an autodidact meets a dilettante…

Well, maybe not quite

I’m writing this because of some remarks made in the workplace which – well, let’s just say they set my sceptical antennae working overtime. They were claims made about the bubonic plague, of all things.

Bubonic plague, dubbed the Black Death throughout European history, is a zoonotic disease, which means it spreads from species to species – in this case from rodents to humans via fleas. Actually there are three types of ‘black death’ plagues, all caused by the enterobacterium Yersinia pestis, the others being the septicemic plague and the pneumonic plague. Other zoonotic diseases include ebola and influenza. Flea-borne infections generally attack the lymphatic system, as does bubonic plague. The term ‘bubonic’ comes from Greek, meaning groin, and the most well-known symptom of the disease were ‘buboes’, grotesque swellings of the glands in the groin and armpit.

It wasn’t called the Black Death for nothing (the blackness was necrotising flesh). It’s estimated that half the European population was wiped out by it in the 14th century. If untreated, up to two-thirds of those infected will be dead within four days. With modern antibiotic treatments, the mortality rate is of course greatly reduced. The broad-based antibiotic, streptomycin has proved very effective. Of course treatment should be immediate if possible, and prophylactic antibiotics should be given to anyone in contact with the infected.

The plague is first known to have stuck Europe in the sixth century, at the time of Justinian. The Emperor actually caught the disease but recovered after treatment. It’s believed that the death toll was very high, but little detail has been recorded. The fourteenth century outbreak appears to have originated in Mongolia, from where it spread through Mongol incursions into the Crimea. An estimated 25 million died in this outbreak from 1347 to 1352.  More limited outbreaks occurred in later centuries, and the last serious occurrences in Europe were in Marseille in 1720, Messina (Sicily) in 1743, and Moscow in 1770. However it emerged again in Asia in the nineteenth century. Limited for some time to south-west China, it slowly spread from Hong-Kong to India, where it killed millions of people in the early twentieth century. Infected rats were inadvertently transported to other countries by trading vessels, resulting in outbreaks in Hawaii and Australia. By 1959, when worldwide casualties dropped to under 200 annually, the World Health Organisation was able to declare the disease under control, but there was another outbreak in India in 1994, causing widespread panic and over 50 deaths.

So that’s a v brief history of the rise and fall of bubonic plague, but I’m interested in looking at early treatments and the discovery of its cause. For the fact is that, even in 1900, when the plague first came to Australia, there was no clear consensus among the experts as to its means of transmission, with many believing that it was as a result of contact with the infected. However, a growing body of evidence was showing a connection with epizootic infection in rats, and as it happened, work done by Australian bacteriologists Frank Tidswell, William Armstrong and Robert Dick, working for a new public health department in Sydney under Chief Medical Officer John Ashburton Thompson, established as a direct result of the plague outbreaks in Sydney from 1900 to 1925, contributed substantially to the modern understanding of Yersinia pestis and its spread from rats to humans. This Australian work was another step forward in the germ theory of disease, first suggested by the French physician Nicolas Andry in 1700, and built upon by many experimental and speculative savants over the next 150 years. The great practical success of John Snow’s work on cholera, followed by the researches of Louis Pasteur and Robert Koch, established the theory as mainstream science, but zoonotic infections, especially indirect ones where the infection passes from one species to another by means of a vector, have always been tricky to work out.

In fact it was in Hong Kong that the Yersinia pestis bacterium was identified as the culprit. A breakout of plague occurred there in the 1890s, and Alexandre Yersin, a bacteriologist who had worked under both Pasteur and Bloch, was invited to research the disease. He identified the bacterium in June 1894, at about the same time as a Japanese researcher, Kitasato Shibasaburo. The cognoscenti recognise that both men should share the honour of discovery. 

