Smallpox, Syphilis and Salvation

by Sheryl Persson

  Death is even faster with the septicaemic form of plague which is almost always fatal. Without treatment, victims usually die within 24 hours of the onset of symptoms. Victims of septicaemic plague do not develop buboes because the bacilli enter the bloodstream directly. Like bubonic plague, the septicaemic variety may be caused by flea bites or from direct contact with infective materials through cracks in the skin. There is haemorrhaging into the skin and other organs which creates black patches on the skin and in some cases red bite-like bumps as well. Today treatment with antibiotics can reduce the mortality rate of septicaemic plague dramatically to around 5 per cent.

  In all three forms of the plague, internal bleeding causes large bruises to appear on the skin hence the appellation the Black Death. As there was no way to distinguish one form from another in the fourteenth century, many scientists and historians believe that the more contagious and virulent pneumonic and septicaemic varieties were present as well as the bubonic form during the pandemic, which not only increased the pace of infection but also facilitated the rampant spread of the disease into inland areas of many countries.

  As is the nature of scientific enquiry and debate there are also claims that the plague that swept through England during the great pandemic was not plague at all and certainly not bubonic plague. A BBC news article published in 2002 discusses the proposition by anthropologists from Penn State University in the United States that the spread of the Black Death was far too rapid to have been bubonic plague and that the geographic reach of the disease supports this.[7] In England, for example, plague made its way along roadways and navigable rivers and its progress was not slowed by natural geographical barriers that would prevent the movement of rodents and thus the spread of bubonic plague.

  Further to this the anthropologists, who subscribe to the theory that bubonic plague becomes rampant in the rat population before being carried to humans by rodent fleas, had found no historical records that referred to dead rats in sufficient numbers. Their conclusion was that the Great Mortality was not bubonic plague but could have been caused by any number of infectious organisms and was probably transmitted through person-to-person contact, not fleas. Because these findings were based on historical records, a bacteriologist at the London School of Hygiene and Tropical Medicine dismissed them as unscientific speculation. He suggested that unless bacterial DNA from that time could be found, tested and compared with various strains of plague bacteria that exist now, then the debate could not be resolved.

  Debate is healthy and there is certainly an ongoing fascination with the Black Death amongst scientists, which says much about the status of this disease in history and the horror surrounding it. Susan Scott, a historical demographer, and Christopher J. Duncan, Emeritus Professor of Zoology in the School of Biological Sciences at the University of Liverpool in the United Kingdom, have also challenged the belief that the Black Death pandemic in the 1300s and the Great Plague of London in 1665 were bubonic plague.[8] Their book, Biology of Plagues, published in 2001, combines epidemiology, molecular biology and computer modelling with historical records to show that rats were not the source of infection. Scott researched the parish records of the English town of Penrith in Cumbria and discovered that the disease that reached this remote spot during the Middle Ages was spread by person-to-person contact and was unlikely to be any form of plague but it may have been the dreaded Ebola virus.

  So, was the fearsome bubonic plague responsible for inestimable deaths in the Middle Ages? The consensus is that because of the rapidity and extent of its spread and the range of symptoms that have been recorded, the Black Death was in fact a combination of all three forms of the plague.

  THE GREAT MORTALITY RESHAPES MEDIAEVAL EUROPE

  In mediaeval times people believed that the Black Death was a punishment from God. As we now know, the cause was far more terrestrial than celestial. In towns and cities people lived cheek by jowl in squalid, unhygienic conditions and knew nothing about infection and contagious diseases, although there was a common belief that rats caused the disease in some way. Streets littered with refuse and sewage provided a perfect breeding ground for rodents and they carried plague fleas into shops, houses and churches. Fleas bit into their victims, literally injecting them with bubonic plague. The problem of contagion was further exacerbated by the unhygienic disposal of bodies and those who handled the plague-infested dead were particularly at risk.

