In some ways Nature favored Egypt because, unlike Mesopotamia, which stood on an open plain and was unprotected from marauding tribes, the deserts that bordered the Nile discouraged invasion, and so the people lived in relative security. The villages shared the river and merged into cities. To tap the bounty of the Nile required the cooperation and organization of the people, with social and political structures developing therefrom. All power was invested in the pharaohs, who were both kings and gods. Below the pharaoh was a vast bureaucracy that rested on the shoulders of the workers and the peasantry. Egypt’s people, however, who built enduring stone monuments for their pharaohs, were racked with a debilitating disease, snail fever. And although medical science began in Egypt, the doctors and surgeons could not keep this disease at bay. There is a reason for this: the early civilizations of Egypt and those of the Fertile Crescent (Sumer, Assyria, and Babylon) were based on agriculture, and this agriculture required irrigation and/or natural flooding by the rivers. Irrigation farming, especially in the tropics, created conditions favorable for the transmission of snail fever caused by the blood fluke. Blood fluke disease—the plague of the pharaohs—is not a fatal disease, as is malaria or yellow fever; it is, however, a corrosive disease. And although there may have been a time when the natural flooding of the Nile River made snail fever a seasonal problem, once there was irrigation it became a year-round problem, since infections could be acquired from the standing water in the irrigation channels. Consequently, as William McNeill wrote in his book Plagues and Peoples,
there was a listless and debilitated peasantry handicapped … for the … demanding task of resisting military attack or throwing off alien political domination and economic exploitation. Lassitude and chronic malaise … induced by parasitic infections was conducive to successful invasion by the only kind of large-bodied predators human beings have to fear: their own kind, armed and organized for war and political conquest.
McNeill also suggested that the rule of the pharaohs may have been due to the power of the snail and the blood fluke and malaria—the classic plagues of Egypt—which debilitated the populace.
And so it was that snail fever did its work. By 660 B.C., Egypt became subject to internal political dissension and to attack by their iron-armed neighbors (the Assyrians), and their civilization, based on agriculture and copper weapons, began to collapse. The Persians overran Egypt in 525 B.C. The cause of snail fever, the disease that set the Egyptian civilization on its inexorable downward spiral, was unknown to the ancient Egyptians because the transmission stages of the parasite (eggs, miracidia, and cercaria) are microscopic; in addition, the adult worms themselves are tiny and live within the small blood vessels, and so they were unnoticed for thousands of years.
Search for the destroyer
Blood fluke disease, also known as snail fever and endemic hematuria, involves feces or urine, water, snails, and a flatworm. The first Europeans to experience the disease on any scale appear to have been the soldiers of Napoleon’s army during the invasion of Egypt (1799-1801). The symptoms of the disease, bloody urine, were rife among the soldiers. Baron Jean Larey, a military surgeon, noted its high frequency in the men; he believed, however, that the excessive heat during the long marches was the cause. The connection between hematuria and a parasite did not occur until 1851. In that year Theodor Bilharz, a German physician working in Egypt, while carrying out an autopsy on a young man, made a startling discovery: worms were found in the blood vessels, a location never before encountered (Fig. 3.2E). He named the worm Distomum (meaning “two mouths”) haematobium (from the Greek words haema, meaning “blood,” and bios, meaning “to live in”). In 1858 the name was changed to Schistosoma (from the Greek words schisto, meaning “split,” and soma, meaning “body”). Today, blood fluke disease is called schistosomiasis or bilharzia, the latter in honor of Bilharz’s discovery. (During World War I, British soldiers found it easier to call the disease “Bill Harris.”)
In 1851, Bilharz reported that he had seen microscopic eggs with a pointed spine in the female worm (Fig. 3.2C), and in the following year he observed these eggs in the bladder; within the egg he observed a small, motile embryo. He also found that the eggs would hatch to release a small ciliated larva (Fig. 3.2F) that swam around for about an hour and then disintegrated. This work was confirmed in 1863 when John Harley, a London physician, examined a patient with hematuria who had previously lived in the Cape of Good Hope in South Africa. Examining the blood-tinged urine in a drop of water under the microscope, he found schistosome eggs, and several of these hatched to give progeny that swam by using their cilia (Fig. 3.2G). But there remained a puzzle: how was the infection transmitted? Bilharz and others were aware that flukes closely related to Schistosoma had intermediate stages in snails, but when Harley examined snails from a region where schistosomiasis was prevalent, he found no evidence of larval stages. Despite this failure, the suspicion remained that humans acquired the infection either by eating infected snails or by drinking water containing the ciliated larva called miracidia. In 1870, Spencer Cobbold, working in London, obtained eggs from a young girl living in the Cape of Good Hope and found that although the eggs would not hatch in urine, they did so in fresh or brackish water. Then, in about 1904, Japanese physicians found that a related blood fluke, named Schistosoma japonicum, could also infect humans, but this species had eggs without a spine. In 1905, Patrick Manson discovered another type of schistosome egg, one with a spine on its side (Fig. 3.2D); this was in the feces of an Englishman who had lived in the West Indies but had never visited Africa; this new type was duly named Schistosoma mansoni. Now there were three known species of human-infecting blood flukes.
The life cycle and mode of transmission of the schistosome to a human were first demonstrated between 1908 and 1910 in Japan. Fujinama and Nakamura found that when the tails of mice were immersed in water from rice fields known to have a high incidence of bilharzia, they became infected with S. japonicum. Shortly thereafter it was possible to show that the miracidia were able to penetrate freshwater snails in the rice paddies, and Ogata found that a tailed larva (called a cercaria) emerged from infected snails and could directly penetrate the skin of mice (Fig. 3.2G). This suggested that species other than S. japonicum might have a similar life cycle. At the outbreak of World War I the British became concerned about the potential deleterious effects of schistosomiasis on their troops in Egypt. In 1915 the British War Office sent Robert Leiper to Cairo “to investigate bilharzia … and advise as to preventive measures to be adopted.” Leiper collected freshwater snails, identified them, and determined whether they were infected, either by allowing the snails to release cercaria or by dissecting the snails to find other larval stages (called sporocysts). Within weeks he and his team identified the snails Bulinus and Biomphalaria as the vectors. (Because the snail vector is critical to transmission, schistosomiasis is called “snail fever.”) Leiper went on to show, by placing the tails of the mice in cercaria-infested water, that the skin of mice could be directly invaded by the cercaria. This suggested that the infection was acquired by bathing in infested water. But could the infection also be acquired by ingestion? Because Leiper was able to show that when cercaria were placed in dilute hydrochloric acid (similar in concentration to that found in the human stomach) they were killed, this route of infection seemed most unlikely. Leiper was also able to show that the adult S. mansoni and S. haematobium were different from one another and that cercaria hatched from Biomphalaria produced eggs with lateral spines whereas those from Bulinus produced eggs with a terminal spine. The pathology of the two species was also found to differ: S. mansoni remained in the liver and laid its eggs there, whereas S. haematobium early in its development left the liver for the veins surrounding the bladder. Thus, 65
