Drugs, fleas, race, and disease

Illustration based on a photo in The American Museum Journal, published in the early 1900s. The text with it reads, “The rat and dog flea, Lamopsylla cheopis, is the ‘plague flea’ but they live on the rat also and thus may carry plague germs. . . ”
Illustration based on a photo in The American Museum Journal, published in the early 1900s. The text with it reads, “The rat and dog flea, Lamopsylla cheopis, is the ‘plague flea’ but they live on the rat also and thus may carry plague germs. . . ”Heather Hopp-Bruce/globe staff

The signature moment of Chris Christie’s presidential campaign to date came during the six and a half minutes he spoke of his mother’s lifelong battle with tobacco that preceded her death from lung cancer. On an October campaign stop at Shooter’s Tavern in Belmont, N.H., he also talked about an old friend, hooked on opioids, watching as that life unraveled. He talked about responsibility and blame.

The point, Christie said, was that no one told his mom that her addiction was her fault. Nobody said “she’s getting what she deserves,” the candidate recalled. Not so for his friend. “If it’s heroin or cocaine or alcohol, we say, ‘they decided it. They’re getting what they deserved.’ ” In perhaps the most pointed rhetoric a Republican could use, he added, “It’s easy to be pro-life for the nine months you’re in the womb,” but the test was what happens from there. “The 16-year-old teenage girl on the floor of the county lockup, addicted to heroin, I’m pro-life for her, too.”


Such openness is purely welcome. Christie demands that his listeners recognize addiction not as a character defect, but an accident of nature. Bad luck. A disease. It got his mom, it got his friend, it could grab anyone, and we should, he says, find the best ways we can to help those whom addiction afflicts.

Yet there are roughly 300,000 Americans in prison for drug offenses, including half of all federal inmates. For many, their addiction led to prosecution, conviction, incarceration. Those prisoners are disproportionately black and brown men. So what happened — what had to take place — to transform their crimes into a malady? Why — and why now — have Christie and many others come to demand that we see a heroin addict as an object not of scorn but of compassion?

One answer comes from Wong Chut King, lying desperately ill in a basement room in San Francisco in early March 1900. The historian Gunther B. Risse has documented what little is known about him: Born around 1859 in Guangdong Province, he immigrated to California in his 20s. For about two decades, his life was almost completely circumscribed within the dozen blocks of Chinatown’s narrow streets and alleys.


Sometime around the turn of the new century, he fell ill. He turned to a traditional Chinese healer, who may have diagnosed him with a bladder ailment. Weeks passed. Wong consulted another healer. A lump in his groin suggested venereal disease. Whatever treatment he endured failed. His fever spiked. He began to vomit. Diarrhea wracked his body. Finally, he was taken from his room to his deathbed in the coffin shop. On March 6, he died.

Death brought Wong into contact with Western medicine for the first time. Frank Wilson, San Francisco’s assistant health officer, discovered that the lump in Wong’s groin was discolored, black. Samples taken from that bubo ultimately confirmed what Wilson suspected. Wong Chut King’s killer was bubonic plague — the Black Death.

Wong is the first known victim of the San Francisco plague outbreak of 1900 to 1904. From the start of the outbreak, the specter of such a legendary killer ignited a hunt for whom was to blame for the disaster. Given who fell ill — and where — there was an obvious culprit.

For most of its history, Chinatown had served as San Francisco’s scapegoat for just about any social ill. Fearing cholera in the summer of 1854, The Daily Alta warned readers of “this outlandish, beastly race . . . flocking to our shores, thick as locusts,” adding that “whatever may be thought of them, mentally, morally, or physically, all are agreed that they are notoriously filthy.” In 1876, Dr. J. L. Meares, San Francisco’s public health officer, attributed a smallpox outbreak to Chinatown’s “laboratory of infection — situated in the very heart of our city, distilling its deadly poison by day and by night and sending it forth to contaminate the atmosphere of the streets and houses of a populous, wealthy, and intelligent community.” Those who lived there were “unscrupulous, lying, and treacherous” and “a social, moral, and political curse to the community.”


Despite such moralizing pathology, the late 19th century saw the basic biology of infectious diseases, including the plague, coming into focus. The bacterium that causes the disease was identified in 1894. An experimental vaccine followed in 1897, while the fact that rats had some connection to plague outbreaks became increasingly clear, though exactly what their role might be remained unknown. Finally, in 1898, the French physician Paul-Louis Simond discovered that fleas carried the disease to rodents, and from there to people — though, crucially, that result would not be generally accepted for several years to come.

Once the plague hit San Francisco, though, neither epidemiology nor microbial biology shook the basic paradigm. Damn the bacteria: The Chinese were “a foreign community, perpetuated in filth,” as Dr. John Williamson, the president of the San Francisco Board of Health, wrote in 1901. To US Surgeon General Walter Wyman, the plague was an “oriental disease, peculiar to rice eaters.” Faced with such a threat, said Williamson, “Chinatown . . . cannot be rendered sanitary except by total obliteration.”

