Flush, p.16
Flush, page 16
Under a section on health and nutrition recommendations, the report nevertheless suggested that the relative abundance of Bacteroides species in my gut indicated that my diet was too high in saturated fats. Six weeks into a successful diet in which I had minimized my fat intake, I was a bit skeptical of the suggestion and wary of what the company would offer to improve my “healthy gut ratios,” given that Sun Genomics also offers personalized probiotics. The report did find that several probiotic species had already made themselves at home (“Keep up the good work,” it said, echoing one of my poop-tracking apps). One, Streptococcus thermophilus, likely came from the yogurt I was regularly eating for breakfast. More surprising was the complete absence of many others, including all ten of the species in the probiotic supplement I was taking. Either the species weren’t viable or didn’t take to my gut, even as temporary residents.
The vast majority of my gut species were commensal microbes thought to have a benign effect on the microbiome, though most of them remain poorly characterized. I harbored a small amount of E. coli bacteria, which I found oddly pleasing despite the variable nature of the potential pathogen, given that I had studied the species for so long. I also hosted a small amount of the archaeal species Methanobrevibacter smithii, which digests some leftovers of bacterial fermentation and produces methane. And then the report took a sharp turn. On the small list of unfavorable microbes, I saw a familiar and disturbing name: Clostridioides difficile. After writing so much about the horrors of C. diff, I was shocked to see the pathogen listed as a resident in my own gut, making up about 0.6 percent of my microbiome. I was apparently an asymptomatic carrier who didn’t suffer ill effects from the microbe after being colonized by it. Mystified about how I might have been exposed, I was unsettled to learn that I could remain colonized for months. When I talked with two microbiome researchers about it, though, they weren’t surprised at all; a scientist from Floré told me it was rare for her to see a report that didn’t include C. diff, given the ubiquity of the bacterial spores in hospitals, clinics, and doctors’ offices. Healthy people commonly carry the pathogen in low abundance, agreed microbial ecologist Sean Gibbons (although published estimates have varied widely; one Japanese study reported a colonization rate of 17.5 percent among 120 asymptomatic volunteers). My lack of symptoms, Gibbons explained, meant that the ecology of my commensal microbial community was keeping it in check: a planted garden crowding out the weeds.
In one of her talks, Lynch likened algae overgrowth in Lake Erie to disturbances in the human gut. She told me she’s always viewed human health and disease and our relationship to our microbiome through the framework of ecology: How do complex ecosystems develop and respond to disruptions, whether in a lake or a gut, and what’s their capacity for resilience? It’s a far more nuanced and intricate view of health and development than the quick fixes we’re often sold by marketers.
In Whorton’s historical treatise on constipation, he writes that doctors of the late 1800s and early 1900s were generous with their prevention advice. Even so, “recommendations to eat more fruits, vegetables, and whole grains; to be more active physically; and always to respond promptly to nature’s morning call to evacuate seemed to many people to require more self-discipline and sacrifice than they cared to exercise. The public, anxious about autointoxication, thus fell easy prey to all manner of marketers of anticonstipation foods, drugs, and devices.” More than a century later, a proliferation of gut- and poop-based tests can similarly project a mirage of easy answers and oversimplified value judgments on what’s good or bad when the reality is far messier. Instead, David said, it may be more useful to take a conservationist approach to the microbiome and think about how to manage our own inner ecosystem.
I was reminded of environmental writer Emma Marris, who argues in Rambunctious Garden that as the most influential creatures on the planet, we’ve fundamentally changed even the most remote landscapes. We have damaged or destroyed much of the environment, true. But we’ve also distanced ourselves from what we imagine to be the remaining bits of untouched wilderness, not understanding that our fates are already intertwined. “We have hidden nature from ourselves,” she writes. Preserving what remains, she argues, will require a hybrid strategy in which we accept our role as change agents in the world around us and embrace our responsibility as caretakers for a vast, half-wild garden.
The gut envisioned by hucksters and schemers has long been a dark, dangerous, and disgusting place full of poison and corruption. A sewer or tube full of toxins to be cleansed and expelled. But if it’s more like a half-wild garden, maybe it’s time we all become committed gardeners. Apps and tests and supplements, if backed by science and used wisely, can help point out imbalances and problem spots but they can’t replace the actual grunt work of tending to our inner flora. Some of the complicated patterns in poop clearly require more research to decipher the signs of trouble. For the rest, we already have our sense and senses to heed the burst of signals floating in the toilet bowl. Best of all? Our own built-in technology will never be obsolete.
WE BEGAN OUR HUNT FOR the killer on a cloudy morning in July near the corner of East Wright Avenue and East T Street in Tacoma, Washington. Past a parked Winnebago with a blue and green Seattle Seahawks football blanket as a privacy curtain for a side window. Then down to the bottom of a large catchment system in one of Tacoma’s poorest neighborhoods.
