegrass. We have seen brown patch kill turf right to the line between high and low level plots. In addition, we found that nitrogen influences the severity of infection by Piricularia on St. Augustinegrass (Freeman, 1964). Adding a high rate of soluble nitrogen dramatically increases the infection of this grass. Conversely, we found that giving bermudagrass a high rate of nitrogen fertilizer retards the development of dollar spot. In fact, this is becoming the ac- cepted method of controlling dollar spot in bermudagrass in Florida. Recently, we have obtained indications that high rates of nitrogen also retard development of Pythium blight. Piricularia Leaf Spot We are also studying how nitrogen affects disease severity. We became interested in this aspect a few years ago while studying Piricularia m St. Augustinegrass. I was studying the influence of rates of nitrogen on disease severi- ty starting out at the zero rate and increasing to 1, 2, 4 and 8 lbs of nitrogen per 1,000 sq ft. Based on leaf-spot counts, there was a significant increase in disease severity with the addition of 1 lb of nitrogen per 1,000 sq ft. Then there was a leveling-off of the disease without a significant in- crease between 1-2 lbs. However, another significant in- crease occurred between 2-4 lbs. A slight, but not signif- icant drop occurred between the 4-8 lbs rates. Therefore, we had a stair-step arrangement of increasing disease se- v e r i ty with increasing rates of nitrogen. Since this disease was v e ry similar to the rice blast disease in which nitrogen content of the plant was correlated with disease severity, we decided that we would check the nitrogen content of the plant. We found the content of total nitrogen followed v e ry closely the curve which we had estab- lished for the number of leaf spots - 0.96. With amino acids, the correlation dropped to 0.92, but that is still a high posi- tive correlation. Then we checked the content of individual amino acids and found that the bulk of the increase in amino acids came f r om aspartic acid, glutamic acid, alanine and the amidesasparagine and glutamine. Glutamine immediately became of interest to us be- cause it had been implicated in the rick blast disease as be- ing a factor influencing infection. We checked for effects of glutamine and found it stimulates germination of Piricularia spores. We have not been able, however, to change the de- gree of disease severity using glutamine, either by spraying it on with spores or allowing the plant to take up excessive amounts of the amide. Consequently, we are not sure that we have established the exact reason f or increased infection under increased nitrogen fertility. However, our data strong- ly suggest that nitrogen metabolism of the host affects its disease reaction. Dollar Spot Another disease we have been interested in is dollar spot on turfgrasses. Dollar spot is exactly the opposite to e P iric u- la ria leaf spot. High nitrogen retards the de- velopment of this disease. Nitrogen fertilization has a dra- matic effect on the incidence of dollar spot in bermudagrass. For all practical purposes, the disease can be controlled with nitrogen fertilizer. In our studies, we used ammonium nitrate at 1 lb of N per 1,000 sq ft. There was a little dollar spot in nitrogen treated plots, but only in the tips of leaf I really don!t know blades and was of no practical concern. what the nitrogen is doing; it may be making the grass more resistant, or simply stimulating the grass to outgrow the fungus. Endo (1966) has postulated that disease reduction is due to the fact that the dollar spot organism requires a nitrogen base to establish a parasitic relationship. There is more senescent tissue in unfertilized grass to provide this nitrogen base. In other words, senescent tissue pro- vides the nitrogen base for the dollar spot organism to attack the grass. With this in mind, we became interested in the effect of nitrogen nutrition on S. homoeocarpa. We checked various rates and sources of nitrogen for their effect on the growth of S. homoeocarpa in liquid cultures. The optimum rate for growth was found to be 0.5 g of N per liter. Once the optimum rate was established, several sources of nitrogen were tested at this rate. It was found that the dollar spot organism can utilize nitrate sources of nitrogen better than the ammonical sources. Casein hydro- lysate was the best source tested. Since the nitrogen in casein hydrolysate is derived f r om a mixture of amino acids, aspartic and glutamic acids, were v e ry good sources for the growth of S. homoeocarpa. The amides of these two acids, glutamine and asparigine, were also very good sources of nitrogen. Leucine and alanine were the best sources f r om among the neutral amino acid group. Methionine was lowest in this group. When the basic amino acids were tested, we found that the fungus did not grow in lysine treatment. We didn't know whether it couldn't utilize lysine as a nitrogen source or whether lysine was inhibitory. Therefore, we added sodium nitrate to the lysine treatments under the assumption that, if it had been inability on the part of the fungus to utilize the lysine as a nitrogen source, adding sodium nitrate would It didn't grow, so we assumed would allow the fungus to grow. that lysine was inhibitory. We later found that casein hydro- lysate will overcome the inhibitory effect of lysine on the growth of Sclerotinia. We had wanted to postulate that lysine was instrumental in making the high nitrogen fertilized grass more resistant to disease. But this last finding confused our thinking on this point. We later found that several other amino acids would counteract lysine inhibition, so it is very doubtful that lysine is actually acting to make the grass resistant. Pythium Blight We also were interested in the effect of nitrogen on Pythium because we find that increasing nitrogen fertilization of ryegrass reduces disease severity. Disease severity is reduced as the nitrogen rate is increased. Our preliminary tests were carried out in a homogenous soil that may have contained varying degrees of nitrogen. Later, tests were carried out in growth chambers in liquid culture, so we could more accurately control our nitrogen source and inoculation procedures. Results f r om these tests were similar to those in soil. This nitrogen-disease relationship was first brought to our attention when many of the golf courses who used am- monium nitrate during the winter months had less disease damage than those using organic sources that release the nitrogen slower. or slow release sources of nitrogen were used during the winter, had more Pythium damage than courses where in- organic or faster release sources were utilized. Our r e- sults had given us an insight as to why this was happening. This work is still in the embryonic stage, but we are rather excited about the potential that we have for control of this serious disease by manipulating the nitrogen fertilization program. Again, we don't know how the nitrogen affects a change in disease severity. In other words, courses on which organic References Cited Endo, R. M. 1966. Control of dollar spot of turfgrass by nitrogen and its probable bases. Phytopathology 56:877 (Abstr.) Freeman, T. E. 1964. Influence of nitrogen on severity of Piricularia grisea infection of St. Augustine- grass. Phytopathology 54:1187-1189. Freeman, T. E. 1967. Diseases of southern turfgrasses. Fla. Agric. Expt. Sta. Bui. 713A (technical). Revised May, 1969. DISCUSSION PERIOD Dr. Altman: I would just like to clarify one thing with r e- gards to your winter brown patch and our summer brown patch. I think we are all in the same boat since Alaska is part of the country and Colorado is now considered in the South, too. But our summer daytime temperatures are be- tween 80 and 90 degrees and I think you mentioned this as your winter temperatures. Our evening temperatures are 55 degrees, so we are talking about the same temperatures at different times of the year. D r. Freeman: You1 re right about that. W e ' re talking about the same kind of conditions. During the summer our day temperatures often exceed 90 degrees in June, July, August and into September. Your summer conditions, in reality, are v e ry close to our winter conditions. M r. Gabert: spot? Also, is there a control for it? Is St. Augustine leaf spot called gray leaf Dr. Freeman: Yes. We find several fungicides will control it. In fact, most of the turf fungicides will adequately control It's a matter of timing the application. The gray leaf spot. disease occurs during the summer months in Florida when we have rain practically every day. The grass is growing v e ry rapidly and it is important to keep the fungicide on the leaf surface, as a protective measure. Practically all the turf fungicides, such as thiram and mercuries, will give adequate control. D r. Harrison: When you were reducing the amount of dollar spot with nitrogen, in what f o rm were you applying the nitro- gen? Was that a liquid or a soluble? D r. Freeman: 1 lb/1 ,000 sq ft, in this particular test. It was a soluble source. Ammonium nitrate, D r. Endo: Your results with Pythium were very interest- ing. Do you think that nitrogen is affecting mycelial growth, infection, or subsequent colonization? I don't know. We first noticed this with am- I had thought, at first, we were affecting Dr. Freeman: monium nitrate. the growth of the parasite. Perhaps we were getting am- monium released that was toxic to it. But we have done this outside the growth chamber. Right now I have a tend- ency to think it is making the grass more resistant. Dr. Endo: Have you looked at those plants microscopically? Did they have as much mycelium growing on the surface? Dr. Freeman: No. In fact this is what we based most of our criteria for disease development on, the size of the disease spots. The actual disease spots are smaller, and there is not as much mycelium growing on the surface. Dr. Endo: Pythium aphanidermatum is really unique because it's one of the few species of Pythium that emerges f r om the soil to attack the foliage, even mature tissues. Do you know if the fungus requires a food base in the f o rm of an infected lower leaf before it can attack the rest of the foliage, or can it grow abundantly as mycelium without it? I think the latter would be right. We get very Dr. Freeman: abundant growth of this fungus over the entire plant tissue. Under ideal disease conditions, it's really an aerial blight- ing in which the fungus grows profusely over the surface of the plants. Dr. Endo: That suggests to me that, somehow, turf is pro- viding abundant exogenous nutrients to nourish hyphal growth. Dr. Freeman: That's correct. Mr. Simmons: Do you get this same disease during the sum- mer and on warm season grasses? I should have pointed this out. Bermudagrass Dr. Freeman: is the only one we found that is susceptible to Pythium, and we have tested all of our warm season grasses. least severe on ryegrass. Pythium is not as much concern during the summer months because the grass is more r e- sistant, but we get a lot of damage f r om this disease on our It is bermudagrasses when we overseed. We have been wonder- ing about this recently because we are seeing more and more of it. Certainly, with the affinity of the fungus for high temper- ature, it would be really rough if bermudagrass were as sus- ceptible as overseeded grasses. Dr. Altman: Have you compared an ammonium sulfate with ammonium nitrate for control effectiveness? Dr. Freeman: Yes, in the case of Pythium blight we did this and they seemed to work the same way, but we got damage to grass with ammonium sulfate under the test system employed. Dr. Altman: What kind of damage did you get? Dr. Freeman: We got physical damage f r om the toxicity of the ammonium sulfate. Dr. Altman: What was the pH of the soil in the outside field plots where you were getting some control? Dr. Freeman: In most cases the pH was 6 to 6.5. Dr. Altman: Did you compare ammonium nitrate and ammon- ium sulfate? I have not for dollar spot, but Dr. Horn has Dr. Freeman: made studies on this comparison. He found that it works quite well and, in fact, he thinks the sulfate has something to do with the control of the dollar spot, as well as the nitro- gen. trol using ammonium sulfate. In other words, he can get an increase in disease con- Dr. Altman: We made a comparison and found where Hel- minthosporium occurs in the leaf spot phase, there was less disease with the ammonium sulfate f e r t i l i z er than ammonium nitrate. Dr. Freeman: This is what we find with dollar spot, too. I don!t know about Helminthosporium. We are just beginning a project on the effect of nitrogen on Helminthosporium disease in bermudagrass. TURFGRASS DISEASES IN WESTERN C A N A DA Jack B. LeBeau, Head Plant Pathology Section Agricultural Research Station Canada Department of Agriculture Lethbridge, Alberta, Canada At Lethbridge, Alberta, we are doing considerable research on turfgrasses, principally on species suitable for putting and bowling greens. The construction of new golf courses and the conversion of greens f r om sand to grass on established courses in Canada have greatly increased the culturing of grass species that are highly susceptible to win ter injury. Consequently, there is a greater need for effect- ive methods of grass culture designed to produce greens of good quality in the early spring. I have been testing variet- ies and techniques for winter protection of turfgrass for the past ten years. Turfgrass