Well over three hundred years have gone by since the plague died out as an indigenous disease in Britain. It lingers on only as a rare rural infection in Madagascar, Tanzania, Kenya, Zaire, Botswana, Uganda, Bolivia, Brazil, Peru, the US, Vietnam, China, Mongolia, Kazakhstan and Burma. Worldwide, the annual number of human cases rarely exceeds a couple of thousand. As the Oxford Textbook of Medicine says: ‘The major animal reservoirs are urban rats as well as rural rodents including ground squirrels and prairie dogs. The Oriental rat flea Xenopsylla cheopis is the most efficient vector. When bitten by a rodent flea humans become an accidental host and play no role in disease transmission except in rare epidemics of pneumonic plague.’
Our understanding of Yersinia pestis and its doings is very incomplete. We still cannot explain why the plague caused havoc in London in 1665 but not in 1664, or why it faded away in 1666; or why epidemics of pneumonic plague – the only form of the disease that spreads easily from person to person – are rare; or why they happen at all.
Contemplating historical uncertainties about the plague has useful contemporary by-products. Those trying to estimate how many it killed in the mid-14th century face exactly the same problems as those trying to discover how many Iraqis have died violent deaths since the invasion of March 2003. In both cases the machinery needed to collect accurate mortality data was absent: in medieval Europe because it had not yet been developed, and in Iraq because it was deliberately destroyed. People continue to die from natural causes during epidemics, wars and insurrections, so the problem is to determine the excess mortality. When there are no reliable sources of information for the population as a whole, this is very hard. But the difficulty is made even greater by the desire of some estimators and users of estimates to force the figures in particular directions. As Hastings Rashdall put it in The Universities of Europe in the Middle Ages: ‘The medieval mind was prone to exaggerate, especially where figures are concerned. It delighted in good round numbers, and was accustomed to make confident statements entirely without adequate data.’ So John Wyclif’s claim in the 1370s that Oxford had once had 60,000 students but that after the Black Death the number had fallen to fewer than 3000 can be confidently dismissed.
The estimate of 98,000 post-invasion excess deaths in Iraq, made by Les Roberts and his colleagues and published in the Lancet last November, has come in for similar criticism. Tony Blair prefers figures from the Iraqi Ministry of Health showing that 3853 civilians were killed between April and October 2004, and his government refers with statistical approval to the Iraqi Body Count Database, which reports 16,352 civilian deaths by 1 November, 2004 – about half the number killed by aerial attack on London during the Second World War. Roberts’s figures have been criticised on two grounds: that he multiplied up from a random sample of population clusters to get a figure for the whole country, and that the people in the clusters his team interviewed were not representative of the nation as a whole. The first is an entirely respectable statistical technique; by attacking it, politicians demonstrate only their ignorance. The second, however, is reasonable comment: extrapolators always wish that their samples were larger. But interviewing families in Iraq in 2004 was very risky. In principle, similar problems attend studies on the Black Death. ‘Although most statements of the number of victims are unreliable,’ August Hirsch wrote in his Handbook of Geographical and Historical Pathology (1881), ‘yet there is information as to the mortality given for a few small centres, which may be trusted, and may serve as an approximate measure of the mortality in general.’
Medieval records are still being profitably mined for evidence of this kind. In Late Medieval Oxford (1992), W.J. Courtenay concluded that
the rate of mortality among known students and masters in the faculty of theology (of Oxford) seems to have paralleled the rate of 25-27 per cent for the upper levels of English society (the episcopate and tenants in chief) not the rate of 40 per cent which can be documented for the rural poor and the clergy who served in urban and rural areas.
The resilience of medieval organisations is demonstrated by their ability to survive despite such mortality rates. Universities continued to be founded in this period, including Florence (1349), Perpignan (1350), Huesca (1354), Siena (1357), Pavia (1361), Cracow (1364), Orange (1365) and Vienna (1365). In Cambridge, Gonville Hall, Trinity Hall and Corpus Christi College were founded in 1348, 1350 and 1352 respectively.
