Ergot

Ergot (pron. /ˈɜːrɡət/ UR-gət) or ergot fungi refers to a group of

fungi of the genus Claviceps.[1] Ergot

The most prominent member of this group is Claviceps purpurea

("rye ergot fungus"). This fungus grows on rye and related plants,
and produces alkaloids that can cause ergotism in humans and
other mammals who consume grains contaminated with its fruiting
structure (called ergot sclerotium).[2][3]

Claviceps includes about 50 known species, mostly in the tropical

regions. Economically significant species include C. purpurea
(parasitic on grasses and cereals), C. fusiformis (on pearl millet,
buffel grass), C. paspali (on dallis grass), C. africana[4] (on
sorghum), and C. lutea (on paspalum).[5] C. purpurea most
commonly affects outcrossing species such as rye (its most
common host), as well as triticale, wheat, and barley. It affects
oats only rarely.

C. purpurea has at least three races or varieties, which differ in Claviceps purpurea
their host specificity:[6] Scientific classification
G1 — land grasses of open meadows and fields; Kingdom: Fungi
G2 — grasses from moist, forest, and mountain habitats; Division: Ascomycota
G3 (C. purpurea var. spartinae) — salt marsh grasses
(Spartina, Distichlis). Class: Sordariomycetes
Order: Hypocreales
Contents Family: Clavicipitaceae

Life cycle Genus: Claviceps

Tul., 1853
Evolution
Effects on humans and other mammals Species
History
Saint Anthony's fire and the Antonites About 50, including:
Claviceps africana
Usage in gynaecology and obstetrics
Claviceps fusiformis
Speculated cause of hysterics and hallucinations Claviceps paspali
Claviceps purpurea Claviceps purpurea
Claviceps sorghi
Claviceps africana
Claviceps zizaniae
Claviceps paspali Claviceps lutea
See also
References
External links
Life cycle
An ergot kernel, called a sclerotium, develops when a spore of fungal species of the genus Claviceps infects
a floret of flowering grass or cereal. The infection process mimics a pollen grain growing into an ovary
during fertilization. Infection requires that the fungal spore have access to the stigma; consequently, plants
infected by Claviceps are mainly outcrossing species with open flowers, such as rye (Secale cereale) and
ryegrasses (genus Lolium). The proliferating fungal mycelium then destroys the plant ovary and connects
with the vascular bundle originally intended for seed nutrition. The first stage of ergot infection manifests
itself as a white soft tissue (known as sphacelia) producing sugary honeydew, which often drops out of the
infected grass florets. This honeydew contains millions of asexual spores (conidia), which insects disperse to
other florets. Later, the sphacelia convert into a hard dry sclerotium inside the husk of the floret. At this
stage, alkaloids and lipids accumulate in the sclerotium.

Claviceps species from tropic and subtropic regions produce macro- and microconidia in their honeydew.
Macroconidia differ in shape and size between the species, whereas microconidia are rather uniform, oval to
globose (5x3μm). Macroconidia are able to produce secondary conidia. A germ tube emerges from a
macroconidium through the surface of a honeydew drop and a secondary conidium of an oval to pearlike
shape is formed, to which the contents of the original macroconidium migrates. Secondary conidia form a
white, frost-like surface on honeydew drops and spread via the wind. No such process occurs in Claviceps
purpurea, Claviceps grohii, Claviceps nigricans, and Claviceps zizaniae, all from northern temperate
regions.

When a mature sclerotium drops to the ground, the fungus remains dormant until proper conditions (such as
the onset of spring or a rain period) trigger its fruiting phase. It germinates, forming one or several fruiting
bodies with heads and stipes, variously coloured (resembling a tiny mushroom). In the head, threadlike
sexual spores form, which are ejected simultaneously when suitable grass hosts are flowering. Ergot
infection causes a reduction in the yield and quality of grain and hay, and if livestock eat infected grain or
hay it may cause a disease called ergotism.

