By Fritz Gerlich
Posted in Slate's Fray
You learned in school, as I did, that the Black Death, now known as bubonic plague, ravaged Europe in the 14th century, killing a third of its population. You also learned that the people of that time were helpless to contain the spread of the disease because they did not realize that the source of the infection was fleas carried by rats.
This has been, for about a century, the standard view of the greatest natural disaster in history. It has been increasingly questioned during the last 25 years, and I would judge that the critics have the stronger side of the argument.
The critics, whose views are conveniently summarized in Susan Scott and Christopher Duncan's Return of the Black Death, maintain that (1) the Black Death was not bubonic plague, but most likely a viral hemorrhagic diease similar to Ebola, Marburg and similar viral illnesses observed in Africa in this century, and (2) that it was not spread by rats and fleas, but by "droplet" transmission from one person to another--i.e., by coughs and sneezes, possibly by other body fluids as well.
As to the first issue, bubonic plague has been extensively studied in modern times. Its pathogen is the bacterium Yersinia pestis, first identified during an outbreak in India at the end of the 19th century. The plague is unquestionably a serious illness, causing high fever, terrible thirst, and the formation of "buboes," or swollen, painful lymph nodes. Before the advent of antibiotics, it was lethal to about 20% of sufferers. It is easily cured with the right antibiotics.
The "reservoir" of Yersinia, the place in nature that it survives between epidemic outbreaks that kill large numbers of its hosts, is wild rodent populations, many of whom do not seem to be affected by it. The standard theory is that fleas bite infected wild rodents, then are transfered to rodents that interact with people, as on farms or the edges of cities. When the flea bites the "domestic" rodent, it transfers the bacterium to it, thus moving the disease within range of man. Eventually another flea transfers the infection from the domestic rodent to a human victim. If this happens on a large enough scale, an epidemic results.
With this mode of transmission, bubonic plague is not especially contagious between people. Sufferers are typically not quarantined but are treated in open hospital wards. The plague is known, however, to have a somewhat uncommon communicable form, called "pneumonic plague." This occurs when the bacterium is widespread inside a patient and damages his lungs sufficiently to be expelled with his breath. (This cannot happen as long as the pathogen remains blood-borne; it can then be transfered only by a transfer of blood.) If it is then inhaled by someone else, it establishes itself in that person's lungs, and an extremely swift, destructive and invariably fatal illness follows. Modern studies indicate that bubonic plague turns pneumonic in about five per cent of cases. Those cases, of course, must be quarantined.
Why has this well-characterized and easily-contained modern disease been thought to be identical with the pandemic disease that killed a third of Europe in the 14th century (and continued to appear in more localized epidemics until the late 17th century)? The reasons surprisingly slender. The principal reason that the identification was made a century ago was simply that buboes are seen in the modern disease, and buboes were described as one of the most prominent symptoms of the historical plague. Buboes, however, are merely grossly swollen and discolored lymph nodes. Some swelling of lymph nodes happens in most infectious illnesses, and full-fledged buboes are observed in serious infectious illnesses besides bubonic plague. They are observed, for example, in some of the African hemorrhagic fevers.
As the controversy over the pathogen of the historical plague heated up, researchers sought to answer the question by biochemical analyses of samples thought to come from old plague victims. The results have been inconclusive. Some samples, it is claimed, did indeed contain DNA associated with Yersinia. But in other studies, not a single sample was found that could be confidently identified as Yersinia. (Some of the difficulty of analyzing ancient DNA is illustrated by a study that extracted DNA from a Viking tooth: DNA of over 20 different individuals was detected.) The critics raise sampling issues as well. It is not terribly easy, hundreds of years later, to be sure that a given skeleton belonged to a victim of the Black Death, either in its debut appearance or a later one. Some of the sites studied had been used as burial sites for almost a thousand years. There were other infectious illnesses that caused epidemics and led to mass burials. Some of the localities under study are known to have suffered localized outbreaks of bubonic plague--the modern illness--at later times; possibly upper levels in a burial site contaminated lower levels.
