1348 was the year bubonic plague arrived in Dublin having landed at the nearby ports of Howth and Drogheda. It then ripped through the capital; killing perhaps half the population. It wasn't only Ireland: plague was a pandemic across the whole of Europe, in the process of killing 20 million people or about a third of the population wherever it appeared, destroying the laboring classes and everyone else indiscriminately, destablising society and leading to a spiral of wage inflation among the survivors. As with the Bald's eye-salve story last week, we know now, from contemporary descriptions, that the disease is caused by a gamma proteobacteria bacterium, Yersinia pestis, quite closely related to Escherichia coli, Vibrio cholerae and Salmonella typhimurium which are all 'enterics'. Any one of those enterics can be fatal usually because your immune system tries to flush the pathogens out of the gut until you run out of fluid. Even the assaults of V. cholerae, the the most aggressive [hey cholera vs a gentle run] of the three, can be weathered if you have access to clean water to replace fluid loss. IV saline drip and as much by mouth as you can hold down: you may be losing 20 lt of fluid per day, so that's a lot of cups of tea.
Yersinia pestis, today's guest on The Blob, kills in a very different manner. It is acquired in two ways, neither of them by ingestion: a) the bite of a flea or b) breathing in droplets coughed up by someone already frothing Yersinia from the lungs. Once acquired Y. pestis migrates to the lymph-nodes most prominently in groin, arm-pit and under each ear there multiplying rapidly. The immune system reacts aggressively and between the two warring parties, there is significant tissue-damage and necrosis causing the lymph-nodes to swell up, turn into black 'buboes' and leak blood and pus to the exterior. Bits of necrotic tissue get into the blood stream where they cause blockages in capillaries, particularly in the extremities, leading to further necrosis and horrible black sub-cutaneous 'bruises'. The distinctive colour gave the infection the title Black Death. These lesions are leaky, as are the linings of the lungs, so the disease propagates rapidly to people in the vicinity. This 'pneumonic' plague is particularly virulent and kills 90-100% of those displaying symptoms. Whatever about your groin, you can't survive long when your lungs are rotting.
1665 was when the Black Death arrived in London, as recorded by Samuel "Diary" Pepys and also as 'faction' in Daniel "Crusoe" Defoe's Journal of the Plague Year in which he channelled his Uncle Henry Foe's recollections of being an adult in that year: Defoe himself was a tot of 5 in 1665. But Defoe also beefed up the account with research, including data from bills of mortality, anecdotes with the ring of truth and vivid descriptions of the disruption to normal life. The Great Plague of London was no respecter of class and at least one excavation has revealed otherwise perfectly healthy [and so by inference, rich] people all dead within the time-frame of the pestilence. English school-boy history records that the Great Fire of London in 1666 was providential in burning the last residues of plague off into the atmosphere.
The other famous story of 1665 is that of Eyam, a village in the English Peak District, which voluntarily quarantined itself to limit the spread of bubonic plague to neighboring parishes. They communicated with outsiders [they had money but needed food] by agreeing to exchange materials at designated places on the periphery of the village. The money was left in a vinegar-filled trough, in the belief that this would sterilise it; remember that this was 300 years before Alexandre Yersin, Louis Pasteur and others twigged that disease was caused by germs. Remarkably, some of the citizens of Eyam, including the gravedigger and the vicar and a mother who buried all six of her children, seemed to be immune to the infection.
Stephen J O'Brien [previously on cheetahs and HIV] has been interested in Eyam because of his interest in CCR5 and its delta32 mutation that confers resistance to HIV, which I mentioned in the earlier piece as being really important for resistance to the modern scourge. But SJO'B couldn't account for the prevalence for the mutant form by looking at modern selective pressures such as HIV; he did some nifty analysis on the distribution of the mutant and reckoned it got a jolt in the arm 650 years ago. Or rather those people who didn't have the mutation got a bad case of death, which meant that delta32ists became more common in the (diminished) population. 650 years ago is 1348! In 1665, Yersinia pestis was on the march again and there is a suggestion that, bad as the bills of mortality were, they weren't as devastating as during the Black Death of 1347-1351. Could that be because delta32 had become more common in the population? Could it further be that the survivors of the killing fields of Eyam were richer in genes carrying the delta32 mutation? This documentary [50 minutes] investigates the issues, describes some of the scientific methods, and also gives results: which turn out to (modestly) support the hypothesis that the Black Death was a driver in the evolution of CCR5. Go Steve!