Jump to content
RemedySpot.com

Re: Re: Salem Witch Trials/Mold induced Psychosis

Rate this topic


Guest guest

Recommended Posts

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed & pubmedid=1593300\

8

Appl Environ Microbiol. 2005 June; 71(6): 3106‒3111.

doi: 10.1128/AEM.71.6.3106-3111.2005.

Copyright © 2005, American Society for Microbiology

Abundant Respirable Ergot Alkaloids from the Common Airborne Fungus

Aspergillus fumigatus

G. Panaccione* and M. Coyle

Division of Plant & Soil Sciences, Genetics & Developmental Biology Program,

West Virginia University, town, West Virginia 26506-6058

Corresponding author. Mailing address: Division of Plant & Soil Sciences,

401 Hall, West Virginia University, town, WV 26506-6058. Phone:

(304) 293-3911, ext. 2235. Fax: (304) 293-2872. E-mail: danpan@....

Received September 17, 2004; Accepted December 20, 2004.

Abstract:

Ergot alkaloids are mycotoxins that interact with several monoamine

receptors, negatively affecting cardiovascular, nervous, reproductive, and

immune systems of exposed humans and animals. Aspergillus fumigatus, a

common airborne fungus and opportunistic human pathogen, can produce ergot

alkaloids in broth culture. The objectives of this study were to determine

if A. fumigatus accumulates ergot alkaloids in a respirable form in or on

its conidia, to quantify ergot alkaloids associated with conidia produced on

several different substrates, and to measure relevant physical properties of

the conidia. We found at least four ergot alkaloids, fumigaclavine C,

festuclavine, fumigaclavine A, and fumigaclavine B (in order of abundance),

associated with conidia of A. fumigatus. Under environmentally relevant

conditions, the total mass of ergot alkaloids often constituted >1% of the

mass of the conidium. Ergot alkaloids were extracted from conidia produced

on all media tested, and the greatest quantities were observed when the

fungus was cultured on latex paint or cultured maize seedlings. The values

for physical properties of conidia likely to affect their respirability (i.e.,

diameter, mass, and specific gravity) were significantly lower for A.

fumigatus than for Aspergillus nidulans, Aspergillus niger, and Stachybotrys

chartarum. The demonstration of relatively high concentrations of ergot

alkaloids associated with conidia of A. fumigatus presents opportunities for

investigations of potential contributions of the toxins to adverse health

effects associated with the fungus and to aspects of the biology of the

fungus that contribute to its success.

The ergot alkaloids are a complex family of indole-derived alkaloids that

have a long history of association with human suffering. The contamination

of rye and other grain crops with alkaloid-rich sclerotia of the ergot

fungus Claviceps purpurea was responsible for gangrenous and convulsive

forms of ergotism known as St. 's fire or holy fire (19). Other ergot

alkaloid-producing fungi, such as the closely related Neotyphodium spp.

endophytes of forage grasses, negatively affect agriculture by reducing

animal productivity and health (2, 22). The ability of different ergot

alkaloids to act as partial agonists or antagonists of various serotonin,

dopamine, and α-adrenaline receptors results in effects on nervous,

circulatory, reproductive, and immune systems, leading to high or low blood

pressure, muscle contractions, reduced fertility, disturbances in sleep-wake

cycles, lowered immune responses, and, at high doses, hallucinations and

gangrene of the extremities (14, 16, 22, 25, 31).

Screening analyses of other fungi for ergot alkaloids have identified

several distantly related fungi as potential sources (13, 17, 29). Among

these fungi, the best characterized is Aspergillus fumigatus. This fungus

was first noted to produce the ergot alkaloid festuclavine and two novel

derivatives of festuclavine, fumigaclavine A and fumigaclavine B, in

semidefined broth culture (29). Later, Cole et al. (3) described an

additional festuclavine derivative, fumigaclavine C, from broth cultures of

A. fumigatus originally isolated from moldy silage.

A. fumigatus is associated with several human health issues. It is the most

common airborne fungal pathogen of humans (6, 18). It can cause invasive

aspergillosis in immunocompromised individuals, and the resulting mortality

rate is >50%. In immunocompetent individuals, this fungus can colonize

preexisting cavities in the lungs or sinuses without penetrating into

tissues, a condition known as aspergilloma or fungus ball (6, 11, 18). A.

fumigatus also is associated with air quality issues in indoor environments

and near composting facilities (11, 12, 27). The presence of conidia of A.

fumigatus and of several other fungi in such environments has been loosely

associated with respiratory allergic symptoms and miscellaneous other

ailments, but causal associations have not been demonstrated.

Most mycotoxin-producing fungi produce their toxins in the substrate in

which they grow, and ingestion of the contaminated substrate is required for

intoxication. Although less frequently documented, the presence of

mycotoxins in or on conidia of the producing fungus provides the potential

for delivery of mycotoxins via the alternate and less voluntary route of

inhalation. For example, the black mold fungus Stachybotrys chartarum

contains trichothecenes associated with its spores (28).

Our objectives in this study were to determine if conidia of A. fumigatus

contain ergot alkaloids in a respirable form, to quantify ergot alkaloids

associated with conidia produced on several environmentally relevant

substrates, and to measure physical properties of conidia likely to affect

their respirability. Detection and quantification of ergot alkaloids

associated with conidia are prerequisites for investigations of potential

contributions of the alkaloids to adverse human health effects or to other

aspects of the biology of the fungus.

Results:

Identification and quantification of ergot alkaloids associated with conidia

of A. fumigatus. Several compounds from simple 80% methanolic extracts of

conidia from PDA-cultured A. fumigatus produced large fluorescent peaks when

they were analyzed by HPLC with excitation and emission wavelengths of 272

nm and 372 nm, respectively (Fig. 1). Electrospray ionization-mass

spectrometry of the compound in peak C (Fig. 1), which had the greatest area

and was the most nonpolar of the alkaloids analyzed, revealed an ion at m/z

367 whose mass corresponded to the mass of [fumigaclavine C + H]+, which had

previously been described from broth cultures of A. fumigatus (3). Treatment

of this compound with 1 M NaOH resulted in a more polar compound (Fig. 1,

peak dC) that yielded an ion at m/z 325 whose mass corresponded to the mass

of [deacetylated fumigaclavine C + H]+.

Similarly, the compound represented by peak A (Fig. 1) yielded an ion at m/z

299 in its native form, which was consistent with the proposed identity as

fumigaclavine A, and it was converted after treatment with NaOH to a more

polar compound (Fig. 1, peak dA) with an ion at m/z 257, which was

consistent with [deacetylated fumigaclavine A + H]+. Peak B, which

cochromatographed with experimentally deacetylated fumigaclavine A (Fig. 1),

is proposed to be fumigaclavine B, which is identical to deacetylated

fumigaclavine A (3, 29). Small quantities of fumigaclavine B also were

detected in untreated extracts of A. fumigatus conidia (Fig. 1, peak B). The

compound in peak F (Fig. 1) yielded an ion at m/z 241 when electrospray

ionization-mass spectrometry was used and was not affected by NaOH

treatment. These characteristics are consistent with identification of this

compound as festuclavine, which was characterized previously from culture

extracts of A. fumigatus (29).