What about descriptions of the disease itself? How do they tally with the modern one? They tally in some respects and not in others. Fever and buboes have been mentioned. Another is spots, which may be red, purple, black, or mixed in color, that appear across portions of the body of most victims. Another is violent vomiting, sometimes of blood. But these symptoms are not unique to bubonic plague--all four may be found in other illnesses, including some hemorrhagic illnesses. There are also discrepancies between the historic plague symptoms and those of modern bubonic plague. One is a difference in lethality. As noted, modern bubonic plague kills about 20% of its victims; others may have a case so light as not to require any medical attention. The historical plague appears to have been much more lethal--something closer to 90% of its victims did not survive. Also, modern autopsies of bubonic plague victims indicate some, but not extensive, degradation of the internal organs. The few descriptions of autopsies of historical plague victims, however, indicate a shocking degree of internal damage--the whole viscera "rotten," "stinking," "full of pus and black fluid," etc. (These descriptions are from 17th century outbreaks.) This tallies better with modern hemorrhagic disease, in which victims die a ghastly death from literal decomposition of their organs.
The greatest discrepancy, however, lies in the factors pertaining to the transmission of the diseases. Modern bubonic plague is documented to have a very short incubation period--i.e., the interval between exposure and first symptoms--of two to six days. This is not consistent with what can be deduced about the spread of the Black Death and its aftershocks.
To begin with, the Black Death overwhelmed all of Europe in an incredibly short time--less than three years. It first appeared at Messina, in Sicily, in October, 1347. From there it radiated northwestwards, reaching Scandinavia and Ireland in 1350. It is possible to draw arc-like lines on a map of Europe, centered on Italy, that show roughly where the plague had been reported by a given date. Of course the actual transmission was more complicated than that. In some places the disease clearly traveled by land and in others by water, and so traveled at different rates. There were also areas that were never touched, or touched only lightly. But the plague kept its basic south-to-north and east-to-west directionality throughout, and it conquered Europe with a relentlessness and a speed that are amazing for times before any kind of automated travel. In fact, most people in the 14th century wouldn't have traveled farther than a few miles from their homes in their lives.
A short incubation period is not consistent with such reach, speed and lethality. A victim who became deathly ill within six days after exposure could not travel that far in the 14th century, when most people walked and even a rider not in a hurry would typically cover perhaps 20 miles per day. Sea voyages under some conditions might be faster, but then they might also be long and arduous, also. The ship that is supposed to have brought the Black Death to Europe had sailed from the Crimea, where some type of plague was reported raging. The voyage could not have taken less than four weeks. Yet the sailors were reported as asymptomatic when they arrived.
What is consistent with reach, speed and lethality is a much longer incubation period, during which the victim is infected and infectious, and does not know it. He, or she, may travel much farther and expose many more people, before succumbing. The effect multiplies geometrically as the chain of transmission lengthens. The greatest single reason that AIDS became a world-wide epidemic is its extraordinarily long incubation period--about 10 years. By the time the first cases were identified, literally millions of people were already infected. There was very little hope of getting on top of the disease by then, except by some type of cure, which has not yet been found.
Scott and Duncan present a fairly convincing argument that the historical plague had an incubation period of slightly more than 30 days. Their data come from English parish records of the 15th and 16th centuries. These records, in some places, meticulously recorded every single case of plague, the date the individual became ill, and the date s/he died (or recovered). In some places, they contain other information, such as who nursed whom, and who lived near whom. (There are no comparable data for the Black Death itself, but the symptoms of the disease were the same, and the later chroniclers seemed to have no doubt that they were witnessing the same disease.) By an extensive (and tedious) drawing of timelines, family relationships, and placement of homes, it is possible for them to show that people in all probability had to be exposed to the illness around a month before they themselves became ill.
Scott and Duncan note an interesting correspondence of their conclusion about incubation with historical fact. When the Black Death first hit Europe, some Italian cities imposed quarantines on suspected persons of 30 days. Fairly rapidly, this was changed to 40 days--and at 40 it stayed, not only in Italy but throughout Europe, and not only during the original plague but for three centuries after. While no contemporary source gives a specific reason for 40 days, it is a reasonable assumption that authorities observed that 40 days worked, 30 did not. Scott and Duncan compute that the average duration of the illness, from first symptom to death, was five days. Added to the 32 days they allow for incubation, the whole course of the illness would be 37 days, which would render the original 30-day quarantine ineffective, but fall within the 40-day quarantine. It also fits the anecdote about the Crimea-Messina connection. With a 32-day incubation period, the disease would have permitted the ship to make the voyage and the sailors still to look well when they arrived.