Black and protruding sclerotia of C. purpurea are well known. However, many tropical ergots have brown
or greyish sclerotia, mimicking the shape of the host seed. For this reason, the infection is often overlooked.

Insects, including flies and moths, carry conidia of Claviceps species, but it is unknown whether insects play
a role in spreading the fungus from infected to healthy plants.[7]

Evolution
The evolution of plant parasitism in the Clavicipitaceae dates back at least 100 million years, to the early-
mid Cretaceous. An amber fossil discovered in 2014 preserves a grass spikelet and an ergot-like parasitic
fungus. The fossil shows that the original hosts of the Clavicipitaceae could have been grasses. The
discovery also establishes a minimum time for the conceivable presence of psychotropic compounds in
fungi.[8][9] Several evolutionary processes have acted to diversify the array of ergot alkaloids produced by
fungi; these differences in enzyme activities are evident at the levels of substrate specificity (LpsA), product
specification (EasA, CloA) or both (EasG and possibly CloA).[10] The “old yellow enzyme,” EasA, presents
an outstanding example. This enzyme catalyzes reduction of the C8=C9 double-bond in chanoclavine I, but
EasA isoforms differ in whether they subsequently catalyze reoxidation of C8–C9 after rotation.[10] This
difference distinguishes most Clavicipitaceae from Trichocomaceae, but in Clavicipitaceae it is also the key
difference dividing the branch of classical ergot alkaloids from dihydroergot alkaloids, the latter often being
preferred for pharmaceuticals due to their relatively few side effects.[10]

Effects on humans and other mammals

The ergot sclerotium contains high concentrations (up to 2% of dry
mass) of the alkaloid ergotamine, a complex molecule consisting of
a tripeptide-derived cyclol-lactam ring connected via amide linkage
to a lysergic acid (ergoline) moiety, and other alkaloids of the
ergoline group that are biosynthesized by the fungus.[11] Ergot
alkaloids have a wide range of biological activities including effects
on circulation and neurotransmission.[12]

Ergot alkaloids are classified as:

1. derivatives of 6,8-dimethylergoline and

2. lysergic acid derivatives.[13]

Ergotism is the name for sometimes severe pathological syndromes

affecting humans or other animals that have ingested plant material
containing ergot alkaloid, such as ergot-contaminated grains. The
Hospital Brothers of St. Anthony, an order of monks established in
1095, specialized in treating ergotism victims[14] with balms
containing tranquilizing and circulation-stimulating plant extracts.
The common name for ergotism is "St. Anthony's Fire",[14] in
reference to this order of monks and the severe burning sensations in
the limbs which was one of the symptoms.[15] There are two types of Ergot-derived drug to stop
postpartum bleeding
ergotism, the first is characterized by muscle spasms, fever and
hallucinations and the victims may appear dazed, be unable to speak,
become manic, or have other forms of paralysis or tremors, and
suffer from hallucinations and other distorted perceptions.[16] This is caused by serotonergic stimulation of
the central nervous system by some of the alkaloids.[16] The second type of ergotism is marked by violent
burning, absent peripheral pulses and shooting pain of the poorly vascularized distal organs, such as the
fingers and toes,[16] and are caused by effects of ergot alkaloids on the vascular system due to
vasoconstriction, sometimes leading to gangrene and loss of limbs due to severely restricted blood
circulation.