The absorbance spectra for these compounds (data not shown) and their

relative retention times on C18 silica were consistent with their proposed

identities. Analyses of the same conidial extracts with an excitation

wavelength of 310 nm and an emission wavelength of 410 nm did not result in

detection of any of the previously characterized lysergyl-derived ergot

alkaloids (data not shown). Conidia collected on the inner lid of a petri

dish and conidia aerosolized and collected on filters under a vacuum yielded

the same spectrum of ergot alkaloids.

To relate the quantities of ergot alkaloids to the spore mass and to

investigate the buoyancy of A. fumigatus conidia, physical properties of

conidia were measured (Table 1). The conidia of A. fumigatus were

significantly smaller, lighter, and less dense than those of some other

common Aspergillus species and the black mold fungus S. chartarum (Table 1).

(Although the ranges of diameters for conidia of Aspergillus species are

well established [26], we determined means and report them here so that our

calculations of density were based on the volume and mass of the same

collections of conidia.) Cultures of A. fumigatus on PDA sporulated

abundantly; a 2-month-old, 85-mm culture contained 5.8 × 1010 conidia.

Each of the four defined ergot alkaloids was quantified in extracts of

defined numbers of conidia with defined conidial masses (Table 2). Ergot

alkaloids accounted for 1.1% of the mass of conidia of A. fumigatus isolate

WVU1943 grown on PDA, whereas conidia of isolate WVU2026 appeared to contain

slightly lower quantities of ergot alkaloids, although the difference was

not statistically significant. Both isolates accumulated the same array of

ergot alkaloids when they were cultured on latex-based paint (Table 2).

Isolate WVU2026 contained significantly more total ergot alkaloids when it

was cultured on paint than when it was cultured on PDA; isolate WVU1943 also

contained abundant total ergot alkaloids when it was cultured on paint, but

the difference compared to the culture on PDA was not statistically

significant. Colonies on paint were relatively small and consisted mainly of

conidiophores and conidia along with very little vegetative hyphae. Cultures

on water agar (also mostly conidiophores and conidia) still accumulated

ergot alkaloids despite the limited exogenous nutrients in this medium.

However, the concentrations of ergot alkaloids extracted from the water

agar-derived conidia were generally lower than the concentrations extracted

from conidia produced on the other substrates. The same set of ergot

alkaloids also was detected in or on conidia of cultures grown on cultured

maize seedlings (on which the fungus colonized mainly the residual scutellum

and kernel tissue), where they accumulated to relatively high levels, and on

sterilized pistachio shells (on which the fungus grew poorly), where the

concentrations of ergot alkaloids were relatively low (Table 2).

The yield of ergot alkaloids recovered after a more harsh extraction

procedure was assessed in a separate experiment. Breaking of ~63% of the

conidia by bead beating followed by a 1-h extraction in 80% methanol

resulted in a 38% increase in the total yield of ergot alkaloids compared to

the ergot alkaloids extracted from unbeaten conidia.

Discussion:

Our results demonstrate that high levels of certain ergot alkaloids are

associated with conidia of A. fumigatus. The alkaloids are present in or on

conidia produced by cultures grown on a variety of substrates. Moreover, the

conidia of A. fumigatus are smaller, lighter, and less dense than those of

closely related species. These physical properties may promote the

aerosolization and buoyancy of the conidia, which serve as vehicles for the

alkaloids.

Whether the ergot alkaloids are on the surface of the conidia, contained

within the conidia, or in both locations cannot be answered definitively

with the available data. The majority of the ergot alkaloids were easily

extracted from intact conidia, which suggests a surface location. A

bead-beating treatment that physically disrupted the spore wall increased

the amount of alkaloid extracted by 38%. However, in addition to cell

breakage, this treatment also more vigorously extracted any surface

compounds. The data from this more disruptive extraction also indicate that

the values in Table 2 represent minimum values for conidium-associated

alkaloids. The question of the location of the ergot alkaloids relative to

the spore surface may not be significant from a health perspective. In

immunocompetent individuals, inhaled conidia are likely to be killed and

lysed by macrophages (18), releasing any mycotoxins contained in them.

Conidia that are not killed and lysed present a threat of infection and

probably additional toxin production. A role for ergot alkaloids in invasive

aspergillosis has not been investigated. Such studies would be facilitated

by comparison of wild-type isolates with the ergot alkaloid-deficient

mutants described in the accompanying paper (4). In the absence of

infection, conidia may serve as vehicles for exposure to ergot alkaloids.

The issue of health risks posed by inhalation of mycotoxin-containing

conidia is complex and is affected by several factors, including the

physical nature of the conidia with respect to their potential for dispersal

and inhalation and the production of mycotoxins on environmentally relevant

substrates. The conidia of A. fumigatus have properties that appear to

facilitate their dispersal and inhalation. The 2.8-μm diameter of conidia is

small enough for them to penetrate deep into the alveoli of the lungs (18).

The low specific gravity of the conidia (0.24) probably promotes efficient

air dispersal. For comparison, the conidia of the trichothecene producer S.

chartarum, which have generated considerable health concerns (10, 28), have

a mass that is 48 times greater and a specific gravity that is four times

greater than those of conidia of A. fumigatus.

Ergot alkaloids were detected on all media tested, including environmentally

relevant substrates such as latex paint, two different plant materials, and

water agar (representative of moist, nutritionally poor environments). The

reported concentrations of ergot alkaloids associated with conidia produced

on substrates other than PDA were based on the number of conidia extracted

and a value for conidial mass determined from conidia produced on PDA. Thus,

these values were based on the assumption that conidia produced on any of

the alternate substrates have the same mass

conidia produced on PDA. We contend that this is a reasonable assumption.

However, if the mass of each conidium were in fact greater on a natural

substrate than on PDA, then the calculated values for the amount of ergot

alkaloid per conidium would be lower. Conversely, if the conidial mass were

lower on a natural substrate than on PDA, then the alkaloid concentration

would be greater than that shown in Table 2.

A more complicated factor in determination of the health risks associated

with conidial mycotoxins is the issue of whether the toxins are encountered

in quantities sufficient for them to exert their effects. There are at least

three components to this issue, including (i) the concentration of mycotoxin

in each conidium, (ii) the number of conidia encountered, and (iii) the

toxicity of the mycotoxins.

Concentrations of ergot alkaloids that exceed 1% of the mass of the A.

fumigatus conidia are relatively high for fungal natural products. There are

few data available for direct comparison, because most mycotoxin data are

expressed as mass of toxin per unit volume of culture. Data for respirable

trichothecenes from S. chartarum (28) revealed a mean of 17 ng of

trichothecenes per mg of dust aerosolized from S. chartarum cultured on

rice. Assuming that conidia, which constituted 85% of the particles in the

aerosolized dust (28), contributed 85% of the mass of the dust sample, then

0.002% of the conidium mass was trichothecenes.

