Know when your crop is potentially at risk.

Sunflower Disease Models


The fungus causing Downy mildew in sunflowers is known under the names Plasmopara halstedii or Plasmopara helianthi. The fungal pathogen complex infects a wide range of genera in the family Asteraceae, including wild and cultivated species of Helianthus. The disease is present wherever sunflowers are grown.

Life Cycle

Starting from a single oospore that germinates and gives rise to a zoosporangium, zoospore differentiation and release are the subsequent steps of development. In the presence of free water, the zoospores move to infection sites (root, hypocotyl) soon if available. Following encystment and germ tube elongation (the latter usually terminates in an appressorium against a host cell) the fungus develops an infection structure (infection peg) for direct penetration. Under experimental conditions, it was demonstrated that germ tubes do not usually form appressoria in water but they do so in the presence of host cells (Gray et al., 1985). After penetration, the fungus grows intracellularly and then intercellularly, and once being established in a susceptible host (compatible) it starts to colonize the entire plant systemically by growing preferably toward the shoot apex and, to a lesser extent, in the direction of the root. When conditions are favourable, asexual sporulation takes place on affected leaves and occasionally on below-ground tissues. Fully developed sporangia disseminate by wind and, since they are short-lived and sensitive to drought and direct sunshine, their survival depends on the current weather situation. Oospores are also produced in infected plant parts, primarily in root and lower stem tissues, whereas leaves and upper plant parts, except seeds, are free from these resting spores (Sackston, 1981; Virányi, 1988; Onan and Onogur, 1991). The most susceptible stage of host development is between germination and emergence (Meliala et al. 2000).

Survival and Source of Inoculum

With respect to the primary infection, P. halstedii is a soilborne pathogen. Its oospores serve as primary inoculum to underground tissues of young sunflower seedlings. It may also be windborne, causing secondary infection of leaves and/or inflorescence. If the latter is the case, the fungus might also be seedborne: the affected seeds carrying mycelium and/or oospores internally. Oospores develop mainly in root and lower stem tissues of mildewed plants, with or without visible symptoms and, with plant residues of the preceding sunflower crop, they come into the soil. Oospores are long-lived and are able to survive for at least 6-8 years (Sackston, 1981; Virányi, 1988). It is generally thought that oospores mainly germinate under wet conditions. However, only a few results on the germination dynamics have been available so far. A low-temperature shock prior to wetness and the presence of host exudates released by roots were shown to enhance the germination process (Delanoe, 1972). In another report (Spring & Zipper 2000), no such temperature effects could be observed and freshly developed oospores were reported to germinate spontaneously in water within a period of 10-30 days, but at a highly variable rate (1-17%).

However, secondary infection is considered as an important factor in the spreading of the disease in certain regions under favourable environmental conditions. Apart from the fact that secondary infection of inflorescence may give rise to latent infection of seeds by P. halstedii (Sackston, 1981), from local leaf lesions the fungus is able to proceed and grow into the stem causing systemic infection (Spring 2001).


The nature of the inoculum (oospore or zoospore), weather variables (relative humidity, temperature), infection site (age of tissue), as well as cultivar reaction are factors that influence or determine the infection process, disease incidence, and severity. Zoospores, originating from either sexual or asexual sporulation, require free water for retaining viability and capability of moving toward infection sites. Consequently, rainfall or intensive irrigation will be a prerequisite for the initiation of infection. It was shown by several studies that if there was enough rain or corresponding water supply during the first two weeks after sowing, the incidence of primary infection from the soil increased. However, the duration of time that favours infection is relatively short and even susceptible sunflowers become resistant with age (Sackston, 1981). Tourvieille et al. (2008a) found that the risk of downy mildew attack appeared greatest if there was heavy rainfall when sunflower seedlings were at their most susceptible stage, whereas heavy rainfall before sowing or after emergence had no effect on the percentage of diseased plants. Göre (2009) that low temperature and extensive spring rains in approximately 85% yield loss and lower quality of sunflower production in the Marmara region of Trace. Besides environmental conditions, disease intensity may also be influenced by the aggressiveness of the pathogen population. Sakr et al. (2009) were able to differentiate the two pathogen strains in terms of their aggressiveness based on the population’s latent period and sporulation density.

Seedborne Aspects

P. halstedii has been found to occur in sunflower seeds from naturally infected plants, either as mycelium or oospores (Novotel’nova, 1966). Doken (1989) reported that the mycelium was only found in the testa and in the inner layer of the pericarp; it was absent from the embryo. Following artificial inoculation, Cohen and Sackston (1973) confirmed that sunflower buds inoculated with P. halstedii became systemically infected and produced infected seeds. Oospores were observed in seeds of inoculated and naturally infected plants in the field. Other records of seed infection are known from Iran (Zad, 1978), Turkey (Döken, 1989) and Germany (Spring, 2001). The fungus usually invades the ovary and the pericarp but fails to grow into the embryo (Novotel’nova, 1966; Döken, 1989). Seed infection regularly occurs in systemically infected plants if they survive up to the flowering stage. In such cases, the development of the embryo is often retarded or inhibited. Moreover, such plants are dwarf and will seldom be harvested. They may increase the local stock of oospores in a field, but for the seed-derived long-distance dispersal of the pathogen they appear to be less important than seeds from late infected symptomless plants (Spring, 2001). The latter type of infection is very dependent on the weather conditions during the flowering process. Thus in dry years the number of pathogen-contaminated seeds is very low and may not exceed several in one thousand, but may be much higher after a cool and humid period in June/July. For example, Spring (2001) found that close to 10% of seeds from a field in Germany were contaminated and Döken (1989), under favourable experimental conditions, observed fungal structures in 28% of the seeds examined.