After Wong’s death, San Francisco authorities did attempt to impose a total blockade on Chinatown and then a forced vaccination campaign, both of which were blocked in court. Nonetheless, the belief that San Francisco’s plague was an essentially Asian disease persisted, culminating in a move to control the public movements of “Asiatics or other races particularly susceptible to the disease.” Officers to enforce the travel bans guarded common exits from the city and state borders with Arizona, Nevada, and Oregon.


The country’s centurylong war on drugs began at roughly the same time as San Francisco confronted the plague — and it too was framed with the lens of race. To get Southern Democrats on board with strict narcotics laws, for example, one of the early drug warriors declared that cocaine was “often the direct incentive to the crime of rape by Negros of the South and other sections of the country.” Opium had long been the Chinese drug, and the Great Depression pushed things further. Mexican immigrants were linked to marijuana, which somehow forced them to commit terrible crimes.

In its current phase, the ongoing drug war still braids together those strands of racial fear and a view of addiction as inherently and voluntarily criminal. The sentencing distinction between crack and powdered cocaine, for example — only eased at the federal level in 2010 — fell on a racial divide, with the result that while “blacks and whites use drugs at roughly the same rates . . . yet by the close of the 20th century, prison was a more common experience for young black men than college graduation or military service,” as Ta-Nehisi Coates wrote in “The Black Family in the Age of Mass Incarceration.”


 New Jersey Governor Chris Christie spoke during a visit to the Turning Point addiction facility with members of Christie’s Facing Addiction Task Force in September in Paterson, N.J.
New Jersey Governor Chris Christie spoke during a visit to the Turning Point addiction facility with members of Christie’s Facing Addiction Task Force in September in Paterson, N.J.CARMINE GALASSO/THE RECORD OF BERGEN COUNTY VIA AP

Now, enter Chris Christie with his Damascene moment. For him, addiction ceased to be someone else’s sin.

More broadly, views like Christie’s are gaining traction because, in essence, drug use in white America has burst into public view. This November, a study by the economists Anna Case and Angus Deaton, the 2015 Nobel laureate, hinted at a reason. Segmenting the American population by race or ethnicity and age, they found that every cohort but one has seen a drop in death rates between 1999 and 2014. There was just one exception: middle-aged non-Hispanic whites — those between 45 and 54 years old — with the strongest effect seen in the least educated.

Subsequent criticism has revised some of Deaton and Case’s analyses, but the basic picture remains: Most Americans are seeing death rates fall; middle-aged whites are not. There is no single clear cause for this result — but Deaton and Case write that “suicide, drug and alcohol poisoning . . . and chronic liver diseases and cirrhosis” have been “persistent and large enough” to kill this cohort at rates high enough to produce a demographic picture not seen in the rest of the American population or in comparable groups in other developed nations.

The larger question, of course, is why middle-aged whites would be drinking and drugging and shooting themselves to death. The most common answer has been that Case and Deaton found a demographic portrait of white despair. Economic insecurity, the crash of 2007-08, globalization, and rapid social change have derailed whites of a certain age. In Deaton’s phrase, the men and women in this cohort have “lost the narrative of their lives.” As Paul Krugman writes, this seems to be a tale of the destruction of deeply held expectations, accumulating into what he believes is “something terrible . . . happening to our country.”

To which there’s an obvious reply: This terrible thing has been happening for a long time — just not (so much) to white people. For one measure: The wealth gap between white and African-American households tripled between the middle of Ronald Reagan’s presidency and the end of George W. Bush’s — and black wealth crashed in the wake of the crash of 2008. The data Case and Deaton deploy show that middle-aged black mortality, though improving, still exceeds that of comparable white men and women. Belaboring the obvious: The terrible ills that Deaton and Case suggest may drive white Americans to despair are hardly breaking news to lots of people whose fate does not usually dominate the headlines.

In life, Wong Chut King was invisible to most of those with whom he shared his city. When he died, Wong reinforced what white San Francisco already believed: The Chinese in their midst were a reservoir of pestilence, a moral and physical danger to the white city beyond Chinatown. San Francisco’s first plague outbreak persisted until 1904, producing an official death toll of 113, of whom 107 were Chinese.

By the end of the epidemic, San Francisco officials had, at least in part, ceased to racialize the disease, emphasizing instead killing rats and moves to line Chinatown’s basements with concrete, the better to seal its buildings against rodents. When plague returned to the Bay Area (but not to Chinatown) in 1907, disease control efforts had swung almost entirely to one informed by the biology of the disease. What had been an indictment of the filth and moral squalor of some of San Francisco’s poorest now became an exercise in rat and flea control; a crime had become a disease.

It counts as progress that Chris Christie can ponder the death of someone he loved, a middle-aged white man addicted to opioids, and bear witness to the realization that addiction is not simply a failure of will, not a sign of moral failure, no mark of Cain. Now, he tells us — and it’s true — that what was seen as sin is better understood as misfortune, that those suffering did not choose to suffer. What’s intolerable is the time it has taken to get from there to here.

Thomas Levenson is a professor of science writing at MIT and an Ideas columnist. His latest book is “The Hunt for Vulcan.”