Chemistry and pharmacology · Last reviewed 2026-10-18
Claviceps purpurea, ergot of rye: life cycle, alkaloids and food safety limits
Claviceps purpurea is a fungus that infects the young flowers of rye and about 400 other grasses and replaces the grain with a dark, hard sclerotium, the ergot, which contains ergot alkaloids such as ergotamine and ergometrine. Because those alkaloids poison people and animals, the European Union caps ergot sclerotia in unprocessed cereal grains at 0.2 g per kg and sets maximum levels for ergot alkaloids in milling products under Regulation (EU) 2023/915. [1, 2]
Key takeaways
- C. purpurea infects only young grass ovaries, mimicking pollen-tube growth, and turns the grain into a sclerotium.
- Its cycle has two spore stages: windborne ascospores in spring, then conidia in sticky honeydew spread by insects and rain.
- Sclerotia overwinter, need weeks of cold, and germinate into tiny mushroom-like stromata as grasses flower.
- EFSA assessed 12 ergot alkaloids in 2012 and set a group tolerable daily intake; EU limits for rye tighten in 2025 and 2028.
- What looks like one species is several: rye ergot in the strict sense is now separated from cryptic relatives on wild grasses.
A parasite of grass flowers
Claviceps purpurea is a ubiquitous pathogen of cereals and grasses. It shows strict organ specificity, attacking only young grass ovaries, and appears to get in by mimicking pollen tubes: no resistance genes are known and no effective resistance reaction is seen in the early stages of infection. [3] Inside the plant it behaves as a true biotroph, living on its host without killing it, although it can easily be grown in culture. [3]
There are about 40 species of Claviceps. C. purpurea is found across most temperate regions and has a very broad host range of about 400 grass species, including the cereals and all the temperate forage grasses; its economically most important host is rye. Related species cause ergot in sorghum (C. africana) and pearl millet (C. fusiformis). [1]
Molecular work has split what was called C. purpurea into several species. C. purpurea in the strict sense is the typical rye ergot; C. humidiphila infects grasses of damp places, C. spartinae grasses of salt marshes, and C. arundinis reeds and moor grass. [4]
The life cycle: ascospores, honeydew, sclerotia
- Spring infection. Windborne ascospores land on the feathery stigmas of flowering grasses, germinate and infect the ovary within about 24 hours. Hyphae grow down to the base of the ovary. [1]
- Honeydew. In the infected ovary the fungus produces masses of asexual spores (conidia) in a sticky, syrup-like fluid called honeydew. Insects, especially flies and moths, are attracted to it and carry it to other flowers; rain splash, head-to-head contact and farm machinery also spread it. Cereals are mainly infected this way, from wild grasses growing in or near the field. [1]
- Sclerotium. Honeydew stops when the sclerotium starts to form. Sclerotia mature in four to five weeks and replace the seed. Each has whitish storage tissue inside a dark outer cortex that protects it from drying, ultraviolet light and other stresses. [1]
- Winter and spring. Some sclerotia are harvested with the grain; others fall to the ground. They need at least 25 days at 0 to 10 degrees C, then germinate in spring, just before grasses flower, into one or several small mushroom-shaped stromata whose sexual fruiting bodies release the next season's ascospores. [1]
That two-host-stage pattern explains the standard advice: wild and weedy grasses at field margins are the first source of inoculum in spring, so cutting or controlling them before they flower reduces infection. [1]
What is in an ergot
The sclerotia contain ergot alkaloids, which can cause severe intoxication in mammals. [3] The main ones are ergopeptines such as ergotamine, ergocristine, ergocryptine and ergocornine, plus the simple amide ergometrine; in sclerotia from some wild grasses, lactam relatives called ergopeptams are the predominant alkaloids. [5, 6] How the fungus assembles these molecules is described in ergot alkaloid biosynthesis and the families are compared in the classes of ergot alkaloids.
The same chemistry is also an industry. Ergot alkaloids for medicines are produced either by field cultivation of ergot-infected rye or by submerged industrial fermentation of the fungus; in 2010 world production was about 20,000 kg, roughly half from field cultivation. [7] They are the starting point for migraine, obstetric and dopamine-agonist drugs, described in ergot alkaloid pharmacology.
