movable metal type was one way that this was accomplished.
Another was to employ an economy of scale in sea- and oceangoing transport vessels. Bigger ships with smaller crews could remain at sea for longer periods of time and would be able to sail directly from port to port, but this would require better ship construction, improvements in navigational instruments, and new business enterprises such as maritime insurance to protect the investment in cargo and the ship. As a consequence, merchants such as bankers and craftsmen became more powerful. The new economy became more diversified, there was a more intensive use of capital, technological innovations became more and more important, and there was a greater redistribution of wealth. In time the aristocracy found it had to yield power to the masses. The social and economic fabric of Europe began to be altered, and it was the Black Death that instigated such change.
Finding the Killer
As plague raged through medieval Europe, it became increasingly apparent that this disease was contagious. Even if Fracastoro’s idea of “seeds of contagion” was accepted, however, at this time there would still be no means to identify precisely the causative agent. Identifying the “seed” would not only require a technological innovation; it would also require a change in the concept of infectious (contagious) diseases. Three centuries after Fracastoro’s theory of contagion, the concept that disease could result from the invasion of the body by microbes or germs—the germ theory of disease—was established. And with a 17th-century technological innovation, the microscope, it was actually possible for humans to see germs! Two schools of thought, one in France under the leadership of Louis Pasteur (1882-1895) and the other in Germany, led by Robert Koch (1843-1910), were responsible for firmly grounding the germ theory, and for all of their lives these two microbe hunters remained fierce competitors (see p. 418).
As plague ravaged China during the third pandemic, Pasteur dispatched Alexandre Yersin (1863-1943), a Swiss-born member of the French medical colonial corps, to Hong Kong to study and attempt to isolate the germ of plague. Yersin arrived when the epidemic was in full force and was given a small table in a dark corridor next to a patients’ room, where he could leave his microscope, notebook, stains, pipettes, and a few cages with guinea pigs, mice, and rats. At first Yersin was not permitted access to the morgue, but through connivance and bribery he was finally able to visit the morgue for a few minutes to examine a sailor who had just died from plague. Yersin punctured the bubo on the dead soldier’s thigh (Fig. 4.6A) with a sterile needle and removed some fluid; he then examined the fluid under the microscope, inoculated a few guinea pigs, and sent the remainder to the Pasteur Institute in Paris. On June 24, 1894, he wrote Pasteur that the fluid was full of rod-shaped bacilli (Fig. 4.6B) that stained poorly with Gram stain; i.e., they were Gram negative. (Gram stain consists of a tincture of crystal violet. After bacteria are killed and washed, some lose the dye whereas others retain the purple color; the former are called Gram-negative and the latter Gram-positive bacilli.) Yersin also wrote: “without question this is the microbe of plague.” A few days later Yersin found that the guinea pigs he had injected with the fluid that he had aspirated from the bubo had died, and that their bodies swarmed with the same bacilli. Yersin was intrigued by the large number of dead rats in the streets of Hong Kong, as well as in the hospital corridors and the morgue. When he examined some of these dead rats, he found the same bacilli to be present. He correctly concluded that plague infects both rats and humans. At about the same time, Koch, convinced that plague was caused by a microbe, sent his associate Shibasaburo Kitasato and a large number of assistants as well as abundant equipment to find the plague germ. Kitasato did culture a bacterium from the finger of a sailor who had died from plague, but it was Gram positive. Further, Kitasato was never able to prove that this bacillus could produce plague in humans or other animals. Bubonic plague, caused by a rod-shaped, Gram-negative bacterium, was named Yersinia pestis after its discoverer, Alexandre Yersin (although Pasteurella pestis was the name used before 1970).
Figure 4.6 A. Bubo of bubonic plague (courtesy of CDC, 1993) and B. the causative agent, Yersinia pestis, stained and seen with light microscope (courtesy CDC)
Finding the Vector
Yersin discovered the plague microbe, but he did not find the means whereby the disease could be transmitted. He asked himself: was it airborne, or did it have to do with rat feces or dried rat urine? The answer to the question came from Paul-Louis Simond (1858-1947), a French army physician who was sent by Pasteur to Vietnam and India to follow up on Yersin’s observations. Simond noted that not only were there large numbers of dead and dying rats in the streets and buildings, but that 20 laborers in a wool factory who had been cleaning the floor of dead rats had died of plague, while none of the other factory workers who had no contact with rats became ill. He began to suspect that there must be an intermediary between a dead rat and a human, and that the intermediary might be the rat flea Xenopsylla cheopis (Fig. 4.7). Simond found that healthy rats groomed themselves and had few fleas, but that sick rats unable to groom their fur had many; and when the rats died, the fleas moved off onto other healthy rats or onto humans. To prove this he did an experiment: a sick rat was placed at the bottom of a jar, and above this he suspended a healthy rat in a wire mesh cage; although the healthy rat had no direct contact with the plague-infected one, it did become infected by exposure to its fleas (which he determined could jump as high as 4 in. without any difficulty). As a control Simond placed a sick rat without fleas together with healthy rats in a jar. None of the healthy ones became sick, but when he introduced fleas into the jar, the healthy rats developed plague and died. On June 2, 1898, he wrote Pasteur that the problem of plague transmission had been solved.
Figure 4.7 Flea as seen with the scanning electron microscope. Courtesy CDC/Janice Haney Carr
The most common scenario for the origins of the Black Death, i.e., the second pandemic, is that its source was microbes left over from the first pandemic (the Justinian plague) that had moved eastward and remained endemic for 7 centuries in voles, marmots, gerbils, and the highly susceptible black rats (Rattus rattus) of the arid plateau of central Asia (roughly corresponding today to Turkestan). Plague-infected rats moved westward along the caravan routes between Asia and the Mediterranean known as the Silk Road, and in this way plague traveled from central Asia, around the Caspian Sea, to the Crimea. There the rats boarded ships and moved from port to port and country to country, spreading plague to the human populations living in filthy, rat-infested cities. This has been described poetically in Robert Browning’s poem “The Pied Piper,” which is based on a legend that on June 26, 1284, the German city of Hamelin became infested with rats. A Pied Piper comes to Hamelin and agrees to rid the city of rats for payment of a large sum of money. He is able to enchant the rats by playing his flute, leading them to the river, where they drown. But when the city fathers refuse payment, the Pied Piper leads the children to a cave, where they disappear. Versions of the tale were gathered by the Grimm brothers (1812), and this plague-inspired tale has over time come to have a moral interpretation: evil will befall those who do not carry out their promises.
Simond’s hypothesis was that the transmission of plague was from the black rat (R. rattus) via the rat flea (X. cheopis) to humans. This has been the accepted scenario for decades. Recently, however, this