failures are often traced to the wrong se- lection of grass strains for the location. Monocultures of grass in golf greens scarcely exist in the Canadian prairies Most greens have been initiated with the Colonial type of bentgrass. These soon undergo succession to annual blue- grass and various wild strains of creeping bent. All greens in western Canada eventually contain mixtures of these types with the predominant species being annual bluegrass. The more northerly the area, with severe winter conditions the more rapidly this succession occurs. Most golf course superintendents accept this succession as inevitable. I am still of the opinion that with proper management, a monocul ture of a suitable grass can be maintained in golf greens in western Canada. Winter Survival Winter-killing of turfgrass seldom results from sub- zero temperatures alone; it is also caused by desiccation or attack by low-temperature fungi. These psychrophilic patho- gens cause a disease commonly called snow mold. One of the most serious effects of winter-killing is the invasion of the killed-out areas by weeds and undesirable grasses. Canadians swarm to golf courses and other r e c r e- ational grounds after the long winter and sports turf should be ready for use. The most important practices in golf and bowling green culture are those that will bring grass through the winter in a healthy condition. Poor greens discourage golfing and many clubs charge only half the regular fee until the greens are suitable for play. during the winter, it is often July in the Canadian prairies before the turf recovers sufficiently to be suitable for play. Often the grass is damaged so badly that seeding or sodding is required to reestablish the turf. If grass is severely damaged Reaction of Species Grasses suitable for golf and bowling greens are generally more susceptible to damage f r om low tempera- tures and snow mold than grasses used for lawns or r e c r e- ational grounds. Grasses that are resistant to cold injury and desiccation are also resistant to snow mold. None of the grasses suitable for bowling and golf greens survives the severe winters of the Canadian prairies uninjured, although some strains are more resistant than others to winter damage. Creeping bentgrass (Agrostis palustris Huds.), for example, is more resistant to cold injury than annual bluegrass (Poa annua L.). Grasses suitable for golf greens on the Canadian prairies are chosen not only for winter hardiness, but also for player acceptance and ease of management. Henderson creeping bentgrass, for example, is winter hardy but does not meet the requirements of player acceptance or easy management. Results f r om experimental plots should not be considered as final, subject to performance under play- ing conditions. Several strains of creeping bentgrass are being tested in Alberta f or golf-green culture. The most promising strains are: Northland, Waukanda, Toronto, Penncross, Congressional and Cohansey. Penncross and Northland have been tested in Alberta on modern golf courses. To date, Northland has met all requirements better than Penncross. Northland has shown good resistance to cold injury and snow mold, and persisted as a pure stand for five years in greens at the Willow Park Golf Club at Calgary, Alberta. The greens at Willow Park are under close observation for winter sur- vival, resistance to invasion by annual bluegrass and play- er acceptance. Northland does not solve all problems involved in culture of greens for the prairie region. If managed pro- perly, however, it is recommended for our northern cli- mate. On the other hand, it is not suitable for warmer regions with humid summers. Northland is vigorous and must be thinned periodically, but this is not a difficult task with modern thinning equipment. It is easier to thin grass than to grow it, particularly when spring temperatures are below optimum for growth. Turf Protection Various methods for protecting turfgrass during the winter are in use in Canada and the United States. Grass is protected f r om snow mold by the application of inorganic m e r c u ry compounds once or twice in the autumn. Greens are protected f r om desiccation and cold injury by covering with manure, peat moss, brush, polyethylene or fiber glass. Watson et al. (I960) made a major contribution to the protection of turf in winter with their work on polyethy- lene covers for turfgrass during the winter. Their techni- ques are being widely used in the northern United States and in Canada to prevent winter-killing on golf greens. The cover prevents extreme drops in soil temperature and lessens cold injury and damage caused by snow mold and desiccation. In southern Alberta, polyethylene covers in- creased the effectiveness of inorganic mercurial fungicides f or control of snow mold. Less than half the recommended rate was adequate to control the disease when the turf was covered with polyethylene sheets immediately after the treat- ment. The use of covers for protection, however, has several disadvantages. These are (a) the plastic covers are difficult to fasten securely to the ground in windy regions; (b) the grass is not always protected; ( c) the cover cannot be removed safely in the spring until threats of damage by freezing are over; (d) grass often grows rapidly under the cover but cannot be clipped; (e) considerable labor and expense are required to supply and maintain covers each year, and ( f) turfgrass is not usable during the long period of cover. Treatment of turf with fungicides and the use of v a r- ious types of soil-insulating materials have reduced winter- killing. These techniques have many disadvantages and do not always produce the desired results. Soil warming below the surface appears to be a solution to this problem. Results f r om experiments conducted at Lethbridge, Alberta, since I9 60, indicate that turf heating with electri- cal cables can ensure winter survival of non-hardy turfgrass. Snow mold and other causes of winter-killing were controlled by raising the temperature of the soil a few degrees during cold periods. Minimum temperatures at a one-inch depth in turf plots were maintained by thermostatically controlled soil-heating cables (LeBeau, 19 64). Results also indicate that consumption of electrical energy required to bring turf- grass through the winter in a healthy condition is in the eco- nomic range. Turfgrass held at minimum temperatures of 3° and 6°C. was severely damaged by excessive heat and electrical consumption was uneconomical, whereas turfgrass held at minimum temperatures of 0° and -3°C. survived the winter in good condition and electrical consumption was economical. The temperature in the unheated plots dropped to -11°C. in December. electrical power required to maintain minimum temperatures above 13°C. These periods occurred when low air temper- ature coincided with limited snow cover. In only two periods of the winter was The first practical test of turf heating in Canada was initiated in 19 66 when electrical cables were installed under a putting green at the Banff Springs Golf Course. The pro- ject is a joint venture of the Canada Agriculture Research Station at Lethbridge, the Canadian Pacific Railway Com- pany, the Calgary Power Company and the Canadian Gen- eral Electric Company. Soil warming is still in the experimental stage in Canada. We have neither promoted nor condemmed it as a practical method for turf culture because the answers are not complete. The results from our experiments at Banff indicate that the cost of installation and operation of electri- cal heating systems for golf greens appears to be within the economical range for high-budget golf courses. Increased Growth Response (I.G.R.) Partial sterilization of soil has increased the pro- duction of alfalfa, winter cereals and sugar beets (Altman and King, 1965; Buchenaw, 1963; Webster et al., 1967). R e- cently, at Lethbridge, we have demonstrated I.G.R. in turfgrass. In addition to controlling snow mold with m e r- curic chloride, the partial sterilization with this chemical has stimulated the growth of the grass in early spring. The chemical treatments were made in the fall. Snow Mold Identification and Control In central Alberta, snow mold is caused by an un- identified low-temperature Basidiomycete. Dead patches in early spring on golf courses, bowling greens aiid lawns are often caused by this pathogen; however, similar damage to turfgrass may result from desiccation, trampling and frost injury. A simple method for distinguishing snow mold f r om these other types of injury seemed desirable. The synthesis of hydrogen cyanide (HCN) by the Basidiomycete has been demonstrated" under artificial conditions. The production of this gas by the fungus suggested a quick method for identify- ing the disease. It was considered that chemical tests that established the presence of HCN in turf samples would dif- ferentiate between damage attributable to the snow mold pathogen and that caused by the other factors noted above. A ll samples taken in April f r om areas containing infected plants gave positive tests for HCN, whereas the con- trols showed no trace of cyanide. Samples taken in early A p r il gave stronger tests for HCN than those removed later in the month, but those taken in May failed to give positive tests. Hydrogen cyanide apparently was not fixed in the plant tis- sue or soil and was volatilized as soon as the temperatures Isolation results confirmed the presence rose in the spring. of the low-temperature Basidiomycete in all samples contain- ing HCN. Fungicidal Treatments of Turfgrass for Snow Mold Inorganic mercury compounds have proven to be ef- fective fungicides against snow mold organisms prevalent in Canada. A mixture of corrosive sublimate (Hg Cl2) and cal- omel (Hg2 CI2) is generally recommended and is sold under several trade names. Companies merchandise these two chemicals in mixtures on the assumption that the more sol- uble corrosive sublimate is readily available to control snow mold in the fall, whereas calomel, being sparingly soluble, persists longer and is more effective in the spring. To test the validity of this hypothesis, an experiment was conducted. Plots of Agrostis tenuis L, 8 ft sq infested with snow mold were treated in the fall. Calomel and corros- ive sublimate were applied at the same rate (mercury equi- valent) and at half the rate of the mixture (Calo-Clor). The treatments were replicated three times and the plots were rated for survival the following spring. The results pro- vided no evidence to support the view that a combination of the two forms of mercury is more effective than either one used alone. Tests with other chemicals are also conducted every year. Some organic compounds are showing promise, parti- cularly when two or more applications are made in the fall. F a i ry Rings Nitrogen fertilizers and fungicides may be beneficial in the control of fairy ring; however, the results of our study showed that complete soaking of the infected area was the essential factor. Fairy rings are most severe on grass inhabited soils that are dry and low in fertility. This state- ment is often disputed by home owners and park superin- tendents who claim they have supplied their lawns with suf- ficient amounts of fertilizer and water and are still plagued with fairy rings. The disease is prevalent on golf course fairways but seldom occurs on the greens, and the latter are fertilized and watered more heavily than any other turf area. In recommending soaking as a method of control, it should be stressed how difficult it is to penetrate a well developed fairy ring with water. The soaking should be done by persistent watering each day for at least a month until the ring is soft. The fungus does not develop under these extremely wet conditions and gradually disappears. The reaction may be due to increased bacterial and fungal ac- tivity in the soil leading to the destruction of M. oreades or to the hydrophobic property of the pathogen. References Cited Altman, J. and M. T. King 1965. Changes in plant growth with chemicals used as soil fumigants. Plant Dis. Reptr. 49:600-602. Buchenaw, G. W. 1963. Winter survival of wheat in chloro- picrin treated soil. Plant Dis. Reptr. 47:602-604. LeBeau, J. B. 1964. Control of snow mold by regulation of winter soil temperature. Phytopathology. 54:693-696. Watson, J. R., H. Krall and L. Wicklund I960. Protecting golf greens against winter-kill. Golf Course Reptr. 28:10. Webster, G. R., S. V. Khan and A. W. Moore. 