But was the plague the work of Yersinia pestis? Some 21st-century sceptics think not. The rate at which the disease spread from place to place during the plague epidemics in the 14th and 17th centuries, and contemporary records of the symptomatology and mortality of the disease, have persuaded Susan Scott and Christopher Duncan (and others) that another parasite must have been at work. There can be no doubt that not everyone who died during these outbreaks died of the plague itself. But the sceptics dismiss strong evidence of Yersinia pestis too lightly. Pepys describes an infected servant as having a ‘bubo on his right groin and two spots on his right thigh’, which fits a Yersinia pestis infection perfectly. And a hundred years earlier, the account of the clinical features of the plague given in the first medical book published in Scotland, Ane Breve Descriptionn of the Pest by Gilbert Skeyne of Kings College, Aberdeen, is just as clear: ‘There are many signs which show a man infected by plague . . . behind the ears, under the armpits, or near their private parts most frequently appear abscesses called buboes.’ Compare this account with J.W.H. Chun’s account, in Plague: A Manual for Medical and Public Health Workers (1936), of cases diagnosed bacteriologically in the pre-antibiotic era, an account personally informed by Chun’s work in the Manchurian epidemics of 1910-11, 1920-21 and 1928: ‘In addition to general symptoms (sudden onset of fever, thirst, vomiting, diarrhoea, headache and prostration) . . . swellings appear in the lymphatic glands. The usual places are the groin, axilla, or side of the neck . . . The skin over the bubo is hot and red . . . the glandular mass is very painful and tender to the touch.’ The combination of general prostration and localised buboes points to Yersinia pestis and nothing else.
Yet, as Chun makes clear, plague can take other clinical forms. Infection can be mild, or septicaemic (the patient is overwhelmed before buboes appear), or pneumonic, another lethal form in which the patient’s bloody sputum is loaded with plague bacilli, making it and them dangerous to other people. Some mortally ill patients became agitated and tried to run away, usually hampered by a staggering gait. All these 20th-century features appear regularly in accounts of historic plagues. And there is evidence from the grave, too. Didier Raoult and colleagues have examined 14th-century skeletons from extramural multiple burials at Montpellier and found Yersinia pestis DNA. The sceptics say that the remains may have been contaminated. It’s possible, but unlikely; these positive results should not be dismissed lightly.
Lloyd and Dorothy Moote and Wendy Orent don’t doubt that Yersinia was responsible. Lloyd Moote is a historian of the 17th century, Dorothy Moote a microbiologist and teacher. Their aim was to supplant Defoe’s Journal of the Plague Year – a fictional account based on real documents but passed off as a rediscovered eyewitness account – with an unembellished story of the events in London from 1664 to the beginning of 1666. The Mootes’ enthusiasm at their archival discoveries flavours their lively account of the Plague Year as increasing numbers of Londoners died in the hot summer – the epidemic peaked in August and September 1665.
The Mootes give prominent acknowledgments to British medical historians. Wendy Orent has turned instead to American and Russian microbiologists and epidemiologists. Although her account takes a wide-ranging historical approach, the thread running through it is the Soviet biological weapons programme. Marmots, susliks, tarabagans (furry rodents that live in Central Asia), great gerbils, rats and prairie dogs all make an appearance as the wild hosts of Yersinia pestis. ‘The Oriental rat flea, Xenopsylla cheopis,’ she says, ‘haunts this book like a tiny destroying angel.’ It is the best transmitter of the bacterium from rat to rat, or from rat to human, because when the flea has fed on a plague sufferer, the bacterium grows in its stomach, blocking it. The hungry flea then feeds again, regurgitating Yersinia in its saliva into the new host as it tries to take its next meal.
Orent’s account is enlivened by her descriptions of plague scientists such as Alexandre Yersin, the Swiss-born co-discoverer of the plague bacillus in Hong Kong in 1894 and, later, the director of the Pasteur Institute at Nha Trang in Vietnam, where he died in 1943. Orent is probably right to say that Yersin’s demonstration of the bacterium was clearer than the one given at the same time by Shibasaburo Kitasato, also in Hong Kong, but her claim that Yersin was the superior scientist is unfair. Kitasato was the first, in 1889, to grow the tetanus bacillus – a technical tour de force which ranks him at the top of the class, too, along with Charles Rothschild, who discovered Xenopsylla cheopis in the Sudan in 1901. ‘A grand time up at Shendi some 100m north of Khartoum,’ Rothschild wrote home. ‘We bagged 600 mammals and birds, 500 fleas and a fair lot of Coleoptera and Lepidoptera. The faalin Arabs are weird folk . . . They sew their unmarried women folk up to ensure their keeping virtuous. They also preserve the penis of the crocodile in honey and eat it as an aphrodisiac.’ Rothschild – the father of Miriam Rothschild, also an entomologist, who died in January – described about five hundred new species and subspecies of flea, and had three genera and seven species as well as a tick, a fly and a spider named after him.
