Desarrollo del Objetivo 3

caused a loss of adequate blood supply to the limbs. This ultimately resulted in gangrene. The highly disfigured extremities became blackened, as if they had been charred by ‘holy fire’. At times the illness reached plague proportions, and in the eleventh century the order of St Anthony was established to care for the tragically crippled survivors.

There was also a convulsive form of the disease (ergotismus convulsivus) characterised by excruciating pain that resulted from dramatic changes in nervous system function. The severely afflicted were described as suffering terribly, with profuse sweating, violent retching and ‘shrieking in agony’. Medical historians noted that seizures were not characteristic of the disease in areas where the diet contained large amounts of milk and butter.

The proposal was put forward that diets deficient in vitamin A predisposed toward the convulsive form of the disease, although this was never confirmed (Lee 2009a; Burn 1962).

Despite a distressing familiarity with its devastating consequences it took centuries before the cause was properly identified, when practical steps could be taken to find a permanent solution.

In the early 1700s the link between rye and a fungal infection was suggested, but for the next century outbreaks surfaced periodically. In January 1723, a letter from Jacques de Campredon, the French Ambassador to Russia, gave disturbing and horrifying insights into an epidemic that was sweeping through a region of Russia at that time:

Already 20,000 persons have died in the neighbourhood of Nijny. At first they thought it was the plague, but the doctors who were sent there, after having made a careful examination, reported that it was not an infectious disease, but that it arose from bad grain which the people had eaten. The grain is reddish and looks very like tares [a type of weed or plant commonly called vetch], spoilt as far as one can judge by the venomous fogs. As soon as people have eaten this bread they become stupefied, with great contractions of the nerves, so that those who do not die on the same day lose their hands and their feet. These fall off in the same way as they do in this country when hands and feet are frozen.

None of the remedies which are used in infectious

diseases do any good to those affected, and only those escape who have had good food and have eaten other bread’ (Burn 1962).

It was not until 1853 that Louis René Tulasne was able to describe the life cycle of the fungus. Soon afterwards (1856) another French botanist, one Monsieur Durien, was able to infect rye flowers with Claviceps spores and the mystery of grain contamination was unravelled. Importantly, it was established that two climatic conditions were essential for this to occur: a wet season allowing germination of the fungal sclerotia, followed by a dry, windy spell that permitted dissemination of the spores to the rye flowers (Lee 2009a).

Ergot was regarded with great dread, and justifiably so. Many doctors would not countenance the use of such a dangerous remedy – despite the fact that midwives continued to employ it. One would assume that such a potent drug would have been deployed very carefully. Incorrect administration could easily result in still births and maternal death. There can be no doubt that its unwise use by the inexperienced would have resulted in disability and tragedy. The admonitions of the herbalist Maude Grieve (1931) have a brevity that belie the many errors which preceded the limitations ultimately placed on Ergot’s use in conventional medicine: ‘Its long-continued use is dangerous, resulting sometimes in gangrene, and it should only be used in the hands of fully qualified practitioners’. She also warned that in bleeding disorders ‘its use should be restricted to cases of uterine haemorrhage, as it has been found to raise blood pressure in pulmonary and cerebral haemorrhage’.

Until 1808 orthodox medicine took little notice of the properties of the fungus. Indeed, it is quite possible that Ergot-based drugs would never have been developed had its value not been re-discovered in America – albeit its incautious use by untutored medical personnel was to be fraught with tales of disaster and death. A letter to the Medical Repository of New York by John Stearns in 1808 entitled ‘An Account of the Pulvis Parturiens, a Remedy for Quickening Childbirth’²², was to trigger a whole new era in its use. Stearns had learned of the use of Ergot

from an old woman who had migrated from Germany.

She had been using it for several years, with a great deal of success, to facilitate cases of prolonged labour. These details sparked a great interest within the profession.

During the 1800s it became readily available on an international scale. The first pharmacopoeia to officially list the drug was that of the United States in 1820 which, fortunately, recommended a standard alkaloid content.²³ Ergot entered into the London Pharmacopoeia in 1836. The preparations used elsewhere were not as reliable, leading to significant differences in its efficacy.

These discrepancies would not be resolved until the discovery of ergometrine, with the chemistry of Ergot being resolved in substantial detail in the mid to late 1900s (Lee 2009).

Stearns’ advice was tragically ignored by many once it came into popular use – despite repeated warnings regarding the consequences of excessive prescribing and an emphasis on the use of restricted doses. By 1822 the physician David Hosack was to comment that Pulvis ad Mortem, ‘death powder’, would be a more appropriate name than Pulvis ad Partum, due to the high rate of infant deaths associated with inappropriate use. Its deliberate use as an abortifacient could be equally catastrophic (Lee 2009a; Burn 1962).

A condition known as ‘ergotism’ could also result.

This was a form of chronic poisoning characterised by the same symptoms as the plagues familiar in Europe – nervous system malfunction, muscular spasms, cramping, and blood supply deficits resulting in gangrene. A particularly ill-fated discovery was its sedative effects on the central nervous system. This increased the chances of even more widespread medical disasters because it led to Ergot’s indiscriminate use in numerous ‘nervous’

conditions in women: anxiety, hysteria, amenorrhoea (lack of menses) and other menstrual disorders. It was also inappropriately used for treating asthma, as an antihidrotic (to reduce night sweats), and a lactagogue (to promote milk secretion in lactating women). Fortunately, after the disastrous side-effects of the remedy once again manifested, medical practice eventually heeded Stearns’

recommendations. It was restricted to the treatment of post-partum haemorrhage – although one can only

wonder at the degree of suffering that its incautious use had already inflicted.

Ergota from British Pharmacopoeia 1914.

Ergota from British Pharmacopoeia 1867 (note the expanded detail regarding its clinical use in the earlier entry).

22 The old name for Ergot used by midwives was Pulvis ad Partum, i.e.

powder of birth.

23 The amount of active constituents in the sclerotia can vary considerably:

0.01–1.0% making the dosage extremely difficult to evaluate (Haarmann 2009).