Read Plagues in World History Online
Authors: John Aberth
Tags: #ISBN 9780742557055 (cloth : alk. paper) — ISBN 9781442207967 (electronic), #Rowman & Littlefield, #History
In the same way, the most effective therapy for cholera, direct injection of saline solution into the veins of the victim, was devised and successfully tested as early as 1832 by an obscure physician from Leith, England, Thomas Latta.24 To this day, fluid replacement therapy is the most widely used treatment for cholera, especially as the bacteria develop resistance to antibiotic drugs, such as tetracy-cline.25 Yet, because Latta’s chemically based therapy did not fit easily into any existing medical tradition, such as the humoral theory, it was not widely adopted during his own lifetime. Meanwhile, some spectacularly unsuccessful, and indeed quite harmful, treatments were being employed, such as bleeding (still practiced as late as the Hamburg epidemic in 1892) and administration of laxa-tives and other purgatives, which, while perhaps endorsed by long tradition going back to ancient times, had exactly the opposite desired impact in a disease Cholera y 109
that was already draining the body’s available fluids. Other “remedies” were simply bizarre, such as bunging up the anus with beeswax in a futile attempt to stem the involuntary gastrointestinal flow.26 All this demonstrates that, while the means of prevention and cure of a disease may be prematurely available to human society, it does not always have the wisdom, foresight, or perhaps the mere psychological readiness to avail itself of them.
C H A P T E R 5
y
Influenza
Influenza is a viral disease, like smallpox, but the viruses that cause influenza are far more unstable genetically than
Variola major
and
minor
, and consequently there are far more, ever-shifting varieties of the microbe that make it a much more challenging disease to combat by means of vaccination. Like a “moving target,” influenza viruses are constantly mutating in the process of replicating copies of their RNA (ribonucleic acid) that they can only achieve by invading a host cell in order to harness its biological machinery; it is estimated that within a single cel an influenza virus can manufacture and then release up to a hundred copies of itself within five or six hours. It is because of this high rate of reproduction (without any ability to “proofread” or correct copies of its genes as in the case of deoxyribonucleic acid, or DNA) that influenza viruses remain so elusive, since the protein molecules or antigens comprising the viruses’ outer coat or capsid, which are recognized and engaged by the antibodies of our immune defense system, are constantly evolving in both minor and major ways, known respectively as antigenic
drift
and antigenic
shift
. For this reason, we will probably never “conquer,” or entirely eliminate, influenza as was achieved against smallpox in the 1970s, and in this respect, influenza is more akin to the human immunodeficiency virus (HIV) that causes AIDS (acquired immune deficiency syndrome) and that will be the focus of the next chapter. Interestingly enough, it has also been recently discovered that the influenza virus can target and suppress the body’s immune system, much as HIV does in AIDS, in order to give the virus time to replicate within the lungs.
Due to their complexity, influenza viruses have earned an elaborate classification system whereby they are divided into three main “types,” known as A, B, and 111
112 y Chapter 5
C (based on the nucleoprotein antigen), of which the type A viruses are the only ones known to cause large-scale pandemics in humans. Within type A, influenza viruses are further classified on the basis of their outer protein coats that allow them to enter and exit a host cell: these are the hemagglutinin (H) and neuramin-idase (N) glycoproteins, of which fifteen varieties are known of the former and nine of the latter. This is how various influenza viruses get their names in the news and other literature that talk about the agents responsible for particular pandemics; for example, the H1N1 virus is believed to have caused both the 1918–1919
pandemic and the recent one that made the rounds in 2009. What is not so clear is if influenza viruses only drift and shift in a cyclical manner, within the relatively limited number of antigenic combinations identified thus far, or if we are doomed to encounter ever new proteins as these constantly evolve.1
Influenza is perhaps the most contagious of any infectious disease we know of; it is more transmissible than smallpox because influenza viruses, like the rhi-noviruses that cause the common cold, specifically target cells in the upper and lower respiratory tract, although they can subsequently be distributed to other parts of the body, such as the brain and central nervous system, where they cause other symptoms typically associated with the disease. Influenza is therefore particularly well suited to person-to-person communication by means of sneezing, coughing, or simple breathing. And since a virus is five hundred times smaller than a bacterium, many more infectious agents are emitted by a victim of influenza with each cough or sneeze than one afflicted with a bacterial respiratory disease such as pneumonic plague or tuberculosis; this makes it far more likely not only that a person nearby will contract influenza but also that it will penetrate deeper into the lungs where it cannot easily be ejected by the cough reflex.