What is fascinating, though, is that the spread of plague from Asia in the 1890s to various ports of the world in the earlier 20th century was very different from the spread of earlier pandemics. Did this have anything to do with science or human practices? Well, what follows is drawn from by far the most comprehensive analysis of the disease I’ve found online, Samuel Cohn’s ‘Epidemiology of the Black Death and successive waves of plague’, in the Cambridge Journal of Medical History.

Cohn’s research and analysis casts credible doubt on the whole plague story, specifically the assumption that we’re dealing with one disease, from the sixth century through to modern outbreaks. He recounts the standard story of three separate pandemics, in the sixth century with a number of recurrences, ditto in the fourteenth century, and in the nineteenth. However, the epidemiology of the most recent pandemic, definitely attributed to Y Pestis and its carrier the Oriental rat flea, Xenopsylla cheopis, is substantially different from that of pandemics one and two, a fact which, according to Cohn, has been obscured by inaccurate analysis of the records. Cohn’s own analysis, it must be said, is fulsome, with 30 pages of references in a 68-page online essay. He doesn’t have a solution as to what caused the earlier pandemics, but he asks some cogent questions. For my own understanding’s sake, I’ll try to summarise the issues in sections.

speed of transmission

 Pandemic 3, if we can call it that, was a much slower mover than the previous two. It seems to have sprung up in China’s Yunnan province from where it reached Hong Kong in 1894. It was noted in the early 20th century that Y pestis was travelling overland at a speed of only 12 to 15 kilometres a year. This can be explained by the fact that Y pestis is a disease mainly of rats, though other rodents can also be infected, and rats don’t move far from their home territories. At this rate pandemic 3, even in a world of railways, cars, and dense human populations, would have taken some 25 years to cover the distance that pandemic 1 covered in 3 months. Pandemic 1 made its first appearance in an Egyptian port in 541 and quickly spread around the Mediterranean from Iberia to Anatolia. Within two years of first occurrence it had reached to the wastelands of Ireland and eastern Persia. Pandemic 2, believed to have originated in India, China or the Russian steppes, made its first European appearance in Messina, Sicily in 1347. Within three years it had impacted most of continental Europe, and had even reached Greenland. The fastest overland travel recorded for plague occurred in 664 (pandemic 1), when it took only ninety-one days to travel 385 kilometres from Dover to Lastingham (4.23 km a day)— far faster than anything seen from Y pestis since its discovery in 1894. Pandemic 2’s speed was similar, as Cohn details it:

like the early medieval plague, the “second pandemic” was a fast mover, travelling in places almost as quickly per diem as modern plague spreads per annum. George Christakos and his co-researchers have recently employed sophisticated stochastic and mapping tools to calculate the varying speeds of dissemination and areas afflicted by the Black Death, 1347–51, through different parts of Europe at different seasons. They have compared these results to the overland transmission speeds of the twentieth-century bubonic plague and have found that the Black Death travelled at 1.5 to 6 kilometres per day—much faster than any spread of Yersinia pestis in the twentieth century. The area of Europe covered over time by the Black Death in the five years 1347 to 1351 was even more impressive. Christakos and his colleagues maintain that no human epidemic has ever shown such a propensity to cover space so swiftly (even including the 1918 influenza epidemic). By contrast to the spread of plague in the late nineteenth and twentieth centuries the difference is colossal: while the area of Europe covered by the Black Death was to the 4th power of time between 1347 and 1351, that of the bubonic plague in India between 1897 and 1907 was to the 2nd power of time, a difference of two orders of magnitude.

All of which raises the question – why was pandemic 3 so much slower than the others? Could it be that Y pestis wasn’t the cause of the earlier pandemics?

mode of transmission

We know that Y pestis is a disease of rats,  and we know that the Black Death was all about rats, so that’s an obvious connection, no? Well, according to Cohn, what we think we know is just wrong. ‘… no scholar has found any evidence, archaeological or narrative, of a mass death of rodents that preceded or accompanied any wave of plague from the first or second pandemic.’ I must say I found this incredible when I first read it, yet Cohn seems to have investigated the sources thoroughly.