Yersin, Kitasato and Rothschild made their discoveries during the third plague pandemic (the first was the Justinian, starting in 542; the second began with the Black Death), which provided the clinical material and political stimulus to work out the natural history of the disease. Starting towards the end of the 19th century, the pandemic ground on into the first quarter of the 20th. It killed 12.5 million people in India. The Plague Research Commission there showed the connection between humans, rats, fleas and Yersinia pestis. Now the ‘two spots on the right thigh’ and a ‘bubo on the right groin’ described by Pepys could be explained. The first were infected flea bites; the second the consequence of the spread of the bacterium up the leg into the inguinal lymph glands.
The third pandemic was worldwide. It reached its furthest north in August 1900 when it killed the wife and grandchild of a dock labourer who lived on the south side of Glasgow. Four people were infected at the wake, and by the end of September there had been 16 deaths out of 36 cases. Wakes were banned, houses and closes were whitewashed, and rats were hunted: 18 with plague were found. Medals were presented to hospital staff when the last patient had been discharged. The disease returned the following autumn, however, with nine cases in its original location, and one at a city-centre hotel, where infected rats were found. It was last imported in 1911, when a foreign seaman on a ship docked in Govan fell ill. It has never been back, a welcome reduction in Scottish biodiversity.
But rodents and their fleas have been more active elsewhere. For example, the Gallup Indian Medical Center in western New Mexico saw 19 cases of bubonic plague and eight of septicaemic in Navahos between 1965 and 1989. And in Madagascar an outbreak in 1997 showed the danger of ‘complementary’ medicine as well as wakes. A woodcutter developed bubonic plague and consulted a traditional healer. As part of his therapy the healer made a cut over the patient’s abdomen and sucked some of his blood. The patient died early next morning. The healer fell ill and died four days later, having infected his wife and son and another of his patients. They also died. Eight others who attended the healer’s funeral fell ill, as well as the son and wife of one of them, their nurse, and the son of the healer’s second patient. In total eight of the 18 cases died. But only 8.4 per cent of possible contacts were infected.
Plague is nasty when it breaks out, but outbreaks don’t last long. Modern conditions are not right for a pandemic. But they are still in place for panic. In 1994, there was a pneumonia outbreak in Surat, in India, after torrential rains had caused the river Tapti to flood the city. Plague was suspected. Trains, buses and lorries filled with immigrant workers leaving ‘Diamond City’ as fast as they could. The doctors had already gone. An anonymous, highly placed official was quoted in the Hindustan Times as saying: ‘We already know that the Surat strain was not Indian. We cannot rule out the possibility of militants purchasing the organism from a Kazakhstan company and releasing it in Surat.’ Fifty-six people died in the outbreak, which subsided as mysteriously as it had begun. Whether it was plague is difficult to say: Yersinia pestis was never isolated from any of the cases.
Orent takes a pessimistic view of bioterrorism and plague. She believes her ex-Soviet informants when they tell her that they discovered how to develop and grow particularly lethal strains of Yersinia pestis. We should be sceptical about such claims, however. Orent reminds us of the malign influence of Trofim Lysenko on Soviet biology. His brand of Lamarckism made Soviet biology second-rate and it is taking a long time to recover.
The Soviets were not alone in considering the military use of Yersinia pestis. Geoffrey Bacon, a scientist in the Microbial Genetics Section of the UK War Department’s Microbiological Research Establishment at Porton Down, died in 1962 of plague caught at work.
Plague in the 21st century is a shadow of its former self. As a pandemic threat it has been replaced by influenza (which needs neither rats nor fleas) and as a microbial killer by HIV (which needs only unprotected sex). It is much more of a threat to prairie dogs than to people, and is in essence a rarity, with very specialised risk factors for catching it (closeness to rodents). Its grand resurgence is improbable: soap and water have seen to that.