Effect on Seed Quality

Sunflower seeds produced in downy mildewed plants are either under-developed, colourless or, rarely, they look healthy. Even in the latter case, such infected seeds are of poor quality; they produce abnormal seedlings and the germination rate is low (Döken, 1989).

For further information have a look at the homepage of CABI.

Model in FieldClimate

Used sensors: soil temperature, precipitation, leaf wetness, air temperature and relative humidity.

We start to calculate the infection progress, when temperature is between 6 and 32°C with optimum from 18 to 24°C and soil temperature are above 10°C. Further on wet conditions are favourable for the disease (rain event, relative humidity above 70%).

Makrosporangia are formed at soil temperatures above 10°C and precipitation (rel. humidity more than 70%). Reset is if relative humidity falls below 50%.

If Makrosporangia are fully developed – the calculations for a soil infection or an air infection (in the graph called primary infection) start (under leaf wetness conditions).

Sporangia are formed under humid conditions (more than 95% r.h.), in darkness and temperatures above 12°C. Reset is during the day and when sporangia are not fully developed.

If Sporangia are fully developed the calculation of the secondary infection starts in dependance of the air temperature.

In the Graph you see at the end of April a long-lasting humid period, which lead to the formation of macrospores and a soil infection (primary root infection). An air infection (called primary infection here) was not determined on the first of May, but conditions have been favourable so it was determined on the 2nd of May. If sunflower seedlings are in a sensitive stage at that time (just sown) control measurements have to be into account ( prophylactic systemic fungicides, mostly phosphoric acids).


Achbani EH, Lamrhari A, Serrhini MN, Douira A, Tourvieille de Labrouche D, 1999. Evaluation of the efficacy of seed treatments against Plasmopara halstedii. Bulletin OEPP, 29(4):443-449; 15 ref.

Achbani EH, Tourvieille D, 1993. Le tournesol au Maroc. Phytoma, 448:30-32.

Agrawal SC, Gupta RK, Prasad KVV, 1991. A case of downy mildew of sunflower in Madhya Pradesh. Journal of Oilseeds Research, 8(1):126

Albourie JM, Tourvieille J, Labrouhe DTde, 1998. Resistance to metalaxyl in isolates of the sunflower pathogen Plasmopara halstedii. European Journal of Plant Pathology, 104(3):235-242; 27 ref.

Albourie JM, Tourvieille J, Tourvieille de Labrouhe D, 1998. Metalaxyl resistance in French isolates of downy mildew. In: Gulya T, ed. Vear F, ed. Proc. Third Sunflower Downy Mildew Symposium, Fargo, USA: ISA, 235-242.

Bán R, Kovács A, Körösi K, Perczel M, Turóczi G, 2014. First report on the occurrence of a new pathotype, 714, of Plasmopara halstedii (sunflower downy mildew) in Hungary. Plant Disease, 98(11):1580-1581.

Bán R, Kovács A, Perczel M, Körösi K, Turóczi G, 2014. First report on the increased distribution of pathotype 704 of Plasmopara halstedii in Hungary. Plant Disease, 98(6):844.

Batinica J, Bes A, Dimic N, Numic R, Radman L, Ristanovic M, Vaclav V, 1973. A contribution to the knowledge of harmful fauna and the causes of diseases of sunflower in the area of its cultivation in the republic of Bosnia and Hercegovina. Radovi Poljoprivrednog Fakulteta Univerziteta u Sarajevu, 21/22(24/25):203-210

Berlese AN, De-Toni JB, 1888. Phycomycetteae. In: Sylloge fungorum, VII:242.

Bohár G, Vajna L, 1996. Occurrence of microscopic fungi pathogenic to Ambrosia artemisifolia var. elatior (L.) Descourt. in Hungary. Növényvédelem, 32:527-528.

Borovkov AY, McClean PE, 1993. A tandemly repeated sequence from the Plasmopara halstedii genome. Gene, 124(1):127-130

Borovkova IG, Borovkov AY, McClean PE, Gulya TJ, Vick BA, 1992. Restriction fragment length polymorphisms and RAPD markers in DNA of Plasmopara halstedii, the downy mildew fungus of sunflower. Proceedings of the 13th International Sunflower Conference Volume 2, Pisa, Italy, 7-11 September 1992., 1420-1425; 9 ref.

Bouterige S, Robert R, Bouchara JP, Marot-Leblond A, Molinero V, Senet JM, 2000. Production and characterization of two monoclonal antibodies specific for Plasmopara halstedii. Applied and Environmental Microbiology, 66(8):3277-3282; 33 ref.

Bouterige S, Robert S, Marot-Leblond A, Senet JM, 2000. Development of an ELISA test to detect Plasmopara halstedii antigens in seed. In: Proc. 15th Int. Sunflower Conference Toulouse, France: ISA (F):44-49.

CABI/EPPO, 1998. Distribution maps of quarantine pests for Europe (edited by Smith, I. M. and Charles, L. M. F.). Wallingford, UK: CAB International, xviii + 768 pp.

CABI/EPPO, 2014. Plasmopara halstedii. Distribution map. Distribution Maps of Plant Diseases, No.October. Wallingford, UK: CABI, Map 286 (Edition 6).

Choi YJ, Park MJ, Shin HD, 2009. First Korean report of downy mildew on Coreopsis lanceolata caused by Plasmopara halstedii. Plant Pathology, 58(6):1171.

CMI, 1988. Distribution maps of plant diseases. Map No. 286. Wallingford, UK: CAB International.

Cohen Y, Sackson WE, 1974. Seed infection and latent infection of sunflowers by Plasmopara halstedii. Canadian Journal of Botany, 52:231-238.

Delanoe D, 1972. Biologie et epidemiologie du mildiou du tournesol (Plasmopara helianthi Novot.). CETIOM Informations Techniques, 29:1-49.

