Bubonic vs pneumonic plague: what was the difference?

The Black Death is often described as if it were a single disease with a single set of symptoms. In fact, the medieval pandemic involved at least three clinical forms of the same disease, each caused by the same bacterium, Yersinia pestis, but each produced by a different route of infection, and each with a different pattern of symptoms and mortality. The differences between the three forms are essential to understanding both the speed of the Black Death’s spread and the terror it inspired. The form of the disease a patient developed was, in many cases, the difference between a painful recovery and a death within twenty-four hours.

The wider context of the pandemic is set out in the overview of the Black Death. The geographical spread of the disease is treated in How did the Black Death spread across Europe?. The medical response is examined in Medieval medical responses to the Black Death. The recurring waves of plague that followed the original pandemic are discussed in Why did the plague return in waves?.

A Single Bacterium, Three Diseases

All three forms of plague are caused by Yersinia pestis, a bacterium that was identified in 1894 by the French-Swiss bacteriologist Alexandre Yersin during an outbreak of plague in Hong Kong. The bacterium lives primarily in rodents, and it is transmitted to humans through the bite of an infected flea. The most important rodent reservoir in medieval Europe was the black rat (Rattus rattus), a species that lived in close association with humans, infesting houses, granaries, and ships. The most important flea vector was Xenopsylla cheopis, the Oriental rat flea, which would readily feed on humans when its preferred rat hosts died.

Once the bacterium enters the human body, it can produce three different clinical pictures, depending on the route of infection. The most common, accounting for the bulk of cases in any given outbreak, is bubonic plague, which results from the bite of an infected flea. The second is pneumonic plague, which results from the inhalation of respiratory droplets from an infected person. The third is septicemic plague, which results from a massive infection of the bloodstream, often as a complication of the bubonic form. The three forms are not, in 14th-century Europe, sharply distinct. A patient with bubonic plague may develop pneumonic or septicemic complications, and a patient with primary pneumonic plague may develop septicemia. The clinical categories are useful for diagnosis and for epidemiological analysis, but they are not exclusive.

The identification of Yersinia pestis as the cause of the Black Death was one of the great achievements of nineteenth- and twentieth-century medical science. The identification was, however, complicated by a long historiographical debate, in which some historians, notably Graham Twigg in The Black Death: A Biological Reappraisal (1984) and John Kelly in The Great Mortality (2005), argued that the Black Death was not, in fact, plague. The argument was based on the apparent speed of the medieval outbreaks, on the absence of rat mortality in some accounts, and on the description of the symptoms in the chronicles. The argument is now largely rejected. The genetic work of Mark Achtman and others, summarised in a series of papers in Nature in 2010–2011, has shown that the medieval plague was caused by a strain of Yersinia pestis that is closely related to the modern strains, and the epidemiological work of Ole J. Benedictow has shown that the speed of the medieval outbreaks is consistent with a modern understanding of plague epidemiology.

The Bubo and Its Symptoms

Bubonic plague is the form that gives the Black Death its most characteristic symptom, the painful swelling called a bubo. The bubo is a swollen lymph node, usually in the groin, the armpit, or the neck, where the bacteria have been filtered out of the lymph after multiplying at the site of the flea bite. The swellings can be as large as an egg or even an orange, and they are intensely painful, hot to the touch, and often dark blue or black with the bleeding that occurs beneath the skin. It is this feature, more than any other, that gave the disease its later popular name.

The other symptoms of bubonic plague develop within two to six days of the original flea bite, the period known as the incubation period. The patient develops a high fever, often with violent chills. There is a profound headache, a sense of weakness, and a general aching of the limbs. The buboes begin to swell, and the patient may vomit blood. The mental state is often affected, with confusion, delirium, and vivid visions. The pulse weakens, the breath comes in short gasps, and the patient often complains of an unquenchable thirst. Death, when it comes, usually comes on the third to fifth day of illness, and is preceded by a deep coma.

