Guest guest Posted December 27, 2006 Report Share Posted December 27, 2006 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 . 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. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 28, 2006 Report Share Posted December 28, 2006 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 > __________________________________________________ Quote Link to comment Share on other sites More sharing options...
Guest guest Posted December 28, 2006 Report Share Posted December 28, 2006 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> > > ... > Quote Link to comment Share on other sites More sharing options...
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