PPM point 8.2
Data Sheets on Pests recommended for regulation as quarantine pests
This data sheet is based on a CPC data sheet
Name: Claviceps africana Freder., Mantle & De Milliano
Synonyms: Sphacelia sorghi McRae
Notes on taxonomy and nomenclature: In 1991, ergot in Zimbabwe was described as a new species, C. africana, quite distinct from C. sorghi (Frederickson et al., 1991). Ergot on sorghums worldwide had been assumed to be C. sorghi prior to this. Earlier reports of C. sorghi in Africa are erroneous and are considered to refer to C. africana
Common name: CYSDV (acronym)
English : ergot, sorghum ergot, sugary disease, India: Asali
Bayer computer code: CLAVAF
EU Annex designation: No status.
Individual florets of the inflorescence are affected by sphacelia/sclerotia and honeydew; the panicle, seeds, leaves and stalks are affected by honeydew.
Sorghum bicolor (common sorghum)
Sorghum halepense (Johnson grass)
Originally present in Asia and Africa. Recently discovered in India but was probably present there for a long time.
Introduced in 1995 into Brazil and rapid spread through the central and southern part of the country.
By 1996 found in Argentina, Bolivia, Colombia, Paraguay, Venezuela. In April 1996 in Australia (southern Queensland) where it spread over 60,000 km2 in 3 weeks.
By February 1997, found in Honduras, Dominican Republic, Haiti, Jamaica, Puerto Rico and Mexico.
By March 1997, found for the first time in Texas, USA, and later in Kansas, Florida, Georgia, Nebraska, Oklahoma.
Asia: Present (India, Japan, Thailand, Yemen)
Africa: Present (Angola, Botswana, Burundi, Ethiopia, Ghana, Kenya, Lesotho, Malawi, Mozambique, Nigeria, Rwanda, Senegal, South Africa, Tanzania, Uganda, Zambia, Zimbabwe).
North America: Mexico, USA (Florida, Georgia, Kansas, Mississipi, Nebraska, Oklahoma, Texas).
Central America: Dominican Republic, Haiti, Honduras, Jamaica, Puerto Rico.
South America: Argentina, Bolivia, Brazil (Goias, Minas Gerais, Santa Catarina, Sao Paulo) Colombia, Paraguay, Uruguay, Venezuela.
Oceania: Australia (New South Wales, Queensland).
Genetic studies are suggesting that Africa could be a possible origin for the clones introduced into the Americas, and Asia for those introduced into Australia.
Macroconidia germinate on the stigmatic hairs of unpollinated ovaries Germination occurs in the range 14-32°C, optimum 20°C (Frederickson, 1990). Hyphae grow down the inner ovary wall to the base, occupying the tissues adjacent to the rachilla, which provides the necessary nutrients to support the massive proliferation of hyphae. By day 4 the ovule has been invaded and hyphae simultaneously emerge onto the ovary surface. All but the very apex of the ovary is colonized. The incubation period before disease symptoms appear (the sphacelium) is 6-12 days (Frederickson, 1990); the optimum temperature for disease development is 20°C (McLaren and Wehner, 1990).
Spores, in honeydew, are exuded about a day after the sphacelia become obvious (c.f. C. sorghi where honeydew appears long before the sphacelia are visible). Under conditions of high relative humidity, macroconidia at the honeydew surface germinate iteratively to produce aerially-supported secondary conidia, rendering the honeydew white in appearance (Frederickson et al., 1989, 1993). Secondary conidiation is a prominent feature of C. africana epiphytotics across the world. Secondary conidia are wind-borne spores. Autoinfection and many secondary cycles are possible in a season, even from a small initial inoculum. Inoculum may thus rapidly build up and spread to cause high disease incidence and severity. At the end of the cropping season the pathogen exists in the form of sphacelia and sclerotia and either may enable survival.
In normal seed store conditions conidial viability decline to zero after about 4 months (Odvody et al., 1999). Honeydew on seed is one potential source of infection which can be eliminated by seed treatment with captan (Dahlberg et al., 1999).
Sclerotia have only been experimentally germinated with difficulty to produce the teleomorph (Frederickson et al., 1991) and they may be less important than the conidia for survival.
The sclerotial tissues of C. africana produce alkaloids that can have adverse effect on animals (pigs, poultry). Toxicity differs between the 'west' strain in Africa and the Americas and the 'east' strain in Australia and India (Pazoutova et al., 2000).