I stopped with the others in front of a maintenance hole cover under a highway overpass. The waste stream from an estimated 15,000 to 18,000 city residents flows past this point in the sewer line, and we were hoping that the assassin hiding within might betray its presence. Steven George, an environmental technician with the city, lifted the cover with a metal hook and then shone a flashlight into the murk below. His work colleague, Haley Abbruscato, was already busy taping a folded industrial paper towel around the end of an extension pole called Mr. LongArm to form a kind of oversized swab.
Casey Starke, an undergraduate researcher overseeing the reconnaissance mission, peered down the hole in search of some suitable buildup for Abbruscato to sample and singled out a small concrete bench just above the flow. Problem spots in the sewer system like overhangs and ninety-degree turns, he said, tend to concentrate solid matter and make for prime sampling locations. With the target identified, Abbruscato lowered the pole until it made contact and then slowly turned it to get her sample. Up again, and she had clearly hit the mark.
Starke opened a clear plastic tackle box that doubled as a portable test kit, with blue gloves, sterile Q-tips, and a tray of carefully labeled polypropylene tubes filled with a buffer that both inactivates the SARS-CoV-2 virus and preserves its genetic material. The stench was unmistakable through our face masks as he dabbed at the pole’s soiled swab with a Q-tip before transferring the sample to a tube. “This is a very ripe site, isn’t it,” he said matter-of-factly.
“It is,” Abbruscato agreed.
“But unfortunately, that correlates to good sample types,” he said.
“So the riper the better?” I asked.
“Yeah, that’s unfortunately what I’ve got to work with.”
“Usually, you go for the greasy, nasty, gunky stuff,” Abbruscato explained. “So if it smells real bad, it’s probably in there.” By it, she meant the killer in the sewer. Not the horrifying It of Stephen King’s wicked imagination but an even more murderous villain that had wiped out more than 138,000 Americans by that point.
Starke, an aspiring doctor with an avid interest in epidemiology, was volunteering with a nonprofit biotech start-up called RAIN Incubator. The pilot project would help determine whether the team could accurately detect genetic material from the SARS-CoV-2 virus at two wastewater treatment plants and five other strategic points across Tacoma and correlate the signal trends to the county’s heat maps of COVID-19 cases. The goal was to combine the test results with socioeconomic data to point out the most vulnerable hotspots and help public health officials determine where to direct more resources. The researchers had their work cut out for them, but if the pilot project proved itself, the city could be further subdivided into areas that drain into some three dozen pump stations where the sewage is pulled to higher ground and from which sludge could be easily collected. “It’s ready made for epidemiology,” Starke said.
Just as your poop can reveal plenty about what’s happening within your gut, a community stool sample can illuminate what may be lurking within an entire population. The growth of wastewater-based epidemiology, turbocharged by the desperate need to get a better handle on a devastating pandemic, could establish the methods and infrastructure for tracking other deadly pathogens and dangerous drugs like the highly addictive opioid painkillers that have fueled a parallel epidemic. Cities across the globe geared up to read these stories in the sewer in the spring and summer of 2020, as hundreds of researchers converged upon the realization that a relatively low-tech surveillance method might give them a critical early warning.
The precedent, in fact, had been set more than eighty years earlier. In the summer of 1939, polio raged around the world and a team of investigators from Yale University set out to conduct tests in three cities with large epidemics: Charleston, South Carolina; Detroit, Michigan; and Buffalo, New York. They had tried before, unsuccessfully, to confirm the presence of the poliovirus in sewage during a 1932 epidemic in Philadelphia and again in 1937 in New Haven, Connecticut.
But this time, they struck gold, first in July when they sampled from a Charleston pumping station that collected sewage from a hard-hit district as well as a nearby isolation hospital. In the crude confirmatory experiments of the time, the researchers inoculated two rhesus macaques with a sample of the sewage, upon which both monkeys developed polio. To confirm their findings, the researchers used tissue from the central nervous system of the stricken animals to inoculate additional monkeys (and occasionally other lab animals), which subsequently developed the clinical signs of polio as well. As in humans, the virus signaled its presence in the monkeys through a fever, spinal cord lesions, and acute flaccid paralysis—a fast-progressing weakness or paralysis in the arms, legs, and even lungs. Tests conducted later in the summer when the epidemic had waned and again in the fall came back negative.
In Detroit, the researchers conducted the first successful wastewater test from a single building when they sampled sewage from a basement trap where the sewer pipe left an isolation hospital. On three occasions in August and September, their inoculation tests in monkeys confirmed the presence of infectious poliovirus. The team also made the first comparison between positive sewage test results and the concurrent burden of polio cases in the hospital’s isolation wards. The investigators had less luck in Buffalo despite the city’s ongoing epidemic. But they inadvertently demonstrated the blunt cruelty of such early experiments and the danger posed by other toxins and pathogens in wastewater when they inoculated monkeys with sludge collected from a treatment plant. “The sludge material proved unusually toxic in that both of the monkeys inoculated with relatively small doses of it, promptly died,” the authors noted. Another ten monkeys died from bacterial infections contracted during the series of experiments.
