A Chemical Examination of the Isenheim Altar: Role Played in History by Horned Rye (2)

  • ChemPubSoc Europe Logo
  • DOI: 10.1002/chemv.201200135
  • Author: Klaus Roth and Sabine Streller
  • Published Date: 04 December 2012
  • Source / Publisher: Chemie in unserer Zeit/Wiley-VCH
  • Copyright: Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim
thumbnail image: A Chemical Examination of the Isenheim Altar: Role Played in History by Horned Rye (2)

The Isenheim altar is counted among the most beautiful altarpieces in all of Western art (Fig. 1). Most especially moving is a cripple covered with boils and apparently beset with unspeakable pain. These are consequences of “St. Anthony’s Fire”, a condition that occurred in epidemic proportions, and led to the deaths of countless victims. It was a matter of centuries before “St. Anthony’s Fire” was finally recognized as the result of poisoning through the ergot fungus, thriving on the rye that served widely as a basis for bread. Here we examine the disastrous influence that alkaloids from ergot have had in human history.




What is an Ergot-infected Kernel of Grain?

For a long time, a kernel of grain (usually rye) infected with ergot was taken simply to be a kernel that had become altered somehow such that it grew much too large. This interpretation led to the designation “Secale cornutum” (“horned rye”), still common in the world of pharmacy. Carl von Linné (1707–1778) speculated that a type of thrips—Thrips physapus, a tiny sucking insect that commonly infested gladioli and dahlias—was perhaps also injurious to rye kernels, leading to the development of ergot.


At the beginning of the 19th century, Joseph Henry Léveillé recognized that ergot represented a malformation of the ovule, caused in turn by a fungal infestation. In 1852, the mycologist Louis René Tulasne clarified the developmental cycle of this fungus, with its various manifestations [9]; he also assigned it the name Claviceps purpurea. Claviceps translates literally into “key head”. The second part of the name, purpurea, is easier to explain, however: the outside of ergot is often violet in color, and its fruiting bodies frequently display a luminous pink hue.


All the members of the Claviceps genus live as parasites on grasses, and Claviceps purpurea in particular has been found on 400 different grass species, rye being the best known of the host plants.




Life-cycle of the Fungus, Starting with the Sclerotium

The “sclerotium” (in German, the “Mutterkorn”) is the persistent form of the fungus (Fig 5). Some of the sclerotia produced in rye fall to the ground even before harvest time, and survive the subsequent winter there. Only after this long period of dormancy at low temperature [10] is the fungus capable of developing further. Spring, when the grasses bloom, is when the pink fruiting bodies, as many as 20 in number, sprout from an old sclerotium.

The development of Claviceps purpurea

Figure 5. The development of Claviceps purpurea.


In order to ensure sprouting in this subsequent springtime, a sclerotium requires a 6–8 week period of temperatures of 2–4 °C (36–39 °F) during the winter. Spores (ascospores [11]) develop in the heads of these fruiting bodies, within an ascus. “Ascus” (lat. tube) is responsible for the name assigned to the entire ascomycota (sac fungi) subdivision of the eumycota, which includes the more familiar truffles and morels. When the spores are ripe, they are catapulted a distance up to 10 cm out of the sclerotia, and then typically distributed by the wind.


If a spore encounters one of the 60–80 blossoms on a rye stalk, it sends out a germ tube, and this becomes ingrown into the rye fruiting body (primary infection).


Infection by sclerotia is possible only with an unpollinated blossom. The infested fruiting body soon becomes completely ingrown with fungus, and results in a dirty white, soft mass: the mycelium. Initially, out of this fungal mycelium, spores known as conidia are pinched off. Simultaneously with conidia formation, the infested fruiting body gives off a sweet, sticky, murky-brown liquid known as the “honeydew”.


Sugar-containing excretions from cereal blossoms infested with ergot are also referred to as “vegetational honeydew”. Animal honeydew is better known. This also consists of sugar-containing excretions, generally from insects, e.g., aphids or scale insects.


