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Remarks (public):For a complete description including images see www.cababstractsplus.org/dfb 
Remarks (internal):The conidial state of L. nodorum is kept distinct from S. avenae Frank f.sp. triticea T. Johnson by Sprague (1950). It has smaller conidia than S. avenae and S. avenae f.sp. triticea. These three fungi are readily distinguished from S. tritici (CMI Descript. 90) which has conidia up to 70 µm long and 1·5-2 µm wide. Muller (1952) distinguishes L. nodorum from L. tritici (Gar.) Pass. which has smaller ascospores (16-20 x 4 µm). Ascospores constantly giving rise to S. nodorum conidia in culture had a mean size (20·5 x 4 µm) only slightly above the range for L. tritici. Glume blotch was first reported from England in 1845 and was later found to be common throughout Europe, where yield losses up to 50% have been recorded in epiphytotics favoured by prolonged periods of rainfall during the summer months (July > 3 in.). Severe outbreaks during the past 15 yr. have been reported from Czechoslovakia, Switzerland, West Germany, Austria, U.S.S.R., Poland and the Netherlands (29: 611; 36: 310; 37: 227, 337, 470; 43: 714) as well as from South India and South Africa (33: 75; 34: 220). Serious damage has also been reported from South America where an epiphytotic was recorded in Argentina in 1940 (Marchionatto, 1941). Losses continued to be heavy during the ensuing 10 yr. particularly after rainy weather in the spring and exceeded that due to Septoria tritici which was also present (27: 413; 30: 514). Cultural methods of control include the use of healthy seed, early maturing varieties, crop rotation, sanitation and ploughing under volunteer wheat plants in the autumn (37: 33; 38: 403). Short plants are more subject to infection than tall, and factors contributing to lodging or late tiller formation, such as winter injury, encourage an increase in disease (37: 32; 38: 139). Excess N delays host development and increases probability of attack (39: 566; 42: 315) while the addition of P, K and Mg to fertilizer mixtures has improved control (37: 33). No wheat is immune but some varieties appear less susceptible than others (2: 211; 33: 75; 37: 32, 33; 38: 139, 403; 39: 566). A laboratory test for resistance using germinating seed has been described (Kietreiber, 1964). Seed treatments based on hot-water or organo-mercurial dusts give only partial control as other sources of primary infection such as infected stubble occur in the field (2: 211; 37: 32; 39: 466; 42: 756).
 
Description type:Non-original description 
Description:Leptosphaeria nodorum Muller, Phytopath. Z. 19: 409, 1952.
Conidial state:
Septoria nodorum (Berk.) Berk., in Berkeley & Broome, 1850.
= Depazea nodorum Berk., 1845.
= Hendersonia nodorum (Berk.) Petrak, 1947.
= Septoria glumarum Pass., 1879.
= Phoma hennebergii Kahn, 1877.
= Macrophoma hennebergii (Kuhn) Berl. & Vogl., 1886.
Ascocarps immersed, globose, finally depressed, mid brown to black, 150-200 µm diam.; wall up to 5 cells thick, composedof thick-walled, brown, pseudoparenchymatic cells; ostiole slightly papillate, 15 µm diam. Asci clavate, cylindrical or curved,shortly stipitate, 8-spored, 47,5-65 x 8-10 µm; ascus wall thick, bitunicate. Ascospores fusoid, subhyaline to pale brown, 3-septate, constricted at the septa, penultimate cell swollen, 19,5-22,5 x 4 µm. Pseudoparaphyses filiform, hyaline, septate. Pycnidia immersed, globose, honey brown, becoming darker, epiphyllous, 140-200 µm diam.; wall up to 5 cells thick, composed of thin-walled, honey yellow, pseudoparenchymatic cells, somewhat larger and thicker-walled near the ostiole, which is slightly papillate and measures up to 25 µm diam. Conidiogenous cells formed from the inner cells of the pycnidialwall, shortly obpyriform, hyaline, non-septate, undifferentiated, 4-6 x 6 µm. Conidia hyaline, cylindrical, straight, sometimesirregularly curved, mostly 3-septate, apex and base obtuse, 22-30 x 2,5-3 µm.
Hosts: On Triticum spp. Also on many other genera in the Gramineae including Agropyron, Cinna, Dactylis, Deschampsia, Elymus, Festuca, Glyceria, Hordeum, Hystrix, Lepturus, Melica, Poa, Psamma, Secale, Stipa (Sprague, 1950).
Disease: Glume blotch of wheat. Causes discoloured to brown lesions on glumes, culms and leaves. Leaf lesions are 1 cm long, elongated, elliptical, golden brown, surrounded by a diffuse, lighter margin becoming darker and bearing pycnidia. Similar brown lesions occur on glumes where they spread from the apices downwards, and bear pycnidia and perithecia. Perithecia are also formed on dead glumes and culms. The heads of wheat may become blackened, producing shrivelled kernels of abnormal structure. Germinating seedlings may also be attacked with subsequent loss of vigour.
Geographical distribution: Africa (Ethiopia, Kenya, Malawi, Morocco, Rhodesia, South Africa, Tanzania, Uganda, Zambia); Asia (China, Formosa (Taiwan), India, Japan, U.S.S.R.); Australasia (Australia, New Zealand); Europe (Austria, Belgium, Bulgaria, Czechoslovakia, Denmark, France, Germany, Great Britain, Greece, Ireland, Italy, Latvia, Netherlands, Norway, Poland, Portugal, Rumania, Spain, Sweden, Switzerland, U.S.S.R., Yugoslavia); North America (Canada, U.S.A.); South America (Argentina, Bolivia, Brazil, Uruguay). (CMI Map 283, ed. 2, 1954; Herb IMI.)
Physiological specialization: Weber (1922) found isolates from wheat, rye and Poa pratensis were cross inoculable on all of these three hosts but not on eight other genera tested which included Agropyron and Hordeum. Machacek (1945) found evidence for the existence of separate strains in Eastern and Western Canada and Thomas (1962) recognized 4 biotypes among 18 isolates tested on 4 differential wheat hosts in the United States.
Transmission: Frequently seed-borne (Noble et al., 1958; Hewett, 1965), persisting in a viable condition in seed up to 7 yr. in Canada (31: 596). Also surviving in wheat stubble and crop residues and after 1 yr. in straw kept in dry storage (43, 4g, 2589). Conidia have remained viable in pycnidia after 18 months in the open (Weber, 1922).
Literature: Weber, Phytopathology 12: 537-585, 1922 [36 refs]; Sprague, Diseases of Cereals and Grasses in North America, New York: Ronald Press Co., 1950 [23 refs]; Richards, Phytopathology 41: 571-578, 1951; Muller, Phytopath. Z. 19: 409-411, 1952 (taxonomy & disease); Shaw, Proc. Linn. Soc. N.S.W. 78: 122-130, 1953 (cytology); Marchionatto, Int. Bull. Pl. Prot. 15: 113M-114M, 1941; Scharen, Phytopathology 54: 300-303, 1964 (epidemiology); Noble, Handbook on Seed Health Testing, Series 3, Sheet 19 (Pre-print 1965); Noble et al., An annotated list of seedborne diseases 1958; Hewett, Trans. Br. mycol. Soc. 18: 59-72, 1965 [31 refs] (incidence on wheat seed); Machacek, Phytopathology 35: 51-53, 1945; Thomas, Diss. Abstr. 23: 789, 1962 (physiologic specialization); Kietreiber, Pflanzenschutzberichte 31: 179-188, 1964 (laboratory test for resistance).

 
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