Splendid Exchange, A

by Bernstein, William L

  Of the two, Cairo was described by European travelers as the more vibrant, with narrow, winding streets filled with traders from Turkey, Arabia, Yemen, Persia, Italy, France, and India and reeking of the aromatic treasures of the Orient. Then, as now, traders took time off from bazaars pulsating with the rhythms of commerce to ride out to gawk at the Pyramids: “All along the way from Cairo were gardens full of date palms, orange, lemon, and pomegranate trees—a delight to the eye.”34

  The origins of the Karimi are lost to history, and their commercial interactions are equally opaque, but they form the essential link in our understanding of the medieval world’s greatest source of concentrated wealth. The historical record suggests that sometime around 1150, toward the end of the Fatimid Empire, this group reached a critical mass, possibly by virtue of its ability to purchase the protection of the Fatimid navy in the pirate-infested waters of the Red Sea and Bab el Mandeb. Smaller traders, such as the Jewish merchants of the Geniza papers, could not afford such expensive naval cover and were probably muscled aside by the Karimi. It is not known whether the Karimi were originally Hindu or Muslim, Indian or Egyptian, or even whether they were primarily merchants or shipowners, although according to the preponderance of the data they were the latter. The Indian and Hindu origins of the group are suggested by the fact that the term seems to derive from the Tamil word for business affairs, karyam.35

  Somehow, by the Mamluk period the Karimi had evolved into a predominantly Arab Muslim, but by no means exclusively Egyptian, group known far and wide as “the merchants of pepper and spices,” and had obtained command of the trade between Yemen and Egypt. A cooperative group of family enterprises handed from father to son and bound together by the commercial and social strictures of Islam and the special requirements of the spice trade, they established huge funduqs all along their long supply lines through the Red Sea. Based primarily at its ends in both Yemen and in Egypt, this chain snaked through many ports and way stations along the familiar ancient route that ran up the Red Sea to its Egyptian coast, across the desert by caravan, and then down the Nile. One thirteenth-century merchant, Muhammad bin Abd al-Rahman bin Ismail, spent his life shuttling among Syria, Mecca, Egypt, Iraq, and the Gulf states—nothing special for the time—but also made three separate journeys to China. He began his career worth five hundred dinars and ended it worth fifty thousand.36

  Throughout the Muslim world, to “resemble the merchants of the Karimi” carried the same meaning as “rich as Rockefeller” in the early twentieth century. Many Karimi fortunes were estimated in excess of a million dinars, and one merchant—Yasir al-Balisi—was worth about ten million dinars, or nearly a half billion dollars in today’s money, an almost unimaginable amount of wealth in the preindustrial world.37 Karimi money built many a mosque, school, and hospital in Alexandria, Cairo, Mecca, and Jeddah. But by far the largest flows of Karimi money went to the state for military operations. When the Syrians rose against the Mamluks in 1352, and when the murderous Tamerlane threatened the Levant in 1394, three leading Karimi merchants financed Egyptian victories.38

  Eventually, like all empires, the Mamluks grew greedy, corrupt, and unable to keep their hands out of the till; in 1428 Sultan Barsbay seized the spice monopoly from the Karimi and reduced them to the status of agents. In 1453, the Ottomans finally took Constantinople and shut off all trade with the Christians, but by then the jig was nearly up for the Muslim-Italian spice trade. The Portuguese were by then crawling down Africa’s western coast; Bartholomew Diaz would double the southern cape in 1488, and a decade later da Gama would break into the Indian Ocean, ending forever the Muslim monopoly of Asian trade with the West.

  The most momentous and lasting legacy of the spice-slave trade exploded out of a lethal gift bestowed by the Mongols on the Genoese at their newly established Black Sea port of Kaffa. Remember that name, for it would resonate with the deaths of millions of Europeans, the collapse of Mongol rule in Asia, the erosion of the Muslim trading empire, and ultimately, the phoenixlike rise of the West.