  Medical knowledge was minimal and superstition was rife. As a result people would try anything to save themselves from falling victim to plague. One extreme measure was flagellation.[9] To show devotion to God, people whipped themselves viciously in the hope that their sins would be forgiven, sparing them a gruesome death. Mediaeval literature is littered with macabre illustrations of flagellants with their whips.

  As the Great Mortality diminished populations throughout Europe, the established order of mediaeval society was utterly disrupted. Crops rotted, fields went unploughed and farm animals died because there was no one to tend them. The inhabitants of towns and cities faced food shortages because the surrounding villages could not provide them with enough food. Grain farming became less popular because the noble class who owned the land had turned to sheep farming, which was less labour intensive. Inflation was rife and exorbitant food prices created additional hardship for the poor.

  Those who survived the Black Death believed that they had been chosen by God and began to question the status quo. The feudal system under which they lived was restrictive and had been introduced to tie peasants to the land. Peasants could not leave their village without their lord’s permission. As labour shortages became critical due to the plague, laws were relaxed and peasants began to move to areas where work was available, some even demanding higher wages. There came a realisation amongst the nobility that the system they relied on to maintain power was breaking down. In England the Statute of Labourers was introduced in 1351 to limit wages that could be paid and received and to reinstate the law restricting the movement of peasants. The resultant anger and discontent led to the Peasants Revolt of 1381.

  Although it may seem paradoxical, it is believed that the Great Mortality was immortalised in the original version of the English nursery rhyme ‘Ring-a-ring o’ roses’.[10] The ‘roses’ refer to the red spots that appear on a victim’s skin over the buboes; ‘A-tishoo! A-tishoo!’ mimics the flu symptoms and ‘We all fall down!’ reflects the swift death that accompanies the pneumonic form of plague. The song may also allude to the fact that the plague made everything fall down—the political, economic and social structures of many countries.

  The Black Death continued to strike parts of Europe throughout the fourteenth, fifteenth and sixteenth centuries with varying degrees of intensity and fatality. In May 1665 the famous, or infamous, Great Plague of London began. Only 43 people died during May of that year but the death toll for June was 6137. This figure almost trebled in July when 17,036 succumbed. The mortality rate doubled again in August, with a staggering 31,159 deaths. Then in 1666 a fire, the Great Fire of London, raced through the city purging it of its infestation of plague-carrying rats and fleas and the slums that harboured them. With widespread destruction came temporary salvation.

  In 1679 plague devastated central Europe and erupted again in England but this was the last major outbreak ever experienced there. During the eighteenth century outbreaks of bubonic plague in the rest of Europe also diminished, probably partly due to improvements in public hygiene and sanitation. Gradual genetic adaptation which provided humans with resistance to the disease may also have contributed to stopping the spread of plague.

  The Black Death had not finished with other parts of the world, however. A third bubonic plague pandemic began in China in 1855 and by 1877 had become a serious problem in India, China and Russia, ultimately killing more than 12 million people in India and China alone.[11] There were two likely sources for this pandemic. The bubonic form of plague was carried around the world via ocean-going tra
de which transported infected people and cargoes infested with rats and fleas. A more virulent strain that was rampant in Manchuria and Mongolia was probably pneumonic, highly contagious from person to person.

  The pandemic persisted in China and India until the mid 1890s and it was because of this continuing threat that Alexandre Yersin and Shibasaburo Kitasato set off with their research teams to go microbe hunting in Hong Kong in the hope of finding the cause of the plague. What was to follow is as intriguing as fiction.

  THE HUNT FOR THE CAUSE

  Alexandre Emile Jean Yersin was born in 1863 in the Swiss town of Aubonne, not far from Lake Geneva. His father, who had been a professor of natural history, died a few days before his birth. As a child, Alexandre showed an aptitude for scientific studies and had a keen interest in nature (a recurrent theme), often spending time collecting and studying insects. Yersin received his secondary education in Lausanne and began his early medical education at the university there but later attended the University of Marburg and completed his training at the Paris Faculty of Medicine.

