Between Hope and Fear

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by Michael Kinch


  The Seleucids were not only humbled by the Romans, but the revelation of their inherent impotence rendered them subject to intermittent cycles of discontent, civil war, and then insurrection. Repeatedly, new pretenders promised to restore the glory of earlier days, only to be later disabused of the notion by the superior arms of neighboring Roman forces.

  Although not a direct vassal of Rome, the reduced Seleucid “empire” was well within the Roman sphere of influence, and Seleucid leaders remained constantly on tenterhooks in recognition that restiveness in the Levant could cause their larger neighbor to snuff out what remained of their fledgling yet marginally independent realm. Unfortunately for the Seleucids, the chaos that continues to characterize the Tigris and Euphrates river valleys even today has ancient roots, and the Seleucids were no better at quelling unrest than any other occupying power, before or since. By the beginning of the 1st century B.C.E., Seleucia had devolved into a failed state manipulated by larger neighbors to the south (the Ptolemaic Egyptians, a Hellenistic colony) and north (Pontus and Armenia), who sought ways to distract and bleed forces from their mutually shared Roman enemy.

  Eventually, these distractions drove Pompey, the great military general and member of the ruling triumvirate (along with Julius Caesar and Marcus Licinius Crassus), to put an end to the Seleucid nuisance once and for all. The utter eradication of the Seleucids and the subsequent carving up of their remaining lands at last quieted some of the disorder as the Romans ceded the lands of Seleucia to other vassal states and minor regional powers.

  The Parthians were one example of a minor client state that benefited from the fall of Seleucia. These people arose from a group of nomadic tribes in the north and eastern regions of Persia, and they had been a long-standing rival of the Seleucids. The weakening and eventual elimination of the Seleucids by the Romans provided an opportunity for the Parthians to expand their holdings. The lands encompassing Seleucia transferred into Parthian hands. As it was with the Seleucids, however, the term empire is an overstatement, as the Parthian holdings were arguably more a confederation of satraps and lacked a strong central power.

  Consequently, the Romans were again faced with instability on their strategic southeastern flank, this time from the Parthians. This required intermittent reintroduction of forces to police the regions of the Fertile Crescent over the next two centuries. An otherwise humdrum round of local interdiction in the mid-2nd century C.E. would unexpectedly undermine the mighty Roman Empire and catalyze its downfall.

  Gaius Avidius Cassius was the scion of a powerful family with a strong and prestigious bloodline on both sides.14 His father was a Roman politician, whose maternal ancestors included Herod the Great, Gaius Cassius Longinus (the same Cassius as profiled by Shakespeare, whose intrigues culminated in the assassination of Julius Caesar), and Gaius Octavius (father of Caesar Augustus). Gaius Avidius Cassius embodied a genetic lineage that encompassed both the major protagonist and antagonist in the Roman transition from republic to empire. In a world not known for outbreeding, his maternal lineage included both Cassius and Octavius, as well as Marcus Vipsanius Agrippa, an architect of notable fame and the general who plotted the defeat of Mark in the Battle of Actium.

  Given his high birth and marshal familial history, it is unsurprising that Gaius Avidius Cassius, who was born in Syria, rose quickly through the military ranks. In 161, he was commanded to lead Roman legions to quell an uprising by the Parthians and to sack their capital in Ctesiphon. During this campaign, he marched his troops down the Euphrates River valley and attacked the Parthians at the town of Seleucia (just across the river from Ctesiphon) in the year 165. A few days after a pivotal battle in which his troops decisively defeated the Parthians, a small number of soldiers began to fall ill with symptoms that included fever, diarrhea, and eruptions of the skin. Looking at the geography (the same location where Alexander’s army had encountered the same disease), symptoms, and rapid spread of the disease, modern epidemiologists have largely concluded that smallpox was again responsible for the outbreak.15, 16 Within weeks, this so-called Antonine Plague (later named because it began during the reign of Emperor Marcus Aurelius Antoninus) would begin to burn up and through the empire.