  6

  THE DISEASE OF TRADE

  Kaffa resembled a medieval version of the American frontier railhead, the last European city before the border with the vast Mongol khanates that spread all the way east to China. Around 1266, the Horde—the Mongol empire of northwestern Asia and eastern Europe—sold the city’s site to the Genoese, who valued its location on the Crimean Peninsula at the western terminus of the Silk Road. From Kaffa’s wharves, merchants shipped slaves to Egypt and the luxuries of the Orient to Italy, France, and even the Atlantic ports of northern Europe.

  The Mongols, observing Kaffa’s prosperity under the Italians, suffered from seller’s regret. They could not resist ravaging it, and an epic tug-of-war over this newly valuable piece of real estate ensued. The Horde’s khan, Toqtai, found his pretext for plunder in the enslavement and exportation of his Turkic brothers and sisters. In 1307 he arrested the Italian residents in his capital at Sarai, some seven hundred miles east of Kaffa; later that same year, the Horde besieged Kaffa itself. The Italians resisted until 1308, when they burned and abandoned the city. After the Mongols had completed their pillage, the Genoese rebuilt it.

  Just east of Kaffa, and thus more exposed to the Horde, was the Venetian slave-buying outpost of Tana. When it was bombarded in 1343, the Italians there fled west to Kaffa and presented Kipchak, the local Turkic ally of the Horde, with an even fatter opportunity. Over the next three years, Kipchak intermittently besieged Kaffa with his fearsome catapults. He failed. After the disaster of 1308, the Genoese had strengthened the city’s maritime lifeline through the Bosphorus and had reinforced its ramparts with a set of two massive concentric walls.

  Unbeknownst to either side, a doomsday weapon had just arrived from the East to inflict defeat on both sides. Initially, it devastated the attackers and provided blessed relief to the Italians huddled in Kaffa. But soon enough, it killed the defenders too, and then sailed silently south on Genoese galleys to visit ashen ruin, first on Europe and next on the realm of the Prophet.

  The plague bacillus, Yersinia pestis, like many human pathogens, spends most of its time in an “animal reservoir,” a population of chronically infected rodents. During the medieval period, the ground squirrels and marmots of the Himalayan foothills, the Asian steppes, and the Great Lakes region of Africa served this function for the bacillus. Probably the most important of these animals was the tarabagan, a burrowing animal that most resembles an obese squirrel, grows to two feet in length, weighs up to eighteen pounds, and hibernates in winter.

  For millennia, the local inhabitants of the steppe kept their distance from infected rodents, easily identified by their sluggish behavior. Occasionally, however, this cultural barrier to infection broke down, most often when outsiders unfamiliar with local custom hunted the diseased animals. When this occurred, the black death seared the land.1

  We owe our modern appreciation of the origins and historical effects of infectious disease to the great historian William H. McNeill of the University of Chicago. Sometime around 1955, while reviewing the defeat of the Aztecs by Hernán Cortés in 1521, he puzzled over how a population of millions, many of them fierce and ruthless fighters, could have been defeated by a force of only six hundred Spaniards. True, the horses, guns, and steel swords of the Europeans conferred a great advantage, but McNeill sensed that something else must have been going on.

  In fact, the Aztecs had defeated Cortés the year before at the capital city of Tenochtitlán and forced the Spanish to retreat—the infamous noche triste. Four months later, a smallpox epidemic swept through the Aztec nation. When McNeill came across mention of the death from smallpox of the victorious Aztec commander, the steel trap of his mind snapped shut: in an instant, he grasped the role of disease in the Spanish conquest of America and opened up a new dimension in our understanding of world history.

  McNeill realized that what had happened both in Tenochtitlán and in Europe two centuries earlier were identical p
henomena—the catastrophic introduction of a new disease into a population lacking immunity to it. He elucidated the mechanics of these collisions of civilizations, in which trade often provided the primary motive force.