Using a different isolate of the same fungal species and measuring only the

most abundant trichothecene, Nikulin et al. (21) reported 0.1 pg of

satratoxin H per conidium. Based on a mass of 140 pg per conidium (Table 1),

satratoxin H accounted for 0.0007% of the conidial mass. Another source of

alkaloid data based on fungal mass is the poisonous mushroom literature. For

example, in basidiocarps of Amanita muscaria ibotenic acid accounts for

0.45% of the dry weight and muscimol accounts for 0.036% (30) (assuming that

12.5 mg [fresh weight] of basidiocarp yields 1 mg [dry weight] [9]).

Amatoxins have

been found to account for 0.1% to 0.7% of the dry weight of Amanita

phalloides basidiocarps (9). In a more relevant example, ergot sclerotia of

field-grown C. purpurea contain 1% to 2% ergot alkaloids by mass (5, 20).

The number of A. fumigatus conidia available in the air depends on the

substrate and the environment in which the fungus is growing. Under

favorable conditions the fungus can sporulate prolifically. A typical

culture of A. fumigatus on PDA can yield ~109 conidia per cm2 of culture

surface area. The number of viable A. fumigatus conidia per m3 of air ranges

from 0 to 200 CFU in clean environments (27) to 107 CFU near composting

facilities (12) to 1011 CFU near moldy hay or other stored organic materials

(27). If the intake rate was 0.63 m3 of air per h (32), the conidial ergot

alkaloid content was 1% by mass, and there was no further ergot alkaloid

production after inhalation of the fungus, the ergot alkaloid dose would

range from 3.7 pg per h (at 200 CFU/m3) to 180 ng per h (at 107 CFU per m3)

to 1.8 mg per h (at 1011 CFU per m3).

An interesting point of reference is that an ingested dose of the illicit

and highly active ergot alkaloid lysergic acid diethylamide (LSD) can range

from hundreds of nanograms to hundreds of micrograms (1), but based on U.S.

Drug Enforcement Agency data the dose is frequently in the range from 20 to

80 μg

( http://www.nida.nih.gov/Infofax/lsd.html ).

To inhale a comparable mass of A. fumigatus ergot alkaloids in 1 h would

require exposure to 107 to 1010 CFU per m3. Such high concentrations of

conidia are encountered only rarely. A more practical issue to consider is

whether there are potential health effects of a less remarkable nature (e.g.,

effects on depression, blood pressure, or sleep-wake cycles) that are

associated with chronic daily doses of ergot alkaloids in the nanogram to

microgram range. This issue has not been investigated.

The toxicity of the particular ergot alkaloids associated with A. fumigatus

conidia has not been studied extensively, but the available data suggest

that these mycotoxins have considerable biological activity. Similar to

other ergot alkaloids that have been studied, festuclavine interacts with

receptors for serotonin, dopamine, and α-adrenaline (7, 14, 24, 25).

Festuclavine and synthetic derivatives of festuclavine also are cytostatic

in in vitro assays with several bacteria and mouse lymphoma cell lines (7,

8). Moreover, festuclavine is unique among the naturally occurring ergot

alkaloids in that it is directly mutagenic in the Ames test (15). In the

only published animal study of fumigaclavine C, ingestion of relatively

crude preparations of this ergot alkaloid greatly reduced feed intake by

treated calves and caused hemorrhagic enteritis of the small and large

intestines, as well as patchy interstitial thickening of alveolar walls of

the animals (3).

Demonstration of the presence of ergot alkaloids at relatively high

concentrations in or on conidia of A. fumigatus does not ipso facto indicate

that the toxins play a role in pathogenesis, other health effects, or any

specific aspect of the biology of the fungus. However, it does raise

interesting questions for further research. Studies with ergot

alkaloid-deficient mutants, such as the dmaW knockout strain described in

the accompanying paper (4), should be useful for assessing the contribution

of ergot alkaloids to virulence to animals or potential contributions of the

alkaloids to the ecological success of A. fumigatus. Since minimization of

the mass of a conidium appears to have been selected for in this fungus, the

presence of alkaloids in quantities that exceed 1% of the mass of the

conidium should have been selected against unless they provided some

advantage to the fungus.

Link to comment
Share on other sites

KC--I am so glad you were able to post these articles on the trials. It makes

you wonder about all the people locked away forever in institutions--maybe they

were reacting or actually poisoned by mold or something or a combination of

things. Jane ANN

tigerpaw2c <tigerpaw2c@...> wrote:

Ergotism: The Satan Loosed in Salem?

Convulsive ergotism may have been a physiological basis for the

Salem witchcraft crisis in 1692.

http://web.utk.edu/~kstclair/221/ergotism.html

Linnda R. Caporael

From Science Vol. 192 (2 April 1976)

Numerous hypotheses have been devised to explain the occurrence

of the Salem witchcraft trials in 1692, yet a sense of bewilderment

and doubt pervades most of the historical perspectives on the

subject. The physical afflictions of the accusing girls and the

imagery of the testimony, therefore, is dismissed as imaginary in

foundation. One avenue of understanding that has yet to be

sufficiently explored is that a physiological condition,

unrecognized at the time, may have been a factor in the Salem

incident. Assuming that the content of the court records is

basically an honest account of the deponents' experiences, the

evidence suggests that convulsive ergotism, a disorder resulting

from the ingestion of grain contaminated with ergot, may have

initiated the witchcraft delusion.

Suggestions of physical origins of the afflicted girls' behavior

have been dismissed without research into the matter. In looking

back, the complexity of the psychological and social factors in the

community obscured the potential existence of physical pathology,

suffered not only by the afflicted children, but also by a number of

other community members. The value of such an explanation, however,

is clear. Winfield S. Nevins best reveals the implicit

uncertainties of contemporary historians (1: 2, p. 235).

. . . I must confess to a measure of doubt as to the moving causes

in this terrible tragedy. It seems impossible to believe a tithe of

the statements which were made at the trials. And yet it is equally

difficult to say that nine out of every ten of the men, women, and

children who testified upon their oaths, intentionally and wilfully

falsified. Nor does it seem possible that they did, or could invent

all these marvelous tales, fictions rivaling the imaginative genius

of Haggard or Jules Verne.

The possibility of a physiological condition fitting the known

circumstances and events would provide a comprehensible framework

for understanding the witchcraft delusion in Salem.

Background

Prior to the Salem witchcraft trials, only five executions on

the charge of witchcraft are known to have occurred in Massachusetts

(3, 4). Such trials were held periodically, but the outcomes

generally favored the accused. In 1652, a man charged with

witchcraft was convicted of simply having told a lie and was fined.

Another man, who confessed to talking to the devil, was given

counsel and dismissed by the court because of the inconsistencies in

his testimony. A bad reputation in the community combined with the

accusation of witchcraft did not necessarily insure conviction. The

case against Godfrey of Andover, a notorious character

consistently involved in litigation, was dismissed. In fact, soon

after the proceedings, Godfrey sued his accusers for defamation and

slander and won the case.