Delen N, Onogur E, Yildiz M, 1985. Sensitivity levels to metalaxyl in six Plasmopara helianthi Novot. isolates. Journal of Turkish Phytopathology, 14(1):31-36

Delos M, Penaud A, Lafon S, Walser P, De Guenin MC, Tourvieille J, Molinero V, Tourvieille D, 1997. Le mildiou de tournesol – Une maladie toujours d’actualitT. Phytoma, 495á:15-16.

Doken MT, 1989. Plasmopara halstedii (Farl.) Berl. et de Toni in sunflower seeds and the role of infected seeds in producing plants with systemic symptoms. Journal of Phytopathology, 124(1-4):23-26

Duarte LL, Choi YJ, Barreto RW, 2013. First report of downy mildew caused by Plasmopara halstedii on Gerbera jamesonii in Brazil. Plant Disease, 97(10):1382.

EPPO, 2014. PQR database. Paris, France: European and Mediterranean Plant Protection Organization.

European and Mediterranean Plant Protection Organization, 2008. Plasmopara halstedii. Bulletin OEPP/EPPO Bulletin, 38(3):343-348.

Garcia GM, Gulya TJ, 1991. Sunflower downy mildew race distribution in North Dakota and Minnesota. In: Proceedings of the 1991 Sunflower Research Workshop, Fargo, USA: National Sunflower Association, 3-5.

Giresse X, Labrouhe DTDe , Richard-Cervera S, 2007. Twelve polymorphic expressed sequence tags-derived markers for Plasmopara halstedii, the causal agent of sunflower downy mildew, 7:1363-1365.

Göre ME, 2009. Epidemic outbreaks of downy mildew caused by Plasmopara halstedii on sunflower in Thrace, part of the Marmara region of Turkey. Plant Pathology, 58(2):396.

Gray AB, Sackston WE, Thauvette L, 1985. The development of infection structures of Plasmopara halstedii in suspensions of sunflower cells. Canadian Journal of Botany, 63(10):1817-1819

Gray B, Sackston WE, 1983. Studies of tissue cultures and cell cultures of sunflower inoculated with Plasmopara halstedii. Canadian Journal of Plant Pathology, 5:206.

Greathead DJ, Greathead AH, 1992. Biological control of insect pests by insect parasitoids and predators: the BIOCAT database. Biocontrol News and Information, 13(4):61N-68N.

Gullino ML, Garibaldi A, 1988. Cryptogamous diseases of the principal pot-cultivated flower plants. Panorama Floricolo, 13(5):4-8.

Gulya TJ, 1995. A simple method to assess root response of downy mildew “resistant” sunflower lines. In: Proceedings of the 17th Sunflower Research Workshop, Fargo, USA: National Sunflower Association, 63-66.

Gulya TJ, 1995. Proposal for a revised system of classifying races of sunflower downy mildew. In: Proceedings of the 17th Sunflower Research Workshop, Fargo, USA: National Sunflower Association, 76-78.

Gulya TJ, 1996. Sunflower diseases in the Northern Great Plains. In: Proceedings of the 18th Sunflower Research Workshop, Fargo, USA: National Sunflower Association, 24-27.

Gulya TJ, 2000. Metalaxyl resistance in sunflower downy mildew and control through genetics and alternative fungicides. In: Proc. 15th Int. Sunflower Conference Toulouse, France: ISA (G):16-21.

Gulya TJ, 2007. Distribution of Plasmopara halstedii races from sunflower around the world, 3:121-134.

Gulya TJ, Rashid KY, Masirevic SM, 1997. Sunflower Diseases. In: Schneiter AA, ed. Sunflower Technology and Production. Number 35 in the series Agronomy. Wisconsin, USA: Amer. Soc. Agronomy, 263-379.

Gulya TJ, Sackston WE, Viranyi F, Masirevic S, Rashid KY, 1991. New races of the sunflower downy mildew pathogen (Plasmopara halstedii) in Europe and North and South America. Journal of Phytopathology, 132(4):303-311

Gulya TJ, Tourvieille de Labrouhe D, Masirevic S, Penaud A, Rashid K, Viranyi F, 1998. Proposal for standardized nomenclature and identification of races of Plasmopara halstedii (sunflower downy mildew). In: Gulya T, ed. Vear F, ed. Third Sunflower Downy Mildew Symposium. Fargo, USA: ISA, 130-136.

Gulya TJ, Virányi F, Nowell D, Serrhini MN, Arouay K, 1996. New races of sunflower downy mildew from Europe and Africa. In: Proceedings of the 18th Sunflower Research Workshop, Fargo, USA: National Sunflower Association, 181-184.

Gulya TJ, Woods DM, Bell R, Mancl MK, 1991. Diseases of sunflower in California. Plant Disease, 75(6):572-574

Hall G, 1989. Unusual or interesting records of plant pathogenic Oomycetes. Plant Pathology, 38(4):604-611

Harmon PF, Dunkle LD, Latin R, 2003. A rapid PCR-based method for the detection of Magnaporthe oryzae from infected perennial ryegrass. Plant Disease, 87(9):1072-1076.

Heller A, Rozynek B, Spring O, 1997. Cytological and physiological reasons for the latent type of infection in sunflower caused by Plasmopara halstedii. Journal of Phytopathology, 145(10):441-445; 15 ref.

Henning AA, Franca Neto JB, 1985. Physiological race and sources of resistance to downy mildew (Plasmopara halstedii (Farl.) Berlese et de Toni) in Brazil. In: Proceedings of the 11th International Sunflower Conference, Mar del Plata, Argentina: Volume 2, 407-409.