  The plague spread quickly by exploiting the same innovations that facilitated the growth of the empire during the Pax Romana. A combination of improved transportation, urbanization, and emigration propagated the expansion of smallpox from a localized epidemic to an empire-wide pandemic. Evidence these improvements accelerated the disease is supported by the fact that within a year following the occupation of Seleucia, the Greco-Roman physician Galen described the symptoms of the disease (facilitating the attribution to smallpox by epidemiologists two thousand years later) as it struck the city of Rome in 166.17 Undoubtedly, the higher population density that had been facilitated by improved building technologies and urbanization unintentionally expedited transmission of the pathogen among the citizenry. The exact extent and impact of the Antonine Plague remains a subject of academic disagreement, but virtually all concur as to its devastation. Low estimates of the plague’s mortality rate cite 7–10 percent of those infected, which would translate into approximately three to five million people killed across the empire (though census figures are unreliable, given the large number and mobility of citizens, slaves, and emigrants within the expansive empire).18 At the other extreme, the 19th-century German historian Otto Seeck claims the Antonine Plague killed more than half the population of the Roman Empire within the fifteen-year period spanning 165–180.19 Putting this into perspective, a comparable plague in the modern United States would cause more than 150 million deaths, which would be equal to the deaths of every person in forty-three states (all save Ohio, Pennsylvania, Illinois, Florida, New York, Texas, and California).

  Without question, the plague altered day-to-day life for virtually all living in the empire. A leading 19th-century historian of Roman law and economics concluded, “The ancient world never recovered from the blow inflicted on it by the plague which visited it in the reign of Marcus Aurelius.”20 Among other things, the living and dying were preyed upon by charlatans. Quack remedies for the plague proliferated and took advantage of a terrified populace. Such behavior is alluded to by the Emperor Marcus Aurelius, who, in his Meditations, conveyed that the disease was less deadly than the lies and malicious intent of those lacking understanding of the pestilence.21 Sadly, the emperor himself would ultimately be counted among the victims of the plague, succumbing to the disease in the year 180. His death brought an end to a period characterized as the rule of the Five Good Emperors: Nerva, Trajan, Hadrian, Antoninus Pius, and Marcus Aurelius.22 Thereafter, a suffering nation was governed by a series of selfish, imperious, and ineffectual leaders, dooming the Western world’s only superpower.

  The Spotted History of Smallpox

  As historically devastating as the Antonine Plague was, it was hardly the first time that humanity, or even the Mediterranean basin, had experienced the desolation caused by smallpox. Modern genetic-based modeling suggests the disease jumped from a rodent to humans between 16,000 and 48,000 years ago, somewhere in or near the Gold Coast of Africa.23 From there, the disease began a relentless northeastern progression through Egypt and the Middle East, into the Caucasus and China. Despite and perhaps because of the familiarity of our species with smallpox, which might have seemed commonplace to many, descriptions of the disease are largely undocumented by most of the oldest extant written sources, such as the Old Testament or Egyptian papyri. However, lesions consistent with smallpox have been detected on Egyptian mummies, including that of Ramses V, who died more than a millennium before the Antonine Plague.24 The high density of people in the Nile River valley likely facilitated the propagation of the disease, and trading with other civilizations perpetuated its spread throughout the ancient world. Another river valley, that of the Indus in modern-day India, also hosted endemic smallpox, and trade with the ancient Egyptians or Chinese might have introduced the pat
hogen to the subcontinent.25