Food safety: the EFSA opinion
In 2012 the European Food Safety Authority's panel on contaminants assessed ergot alkaloids in food and feed using more than 20,000 analytical results. It based its assessment on the main C. purpurea alkaloids (ergometrine, ergotamine, ergosine, ergocristine, ergocryptine and ergocornine, and their -inine epimers), took the vasoconstrictive effect seen in a rat feeding study of ergotamine as its reference point, and set a group acute reference dose and a group tolerable daily intake for the sum of these alkaloids. [5]
The panel concluded that the available data did not indicate a concern for any population group, while noting that the exposure estimates covered a limited number of foods; for livestock on normal diets it judged the risk of toxicosis low. [5]
EU maximum levels in Regulation (EU) 2023/915
Regulation (EU) 2023/915, which replaced Regulation (EC) No 1881/2006, sets the limits, as amended by Regulation (EU) 2024/1808. Alkaloid limits apply to the lower-bound sum of the same six alkaloids and their -inine epimers. [2]
| Product | Limit | Notes |
|---|---|---|
| Ergot sclerotia, unprocessed cereal grains (except maize, rice and rye) | 0.2 g/kg | Applies to grain placed on the market for first-stage processing |
| Ergot sclerotia, unprocessed rye grains | 0.2 g/kg | From 1 July 2025; previously 0.5 g/kg |
| Ergot alkaloids, low-ash milling products of barley, spelt and oats | 50 µg/kg | From 1 July 2024; previously 100 µg/kg |
| Ergot alkaloids, low-ash wheat milling products | 100 µg/kg | Falls to 50 µg/kg from 1 July 2028 |
| Ergot alkaloids, rye milling products and rye for the final consumer | 500 µg/kg | Falls to 250 µg/kg from 1 July 2028 |
| Ergot alkaloids, wheat gluten | 400 µg/kg | |
| Ergot alkaloids, processed cereal-based food for infants and young children | 20 µg/kg |
Member States and interested parties must report occurrence data on ergot sclerotia and ergot alkaloids in rye and on ergot alkaloids in other cereal milling products to EFSA every year. [2] Grain cleaning matters: sorting sclerotia out of harvested grain with optical sorters works but is expensive and slow. [1]
The human history of ergot poisoning, from St Anthony's fire to modern outbreaks, is told in ergotism through history.
Questions and answers
What is ergot of rye?
Ergot is the sclerotium of the fungus Claviceps purpurea: a hard, dark body that replaces an infected grain in rye or another grass and contains ergot alkaloids such as ergotamine and ergometrine. It forms four to five weeks after the fungus infects the flower. [1, 3]
How does ergot spread in a field?
Primary infection comes from windborne ascospores released in spring by sclerotia that overwintered in the soil; the infected flowers then exude honeydew full of conidia, which insects (especially flies and moths), rain splash and machinery carry to other flowers. [1]
What is the EU limit for ergot in rye?
Under Regulation (EU) 2023/915 as amended, unprocessed rye grain may contain at most 0.2 g of ergot sclerotia per kg from 1 July 2025, and rye milling products at most 500 µg/kg of ergot alkaloids, falling to 250 µg/kg from 1 July 2028. [2]
References
- Miedaner T, Geiger HH (2015). Biology, genetics, and management of ergot (Claviceps spp.) in rye, sorghum, and pearl millet. Toxins 7(3):659-678. doi:10.3390/toxins7030659 PubMed 25723323
- Commission Regulation (EU) 2023/915 of 25 April 2023 on maximum levels for certain contaminants in food and repealing Regulation (EC) No 1881/2006, Annex I point 1.8 and Article 8, consolidated text of 1 July 2025 (including Regulation (EU) 2024/1808). EUR-Lex, checked 18 October 2026. Official text
- Tudzynski P, Scheffer J (2004). Claviceps purpurea: molecular aspects of a unique pathogenic lifestyle. Molecular Plant Pathology 5(5):377-388. doi:10.1111/j.1364-3703.2004.00237.x PubMed 20565614
- Pažoutová S, Pešicová K, Chudíčková M, Šrůtka P, Kolařík M (2015). Delimitation of cryptic species inside Claviceps purpurea. Fungal Biology 119(1):7-26. doi:10.1016/j.funbio.2014.10.003 PubMed 25601146
- EFSA Panel on Contaminants in the Food Chain (CONTAM) (2012). Scientific Opinion on Ergot alkaloids in food and feed. EFSA Journal 10(7):2798. doi:10.2903/j.efsa.2012.2798
- Uhlig S, Petersen D (2008). Lactam ergot alkaloids (ergopeptams) as predominant alkaloids in sclerotia of Claviceps purpurea from Norwegian wild grasses. Toxicon 52(1):175-185. doi:10.1016/j.toxicon.2008.05.002 PubMed 18639312
- Hulvová H, Galuszka P, Frébortová J, Frébort I (2013). Parasitic fungus Claviceps as a source for biotechnological production of ergot alkaloids. Biotechnology Advances 31(1):79-89. doi:10.1016/j.biotechadv.2012.01.005 PubMed 22261014