Arthur Tudor died at the young age of 15 on April 2, 1502 at Ludlow Castle in Wales. It is springtime here, and Wales is covered with wildflowers and fields full of woolly little lambs. It seems exceptionally sad that Arthur died at this time of year, when he was a newlywed and also just entering the spring of his life.
Adding to the tragedy of his death is that no one is sure exactly why he died. A contemporary source records that Arthur’s ailment was “the most pitiful disease and sickness, that with so sore and great violence had battled and driven, in the singular parts of him inward, [so] that cruel and fervent enemy of nature, the deadly corruption, did utterly vanquish” (Starkey, 2003:76) the teenage prince. The onslaught of the illness that killed him began on March 27, 1502 and final breath Arthur took was less than a week later. What could have killed him in such a short space of time?
Thomas Penn’s biography of Henry VII states that the newlywed prince died of the sweating sickness, but the course of the sweating sickness – whether to resumed health or to the grave – went much faster. As Claire Ridgeway explained in her treatise Sweating Sickness in a Nutshell, the illness “lasted 24 hours, more or less”. Since it took Arthur almost a week to succumb, it was either an oddly long time for the sweating sickness to progress or it wasn’t sweating sickness at all. Influenza and/or pneumonia could have certainly caused it in that space of time, but Arthur’s physicians would have known and named either condition (Ricks, 2009; Wallis, 2010).
Testicular cancer has also been suggested as a reasonable explanation for Arthur’s rapid decline (Starkey, 2003:76-77), but the odds are good that one of his physicians would have noticed and tried to treat a tumorous mass on Arthur’s scrotum – especially if the prince’s health was failing. Medieval physicians were aware of cancer and its progression, looking for “morbid swellings that were hard, spread quickly … and eventually produced ulcers that corroded the flesh” (Wallis, 2010:344). Moreover, health care professionals past and present quickly learn the ‘cancer smell’ that comes with end stage cancer, “which somewhat resembles the scent of lilac or jasmine, mixed with an intolerably fetid odor” (Smith, 1855:96) or “rotting flesh, but even more pungent” (Gunter, 2012). Like influenza or pneumonia, Arthur’s doctors could have probably named the disease for what it was, even though they were helpless to treat it.
Other historians have speculated that Arthur’s death was the result of consumption (Whitelock, 2010:10), but if so it was again another surprisingly rapid case tuberculosis. A Spanish physician in Katherina of Aragon’s household reportedly diagnosed the prince with “tisis, a Spanish catchall word covering everything from pulmonary tuberculosis to any wasting, feverish disease the produced ulceration of some bodily organ” (Tremlett, 2010:91). If this was the case, why didn’t any of the prince’s doctors notice it? Certainly tuberculosis was a disease which any medieval physician would have recognized (Magner, 1992; Crabtree, 2013). Could his disease have only produced consumptive-like symptoms a few weeks prior to his death?
I think it might have been genetic. Like his older brother Arthur, both Henry VIII’s sons that survived infancy died in their mid teens. God knows that genetic conditions could flourish in a closed breeding population like the nobility. This is the theory I put forth in my book, Edward VI in a Nutshell.
In the book I argue that Arthur, Edward VI, and Henry Fitzroy had atypical cystic fibrosis, which usually doesn’t show up until later in childhood or when the patient is in his teens. Atypical cystic fibrosis would also explain why some eyewitnesses saw Arthur as healthy while he simultaneously developed a reputation for being ‘delicate’; his perceived health would depend on whether his atypical CF was causing him issues at the time and if you were aware of his chronic cough and/or indigestion. Moreover, CF can look a hell of a lot like tuberculosis to the untrained eye — the patient can suddenly go downhill fast. Doctors would have known TB well enough to know it wasn’t quite TB that killed the patient, but they wouldn’t have had any idea of what it really was. CF can also involve copious amounts of malodorous sweat, which may explain why they thought Arthur might have had some weird form the sweating sickness.
As many as 1/25 people of Northern European decent are carrying the recessive gene, so it wouldn’t be very far-fetched for cousins (albeit distant) Henry VII and Elizabeth of York to both have the gene. Neither it is beyond belief that both Bessie Blount and Jane Seymour, both descendants of minor Plantagenet houses, had the recessive genes as well.
What do you think killed the Prince Arthur?