The scientists had, however, demonstrated that a lethal virus could be tracked through a community’s sewers, and other researchers quickly took note. “As soon as we were informed of this discovery, it seemed to us important to get it verified,” wrote a team of Swedish researchers who began testing the sewage of Stockholm during an outbreak in the city that same year. The scientists not only verified the earlier results by detecting polio in a sample collected that October, but also determined that the virus could retain its virulence for weeks. After storing the sewage sediment at roughly thirty-nine degrees Fahrenheit for two months, the scientists used it to successfully infect macaques. The authors argued that sewage that hadn’t been disinfected was posing an imminent public health threat, adding to the growing consensus that polio was a water-borne disease. “Hence the serious consequence that during those periods when infantile paralysis is epidemical, we have to reckon with the sewage as an important source of infection, from which the disease can spread over vast areas,” they wrote.
But wait, a French researcher responded. What about an animal vector like, say, sewer rats? In a droll bit of Scandinavian shade, the Swedish scientists roundly rejected the suggestion: “This idea may, of course, appear plausible if one considers the extraordinary abundance of rats prevailing in certain parts of the Paris sewers.” But in the closed drains of Stockholm’s sewer system, they asserted, “the rat has certainly no prospects of existence, still less of propagating.” That would be welcome news indeed to the residents of what some have more recently called “the rat capital of Scandinavia,” and to the listeners of Radio Sweden, which warned that a record invasion in Stockholm was being abetted in part by enterprising rats that were entering homes through the “protected environment” of sewer pipes.
The Swedish researchers similarly—and wrongly—dismissed the idea that insects could be carriers: “These arthropodes certainly very unwillingly, if ever, look for such a vehicle as sewage when they are about to lay their eggs.” Au contraire, as we saw from Mark Benecke’s forensic entomology. Amid the missteps, the authors introduced an important concept: “One possibility presupposes the presence of a considerable number of healthy virus carriers living within the drainage area whence the infected sewage came.” The idea of a silent outbreak was born, if deemed much less likely than the possibility that a living being, perhaps a single-celled protozoa, was somehow enabling the virus to multiply in the sewer.
Joseph Melnick, a pioneer of virology, environmental surveillance, and polio vaccine research, poured cold water on the idea that sewage was playing a direct role in the spread of the disease in a 1947 paper. But he championed the idea that determining the existence or nonexistence of virulent poliovirus in the sewer—a binary yes-no signal—could provide critical epidemiological information about whether it was present only during epidemics or all the time in urban environments. As scientists now know, only about one in every 200 polio infections leads to paralysis. Even so, the virus can efficiently replicate in the intestinal tract of both symptomatic and asymptomatic carriers and spread to others who ingest virus-laden fecal particles or are indirectly exposed through contaminated food or water. In the sewer, signs of the virus can track the rise and retreat of local outbreaks even in the absence of clear cases.
In 2021, polio was still endemic in Pakistan and Afghanistan, the last holdouts of a disease that has stubbornly resisted decades of effort to fully eradicate it from the planet. But periodic outbreaks of both the wild virus and a form that can occasionally escape from oral vaccines made with live but weakened versions of the virus have hit other countries. Israel has conducted sewage-based environmental surveillance for polio since 1989, with monthly samples collected and tested at sentinel sites across the country. In May 2013, wastewater monitors picked up signs of wild poliovirus type 1, the first time it had been detected in Israel since 1988. Investigators soon traced the silent outbreak to the southern city of Rahat, the largest predominantly Bedouin community in the country. Public health officials launched a vaccination campaign and the outbreak subsided in 2014. In a little more than six months, however, an estimated 60 percent of susceptible individuals, mainly children under the age of ten, had been infected in the community.
Surveillance systems in Israel and elsewhere have also had to account for chronic shedding of poliovirus particles by immunocompromised individuals who cannot fully clear the intestinal infection. Through the end of 2019, the World Health Organization had tallied nearly 150 cases of prolonged or chronic shedding from individuals who had been infected with polio through an attenuated vaccine and who represented potential reservoirs of disease. In one exceedingly rare but remarkable example, researchers were tracking a man in the UK who, at last count, had been continually shedding virulent poliovirus particles through his poop for more than thirty years.
The ability of poop-based surveillance to sketch out the contours of diet, disease, and even drug habits clearly raises ethical questions about who deserves to know what we’re carrying around with us and when the public good outweighs personal privacy. In aggregate, though, testing wastewater may afford a measure of anonymity that monitoring cell phone use and personal health data doesn’t. David Hirschberg, RAIN Incubator’s founder, told me that because poop is so widely devalued, people are far more likely to agree to surveillance of wastewater samples than blood samples. As he put it, “I think people are done with their shit.”
Roughly 40 percent of people infected with the SARS-CoV-2 virus shed it in their feces, potentially allowing sensitive tests of pooled sewage samples to detect even a handful of cases that might otherwise go undetected. Results can be available within a few hours of when a sample arrives at a lab for testing. Compared to clinically confirmed COVID-19 cases, multiple researchers have agreed, daily sewage tests can provide a head start of about a week in detecting the virus in a community. This monitoring requires a public sewer system, of course, and more than one-fifth of US households use private septic systems instead. Similar pooled tests, though, have also worked on wastewater samples from cruise ships and commercial airplanes.