The supposed witchcraft at Salem Village was not initially

identified as such. In late December 1691, about eight girls,

including the niece and daughter of the minister, Parris,

were afflicted with unknown " distempers " (1, 4-6). Their behavior

was characterized by disorderly speech, odd postures and gestures,

and convulsive fits (7). Physicians called in to examine the girls

could find no explanation for their illness, and in February one

doctor suggested the girls might be bewitched. Parris seemed loath

to accept this explanation at the time and resorted to private

fasting and prayer. At a meeting at Parris's home, ministers from

neighboring parishes advised him to " sit still and wait upon the

Providence of God to see what time might discover " (6, p.25).

A neighbor, however, took it upon herself to direct Parris's

Barbados slave, Tituba, in the concocting of a " witch cake " in order

to determine it witchcraft was present. Shortly thereafter, the

girls made an accusation of witchcraft against Tituba and two

elderly women of general ill repute in Salem Village, Good and

Osborn. The three women were taken into custody on 29

February 1692. The afflictions of the girls did not cease, and in

March they accused Martha Corey and Nurse. Both of these

women were well respected in the village and were covenanting

members of the church. Further accusations by the children

followed.

Examinations of the accused were conducted in Salem Village

until 11 April by two magistrates from Salem Town. At that time,

the examination were moved from the outlying farming area to the

town and were heard by Deputy Governor Danforth and six of the

ablest magistrates in the colony, including Sewall. This

council had no authority to try accused witches, however, because

the colony had no legal government--a state of affairs that had

existed for 2 years. By the time Sir Phips, the new

governor, arrived from England with the charter establishing the

government of Massachusetts Bay Colony, the jails as far away from

Salem as Boston were crowded with prisoners from Salem awaiting

trial. Phips appointed a special Court of Oyer and Terminer, which

heard it first case on 2 June. The proceedings resulted in

conviction, and the first condemned witch was hanged on 10 June.

Before the next sitting of the court, clergymen in the Boston

area were consulted for their opinion on the issues pending. In an

answer composed by Cotton Mather, the ministers advised " critical

and exquisite caution " and wished " that there may be as little as

possible of such noise, company and openness as may too hastily

expose them that are examined " (2, p.83). The ministers also

concluded that spectral evidence (the appearance of the accused's

apparition to an accuser) and the test of touch (the sudden

cessation of a fit after being touched by the accused witch) were

insufficient evidence for proof of witchcraft.

The court seemed insensitive to the advice of the ministers, and

the trials and executions in Salem continued. By 22 September, 19

men and women had been sent to the gallows, and one, Giles Corey,

had been pressed to death, an ordeal calculated to force him to

enter a plea to the court so that he could be tried. The evidence

used to obtain the convictions was the test of touch and spectral

evidence. The afflicted girls were present at the examinations and

trials, often creating such pandemonium that the proceedings were

interrupted. The accused witches were, for the most part, persons

of good reputation in the community; one was even a former minister

in the village. Several notable individuals were " cried out " upon,

including Alden and Lady Phips. All the men and women who were

hanged had consistently maintained their innocence; not one

confessor to the crime was executed. It had become obvious early in

the course of the proceedings that those who confessed would not be

executed.

On 17 September 1692, the Court of Oyer and Terminer adjourned

the witchcraft trials until 2 November; however, it never met again

to try that crime. In January 1693 the Superior Court of

Judicature, consisting of the magistrates on the Court of Oyer and

Terminer, met. Of 50 indictments handed in to the Superior Court by

the grand jury, 20 persons were brought to trial. Three were

condemned but never executed and the rest were acquitted. In May

Governor Phips ordered a general reprieve, and about 150 accused

witches were released. The end of the witchcraft crisis was

singularly abrupt (2, 4, 8).

Tituba and the Origin Tradition

Repeated attempts to place the occurrences at Salem within a

consistent framework have failed. Outright fraud, political

factionalism, Freudian psychodynamics, sensation seeking, clinical

hysteria, even the existence of witchcraft itself, have been

proposed as explanatory devices. The problem is primarily one of

complexity. No single explanation can ever account for the

delusion; an interaction of them all must be assumed. Combinations

of interpretations, however, seem insufficient without some

reasonable justification for the initially afflicted girls'

behavior. No mental derangement or fraud seems adequate in

understanding how eight girls, raised in the soul-searching Puritan

tradition, simultaneously exhibited the same symptoms or conspired

together for widespread notoriety.

All modern accounts of the beginnings of Salem witchcraft

begin with Parris's Barbados slave, Tituba. The tradition is that

she instructed the minister's daughter and niece, as well as some

other girls in the neighborhood, in magic tricks and incantations at

secret meetings held in the patronage kitchen (2, 4, 8, 9). The odd

behavior of the girls, whether real or fraudulent, was a consequence

of these experiments.

The basis for the tradition seems two-fold. In a warning

against divination, Hale wrote in 1702 that he was informed

that one afflicted girl had tried to see the future with an egg and

glass and subsequently was followed by a " diabolical molestation "

and died (6). The egg and glass (an improvised crystal ball) was an

English method of divination. Hale gives no indication that Tituba

was involved, or for that matter, that a group of girls was

involved. I have been unable to locate any reference that any of

the afflicted girls died prior to Hale's publications.

The other basis for the tradition implicating Tituba seems

to be simply the fact that she was from the West Indies. The

Puritans believed the American Indians worshiped the devil, most

often described as a black man (4). Curiously, however, Tituba was

not questioned at her examination about activities as a witch in her

birthplace. Historians seem bewitched themselves by fantasies of

voodoo and black magic in the tropics, and the unfounded supposition

that Tituba would inevitably be familiar with malefic arts of the

Caribbean has survived.

Calef (7) reports that Tituba's confession was obtained

under duress. She at first denied knowing the devil and suggested

the girls were possessed. Although Tituba ultimately became quite

voluble, her confession was rather pedestrian in comparison with the

other testimony offered at the examination and trials. There is no

element of West Indian magic, and her descriptions of the black man,

the hairy imp, and witches flying through the sky on sticks reflect

an elementary acquaintance with the common English superstitions of

the time (9-11).

Current Interpretations

1) Fraud. Various interpretations of the girls' behavior

diverge after the discussion of its origins. The currently accepted

view is that the children's symptoms of affliction were fraudulent

(4, 8, 12). The girls may have perpetrated fraud simply to gain

notoriety or to protect themselves from punishment by adults as

their magic experiments became the topic of rumor (2). One author

supposed that the accusing girls craved " Dionysiac mysteries " and

that some were " no more seriously possessed that a pack of bobby-

soxers on the loose " (8, p.29). The major difficulty in accepting

the explanation of purposeful fraud is the gravity of the girls'

symptoms; all the eyewitness accounts agree to the severity of the

affliction (6, 10, 11, 13).