1967. Poor growth on some Alberta soils. Agron. J. 59:37-41. DISCUSSION PERIOD Dr. Altman: You stated that fairy rings can be controlled by soaking the area and applying a high rate of nitrogen. How long does this control last with flooding? Dr. LeBeau; feeding and watering program. It will last as long as you maintain a regular I've heard of this and tried it but had only a Dr. Altman: temporary effect, sort of a masking effect. Do you suggest that you can get permanent control? I would suggest this. My argument reverts Dr. LeBeau: back again to the fact that you don!t get f a i ry rings on well watered and fertilized golf greens. On the other hand, this may be too much water to ask homeowners to put on their lawn. I do know that lack of water and nitrogen are impor- tant. Lawns on a slope, where it's difficult to get proper irrigation and runoff occurs are very susceptible to fairy ring. Occasionally you will find a fairy ring on a golf green located in a high, dry area. Dr. Endo: When you get threads of hyphae growing through the soil, they are quite water repellent, aren't they? Dr. LeBeau: Yes, very difficult to soak. Dr. Endo: Do surfactants help? Dr. LeBeau: Surfactants weren't used, but they probably would help. We just wanted to see if we could get control with persistent watering, and I mean really persistent watering. We didn't even use a probe, but we did use a hand aerifier and punched holes in the ring. Then we watered and soaked it everyday. We kept this up until it got real mushy. Dr. Endo: Every day for how long? Dr. LeBeau: Well, I shouldn't say everyday. was every second day. finished. It took about a month before we It probably Dr. Endo: How about IGR? Do you have any idea what caused it? I don't know. Dr. LeBeau: ents, but it's more than that. On the sick alfalfa problem they are finding out they are getting stimulation and nodu- lation on the alfalfa after soil sterilization. It may be a release of nutri- Dr. Endo: Do you know if the roots of your plants that have shown this IGR have mycorrhiza? I don't know. Dr. LeBeau: this phenomenon. I am saying that it occurs on turf grass as well as on alfalfa, winter wheat, sugar beets and other winter cereals. I haven't done any research on Dr. Fenwick: You stated that the one-shot application for control of severe snow mold is no longer recommended. What do you recommend? It is a little premature to say exactly, but we Dr. LeBeau: are working with inorganic and organic mercurials. We are convinced, f r om our experiments this year, that two or three applications in the fall offer much better control. For exam- ple, w e ' re not getting bad results with Panogen. Using one- shot applications of six ounces of Panogen per thousand, we didn't get good control, perhaps 50-60% control. But if we put three applications at three ounces, and Panogen is a relatively cheap fungicide compared with inorganic mercur- ials, we get much better control. With our inorganic m e r- curials, either mercuric or mercurous chloride, we find that we need at least two applications. For the exact timing, we want to get some trials out in various areas of western Canada. Say we were going to put treatments on September 15th, the end of September and again on October 15th. If we are going to do this at eight locations, we need some cooper- ative trials. really needed. Even though a lot of people are treating, they I think uniform testing is something that is I think the time of appli- are just not getting good results. cation is very important. I realize that extra applications take a little more labor, but if you could get good control with a fungicide at about a tenth of the cost of inorganic m e r- curials, the savings might apply toward your extra labor costs. Mr. Gabert: On that unidentified Basidiomycete, were you able to get spores f r om it or get in it to grow culture? I refuse to even think about it. Dr. LeBeau: a lot of time trying to get that pathogen to sporulate. we don't know how it over-summers. We have never seen spores and we don't know how the pathogen is disseminated. A ll we know is that it is ubiquitious throughout the Canadian prairies. I have wasted In fact, Dr. Worf: your snow mold problems? Is the Typhula organism associated with any of Dr. LeBeau: Typhula is sporadic and does occur, but it certainly is of very minor importance in our area. Dr. Worf: You mentioned the HCN content of Marasmius. Do you associate the HCN with a part of a pathogenic relat- ionship there? I don't. I would not speculate that HCN is the Dr. LeBeau: toxic principle in Marasmius. the soil as well as in the mycelium and in the fruiting struc- tures. However, I have not associated it at all with patho- gensis. lation, the green effect you get in the rings. It may have something to do with that nitrogen stimu- I know it produces HCN in I would like to respond very briefly to your com- Dr. Altman: ment about this increased growth response (IGR) and a little bit of the work that Ifve done. There is a stimulation in r e- lease of nitrogenous compounds, including several amino acids and ammonia. change that occurs in treated soil. There is also a predom- inance of saprophytic Corynebacterium that contributes to this stimulation. have done this on many occasions. In addition, there is a micro-ecological It can be isolated and grown in vitro. I Dr. Long: Dr. Ferguson, at the University of Manitoba, indicated that, if he used a wood fiber material to cover bent greens, he was able to reduce the activity of the low temper- ature Basidiomycete. I'm not sure whether this was in com- bination with a fungicide or not, but he said it was quite effective. A re you familiar with the work there? I know some of the superintendents I know Dr. Ferguson quite well, but I don't Dr. LeBeau: know of this experiment. are using a seaweed type of product for covering turf and I would certainly think Dr. Ferguson has treated the turf with a fungicide, too. Any covering I have seen does not reduce snow mold infection; it usually stimulates it, unless there is some fungicidal action. A polyethylene cover c e r- tainly would increase the efficiency of mercurial fungicides. This covering may reduce the loss of the chemical or raise the soil temperature. I don't know which of these two factors are responsible for increasing the efficiency of the fungicide. Mr. Simmons: Could you time treatments at the end of the season when the snow is melting, or has melted, and obtain control of snow mold? Dr. LeBeau: No, but we used to think this could be done. I'd say you can with Fusarium nivale because it comes later. With low temperature Basidiomycete we get maximum HCN production, starting the first part of January, and by the middle of February and early March the damage has been done. they will die with the snow melting. I wouldn't say that the plants were all killed then, but Mr. Simmons: We seem to notice f r om some of our work here that good control will occur all the way up to that final snow melt. Then some disease will occur after that time. In a lot of cases, this is masked. You know Dr. LeBeau: the grass will come through and look pretty nice when the snow first melts. is still occurring. With this Basidiomylete, however, its too late to control the disease in the spring. If the snow stays for a long time, damage Dr. Lukens: true they are rarely seen in putting green turf. However, I have one comment about fairy rings. It's It was a new course that was In several years ago I tried to control f a i ry rings in Penncross greens on one golf course. carved out of wooded land on a hilltop in Connecticut. about four years, f a i ry rings popped up all over the place-- fairways, tees and greens. The superintendent was able to stop the symptoms with a wetting agent and water on the greens for about two years. Later, in spite of those treat- ments, the grass wilted and the typical fairy rings reappeared. Shortly thereafter, I ran many treatments, some where the fungicide in water was injected under pressure beneath the sod with a tree-feeder needle; other treatments were drenched on the turf. Nothing we did seemed to stop the grass f r om wilting out. The problem is still there. Dr. LeBeau: This is very unusual. We've had them all over the fairways on our courses, but very rarely on the greens. Dr. Endo: Dr. Lukens, were you referring to Marasmius, or Lepiota? Does this treatment work for Lepiota, also? Dr. Lukens: We were concerned with Marasmius. know about Lepiota. I donft ST. AUGUSTINE DECLINE (SAD) -- A N EW LAWNGRASS DISEASE Robert W. Toler Department of Plant Sciences Texas A & M University- College Station, Texas, 77840 Lawn and turfgrass production is a major enterprise in Texas. These grasses represent a permanent investment in better living, the value of which cannot be calculated in dollars alone. Cost of turf and lawn maintenance in Texas annually is estimated at $211 million (Holt et al., 1964). It is also estimated that 41% of the home lawns in Texas are in bermuda, 56% in St. Augustine and 3% in other grasses. Along the Gulf Coast of Texas, 96% of the lawns are in St. Augustine. The first account of a virus disease of St. Augustine- grass (Stenotaphrum secundatum) was reported by Todd (1964). He described the disease as being transmitted by mechanical means f r om St. Augustinegrass to sugarcane and sorghum, and back to St. Augustinegrass. Todd also deter- mined the mosaic virus strain infecting St. Augustinegrass to be an undescribed strain similar to that which occurs in sugar cane variety F 31-407. The effect of the disease on St. August ine was not known at that time. Abbott and Tippett (1964) reported that St. Augustine- grass grown f r om stolons and inoculated with an airbrush became infected with strains of A, B, D and H of sugarcane mosaic virus (SCMV). The virus was transmitted f r om St. Augustinegrass back to sugarcane. A natural infection of the mosaic disease had been observed on St. Augustine in Louisiana. Dale ( 1966) reported St. Augustinegrass seedlings mechanically inoculated with maize dwarf mosiac virus ( M D M V) and SCMV resulted in 80% and 76% infection, r e- spectively. MDMV has been shown to be similar in many r e- spects to SCMV and the viruses have been shown to be serologically related (Williams and Alexander, 19 65). Although the two viruses are similar, they do differ in one respect. MDMV will readily infect Johnsongrass, both in nature and experimentally. SCMV has not been found on this plant in nature, and in only one instance has infection f r om mechanical inoculation been reported (Abbott and Tippett, 1964). In Texas, the new mosaic disease of St. Augustine- grass was first observed in the Lower Rio Grande Valley in 1966 ( T o l er et al., 1969). By May of 1969 the disease had been observed in 13 counties in Texas (Fig. 1). Grain sorghum (Sorghum vulgare) is a host for both MDMV (Abbott and Tippett, 1964; Kuhn and Kozelnicky, 19 68; Sehgal, 19 66; Shepherd, 1965) and SCMV (Dale, 1966; Sum- mers et al., 1948; Todd, 1964), but has not been demonstrated to be a host for the agent causing decline in St. Augustine- grass. $ $$ Positive Identification of SAD Fig. l County map showing distribution of S t. Augustine Decline (SAD) in Texas during 1969. F i g. 2 Symptoms of S t. Augustine Decline (SAD) on S t. Augustine (Stenotaphrum recundatum). Healthy leaf on the left; three infected leaves on the right. The symptom of the new disease in St. Augustine is a chlorotic mottling (Fig 2). The mottling becomes more severe until the leaves are yellow. Stolon growth is retard- ed and shortened internodes may be observed. In advanced stages, necrosis of leaves and stolons occurs causing dead patches in the turf. These areas are soon invaded by weeds and other grasses. Symptoms of St. Augustine infected with MDMV are similar to those infected with SCMV. Within two weeks after inoculation with MDMV or SCMV, elongated chlorotic and green islands develop in contrast to the chlorotic nottled ap- pearance for the mosaic condition under current investiga- tion. The SAD disease appears to be caused by a new virus or a mutated strain of an existing virus. The morphology of MDMV and SCMV are very simi- lar. Williams and Alexander ( 1965) reported MDMV parti- cles to be flexuous or semi-flexuous rods 750 mu in length. F r a z i er et al. ( 1965) demonstrated SCMV particles to be long, sinuous particles with a mean length of 743 mu. Other researchers have found the mean length to be 755 mu (Pirone and Anzalone, 1966). Maize dwarf mosaic virus has a non-persistent or stylet-borne relationship with its aphid vectors (Messieha, 1967). The corn leaf aphid, Rhopalosiphum maidis (Fitch), has been found to be one of the principal vectors of MDMV ( T o l er et al., 1967). Physical property studies by Shephard ( 1965) have n ot at 10-3. Extracted sap held at room temper- shown the virus to be thermally inactivated in 10 minutes at 55°C, but not at 50*C. Infectivity was retained at dilutions of 10-2, ature was infectious after one day but not after two days. MDMV has properties similar to those of SCMV (Ross, 1964). The host range of MDMV has been found to be similar to that of SCMV. Shephard ( 1965) reports that host range for both viruses is limited to the Gramineae. Losses Figure 1 shows the distribution of SAD in Texas. In Nueces County, it is estimated that 85% of the lawns are in- fected. Severity of the disease in infected lawns ranged f r om trace amounts to as high as 100%. In Corpus Christi alone, the loss to homeowners is estimated at $18 million. Symptoms in St. Augustinegrass Symptoms of this disease can be used as the diag- nostic characteristic in identifying the problem. The first symptom is a mottled appearance of the infected leaves that could be described as spotted or stippled. The mottled condition appears as small chlorotic spots in a green leaf. As symptoms progress, these spots coalesce and larger mot- tled spots occur. The entire leaf may eventually be o v e r- come with chlorosis. This disease should not be confused with iron chlorosis. With iron chlorosis, a yellow streaking runs parallel with the leaf veins. During the second year of infection, the grass con- tinues to become chlorotic and weakened to the extent that weeds and grasses begin to invade the lawn. Very slow growth is noted and numerous chlorotic leaves are observed. Any new growth is slightly chlorotic and mottled. During the third year after infection, the grass thins out and begins to die in large patches. The leaves generally begin to die first, then the