Multiply drug-resistant TB had arrived. Microbes had emerged that were so broadly resistant to antibiotics that, in practical terms, they were invulnerable.
Tuberculosis didn’t reemerge overnight in the United States. On the contrary, the new mutant microbes made numerous tentative incursions into the Homo sapiens population over a period of years. It wasn’t a surprise attack.
It almost seemed as if human beings were deliberately ignoring the plentiful warning signs.
Though tuberculosis had never disappeared, its incidence had declined steadily in the United States since the 1880s, and hit record lows following the introduction of antibiotic treatment. The robust Mycobacterium tuberculosis was impossible to eradicate, as half the world’s population at any given time was infected with the bacteria. For most people M. tuberculosis infection was a benign event: the microbe was kept in check by the immune system and the individual never, throughout his or her life, fell ill.
On average, infected people had a 10 percent chance of developing active disease sometime during their lives, and a 1 percent chance of coming down with a lethal TB illness. Thus, statistics would indicate that about 2 billion human beings were infected with the microbe in 1988; 200 million would during their lives suffer tuberculosis and 2 million would die of the disease.
But those neatly averaged numbers belied the true nature of the risks of TB and the disease’s extremely unequal distribution worldwide.
From the earliest days of Western tuberculosis research, scientists and physicians had recognized that the microbe moved hand in hand with poverty. Though there were famous cases of TB among more affluent individuals, most of the world’s tuberculosis victims had always been the poorest citizens.
The nature of the association between TB and poverty was hotly debated throughout the nineteenth and twentieth centuries,132 but the salient points were clear. The M. tuberculosis bacterium was, like its close cousin the M. leprae, which caused Hansen’s disease, an extremely slow-growing microbe that under most circumstances spent its life either under attack from the human immune system or lying low, causing no disease. Its best hopes of vigorously reproducing, developing a large microbial colony within a human being, and causing disease lay with either a diminished host immune capacity or continuous reinfection of the human being.
Diminished immune systems were plentiful wherever Homo sapiens lived in squalor and poverty. Malnutrition played an important role, though chronic infections with other microbes, such as tropical parasites, influenza, and amoebas, were also factors. Any ailment that taxed the immune system could create opportunities for M. tuberculosis.
M. tuberculosis exploited vulnerabilities. It was an opportunist. For decades it might silently lurk inside a Homo sapiens awaiting a moment when defenses were down, and then, when the victim’s immune system was preoccupied with malaria or cancer, famine or pneumonia, it would strike.
It was also possible for people living in densely crowded situations to be continuously reexposed to the M. tuberculosis exhaled by others, which greatly increased their risk for developing an active case of the disease. That was why TB had historically been so strongly linked with urbanization and, in particular, slum housing and institutionalization.
Certainly it could have been predicted that the arrival of a new disease that produced severe immune deficiency and struck particularly hard in communities of poverty would spawn a reemergence of tuberculosis. If such communities had already been witnessing a slow, steady rise in TB cases, well before the new wave of immunodeficiency arrived, a resurgence of tuberculosis seemed a virtual certainty, unless public health mitigating actions were taken.
In 1947, when antibiotic therapy for TB was still considered a novel treatment and disease prevention technique, 134,946 cases of tuberculosis were reported in the United States. By 1985 the uses of streptomycin, rifampin, isoniazid, and other antibiotics, coupled with an aggressive public health effort to identify and treat TB cases, had brought the U.S. caseload down to 22,201. Fewer than 30,000 Americans had actually contracted tuberculosis each year since 1977, and the majority were elderly individuals of European descent who had carried the M. tuberculosis microbes in their bodies for decades, only falling ill as their aging immune systems failed to keep the bacteria in check.
Well before the actual numbers of TB cases began to swell, the demographics of the disease shifted. Between 1961 and 1969 more than 80 percent of all active TB cases in the United States were among people over sixty-two years of age, most of them readily treated without hospitalization through basic long-term antibiotic therapy. During that time the U.S. federal government spent $69,287,996 on TB control.133
Between 1975 and 1984, however, the numbers of active TB cases reported among elderly Americans and Caucasians of all ages declined sharply. White male cases dropped 41 percent, white female cases 39 percent. In contrast, though TB was declining across the board, its downturn among non-whites was far slower: only 25 percent for males and 26 percent for females. And the age distribution of cases had shifted: by 1984 only 29 percent were over sixty-two years of age. In the non-white population less than one out of every five active TB cases that year involved a person over sixty-two and fully 20 percent were between the ages of twenty-five and thirty-four. 134
As early as the mid-1970s, Lee Reichman, then head of tuberculosis control for New York City, was seeing a marked increase in active cases among injecting drug users and vagrants living in Harlem, most of them young men. Reichman’s attempts to sound alarms about the new trend were muffled by a medical establishment that had already written TB off as a historical artifact. 135
There were other clear warning signs. Between 1980 and 1986 five different surveys documented a relationship between the rise of homelessness in America and surges of TB in young adult populations. The spread of tuberculosis within emergency homeless shelters was demonstrated, and it was even clear to the CDC by 1984 that new mutant strains of drug-resistant TB were spreading among the urban indigent. 136 A striking 1980 study of young adult men living in subsidized single-room occupancy housing for the otherwise homeless in New York City found that 98 of 101 came up positive in skin tests for TB infection, and 13, or 6 percent, had active disease as measured by laboratory analysis of their sputum. The 13 were carrying contagious pulmonary disease, meaning they could exhale the microbes onto others.137
By 1986 nearly half of all active TB cases reported in the United States were among nonwhites, most of them African-American. There could be no doubt that dramatic changes were underway by the mid-1980s. Tuberculosis had clearly shifted to younger, predominantly African-American and urban populations. Geographically, it had shifted from areas such as Virginia to New York City, Miami, and scattered urban sites. The CDC itself noted the shift in 1986, which coincided with the first upward trend in TB cases reported in the United States since 1953. The agency also believed that “HIV infection may be largely responsible for the increase in tuberculosis in New York City and Florida.â€138
From the beginning of the AIDS epidemic, researchers in both the United States and Haiti had noted that HIV-positive Haitians had a high rate of tuberculosis. Indeed, published reports stated as early as 1982 that Haitians suffering from AIDS in Port-au-Prince were more likely to die of tuberculosis than of any other opportunistic infection. But American officials took little notice of this observation. Like their counterparts throughout the Western world, U.S. physicians tended to view the TB risk for people with HIV as a Third World problem.
