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Plantwise Technical Factsheet

headblight of maize (Gibberella zeae)

Host plants / species affected
Acacia mearnsii (black wattle)
Alopecurus pratensis (meadow foxtail)
Avena sativa (oats)
Azadirachta indica (neem tree)
Beta vulgaris var. saccharifera (sugarbeet)
Cucurbita pepo (marrow)
Dianthus (carnation)
Gardenia jasminoides (cape jasmine)
Glycine max (soyabean)
Gossypium (cotton)
Hordeum vulgare (barley)
Hyacinthus orientalis (hyacinth)
Jatropha curcas (jatropha)
Linum usitatissimum (flax)
Lolium multiflorum (Italian ryegrass)
Lupinus (lupins)
Mangifera indica (mango)
Medicago (medic)
Medicago littoralis (strand medick)
Miscanthus × giganteus
Musa x paradisiaca (plantain)
Nicotiana tabacum (tobacco)
Oryza sativa (rice)
Panicum miliaceum (millet)
Pennisetum glaucum (pearl millet)
Phalaris canariensis (Canarygrass)
Phaseolus vulgaris (common bean)
Pinus sylvestris (Scots pine)
Pisum (pea)
Rubus idaeus (raspberry)
Secale cereale (rye)
Setaria italica (foxtail millet)
Solanum (nightshade)
Solanum tuberosum (potato)
Sorghum bicolor (sorghum)
Trifolium (clovers)
Triticum aestivum (wheat)
Vaccinium (blueberries)
Vicia faba (faba bean)
Vitis vinifera (grapevine)
Zea mays (maize)
Zingiber officinale (ginger)
List of symptoms/signs
Inflorescence  -  discoloration panicle
Inflorescence  -  twisting and distortion
Leaves  -  abnormal colours
Roots  -  cortex with lesions
Roots  -  necrotic streaks or lesions
Roots  -  rot of wood
Roots  -  soft rot of cortex
Seeds  -  discolorations
Seeds  -  lesions on seeds
Stems  -  dieback
Stems  -  discoloration of bark
Stems  -  internal discoloration
Stems  -  internal red necrosis
Stems  -  mould growth on lesion
Stems  -  wilt

Gibberella stalk rot
Leaves on early-infected plants suddenly turn a dull greyish-green while the lower internodes soften and turn tan to dark-brown. Diseased tissue within the stalks often shows a pink to reddish discoloration. The fungus causes shredding of the pith and may produce small, round, black perithecia superficially on the stalks. Lesions may develop concentric rings.

Gibberella (red) ear rot
A reddish mould, often at the ear tip, is the characteristic sign of Gibberella ear rot. Early infected ears may rot completely, with the husks adhering tightly to the ear and a pinkish to reddish mould growing between the husks and ear.


G. zeae can affect sorghum at all growth stages. Lesions vary in size from small, circular spots to elongated streaks. They may be light-red to dark-purple. Lesions may be found in the interior and on exterior tissues of roots, stalks, seeds and peduncles. Dark red discoloration of the cortex of seedling roots is often observed, and the fungus may spread to other root and stalk tissue during the growing season (Frederiksen, 1986). In seedlings and young plants, leaves turn brown and the plants wither and die; under very humid conditions whitish-yellow mycelium develops, which later becomes salmon-pink.

In older plants, the pathogen invades the vascular bundles and inner tissues of the stalk which then become reddish. Early-infected flowers or young grain may be destroyed; mature grains may become covered with mycelium, but are not destroyed (Tarr, 1962).


G. zeae may produce a reddish appearance on affected seeds. Discoloration of definite areas of the seed, appearing as brown spots, or covering the entire surface of the seed, may also occur.

The fungus causes the formation of spots on the surface of the husks which are at first white, but later become yellow and salmon or carmine. Infected grains are light, shrunken and brittle. Nodes of stems are attacked, causing them to rot, turn black and disintegrate. Stems wilt, break and lodge (Padwick, 1950).


Blighted seedlings are characterized by a light-brown to reddish-brown water-soaked cortical rot and blight before or after emergence. Head blight is conspicuous before the spikes mature. Infected spikelets first appear water-soaked; this is followed by the loss of chlorophyll, giving a final bleached straw colour.