The contemporary descriptions of the symptoms are vivid and consistent. The Avignon-based physician Guy de Chauliac, personal doctor to Pope Clement VI and himself a survivor of the Black Death, described the buboes in his Chirurgia Magna (1363) as “stony” and noted that the patient would “wander in his mind” and “spit blood.” The Florentine chronicler Marchionne di Coppo Stefani described the disease in the Cronaca fiorentina: “the patients had large buboes under the arms and in the groins, and these were followed by putrid fever, and the patients died in three days.” The Sienese chronicler Agnolo di Tura recorded that “the breath became fetid” and that the patients “vomited blood.” The consistency of the accounts is one of the strongest pieces of evidence that the Black Death was, in fact, bubonic plague.

The case-fatality rate of untreated bubonic plague is high, generally estimated at 30% to 90%. In a population with no acquired immunity, such as fourteenth-century Europe, the death rate among those infected is likely to have been at the higher end of this range. The mortality of the Black Death in 1348 was therefore a function both of the high case-fatality rate of the disease and of the lack of acquired immunity in the population. The two factors reinforced each other, and the result was a mortality that has no parallel in the modern history of plague.

Pneumonic Plague: The Breath-Borne Killer

Pneumonic plague is the most lethal and the most contagious form of the disease. It is caused when the bacterium infects the lungs, either as a primary infection (acquired by inhaling respiratory droplets from another infected person) or as a secondary infection (when the bacteria from a bubonic infection spread to the lungs through the bloodstream). The symptoms are those of a violent pneumonia: a high fever, a painful cough, the expectoration of blood, and a profound difficulty in breathing. The patient often turns blue from lack of oxygen, and death usually occurs within two to three days.

Pneumonic plague is, crucially, transmissible directly from person to person. The respiratory droplets produced by coughing and sneezing contain the bacteria, and a person standing within a meter or two of an infected patient can become infected simply by breathing. The case-fatality rate of pneumonic plague, in the absence of treatment, is essentially 100%. Medieval doctors, who could do nothing for bubonic patients, were completely helpless in the face of pneumonic plague. The chronicler Marchionne di Coppo Stefani described a case in Florence in which a priest “began to spit blood, and within a day he was dead, and all those who had been near him died in the same way.” The passage is one of the most often quoted descriptions of pneumonic plague in the medieval chronicles.

The relative role of pneumonic plague in the Black Death of 1347–1351 is debated. The historian Ole J. Benedictow, in The Black Death 1346–1353 (2004), argued that pneumonic plague played a much larger role in the medieval pandemic than had previously been thought, and that the pneumonic form was responsible for the speed of the Black Death’s spread. The historian Samuel K. Cohn Jr., in The Black Death Transformed (2002), argued the opposite, on the basis of the chroniclers’ emphasis on the buboes, and suggested that pneumonic plague was a relatively rare complication of bubonic plague. The most likely truth is that the original Black Death involved a mix of bubonic and pneumonic cases, and that pneumonic cases became more common in the winter months, when the bubonic cycle slowed and person-to-person transmission became the dominant mode of spread. The modern epidemiological work on the spread of plague in the Indian outbreaks of the late nineteenth and early twentieth centuries, and on the Madagascar outbreaks of the late twentieth century, suggests that a mixed epidemic is the most common form of large-scale plague outbreaks.

Septicemic Plague: The Black Blood

Septicemic plague is the rarest and the most rapidly fatal of the three forms. It is caused when the bacteria enter the bloodstream directly, often through a flea bite or a cut, and multiply so rapidly that the body’s defences are overwhelmed within hours. The symptoms are a high fever, abdominal pain, vomiting of blood, and a profound shock. The skin often turns black as the tissues die. Death usually occurs within twenty-four hours of the first symptoms, often before any buboes have had time to form.