Upham (4) appears to accept the contemporaneous descriptions

and ascribes to the afflicted children the skills of a sophisticated

necromancer. He proposes that they were able ventriloquists, highly

accomplished actresses, and by " long practice " could " bring the

blood to the face, and send it back again " (4, vol.2, p.395). These

abilities and more, he assumes, the girls learned from Tituba. As

discussed above, however, there is little evidence that Tituba had

any practical knowledge of witchcraft. Most colonists, with the

exception of some of the accused and their defenders, did not appear

even to consider pretense as an explanation for the girls'

behavior. The general conclusion of the New Englanders after the

tragedy was that the girls suffered from demonic possession (2, 6,

9).

2) Hysteria. The advent of psychiatry provided new tools

for describing and interpreting the events oat Salem. The term

hysteria has been used with varying degrees of license (2, 8, 9,

14), and the accounts of hysteria always begin in the kitchen with

Tituba practicing magic. Starkey (8) uses the term in the loosest

sense: the girls were hysterical, that is, overexcited, and

committed sensational fraud in a community that subsequently fell

ill to " mass hysteria. " Hansen (9) proposes the use of the word in

a stricter, clinical sense of being mentally ill. He insists that

witchcraft really was practiced in Salem and that several of the

executed were practicing witches. The girls' symptoms were

psychogenic, occasioned by guilt at practicing fortune-telling at

their secret meetings. He states that the mental illness was

catching and that the witnesses and majority of the confessors

became hysterics as a consequence of their fear of witchcraft.

However, if the girls were not practicing divination, and if they

did indeed develop true hysteria, then they must all have developed

hysteria simultaneously -- hardly a credible supposition.

Furthermore, previous witchcraft accusations in other Puritan

communities in New England had never brought on mass hysteria.

Psychiatric disorder is used un a slightly different sense in

the argument that the witchcraft crisis was a consequence of two

party (pro-Parris and anti-Parris) factionalism in Salem Village

(14). In this account, the girls are unimportant factors in the

entire incident. Their behavior " served as a kind of Rorschach test

into which adults read their own concerns and expectations " (14,

p.30). The difficulty with linking factionalism to the witch trials

is that supporters of Parris were also prosecuted while some non-

supporters were among the most vociferous accusers (2, 14). Thus,

it becomes necessary to resort to projection, transference,

individual psychoanalysis, and numerous psychiatric disorders to

explain the behavior of the adults in the community who were using

the afflicted children as pawns to resolve their own personal and

political differences.

Of course, there was fraud and mental illness at Salem. The

records clearly indicate both. Some depositions are simply fanciful

renditions of local gossip or cases of malice aforethought. There

is also testimony based on exaggerations of nightmares and

inebriated adventures. However, not all the records are thus

accountable.

3) Physiological explanations. The possibility that the

girls' behavior had a physiological basis has rarely arisen,

although the villagers themselves first proposed physical illness as

an explanation. Before the accusations of witchcraft began, Parris

called in a number of physicians (6, 7). In an early history of the

colony, Hutchinson wrote that " there are a great number of

persons who are willing to suppose the accusers to have been under

bodily disorders which affected their imagination " (12, vol. 2,

p.47). A modern historian reports a journalist's suggestion that

Tituba had been dosing the girls with preparations of jimsonweed, a

poisonous plant brought to New England from the West Indies in the

early 1600's (8, footnote on p.284). However, because the Puritans

identified no physiological cause, later historians have failed to

investigate such a possibility.

Ergot

Interest in ergot (Claviceps purpura) was generated by

epidemics or ergotism that periodically occurred in Europe. Only a

few years before the Salem witchcraft trials the first medical

scientific report on ergot was made (15). Denis Dodart reported the

relation between ergotized rye and bread poisoning in a letter to

the French Royal Academie des Sciences in 1676. Ray's mention

of ergot in 1677 was the first in English. There is no reference to

ergot in the United States before an 1807 letter by Dr. Stearns

recommending powdered ergot sclerotia to a medical colleague as a

therapeutic agent in childbirth. Stearns is generally credited with

the " discovery " of ergot; certainly his use prompted scientific

research on the substance. Until the mid-19th century, however,

ergot was not known as a parasitic fungus, but was thought to be

sunbaked kernels of grains (15-17).

Ergot grows on a large variety of cereal grains--especially

rye--in a slightly curved, fusiform shape with sclerotia replacing

individual grains on the host plant. The sclerotia contain a large

number of potent pharmacologic agents, the ergot alkaloids. One of

the most powerful is isoergine (lysergic acid amide). This

alkaloid, with 10 percent of the activity of a D-LSD (lysergic acid

diethylamide), is also found in ololiuqui (morning glory seeds), the

ritual hallucinogenic drugs used by the Aztecs (15, 16).

Warm, damp, rainy springs and summers favor ergot

infestations. Summer rye is more prone to the development of the

sclerotia than winter rye, and one field may be heavily ergotized

while the adjacent field is not. The fungus may dangerously

parasitize a crop one year and not reappear again for many years.

Contamination of the grain may occur in varying concentrations.

Modern agriculturalists advise farmers not to feed their cattle

grain containing more than one to three sclerotia per thousand

kernels of grain, since ergot has deleterious effects on cattle as

well as on humans (16, 18).

Ergotism, or long-term ergot poisoning, was once a common

condition resulting from eating contaminated rye bred. In some

epidemics it appears that females were more liable to the disease

than males (19). Children and pregnant women are most likely to be

affected by the condition, and individual susceptibility varies

widely. It takes 2 years for ergot in powdered form to reach 50

percent deterioration, and the effects are cumulative (18, 20).

There are two types of ergotism--gangrenous and convulsive. As the

name implies, gangrenous ergotism is characterized by dry gangrene

of the extremities followed by the falling away of the affected

portions of the body. The condition occurred in epidemic

proportions in the Middle Ages and was known by a number of names,

including ignis sacer, the holy fire.

Convulsive ergotism is characterized by a number of

symptoms. These include crawling sensations in the skin, tingling

in the fingers, vertigo, tinnitus aurium, headaches, disturbances in

sensation, hallucination, painful muscular contractions leading to

epileptiform convulsions, vomiting, and diarrhea (16, 18, 21). The

involuntary muscular fibers such as the myocardium and gastric and

intestinal muscular coat are stimulated. There are mental

disturbances such as mania, melancholia, psychosis, and delirium.

All of these symptoms are alluded to in the Salem witchcraft

records.

Evidence for Ergotism in Salem

It is one thing to suggest convulsive ergot poisoning as an

initiating factor in the witchcraft episode, and quite another to

generate convincing evidence that it is more that a mere

possibility. A jigsaw of details pertinent to growing conditions,

the timing of events in Salem, and symptomology must fit together to

create a reasonable case. From these details, a picture emerges of

a community stricken with an unrecognized physiological disorder

affecting their minds as well as their bodies.

