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April 7 - April 9, 2020
One man who lived on the upper floor at 38 Silver Street kept twenty-seven dogs in a single room. He would leave what must have been a prodigious output of canine excrement to bake in the brutal summer sun on the roof of the house.
The streets flex with the Victorian equivalent of rush hour, rising at daybreak and then subsiding with nightfall; streams of people pour into each daily service at St. Luke’s; small queues form around the busiest street vendors. In front of 40 Broad Street, as baby Lewis suffers only a few yards away, a single point on the sidewalk attracts a constant—and constantly changing—cluster of visitors throughout the day, like a vortex of molecules winding down a drain. They are there for the water.
THE BROAD STREET PUMP HAD LONG ENJOYED A REPUTATION as a reliable source of clean well water. It extended twenty-five feet below the surface of the street, reaching down past the ten feet of accumulated rubbish and debris that artificially elevated most of London, through a bed of gravel that stretched all the way to Hyde Park, down to the veins of sand and clay saturated with groundwater. Many Soho residents who lived closer to other pumps—one on Rupert Street and another on Little Marlborough—opted to walk an extra few blocks for the refreshing taste of Broad Street’s water.
The coffeehouse down the street brewed its coffee with pump water; many little shops in the neighborhood sold a confection they called “sherbet,” a mixture of effervescent powder with Broad Street water. The pubs of Golden Square diluted their spirits with pump water.
With temperatures reaching the mid-eighties in the shade on those late-August days, and no wind to freshen the air, the collective thirst for cool well water must have been intense.
There is something remarkable about the minutiae of all these ordinary lives in a seemingly ordinary week persisting in the human record for almost two centuries. When that chemist’s son spooned out his sweet pudding, he couldn’t possibly have imagined that the details of his meal would be a matter of interest to anyone else in Victorian London, much less citizens of the twenty-first century. This is one of the ways that disease, and particularly epidemic disease, plays havoc with traditional histories.
epidemics create a kind of history from below: they can be world-changing, but the participants are almost inevitably ordinary folk, following their established routines, not thinking for a second about how their actions will be recorded for posterity.
for Londoners, the specific menace of cholera was a product of the Industrial Age and its global shipping networks: no known case of cholera on British soil exists before 1831.
Sanskrit writings from around 500 B.C. describe a lethal illness that kills by draining water from its victims. Hippocrates prescribed white hellebore blooms as a treatment. But the disease remained largely within the confines of India and the Asian Subcontinent for at least two thousand years.
In 1817, the cholera “burst forth…with extraordinary malignity,” as the Times reported, tracking through Turkey and Persia all the way to Singapore and Japan, even spreading as far as the Americas until largely dissipating in 1820. England itself was spared, which led the pundits of the day to trot out an entire military parade of racist clichés about the superiority of the British way of life.
In 1829, the disease began to spread in earnest, sweeping through Asia, Russia, even the United States. In the summer of 1831, an outbreak tore through a handful of ships harbored in the river Medway, about thirty miles from London.
William Sproat, the first Englishman to perish of cholera on his home soil.
By outbreak’s end, in 1833, the dead in England and Wales would number above 20,000. After that first explosion, the disease flared up every few years, dispatching a few hundred souls to an early grave, and then going underground again.
But the experience was largely dominated by one hideous process: vast quantities of water being evacuated from his bowels, strangely absent of smell and color, harboring only tiny white particles. Clinicians of the day dubbed this “rice-water stool.” Once you began emitting rice-water stools, odds were you’d be dead in a matter of hours.
One of cholera’s distinctive curses is that its sufferers remain mentally alert until the very last stages of the disease, fully conscious both of the pain that the disease has brought them and the sudden, shocking contraction of their life expectancy.
Most of this is, to a certain extent, conjecture. But one thing we know for certain: at one p.m. on Friday, as baby Lewis suffered quietly in the room next door, Mr. G’s heart stopped beating, barely twenty-four hours after showing the first symptoms of cholera. Within a few hours, another dozen Soho residents were dead.