  Some modern historians speculate that the Plague of Athens might have arisen from a smallpox pandemic that had its beginnings in Egypt.26, 27 This particular plague stands out in history because it arose in the midst of, and influenced the outcome of, the Peloponnesian War. As an overly brief summary of that conflict, the two antagonists, Sparta and Athens, utilized very different strategies centered upon their individual strengths. Sparta was a land power, and their soldiery was feared throughout the region. In contrast, the Athenians were a seafaring power that flourished largely because of trade with the many other city-states and civilizations found throughout the Mediterranean world. The Athenian leadership recognized the mutual mismatch: Athens could not compete with Sparta on the land, and Sparta was no match for the Athenian fleet. In response, the celebrated Athenian leader Pericles adopted an approach of building great defensive embattlements around Athens and succoring the city with seaborne supplies. The surrounding farmlands were to be harvested and the farmers brought inside the massive fortress with the intention of waiting out the inevitable Spartan sieges. Pericles was confident in this approach, as Athens could be provisioned by trade with other coastal city-states, while the Spartans would be compelled to squander precious manpower and resources on maintaining the siege.

  Pericles could not have realized that his innovative strategy would be undermined by unwanted microbial guests. As documented by the father of modern history, Thucydides, the plague was rumored to have started in Ethiopia before entering the Hellenized lands of Egypt, which was a major trading partner for Athens. Thus, a Periclean strategy based on trade with Egypt and other Greek city-states hastened and magnified the spread of disease. Compounding the issue, a high population, which was exacerbated by the refuge granted to the peoples outside the Athenian defensive walls, increased the efficiency of transmission once it gained a toehold within the Athenian redoubt. The spread of the disease was so rapid and pronounced that the besieging Spartans became disconcerted by the constant burning of funeral pyres within Athens and lifted the cordon. Their fears further caused them to temporarily suspend all military and nonmilitary interactions with the Athenians in an attempt to prevent the infection from spreading to their own camps.

  Based on written reports and mass graves excavated in the area, the victims of the Plague of Athens might have included more than half the Athenian population. Prominent among these were the great leader Pericles himself, who was joined in death by his entire family. Despite the lifting of the siege, the disease combined with the sudden loss of Pericles’s leadership to undercut the influence of the Athenian resistance to Sparta thereafter. Indeed, Thucydides writes that the social fabric of Athens disintegrated during the epidemic as citizens stopped respecting authority and obeying the law and social conventions, such as caring for afflicted family and neighbors and following religious authority. The societal unrest effectively neutered the once-mighty Athenians for at least a generation. The Plague of Athens was unquestionably a disaster for the Western world. While smallpox seemed to have played a role, additional or alternative microbial pathogens, such as typhoid fever and typhus, likely also contributed to the epidemic.28 Indeed, the lowering of individual and public health by one disease, especially during times of war, often encourages the rapid expansion, and synergy with, other infectious diseases. Nonetheless, these results suggest smallpox might have played a role in destroying both of the great pillars of ancient Western civilization.

  A New World

  Through a combination of luck and circumstance, new microbial pathogens are constantly challenging hosts new and old. A virus that lives in one species, say a bird, might change (mutate) ever so slightly such that it can now infect a human. Alternatively, a virus-infected member of one species might introduce the disease to another, for example by serving as its prey. Many such examples have and will continue to occur, as evidenced by an ongoing avian influenza (H5N1) epidemic throughout much of Asia, as well as the recently established monkey-to-human transmission of HIV (most likely the result of a hunter being bitten by bush meat) in the early 20th century. We will return to this subject in greater detail in subsequent chapters, but the dynamism of infectious disease has been and will remain a constant feature afflicting human civilization.

  A long-standing theory of infectious disease epidemiology is that the introduction of a new pathogen into a population or species conveys a more pathogenic or deadly form of disease. One tenet of this idea holds that if a particular microbe became too aggressive, in its frenzy to feed it would likely kill or incapacitate its host in a short enough time that its food would be exhausted before the pathogen could be propagated to its next victim (and so the first meal would be its last). Such a high-morbidity and -mortality virus would “burn itself out.” Such outbreaks would therefore remain local and easily maintained, much as we had seen with the Ebola virus until recent years.

  Following this line of logic, a less lethal form of a microbe may ironically cause a more dangerous disease to the larger population. Viewed a different way, more danger can arise when a pathogen becomes slightly less obnoxious so that it does not kill the host until after it can spread to others. If the disease is easily spread and death or sterility (i.e., the failure of the host to reproduce) is the outcome, then the microbe could again destroy the entire host species, its food source, in a relatively short period of time. Thus, a well-mannered and long-term-minded pathogen will seek to farm its food and harvest only when needed.