During warm, humid weather, conidial development is abundant and the infected spikelets show a pink or salmon-pink cast, especially at the base and in the crease of the kernel. Infection may spread to adjacent spikelets or through the entire spike. The infected kernels become shrivelled, with a scabby appearance due to the tufty mycelial outgrowths from the pericarp. Infected kernels range in colour from white to pink to light-brown, depending upon the time of infection and environmental conditions during disease development (Dickson, 1947).


Restricted, reddish-brown cortical lesions occur when infected seed is sown in cool, moist soil. In warm soil, seedling blight may occur before or after emergence. During later stages of plant development, crown and basal culm rot are commonly observed.


Spikes are dwarfed and compressed with infected spikes closed rather than spread. All or part of the spike is infected. Hulls (lemma and palea) are light to dark-brown with a dead, lustreless surface (Dickson, 1947). Conidial or perithecial masses commonly develop on the surface, especially during moist weather. Kernels are shrunken and light brown in colour. The pericarp surface is rough or scabby in appearance. In Manitoba, definitive, reliable symptoms of Fusarium head blight infection in harvested barley (and oat) were often absent (Clear et al., 1996).
Prevention and control

Cultural Control and Sanitary Methods

In the irrigated area of central Shaanxi Province, China, cultural factors contributing to severity of outbreaks of scab in wheat include susceptibility of the host, irrigation changes and intensive cultivation of summer maize crops (Shang et al., 1987). In Canada, ploughing-disking in spring significantly reduced maize stalk rot by G. zeae (Hudon et al., 1990).

In Germany, FHB incidence in spring wheat was reduced by ploughing under infected stubble residues and by nitrolime application (Yi-CuiLin et al., 2001). Krebs et al. (2000) found that in winter wheat tilllage using a mouldboard plough reduced the grain contamination with F. graminearum and the DON-content by 80%. In no-tillage treatments, rape as the previous crop reduced the F. graminearum incidence and the DON-content by 90% compared to maize as the preceding crop.

The incidence of maize cob rot caused by G. zeae was determined over two seasons under different tillage systems at various localities in South Africa. Tillage had no effect on cob rots caused by Fusarium species (Flett and Wehner, 1991). Seed conditioning with gravity separation has been shown to improve germinability and emergence rates of Fusarium infected wheat seed in Iowa (Gutormson et al., 1993).

Several studies have examined the effect of tillage practice on head blight development. Tillage systems that leave the most residues on the soil are expected to produce the greatest amount of inoculum and cause the highest severity of FHB. Tillage and crop rotation were recommended as means of reducing inoculums (Khonga and Sutton 1988). However, in Saskatchewan, zero till did not result in fields with higher levels of FHB compared with conventional till, while minimum till generated more severely diseased fields (Fernandez et al. 2001).

Significant differences were found in disease incidence and severity and in DON content of grain in a Minnesota study that examined the effects on disease levels of moldboard plow (~10% residue retained), chisel plow (~30% residue retained), and zero till (~65% residue retained) (Dill-Macky and Jones 2000). The distances were small but significant: disease incidences in moldboard plow, chisel plow, and zero-till plots were 64%, 72%, and 71%, respectively; disease severities, 16%, 20%, and 21%, respectively; and DON levels, 8.1, 10.6, and 11.1 ppm, respectively. The results of a 3-year tillage study in Ontario were inconclusive, with observations that G. zeae persists on debris under both till and zero-till conditions and that other factors such as rotation and cultivar susceptibility are likely to be more important than tillage practice (Miller et al. 1998). Conclusions as to the effects of rotations are somewhat similar. Where differences were found, levels of disease on wheat following crops other than cereals or maize were significantly different, but small (Dill-Macky and Jones 2000).

Host-Plant Resistance

Wheat cultivars exist with moderate degrees of resistance to G. zeae (Nass et al., 1995). Winter and spring wheats both show a range of resistance (4-58% and 12-58% infection respectively) (Rodemann et al., 2001). Extensive studies are in progress to obtain higher levels of resistance by understanding inheritance and mechanisms of resistance (Wang et al., 1994; Mesterhazy, 1995; Singh et al., 1995). Barley has at least one cultivar with known resistance; this cultivar was used to map quantitative trait loci (QTL) on the genome that were associated with low FHB and DON levels (Ma et al., 2000) Three QTLs on different chromosomes were suggested as being useful for marker-assisted selection. A cultivar with intermediate level resistance to G. zeae has been released commercially (Rasmusson et al., 1999). A study of QTL in Chinese spring wheat crosses by (Ittu et al., 2000) showed gliadin loci on chromosomes 1B and 1D to be markers associated with resistance to FHB. Selection for genotypes possessing these genetic markers in this population would increase the probability of obtaining lines with higher resistance to FHB.