Cholera is a species of bacterium, a microscopic organism that consists of a single cell harboring strands of DNA. Lacking the organelles and cell nuclei of the eukaryotic cells of plants and animals, bacteria are, nevertheless, more complex than viruses, which are essentially naked strands of genetic code, incapable of surviving and replicating without having host organisms to infect.
More impressive than their sheer number, though, is the diversity of bacterial lifestyles. All organisms based on the complex eukaryotic cell (plants, animals, fungi) survive thanks to one of two basic metabolic strategies: photosynthesis and aerobic respiration. There may be astonishing diversity in the world of multicellular life—whales and black widows and giant redwoods—but beneath all that diversity lie two fundamental options for staying alive: breathing air and capturing sunlight.
Without the metabolic innovations pioneered by bacteria, we would literally have no air to breathe. With the exception of a few unusual compounds (among them snake venom), bacteria can process all the molecules of life, making bacteria both an essential energy provider for the planet and its primary recycler.
Viewed through an electron microscope, the bacterium looks somewhat like a swimming peanut—a curved rod with a thin, rotating tail called the flagellum that propels the organism, not unlike the outboard motor of a speedboat. On its own, a single V. cholerae bacterium is harmless to humans.
Because our minds have a difficult time grasping the scale of life in the microcosmos of bacterial existence, 100 million microbes sounds, intuitively, like a quantity that would be difficult to ingest accidentally. But it takes about 10 million bacteria per milliliter of water for the organism’s presence to be at all detectable to the human eye.
A glass of water could easily contain 200 million V. cholerae without the slightest hint of cloudiness.
V. cholerae needs to find its way into your small intestine. At that point, it launches a two-pronged attack. First, a protein called TCP pili helps the bacteria reproduce at an astonishing clip, cementing the organisms into a dense mat, made up of hundreds of layers, that covers the surface of the intestine.
the bacteria inject a toxin into the intestinal cells. The cholera toxin ultimately disrupts one of the small intestine’s primary metabolic roles, which is to maintain the body’s overall water balance. The walls of the small intestine are lined with two types of cells: cells that absorb water and pass it on to the rest of the body, and cells that secrete water that ultimately gets flushed out as waste. In a healthy, hydrated body, the small intestine absorbs more water than it secretes, but an invasion of V. cholerae reverses that balance:
The expelled fluids contain flakes from the epithelial cells of the small intestine (the white particles that inspired the “rice water” description). They also contain a massive quantity of V. cholerae.
an accidental ingestion of a million Vibrio cholerae can produce a trillion new bacteria over the course of three or four days. The organism effectively converts the human body into a factory for multiplying itself a millionfold. And if the factory doesn’t survive longer than a few days, so be it. There’s usually another one nearby to colonize.
THE ACTUAL CAUSE OF DEATH WITH CHOLERA IS DIFFICULT to pinpoint; the human body’s dependence on water is so profound that almost all the major systems begin to fail when so much fluid is evacuated in such a short period of time. Dying of dehydration is, in a sense, an abomination against the very origins of life on earth.
Fertilization for all animals takes place in some form of water; embryos float in the womb; human blood has almost the same concentration of salts as seawater.
The first significant effect of serious dehydration is a reduction in the volume of blood circulating through the body, the blood growing increasingly concentrated as it is deprived of water.
Because the brain continues to receive a sufficient supply of blood in this early stage, the cholera victim retains a sharp awareness of the attack that V. cholerae has launched against his body.
The mind grows hazy; some sufferers become lightheaded or even pass out. The terrible evacuations of rice-water stools continue. By now, the cholera victim may have lost more than ten percent of his body weight in a matter of twenty-four hours.
waste products accumulate in the blood, fostering a condition called uremia. The victim slips into unconsciousness, or even a coma; the vital organs start to shut down.
the organisms wants a certain environment because the setting allows it to reproduce more effectively than other environments: a brine shrimp desires salty water, a termite desires rotting wood.
what the Vibrio cholerae bacterium desires, more than anything, is an environment in which human beings have a regular habit of eating other people’s excrement. V. cholerae cannot be transmitted through the air or even through the exchange of most bodily fluids. The ultimate route of transmission is almost invariably the same: an infected person emits the bacteria during one of the violent bouts of diarrhea that are the disease’s trademark, and another person somehow ingests some of the bacteria, usually through drinking contaminated water.