  As a consequence of these dynamics, a microbe is best served if its virulence or ability to infect the host is moderated (known as attenuation). Clearly, microbes are not sentient beings that make conscious decisions to slow their growth or diet. Under the assumption we are all at least vaguely aware of DNA and the ideas of mutation, then this process could offer an explanation. To readers familiar with the concept of genetic mutation, attenuation explains why. Worse still, a well-mannered microbe still faces competition for this same food source from its more obnoxious cousins, who may still be in a frenzied state of feeding. Thus, the microbe encounters a situation that is identical to the economic problem known as the tragedy of the commons, first described by William Forster Lloyd in early Victorian England and popularized by Garret Hardin in the 1960s.29

  Fortunately, a parallel form of evolution in the host species can help resolve the microbial version of the tragedy of the commons. It is widely appreciated that genetic diversity is a good thing. Anyone who has visited a major zoo has likely heard the story of the cheetah, a species where a past population crisis (i.e., where many animals die off) about ten thousand years ago caused a genetic bottleneck—an event that limits genetic variation in a population. This fundamentally threatened the future viability of the entire species.30 Although the causes of the cheetah crisis are not clear, the bottleneck event might have consisted of a sudden environmental change and/or contact with an obnoxious new microbe. Regardless, the genetic diversity of the survivors quickly dropped by at least 75 percent. As a second example, we are well aware of the problems associated with consanguineous mating when siblings or close cousins produce an offspring. Indeed, most modern countries have laws limiting the ability of an individual to marry a close relative, since the progeny of such matings tend to display recessive traits that rarely improve the stock.

  This raises the question of why genetic diversity is so important. Let’s consider an example inspired by mixing and matching a few theological viewpoints: If God created an individual (or two) specifically to live within a privileged environment (the Garden of Eden), then why bother to continue the process of DNA mutation and evolution? The best answer, to which any Buddhist can attest, is that the world is subject to constant change. The future will be peopled by those who can adapt. Another pretty good response to the question derives from the reminder that all individuals (even bacteria, as we will soon see) are constantly forced to fight off pathogens.

  Though we will return to the subj
ect of genetic bottlenecks many times throughout this book, it suffices to say that genetic diversity is one way to increase the likelihood that a species will not be wiped out by a new microbial pathogen. If a population of organisms (let’s say people) is sufficiently diverse from the standpoint of genetics, then the odds are (and it is all a statistical gamble) that some individuals will be more prone to survive an epidemic than others. When a large enough population has sufficient genetic diversity, then a Darwinian-like selection should allow the more robust population bearing a trait (also known as a phenotype) to survive, and perhaps even thrive, in the face of an obnoxious microbe. The survival of both the host and pathogen thus depends on the ability of the host to maintain enough genetic diversity to provide enough time for the microbe to learn how not to destroy its host.

  A comparable form of parallel evolution of both the pathogen and the host has occurred with smallpox. As the virus continued to burn through the Middle East and Europe throughout the Middle Ages, the death toll slowly waned, and those people who were less prone to die (even slightly so) had more of an opportunity to pass along this decreased susceptibility to their progeny. These dynamics progressed towards an equilibrium in which the virus could be stably maintained in the human population without threatening the fundamental survival of the human species. Individuals might succumb to the disease, but mankind itself would survive. As such, the populations of Europe, Africa, and Asia experienced a rapid (known as punctuated) form of evolution over the past few millennia, in which the survivors were somewhat more adapted to survive smallpox than individuals who lived ten thousand years ago would have been. Something very different happened when smallpox was turned loose in a population in which the most susceptible individuals had not been subjected to multiple generations of selection. Such a disaster was experienced just over a half millennium ago all throughout the Western Hemisphere, with tragic consequences.

 

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