(This is why gauze facemasks recommended by Dr. Wu Liande that protected his medical staff during the pneumonic plague outbreak in Manchuria in 1910–1911 proved not so effective against the influenza pandemic in 1918–1919.) In addition, the influenza virus can remain infectious for up to forty-eight hours outside the host, so that one can also contract influenza by breathing in contaminated dust particles or by touching contaminated objects such as doorknobs and utensils and then ingesting the microbial agents on one’s hands. Recent experience with avian flu has likewise demonstrated that influenza can be spread, at least from animals to humans, via the gastrointestinal tract as a result of eating infected poultry products or drinking contaminated water.2
As soon as one or two days from infection, the typical flu symptoms will manifest themselves, which include high fever, chills, headache and other bodily aches and pains, prostration, lethargy, and sometimes vomiting or diarrhea. In the worst-case scenario, bacterial or viral pneumonia will later emerge, due to the fact that a certain amount of synergy exists between flu and pneumonia: flu can Influenza y 113
prepare the way for pneumonic infection and vice versa.3 It is important to note that the victim is infectious even before these symptoms appear, and some people can be infected by flu without showing hardly any signs at all, becoming in effect asymptomatic carriers of the disease.4 But flu symptoms are so general that it is quite difficult to make a positive diagnosis of historical epidemics on that basis alone; usually a pattern of high morbidity accompanied by low mortality that is typical of influenza will confirm its presence in most scholars’ minds.5 Influenza usually runs its course through the human body in three days, after which the patient can generally be expected to make a full recovery. Death from flu is rare, occurring on average in only one-tenth of 1 percent of all victims during most outbreaks; these unfortunates also tend to be either the very young or the very old, people already at high risk in premodern times. The exception, of course, was the 1918–1919 pandemic, when average mortality rates jumped to 2.5 to 5
percent or higher in some places, and many more victims came from among those in the prime of life, roughly between twenty and forty years of age. Morbidity rates for this pandemic were likewise unprecedented for normal influenza, comprising anywhere from 25 to 50 percent of populations, although such statistics are notoriously hard to pin down since cases of sickness were less rigorously reported than actual deaths.6
A seasonality of incidence is also associated with influenza, which strikes typically during the winter months in the northern and southern hemispheres and during the rainy or monsoon seasons in tropical zones. At times, however, influenza can come on in waves, as it did in 1918–1919. In this particular outbreak, historians have noted three successive waves of the disease, a first and mild one occurring in the spring to midsummer of 1918, the second and most severe wave starting almost immediately thereafter in the late summer and autumn, and finally a third and again mild wave during the early months of 1919.7 The flu pandemic that ran its course in the United States during the latter half of 2009
peaked in September and October, rather than during the usual bad months for flu of December and January. A combination of social and environmental factors are thought responsible for flu’s seasonal behavior. Certainly, overcrowding of populations that tend to occur with the onset of bad weather will greatly facilitate spread of influenza, but the virus also does best in conditions of low humidity and sunlight such as we find in winter. Human immune systems are also more likely to be compromised as the body fights off the effects of cold or rain. Yet, a certain amount of mystery remains in this regard: laboratory experiments with mice have found flu behaving seasonally even when conditions of temperature and humidity are equal.8
Such are the bare epidemiological facts about influenza that distinguish it from other infectious diseases we have discussed thus far. Compared to those of 114 y Chapter 5
plague, smallpox, or cholera, its symptoms are not especially memorable, dramatic, or enduring. In most cases, an entire epidemic or even pandemic comes and goes quickly, in a matter of months, leaving behind relatively few to mourn and those at the life-expectant margins of society. This has made it easy for both past and present cultures to overlook influenza, seeing it, perhaps, as no worse than a severe cold. And yet the 1918–1919 pandemic overturned all these expectations about this otherwise seemingly benign disease, for in that one outbreak influenza swept across as many categories of society as the “danse macabre” of plague; in some unforgettable cases, it brought on the heliotrope or blue-black cyanosis of the face so typical of cholera, and it marked its survivors with a trauma as tangible, even if not as visible, as the pockmarks of smallpox. Remarkably, influenza in this particular instance behaved both like the worst of infectious diseases in the minority of cases it did kill, striking with a virulence that invited comparisons with the Black Death,