The neurotropic activities of the ergot alkaloids may also cause hallucinations and attendant irrational
behaviour, convulsions, and even death.[11][12] Other symptoms include strong uterine contractions, nausea,
seizures, high fever, vomiting, loss of muscle strength and unconsciousness. Since the Middle Ages,
controlled doses of ergot were used to induce abortions and to stop maternal bleeding after childbirth.[17]
Klotz offers a detailed overview of the toxicities in mammalian livestock, stating that the activities are
attributable to antagonism or agonism of neurotransmitters, including dopamine, serotonin and
norepinephrine. As well, he shares that the adrenergic blockage by ergopeptines (e.g., ergovaline or
ergotamine) leads to potent and long-term vasoconstriction, and can result in reduced blood flow resulting in
intense burning pain (St. Anthony’s fire), edema, cyanosis, dry gangrene and even loss of hooves in cattle or
limbs in humans. Reduced prolactin due to ergot alkaloid activity on dopamine receptors in the pituitary is
also common in livestock. Reduced serum prolactin is associated with various reproductive problems in
cattle, and especially in horses, including agalactia and poor conception, and late-term losses of foals and
sometimes mares due to dystocia and thickened placentas.[10] Although both gangrenous and convulsive
symptoms are seen in naturally occurring ergotism resulting from the ingestion of fungus infected rye, only
gangrenous ergotism has been reported following the excessive ingestion of ergotamine tartrate.[18] Ergot
extract has been used in pharmaceutical preparations, including ergot alkaloids in products such as Cafergot
(containing caffeine and ergotamine[17] or ergoline) to treat migraine headaches, and ergometrine, used to
induce uterine contractions and to control bleeding after childbirth.[19] Clinical ergotism as seen today
results almost exclusively from the excessive intake of ergotamine tartrate in the treatment of migraine
headache.[18]

In addition to ergot alkaloids, Claviceps paspali also produces tremorgens (paspalitrem) causing "paspalum
staggers" in cattle.[20] The fungi of the genera Penicillium and Aspergillus also produce ergot alkaloids,
notably some isolates of the human pathogen Aspergillus fumigatus,[21] and have been isolated from plants
in the family Convolvulaceae, of which morning glory is best known. The causative agents of most ergot
poisonings are the ergot alkaloid class of fungal metabolites, though some ergot fungi produce distantly
related indole-diterpene alkaloids that are tremorgenic.[10]

Ergot does not contain lysergic acid diethylamide (LSD) but instead contains lysergic acid as well as its
precursor,[22] ergotamine. Lysergic acid is a precursor for the synthesis of LSD. Their realized and
hypothesized medicinal uses have encouraged intensive research since the 1950s culminating on the one
hand in development of drugs both legal (e.g., bromocriptine) and illegal (e.g., lysergic acid diethylamide=
LSD), and on the other hand in extensive knowledge of the enzymes, genetics, and diversity of ergot
alkaloid biosynthetic pathways.[10]

The January 4, 2007 issue of the New England Journal of Medicine includes a paper that documents a
British study of more than 11,000 Parkinson's disease patients. The study found that two ergot-derived
drugs, pergolide and cabergoline, commonly used to treat Parkinson's Disease may increase the risk of leaky
heart valves by up to 700%.[23]

History
Ergotism is the earliest recorded example of mycotoxicosis, or
poisoning caused by toxic molds.[24] Early references to ergot
poisoning (ergotism) date back as far as 600 BC, an Assyrian tablet
referred to it as a 'noxious pustule in the ear of grain'.[25] In 350 BC,
the Parsees described 'noxious grasses that cause pregnant women to
drop the womb and die in childbed'.[25] In ancient Syria, ergot was
called 'Daughter of Blood'.[26] Radulf Glaber described an ailment
he called 'hidden fire' or ignus ocultus, in which a burning of the
limb is followed by its separation from the body, often consuming
the victim in one night.[26] In 1588, Johannes Thallius wrote that it
is called 'Mother of Rye', or rockenmutter, and is used to halt
bleeding.[26]

Human poisoning due to the consumption of rye bread made from

ergot-infected grain was common in Europe in the Middle Ages. The
first mention of a plague of gangrenous ergotism in Europe comes
Ergot on wheat heads
from Germany in 857, following this France and Scandinavia
experienced similar outbreaks;[27] England is noticeably absent from
the historical regions affected by ergotism as their main source of food was wheat, which is resistant to ergot
fungi.[26] In 944, a massive outbreak of ergotism caused 40,000 deaths in the regions of Aquitaine,
Limousin, Perigord, and Angoumois in France.[24] In Hesse in 1596, Wendelin Thelius was one of the first
to attribute ergotism poisoning to grain.[27] In 1778, S. Tessier, observing a huge epidemic in Sologne,
France in which more than 8,000 people died, recommended drainage of fields, compulsory cleaning of
grain, and the substitution of potatoes for affected grain.[27]
Saint Anthony's fire and the Antonites