  Right from the start of his medical career Yersin eschewed routine clinical work and decided to specialise in pathology. He became an assistant to Professor André Cornil, the pathologist at the Hôtel-Dieu Hospital in Paris, and it was while he was here that he suffered an accident that determined his future medical career and brought him in contact with Emile Roux. Yersin cut himself while performing an autopsy on a patient who had died of rabies.[12] An injection of Pasteur’s new rabies vaccine was administered by Emile Roux at the Pasteur Institute and this one event saved Yersin from an agonising death, and changed his life.

  Yersin saw the vaccine as miraculous and he was in awe of Pasteur and the scientists who worked with him. It became Yersin’s ambition to join both them and the quest that was taking place in the major European laboratories to find ways of combating the major diseases that humankind had always accepted as being a part of living and dying. Before joining Pasteur, Yersin spent some months during 1877 in Berlin continuing his bacteriological studies under the tuition of the other demi-god of science, Robert Koch. While there Yersin was able to learn and practise the new research methods and technical aspects of tissue staining that Koch had introduced and it was Yersin who introduced many of these to Pasteur’s laboratory.[13]

  In 1888 Emile Roux hired Alexandre Yersin as his assistant and, having been influenced by Robert Koch, Yersin began his first research project working on tuberculosis and the action of antiseptic and heat treatment on tubercle bacilli. Roux at this time began to focus on diphtheria and invited Yersin to collaborate with him. Some early research had been done on diphtheria and the bacillus had been discovered in 1883. The two scientists spent an arduous three years examining the toxic properties of the diphtheria bacillus and developing a procedure that enabled them to produce diphtheria toxin. During the time that they worked so intensively together Yersin and Roux became good friends. The results of their groundbreaking work were published in three classic papers, one in 1888, the next in 1890 and the last in 1891.

  Although Yersin’s standing in the scientific community was increasing rapidly, once the diphtheria project had been completed he was struck by a desire for travel and adventure, another trait many of the early medical pioneers had in common. He had found it difficult working within the constraints of a laboratory and did not approve of the imperious way in which Louis Pasteur directed the institute. Yersin was described as boyish and admitted to a desire to follow in the footsteps of Dr Livingstone, the British explorer.[14]

  After resigning in 1889, Yersin signed on as a ship’s doctor on a steamer bound for Saigon and Manila. Yersin made several voyages to Saigon, and like Albert Calmette, who had set up the Saigon branch of the Pasteur Institute, became fascinated by Indochina. He happily took charge of the institute when Calmette had to return to France in 1891. This position gave Yersin an opportunity to help fight disease in the country he had come to love and it also meant he could pursue both his scientific interests and his passion for exploration. He did travel to Europe in the winter of 1892 to visit both family and colleagues but found it so depressing and cold that he knew he could never return permanently to a conventional life. Emile Roux had planned a warm welcome for his young friend hoping to lure him back, but he soon became resigned to the fact that Yersin’s heart was now in the Far East.

  Yersin undertook three expeditions to the remote central region of Indochina, the first in 1892. The inveterate explorer often set out with inadequate supplies but despite the many hazards he encountered, which included a violent skirmish between armed Vietnamese and the French colonial authorities, he collected valuable information on the topography, flora and fauna of the region. He discovered the source of the Dong Nai River and the high plateau of Langbiang, where he established the village of Da Lat. The village would eventually become a city and, perhaps regrettably for Yersin, a vacation destination for Europeans. One thing that Yersin never failed to do on his journeys was to treat the sick wherever he found them and he believed it was his moral duty never to ask the poor for payment.

  While Yersin was immersed in his work in and around Saigon, in May 1894, during the third pandemic, plague spread from the mainland of China to the colony of Hong Kong and the death toll began to rise. As an employee of the colonial health service, the Corps de Santé des Colonies, Yersin was sent to Hong Kong to conduct research on the plague. He was not the first bacteriologist to arrive, however. The Japanese government’s mission landed in Hong Kong a few days earlier. Led by the eminent and experienced Shibasaburo Kitasato, the mission was well staffed and well organised and immediately gained the upper hand when they began work on 14 June, the day before Yersin arrived.