Septicemic plague is rarely transmitted directly from person to person. It is essentially a complication of bubonic plague, and it accounts for a small percentage of cases in any given outbreak. It was, however, the most terrifying form of the disease for medieval doctors, who had no way of distinguishing it from bubonic plague until the patient was already dying. The dark discolouration of the skin produced by the disease is one of the possible origins of the name “Black Death,” although the more common explanation is that the name refers to the dark discolouration of the buboes in bubonic plague. The Septicemic form of the disease is described in the chronicles as a particularly rapid form of death, often associated with a profound blackening of the skin.

The modern understanding of septicemic plague is that it is a complication of bubonic or pneumonic plague in which the bacteria overwhelm the immune system and multiply in the bloodstream. The case-fatality rate is essentially 100%, and the disease is usually fatal within twenty-four hours. The disease is rare, but it is a useful reminder that the medieval plague was not a single, well-defined disease, but a spectrum of clinical pictures, each with a different prognosis and a different transmission pattern.

The Course of the Disease in a Medieval Patient

A typical case of bubonic plague in 1348 would have progressed roughly as follows. The patient, having been bitten by an infected flea some days before, would have noticed the first symptoms — fever, chills, headache, and weakness. Within a day or two, the buboes would have begun to swell, and the pain would have become intense. The patient would have complained of thirst and of an internal heat. Within three or four days, the mental state would have begun to deteriorate, with confusion, hallucinations, and a kind of wild delirium. The family and the doctor, who could do little but bleed the patient, apply poultices, and pray, would have watched helplessly as the disease progressed. Death, when it came, would have come suddenly, often in a final convulsion, and the body would have been removed for burial as quickly as possible to prevent further infection.

The treatment of the disease, in 1348, was the standard Galenic treatment of the medieval West: bleeding, purging, sweating, and the application of poultices to the buboes. The treatment is examined in detail in Medieval medical responses to the Black Death. The treatment was, in retrospect, often harmful: bleeding a patient who was already weak from fever and dehydration accelerated the decline. The mortality of patients who were subjected to the full battery of medieval treatments was probably higher than the mortality of those who were simply left alone.

The Mix That Made the Black Death

The differences between the three forms of plague matter for several reasons. First, they help to explain the speed and pattern of the Black Death’s spread. Bubonic plague, transmitted by rat fleas, moves at the speed of rats and ships, which is to say at the speed of medieval trade. Pneumonic plague, transmitted by respiratory droplets, moves at the speed of human contact, which is much faster. The Black Death moved at both speeds simultaneously, and the mix of forms helped the disease to spread rapidly and to penetrate deeply into the population.

Second, the differences help to explain the terror the disease inspired. Bubonic plague, with its high mortality and its gruesome symptoms, was terrifying enough. Pneumonic plague, with its near-100% fatality and its rapid person-to-person spread, was even more terrifying, and the knowledge that a single breath from an infected person could be enough to kill must have made the disease feel like the very embodiment of divine wrath. Septicemic plague, with its rapid and mysterious course, was the most terrifying of all, because there was no warning and no time for the patient to prepare for death.

Third, the differences help to explain the epidemiology of the recurring outbreaks. Bubonic plague, which depends on the rat-flea-human cycle, is more common in the summer and autumn, when the rat population is most active. Pneumonic plague, which depends on person-to-person transmission, is more common in the winter, when people are confined indoors. The mix of forms in any given outbreak is a function of the climate, the season, and the local conditions. The understanding of the mix of forms is one of the most important pieces of knowledge that the modern historian of plague brings to the medieval sources.

References

Benedictow, Ole J. The Black Death 1346–1353: The Complete History. Boydell Press, 2004.
Cohn, Samuel K. Jr. The Black Death Transformed: Disease and Culture in Early Renaissance Europe. Oxford University Press, 2002.
Kelly, John. The Great Mortality: An Intimate History of the Black Death. HarperCollins, 2005.
Twigg, Graham. The Black Death: A Biological Reappraisal. Batsford, 1984.
Horrox, Rosemary, trans. and ed. The Black Death. Manchester University Press, 1994.