In maize, stalk-rot resistance has long been recognized for inbreds and hybrids, and its inheritance extensively studied (Koehler, 1960; Christensen and Wilcoxson, 1966). Resistance also exists among hybrids to ear rotting (Koehler, 1959; Sutton and Baliko, 1981; Atlin et al., 1983; Hart et al., 1984), and vomitoxin production (Hart et al., 1984). A linkage map of maize has been obtained, in which four to five genomic regions are shown to carry factors involved in resistance to G. zeae (Pe et al., 1993). Resistance to ear rot caused by G. zeae in three maize inbred lines has been developed from the breeding line CO272, which appears to carry a single dominant gene for resistance to infection through the silk (Reid and Hamilton, 1996).

Genetic engineering shows some potential to control G. zeae in wheat. Chen et al. (1999) found that transgenic wheat plants resulting from the introduction of the rice thaumatin-like protein gene (tlp) had slower development of scab symptoms than non-transgenic plants following inoculation with conidia of F. graminearum.

In a head scab disease screening program of the Triticeae 1507 accessions representing 93 species from 18 genera were tested using floret inoculation. High resistance was found in mainly perennial genera: Roegneria [Elymus], Hystrix, Agropyron, Kengyilia and Elymus (Wan et al., 1997). Elymus tsukushiensis is a potential source of resistance to scab caused by G. zeae. Wheat breeding lines identified as a disomic substitution lines involving chromosome 3A have shown a high level of resistance to scab with potential in chromosomal engineering and development of improved wheat germplasm for scab resistance breeding (Wang et al., 1999). In a study of wheat using chromosome substitution lines, chromosome 6B appeared to be a major determinant of head blight resistance (Grausgruber et al., 1998).

Biological Control

Pseudomonas fluorescens strain M.3.1. was found by Ventura et al. (1997) to be an effective antagonist of G. zeae in vitro and a potential biocontrol agent. A strain of Streptomyces sp. antagonistic to G. zeae partially attenuated the effect of G. zeae on wheat spikes (Fulgueira et al., 1996). However, the antagonistic effect was not sufficient to prevent the reduction in size and weight of the grains. Perondi et al. (1996) found in field experiments that two strains of Bacillus subtilis, one of Bacillus sp. and the yeast Sporobolomyces roseus all reduced disease severity caused by G. zeae, all giving significant increases in wheat yield (16-31% relative to the untreated control).

B. megatherium (Embr.9790) and B. subtilis (Embr.9786) significantly reduced the FHB disease incidence and severity up to 50% and 67%, respectively in wheat (Luz, 2000). Application of biocontrol agents at anthesis may achieve pathogen control by aborting, curtailing, or delaying germination of G. zeae spores in the infection court of the head (Fernando 2001). These biocontrol agents may be effective both in reducing FHB incidence and severity and in reducing DON levels. Three bacterial strains, H-08, S-01, and L-01, that were isolated from wheat head, stem, and leaf, respectively, caused significant inhibition of G. zeae (Fernando et al. 2002). Bacillus subtilis (Ehrenberg) Cohn strain H-08 reduced disease incidence and severity and maintained high population levels on the head after inoculation under controlled conditions. Lysobacter enzymogenes Christensen & Cook strain C3, a gram-negative bacterium, reduced disease incidence (type-I resistance) and spread (type-II resistance) when applied to spikelets of the wheat head (Jochum and Yuen 2002). Anther-colonizing organisms capable of utilizing tartaric acid, a compound that is poorly metabolized by G. zeae and which could be added to formulations of biocontrol agents, have been shown to reduce FHB (Khan et al. 2001).