Alternative hosts are known and have a proven role in inoculum survival in some parts of the world. In the Americas and Australia, C. africana infections on Johnson grass (Sorghum halepense) and other species of sorghum are common (Ryley et al., 1996; Odvody et al., 1998) and experimental cross-inoculation onto cultivated sorghum and back has been successful. Ergot was first recorded in Texas, USA, in 1997 (Isakeit et al., 1998) and mild winter weather allowed the pathogen to persist in an active form throughout the southern part of the state until the spring of 1998. C. africana has repeatedly survived the winter as active, conidial inoculum in Texas and Mexico every year since (Odvody et al., 2000).
Detection and identification
Individual ovaries between the glumes of some or all sorghum florets are replaced by a soft, white, subglobose-shaped growth of mycelium (sphacelium) from which sticky, liquid droplets of spore-bearing honeydew (thin to viscous, orange-brown or superficially white) may exude. Under conditions of high relative humidity, the copious honeydew is of low viscosity and the surface white. The surfaces of the panicle, seed, leaves, stalk and soil also become smeared by the dripping honeydew and appear conspicuously white. A white, powdery crust forms wherever such honeydew dries. For more information, see Frederickson et al. (1989, 1991).
When the honeydew and sphacelia are colonized by the hyperparasite Cerebella andropogonis, black, spherical, convoluted growths are seen at floret tips (Bandyopadhyay et al., 1998). Upon dissection, a discoloured sphacelium of reduced size is found underneath. Other moulds may also grow on the honeydew.
Sphacelia are white and subglobose, 4-6 x 2-3 mm, forming two types of spore: the oblong macroconidium which has polar vacuoles and a slight central constriction (9-17 x 5-8 Ám), and the spherical microconidium (2-3 Ám diameter). Germination of the macroconidium produces the pyriform secondary conidium (8-14 x 4-6.5 Ám) on the tip of the sterigma-like process (Frederickson et al., 1989, 1991).
The structure popularly called the sclerotium is actually comprised of both sphacelial and sclerotial tissues and is similar in size and shape to the initial sphacelium. The true sclerotial tissues are proximal, spherical to oval in shape and, in contrast to the sphacelium, are firm (even after soaking in water), hydrophobic and contain the alkaloid dihydroergosine. The sclerotial cortex is orange-brown but may appear superficially pink, orange or red due to adherent floral membranes. Germination of the sclerotium gives rise to up to six stromata each with a purple stipe, 8-15 x 0.3-0.6 mm long, and purple capitulum (0.5-1.3 mm diameter). Ascomata (perithecia), 123-226 x 86-135 Ám, the cylindric asci in situ are 140 x 3-4 Ám and the eight ascospores up to 45 x ca 1 Ám in situ (Frederickson et al., 1991).
Two other species of Claviceps, C. sorghi (Kulkarni et al., 1976) and C. sorghicola (Tsukiboshi et al., 1999) infect sorghum and overlap in distribution with C. africana. Both C. sorghi and C. sorghicola form elongate sphacelia and sclerotia, whereas those of C. africana are subglobose. The sori of covered kernel smut (Sporisorium sorghi [Sphacelotheca sorghi]) and long smut (Tolyposporium ehrenbergii) are sometimes confused with C. africana sphacelia. However, in these fungi the sack-like sori comprise a smooth, cream to grey outer covering or peridium enclosing the powdery-black teliospores (Frederiksen, 1986; Hilu, 1986). The sphacelia are devoid of an outer covering, being solid, spongy bodies with convolutions which are the microscopic spore-bearing cavities.
Detection and inspection methods:
In the field, C. africana infection is usually obvious from the dripping of honeydew from infected florets and honeydew deposition on the panicle, leaves, stalk and soil. Often the panicle is spectacularly white (see Symptoms). The pathogen is less easily detected in seed batches and poses potential problems for seed exchange.
Seed lots are examined by at least a x10 magnification for the presence of sphacelia: cream-white to grey cushions of fungal growth. (Alderman et al., 1999; Frederickson et al., 1999). If present at the base of sphacelia, sclerotial tissues are red-brown and oval-spherical in shape. Host tissues (lemma, palea, glumes) may be attached. (c.f. Sclerotia of the Indian C. sorghi are thin, cylindrical and elongate; sclerotia of the Japanese Claviceps sorghicola are conical, elongate and purple-black).