and
like any other flu outbreak in terms of the usual pattern of low mortality and high morbidity: horrifying as the deaths from flu were, the vast majority of people still recovered from or did not get the disease. In a sense, here was influenza on the grand scale, with a much higher incidence of the disease than normal and across a broader spectrum of the population, accompanied by a higher mortality rate within that subgroup, in a particularly far-reaching pandemic that left practically no part of the world, even in its remotest spaces, untouched. In other words, influenza was still influenza, only this time morphed into a monstrous version of itself that, of necessity, impinged upon the consciousness of all. Although the historian Alfred Crosby has dubbed it the “forgotten pandemic” among its own contemporary generation, the outbreak of 1918–1919 has since cast a long shadow over almost every subsequent pandemic threat of influenza.9 It is quite simply the deadliest single outbreak of disease in history, surpassing even the Black Death in terms of sheer numbers of people directly killed by its onslaught, with the most recent estimates ranging anywhere from fifty to one hundred million dead worldwide. Why and how this happened are mysteries that are still in the process of being answered.
Before we get to the infamous 1918–1919 pandemic, however, it is advisable to trace the prior history of this disease. Influenza viruses have been around for millions of years, where their natural host reservoir has been and continues to be ducks and other aquatic wildfowl, which are generally immune to the disease and instead act as carriers, continually shedding viruses in their feces. When humans began domesticating ducks around four thousand years ago, the influenza virus was then able to make this species leap, even though the current human strains of influenza had already emerged toward the start of the Neolithic age another four thousand years earlier. As humans domesticated other animals, particularly pigs and chickens, influenza was able to make its endemic home in human Influenza y 115
populations across much of the ancient world. (In addition to the above species, influenza epidemics are also known to afflict horses, dogs, and cats.) However, the source of most new outbreaks of human influenza, both then and now, is thought to be China and Southeast Asia, due to its ancient practice of rice growing and fish farming, where live ducks living in the water were used for weeding and their feces as fertilizer and fish food. When pigs were added to this microbial stew, passage of the influenza virus from animals to humans became much easier, since pigs, having an anatomy much closer to humans than do birds, were able to be infected by both human and avian strains of influenza and thus became a kind of “mixing bowl” for emerging flu pandemics.10 Yet, the influenza virus can and does pass directly from birds to humans, and indeed this is what is now thought to have occurred during the influenza pandemic of 1918–1919, as well as in the current outbreaks of avian flu that have menaced the world for at least the past decade.
The ancient Greek physician Hippocrates provides perhaps our first written description of influenza in his
Epidemics
composed sometime during the fourth century B.C.E., and down through to the Middle Ages flu outbreaks may have been subsumed under references to “fevers,” “rheums,” and “catarrhs.” The term “influenza” itself was apparently first introduced from the Italian in 1504 to describe any general disease epidemic that afflicted large numbers of people due to the “influence” of the stars; the modern sense of the word does not seem to emerge, however, until the eighteenth century, when the “grippe” also came into usage to refer to the disease. Some convincing descriptions of influenza epidemics in Britain and Europe can be produced for the sixteenth and seventeenth centuries, but it is quite likely that any such outbreaks were sporadic and not very widespread.11 There may be any number of reasons for this. One explanation that has not been considered thus far is that, at this time, health manuals, plague treatises, and dietary regimens all advised that people steer clear of waterfowl, such as ducks and geese, not only on the grounds that their “watery” meat would produce watery, easily corruptible blood but also because they fed on unclean, noxious things in often foul, stagnant waters.12 While of course ignorant of the fact that waterfowl were the natural hosts of the influenza virus, such medical prescience may nonetheless have limited the opportunities for the virus to become endemic in human populations, at least in Europe, where this advice was proffered. Moreover, human traffic to the Far East, presumably the ancient home of influenza, would have taken too long and would not have been of high enough volume to really sustain too many pandemics.