Hong CX, 2006. Downy mildew of Rudbeckia fulgida cv. Goldsturm by Plasmopara halstedii in Virginia. Plant Disease, 90(11):1461. HTTP://

Hua Z, Ma G, 1996. A review of sunflower diseases research of China. In: Proceedings of the 14th International Sunflower Conference, Beijing, China: ISC-LAAS, 754-759.

Intelmann F, Spring O, 2002. Analysis of total DNA by minisatellite and simple-sequence repeat primers for the use of population studies in Plasmopara halstedii. Canadian Journal of Microbiology, 48(6):555-559; 25 ref.

IPPC, 2010. First UK finding of Plasmopara halstedii. IPPC Official Pest Report, No. GBR-23/1. Rome, Italy: FAO.

Jardine DJ, Gulya TJ, 1994. First report of downy mildew on sunflowers caused by Plasmopara halstedii in Kansas. Plant Disease, 78(2):208

Kinga R, Bíró J, Kovács A, Mihalovics M, Nébli L, Piszker Z, Treitz M, Végh B, Csikász T, 2011. Appearance of a new sunflower downy mildew race in the South-East region of the Hungarian Great Plain. (Újabb napraforgó-peronoszpóra rassz megjelenése Magyarországon, a Dél-kelet Alföldi régióban.) Növényvédelem, 47(7):279-286.

Kola K, 1980. Comparative study of sunflower varieties to assess their resistance to fungal diseases in the Zadrima area. Buletini i Shkencave Bujqesore, 19:87-94.

Komjáti H, Walcz I, Virányi F, Zipper R, Thines M, Spring O, 2007. Characteristics of a Plasmopara angustiterminalis isolate from Xanthium strumarium. European Journal of Plant Pathology, 119(4):421-428.

Kucmierz J, 1976. Plasmopara helianthi Novot., a new fungus species for Poland. Fragmenta Floristica et Geobotanica, 22(3):373-375

Labrouhe DDe , Walser P, Serre F, Roche S, Vear F, 2008. Relations between spring rainfall and infection of sunflower by Plasmopara halstedii (downy mildew). Cordoba, Spain, 8-12 June 2008. In: Proceedings of the 17th International Sunflower Conference Vol ed. by Velasco, L.. Saville, Spain: Council of Agriculture and Fishing, 97-102.

Lafon S, Penaud A, Walser P, De Guenin M-Ch, Molinero V, Mestres R, Tourvieille D, 1996. Le mildiou du tournesol toujour sou surveillance. Phytoma, 484:35-36.

Leite RMVBde C, Henning AA, Rodrigues SR, Oliveira MFde, 2007. Detection and variability of Plasmopara halstedii in Brazil and resistance of sunflower genotypes to downy mildew. (Detecção e variabilidade de Plasmopara halstedii no Brasil e avaliação da resistência de genótipos de girassol ao míldio.) Summa Phytopathologica, 33(4):335-340.

Leppik EE, 1966. Origin and specialization of Plasmopara halstedii complex in the Compositae. FAO Plant Protection Bulletin, 14:72-76.

Liese AR, Gotlieb AR, Sackston WE, 1982. Use of enzyme-linked immunosorbent assay (ELISA) for the detection of downy mildew (Plasmopara halstedii) in sunflower. In: Proceedings of the 10th International Sunflower Conference, Surfers Paradise, Australia, 173-175.

Ljubich A, Gulya TJ, 1988. Cotyledon-limited systemic downy mildew infection. In: Proceedings of the 1988 Sunflower Research Workshop, Bismarck, USA: National Sunflower Association, 9.

Masirevic S, 1992. Races of downy mildew (Plasmopara halstedii) on sunflower present in our region and in the world. Zbornik Radova, 20:405-408.

Mayee CD, Patil MA, 1987. Downy mildew of sunflower in India. Tropical Pest Management, 33(1):81-82

Melero-Vara JM, Garcia-Baudin C, Lopez-Herrera CJ, Jimenez-Diaz RM, 1982. Control of sunflower downy mildew with metalaxyl. Plant Disease, 66(2):132-135

Melero-Vara JM, Molinero Luiz L, Merino A, Dominguez J, 1996. Razas de Plasmopara halstedii presentes en Espana y evaluacion de susceptibilidad en hibridos comerciales. In: Proceedings of the ISA Symposium I, Disease Tolerance in Sunflower, Beijing, China: International Sunflower Association, 7-13.

Meliala C, Vear F, Labrouhe DTde, 2000. Relation between date of infection of sunflower downy mildew (Plasmopara halstedii) and symptoms development. Helia, 23(32):35-44.

Molinero-Ruiz ML, Domfnguez J, Melero-Vara JM, 2002. Races of isolates of Plasmopara halstedii from Spain and studies on their virulence. Plant Disease, 86(7):736-740; 28 ref.

Moses GJ, 1989. New occurrence of downy mildew of sunflower in Andhra Pradesh. Journal of Research APAU, 17(1):73

Nandeeshkumar P, Ramachandra K, Prakash HS, Niranjana SR, Shetty H, 2008. Induction of resistance against downy mildew on sunflower by rhizobacteria, 3(4):255-262.

Nandeeshkumar P, Sarosh BR, Kini KR, Prakash HS, Shetty HS, 2009. Elicitation of resistance and defense related proteins by beta-amino butyric acid in sunflower against downy mildew pathogen Plasmopara halstedii. Archives of Phytopathology and Plant Protection, 42(11):1020-1032.

Nandeeshkumar P, Sudisha J, Ramachandra KK, Prakash HS, Niranjana SR, Shekar SH, 2008. Chitosan induced resistance to downy mildew in sunflower caused by Plasmopara halstedii. PMPP Physiological and Molecular Plant Pathology, 72(4/6):188-194.