In 1722, the Russian Tzar Peter the Great was thwarted in his campaign against the Ottoman Empire as his
army, traveling down the Terek steppe, were struck by ergotism and were forced to retreat in order to find
edible grains. A diary entry from the time describes that as soon as people ate the poisoned bread they
became dizzy, with such strong nerve contractions that those who did not die from the first day found their
hands and feet falling off, akin to frostbite.[28] The epidemic was known as Saint Anthony's fire,[14] or ignis
sacer, and some historical events, such as the Great Fear in France during the French Revolution have been
linked to ergot poisoning.[29] Saint Anthony was a 3rd Century Egyptian ascetic who lived by the Red Sea
and was known for long fasting in which he confronted terrible visions and temptations sent from the
Devil.[27] He was credited by two noblemen for assisting them in recovery from the disease; they
subsequently founded the Order of St. Anthony in honor of him.[26] Anthony was a popular subject for art in
the Middle Ages and his symbol is a large blue "T" sewn onto the shoulder of the order's monks,
symbolizing the crutch used by the ill and injured.[30]

The Order of St. Anthony, who were also known as Antonites, grew quickly and hospitals spread through
France, Germany, and Scandinavia and gained wealth and power as grateful patrons bestowed money and
charitable goods to the hospitals.[26] By the end of the Middle Ages, there were 396 settlements and 372
hospitals owned by the order[30] and pilgrimages to such hospitals became popular as well as the donation of
limbs lost to ergotism, which were displayed near shrines to the saint.[26] These hagiotherapeutic centers
were the first specialized European medical welfare systems and the friars of the order were knowledgeable
about treatment of ergotism and the horrifying effects of the poison.[30] The sufferers would receive ergot-
free meals, wines containing vasodilating and analgesic herbs, and applications of Antonites-balsalm, which
was the first transdermal therapeutic system (TTS) in medical history.[25] Their medical recipes have been
lost to time, though some recorded treatments still remain.[30] After 1130 AD, the monks were no longer
permitted to perform operations, and so barber surgeons were employed to remove gangrenous limbs and
treat open sores.[30] Three barbers founded a hospital in Memmingen in 1214 and accepted those who were
afflicted with the gangrenous form of ergotism. Patients were fed and housed with the more able-bodied
individuals acting as orderlies and assistants. Patients with the convulsive form of ergotism, or ergotismus
convulsivus, were welcomed for only nine days before they were asked to leave as convulsive ergotism was
seen as less detrimental. Though the sufferers often experienced irreversible effects, they most often
returned to their families and resumed their livelihoods.[30]

An important aspect to the Order of St. Anthony's treatment practices was the exclusion of rye bread and
other ergot-containing edibles, which halted the progression of ergotism.[26] There was no known cure for
ergotism itself, however there was treatment of the symptoms, which often included blood constriction,
nervous disorder, and/or hallucinations; if the sufferer survived the initial poisoning, his limbs would often
fall off and he or she would continue to improve in health if they halted consumption of ergot.[27] The trunk
of the body remained relatively untouched by the disease until its final stages and the victims, not
understanding the cause of their ailment, would continue to imbibe ergot-laden food for weeks until the
condition reached their digestive system.[30] It is believed that the peasantry and children were most
susceptible to ergotism, though the wealthy were afflicted as well, as at times entire villages relied on tainted
crops for sustenance and during times of famine, ergotism reached into every house.[25] Ergot fungus is
impervious to heat and water, thus it was most often baked into bread through rye flour; though other
grasses can be infected, it was uncommon in Medieval Europe to consume grasses other than rye.[26] The
physiological effects of ergot depended upon the concentration and combinations of the ingested ergot
metabolites, as well as the age and nutritional status of the afflicted individual.[28] The Antonites began to
decline after physicians discovered the genesis of ergotism and recommended methods for removing the
sclerotium from the rye crops. In 1776, the cloisters of the Antonites were incorporated into the Maltese
Knights Hospitaller, losing much of their medical histories in the process and losing the ergotism cures and
recipes due to lack of use and lack of preservation.[30]
Usage in gynaecology and obstetrics