stolons. Host Range Most of the common varieties of St. Augustine tested by manual inoculation have been found susceptible to SAD. SAD failed to reproduce in common bermuda grass, Johnson- grass, wheat, oats, barley, rice, grain sorghum, Kleingrass or corn. However, three millets were found to be suscept- ible: (1) German foxtail; (2) pearl, and (3) proso. Proso m i l- let is the best indicator and is a diagnostically-useful tool. Symptoms appear within 6 days after inoculation and the dis- ease progresses in a lethal manner causing death of the plants in 14 days. Proso is, therefore, an excellent indica- tor host. Diagnostically this cuts identification time f r om 30 days, the normal time necessary for St. Augustine to show SAD symptoms, to only 6 days f r om inoculation to symptom expression in proso millet. Transmission Mechanical transmission with carborundum and buf- f er rubbing is fairly successful. The artist airbrush trans- mission has not been too effective at 100 psi and additional work at varing pressures, flow rates and times are under study. Preliminary studies indicated that lawn mower trans- mission was evident at Edinburg, Texas, three months after inter-planting healthy grass. Soil transmission studies have Insects investigated as vectors without all been negative. evidence of transmission are chinch bugs and leafhoppers, while still under study as possible vectors are mites and walking scale. Pathogen Transmission, host range, symptomology, severity, purification and isolations tentatively indicate the pathogen is a mechanically transmissible virus similar to the rod- shaped sugarcane group. This information will be ulti- mately published upon completion of the studies currently underway on morphology, serology and biochemistry of the infectious particles that have been isolated. Control Studies are underway to evaluate various strains of St. Augustine for tolerance to the SAD disease. Surveys are currently being made to collect clones that have survived in areas heavily infected with SAD. are also being screened f r om the St. Augustine world collec- tion maintained by Dr. G. C. Horn at the University of Florida, Gainesville. Promising clones have been found to be r e s i s- tant to infection f r om mechanical inoculation. This material is being tested for field resistance and will serve as the basis for the new breeding program currently being initiated by Dr. George McBee at College Station, Texas. In addition, genetic sources R e f e r e n c es Cited Abbott, E. V. and R. L. Tippett. 1964. Additional hosts of sugarcane mosaic virus. Plant Dis. Reptr. 48:443. Dale, J. Li. 1966. Infection of St. Augustinegrass with virus causing maize dwarf mosaic. Plant Dis. Reptr. 50: 441. F r a z i e r, N. W., J. H. Freitag, and A. H. Gold. 1965. Corn naturally infected by sugarcane mosaic virus in California. Plant Dis. Reptr. 49:204. Holt, E. C., W. W. A l l en and M. H. Ferguson. 1964. Turf grass maintenance costs in Texas. Texas A g r i. Exp. Sta. B-1027. p. 19. Kuhn, C. W. and G. M. Kozelnicky. 1968. Maize dwarf m o s- aic virus in Georgia. Plant Dis. Reptr. 52:320-322. Messieha, Mimi. 19 67. Aphid transmission of maize dwarf mosaic virus. Phytopathology. 57:9 56-9 59. Pirone, T. P. and L. Anzalone, Jr. 19 66. Purification and electron microscopy of sugarcane mosaic virus. Phy- topathology. 56:371-372. Ross, A. F. 1964. Identification of plant viruses. In Corbett, M. K. and H. D. Sisler. 1964. Plant Virology. Univ. of Florida P r e s s, pp. 68-92. Sehgal, O. P. 19 66. Host range, properties and partial puri- fication of a Missouri isolate of maize dwarf mosaic virus. Plant Dis. Reptr. 50:862-866. Shepherd, R. J. 19 65. P r o p e r t i es of a mosaic virus of corn and Johnsongrass and its relation to the sugarcane mosaic virus. Phytopathology. 55:1250-1256. Summers, E. M., E. W. Brands, and R. D. Rands. 1948. Mosaic of sugarcane in the United States, with special r e f e r e n ce to strains of the virus. U. S. Dept. A g r. Tech. Bull, 955. 124 pp. Todd, E. H. 1964. Sugarcane mosaic on St. Augustinegrass in Florida. Plant Dis. Reptr. 48:442. T o l e r, R. W., C. D. Hobbs and A. J. Bockholt. 1967. Identi- fication, transmission, and distribution of maize dwarf mosaic in Texas. Plant Dis Reptr. 51:777-781. T o l e r, R. W., N. L. McCoy and J. Amador. 1969. A new mosaic disease of St. Augustinegrass. pathology. 59:118. (Abstr.) Phyto- Williams, L. E. and L. J. Alexander. 1965. Maize dwarf mosaic, a new corn disease. Phytopathology. 55: 802-804. DISCUSSION PERIOD Dr. Weihing: What are the characteristics of the particle? Dr. Toler: Some observations have been made and we found a rod-shaped particle. We have also gone through some pur ification procedures and found a straight to slightly flexuous rod. plus. This material is being further purified, and our s e r- ology is under way at present. Also, w e ' re trying to build up a titer. It seems to be fairly long, around 700 millimicrons Dr. Weihing: Do you f e el that the primary transmission of the virus has been mechanical throughout the area, or is there a biological factor? Dr. T o l e r: Most of the disease that we encountered at first was in older lawns, which indicated that probably some type of vector was involved as well as mechanical transmission. Of course, there is always the possibility of vegetative spread f r om the nurseries since we have not surveyed the nurseries nor examined any of them. We know that the virus can be spread quite readily through the stolons and that it is translocated rapidly after infection. Planting ma- terial is a source for spreading it to new areas. We f e el that mowers have been a contributing factor, particularly the rotary mower and the use of custom mowing in areas that are heavily infected. We have worked v e ry closely with some of the lawn-care services. We f e el that the rotary mowers that mow several lawns per day have con- tributed to this rapid spread. However, we still f e el that there is a biological agent, probably an insect of some type, contributing to some of the spread that we can't account for by mowers or by planting infected material. Dr. Wittenbrook: Do you know of any chemical control, how- ever slight, that has been tried on this? Dr. T o l e r: Nothing, other than the nutritional amendments. Dr. Wittenbrook: In a lawn that has been killed by this virus can you come back and clean it off, replant and get a normal lawn that is not infected? Dr. T o l e r: We have some areas in which we have removed the old thatch, fumigated with methylbromide and sprigged in healthy material that was grown f r om seedlings that we had multiplied in isolation. At this time it is still healthy. But this is an isolated area near San Antonio and it is completely surrounded by cactus and mesquite. may not pick up some transmission later on. This is one reason we are checking it for biological agents. We are look- ing for mites and various insects, mostly soil inhabitors and vegetative feeders, to see if we pick up any biological agent that could transmit in the area. I can't guarantee that we Mr. Simmons: Do you see any reason why this virus won't continue to move north? It's moved quite rapidly in the last couple of years Dr. T o l e r: and I see no reason why it cannot continue to move into new areas where St. Augustine is grown. The use of disease-free planting stock and disinfesting mowers may help cut down immediate spread in some areas and your long distant spread by man. I don't anticipate that it will suddenly stop spreading. However, I mentioned we have not, to date, identified a vector. Dr. Harrison: Have you had the chance to check on the possi- bility of nematodes as vectors? Dr. T o l e r: We have. Dr. Thames and Mr. McCoy at Texas A & M have checked some three or four species of nematodes as possible vectors and isolated them in pure cultures. We fed them on the material and moved them into healthy plants. As yet, we have not positively transmitted the virus under these conditions. This does not rule out nematodes as pos- sible vectors. Dr. Harrison: Do you know what species of nematodes were used? Dr. T o l e r: Yes. Dr. Holcomb: You haven't said much about regulation. A re your regulatory people aware of this, or have they been made aware of this in relation to interstate shipment of turf? Dr. T o l e r: They are aware of it, but since this is a different area f r om research, I leave it up to the extension and regu- latory people. Dr. Worf: This is quite timely because I was going to ask the same question. You've indicated some of the problems that would be involved with trying to minimize the spread through individual action, but is the area of distribution con- fined to Texas at present and is there a possibility, theoreti- cally, of controlling SAD through quarantine restrictions? Dr. T o l e r: F r om a theoretical standpoint, yes, if the quaran- tine could be made 100% effective. Even though it is not absolute, I would say that it probably would help in slowing the spread, if you could keep the plant materials completely restricted and prevent homeowners f r om shipping samples at random. To date, no other state has reported the disease. Dr. Scott: You mentioned proso millet and foxtail as hosts. Have you found any natural infections in these species? Dr. T o l e r: No, we haven't found any natural infections. The millets are grown in the western part of the state and the Lubbock area in the South Plains. The seed production blocks are in this area. We have not found SAD in our survey of that particular area. However, they are sometimes infected with maize dwarf mosaic virus. Dr. Carlstrom: What about seed transmission? Dr. T o l e r: We have been unable to obtain sufficient seed f r om infected material to get an evaluation on seed transmission of the virus. Dr. Elliott: Would you like to predict whether this is going to be a maize dwarf mosaic or a sugar cane mosaic related virus? Dr. T o l e r: This may be a little difficult. F r om host range arid some of our physical and chemical property studies, it appears to be somewhat different. However, the particle size is within the range of SCMV and MDMV. appear to be a flexuous rod at this time so it makes it diffi- It doesn't cult to speculate until we can make our complete compari- sons and collect our serology data. W e ' ll have to rely more on serology. Dr. Lloyd: Does maize dwarf mosaic virus or sugar cane mosaic virus infect St. Augustinegrass? Dr. T o l e r: Yes, they go to the clones that are also sus- ceptible to SAD. During some phases of the syndrome, they produce a slightly different symptom. The maize dwarf and sugar cane mosaic symptoms appear to be somewhat more broken interveinal lines. In other words, you get more of a broken pattern of lines in green areas that I like to call "green islands." Also, they tend to be more confined to interveinal areas and are somewhat more broken and chlo- rotic in the green areas than grass infected with SAD. SAD tends to show more yellow and more of a block-type of mosaic pattern than we usually find with maize dwarf or sugar cane mosaic in St. Augustine. However, the symptoms alone are not always sufficient to tell them apart. But there is a difference, if it is observed very closely. Symptom comparison as a clinical tool is not as conclusive as use of millet indicators. We have also tried to infect sugar cane unsuccessfully with SAD, at least with the one variety we have inoculated up to this time. We do plan to inoculate other varieties of sugar cane that are known to be sus- ceptible to the different strains of sugar cane mosaic virus. S P E C I AL DISCUSSION SESSION ON TURFGRASS DISEASE PROBLEMS Dr. Long: Dr. Partyka, you mentioned that you would like to have someone elaborate on the use of infrared detecting devices for studying disease infestation development. Would you want to comment on that? D r. Partyka: There is some discussion because I know many of the folks are concerned with evaluating plots. I think most people are aware of disease detection methods. Ifm just wondering whether this could be applied in some method to come up with a uniform reading for losses or es- timates of a disease problem in turf. I think we all realize that there are many complicating factors when you work with turf plots. Rather than making leaf spot counts, or so-called eyeball evaluations, it has been mentioned that disease might be assessed on a more detailed basis with infrared photographs put through a scanning device. This would give some idea as to exact color differences rather than relying on the eyeball method of evaluation. Experiments are being made with other techniques. I think a lot of people are familiar with remote sensing devices. Disease losses are always of concern, but sometimes the question comes up as to whether they're really that important in certain crops. Sometimes, if we knew ex- actly what was involved, we might be able to get more money f or research. Looking ahead to the future, turf and ornamentals are going to be the biggest crops in the country. I have a student who has been doing some work D r. Altman: with infrared. Aside f r om the turf work, I 'm also project leader for sugar beet diseases. In sugar beets the infrared has been picking up growth-response differences following soil fumigation in the field. These infrared pictures can be reproduced. You can detect differences in nitrogen, or ap- parent nitrogen in the leaves. You can also detect differences f r om airplanes. Grain fields infested with rust are