Honeydew, with the conidia, wells up out of the blossoms, and is captured by insects, who then transport the conidia to other blooming grasses that have not yet been infested (secondary infection). Just like ascospores, the newly-arrived conidia attack pistils, and spread sclerotia formation further through the developing crop. The phase of honeydew and conidia formation lasts only about 9–13 days.


The fungal structures next develop further in the fruiting bodies, become consolidated, and produce in place of a kernel of grain a new sclerotium. The cycle is thus closed. If during flowering of the rye there happens to be a period of moist, cool weather, conidia access is facilitated, since pollination is limited, and the blossoms also stay open for days. Precisely such weather conditions encourage secondary infections, and lead to an especially high, and for us dangerous, level of infestation.


In the case of wheat, the situation is very different. In contrast to rye, a wheat bloom can accomplish self-pollination. The blossoms, moreover, are open for only a few minutes, and in moist weather they remain entirely closed, so that infection by sclerotia fungus is impossible [7].


Thanks to knowledge available to us today regarding the lifecycle of this fungus, as well as of the climatic and agricultural prerequisites for a massive attack on a rye crop, we are able in retrospect to interpret many otherwise incomprehensible and appalling patterns of village behavior in the 17th and 18th centuries: responses to a mass poisoning with sclerotium. The truly devilish effects of sclerotium poisoning might be illustrated by the outbreak of witch trials in Salem Village, Massachusetts, USA, in 1692.




The Witches of Salem

Witch trials were rare in the colonies that were later to become the United States, and most of the few that were held were adjudicated to the benefit of the accused, with but one exception: the aforementioned witch trials of Salem Village in the year 1692. Here, 140 people were suspected and then formally charged with witchcraft. Some died during their imprisonment, but 10 women and 8 men over the course of a few weeks were ultimately hanged. These events were seen by many even then as scandalous and disgraceful, and they have since been carefully considered not only from historical, sociological and psychological, but also a scientific-medical perspective.


The tragedy commenced after the cold winter of 1691/92 in Salem Village, a small town near Boston. Elisabeth (Betty), the nine-year old daughter of the village pastor Samuel Parris, began suddenly in February to show peculiar symptoms. She frequently threw herself down, slid under furniture, and suffered from painful cramps. Betty’s eleven-year old cousin Abigail Williams and six additional young girls displayed similar symptoms. They all complained of sharp pains, as though they were being bitten or pecked.


Doctors that were summoned were baffled, unable to find any explanation for the peculiar behavior. In an age when, for everyone, the devil was a real and present being, one who might well intervene in the daily life of any individual, bewitchment of the girls was an obvious potential explanation.


The girls labeled as “bewitched” sought, in response, guilty parties elsewhere, and claimed that other villagers had bewitched them. The accused were the slave Tituba, who worked in the pastor’s household, a beggar-woman named Sarah Good, and Sarah Osborn, a peculiar old woman of the community. All three were arrested.


During the ensuing inquiry, conducted on 1 March 1692, the girls described how spirits of the three women had attacked them. If one of the accused were simply to come in the vicinity of a witness, this girl fainted, or displayed cramp-like spasms, in those days considered clear proof that the accused was a witch. With assurance she need not fear confession that would result in a death sentence, Tituba admitted to being a witch, and described in detail how she, together with her two codefendants, had flown around on broomsticks. The charges against the girls subsequently escalated, in that they were allegedly beset by the spirits of other men and women. Thus, the eleven-year old Ann Putnam testified about how she had harassed the spirit of the four-year old Dorcas Good, daughter of Sarah Good, already accused of being a witch [12]. Thereupon, the four-year old was imprisoned for eight months, and forced to watch her mother being led away to the gallows.


As a result of further allegations against the girls and other townspeople, nearby jails were soon filled with “witches”, both male and female. The actual trials began on 2 June, and only a week later Bridget Bishop was the first to be hanged. By 22 September 1692, 17 more death penalties had been carried out. One of the accused, the 80-year-old farmer Giles Corey, continued to deny all the charges even after a five-month imprisonment in chains, and he refused to cooperate with the court, so that a trial could not formally be conducted. This unseemly behavior was punished as well: on the morning of 19 September a wooden board was laid across the naked man’s breast, and on this board were loaded more and more large stones. The neighbors stood aghast as the 80-year old man slowly came nearer and nearer to death, finally dying around noon. Three days later his wife Martha was hanged, one of the last sacrifices of the witch trials. All those sentenced to death protested their innocence to the very end.


