Plague and Rye
"Plague" as an event in altering the possible course of history looms large in the Roman and Medieval Worlds. Elsewhere on this blog and in the Forum discussion has occurred touching "what the plagues might have been?"That is can we be sure that bubonic plague is the identifiable catastrophic disease? The short answer is no we cant. Bubonic plague might well be a co-factor in a given incidence of plague, a taker of life and a causative factor in economic ruin , but certain other possibilities suggest themselves to us.
Several factors suggest that in the medieval plague two morbid strains of disease were immanent, namely the very visible bubonic element (gross lymphatic swellings in particular) from which some persons survived ; and a further pneumonia like respiratory infection which was possibly co-terminus with the buboes (and possibly not) but nearly always fatal.Hence we might have the appearence of death from an ostentatiously visible disease actually caused by another invisible vector.
One of the most widespread and easily percieved toxins in nature is Ergot of Rye (actually a resting stage in the life of Claviceps purperea )It is actually a sclerotium ie: a dormant hibernating form.As many of you will know the ergot replaces individual ears of rye and was for most of history not recognised as being a separate biological entity(1850 in fact).
One may find ergot everywhere, there are more than 30 species afflicting grasses and there are a lot of grasses! All these species form mycotoxins(as all poisinous fungii), but they dont normally get into the food chain at all. So far so good , what of LSD you ask then ? Well lysergic acid amides can be produced from ergot along with ergotamine and ergocristine, ergot as such holds no "true" LSD but can nevertheless trigger hallucinatory convulsions.
Regrettably happy hippy trips can also be partner to gangrenous ergotism from direct ergot consumption.Ergonovine another ergot product may cause spontaneous abortion (either by accident or design) and also is highly toxic to nursing infants , indeed skilled Germanic Midwives used it from the 16C to ease labour though obviously dosage calculation had to be most exacting. Matossian of the Maryland University has done extensive demographic work into the Medieval era :
http://www.hulford.co.uk/ergot.html
but her findings resonate justifiably to earlier time frames.Ergot produces upward of twenty different alkaloids in different mycotoxinal mixes, infecting host populations in different ways.Given that such a large ,but variable ,range of toxins might be produced by a common, but unrecognised , fungus can we interpret any historical patterns where populations have been weakened (and left in a "morbid" state ) where advetitious infections could thus have been rendered far deadlier ?
Anthropologist James Woods has argued that the Black Death was not in fact bubonic plague, on statistical grounds.The mortality rate recorded from Parish registers shows a 45 fold increase in morbidity, a factor way in excess of the known fatality rate for Plague. Even if the disease had hit a non-immune population the death rate is colossal.Modern plague (and we must infer from the modern as best we can) reaches a high morbidity in the rat population before it spills over into the human sphere.Modern epidemics are always preceeded by a noticeable die off of rodents, and the Black Death attracts no such commentary (and I would be pleased to hear if someone can find any source commenting on the like regarding the Plague of Justinian).Clue patterns are reflected geographically also. cold dry areas tend to be immune.The geographic spread of the Black Death also appears to follow a dissemination pattern in relation to transportation routes.According to Woods the Bubonic Plague can only be reliably identified as late as the early 19th C, the original "Black Death" was a massive killer with a very patchy morbidity distribution...so were those who died actually weakened by some underlying common factor? Hence I offer you immunosuppression by mytotoxins on the commenest of foods...rye. Ergot tends to flourish in damp conditions and the modern disaster of 1666 followed two apallingly wet winters.
So could the early Classical Era plagues be of multiple causation? We have 1. a staple crop(s) subject to various forms of (sometime) toxic parisitism 2. Poor weather , ie: damp winter in a warmish climate 3. Poor storage (ie: partial fermentation). 3. A heavy reliance on the affected crops as a staple for the poor 4. Immune system suppression on a wide scale, spontaneous abortion, infant deaths via toxin ingestion 5. Viral infection from a previously isolated source on top of (4) above ....heavy morbidity.
Food (or mycotoxin) for thought.
ref: Macinnis "The Killer Bean of Calabar"
http://www.amazon.co.uk/Killer-Bean-Calaba...5251&sr=8-1
an excellent ripping yarn collection for the toxophagus.
PS: I was just perusing some toxicology notes regarding the Justinian "episode" and the "episode" was not a single event rather a series of diminishing epidemics spread over a period of (at least ) 100 years starting in 541 CE , this "ripple effect" is evident in all major outbreaks of "Plague" .Epidemologists suggest that the arrival of the second major event (1340 CE ) echoed on for a 300 year epoch of "plagues". Both these episodes profoundly changing social, religious and demographic dynamics.
Lax "Toxin" OUP refers.
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