Nikolov G, 1981. Apron 35 SD, an effective preparation in the control of downy mildew of sunflower. Rastitelna Zashchita, 29(3):40-41

Nishimura M, 1922. Studies in Plasmopara halstedii. J. Coll. Agric, 3(XI):185-210.

Novotel’nova NS, 1966. Downy mildew of sunflower. Moscow, USSR: Nauka.

Onan E, Onogur E, 1989. Downy mildew of sunflower (Plasmopara helianthi Novot.). Ege Universitesi Ziraat Fakultesi Dergisi, 26(1):271-286

Onan E, Onogur E, 1991. Studies on relation between host and pathogen of sunflower downy mildew (Plasmopara helianthi Novot.). Journal of Turkish Phytopathology, 20(1):1-10

Oros G, Viranyi F, 1987. Glasshouse evaluation of fungicides for the control of sunflower downy mildew (Plasmopara halstedii). Annals of Applied Biology, 110(1):53-63

Patil MA, Mayee CD, 1988. Investigations of downy mildew of sunflower in India. In: Proceedings of the 12th International Sunflower Conference, Novi Sad, Yugoslavia: 2:42.

Patil MA, Phad HB, Ramtirthkar MS, 1993. Occurrence and distribution of recently introduced sunflower downy mildew in Maharashtra. Journal of Maharashtra Agricultural Universities, 18(1):129-130

Rahmani Y, Madjidieh-Ghassemi S, 1975. Research on relative resistance of different varieties and inbred lines of sunflower to downy mildew Plasmopara helianthi Novt. in greenhouse and in the experimental field test, 1973. Iranian Journal of Plant Pathology, 11(3/4):96-104; 42-45

Rashid KY, 1991. Sunflower downy mildew in Manitoba. In: Proceedings of the Sunflower Research Workshop, Fargo, USA: National Sunflower Association, 12.

Rashid KY, 1993. Incidence and virulence of Plasmopara halstedii on sunflower in western Canada during 1988-1991. Canadian Journal of Plant Pathology, 15(3):206-210

Rivera Y, Rane K, Crouch JA, 2014. First report of downy mildw caused by Plasmopara halstedii on black-eyed Susan (Rudbeckia fulgida cv. ‘Goldsturm’) in Maryland. Plant Disease, 98(7):1005-1006.

Roeckel-Drevet P, Coelho V, Tourvieille J, Nicolas P, Labrouhe DTde, 1997. Lack of genetic variability in French identified races of Plasmopara halstedii, the cause of downy mildew in sunflower Helianthus annuus. Canadian Journal of Microbiology, 43(3):260-263; 23 ref.

Roeckel-Drevet P, Tourvieille J, Drevet JR, Says-Lesage V, Nicolas P, Labrouhe DTde, 1999. Development of a polymerase chain reaction diagnostic test for the detection of the biotrophic pathogen Plasmopara halstedii in sunflower. Canadian Journal of Microbiology, 45(9):797-803; 27 ref.

Rozynek B, Spring O, 2000. Pathotypes of sunflower downy mildew in southern parts of Germany. Helia, 23(32):27-34; 18 ref.

Rozynek B, Spring O, 2001. Leaf disc inoculation, a fast and precise test for the screening of metalaxyl tolerance in sunflower downy mildew. Journal of Phytopathology, 149(6):309-312; 17 ref.

Ruiz MLM, Dominguez J, Vara JMM, Gulya TJ, 2000. Tolerance to metalaxyl in Spanish isolates of Plasmopara halstedii. In: Proc. 15th Int. Sunflower Conference Toulouse, France: ISA, (G):11-15.

Sackston WE, 1981. Downy mildew of sunflower. In: Spencer DE, ed. The Downy Mildews. London, UK: Academic Press, 545-575.

Sackston WE, 1992. On a treadmill: breeding sunflowers for resistance to disease. Annual Review of Phytopathology, 30:529-551; 123 ref.

Sackston WE, Anas O, Paulitz T, 1992. Biological control of downy mildew of sunflower. In: Abstracts of the American Phytopathological Society North-East Division Meeting, Portland, USA: 33.

Sakr N, Ducher M, Tourvieille J, Walser P, Vear F, Labrouhe DTde, 2009. A method to measure aggressiveness of Plasmopara halstedii (sunflower downy mildew). Journal of Phytopathology, 157(2):133-136.

Says-Lesage V, Meliala C, Nicolas P, Roeckel-Drevet P, Tourvieille de Labrouhe D, Archambault D, Billaud F, 2001. Molecular test to show the presence of mildew (Plasmopara halstedii) in sunflower seeds. OCL – Ole^acute~agineux, Corps Gras, Lipides, 8(3):258-260; 5 ref.

Schuck E, Jobim CIP, 1988. Diseases of sunflower (Helianthus annuus L.) in Viamao and Santo Augusto, Rio Grande do Sul. Agronomia Sulriograndense, 24(2):221-232; 12 ref.

Simay EI, 1993. Incidence of rare microfungi observed in the Budateteny and Cinkota areas of Budapest. Mikologiai Kozlemenyek, 32(1-2):81-89

Skoric D, 1994. Sunflower breeding for resistance to dominant diseases. In: Proceedings of the EUCARPIA Oil and Protein Crops Section, Symposium on Breeding of Oil and Protein Crops, Albena, Bulgaria, 30-48.

Spring O, 2000. Homothallic sexual reproduction in Plasmopara halstedii, the downy mildew of sunflower. Helia, 23(32):19-26; 13 ref.

Spring O, 2001. Nonsystemic infections of sunflower with Plasmopara halstedii and their putative role in the distribution of the pathogen. Journal of Plant Diseases and Protection, 108:329-336.