The brutal death of the 80-year old Giles Corey and the hanging of the universally respected former pastor of Salem, George Burroughs, created such great waves that the newly appointed governor, Sir William Phips, immediately prohibited the conducting of any more witch trials. All pending cases were closed, with no more death penalties—most indeed with acquittals—and all still imprisoned “witches” were pardoned in May 1693.

Ann Putnam was one of the few who later confessed to her own guilt. She was spokeswoman for the girls, and was 11-years old at the time of the trial; at the age of 25 she filed a confession of sorts regarding her denunciation of a total of 62 (!) people [12].


An abbreviated account of the events, as presented here, might well tempt one to shrug off the whole witch hunt as due simply to the fantasies of some pubescent girls, with a resultant mass hysteria. Such a conclusion would be premature, however, because during the witch trials there were also many deaths of adolescents, children, and infants in Salem involving no suspicions of witchcraft. Thus John Putnam, for example, described the death of his eight-week old baby boy:

“I developed this peculiar sort of attacks: but through the grace of God I got over them. Shortly thereafter our poor little baby began to have strange and serious seizures, which continued for two days and two nights. He died a terrible and agonizing death that was enough to melt a heart of stone. By our estimate he spent almost five hours dying.”


These are the typical symptoms of ergot poisoning, and the American psychologist Linda Caporael in 1976 expressed for the first time the conjecture that that is what the girls were actually suffering from; besides the recorded seizure-like cramps, she proposed they were also experiencing neurological disturbances, such as visual disorders and hallucinations, which might perhaps have led to their false accusations [13]. The entire mass hysteria can of course not be attributed solely to the neurological disturbances of a few youths, but the following scientifically grounded puzzle pieces might make a massive ergot-derived poisoning of parts of the population of Salem in fact very probable [14, 15]:

  • The settlers in Massachusetts originally raised wheat. Starting in 1650, however, they experienced major crop losses due to wheat rust, so that starting in 1665 there was increased planting of rye.
  • Tree ring records from the region show that until 1687 the climate was quite mild, and rye harvests were probably good, with little incursion of ergot.


An infestation of ergot that would amount to a threat to humans occurs only when three factors coincide:

  1. A cold winter causes ergot lying on the ground to sprout extensively in the following spring.
  2. A subsequent rainy early summer leads to a low pollen count, with a resulting extended blooming period.
  3. A cold summer with mean temperatures of 17.5–19.0 °C (67–70 °F) leads to maximum alkaloid biosynthesis in ergot.






Table 2.
Radial growth data for trees in New Hampshire, USA, between 1690 and 1729.Radial growth data for trees in New Hampshire, USA, between 1690 and 1729.


Seasonal variation in the width of the growth rings for trees in New Hampshire, just north of Massachusetts, [16] between 1660 and 1729 shows that, for the ten years starting with 1688 (except for 1689), below-average temperatures must have prevailed (Tab. 2).

  • Three concurring eyewitness testimonies argue for the involvement of ergot, because Pastor Parris is said to have administered red communion wafers during a service [17]. A red coloration becomes apparent in rye flour at an ergot content greater than 3 %.
  • A number of cows were said to have displayed unusual cramp-like symptoms, and then to have died.
  • The typical symptoms affected mainly younger townspeople. This also suggests ergot poisoning, since growing young people naturally consume more bread per kg body weight than adults, and babies would ingest the toxic alkaloids through mother’s milk.
  • The distribution of the 22 households experiencing symptoms in Salem Village shows that the fields for all these households would have been perfect for cultivation of rye: moist, acidic, and sandy soil. Moreover, 16 of the fields were located near streams or swamps, and 15 were shaded by adjacent hills, and thus remained always moist, making them ideal for ergot infestation.