Cohn notes that:

while plague doctors of “the third pandemic” discovered to their surprise that the bubonic plague of the late nineteenth and twentieth centuries was rarely contagious, contemporaries of the first suggest a highly contagious person-to-person disease. Procopius, Evagrius, John of Ephesus, and Gregory of Tours characterized the disease as contagious and, in keeping with this trait, described it as clustering tightly within households and families; the evidence from burial sites supports their claims.

Pandemic 2 made the word contagium popular among the general public, and the incredible speed of transmission became one of the principle signs of the Black Death, differentiating it, for example, from smallpox, which had some similar physical characteristics. This contagion suggests person to person contact, more typical of pneumonic plague, which is highly infectious and can be transmitted through coughing and sneezing. A later chronicler of pandemic 2, Richard Mead, writing in the 1700s, advised against crowding plague sufferers in hospitals, as it ‘will promote and spread the Contagion’. However, those treating pandemic 3 noted, to their surprise, that plague wards were the safest places to be, and that this particular plague rarely took on the pneumonic form.

Cohn notes that the earlier pandemics were often associated with famine. For example in Alexandria and Constantinople in 618 and 619 famine preceded the plague and appeared to spark it into life. However, pandemic 3, definitely caused by Y Pestis, tended not to thrive in situations of dearth and was instead fed by increased yields. Such yields lead to higher rat populations, and higher rates of possibly infected rat fleas and so higher rates of transmission to humans.

death rates

According to contemporary accounts the first pandemic wiped out entire regions, decimating the inhabitants of cities and the countryside through which it so swiftly passed.  These accounts are backed up by archaeological and other evidence. It’s pretty clear that millions died in the second pandemic too. Compare this to the third pandemic, which spread so slowly and was limited to coastal areas and even just shipping docks. Restricted to temperate zones, this last pandemic resulted in deaths in the hundreds, with never more than 3% of an affected population dying.

symptoms

Although few quantitative records describe the signs or symptoms of plague for pandemic one, those that do (and Cohn cites 6 different ancient authors) are in general agreement in their descriptions of ‘swellings in the groin, armpits, or on the neck just below the ear’, the classic symptoms of bubonic plague. Procopius of Caesaria also observed that victims’ bodies were covered in black pustules or lenticulae. Pandemic 2, which begins with the Black Death of 1347-52, is marked, on the other hand, by extensive records, both professional and popular – writings about it were amongst the first forms of popular literature.

range and seasonality

Another problem for the view that this has all been the doing of Y pestis, is that pandemics 1 and 2 could strike all year round, but generally settled into a pattern of prevailing in summer in the southern Mediterranean and the Near East, which is not the best season for the flea vector X cheopis. The seasonal cycle of modern plague is quite different, and the range is much more limited.

So all this opens up a mystery. Scientists are agreed that we don’t have a clear-cut story of Y pestis causing horrific disease through rats and fleas over millennia (archaeological and other evidence suggests that rats were scarce in 14th century Europe) , but they’re much in disagreement about what the real story might be. If not Y pestis, then maybe a hemorrhagic virus (one of which causes ebola). Such viruses are notorious for their rapid transmission, their resurgences and their high mortality rates. Pneumonic plague,  the more infectious, lung-infecting form of plague may also be implicated, but this doesn’t appear to agree with most of the described symptoms of pandemics 1 and 2. Other types of fleas, not associated with rats, as well as lice, are also being considered as possible vectors. Some geneticists believe that a variant of Y pestis may have been responsible. It looks as if genetic analysis is the most likely pathway to finding a solution.

This article got started, as I wrote at the beginning, because someone keen on naturopathy said something about bubonic plague in our staff room. Some plant she brought in, which had great anti-oxidant properties (she clearly hasn’t kept up with the latest findings on anti-oxidants) was also a cure for bubonic plague, or maybe it was a variant of the plant, and the person who discovered the secret of its healing properties died suddenly (presumably not from plague) and the secret was lost to us for centuries…