Midwives and very few doctors in Europe have used extracts from ergot for centuries:

1. In a Nürnberg manuscript of 1474 powdered ergot was prescribed together with Laurel-fruits
and rhizomes of Salomon’s seals to cure »permutter« or »heffmutter«, that means pain in the
lower abdomen caused by the »uprising of the womb«[31]
2. In a printed book of 1582 the German physician Adam Lonicer wrote, that three sclerotia of
ergot, used several times a day, were used by midwives as a good remedy in case of the
»uprising and pain of the womb« (»auffſteigen vnd wehethumb der mutter«)[32]
3. Joachim Camerarius the Younger wrote in 1586, that sclerotia of ergot held under the tongue,
would stop bleeding[33]

To prove, that ergot is a harmless sort of grain, in 1774 the French pharmacist Antoine-Augustin Parmentier
edited a letter, he had received from Madame Dupile, a midwife of Chaumont-en-Vexin. She had told him,
that if uterine contractions were too weak in the expulsion stage of childbirth she and her mother gave
peeled ergot in an amount of the filling of a thimble solved in water, wine or broth. The administration of
ergot was followed by a mild childbirth within 15 minutes.[34] The French physician Jean-Baptiste
Desgranges (1751–1831) published in 1818, that in 1777 he had met midwives in Lyon, who successfully
treated feeble uterine contractions by administering the powder of ergot. Desgranges joined this remedy into
his therapeutic arsenal. From 1777 to 1804 he was successful in alleviating childbirth for more than twenty
women by the administration of the powder of ergot. He never saw any side-effect of this treatment.[35]

In 1807 Dr. John Stearns of Saratoga County wrote to a friend, that he had used over several years a »pulvis
parturiens« with complete success in patients with »lingering parturitation«. This »pulvis
parturiens« consisted of ergot, that he called a »spurious groth of rye«. He boiled »half a drachm« (ca. 2g) of
that powder in half a pint of water and gave one third every twenty minutes, till the pains commenced.[36] In
1813 Dr. Oliver Prescott (1762–1827) of Newburyport published a dissertation "on the natural history and
medical effects of the secale cornutum,” in which he described and analysed the experience he had gathered
over five years while using ergot in cases of poor uterine action in the second stage of labour in
childbirth.[37]

The 1836 Dispensatory of the United States recommended »to a woman in labour fifteen or twenty grains
[ca. 1 to 1,3g] of ergot in powder to be repeated every twenty minutes, till its peculiar effects are
experienced, or till the amount of a drachm [ca. 3,9g] has been taken«.[38]

In 1837 the French Codex Pharmacopee Francaise required ergot to be kept in all pharmacies.[39]

Low to very low evidence from clinical trials suggests that prophylactic use of ergot alkaloids, administered
by intravenous (IV) or intramuscular (IM) in the third stage of labor, may reduce blood loss and may reduce
the risk of moderate to severe hemorrhage following delivery, however this medication may also be
associated with higher blood pressure and higher pain.[40] It is not clear of oral ergo alkaloids are beneficial
or harmful as they have not been well studied.[40] A 2018 Cochrane Systematic Review concluded that other
medications such as oxytocin, syntometrine and prostaglandins, may be preferred over ergot alkaloids.[40]