Chemical Control

Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:


Many plant species are affected by G. zeae, but those of major economic importance include maize, and small grains, particularly wheat, barley, rye and triticale. The fungus attacks the cob or cereal spikes resulting in pink ear rot of maize, lightweight, chalky-white Fusarium damaged kernels (FDK) of wheat, and shrunken discoloured kernels of other grains. Losses are not restricted to yield and quality however, but are incurred throughout the grain industry by millers, bakers, pasta makers, maltsters, brewers and feedlot operators (Gilbert and Tekauz, 2000; Tekauz et al., 2000). In addition to yield loss, Gibberella ear rot causes the production of mycotoxins in diseased ears and kernels that contaminate animal and human food. Of particular concern are vomitoxin that causes a vomiting syndome, zearalenone that causes hyperoestrogenism and the tricothene toxin, T-2-toxin. Various surveys have shown that these mycotoxins cause extensive contamination of maize and wheat grain throughout the world (Tuite et al., 1990; Leonov et al., 1994). A survey of storage facilities in Queensland, Australia in 1983, showed that 4-deoxynivalenol was detected in nearly all pooled maize samples representing bulk wheat at concentrations ranging from trace amounts to 1.7 mg/kg. The highest concentration of zearalenone detected in a pooled wheat sample was 0.04 mg/kg. In a few samples representing individual wheat deliveries and with up to 2.8% by weight of pink grains, 4-deoxynivalenol concentration ranged up to 11.7 mg/kg and zearalenone up to 0.43 mg/kg (Blaney et al., 1987). A survey of commercial small cereal grains in Minnesota, North Dakota and South Dakota in 1993-1994 by Jones and Mirocha (1999) detected deoxynivalenol (DON) [vomitoxin] in 493 of 500 samples of wheat, 100 out of 100 six-row barley samples and in 28 samples of oats. In an evaluation of semolina milling and pasta-making quality in ten durum wheat cultivars harvested in Manitoba, Dexter et al. (1997) found that the retention of vomitoxin in the semolina was ca 50% and the semolina yield was lower than in unaffected grain.

In a survey of maize cobs with Fusarium ear rot in Poland from the 1986 season, all investigated cobs contained vomitoxin (range 18.0-131.5 mg/kg) and zearalenone (range 0.38-2.17 mg/kg) (Perkowski et al., 1991). Deoxynivalenol (DON), the main mycotoxin produced by G. zeae, destroys starch granules and endosperm proteins (Bechtel et al., 1985; Nightingale et al., 1999). DON accumulated in G. zeae infected barley grain can persist in malt and beer (Prom et al., 1999). In wheat, germination is impaired causing further losses to seed producers (Gilbert and Tekauz, 1995) and sales are lost due to low customer tolerances for FDK (Charmley et al., 1994). Fusarium head blight (FHB) epidemics are sporadic in nature requiring rain or high humidity at flowering, in addition to the presence of susceptible hosts and inoculum. In recent decades, years with severe losses due to FHB have been numerous, and regions recording severe losses appear to have increased. The disease, caused by G. zeae, is prevalent in areas with continental climates such as parts of Asia (China, Japan), North and South America (Canada, USA, Mexico, Uruguay, Argentina) and Europe (Bulgaria, Germany, Hungary, Italy, Poland, Romania, Russia, Yugoslavia) (Parry et al., 1995). In temperate or maritime regions the disease is usually caused by Fusarium culmorum.

Wheat and Barley


Approximately 6.7 to 7.0 million hectares in 20 provinces, representing 25% of the total wheat acreage, are affected by FHB (Wang, 1996; Chen et al., 1997). The disease is most severe in the mid- to lower reaches of the Yangtze River valley (Xu et al., 2000). During the period 1950 to 1990 there were 12 years with moderate epidemics when losses ranged from 10 to 20%. Severe epidemics were reported as numbering three between 1957 and 1979 (Xu et al., 2000) or seven between 1950 and 1990 (Wang, 1996), when the incidence of diseased heads reached 50 to 100% and yield loss was estimated to be approximately 40%.


More than 10,000 ha, corresponding to 4-7% of the total wheat production area, are affected by FHB in an average year, including 20 and 5% of the wheat growing regions of Kyushu and Hokkaido, respectively (Ban, 1997). In 1996, a severe outbreak affected close to 27% of Japan's wheat growing area. In Hokkaido in that year, more than 40% of the crop was damaged and yields were reduced by 20% (Li et al., 2000).