1) Growing conditions. The common grass along the Atlantic

Coast from Virginia to Newfoundland was and is wild rye, a host

plant for ergot. Early colonists were dissatisfied with it as

forage for their cattle and reported that it often made the cattle

ill with unknown diseases (22). Presumably, then, ergot grew in the

New World before the Puritans arrived. The potential source for

infection was already present, regardless of the possibility that it

was imported with the English rye.

Rye was the most reliable of the Old World grains (22) and

by the 1640's ot was a well-established New England crop. Spring

sowing was the rule; the bitter winters made fall sowing less

successful. Seed time for the rye was April and the harvesting took

place in August (23). However, the grain was stored in barns and

often waited months before being threshed when the weather turned

cold. The timing of Salem events fits this cycle. Threshing

probably occurred shortly before Thanksgiving, the only holiday the

Puritans observed. The children's symptoms appeared in December

1691. Late the next fall, 1692, the witchcraft crisis ended

abruptly and there is no further mention of the girls or anyone else

in Salem being afflicted (4, 9).

To some degree or another all rye was probably infected with

ergot. It is a matter of the extent of the infection and the period

of time over which the ergot is consumed rather than the mere

existence of ergot that determines the potential for ergotism. In

his 1807 letter written from upstate New York, Stearns (15, p. 274)

advised his medical colleague that, " On examining a granary where

rye is stored, you will be able to procure a sufficient quantity [of

ergot sclerotia] from among that grain. " Agricultural practice had

not advanced, even by Stearns's time, to widespread use of methods

to clean or eliminate the fungus from the rye crop. In all

probability, the infestation of the 1691 summer rye crop was fairly

light; not everyone in the village or even in the same families

showed symptoms.

Certain climatic conditions, that is, warm, rainy springs

and summers, promote heavier than usual fungus infestation. The

pattern of the weather in 1691 and 1692 is apparent from brief

comments in Sewall's diary (24). Early rains and warm

weather in the spring progressed to a hot and stormy summer in

1691. There was a drought the next year, 1692, thus no

contamination of the grain that year would be expected.

2) Localization. " Rye, " continues Stearns (15,

p.274), " which grows in low, wet ground yields [ergot] in greatest

abundance. " Now, one of the most notorious of the accusing children

in Salem was Putnam's 12-year-old daughter, Ann. Her mother

also displayed symptoms of the affliction and psychological

historians have credited the senior Ann with attempting to resolve

her own neurotic complaints through her daughter (8, 9, 14). Two

other afflicted girls also lived in the Putnam residence. Putnam

had inherited one of the largest landholdings in the village. His

father's will indicates that a large measure of the land, which was

located in the western sector of Salem Village, consisted of swampy

meadows (25) that were valued farmland to the colonists (22).

Accordingly, the western acreage of Salem Village, may have been an

area of contamination. This contention is further substantiated by

the pattern of residence of the accusers, the accused, and the

defenders of the accused living within the boundaries of Salem

Village (Fig. 1). Excluding the afflicted girls, 30 of 32 adult

accusers lived in the western section and 12 of the 14 accused

witches lived in the eastern section, as did 24 of the 29 defenders

(14). The general pattern of residence, in combination with the

well-documented factionalism of the eastern and western sectors,

contributed to the progress of the witchcraft crisis.

The initially afflicted girls show a slightly different

residence pattern. Careful examination reveals plausible

explanations for contamination in six of the eight cases.

Three of the girls, as mentioned above, lived in the Putnam

residence. If this were the source of ergotism, their exposure to

ergotized grain would be natural. Two afflicted girls, the daughter

and niece of Parris, lived in the parsonage almost exactly in

the center of the village. Their exposure to contaminated grain

from western land is also explicable. Two-thirds of Parris's salary

was paid in provisions; the villagers were taxed proportionately to

their landholding (4). Since Putnam was one of the largest

landholders and an avid supporter of Parris in the minister's

community disagreements, an ample store of ergotized grain would be

anticipated in Parris's larder. Putnam was also Parris's closest

neighbor with afflicted children in residence.

The three remaining afflicted girls lived outside the

village boundaries to the east. One, Hubbard, was a

servant in the home of Dr. Griggs. It seems plausible that the

doctor, like Parris, had Putnam grain, since Griggs was a

professional man, not a farmer. As the only doctor in town, he

probably had many occasions to treat Ann Putnam Sr., a woman known

to have much ill health (2, 4). Griggs may have traded his services

for provisions or bought food from the Putnams.

Another of the afflicted, Churchill, was a servant in

the house of a well-off farmer (25). The farm lay along that

Wooleston River and may have offered good growing conditions for

ergot. It seems probable, however, that 's affliction was a

fraud. She did not become involved in the witchcraft persecutions

until May, several months after the other girls were afflicted, and

she testified in only two cases, the first against her master. One

deponent claimed that later admitted to belying herself and

others (11).

How Warren, a servant in the Proctor household, would

gain access to grain contaminated with ergot is something of a

mystery. Proctor had a substantial farm to the southeast of Salem

and would have had no need to buy or trade for food. Both he and

his wife were accused of witchcraft and condemned. None of the

Proctor children showed any sign of the affliction: in fact, three

were accused and imprisoned. One document offered as evidence

against Proctor indicated that stayed overnight in the village

(11). How often she stayed or with whom is unknown.

's role in the trials is particularly curious. She

began as an afflicted person, was accused of witchcraft by the other

afflicted girls, and then became afflicted again. Two depositions

filed against her strongly suggest, however, that at least her first

affliction may have been a consequence of ergot poisoning. Four

witnesses attested that she believed she had been " distempered " and

during the time of her affliction had thought she had seen numerous

apparitions. However, when was well again, she could not say

that she had seen any specters (11). Her second affliction may have

been the result of intense pressure during her examination for

witchcraft crimes.

Ergotism and the Testimony

The utmost caution is necessary in assessing the physical

and mental states of people dead for hundreds of years. Only the

sketchiest accounts of their lives remain in public records. In the

case of ergot, a substance that affects mental as well as physical

states, recognition of the social atmosphere of Salem in early

spring 1692 is basic to understanding the directions the crisis

took. The Puritans' belief in witchcraft was a totally accepted

part of their religious tenets. The malicious workings of Satan and

his cohorts were just as real to the early colonists as their belief

in God. Yet, the low incidence of witchcraft trials in New England

prior to 1692 suggests that the Puritans did not always resort to

accusations of black magic to deal with irreconcilable differences

or inexplicable events.

The afflicted girls' behavior seemed to be no secret in

early spring. Apparently it was the great consternation that some

villagers felt that induced Sibley to direct the making of the

witch cake of rye meal and the urine of the afflicted. This

concoction was fed to a dog, ostensibly in the belief that the dog's

subsequent behavior would indicate the action of any malefic magic

(14). The fate of the dog is unknown; it is quite plausible that it

did have convulsions, indicating to the observers that there was

witchcraft involved in the girls' afflictions. Thus, the

experiments with the witch cake, rather than any magic tricks of

Tituba, initiated succeeding events.