Though ergot was known to cause abortions in cattle and humans, it was not a recognized use for it as
abortion was illegal in most countries, thus evidence for its use in abortion is unknown.[24] Most often, ergot
was used to speed the process of parturition or delivery, and was not used for the purpose of halting
postpartum bleeding, which is a concern of childbirth.[27] However, until anesthesia became available, there
was no antidote or way of controlling the effects of ergot. So if the fetus did not move as expected, the drug
could cause the uterus to mold itself around the child, rupturing the uterus and killing the child. David
Hosack, an American physician, noted the large number of stillbirths resulting from ergot use and stated that
rather than pulvis ad partum, it should be called pulvis ad mortem.[27] He began advocating for its use to
halt postpartum bleeding. Eventually, doctors determined that the use of ergot in childbirth without an
antidote was too dangerous. They ultimately restricted its use to expelling the placenta or stopping
hemorrhage. Not only did it constrict the uterus, ergot had the ability to increase or decrease blood pressure,
induce hypothermia and emesis, and influence pituitary hormone secretions.[24] In 1926, Swiss psychiatrist
Hans Maier suggested to use ergotamine for the treatment of vascular headaches of the migraine type.[16]

In the 1930s, abortifacient drugs were marketed to women by various companies under various names such
as Molex pills and Cote pills. Since birth control devices and abortifacients were illegal to market and sell at
the time, they were offered to women who were "delayed". The recommended dosage was seven grains of
ergotin a day. According to the United States Federal Trade Commission (FTC)[41] these pills contained
ergotin, aloes, Black Hellebore, and other substances. The efficacy and safety of these pills are unknown.
The FTC deemed them unsafe and ineffective and demanded that they cease and desist selling the product.
Currently, over a thousand compounds have been derived from ergot ingredients.[16]

Speculated cause of hysterics and hallucinations

It has been posited that Kykeon, the beverage consumed by participants in the ancient Greek Eleusinian
Mysteries cult, might have been based on hallucinogens from ergotamine, a precursor to the potent
hallucinogen lysergic acid diethylamide (LSD), and ergonovine.[42][16]

British author John Grigsby contends that the presence of ergot in the stomachs of some of the so-called
'bog-bodies' (Iron Age human remains from peat bogs Northeast Europe, such as the Tollund Man) is
indicative of use of Claviceps purpurea in ritual drinks in a prehistoric fertility cult akin to the Greek
Eleusinian Mysteries. In his 2005 book Beowulf and Grendel, he argues that the Anglo-Saxon poem Beowulf
is based on a memory of the quelling of this fertility cult by followers of Odin. He writes that Beowulf,
which he translates as barley-wolf, suggests a connection to ergot which in German was known as the 'tooth
of the wolf'.[43]

Linnda R. Caporael posited in 1976 that the hysterical symptoms of young women that had spurred the
Salem witch trials had been the result of consuming ergot-tainted rye.[44] However, Nicholas P. Spanos and
Jack Gottlieb, after a review of the historical and medical evidence, later disputed her conclusions.[45] Other
authors have likewise cast doubt on ergotism as the cause of the Salem witch trials.[46]

Claviceps purpurea
Mankind has known about Claviceps purpurea for a long time, and its appearance has been linked to
extremely cold winters that were followed by rainy summers.

The sclerotial stage of C. purpurea conspicuous on the heads of ryes and other such grains is known as
ergot. Favorable temperatures for growth are in the range of 18–30 °C. Temperatures above 37 °C cause
rapid germination of conidia. Sunlight has a chromogenic effect on the mycelium, with intense coloration.
Cereal mashes and sprouted rye are suitable substrates for growth of the fungus in the laboratory.

Claviceps africana
Claviceps africana infects sorghum. In sorghum and pearl millet, ergot became a problem when growers
adopted hybrid technology, which increased host susceptibility.[16] It only infects unfertilized ovaries, so
self-pollination and fertilization can decrease the presence of the disease, but male-sterile lines are
extremely vulnerable to infection. Symptoms of infection by C. africana include the secretion of honeydew
(a fluid with high concentrates of sugar and conidia), which attracts insects like flies, beetles, and wasps that
feed on it. This helps spread the fungus to uninfected plants.