Baking Experiments with Ergot

In historical sources one finds over and over again accounts of bread contaminated with ergot. During the baking process there is said to arise a peculiar odor reminiscent of a salt solution in which herring have been pickled, and some of the bread is reported to have turned out blood red. On the other hand, cases are described in which bread containing ergot was enthusiastically eaten because it was said to have tasted especially good: “a great epidemic broke out in 1908 within the Rumanian population in Komitat Bihar, and it could not be curbed despite warnings and explanations from the authorities, because the people ate ergot-containing bread especially gladly since it tasted so good” [6].


In an attempt at clarification, the present authors carried out their own baking trials, followed by a tasting.

In two baking tests, first using 100 g of the Aurora baking mix “Saftiges Kornbrot” (“luscious three-grain bread”) (Fig. 6, upper left) and then 90 g of baking mix together with 10 g of ergot, ground in a hand mill (Fig. 6, upper right), each batch was worked into a dough. Both dough preparations were then formed into bread rolls and baked for 40 minutes.


Baking experiments with ergot

Figure 6. Baking experiments with ergot.


The smells from the two bread rolls during baking were essentially identical, although in the one containing ergot a weak scent reminiscent of hay was discernible.


A difference in color was obvious, but no blood-red coloration was observed. Both the ergot-containing dough and the corresponding baked rolls proved a bit darker than their counterparts.


A comparative taste test showed clear differences. Rolls containing ergot had a tangier flavor—two of the study participants described it as “sourer”—relative to the “normal” rolls.


The bottom line: In our tests, no unpleasant optical or other sensory effect could be discerned in the finished baked rolls by any of our subjects.
The next part looks at the isolation and structural determination of the potent ergot alkaloids, chemical knowledge that guarantees we can enjoy our daily bread without harm



References

[9] E. Mühle, K. Breuel, Das Mutterkorn, A. Ziemsen Verlag, Lutherstadt Wittenberg, Germany, 1977.
[10] H. Mielke, Mitteil. Biol. Bundesanstalt 2000, 375, www.bba.de/veroeff/mitt/pdfs/mitt375.pdf.
[11] H. Dörfelt, E. Ruske, Die Welt der Pilze, Weissdorn-Verlag, Jena, Germany, 2008.
[12] http://etext.virginia.edu/salem/witchcraft/texts/transcripts.html; www.gutenberg.org/files/17845/17845-h/salem2-htm.html; www.law.umkc.edu/faculty/projects/ftrials/salem/salem.htm; www.law.umkc.edu/faculty/projects/ftrials/salem/ASA_GOOD.HTM
[13] L.R. Carporael, Science 1976, 192, 21.
[14] M.K. Matossian, Am. Sci. 1982, July/August, 355.
[15] M. K. Matossian, Poisons of the Past, Yale University Press, New Haven, USA, 1989.
[16] Tree-Ring chronologies of eastern North America (Eds. E. DeWitt and M. Ames), Laboratory of Tree-Ring Research, Tucson, USA, 1978.
[17] Salem witchcraft papers (Eds. P. Boyer and S. Nissenbaum), Da Capo Press, New York, USA, 1977, 2, 410, 423 and 524; http://etext.virginia.edu/salem/witchcraft/texts/transcripts.html


Prof. Klaus Roth

Freie Universität Berlin, Germany.

Dr. Sabine Streller
Freie Universität Berlin, Germany.


The article has been published in German in:

and was translated by W. E. Russey.



A Chemical Examination of the Isenheim Altar: Role Played in History by "Horned Rye" Part 1

Takes a scientific look at the Isenheim Altar, which depicts the symptoms and treatment of “St. Anthony’s Fire”, the result of poisoning by ergot alkaloids

A Chemical Examination of the Isenheim Altar: Role Played in History by "Horned Rye" Part 3

Looks at the isolation and structural determination of the potent ergot alkaloids, chemical knowledge that guarantees we can enjoy our daily bread without harm



Other articles by Klaus Roth published by ChemViews magazine:

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