The importance of the witch cake incident has generally been

overlooked. Parris's denouncement of his neighbor's action is

recorded in his church records. He clearly stated that, until the

making of the cake, there was no suspicion of witchcraft and no

reports of torturing apparitions (4). Once a community member had

gone " to the Devil for help against the Devil, " as Parris put it,

the climate for the trials had been established. The afflicted

girls, who had made no previous mention of witchcraft, seized upon a

cause for their behavior--as did the rest of the community. The

girls named three persons as witches and their afflictions thereby

became a matter for the legal authorities rather than the medical

authorities or the families of the girls.

The trial records indicate numerous interruptions during the

proceedings. Outbursts by the afflicted girls describing the

activities of invisible specters and " familiars " (agents of the

devil in animal form) in the meeting house were common. The girls

were often stricken with violent fits that were attributed to

torture by apparitions. The spectral evidence of the trials appears

to be the hallucinogenic symptoms and perceptual disturbance

accompanying ergotism. The convulsions appear to be epileptiform

(6, 13).

Accusations of choking, pinching, pricking with pins, and

biting by the specter of the accused formed the standard testimony

of the afflicted in almost all the examinations and trials (26).

the choking suggests the involvement of the involuntary muscular

fibers that is typical of ergot poisoning; the biting, pinching, and

pricking may allude to the crawling and tingling sensations under

the skin experienced by ergotism victims. Complaints of vomiting

and " bowels almost pulled out " are common in the depositions of the

accusers. The physical symptoms of the afflicted and any of the

other accusers are those induced by convulsive ergot poisoning.

When examined in the light of a physiological hypothesis,

the content of so-called delusional testimony, previously dismissed

as imaginary by historians, can be reinterpreted as evidence of

ergotism. After being choked and strangled by the apparition of a

witch sitting on his chest, Londer testified that a black thing

came through the window and stood before his face. " The body of it

looked like a monkey, only the feet were like cock's feet, with

claws, and the face somewhat more like a man's than a monkey . . .

the thing spoke to me . . . " (25, p.45).

ph Bayley lived out of town in Newbury. According to

Upham (4), the Bayleys, en route to Boston, probably spent the night

at the Putnam residence. As the Bayleys left the village,

they passed the Proctor house and ph reported receiving a " very

hard blow " on the chest, but no one was near him. He saw the

Proctors, who were imprisoned in Boston at the time, but his wife

told him that she saw only a " little maid. " He received another

blow on the chest, so strong that he dismounted from his horse and

subsequently saw a woman coming toward him. His wife told him she

saw nothing. When he mounted his horse again, he saw only a cow

where he had seen the woman. The rest of Bayley's trip was

uneventful, but when he returned home, he was " pinched and nipped by

something invisible for some time " (11). It is a moot point, of

course, what or how much Bayley ate at the Putnams', or that he even

really stayed there. Nevertheless, the testimony suggests ergot.

Bayley had the crawling sensations in the skin, disturbances in

sensations, and muscular contractions symptomatic of ergotism.

Apparently his wife had none of the symptoms and Bayley was quite

candid in so reporting.

A brief but tantalizing bit of testimony comes from a man

who experienced visions that he attributed to the evil eye cast on

him by an accused witch. He reported seeing about a dozen " strange

things " appear in his chimney in a dark room. They appeared to be

something like jelly and quavered with a strange motion. Shortly,

they disappeared and a light the size of a hand appeared in the

chimney and quivered and shook with an upward motion (27). As in

Bayley's experience, this man's wife saw nothing. The testimony is

strongly reminiscent of the undulating objects and lights reported

in experiences induced by LSD (28).

By the time the witchcraft episode ended in the late fall

1692, 20 persons had been executed and at least two had died in

prison. All the convictions were obtained on the basis of the

controversial spectral evidence (2). One of the commonly expressed

observations about the Salem Village witchcraft episode is that it

ended unexpectedly for no apparent reason (2, 4). No new

circumstances to cast spectral evidence in doubt occurred. Increase

Mather's sermon on 3 October 1692, which urged more conclusive

evidence than invisible apparitions or the test of touch, was just a

stronger reiteration of the clergy's 15 June advice to the court

(2). The grounds fro dismissing the spectral evidence had been

consistently brought up by the accused and many of their defenders

throughout the examinations. There had always been a strong

undercurrent of opposition to the trials and the most vocal

individuals were not always accused. In fact, there was virtually

no support in the colonies for the trials, even from Boston, only 15

miles away. The most influential clergymen lent their support

guardedly at best; most were opposed. The Salem witchcraft episode

was an event localized in both time and space.

How far the ergotized grain may have been distributed is

impossible to determine clearly. Salem Village was the source of

Salem Town's food supply. It was in the town that the convictions

and orders for executions were obtained. Maybe the thought

processes of the magistrates, responsible and respected men in the

Colony, were altered. In the following years, nearly all of them

publicly admitted to errors of judgment (2). These posttrial

documents are as suggestive as the court proceedings.

In 1696, Sewall made a public acknowledgment of

personal guilt because of the unsafe principles the court followed

(2). In a public apology, the 12 jurymen stated (9, p.210), " We

confess that we ourselves were not capable to understand nor able to

withstand the mysterious delusion of the Powers of Darkness and

Prince of the Air . . . [we] do hereby declare that we justly fear

that we were sadly deluded and mistaken . . . " Hale, a

minister involved in the trials from the beginning, wrote (6,

p.167), " such was the darkness of the day . . . that we walked in

the clouds and could not see our way. "

Finally, Ann Putnam, Jr., who testified in 21 cases, made a

public confession in 1706 (2, p.250).

I justly fear I have been instrumental with others though ignorantly

and unwittingly, to bring upon myself and this land the guilt of

innocent blood; though what was said or done by me against any

person I can truly and uprightly say before God and man. I did it

not for any anger, malice or ill will to any person, for I ahd no

such things against one of them, but what I did was ignorantly,

being deluded of Satan.

One Satan in Salem may well have been convulsive ergotism.

Conclusion

One could reasonably ask whether, if ergot was implicated in

Salem, it could have been implicated in other witchcraft incidents.

The most cursory examination of the Old World witchcraft suggests an

affirmative answer. The district of Lorraine suffered outbreaks of

both ergotism (15) and witchcraft persecutions (4) periodically

throughout the Middle Ages until the 17th century. As late as the

1700's, the clergy of Saxony debated whether convulsive ergotism was

symptomatic of disease or demonic possession (17). Kittredge (3),

an authority on English witchcraft, reports what he calls " a typical

case " of the early 1600's. The malicious magic of Alice Trevisard,

an accused witch, backfired and the witness reported that Alice's

hands, fingers, and toes " rotted and consumed away. " The sickness

sounds suspiciously like gangrenous ergotism. Years later, in 1762,

one family in a small English village was stricken with gangrenous

ergotism. The Royal Society determined the diagnosis. The head of

the family, however, attributed the condition to witchcraft because

of the suddenness of the calamity (29).