  As is all too clear today, commerce and travel (as well as the increased population densities of the modern world) can spread pathogens, both novel and well-established, among continents with frightening speed. In many ways, the situation in the ancient and premodern world was even more dangerous. Back then, the world was an epidemiologic tinderbox consisting of several completely separate geographic “disease pools.” The populations within each pool were reasonably resistant to its organisms, but not to those from other pools; an organism that had been benignly endemic in one nation for millennia could visit apocalypse several hundred miles away. As world commerce blossomed between the fourteenth and eighteenth centuries, the world’s existing disease pools mixed together, with disastrous results. The good news is that today, relatively little further mixing of existing organisms can occur; pandemics result only when an organism from a nonhuman host, such as the HIV virus, mutates and acquires the ability to infect humans. This is a much higher bar than in the pre-Columbian era, when a merchant, sailor, or rodent from a neighboring disease pool could touch off a deadly epidemic.

  McNeill seized on an episode, which began in 1859, when British settlers introduced rabbits into Australia, desiring to alleviate their homesickness for the English countryside and to have a familiar animal to hunt and eat. These adorable animals, unfortunately, found no predators in their new home. They multiplied, as rabbits are wont to do, stripped the continent of its scant and fragile pasturage, and threatened the nascent sheep industry. Fences, poisons, traps, and rifles proved of little use in keeping down the population of a creature that can reproduce just six months after it is born. The situation cried out for a more imaginative remedy.

  In 1950, the Australians introduced the myxoma virus, uniquely lethal to rabbits, into their wild population, which had no prior exposure, and therefore limited resistance, to it. The situation was thus analogous to the Mexican and European experience with smallpox and plague. The ensuing years saw a rabbit holocaust which reduced their numbers by 80 percent; the death rate among infected rabbits was 99.8 percent.

  Just at the point when the rabbit was about to disappear from Australia, natural selection kicked in, favoring those strains of rabbits most resistant to the disease. Further, this process worked equally well from the perspective of the virus. It did the myxoma organism no good to kill its host so rapidly; over time, it became less deadly, so that it lived longer and multiplied more effectively. By 1957, only one-fourth of infected rabbits succumbed. The one-sided relationship between a highly fatal disease and a completely defenseless host had changed into a standoff between a less virulent pathogen and a more resistant population.

  The same process occurs when humans are exposed to new infections. At first, mortality is high, but natural selection results in both a more resistant population and a less lethal pathogen. This process of “disease equilibration,” in which pathogen and host adapt to each other, seems to take about five or six generations—several years in the case of rabbits, and about 100 to 150 years in people. In the human population, such diseases as measles and chicken pox, which were once killers of adults, now affect mainly those who have not yet built up immunity to them, i.e., children. It is also no coincidence that these diseases arose originally from domesticated animals living in intimate proximity to humans: smallpox from cowpox, influenza from hogs, and measles from canine distemper or rinderpest.2

  Plague presents a somewhat more complex case. While the disease has certainly not reached a similar equilibrium in humans—it is nearly as deadly now as it was when it tore through the Old World in the fourteenth century—this matters little to the organism, for whom human infection constitutes a mere sideshow. From the perspective of the plague bacillus, the only hosts that matter are ground rodents such as the tarabagan, millions of which are to this day infected all around the globe. The disease proves rapidly fatal to the creatures as well, but the degree of isolation among these burrowing animals is high enough to slow down colony-to-colony transmission. Only among gerbils in the southwest Asian deserts is plague infection believed to be indolent enough to allow chronic, low-grade infection of individual animals.3 Scientists do not know for sure where the original reservoir population of infected underground rodents first arose; the best guess is somewhere in the Himalayan region of south China.

  If humans, marmots, and ground squirrels were the only hosts of plague, then people would be protected from it by distance; however, two other animals are involved in this deadly disease chain. The first is the flea, whose bite transmits the bacillus from mammal to mammal. Fleas are unable to travel the miles between people and remote underground rodent populations; the second animal, the black rat, provides the essential “bridge” between ground rodent and civilization and allows the ground-animal reservoir to lap on human shores. The bacillus is just as lethal to the flea and the rat as it is to people. All that remains is for the rat to die; the infected fleas then abandon the dead rodent, and, just before they too succumb, span the final few feet to an unlucky human.