Since the early decades of the 20th century FHB has been associated with higher than normal rainfall in the months of June, July and August (Sutton, 1982). In 1980, a severe epidemic in eastern Canada affected both the spring and winter wheat growing areas of Ontario and the Atlantic Provinces (Sutton, 1982). Yield losses of 30-70%, in addition to reduction in quality from contamination by deoxynivalenol (DON), were reported for spring wheat in the Atlantic Provinces (Martin and Johnston, 1982). In western Canada in 1993, southern Manitoba experienced the same epidemic that affected the upper American Midwest. The cost of the epidemic was estimated at $75 million Canadian dollars due to lowered yield and quality (Gilbert et al., 1994) and annual losses associated with the disease have been estimated at $50 million dollars. On barley, FHB has become more important in Manitoba, since 1994. It is now generally found in most fields and in 1998 was nearly equal in severity (6.7%) to wheat (Tekauz et al., 2000). The 1996 winter wheat crop in Ontario was severely infected with FHB, resulting in a 30% yield loss that equates to a 230,000 ton loss in volume. A $CDN 100 million loss was reported for the year resulting from yield loss ($CDN 34.5 million), quality loss ($CDN 33.75 million), marketing ($CDN 11.25 million) and replacement wheat stocks ($CDN 20-30 million) (Schaasfma et al., 2000).


Fusarium head blight, or scab, is not a new disease in the USA. In 1917, 31 of 40 states that were surveyed reported damage from FHB with losses estimated at 288,000 metric tons, primarily from the winter wheat areas of Ohio, Indiana and Illinois. In 1919 losses caused by the disease were estimated at 2.18 million metric tons throughout the USA (reported by McMullen et al., 1997). Losses of 4% for all the USA were attributed to FHB in 1982 (Boosalis et al., 1983). A major epidemic affected 4 million hectares of the spring wheat and barley growing area of the northern Great Plains of North and South Dakota and Minnesota. Yield losses exceeded 6.5 million tons worth $826 million dollars, although total losses associated with the epidemic approached one billion dollars. In subsequent years losses in these states have been estimated at $200-400 million annually (McMullen et al., 1997). In the winter wheat growing states of Ohio, Michigan, Indiana and Illinois, losses were in excess of 300 million dollars in 1995 and 1996 (US Wheat and Barley Initiative). Losses in barley due to FHB are largely due to the presence of DON. In 1996, barley prices in Minnesota dropped to $2.75 from $3.00 per bushel if the mycotoxin was detected and an additional $0.05 for each additional ppm DON detected. Malting barley was sold at feed prices, as low as $2.25 per bushel (Dill-Macky, 1997).


In the latter half of the 20th century, 16 FHB epidemics were recorded in Argentina, the worst occurring in 1945-46, 1978, 1985 and 1993. Predictive models indicate the probability of severe epidemics (incidence >45%) in just over 2 in 20 years in the southeast and in the east of the central-north wheat growing regions. In the central and western zones of the latter region, the probability decreases to 1.5 and 1 year(s) in 20, respectively (de Galich, 1997). Severe epidemics were estimated to result in 20-30% yield losses, although in 1993, in no-till fields following maize, estimated losses were as high as 50%. DON levels exceeding 2 p.p.m. were common in whole samples from primary elevators, port terminal elevators and flour mills (de Galich, 1997). In the southeast wheat growing area, durum wheat production has declined from 20% of all wheat grown to less than 3.5% because of its susceptibility to FHB (de Galich, 1997). In the epidemic years of 1963, 1976, 1978 and 1985 durum crop losses as high as 70% occurred.


The disease was considered sporadic in Uruguay until 1976 when the first of many epidemics occurred (Diaz de Ackermann and Kohli, 1997). Crop production oscillated between 200,000 and 500,000 t between 1990 and 1995 due in part to epidemics of FHB. Yield losses caused by FHB in the epidemic years of 1990, 1991 and 1993 ranged between 0.5 and 31.0%. However, the damage caused under field conditions appears to be more severe than the actual losses; an average of 54% infected heads between 1990 and 1993 only resulted in a 10% yield loss. On the other hand, high levels of DON, 1-5 ppm, were found in wheat with just 12-14% infected kernels (Diaz de Ackermann and Kohli, 1997).