Spring O, Benz A, Faust V, 1991. Impact of downy mildew (Plasmopara halstedii) infection on the development and metabolism of sunflower. Zeitschrift fur Pflanzenkrankheiten und Pflanzenschutz, 98(6):597-604

Spring O, Haas K, 2002. The fatty acid composition of Plasmopara halstedii and its taxonomic significance. European Journal of Plant Pathology, 108(3):263-267; 20 ref.

Spring O, Miltner F, Gulya TJ, 1994. New races of sunflower downy mildew (Plasmopara halstedii) in Germany. Journal of Phytopathology, 142(3-4):241-244

Spring O, Rozynek B, Zipper R, 1998. Single spore infections with sunflower downy mildew. Journal of Phytopathology, 146(11/12):577-579; 7 ref.

Spring O, Zipper R, 2000. Isolation of oospores of sunflower downy mildew, Plasmopara halstedii, and microscopical studies on oospore germination. Journal of Phytopathology, 148(4):227-231; 15 ref.

Spring O, Zipper R, 2006. Evidence for asexual genetic recombination in sunflower downy mildew, Plasmopara halstedii. Mycological Research, 110(6):657-663.

Sudisha J, Niranjana SR, Sukanya SL, Girijamba R, Devi NL, Shetty HS, 2010. Relative efficacy of strobilurin formulations in the control of downy mildew of sunflower. Journal of Pest Science, 83(4):461-470.

Thanassoulopoulos CC, Mappas CB, 1992. First report of downy mildew of sunflower in Greece. Plant Disease, 76(5):539

Tourvieille J, Roeckel-Drevet P, Nicolas P, Tourvieille de Labrouhe D, 1996. Characterization of sunflower downy mildew (Plasmopara halstedii) races by RAPD. In: Proceedings of the 14th International Sunflower Conference, Beijing, 781-785.

Vida R, 1966. Downy mildew of sunflower: a significant return. Növényvédelem, 32:533-535.

Virányi F, 1984. Recent research on the downy mildew of sunflower in Hungary. Helia, 7:35-38.

Virányi F, 1988. Factors affecting oospore formation in Plasmopara halstedii. In: Proceedings of the 12th International Sunflower Conference, Novi Sad, Yugoslavia, Vol, 2:32.

Viranyi F, Gulya TJ, 1995. Inter-isolate variation for virulence in Plasmopara halstedii (sunflower downy mildew) from Hungary. Plant Pathology, 44(4):619-624

Virányi F, Gulya TJ, 1995a. Pathogenic variation in Plasmopara halstedii. In: Abstracts of papers of the 1st International Symposium on Downy Mildew Fungi, Gwatt, Switzerland: Federation of European Microbiological Societies, Ciba-Geigy.

Virányi F, Gulya TJ, 1996. Expression of resistance in the Plasmopara halstedii – sunflower pathosystem. In: Proceedings of the ISA Symposium I, Disease Tolerance in Sunflower, Beijing, China: International Sunflower Association, 14-21.

Viranyi F, Sziraki I, 1986. Establishment of dual cultures of Plasmopara halstedii and sunflower. Transactions of the British Mycological Society, 87(2):323-325

Viranyi F, Walcz I, 2000. Population studies on Plasmopara halstedii: host specificity and fungicied tolerance. In: Proceedings of the 15th International Sunflower Conference Toulouse, France: ISA, (I):55-60.

Walcz I, Bogßr K, Virßnyi F, 2000. Study on an Ambrosia isolate of Plasmopara halstedii. Helia, 23(33):19-24; 8 ref.

Yang SM, Wei SE, 1988. Diseases of cultivated sunflower in Liaoning Province, People’s Republic of China. Plant Disease, 72(6):546

Yorinori FT, Henning AA, Ferreira LP, Homechin M, 1985. Diseases of sunflower in Brazil. In: Proceedings of the 11th International Sunflower Conference, Mar del Plata, Brazil, 459.

Zad J, 1978. Transmission of sunflower downy mildew by seed. Iranian Journal of Plant Pathology, 14(1/4):1-2; 1-7

Zazzerini A, 1978. The spread of Plasmopara helianthi Novot in relation to slope. Phytopathologia Mediterranea, 17(3):153-156

Zazzerini A, 1983. Peronospora disease (Plasmopara helianthi Novot.) of sunflower: physiologic races of the parasite and methods of identifying infected material. Informatore Fitopatologico, 33(2):117-119

Zimmer DE, 1974. Physiological specialization between races of Plasmopara halstedii in America and Europe. Phytopathology, 64(11):1465-1467


Sclerotinia Infection Model

Plant Infection by S. sclerotiorum

Carpogenic germination of sclerotia is stimulated by periods of continuous soil moisture. Apothecia are formed on the soil surface from which ascospores are released into the air. Infection of most crop species is principally associated with ascospores but direct infection of healthy, intact plant tissue from germinating ascospores usually does not occur. Instead, infection of leaf and stem tissue of healthy plants results only when germinating ascospores colonize dead or senescing tissues, usually flower parts such as abscised petals, prior to the formation of infection structures and penetration. Myceliogenic germination of sclerotia at the soil surface can also result in colonization of dead organic matter with subsequent infection of adjacent living plants. However, in some crops, for example sunflower myceliogenic germination of sclerotia can directly initiate the infection process of the roots and basal stem resulting in wilt. The stimulus for myceliogenic germination and infection in sunflower is not known but likely depends on nutritional signals in the rhizosphere derived from host plants.