visible be- cause they emit different color bands of light and you can pick them up. I'm wondering if, in addition to disease, you could use infrared as a possibility for evaluating the fertility level on golf courses and parks. Mr. Brown: Remote sensing has been successful when used in a satellite. The satellite is in a very specific orbit. They take pictures and get the same light intensity everytime it orbits. By the time a plane covers a large area, it may be subjecting itself to different light intensities. ing what instrument could be used that would be portable enough and would not be subjected to these variables? I was wonder- Dr. Wadsworth: Several years ago we got involved in this work on cereal diseases, primarily leaf rust on wheat. This was an aerial reconnaissance photographing mission that took a very close program of ground support to find out ex- actly what the reflectance differences were showing. In our particular case, we found some of the variances in r e f l e c- tance were due to differences in varieties. Without very close ground support, the reflectance differences were not very mean ingful in crops that were maturing at different times. Recent information on the satellite program indicated that differences could now be detected on as little as ten acres. Apparently, considerable progress has been made. Dr. Harrison: Perhaps a little more practical and important to me is the question of rating and reporting of disease inci- dences and the degree of control obtained. The systems I use differ f r om those used by others in determining the degree of control obtained with experimental chemicals on Helminthospor ium leaf spot, dollar spot and brown patch. the people here think it would be desirable to work toward a standardization for determining the degree of control obtained with experimental chemicals for the more common turf disea- ses. I would like to get some opinion f r om the people here and an idea of the different rating or evaluating techniques used. I wonder whether One of the speakers yesterday mentioned that, in the evaluat- ing process, he judged the degree of disease control. Some workers with Helminthosporium leaf spot, for example, pick 100 blades at random and simply count any grass blade that has spots, regardless of the number of spots on that blade. With stripe smut, I know some workers who are counting the number of tillers with smutted leaves per given area of a plot. With dollar spot, three of my assistants evaluate the plots by visual inspection and, to avoid bias, they note their observations on records with the treatments omitted. We use a purely objective rating of the plots for brown patch. With other diseases, we do it in a very subjective sort of way. and whether or not the people though it would be of any val- ue to discuss the topic now. I just wondered how others evaluate disease control I think everybody chooses the means that is Dr. Lukens: most convenient for him. It would be difficult to get us all thinking in the same groove. We do run into problems be- cause one worker reports control with a chemical in one rating system and another reports the same chemical with- out effect. Primarily, they are talking about two different systems of rating disease control. For instance, with stripe smut, my results differed from those of Dr. P. M. Halisky in New Jersey. I was working on a lawn that was heavily infested with stripe smut and looking at it f r om the viewpoint of the homeowner as to what he ex- pected in control and appearance. I counted the number of patches (about the size of silver dollar) blighted with stripe smut. The grass was actually yellow and dying. Dr. Halisky was counting the number of tillers that he found smutted in green turf. Naturally, we drew different conclusions f r om our results. I didn't have to look at blighted tillers in my system because most were blighted. I was evaluating how much area of turf was discolored by disease. Turning to Helminthosporium, I compared several methods of recording data with a view to precision and time required to do the job. I counted the leaf spots per blade and analyzed for chlorophyll. Then I counted the number of square inches in a square foot diagram that contained leaf spot and crown rot. Finally, I estimated visually, using the Horsfall-Barret system, the area of turf brown f r om melting-out. The data all came out about the same when converted to percent con- trol of disease by a particular chemical. The visual estimate was by far the simpliest and quickest way of measuring dis- ease. I base my field data now on the visual estimates of per- cent area brown. Any greater precision that one may get from some other method isn't worth the extra time it takes to get the data. I count the number of leaf spots per unit length of blade in the greenhouse and, in certain situations, the size of the spots is recorded. The number of spots is a measure of infectivity of the fungus whereas the size of the spots mea- sures disease development. However, the time required for collecting data is very substantial. I donft think we can all use one system unless we are rat- ing performance of fungicides on turf. This is where things can be standardized. Some people don't like to use a logar- ithmic visual system, which is an accurate way of measur- ing, because what is measured is one's ability to distinguish between differences. You can smell one rotten apple in a whole bushel as well as you can smell 50 rotten apples. Why not utilize this precision of distinguishing the fine trace and have it reflected in the data? With arithmetical grades, say five equal grades between 0-100, one loses precision near the ends. Since values above 80% are of greater interest in disease control, arithmetical grading is a poor method of visual estimation. It is an aid to all of us that are having to I think this is an important subject worthy of a Dr. LeBeau: few comments. stand up and be counted, and justify our existence. I know this is particularly true in Canada. Currently, we are hav- ing to justify most of our research projects. They have set up a special program to try and develop methods of deter- mining how much loss we get f r om plant diseases in Canada. This, of course, is a very difficult problem. When you are dealing with rust of wheat, it's quite simple. You've got a devastating disease, a chemical method of control, and r e- sistant varieties. Using these, they've made some very accurate estimates and have shown we can lose 100-million bushels of wheat in western Canada f r om rust. When we get into other areas, such as turf and forage crops, estimates are going to be much more difficult. This is an area that we are going to see some action in the future, especially in In Pennsylvania, they claim turf work in the United States. turf is their number one agricultural industry. I think that we need to estimate the loss f r om turf diseases in terms of the gross national product. Not only the value of fungicides, but how many man hours does this add to our dollar value in labor? What does this do to stimulate the economy? I think you can relate the value of turf culture, turf maintenance and installation and it's importance in the national economy. There is room for a survey noting how important it is to con- trol these diseases. The more pressure we can advance for this type of survey - the better we might make our cause look, especially in the area of turfgrass pathology. In Dr. Lukens: A couple of years ago I had the problem of t r y- ing to evaluate the dollar value of turf in Connecticut. addition, I *ried to estimate disease loss from Helminthos- porium blight, the most important disease of bluegrass. When to employ control measures, replace turf, or do noth- ing is questionable? Every man has his own castle and he has his own budget for that castle. Wealthy people may act at the first sign of a loss in aesthetic value. Others go along with a disfigured lawn without giving it any concern. How do you measure dollar loss in this situation? Probably, most homeowners would act if deterioration exceeds 75% in their lawns. I would like to ask a specific question about Dr. Harrison: brown patch, one disease which I have always been very con- cerned about the way I was rating. To those people who have worked, or who are working with any control materials on brown patch, how do you rate your plots for control for brown patch—according to the various materials used? I used a very simple eyeball technique for getting some sort of evalu- ation and tried to put it on a 1 to 10 scale. I'm not sure it is the best method to use. I would like to hear if there are any other methods being used so I can, perhaps, modify my own in order to get a better system of evaluating the amount of Rhizoctonia brown patch. In my system, I give my assis- tants blank copies of the plot plan and ask them to rate the plots weekly as long as the disease is present. Then at the end of 5 or 6 weeks, we try to put the data together on a 1 to 10 scale. A re there any other techniques being used with Rhizoctonia brown patch in particular? I don't think you can get an evaluation of brown Dr. Altman: patch in two weeks. We put fungicide on 50 or 100 sq ft plots and evaluate them every month for the presence of brown patch. Then, by going through approximately a five-month evaluation with fungicides, we can tell if the disease is pre- sent. On a five week basis, all you can do is reduce the size of the smoke ring or the size of the brown patch areas. The disease spreads if you restrict your applications. This would indicate that the time period is a little too short to make a fair evaluation. Dr. Wadsworth: We have carried out a study on the golf course f or a number of years, and our two primary diseases are brown patch and dollar spot. In this case, we use a control- type spray program for one year. Materials that look good at the end of this period go into a preventative program on the golf course the following year. Consequently, we get two years of data on these materials. In our evaluation program we measure the number of square feet of affected turf at i r- regular intervals and put this on a 1,000 sq ft basis, since our plots on the green are not all the same size. This has worked out very well for us. It wouldn't seem to matter what type of system is Dr. Dale: used if it can be converted to a common factor. For exam- ple, in Gould's work I believe he uses the 1 to 5 system in his evaluations. In cooperative corn work in the south, we have all agreed to use a common disease system rating of 1, 3, 5, 7 and 9. If someone does not wish to evaluate this closely, they can use 1, 5 and 9. This can be averaged in with the 1, 3, 5, 7 and 9. As long as people agreed on a sys- tem that can intermesh -- 1 to 10, 1 to 5, or something else -- it would not seem to matter what system is used. In the fungicide-nematocide tests published each Dr. Long: year, different rating procedures are used. It would aid com- munication if a universal rating procedure could be adopted. Dr. Altman: I would like to go back to Dr. LeBeau's comment. Recently I made an estimate of the value of turf on the eastern slope of the Rockies in Colorado. I came up with the figure of $350-million, including both the value of turf and maintenance. A banker and several golf course superintendents independent- ly came up with a figure of $325-million. industry, production is valued at about $35-million, so there is a tenfold difference in value of there two industries. Yet, experiment station support for turf is one-tenth of that for sugar beets. With the turf and ornamental industry expanding, In the sugar beet I think is rather important that we try and come up with a little better selling job in this area. Dr. Carlstrom: One more small point on this. going to be making evaluations on the value of turf disease control as a selling point, I think we should throw in orna- mentals there, too. This would probably comprise 50% of the total disease losses experienced in all crops each year. If we are I believe there is another aspect of reporting Dr. Worf: results that has not been mentioned. We have been talking about comparison of treatments and material for control and, also, in terms of reporting them. literature, one of the common problems in reports giving a comparison of treatments is that there generally isn't a summary indicating whether any of the treatments are ade- quate. In other words, we may compare two dosages. One may be bad and the other one very bad. To a person not aquainted with the situation, such a report doesn't indicate if there is anything really encouraging that should be looked at as a possible control. In pursuing the Dr. Harrison: There were some other points I thought I would like to mention with regard to leaf spot. I know there are several systems being used and I wondered whether any- one felt there were any differences between systems for rating the leaf spot phase. I know some people count the number of leaves with spots, while others actually count the number of spots per leaf. With the same disease, on the other hand, others simply try to estimate the amount of dead turf per plot. has an opinion one way or the other on how that should be done with regards to Helminthosporium leaf spot? I wonder whether or not anyone here Dr. Worf: Our greatest concern hasn't been with the leaf spot phase, but with the damage that occurs as the disease develops in the crown area. we have rather ignored the leaf spot response