C. africana caused ergot disease that caused a famine in 1903-1906 in Northern Cameroon, West Africa, and
also occurs in eastern and southern Africa, especially Zimbabwe and South Africa. Male sterile sorghums
(also referred to as A-lines) are especially susceptible to infection, as first recognized in the 1960s, and
massive losses in seed yield have been noted. Infection is associated with cold night temperatures that are
below 12 °C occurring two to three weeks before flowering.

Sorghum ergot caused by Claviceps africana Frederickson, Mantle and De Milliano is widespread in all
sorghum growing areas, whereas the species was formerly restricted to Africa and Asia where it was first
recorded more than 90 years ago, it has been spreading rapidly and by the mid-1990s it reached Brazil,
South Africa, and Australia. By 1997, the disease had spread to most South American countries and the
Caribbean including Mexico, and by 1997 had reached Texas in the United States.[16]

Claviceps paspali
Claviceps paspali infects wild grasses and could be found on the common grass Paspalum. Like the C.
africana, C. paspali also secretes honeydew which is consumed by bees. The bees then create a honey called
fic'e (Paraguayan Makai Indian language), which is infused with secretions from the plants and has a
pungent aroma. If consumed in high amounts, the honey can cause drunkenness, dizziness and even death.
[47].

See also
Medicinal mushrooms
Universal Laboratories Building: a major producer of ergot

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External links
Claviceps purpurea - Ergot Alkaloid (http://www.entheology.org/edoto/anmviewer.asp?a=37&z
=5)
Ergot article from North Dakota State University, 2002 (http://www.ext.nodak.edu/extpubs/plant
sci/crops/pp551w.htm)
Panaccione DG, Coyle CM (June 2005). "Abundant respirable ergot alkaloids from the
common airborne fungus Aspergillus fumigatus" (https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C1151833). Applied and Environmental Microbiology. 71 (6): 3106–11.
doi:10.1128/AEM.71.6.3106-3111.2005 (https://doi.org/10.1128%2FAEM.71.6.3106-3111.200
 5). PMC 1151833 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1151833). PMID 15933008
(https://pubmed.ncbi.nlm.nih.gov/15933008).
PBS Secrets of the Dead: "The Witches Curse" (concerning the Salem trials and ergot) (http
s://www.pbs.org/wnet/secrets/witches-curse/1498/)
Parkinson's Drugs Can Damage Heart Valves (https://web.archive.org/web/20070106040511/h
ttp://www.healthday.com/Article.asp?AID=600564). HealthDay. January 3, 2007.
McCrea A (January 1931). "The Reactions of Claviceps purpurea to Variations of Environment"
(https://deepblue.lib.umich.edu/bitstream/2027.42/141053/1/ajb209571.pdf) (PDF). American
Journal of Botany. 18 (1): 50–78. doi:10.2307/2435724 (https://doi.org/10.2307%2F2435724).
hdl:2027.42/141053 (https://hdl.handle.net/2027.42%2F141053). JSTOR 2435724 (https://ww
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Bonns WW (July 1922). "A Preliminary Study of Claviceps purpurea in Culture". American
Journal of Botany. 9 (7): 339–353. doi:10.2307/2435269 (https://doi.org/10.2307%2F2435269).
JSTOR 2435269 (https://www.jstor.org/stable/2435269).
Woodcock EF (February 1925). "Observations on the Poisonous Plants of Michigan".
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Prom LK, Lopez JD (2004). "Viability of Claviceps africana Spores Ingested by Adult Corn
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Pažoutová S, Frederickson DE (December 2005). "Genetic diversity of Claviceps africana on
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3059.2005.01255.x (https://doi.org/10.1111%2Fj.1365-3059.2005.01255.x).
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