The short incubation of bubonic plague helps explain why, in well-documented modern appearances, it has been a disease of ports, and has rarely spread more than a few miles from the site of its initial appearance ashore. The disease appears too soon for infected people to get very far and infect very many others.
Both the speed of the Black Death and its universal reach are inconsistent with something else: the alleged transmission by rats and fleas. Epidemiologists know that a disease is spread fastest by person-to-person infection, and that air-borne or droplet-borne diseases will be the most infectious and the swiftest to spread. Bubonic plague, however, is spread chiefly by fleas carried by infected rats. Modern studies have been done on the movement of rodent-borne infections, including bubonic plague. Typically, they spread at the rate of somewhere between one and 12 miles per year. At that rate it would have taken the Black Death about a century to spread all the way across Europe. One reason for this slow movement is that rats, unlike the reservoir rodent species for bubonic plague, are sickened and killed by Yersinia. Given its short incubation period, an infected rat does not have long to pass it to someone else, including a man, depending as it does on its fleas to make the actual transfer. And, in fact, huge rat mortality has been noted in some bubonic outbreaks. None was ever mentioned by observers of the historical plague.
Another fact disfavoring the rat idea is that the people who faced the Black Death and the later attacks of the same disease were very aware that they had to avoid the presence of infected persons. This appeared in such shocking form as husbands abandoning ill wives and parents abandoning sick children, so terrified were they of getting the disease themselves. Medieval and later people could not make a scientific analysis of the plague, but they made common-sense observations to help them avoid it. Their unanimous testimony, by their deeds, is that close personal contact with an infected person put one at greatest risk. Why would they have thought so, if people who had had zero exposure regularly came down with the disease, as would have to have happened if fleas really posed the risk?
Some bubonic defenders point to the pneumonic form to explain the plague's spread. Certainly, pnuemonic plague is a much closer fit with the historical facts than classic bubonic plague is. But its usefulness as an explanation is limited. First, the pneumonic form is uncommon; only five per cent of people would have been infectious under this hypothesis. Both the plague's rapid spread and the universal fear of infected persons it inspired argue against pneumonic plague's being the villain. Furthermore, pneumonic plague does not appear by itself; it is observed only in the context of a wider bubonic epidemic. One reason for its inability to stand alone is its extraordinary lethality: 100% of victims die, and they die within an average of three days after exposure. A disease that does that to its victims simply ensures its own demise, since its hosts die before they can efficiently spread the pathogen.
There is a final bit of evidence against rat-borne bubonic plague causing the Black Death. The plague touched Iceland in the 15th century, killing an estimated 60% of its population. Yet Iceland is known not to have harbored any rats at that time. And fleas do not live in a cold climate. In Alaska, we don't deflea our dogs because we just don't have that problem.
Scott and Duncan are just guessing when they attribute the historical plague to "something very like" the filoviruses of Ebola and Marburg. There is no direct evidence of that, but it is suggested by the symptoms. It appears that the incubation period for these diseases is highly variable, ranging from a few days to over a month, which allows for one of them to have caused the plague, but does not prove it.
Today scientists speak of "emerging diseases," or diseases that either are new or re-emerged after a long time, at least several generations, of dormancy. AIDS was an emerging disease in the 1970's and early 1980's. SARS is another example, and the much-watched avian flu could prove to be another, if it jumps to humans and becomes contagious. The Black Death was the mother of all emerging diseases. No one who lived through it had ever seen anything like it. And while the plague was recognized when it returned in the succeeding centuries, those outbreaks were often spoken of in similar apocalyptic terms, so distinctive and so frightening was the disease. The study of the origins of the Black Death is a major part of how we should understand emerging diseases. Identifying Yersinia as the historical pathogen could lead to preparations that are useless if the Black Death was really something else, and it returns once again.