and placed more emphasis upon the amount of total death that takes place. This is the stage of the disease that the homelawn owner or the golf course superintendent sees and becomes concerned about. I don't know, but I think the question has to do with whether there is a correlation between the amount In our own particular situation, of leaf spot that would occur at one time and the amount of crown rot that would develop, let's say, at a later stage in the development of the disease. D r. Lukens: We consider the leaf spot stage as a minor nuisance. Turf is lost f r om crown infections. We do not recommend the removal of clippings as a measure of dis- ease control. However, in Maryland, people are advised to remove clippings in the spring to reduce the severity of this disease. I didn!t go along with this advice until I v i s- ited this state and saw their bluegrass in the spring. The leaves were plastered with leaf spot. In addition to their unsightly appearance, the infected leaves contributed sub- stantially to the total inoculum. Because of such an over abundance of inoculum for crown rot, it appeared wise to remove leaves under these extreme conditions. Thus, the seriousness of a stage of disease can vary with location. I think your comment begs a question, too, with D r. Worf: respect to Helminthosporium. We've talked a lot about that disease but I wonder if, when we are dealing with these Hel- minthosporium control plots, we should also be taking the time to determine what species is present. I don't want to break the line of thinking with respect to rating systems, but I would be interested in an appraisal of the group here in terms of the relative importance of H. vagans versus sativum, or other species in terms of leaf spot, crown rot or even root rot development. Has there been some definitive work indicating that we might have leaf spot com- ing f r om one Helminthosporium and crown rot f r om another H e lm inth osporium? D r. Partyka: Since w e ' re on leaf spot, I wonder if we should take a closer look at the f e r t i l i z er rates and nutritional aspects of this problem. are building up since we have gone to higher f e r t i l i z er rates. Maybe different types of nitrogen and different times of year, in relationship to application, should be considered a little bit more. It seems that many disease problems D r. Lukens: I will try to answer Dr. W o r f 's question on discerning the several species of Helminthosporium that attack bluegrass. We have isolated H. vagans f r om leaf and Isolates taken crown infections during times of epidemics. in summer are difficult to sporulate in the laboratory, but the few spores produced behave as H. vagans. Crown rot f r om H. vagans and H. sativum have many characteristics in common and both respond to the same control measures. To distinguish between the two may be of little practical value, but may be of academic interest. However, isolates of H. In my talk I have r e f e r r ed to differences in vagans can vary. sporulation with temperature of two isolates f r om leaf spots of the same patch of diseased turf, moreover, one can change morphological characteristics and physiological performance drastically by manipulating cultural procedures. On appraising the performance of fungicides, I find that visual estimates of turf diseases are reliable under many circumstances. Because numerous readings can be obtained, one can assess the performance of a treatment by the rate of change in disease during the season. The effect of treat- ment on the rate of development of diseases yields more information on performance than does data describing the effect of treatment on disease at one time. Also, when con- sidering rate of change, performance is not entirely depend- ent upon the absolute levels of infection. Thus, one can obtain reliable data on the performance of a treatment in seasons of low levels of disease. v aga n s« Dr. Elliott: Back to this question about the different species, I expect people looking for resistant bluegrass varieties would be v e ry interested in knowing what fungus species are involved. According to reports, essentially all of the leaf spot in Maryland is caused by H. dictyoides, not by H. sativum I think you'll find in reports f r om Minnesota or that the species is mainly H. sativum. Since Maryland is neighboring on West Virginia, we thought maybe we had some H. dictyoides on Kentucky bluegrass. We looked quite extensively at bluegrass, not necessarily lawns, but any bluegrass in West Virginia. Ninety-five percent or higher was H. vagans and we never did find H. dictyoides. The only other species we e v er find is H. sativum in bluegrass. It is very important that people know what species they are dealing with before they select a material for disease resistance. I can appreciate Dr. Elliott's remark about the Dr. Lloyd: area around Minnesota because I believe that happens to be North Dakota. H. sativum is the major pathogen in the lawn grasses there. From my own standpoint, I'm interested in the population of H. sativum in this area because it is a pre- dominant pathogen causing kernel black point, leaf blotch and root rot of wheat, barley and durum. I wanted to make a comment on Dr. Freeman: Regarding ratings for disease control, I use a visual rating system. this Helminthosporium species question. On bermudagrass, we run into several species commonly attacking the grass at the same time. One isolation may be Helminthosporium cynodontis and the next may be Helminthosporium stenospi- lum. Quite frequently it's a complex of organisms, at least as far as the Helminthosporium species are concerned on bermudagras s. Dr. Long: Do you use the designation, Helminthosporium ? Dr. Freeman: That's right. Mr. Bangs: Studies are frequently reported on the control of naturally-occurring fungus activity, regardless of which disease we are talking about. In many instances, no disease occurs during the treatment studies. Why don't researchers inoculate the disease plots so there is some disease in every plot studied? Dr. Freeman: We inoculate with Pythium in our test plots, and we do it routinely. Pythium is grown on sterilized oats, then mixed up in a bucket and spread in equal portions over each plot. We assume we are starting with equal inoculum in each plot. It has worked out quite well for us. That's the only one we have been able to successfully inoculate with in the field. I don't know why. I think there is a great danger in this proced- If you just throw out the inoculum Dr. LeBeau: ure if you're not careful. and then put on a control chemical, you may not be getting natural infection. On the other hand, if you can put your inoculum out and build up a disease nursery, and maybe use it next year, it would be more effective. much better if you can get natural infection and have a well replicated experiment rather than using artifical infection. I think it is Dr. Worf: With respect to Helminthosporium, we've had perplexing problems upon occasion. We have felt that, in the absence of disease, the environmental conditions were not appropriate for disease development. Here we would be dealing with an attempt to modify a local environment in order to bring about the onset of disease. we have conducted, we have not felt it was the absence of the inoculum that was limiting disease development. In the research Dr. Long: Dr. Freeman, do you recall whether they inocu- lated the centipedegrass in the brown patch plots at Fort Lauderdale? The infestations were uniform there last year. Dr. Freeman: They did artifically inoculate those plots. How they did it, I don't know. I think this comment about modifying the environment is important. One way they can do it in Fort Lauderdale is to put sand on their St. Aug- ustinegrass, and they will invaribly get brown patch. I tried to inoculate once in the field by covering the plots with burlap for 24 hours, but it was too much trouble. Dr. Long: Some researchers indicate that you get much more uniform and heavier infestations of gray leaf spot if you have a sprig St. Augustine planting with bare soil areas. Sprinkling or rainfall that splatters the soil on to the grass leaves appears to enhance the spread of this disease. Dr. Freeman: This is true with gray leaf spot. It appears the disease is much more severe on young, rapidly growing tissue. Therefore, we can get a very good test by using newly sprigged areas. Then we can get some idea of the num- ber of leaf spots and their prevelence. After a few weeks we can evaluate our disease control by the grass coverage of the various plots. Those that we got the best control in will have the most grass; those with the least control will have the least grass. If one con- Dr. Endo: I think this question of why we donft have more disease epidemics is very important since the turfgrass com- munity represents a kind of maximum expression of the three essential conditions required for disease. siders all the turfgrass acreage, it's remarkable that we don't have more disease. Why is that? Numerous references r e f er to the apparent survival of faculatative fungal parasites in infected turf debris. But I'm not convinced that this debris is always important and is always functioning as a source of inoculum. Since the facultative parasites must complete with the saprophytic micro-organisms in the litter, an understand- ing of the factors that determine the outcome of this competi- tion may be the key to predicting the development of turfgrass diseases caused by facultative fungal parasites. It's very strange that we can not predict the development of disease caused by facultative fungal parasites, only diseases caused by obligate parasites. Why is this? I think it is be- cause the obligate parasite has essentially evolved a life cycle that has removed it f r om competition. Obligate para- sites either produce their spores above the surface of the host, or within the host where it is isolated f r om competing microorganisms. When the spore is airborne, it is essenti- ally isolated f r om competitors. It is well known that spores of the obligate parasite attach and develop best as mycelia in vigorous, actively-growing tissues. This adaptation also serves to remove them f r om competition since few organisms are present on the surfaces of actively growing leaves. Dr. Leben has shown that the surfaces of leaves are remark- ably f r ee of saprophytes until the leaf has attained its' half- life. After this, there is a very rapid build-up of saprophytes and very weak parasites which would compete with facultative parasites for nutrients during their prepenetration and pene- tration stages. The lower senescent leaves of turf are un- doubtedly colonized by a characteristic group of microorgan- isms which may inhibit or favor disease development. I con- sider this question of competition and its outcome as funda- mental to understanding the development of turfgrass diseases. Another important question that Dr. Worf r e f e r r ed to is de- termining the initial sites of infection. Do Helminthosporium infections start on the leaf, the stem base, or on the leaf sheath? Is there a correlation between the amount of leaf infection and the amount of foot rot? I think that when the disease starts to develop in the spring in California, the infection frequently takes place on the leaf sheath. The leaf sheath is a very favorable ecological niche because the sheath clasps the stem and the result is a perfect incubation chamber essentially protected f r om competitors. When suc- cessive leaf sheaths are removed, the mycelium of Helmin- thosporium can be seen growing out of the leaf sheaths and colonizing successive sheaths. It has been made very clear that crown frequently follows. It is imperative, the foot rot stage is the most important. therefore, to separate these two sites of infection and eva- luate this relationship. Infection of the stem base or Dr. Scott: Somewhat in relation to what Dr. Endo was men- tioning, during my work with the cereals using Helminthos - porium sativum, I found that this organism was an extremely poor root pathogen. Very little infection could be obtained by root inoculations; however the leaf sheath, leaf and crown tissues were highly susceptible to infection by this fungus. In all cases I found that crown infections orginated f r om leaf sheath infections. Where I did get root infection with Helmin- thosporium sativum was in the adventitious roots of the crown. The fungus always stopped right at the edge of the crown tissue. leaf sheath infections easily spread into the crown tissues. It never entered into the crown, but the In Nebraska, we had exactly the same experi- Dr. Weihing: ence in following through with the crown an,d root rot of Hel- minthosporium sativum on cereals. The development into the roots never occurred until the plant was under consider- able stress. We see the same thing in bluegrass lawns in our area where they undergo tremendous heat and drought stress during the summer. Throughout this decline, caused by environmental stress, there is rapid involvement of the root system and crowns with Helminthosporium. Dr. Long: Do you think over-saturation of the soil in cool, wet periods could contribute to stress? Dr. Weihing: That certainly could cause stress. I have been trying to decide what would represent Dr. Endo: the best stress o n t u r f g r a s s. Dr. Couch has repeatedly shown that, with three facultative fungal parasites, he produced the most s e v e re disease on t u r f g r a ss