Of course, there can never be hard proof for the presence of

ergot in Salem, but a circumstantial case is demonstrable. The

growing conditions and the pattern of agricultural practices fit the

timing of the 1692 crisis. The physical manifestations of the

condition are apparent from the trial records and contemporaneous

documents. While the fact of perceptual distortions may have been

generated by ergotism, other psychological and sociological factors

are not thereby rendered irrelevant; rather, these factors gave

substance and meaning to the symptoms. The content of

hallucinations and other perceptual disturbance would have been

greatly influenced by the state of mind, mood, and expectations of

the individual (30). Prior to the witch cake episode, there is no

clue as to the nature of the girls' hallucinations. Afterward,

however, a delusional system, based on witchcraft, was generated to

explain the content of the sensory data (31, p.137). Valins and

Nisbett (31, p.141), in a discussion of delusional explanations of

abnormal sensory data, write, " The intelligence of the particular

patient determines the structural coherence and internal consistency

of the explanation. The cultural experiences of the patient

determine the content--political, religious, or scientific--of the

explanation. " Without knowledge of ergotism and confronted by

convulsions, mental disturbance, and perceptual distortions, the New

England Puritans seized upon witchcraft as the best explanation for

the phenomena.

References and Notes

1. I have attempted to use sources that would be readily available

to any reader. The spelling of quotations from old documents has

been modernized to promote clarity.

2. W. S. Nevins. Witchcraft in Salem Village (lin, New York,

1916; reprinted 1971).

3. G. L. Kittredge. Witchcraft in Old and New England (Harvard

Univ. Press, Cambridge, Mass., 1929).

4. C. W. Upham. Salem Witchcraft (Wiggins & Lunt, Boston, 1867;

reprinted by Ungar, New York, 19590, vols. 1 and 2.

5. The number of afflicted girls varies between 8 and 12, depending

on the history consulted. I have restricted the " afflicted girls "

to those eight whose residence in or near Salem Village is known.

They are Ann Putnam, Jr., Warren, Mercy , Churchill,

Betty Parris, Abigail , Hubbard, and Walcott.

6. J. Hale. A Modest Inquire Into the Nature of Witchcraft

(Boston, 1702; facsimile reproduction by York Mail, Bainbridge,

N.Y., 1973).

7. R. Calef, in Narratives of the Witchcraft Cases 1648-1706. G.

L. Burr, Ed. (Scribner's, New York, 1914).

8. M. L. Starkey. The Devil in Massachusetts (Knopf, New York,

1950).

9. C. Hansen. Witchcraft at Salem (Braziller, New York, 1969).

10. S. G. Drake. The Witchcraft Delusion on New England (lin,

New York, 1866; reprinted 1970).

11. W. E. Woodard. Records of Salem Witchcraft (privately printed,

Roxbury, 1864; reprinted by De Capo, New York, 1969).

12. T. Hutchinson. The History of the Colony and Province of

Massachusetts Bay, L. S. Mayo, Ed. (Harvard Univ. Press, Cambridge,

Mass., 1936), vols. 1 and 2.

13. D. Lawson, in Narratives of the Witchcraft Cases 1648-1706, G.

L. Burr, Ed. (Scribner's, New York, 1914).

14. P. Boyer and S. Nissenbaum. Salem Possessed: The Social

Origins of Witchcraft (Harvard Univ. Press, Cambridge, Mass., 1974)

(a map indicating the geography of the witchcraft is on p. 35).

15. F. J. Bove. The Story of Ergot (Barger, New York, 1970).

16. A. Hoffer. Clin. Pharmacol. Ther. 6, 183 (1965).

17. G. Barger. ergot and Ergotism (Gurney & , London, 1931).

18. C. E. Sajous and J. W. Hundley. The Cyclopedia of Medicine

(, Philadelphia, 1937), vol. 5, pp.412-416.

19. Ergot has been used to induce and hasten labor in childbirth;

however, it is generally unsuccessful in procuring abortion. Also,

there is no evidence that epidemics of chronic convulsive ergotism

of the type hypothesized to have occurred in Salem have produced

abortions (17).

20. C. M. Gruber. The Cyclopedia of Medicine, Surgery, Specialties

(, Philadelphia, 1950), vol. 5, pp.245-248.

21. W. C. Cutting. Handbook of Pharmacology: Action and Uses of

Drugs (Appleton-Century-Crofts, New York, 1972).

22. L. Carner. The Beginnings of Agriculture in America (McGraw-

Hill, New York, 1923).

23. R. E. Walcott. N. Engl. Q. 9, 218 (1936).

24. M. H. , Ed. The Diary of Sewall 1674-1729

(Farrar, Straus & Giroux, New York, 1973).

25. P. Boyer and S. Nissenbaum, Eds. Salem Village Witchcraft: A

Documentary Record of Local Conflict in Colonial New England

(Wadswoth, Belmont, Calif., 1972). The editors publish an extremely

useful map adapted from Upham (4).

26. A random selection of almost any testimony in Woodard (11) will

attest to this.

27. Essex County Archives. Salem Witchcraft. Keysar's

testimony from the F. Madigan photostats are transcribed in

the Works Progress Administration verbatim report, vol. 2, p.9.

28. S. H. Snyder. Madness and the Brain (McGraw-Hill, New York,

1974).

29. D. van Zwanenber. Med. Hist. 17, 204 (1973).

30. A. Goth. Medical Pharmacology (Mosby, St. Louis, 1972).

31. S. Valins amd R. Nisbett, in Attributions: Perceiving the

Causes of Behavior, E. et al., Eds. (General Learning Press,

town, N. J., 1972).

32. I thank C. F. and M. B. Brewer for their helpful comments

on the manuscript.

>

> If you google: Salem Witch Trials mold, many articles related to

> possible stachybotrys contamination of their rye grain are to be

> found. Jane

>

__________________________________________________

Link to comment
Share on other sites

Jane,

Thank you -

I am also sure that mold exposure tragedies are part of the cascade of

personal tragedy that made many homeless people originally homeless.

These illnessesend up making people unemployable, and uninsurable and

marginalized.

This makes and keeps many poor people poor.

The effects of these familial tragedies can span generations. They can ruin

lives.

This seems obvious to me..

On 12/27/06, jane mosher <janeannmosher@...> wrote:

>

> KC--I am so glad you were able to post these articles on the trials. It

> makes you wonder about all the people locked away forever in

> institutions--maybe they were reacting or actually poisoned by mold or

> something or a combination of things. Jane ANN

>

> tigerpaw2c <tigerpaw2c@... <tigerpaw2c%40>> wrote:

> Ergotism: The Satan Loosed in Salem?

>

> Convulsive ergotism may have been a physiological basis for the

> Salem witchcraft crisis in 1692.

>

>

http://web.utk.edu/~kstclair/221/ergotism.html<http://web.utk.edu/%7Ekstclair/22\

1/ergotism.html>

>

> ...

>

Link to comment
Share on other sites

Join the conversation

You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

Loading...
×
×
  • Create New...