The infection process

The infection of healthy tissue depends on the formation of an appressorium, which may be simple or complex in structure depending on the host surface. In most cases, penetration is directly through the cuticle and not through stomata. Appressoria develop from terminal dichotomous branching of hyphae growing on the host surface and consists of a pad of broad, multi-septate, short hyphae that are orientated perpendicular to the host surface to which they are attached by mucilage. Complex appressoria are often referred to as infection cushions. Although earlier workers considered the penetration of the cuticle to be a purely mechanical process there is strong evidence from ultrastructural studies that enzymatic digestion of the cuticle also plays a role in the penetration process. Little is known about S. sclerotiorum cutinases, however, the genome encodes at least four cutinase-like enzymes (Hegedus unpublished). A large vesicle, formed at the appressorium tip prior to penetration, appears to be released into the host cuticle during penetration. After penetration of the cuticle, a subcuticular vesicle forms from which large hyphae fan outgrowing over and dissolving the subcuticular wall of the epidermis.

Infection by enzymatic degradation of the epidemic cells: Oxalic acid works in concern with cell wall degrading enzymes, such as polygalacturonase (PG), to bring about the destruction of host tissue by creating an environment conducive for PG attack on pectin in the middle lamella. This, in turn, releases low molecular weight derivatives that induce the expression of additional PG genes. Indeed, overall PG activity is induced by pectin or pectin-derived monosaccharides, such as galacturonic acid, and is repressed by the presence of glucose. Examination of the expression patterns of individual Sspg genes has revealed that the interplay among PGs and with the host during the various stages of infection is finely co-ordinated. (Dwayne D. Hegedus *, S. Roger Rimmer: Sclerotinia sclerotiorum: When ‘‘to be or not to be’’ a pathogen? FEMS Microbiology Letters 251 (2005) 177–184)

Looking for Climate Conditions for Infection of S. sclerotiorum has to take consideration of the apothecia formation, the sporulation, the direct infection by apothecia (even if it does not take place very frequent) and the infection from established mycelia by encymatic degradation of the epidemic cells. Apothecia formation and sporulation takes place if a rain of more than 8 mm is followed by a period of high relative humdiity lasting longer than 20 hours at optimum temperature of 21°C to 26°C.
Direct Infection by Apothecia can be expected after a leaf wetness period followed by 16 hours of relative humidity higher than 90% under optimum 21°C to 26°C (“appressoria infection”). Wheras saprophytic growth followed by encymatic degratation of the epidermic cells (“hydrolytic infection”) can be expected under a slightly lower relative humditiy of 80% lasting for a period of 24 hours under optimum conditions of 21°C to 26°C.


1 Lumsden, R.D. (1976) Pectolytic enzymes of Sclerotinia sclerotiorum and their localization on infected bean. Can. J. Bot. 54,2630–2641.
2 Tariq, V.N. and Jeffries, P. (1984) Appressorium formation by Sclerotinia sclerotiorum: scanning electron microscopy. Trans. Brit. Mycol. Soc. 82, 645–651.
3 Boyle, C. (1921) Studies in the physiology of parasitism. VI. Infection by Sclerotinia libertiana. Ann. Bot. 35, 337–347.
4 Abawi, G.S., Polach, F.J. and Molin, W.T. (1975) Infection of bean by ascospores of Whetzelinia sclerotiorum. Phytopathology 65, 673–678.
5 Tariq, V.N. and Jeffries, P. (1986) Ultrastructure of penetration of Phaseolus spp. by Sclerotinia sclerotiorum. Can. J. Bot. 64, 2909– 2915.
6 Marciano, P., Di Lenna, P. and Magro, P. (1983) Oxalic acid, cell wall degrading enzymes and pH in pathogenesis and their significance in the virulence of two Sclerotinia sclerotiorum isolates on sunflower. Physiol. Plant Pathol. 22, 339–345.
7 Fraissinet-Tachet, L. and Fevre, M. (1996) Regulation by galacturonic acid of ppectinolytic enzyme production by Sclerotinia sclerotiorum. Curr. Microbiol. 33, 49–53.

Practical Use of the Sclerotinia Model

The White Leg Infection Model shows the periods when the formation of apothecia are expected. If these periods are coinsitent with the flowering period of rape seed or canola we have to expect S. sclerotiorum infections during a moist period. The spores formed in the apothecia might be available for one to several days. The opportunity of infections is indicated by the calculation of the infection progress for direct or indirect infections by appressoria or enzymatic cell wall degradation. If the infection progress line reaches 100% an infection has to be assumed. These infections should be covered preventative or a fungicid with a curative action against S. sclerotiorum has to be used.


Grey Mould (Botrytis cinerea) is a devastating disease with a high economic impact in production. B. cinerea infects the flowers and the fruits close to maturity.

The fungal pathogen has a very broad host range, infecting more than 200 different hosts. Fungal growth exists saprophytically and parasitic.


On Sunflowers the pathogen causes a grey mould on the head and stem. There while the leaves start to dry out. These symptoms occur during the maturation of kernels on the head. Brown spots on the backside are seen. These spots are covered by the fungal mycelium and spores, giving the appearance of a powdery. Spores are able to be spread during wet weather conditions.

Black sclerotia deprived of medulla appear on the crop debris after harvesting or directly on the plants if they are harvested too late.

The fungus overwinters during winter on the soil surface or in the soil as mycelium or sclerotia. In springtime, the overwintering form starts to germinate and produce conidia. These conidia are spread by wind and rain and infect new plant tissue.

Germination is possible at relative humidity over 85%. The optimal germinating temperature is 18°C. The fungal pathogen can reproduce multiple times.

Control options: Seed control can protect plants of damping- off. Chemical control is difficult due to the resistance of the pathogen. Therefore attempts are made for natural control strategies with Trichoderma harzianum.

