Ergotism and the Bubonic Plague In order to understand the disease, let us first go over its life history. The bacterium, Yersinia pestis, is the actual pathogenic agent that causes the Bubonic Plague. However, it does not directly infect humans, most commonly, Xenopsylla cheopis, a species of flea that specifically infects rats is the carrier of the disease. Pulex irritans, a flea that typically infects human can carry also carry the disease, but this is uncommon. The disease cycle begins when the bacterium enters the stomach of a flea that has bitten an infected rat and dined on its blood. If the rat host dies of the disease or for some other reason, the flea will have to find another host. If the flea should bite a human and sucks its blood, it regurgitates blood and plague bacilli into the bite site thereby infecting its human host. It was believed that during the High Middle Ages, the 1100s-1200s, Europe was in a period of relatively good health and population growth. However, this ended between 1348-1350, when a major epidemic of the Bubonic Plague struck. It is estimated that 1/3 of Europe’s population died as a result of the plague. Although the death toll on this occasion was high, a depression in the population of Europe lasted until 1490. This puzzled historians since even with such a high number of deaths, population recovery should have occurred by the next generation, unless other factors were involved. Necrosis, bleeding and an ulcerous swollen throat, symptoms of damage to cells in the bone marrow were observed in many victims. These symptoms indicated widespread damage to the human immune system.
Matossian (1988) believed that while deaths could ultimately be attributed to Bubonic Plague, the consumption of grains infected with T-2 or related mycotoxins compromised the immune system and increased the likelihood of death in human and rats. Because of the increase in death of rats, the fleas carrying the disease would require a new host, which in heavily populated area, often was a human host. This led to a higher death rate than might have normally occurred. She also presented evidence, based on what seemed to be selectivity of the disease, based on age and wealth, grain storage and environmental moisture.
The age groups that were most impacted by the plague were children 5-14 years and youths 15-24 years. The latter groups had mortality rates that were three times normal during the plague while the children between 1 to 4 years had a mortality rate of less than average. Matossian believed that age, activity and diet played a major role in the mortality rate. The youngest children during this period tended to be on a diet of porridge, which would normally be boiled long enough to break down the mycotoxin. Those in the age groups with the high mortality rate, because of their growth spurts and activity, consumed more calories per unit body weight than other age groups and therefore consumed more mycotoxin. The poor also had a greater mortality rate than the rich. This can probably be attributed to the ability of the latter groups ability to move away from areas of plague and to be more selective in their diet. The poor were often forced to consume substandard food that more than likely were contaminated with mold during the plague.
The highest incidents of plague occurred in areas where there were large surpluses of grain stored. The large surpluses of grain attracted large populations of rats who were the vector transmitting the plague. There also appeared to be a strong correlation between the occurrence of plague and the amount of rain, humidity and flooding. Areas of Europe where such conditions prevailed were hit hardest with the plague. For example, England had a very wet summer, during 1348, where the mortality was high. However, neighboring Scotland that same year and the plague did not spread widely there, until the wet summer of 1350. Areas that were cold, but dried, such as Iceland, northern Norway and Sweden, Finland, and large areas of Russia and the Balkans escaped the the plague, entirely. Thus, the plague did not find its way throughout Europe, but was rather restricted in its distribution. Matossian cites Graham Twigg (1936) was a historian who believed that the plague was only present in Mediterranean ports and a few cities where there was a dense human and rat population.
Due to the cold and wet years that occurred in 1348-50, in certain areas of Europe, grain crops, which were the staple for Europe at this time, were thought to have been contaminated with T-2 or related toxins that damaged the immune systems of both rats and humans. The damage to the immune systems of both rats and human is believed to be one the contributing factors that led to the high mortality during the Bubonic Plague. However, other causes of depressed immune systems, other than fungal in origin, may also have occurred at this time.
Kicked Out of Heaven Vol. II
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The Untold History of The White Races cir. 700 – 1700 a.d.
666 pages 197 pages
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Kicked Out Of Heaven Vol. II: The Untold History of The White Races cir. 700-1700 a.d. is a 3 volume series that will be released one by one. This book details everything about European society and mentality. In this edition you will find these facts: Alcoholism & The Blue Devils, Insanity & Lead Poisoning, Ergot (LSD) Hallucinations, The Sweating Sickness & Leprosy, The Tobacco Enema & Leeches, The Defloration Mania, The Dancing Mania, The Black Death, The Gravediggers & Body Snatchers, Jews Poisoning the Wells, Millions of Deaths, Folklore & Superstition, Magic Mirrors & Crystal Balls, Witches Dancing in Baby Blood, Pants Made of Human Skin, Necromancy & Ghost Armies, Attacks from The Undead, Lycanthropy & Were-Wolves, Multiple Cases of Vampires, Who is Satan, Lucifer & The Devil!
Bam! Smack! Pow!: Lucifer No. 2: Plague, tumors, and undead mothers.