Since the dawn of civilization, human culture has demonstrated a remarkable knack for diversity, but eating other humans’ waste is as close to a universal taboo as any in the book.
In practice, it’s not impossible for physical contact with a cholera victim to transmit the disease, but the chance of transmission is slight. In handling soiled linens, for instance, an invisible collection of V. cholerae might cluster on a fingertip, where, left unwashed, they might find their way into your mouth during a meal, and shortly thereafter begin their deadly multiplication in your small intestine.
Humans began gathering in urban areas with population densities that exceeded anything in the historical record: fifty people crammed into a four-story townhouse, four hundred to an acre. Cities became overwhelmed with their human filth. And those very cities were increasingly connected by the shipping routes of the grand empires and corporations of the day.
Inevitably, in these sprawling new metropolitan spaces, with their global networks of commerce, lines were crossed: drinking water became laced with sewage. Ingesting small particles of human waste went from being an anomaly to a staple of everyday life.
Bacteria and viruses evolve at much faster rates than humans do, for several reasons. For one, bacterial life cycles are incredibly fast: a single bacterium can produce a million offspring in a matter of hours. Each new generation opens up new possibilities for genetic innovation, either by new combinations of existing genes or by random mutations.
They are not limited to passing on their genes in the controlled, linear fashion that all multicellular organisms do. It’s much more of a free-for-all with the microbes. A random sequence of DNA can float into a neighboring bacterial cell and be immediately enlisted in some crucial new function. We’re so accustomed to the vertical transmission of DNA from parent to child that the whole idea of borrowing small bits of code seems preposterous, but that is simply the bias of our eukaryotic existence.
Bacteria like Vibrio cholerae, then, are eminently capable of evolving rapid new characteristics in response to changes in their environment—particularly a change that makes it significantly easier for them to reproduce themselves.
In environments where the risk of transmission is low, the better strategy is to pursue a low-intensity attack on the human host: reproduce in smaller numbers, and keep the human alive longer, in hopes that over time some bacterial cells will find their way to another intestine, where the process can start all over again.
In a low-transmission environment, lethal strains die out, and mild ones come to dominate the population. In high-transmission environments, the lethal strains quickly outnumber the mild ones.
When the citizens of London and other great cities first began gathering together in such extraordinary number, when they began building elaborate mechanisms for storing and removing their waste, and pulling drinking water from their rivers, they did so with conscious awareness of their actions, with some clear strategy in mind. But they were entirely unaware of the impact that those decisions would have among the microbes: not just in making the bacteria more numerous, but also in transforming their very genetic code.
THE TRAGIC IRONY OF CHOLERA IS THAT THE DISEASE HAS A shockingly sensible and low-tech cure: water. Cholera victims who are given water and electrolytes via intravenous and oral therapies reliably survive the illness, to the point where numerous studies have deliberately infected volunteers with the disease to study its effects, knowing that the rehydration program will transform the disease into merely an uncomfortable bout of diarrhea.
And indeed, one British doctor, Thomas Latta, hit upon this precise cure in 1832, months after the first outbreak, injecting salty water into the veins of the victims. Latta’s approach differed from the modern treatment only in terms of quantity: liters of water are necessary to ensure a full recovery. Tragically, Latta’s insight was lost in the swarming mass of cholera cures that emerged in the subsequent decades.
Those endless notices reflect a strange historical overlap, one we have largely outgrown—the period after the rise of mass communications but before the emergence of a specialized medical science.
You didn’t need an academic degree to share your cure for rheumatism or thyroid cancer with the world. For the most part, this meant that the newspapers of the day were filled with sometimes comic, and almost always useless, promises of easy cures for diseases that proved to be far more intractable than the quacks suggested.
Sometimes the cholera was treated with leeches, based on the humoral theory that whatever seemed wrong with the patient should be removed from the patient: if the cholera sufferer’s blood was unusually thick, thanks to dehydration, then the patient needed to lose more blood.
While these were not quite examples of the cure being worse than the disease—cholera set the bar quite high, as diseases go—many of the proposed remedies exacerbated the physiological crisis that cholera induced.