Conditions for modeling infection

B. cinerea infections are related to free moisture. Therefore in open field production leaf wetness, which is a good indicator, is determined.
Bulger et al. (1987) studied the correlation of leaf wetness periods during flowering and the occurrence of grey mould on the fruits. They found that for a higher risks of infection at 20°C a time period of longer than 32 hours of leaf wetness is needed. At lower temperatures, the leaf wetness periods have to be longer for infection of the disease.

FieldClimate is indicating risk of Botrytis cinerea on the base of leaf wetness periods and the temperature during these periods.

The graph below shows the duration of wet leaves in dependence of the actual temperature needed for a Botrytis infection. If the risk is higher than 0 every leaf wetness period longer than 4 hours will increase the risk by the same relation.
A day with a leaf wetness period shorter than 4 hours is assumed to be a dry day and will reduce the risk by 20% of the actual value.

Practical use of the Grey Mould Model: The model indicates periods with a risk of a Botrytis infection. This risk period during the bloom of strawberry will lead to infected fruits. As longer the risk period lasts and as higher the risk is as higher is the probability and the number of infected fruit. The risk, which can be taken into consideration, depends on the market. Growers, which are selling their fruits to the supermarket will not take any risk, knowing that they are not able to sell infected fruits. While growers, who sell their fruits directly to the people are able to take a higher risk.


Bulger M.A., Ellis M. A., Madden L. V. (1987): Influence of temperature and wetness druation on infection of strawberry flowers by Botrytis cinerea and disease incidence of fruit originating from infected flowers. Ecology and Epidemiology; Vol 77 (8): 1225-1230.

Sosa-Alvarez M., Madden L.V., Ellis M.A. (1995): Effects of temperature and wetness duration on sporulation of Botrytis cinerea on strawberry leaf residues. Plant disease 79, 609-615.



TOMCAST (TOMato disease foreCASTing) is a computer model based on field data that attempts to predict fungal disease development, namely Early Blight, Septoria Leaf Spot and Anthracnose on tomatoes. Field placed data loggers are recording hourly leaf wetness and temperature data. This data where analysed over a 24 hour period and may result in the formation of a Disease Severity Value (DSV); essentially an increment of disease development. As DSV accumulate, disease pressure continues to build on the crop. When the number of accumulated DSV exceed the spray interval, a fungicide application is recommended to relieve the disease pressure.

TOMCAST is derived from the original F.A.S.T. (Forecasting Alternaria solani on Tomatoes) model developed by Drs. Madden, Pennypacker, and MacNab? at Pennsylvania State University (PSU). The PSU F.A.S.T. model was further modified by Dr. Pitblado at the Ridgetown College in Ontario into what we now recognize as the TOMCAST model used by Ohio State University Extension. DSV are: A Disease Severity Value (DSV) is the unit of measure given to a specific increment of disease (early blight) development. In other words, a DSV is a numerical representation of how fast or slow disease (early blight) is accumulating in a tomato field. The DSV is determined by two factors; leaf wetness and temperature during the “leaf wet” hours. As the number of leaf wet hours and temperature increases, DSV accumulate at a faster rate. See the Disease Severity Value Chart below.

Conversely, when there are fewer leaf wet hours and the temperature is lower, DSV accumulate slowly if at all. When the total number of accumulated DSV exceeds a preset limit, called the spray interval or threshold, a fungicide spray is recommended to protect the foliage and fruit from disease development.

The spray interval (which determines when you should spray) can range between 15-20 DSV. The exact DSV a grower should use is usually supplied by the processor and depends on the fruit quality. Following a 15 DSV spray interval is a conservative use of the TOMCAST system, meaning you will spray more often than a grower who uses a 19 DSV spray interval with the TOMCAST system. The trade off is in the number of sprays applied during the season and the potential for difference in fruit quality.

Studies have been initiated at Michigan Staate University to test the disease forecasting system, TomCast, for use in managing foliar blights on carrot. TomCast has been used commercially in tomato production, and has recently been adapted for use in disease management of asparagus. Processing carrots ‘Early Gold’ were planted with a precision vacuum seeder at the MSU Muck Soils Research Farm in three rows 18 inches apart on a raised bed that was 50 feet long. Carrot beds were spaced on 64 inch centers and inrow seed spacing was 1 inch. Each of the four replications of the experiment were located in separate blocks of carrots that consisted of 36 beds. Seventeen treatment beds 20 feet long were randomly placed in a checker board pattern in each replication. Treatments were applied with a CO2 backpack sprayer that was calibrated to deliver 50 gallons per acre of spray solution using 8002 flat fan nozzles. Treatments consisted of an untreated and different schedule applications of Bravo Ultrex 82.5WDG (22.4 oz/A) alternated with Quadris 2.08SC (6.2 fl oz/A). The chemical program was applied on a 10 day calendar program as well as when predicted by the TomCast disease forecaster. Three different prediction thresholds of 15, 20, and 25 DSVs were used to time fungicide applications. When the cumulative daily DSV values reached the determined threshold a spray would be applied. Each treatment regime was initiated at four different levels of disease pressure (0%, trace, 5%, and 10% foliar blight). The first treatments were applied on 2 July and the last application of any treatment was made on 21 September. Ten feet of each center row of the spray blocks were marked before the first application and were used for weekly disease ratings (see graphs, below). Yields were taken from the same ten feet section of row by hand harvesting the carrots and topping and weighing.

This indicates that the first treatment in carrot should be done as soon as we can find the first disease incidence in field. From now on it worked fine by the use of the TomCast model with a threshold of 20 DSV accumulated since the last spray. determines the severity of an Alternaria Infection in two different models:

Source: (Jim Jasinski, TOMCAST Coordinator FOR OHIO, INDIANA, & MICHIGAN)

TomCast Alternaria Model

In dependence of the climatic conditions of hours of leaf wetness and air temperature, values of severity of an Infection (from 0 – 4, see table above) are determined.