Hungary, Romania and Russia

Severe epidemics were recorded in 1970, 1975 and 1985 with more moderate epidemics in 1972, 1978 and 1979. In inoculated trials producing severe infection, yield losses reach 50% or more (Veisz et al., 1995). Annual yield losses ranging from 6-7% to 50%, plus reduction in grain quality, occur annually in Romania (Moldovan and Moldovan, 2000). The disease is also found on wheat in many parts of Russia including the Northern Caucasus, Central Russia, Siberia and the Far East. In the Krasnodar district, three major epidemics occurred between 1985 and 1994 with wheat crop losses of 25-50%. Concentrations of mycotoxin contamination in the grain were 25 times higher than usual and exceeded the permitted level in 25-80% of wheat samples tested (Levitin et al., 1995).


A severe epidemic of FHB was recorded in durum wheat on the Liverpool Plains in New South Wales in 1999 (Southwell et al. 2003). The incidence of disease in individual crops ranged from 2 to 100%.

Maize, Rye and Triticale

Damage to maize from infection by G. zeae is expressed in ear and stalk rots. Actual yield loss data are not available for pink ear rot. Sutton (1982) lists 1972, 1975, 1976 and 1977 as years in which serious epidemics of pink ear rot in maize occurred in eastern Canada. The 1994 growing season in Maryland and Delaware, USA, resulted in a severe outbreak of G. zeae maize ears ('Moore' variety) prior to harvesting and canning. The number of ears visibly infected ranged from <5% to 25% and kernels from the visibly mouldy area of the ears contained DON at levels of approx. 446 mg/g (Wetter et al. 1999). The incidence of zearalenone in grain was high and there were frequent reports of estrogenism in swine fed affected grain. This led to serious losses in swine, especially in reproductive herds. Reid and Sinha (1998) discuss the importance of Gibberella ear rot causing reduction in maize yield and contamination of grain with mycotoxins. Deoxynivalenol (DON) is the predominant trichothecene produced by G. zeae. DON is an immunosuppressant in livestock and induces emesis in swine characterized by vomiting, feed refusal and decreased weight gain.

Yield may be greatly reduced as a result of stalk rot following inoculation with G. zeae. Disease development appears to be influenced by genotype and environment as yield reductions range from 0.9% associated with 33% disease severity in Pakistan (Ahmad et al., 1997) to 57% in Québec, Canada (Hudon et al., 1992). In an earlier study, Wilcoxson (1962) indicated that yields in the USA were reduced by as much as 17% after inoculation with G. zeae. These yield data were all obtained from inoculated trials.

Following inoculation of winter rye with G. zeae and Fusarium culmorum, Miedaner et al. (1993) concluded that overall yield losses of 38, 27 and 16% in relative grain weight/spike, thousand kernel weight, and number of grains/spike, respectively, were similar to those caused by Fusarium head blight in wheat.

Dormann and Oettler (1993) tested the response of triticales to inoculation by G. zeae. On average, the pathogen caused reductions of 50, 28 and 33% in relative grain weight/spike, thousand kernel weight, and number of grains/spike, respectively.


Fusarium stub dieback causes three kinds of losses: reduction in number of flowers, delay in cropping and reduction in grade of flowers. In severe epidemics in commercial greenhouses, the incidence of infection may be greater than 50%. Assuming 10% infection rate in all stubs, Stack (1979) calculated that losses from stub dieback for a 2-year carnation crop would be 1-2% of all flowers.
Related treatment support
Plantwise Factsheets for Farmers
Chen, G.; CABI, 2013, Chinese language
Pest Management Decision Guides
CABI; CABI, 2017, English language
CABI; CABI, 2016, Chinese language
CABI; CABI, 2016, Spanish language
CABI; CABI, 2016, Portuguese language
External factsheets
Bayer CropScience Crop Compendium, Bayer CropScience, English language
Virginia Cooperative Extension - Plant Diseases, Virginia Polytechnic Institute and State University, 2011, English language
CIMMYT Plant Pest and Disease Factsheets, Centro Internacional de Mejoramiento de Maiz y Trigo (CIMMYT) (International Maize and Wheat Improvement Center), English language
PANNAR Seed Factsheets, Pannar Seed (Pty) Ltd, 2009, English language
PANNAR Seed Factsheets, PANNAR Seed (Pty) Ltd, 2009, English language
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