  Shibasaburo Kitasato, who was born in 1853 in Kumamoto on the island of Kyushu in Japan, had been educated at Kumamoto Medical School and completed his medical studies at the Imperial University of Tokyo in 1883. Following this, as a young researcher he did groundbreaking work when he moved to Berlin to work in Robert Koch’s laboratory from 1885 until 1891, research that contributed enormously to the understanding of disease and how the body fights infection. In 1890 Kitasato discovered a method of growing the tetanus bacillus in a pure culture and, with the bacteriologist Emil von Behring, developed tetanus and diphtheria antitoxins, substances that neutralise poisons produced by micro-organisms.

  After returning to Japan in 1891 the respected Kitasato founded an institute for the study of infectious diseases and he was working there when asked by his government to take up the challenge against the plague in Hong Kong as it represented a direct threat to Japan. The authorities in Hong Kong had ignored the early signs of the plague and by the time Kitasato and Yersin began work the disease was spreading rapidly, ravaging the colony. Because of his world-renowned research skills, and because it was in their interest to do so considering the enormity of the crisis, the British government allowed Kitasato unrestricted access to patients and to supplies. He was given personal support by Dr James Lowson, the Superintendent of the Government Civil Hospital, who immediately provided Kitasato’s team with a functioning laboratory.[15]

  Yersin’s situation in Hong Kong was the antithesis of Kitasato’s. There was no laboratory for Yersin. He and his ‘team’, a misnomer really, as there was only Yersin and two assistants, set up what equipment they had in a straw hut. Yersin had even less to work with when one of the assistants disappeared with the meagre funds Yersin had been allotted. Two great minds were trying to solve the same puzzle but any hope of collaboration on Yersin’s part was dashed when he paid a courtesy visit to Kitasato.[16] The meeting failed not just because of language difficulties but because reputations were at stake.

  The odds were stacked very heavily in Kitasato’s favour. Yersin found himself ostracised by the authorities and deliberately obstructed in his research. Because material from autopsies on plague victims was reserved for the Japanese mission, Yersin had great difficulty acquiring the specim
ens he needed to make progress with this research. With all the advantages Kitasato had, it is not surprising that within a few days of his arrival in Hong Kong he had isolated what he believed to be the bacterium that causes bubonic plague. He then confirmed his finding after applying Koch’s postulates to tests on experimental animals. Without delay and using the new communication medium, the telegraph, Kitasato cabled the Japanese Interior Minister and announced his discovery of the bacillus, Pasteurella pestis, to the local English press.

  What is astonishing is that despite his difficulties Yersin seems to have made the same discovery at the same time. However, before Yersin was able to get his findings into print in French journals, Kitasato had sent a paper on 7 July to London and his article appeared in The Lancet on 13 August 1894 complete with photographs.[17] It was barely two months after the discovery.

  And so the controversy about who discovered the bubonic plague bacillus began. People in different parts of the world credited one or the other scientist with the discovery, depending on the source of their information. Since then the validity of Kitasato’s original findings has been the subject of debate and the topic of much scientific literature. In 2002 Edward Marriott published Plague: A story of science, rivalry, and the scourge that won’t go away, in which he tried to piece together the events surrounding the discovery of the plague bacterium and the rivalry between Kitasato and Yersin. (The title also alludes to the fact that the plague, despite the best efforts of science is determined to stay with us.)

  Rightly or wrongly, Kitasato was originally acknowledged as the discoverer of Pasteurella pestis, named after Louis Pasteur, and Yersin’s work was seen as a confirmation of this.[18] It is impossible not to feel some sympathy for Yersin who, with grossly inadequate resources, solved one of the world’s greatest disease mysteries but because of circumstances was sidelined. It is interesting to note, however, that the pendulum has swung and Yersin and Kitasato are now credited with discovering the bacteria at the same time. The public affirmation of this is that since 1970 the bacillus has been known as Yersinia pestis, ‘Yersinia’ after Yersin, and ‘pestis’ after the Great Pestilence.