when plants w e re under moisture stress. Why should that be? H. L. Russell has reported that desiccation causes s e v e re damage to the root cortex and injury to the plasma membrane. Leakage of nut- rients would f o l l ow that germination of dormant fungal struc- tures and byphal growth. Now if moisture stress is placed on a plant, and both old and young leaves a re present, the older leaves would be colonized by s a p r o p h y t i c - m i c r o o r g a n- i s ms and probably would represent unfavorable substrates. On the other hand, young, vigorously growing tissues would tend to lack the population of m i c r o o r g a n i s ms that would compete with our facultative fungal parasites. Some s y m- ptoms of drought a re obvious. The one ingredient n e c e s s a ry f or fungal activity is usually supplied--water. Contrary to what is recommended, many golf courses in California a re watered daily. I told g r o w e rs that it was an ideal disease situation but they frequently claimed a low incidence of dis- ease. It may be that light daily watering f a v o rs the build-up of the litter, inhabiting saprophytic m i c r o - o r g a n i s ms which cpmpete with our facultative fungal parasites. Dr. Scott: As I said e a r l i e r, we found Helminthosporium sativum a v e ry poor root pathogen. . Root infection occurred only under variable soil water conditions in greenhouse studies. Plants w e re watered to soil saturation point, then allowed to dry to near the wilting point b e f o re watering again. Under these conditions, we obtained a s m a ll amount of root infection by Helminthosporium sativum. Where soil moisture was maintained at a constant l e v el near f i e ld capacity, we did not obtain root infection. M r. Simmons: This comment concerns leaf spot. spoken of as a spring disease in most cases. observations here, we f e el that the cool, wet weather condi- tion in the f a ll f a v or leaf spot activity. You will find leaf spot quite active at that t i me and I wonder if this doesn't account f or the f o o t - r ot stage that you see in the spring. As a follow-up, we have found that f a ll applications of certain It's been In many of our fungicides, principally PCNB, will carry over through the winter and provide leaf spot control the following spring. In partial agreement with Dr. Scott are the data Dr. Lloyd: in F. C. Butter's monograph on "Root and Foot Rot Diseases of Wheat." He states that H. sativum has two soil moisture optima: above 60% moisture holding capacity and below 30% are the most favorable optium for Helminthosporium infec- tion. At least in wheat crown and roots. G U T T A T I ON FLUID AND ROOT TIP DEGENERATION IN TURFGRASSES Robert M. Endo Associate Plant Pathologist University of California Riverside, California, 92502 I won't say much about guttation fluid and its effects on disease development because I have done very little additional work on it. However, I believe there are some v e ry important ecological niches in turf that favor the growth of fungal hyphae over the aerial surfaces of grass plants. Guttation fluid may be one means by which fungi obtain the necessary nutrients and energy necessary for mycelial growth and infection. There are at least six facultative fungal parasites affecting turfgrass that are capable of growing and spreading f r om plant to plant by means of ectotrophic hyphae and causing infection. I don't know of any other crop where above ground parts are attached by hyphae of more than one or two facultative fungal parasites. The exogenous source of nutrients and/or food base necessary f or ectotrophic hyphal growth must come f r om somewhere-- but where? Moisture and Drought Stress I think the literature provides us with some clues. Katznelson et al. (1955) have shown that if moisture stress is placed on plant roots, they will exude more amino acids. Russell (1970) has demonstrated that the root cortex of bar- ley collapses after short periods of desiccation. Tukey (1970) has shown that more nutrients are leached f r om the a e r i al organs of plants into water droplets if they are in- jured, and that senescent leaves leak more than immature or mature leaves. Das and Leopold (1964) have indicated that there is an increase in permeability as leaves approach senescence. Others have pointed out that lack of nutrients, water, shading, high temperatures, or any factor that limits growth, initiates senescence. Drought injury appears to offer the best conditions for disease development in turfgrass because the injured leaves, following the application of water to relieve the water stress, tend to leak the nutrients necessary for the germination of dormant fungal structures in the thatch and soil, and the sub- sequent growth of hyphae. If the period of drought stress is prolonged, the activity of competing saprophytes may be r e- duced; especially if soil temperatures were unfavorable for their development (eg 50oF) but still favorable for pathogen development. Although numerous sources of host nutrients, such as guttation fluid, are available to nourish fungal hyphae, it is obvious that competing saprophytes may utilize them In fact, it is highly probable in most cases that the as well. competing microorganisms use the host nutrients more ef- fectively than the parasites do, thereby inhibiting their de- velopment. This is particularly true of guttation fluid oc- curring on a senescent turfgrass leaf. Leben ( 19 65) has shown that as a bean leaf passes its half-life, its surface is rapidly colonized by various species of bacteria, yeast and fungi. A similar situation probably also occurs in turf and could effectively suppress growth, infection and pathogen colonization. the disease development curve for any facultative fungal parasite and compare it with its activity curve, we would probably find that disease development frequently depends upon how well the fungal parasites are doing in their com- petition with competing saprophytic microorganisms. I suspect that if we could examine Root Tip Degeneration Another topic I would like to consider is root tip degen- eration. In California the roots of cool season turfgrasses frequently exhibit a degenerated condition of their root tips. Only the immature cells and tissues manifest this degener- ation; the mature tissues apparently are not affected. The condition is more prevalent during the summer and early fall when soil temperatures are high, and less prevalent during the winter and early spring when soil temperatures are cool. No consistent fungal parasite has been isolated f r om these degenerated root tips and inoculations have not succeeded in reproducing these symptoms, except with the possible excep- tion of Sclerotinia homoeocarpa. Microscopic examination showed that a degenerated root apex is not only swollen due to hypertrophy of the cells, but is occasionally curved. The size of the cells is greatly enlarged in the regions of elongation and differentiation. A f- fected cells are devoid of nuclei and cytoplasm. (Endo and Malca, 19 65) If the meristematic cells at the root apex be- come enlarged they lose the capacity to divide and the root ceases to elongate, the root cap completely disappears and the root becomes truncate. As the root cap cells slough off, they are no longer replaced by additional root cap cells. Since the meristem cells no longer divide, a few immature cells may enlarge to f o rm root hairs near the root apex. Following cellular hypertrophy, the cytoplasm and nuclei dis- appear. This is why I refer to the condition as root tip de- generation. What I don't know is how much damage root tip degen- eration is causing to plants in the field. A few root tips are degenerated prematurely during the winter, but the loss is compensated for by the formation of lateral roots. The root systems of cool season grasses are, however, short and greatly reduced in number during the summer in California. The presence of root tip degeneration further weakens such plants and the high summer soil temperatures suppress the formation and elongation of both new and old roots. In pursuing the cause of root tip degeneration, I have followed K e rr ( 19 56), who showed that Sclerotinia homoeocarpa killed the root tips of pea seedlings. The seedlings were placed in cellophane bags containing soil, and the soil surrounding the bags were inoculated with the fungus. He concluded that the fungus produced a toxin which killed the root tips, since the my- celia of the fungus did not penetrate the cellophane bag. I v e r i- fied K e r r 's results and found that the fungus infested the leaves of bentgrass seedlings very readily, but not the roots. How- ever, the fungus produced a toxin which killed the root tips. Since microscopic examination revealed that the Scler- otinia affected root tips manifested symptoms very similar to root tip degeneration, Dr. Malca and I ( 1965) decided to look further into this problem. We attempted to produce the toxin by growing Sclerotinia homoeocarpa in a synthetic medium con- taining lactose as a carbon source because it caused the least damage to healthy root tips. A f t er seven days, the culture f i l- trate was found to be toxic to the root tips of bentgrass, but microscopic studies showed that the symptoms caused by the toxic factor in the culture filtrate was different f r om that caused by Sclerotinia. When we identified the toxic product, it turned out to be D-galactose. The fungus was utilizing the glucose moiety of lactose, and allowing D-galactose to accum- ulate in the culture filtrate. Guttation Fluid We decided to continue this problem because D - g a l- actose killed root tips of bentgrass at a concentration of 30 ppm in 16 hours and because Stenlid ( 19 57) had not only r e- ported D-galacto se and D-mannose as toxic to root tips, but also galactosamine and glucosamine. A ll of these compounds occur as components of cell walls. Galactose is a component of galactans in hemicellulose, mannose is a component of mannans and glucosamine is a component of chitin. This sug- gested that if the products accumulate for even a brief time in the surface litter following the breakdown of cell walls of plants, insects, and fungi, and are taken up by roots, they might cause root tip degeneration. An anatomical study of galactose-affected root tips revealed; (1) a hypertrophy of all the cells of the root apex; (2) a degeneration and disappearance of the cytoplasm and nuclei, particularly in the cells in the region of elongation; (3) a separation of cells in the region of the procambium, and (4) the presence of two nuclei in some cells, suggesting an inhibition of cell plate formation (Endo and Malca, 19 65). These light microscope effects suggested that D-galactose was inhibiting the synthesis of cell walls. This was also verified in our electron microscope studies of galactose- affected root tips (Endo et al., 1968). These studies reveal- ed that D-galactose inhibited cell plate formation by inhib- iting the formation of vesicles by the dictyosomes and by inhibiting the formation of phragmoplast microtubules. We have also noted that the cell walls are thickened and greatly convoluted, suggesting that the cell wall has somehow been weakened by affecting the activity of the cell wall degrading enzymes that are normally present in cell walls. To date, biochemical studies by Schmitt and Endo ( 1969) have shown that D-galactose does not inhibit respi- ration until 16 hours after treatment. This suggests that galactose is not interfering with energy metabolism. We also found, using radio active glucose, that galactose inhib- ited the incorporation of glucose into pectin, hemicellulose and cellulose, and caused a 20% to 30% increase in cell wall protein. Summary In summary, D-galactose appears to cause root tip degeneration by inhibiting the synthesis of cell walls. Whether it is responsible for causing root tip degeneration of cool season grasses in the field has not been determined. The so-called mat and thatch which consists of fresh and decomposing turfgrass debris does, however, offer uniquely favorable conditions for the break-down of cell wall compo- nents such as D-galactose and D-mannose, glucosamine, " e t c ," which may repress cell wall synthesis. In conclusion, I am interested in learning whether others have observed what I have been calling root tip degen- eration. R e f e r e n c es Cited Das, T. M. and A. C. Leopold. 1964. In_Plant Growth and Development. M c G r a w - H i ll Book Co., New York, (page 200). Endo, R. M., and I. Malca. 1965. Morphological and cyto- histological responses of p r i m a ry roots of bentgrass Sclerotinia homoeocarpa and D-galactose. Phytopathology 55:781-789. Endo, R. M., W. W. Thomson, and Emmylou M. Krausman. 19 68. Effects of D-galactose on the ultrastructure of bentgrass root apices. Can. J. Bot. 46:391-395. Katznelson, H. J., W. Rouatt, and T. M. B. Payne. 19 55. Liberation of amino acids by plant roots in relation to desiccation. Nature (London) 174:1110-1111. K e r r, A. 19 56. Some interactions between plant roots and pathogenic soil fungi. Australian J. Biol. Sei. 9:45-52. Leben, C. 1965. Epiphytic m i c r o - o r g a n i s ms in relation to plant disease. Ann. Rev. Phytopathology 3:209-230. Malca, I. and R. M. Endo. 19 65. Identification of galactose in cultures of Sclerotinia homoeocarpa as the factor toxic to bentgrass roots. Phytopathology 55:775-780. Russell, R. S. 1970. Root systems in plant nutrition. Some new approaches. Endeavor 29:60-66. Schmitt, R. A. and R. M. Endo. 1969. Effects of galactose on barley root apices. Phytopathology 59:1048. Stenlid, G. 19 57. A comparison of the toxic effects of some sugars upon growth and chloride accumulation in young wheat plants. Physiol. Plantarum. 