C. africana can be distinguished from the other sorghum ergot pathogens by the detection of the alkaloid dihydroergosine in sclerotial tissues (Frederickson et al., 1991; Mantle and Hassan, 1994) or by comparison of the nucleotide sequences of ITS1 and part of 5.8S rDNA (Pazoutova et al., 2000). The east and west strains of C. africana could be distinguished by the RAPD banding patterns produced with seven primers (Pazoutova et al., 2000).
Means of movement and dispersal
Studies in Africa and Mexico indicate that sorghum seed from C. africana-infected plants are coated with sugary exudates in which the fungal spores are borne (Mclaren, 1993; Valasquez-Valle et al., 1998) but the role of these seeds, or seed-sphacelia/sclerotia admixtures, in the spread of ergot has not yet been determined. Sorghum is not susceptible at sowing (seed) but only much later at flowering, so a flowering, alternative host would have to present at sowing to permit infection. Even if secondary conidia were produced by iterative germination of macroconidia, the spores, being planted with seed in the ground, would have no inoculum potential. The likelihood of ergot infection resulting from the importation of contaminated seed into an area is very slim compared to infection arising from the dissemination of airborne inoculum (secondary conidia) from relatively local sources (Odvody et al., 2000).
The rapid spread of the disease across vast continental areas in the Americas and Australia are consistent only with wind-borne spread of conidia (Bandyopadhyay et al., 1998). However, windborne dissemination of the pathogen is unlikely to have been responsible for the initial introduction of ergot disease to these countries.
Ergot disease is primarily an economic problem in F1 hybrid seed production. It is particularly severe in male-sterile lines (A-lines) when either non-synchronous flowering of A-line and restorer lines (R-lines) or adverse environmental conditions result in lack of viable pollen and delayed seed set (Bandyopadhyay et al., 1998). Losses of 10-80% have been reported in hybrid seed production field in India and regular annual losses of 12-25% recorded in Zimbabwe (Frederickson and Leuschner, 1997; Bandyopadhyay et al., 1998). It has been estimated that ergot will cost the Australian seed industry A$4 annually (Bandyopadhyay et al., 1998) and in the USA, annual production cost increases due to ergot are projected at $5 million (Anon., 1999).
Cultural Control and Sanitary Methods
Cultural control is not a reliable control method, often depending on the capricious nature of the climate. Field practices aimed at reducing the risk or severity of infection include the removal of infected panicles at harvest, 3-year crop rotations and deep ploughing of field residues. However, despite these measures, a serious epiphytotic occurs every 5-10 years in Zimbabwe (Frederickson and Leuschner, 1997). Increasing the ratio of pollen-producing rows to the male-sterile, female parent, or staggering the planting dates of the pollen donor rows helped reduce ergot by increasing the period when pollen was available (Frederickson and Leuschner, 1997) but only if the weather conditions were favourable for pollination.
There is currently no source of resistance to sorghum ergot for use in the field in A-lines. Resistant fertile sorghums have been reported (Tegegne et al., 1994; Musabyimana et al., 1995) but resistance has proved a function of cleistogamy, or fast and efficient pollination and fertilization (Bandyopadhyay, 1992; Frederickson et al., 1994) with no potential use in A-lines.
Chemical Control and Seed Treatment
Chemical control is barely cost effective, only feasible for controlling disease on the A-lines and unnecessary on the hybrids themselves. The fungicide must be precisely deposited on the stigmas rendering aerial application ineffective so far.
The contamination of C. africana honeydew on infected seeds could be reduced by seed washing but large volumes of water (4 L/15g seed) were required to reduce the concentration to levels which would not affect germination and seedling development (McLaren, 1993). In Texas commercial seed production, air-blowing, screen-cutting (sieving) and use of the gravity table removes almost all sclerotia/sphacelia from seed (DE Frederickson, INTSORMIL, Box 776, Bulawayo, Zimbabwe, personal communication, 2001). Further coating of seed with captan renders conidia in honeydew deposits inviable and prevents germination of conidia from any remaining sphacelial tissues (Dahlberg et al., 1999; Odvody et al., 2000).
Development of IPM Strategies
The integration of several control practices would provide the greatest potential for control. Cultural control alone has little impact on disease. Chemical use in the field is only economically feasible in seed production plots and then only with marginal profit. Fungicide treatment of seed, however, is an effective and economic way to control potential seed-borne, conidial inoculum (Dahlberg et al.,1999; Odvody et al., 2000). Disease forecasting by using weather variables to predict ergot severity is still in its infancy. Combining some form of host genetic resistance with disease prediction and limited fungicide use during high risk periods may be the best strategy for control in the future.
To be completed after PRM
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