  A particular species of flea, Xenopsylla cheopsis, became the crucial link in the chain of death. This unattractive insect has two characteristics that make it particularly well adapted to this role. First, the black rat is its host of choice. Whereas tarabagans seldom come into close contact with humans, the black rat is a so-called “commensal” animal. This term refers to the black rat’s adaptation to close proximity to human habitation by feeding off garbage and discarded food scraps. The black rat also cohabits with tarabagans. This allows Xenopsylla, and the plague bacillus along with it, to hop from tarabagan to black rat. Xenopsylla leaves the rat only under duress, when the rat dies, freeing the flea to transmit the bacillus one final, spectacular step, to humans. Xenopsylla’s second deadly characteristic is that, uniquely among fleas, its digestive system is highly sensitive to the bacillus, which creates intestinal blockage and regurgitation of large amounts of infected material into the rodents and humans it bites.4

  On the death of the rat, Xenopsylla can also find refuge in horses and camels, which become veritable flea hotels.5 Both beasts of burden, as well as a large number of other mammal and bird species, are highly susceptible to the disease.

  As far as the plague bacillus is concerned, Xenopsylla, the black rat, and man are two-bit players, unfortunate innocent bystanders. The organism’s primary mission is to maintain itself in its reservoir population of ground rodents. Worse, successful settled agriculture results in dense, specialized cities, which in turn attract the commensal black rat, specifically adapted to the urban environment.

  The black rat fills its deadly role brilliantly; it not only prefers close company to humans, but is also a world-class climber. Around the time when the Romans and the Han Chinese were in the ascendant, the species began to range far and wide along the Silk Road and the maritime monsoon routes. At some point early in the Common Era, the black rat gained passage to Europe via the mooring ropes of the dhows and Greek vessels plying the monsoon routes.

  The term “plague” itself causes much confusion. Almost certainly, none of the outbreaks recorded in ancient sources were the work of Yersinia pestis. Sumerian sources mention epidemics as far back as 2000 BC, and the first books of the Old Testament, written between 1000 and 500 BC, described divine retribution in the form of outbreaks among the populations of the Fertile Crescent. Modern translators fell on the word “plague” to describe these episodes, but the Bible and other ancient sources rarely gave enough clinical detail to identify the responsible bacteria or viruses.

  On only a few occasions did ancient observers provide enough such detail to identify the source of a specific outbreak. The very first passage in Hippocrates’s Of the Epidemics, written around 400 BC, clearly details an outbreak of mumps (painless swelling
about the ears, hoarseness, cough) on the island of Thasos. Nowhere in his works is found a description suggestive of Yersinia pestis infection.6 The great historian of the Peloponnesian War, Thucydides, described perhaps the most famous epidemic of ancient history, the Athenian plague of 430 BC, which killed about one-fourth of the empire’s army; its causative organism cannot be identified from the text with any accuracy.7

  Outbreaks of infectious diseases regularly savaged Rome—both the republic and the empire, most famously in about AD 166, when Marcus Aurelius’s legions brought back a pathogen from Mesopotamia. Contemporaneous accounts tell of the deaths of up to one-third of the inhabitants of the capital and the destruction of entire armies. Another outbreak struck Rome in the mid-third century and killed as many as five thousand people per day.8 Once again, precise descriptions of these Roman pestilences are lacking; the best evidence suggests that these were the first European invasions of smallpox and measles from their origins in the stockyards and dwellings of the Fertile Crescent.

  The clinical features of the plague caused by Yersenia—swelling in the groin and armpit, high fever, a black hemorrhagic rash, and rapid demise—are distinctive enough that had it occurred in the ancient world before AD 500, we should have record of it. This is even more true of the pneumonic form of the disease, in which airborne person-to-person transmission of the bacillus from coughing can by nightfall devastate entire urban quarters that at sunrise had appeared unaffected.9