12:199-217. Tukey, H. B. 19 70. The leaching of substances f r om plants. Ann. Rev. Plant Physiol. 21:305-324. DISCUSSION PERIOD I have observed root tip degeneration but havenft Dr. Altman: If you recall, Dr. Wilhelm reported on root done much with it. tip degeneration on strawberries a few years ago. I would like to ask you a question. What's the difference between degener- ation and senescence as it occurs in roots? Dr. Wilhelm sug- gested that this was a natural process with strawberry roots. There was a replacement that permitted the strawberry plant to produce a crop after substantial degeneration had occurred. It is probably not a normal dying of roots because Dr. Endo: it happens to seedling and young roots, as well as to old roots. Its distribution pattern does not conform to the age of the roots and itfs much more prevalent on cool season grasses during the warm months. Dr. Lukens: The same question occurred to me when you mentioned that this is most prevalent during your cool season, which is also your wet season, is it not? Dr. Endo: No, it is more prevalent during our warm season. I don't believe root tip degeneration is due to normal aging of the roots. However, I do think that we need to know more about the normal development of roots; how long they live under different conditions, and what effect such factors as clipping, compaction and high soil temperatures have on root longevity. Dr. Lukens: Several years ago, Dr. E. J. Bredakis at the University of Massachusetts studied the relationship between cutting height and root length of fine leaf fescues and blue- grass. Whether the increase in root development was long rootlets or continuous side branching was not explained. Dr. Bredakis found a direct relationship between cutting height and root length. Below two inches, root development was drastically reduced in most grasses. Dr. Endo: Is this greenhouse work? Dr. Lukens: Yes. I think we have to be somewhat cautious about clip- Dr. Endo: ping experiments because one can get quite dramatic effects f r om clipping if the plants are allowed to grow for a period, and then are suddenly clipped. This is a t e r r i f ic stress on the plant. When I did this, many of the root tips died very rapidly. Dr. Lukens: Apparently the tops of all treatments were clipped at the same time. I think frequency of cut was examined, too. Dr. Endo: Did they first allow the plants to become adjusted gradually to the clipping treatments before they imposed a par- ticular clipping schedule? Dr. Lukens: I think clipping was started in the seedling stage. Dr. Altman: You r e f e r r ed to toxicity f r om galactose with root tips. A re you familiar with toxicity as a result of an amino acid. There was some work done in 1941 in which various amino acids were placed on tobacco meristems and frenching was induced. This frenching was attributed to cell wall development elonga- tion as part of the complex involved. Dr. Endo: Yes, I am familiar with Steinberg's work. He reported that quite a number of amino acids would cause frenching and root tip necrosis. We have found that the root tip is very responsive to adverse environmental effects and chemicals. Root growth may be inhibited rapidly under laboratory conditions. Dr. Altman: Have you done any work to evaluate the actual level of root development required to maintain what we consider a nor- mal above ground growth? Dr. Endo: No, but I think that would constitute a good research problem. I have been searching around in my mind as how one could do that. Do you have any suggestions? in trying to find a system where I could remove a predetermined amount of root hairs with detergents, but the experiments failed. (See Endo et al. 1969. Agronomy Journal 61:850-854). I have been interested Dr. Altman: How serious is this root degeneration, in regards to overall crop production or yeild of a particular plant? Dr. Endo: I don't know. California during the hot, dry summer months because such plants succumb readily to heat and moisture stress. I think it is mainly a problem in Dr. Worf: I missed, at the outset, the conditions that brought about your looking at the root system to detect this degenera- tion. I was interested in evaluating the relation of spe- In attempting to study this, Dr. Endo: cies of Pythium to root troubles. I encountered the problem of root tip degeneration. Also, plants that died f r om moisture and heat stress in the summer usually had markedly reduced root systems and the root tips were frequently degenerated. Dr. Worf: Did you perceive any external above ground symptoms then, which initiated your underground inquiry? Dr. Endo: There were some, but these differences were most- ly in reduced vigor, size of plants and number of tillers. There were no obvious pathological lesions on the upper por- tions of the plant. I understood that this work was primarily Mr. Simmons: with the cool season grasses. Have you looked at the warm season grasses, and do they do the same thing at this elevated temperature? Dr. Endo: cause we have few disease problems on them. I haven't looked at the warm season grasses be- Mr. Stottlemyer: When I first looked at those micrographs it reminded me of boron deficiency. ciency has never been shown on grasses, however they look alike and have the same symptoms. Once again, when you have boron deficiency, your zones of elongation and meriste- matic activity disappear. You essentially have differentiation to the root tips. that possibility. I was wondering whether you have ruled out I realize that boron defi- Dr. Endo: No, I haven't ruled out boron deficiency. possibility, since Dr. Dugger has indicated a relationship between boron and sugar transport. It is a E X T R A C E L L U L AR RIBONUCLEASE PRODUCTION BY FUNGI Bill Berkenkamp Plant Pathologist Canada Department of Agriculture Lacombe, Alberta, Canada Ribonuclease or RNase, has been shown to be pro- duced by pathogenic fungi, however, its significance in host- parasite relationships has not been established. In theory, it could play a significant role in the modification and dis- ruption of the host metabolism. A simplified method of qualitatively assaying RNase produced by culturable fungi was developed by utilizing rea- gents to precipitate RNA in media. The test medium was made up using 2 grams of yeast RNA, 20 grams of Bacto Peptone, 15 grams of agar and 1 liter of distilled water. The components were dissolved in water and adjusted to pH 5.4, sterilized at 15 pounds for 20 minutes and poured into petri plates. After cooling, the plates were inoculated with the fungi to be tested and incubated 4-6 days. The plates were then flooded with Uranyl reagent ( 1 grarA uranyl acetate in 100 ml. of 10% perchloric acid) to precipitate any unhydrol- yzed R NA in the agar. Cleared areas around the colonies of fungi demonstrated the presence of RNase activity (Fig. 1). Acetone and HC1 can also be used as reagents for precipitat- ion, however, acetone precipitates other material in addition to RNA. The media must, therefore, be tested before use. HC1 gives a somewhat weaker reaction than Uranyl reagent and lasts for only a few hours. This method was compared with two other methods using liquid cultures. First, turbidometric measurements were made with a Spectronic 20 at 625 mu, on culture f i l- trates containing RNA, after precipitation with Uranyl rea- gent. F i g. 1. Fungi on RNA agar after growth and development with Uranyl Reagent. Cleared areas around RNase active fungi are dark due to black background. Top row left to right: Pseudoplea trifolii, Kabatiella caulivora, Drechslera poae, Stemphyllium loti. Lower row: Sclerotinia sp., Stagonospora meliloti, Hetero- sporium phlei, Drechslera phlei, a positive unidentified contaminant at the bot- tom of left plate. The reduction in turbidity was a measure of RNase activity. Second, an increase in optical density due to sol- uble breakdown products after precipitation and centrifuga- tion was measured with a Beckman DU at 260 mu. Both of these methods were less sensitive and slower, requiring about nine days incubation; however, they were quantitative. The depression of RNase production in liquid may be due to a lack of aeration. The plate tests offer a quick, simple, but only quali- tative assay of culturable micro-organisms for their ability to produce extracellular RNase. Some of the fungi tested and found to produce RNase were: Ascochyta caulicola, A. imperfecta, Alternaría sp., Heterosporium phlei, Kabatiella caulivora and Pseudoplea trifolii. Those not producing RNase were: Bipolaris sorokiniana, Drechslera poae, D. phlei, D. bromi, Fusarium avenaceum, F. oxysporum, F. solani, Sclerotinia trifoliorum, Stagonospora meliloti and Stemphyllium loti. DISCUSSION PERIOD Dr. Lukens: Can RNase be involved in anyway in pathogen- esis ? Dr. Berkenkamp: I would suspect so. Dr. Lukens: Could you give us any idea as to how you feel it acts? Dr. Berkenkamp: Since RNA is the mechanism of action f r om the gene to metabolism, I would say there is a possi- bility of changing the metabolism in favor of the parasite. I would like to prove this, but I don't know how. Dr. Lukens: Is there any work that may suggest this? Dr. Berkenkamp: No, not that I know of. There is quite a bit of work on virus RNase in virus infected plants and some on obligate parasites but, other than production of RNase, nothing on culturable parasites. Dr. Altman: Could you use your assay technique as a means of evaluating purity in a particular fungus? Also, would you be able to evaluate virulence or loss of virulence by this technique? Dr. Berkenkamp: lated to virulence, but not necessarily. I couldn't say. I would expect it to be r e- Dr. Altman: A re the precipitates that come out of these white, opaque areas characteristic for a particular fungus? Dr. Berkenkamp: No, the precipitate is the undegraded RNA. The cleared areas are where RNase has been active in degrading the medium. The result is a fungus colony, a clear area, and the rest of the plate is opaque (precipitated RNA). Dr. Altman: Does a specific fungus give you a different type of a clear area or are they all similar? Dr. Berkenkamp: No, usually t h e y ' re distinct. I compared this with liquid tests and found the plate cultures to be m o re sensitive than those cultured in tubes. In comparing various cultures, some fungi a re positive and others a re negative. T h e re a re some questionable responses in fungi, but p r i m a r- ily it's yes or no, especially if you use the low pH. M r. Gabert: What fungi have you t r i ed with this test? Dr. Berkenkamp: A l a r ge number of legume pathogens, A s c o- chyta imperfecta, Heterosporium phlei causing timothy eye spot, and some fusaria. M r. Gabert: Did you notice any significant d i f f e r e n c es in the amount produced over a given t i me between the different species? Dr. Berkenkamp: The test is not quantitative. If we assume there a re i s o z y m e s, they would have different diffusion rates. The s i ze of the cleared a r e as would not be quantitative. would like to test a l a r ge number of fungi and relate the char- a c t e r i s t i cs of this feature to gain some insight. T o - d a te I haven't tested enough fungi. I Dr. F r e e m a n: You brought up a point concerning the H e l m i n- thosporium classification. Does any one have any comments on this? I know the people in Canada have been working on changing the name of the genus Helminthosporium but does any one here use those new classifications? Do they still speak of Helminthosporium or of Bipolaris and D r e c h s l e r a? Dr. Berkenkamp: Bipolaris is the one that germinates only f r om the end cells of the conidia, and D r e c h s l e ra germinates I 'm not a taxonomist, but I wondered if there f r om any cell. was a reason why these names w e re not acceptable? I would like to know. Dr. F r e e m a n: Maybe all of us a re stuck in our ways. Do you think it is a valid r e c l a s s i f i c a t i o n? Dr. Berkenkamp: I was asking you. Dr. F r e e m a n: I ' ll ask somebody else f or their opinion. I'm not a Dr. Dale: You were talking about Bipolaris. Helminthosporium expert but have done some work with H. spiciferum, somewhat similar to that Dr. Wadsworth did on the spring dead spot disease. In this work, a student studied germination of Bipolaris spores using a range of temperatures. Bipolar germination occurred at some temperatures, but at others, germination was just at one end. Bipolar germination may be a good taxonomic char- acter, however, workers should specify exactly what temperatures are used when studying spore germination. I don't know the answer to Dr. Freeman's question, but believe we need more criteria in classifying Helmintho- sporium. We may need some "lumpers" instead of "split- ters. " Dr. Jackson: Bipolaris and Drechslera are included in Shoemaker's recent classification. He is a Canadian. A re you familiar with him? Dr. Berkenkamp: Yes, but Drechslera was originally de- scribed in Japan by Ito. Dr. Jackson: There seems to be some difficulty in Shoe- maker, Luttrell, Ellis and others agreeing on this group. I think the British Mycology Society has accepted Shoe- maker's classification since it is now used in the Review of Applied Mycology. But because the name Helminthospor- ium is so well known, it is retained for general use.