They were partly right; tuberculosis was an enormous, and escalating, problem in the developing world.
In 1990 Africa’s most famous contemporary hero, Nelson Mandela, developed acute tuberculosis during his twenty-sixth year of imprisonment. Spitting up blood during the bitter Cape Town winter, Mandela was gravely ill. At the age of seventy at the time, Mandela fit three classic risk groups for active tuberculosis: elderly, living in cramped, den
sely populated quarters, and black. In South Africa, 15 percent of infected blacks went on to develop active TB, compared with only 3 percent of whites, largely because of inequities in housing and health care.
As early as 1984, Project SIDA researchers in Zaire had seen a direct link between rising TB rates in that country and the HIV epidemic. Five years later, the World Health Organization’s TB and AIDS programs issued a joint statement calling attention to the linkage and warning of growing parallel pandemics. In particular, the WHO report noted that 60 percent of all AIDS patients in Haiti had active TB, as did 20 to 60 percent of all African AIDS patients (rates varying geographically across the continent). 139
Though many developing countries quickly took steps to follow the WHO recommendations, the United States and most of Western Europe were unmoved.
There were several disturbing facets to Africa’s new TB epidemic—again, offering clues that should have served as warnings to officials in the wealthy nations. Some HIV-positive patients seemed to suffer not only activated disease from long-dormant M. tuberculosis infection but also new infection. That meant the disease was spreading and could be posing an increased risk for general populations, not just those who were infected with HIV.140 Where endemic tuberculosis rates were high, TB was “the single most important opportunistic disease related to HIV infection in the developing world,†according to researchers based in Côte d’Ivoire.141 HIV-positive patients did not respond well to the two cheapest antituberculosis drugs, thiacetazone and streptomycin; the drugs were four times more toxic in people with HIV, even lethal. This posed enormous problems in terms of the cost of tuberculosis treatment. 142 And the relative severity of tuberculosis in HIV-positive people did not vary appreciably with the stage of HIV disease. Indeed, for many Africans tuberculosis was the first ailment that tipped off physicians that they might have AIDS. Thus, hundreds of thousands—perhaps millions—of people in developing countries, who didn’t yet realize that they were infected with HIV, were at tremendous risk for tuberculosis. 143
By 1990 public health experts in some African countries were predicting not only utter defeat in their decades-old tuberculosis control efforts, but also potentially dire economic impacts that would further compound the grim damage the AIDS epidemic was expected to cause.144 On the wall of the Geneva headquarters of the Global Programme on AIDS hung a graph tracking the AIDS and TB epidemics of Burundi, Malawi, Zambia, and Tanzania. The two epidemics tracked in clear tandem, each growing at exactly the same rates.
Despite all these observations the CDC concluded in early 1989 that the goal of eliminating tuberculosis from the United States by the year 2010 remained attainable and the nation’s TB control efforts were essentially on track.145
The following year, however, the CDC’s tone changed to one of alarm as fuller assessment of American TB reports revealed that the decade of the 1980s had witnessed a 28,000-person excess caseload of tuberculosis. Indeed, the downward slope TB had been following since 1953 plateaued in 1984–85 and climbed steadily, so that by the end of the decade the United States had almost as many cases of the disease as had been seen in 1980. The biggest increase was among inner-city African-Americans—TB cases in that group skyrocketed by 1,596 percent between 1985 and 1990.146 Between 1985 and 1991 there was an overall 18.4 percent increase in tuberculosis cases in the United States,147 most of it attributable to the HIV epidemic.148
When the crisis hit, Dr. Karen Brudney was one of those who could say, “I told you so.†Not that it gave her much satisfaction. She was far too overwhelmed with her huge tuberculosis caseload to spend a lot of time wagging her finger at public health bureaucrats. The street-savvy, tough-talking physician made up in spades with attitude for what respect her thin, wiry female frame might otherwise fail to muster from the kinds of clients she served every day in the city’s Lincoln Hospital, located in the Bronx. Equally comfortable conversing in English, Spanish, French, or Haitian Creole, Brudney barked her commands and castigations just as freely to the drug dealers, alcoholics, thieves, and ex-convicts as she did to New York’s model citizens. If any of them took this thirty-something white lady for a pushover, they were in for a big surprise.
On an icy late-winter day in 1992, Brudney paced the hospital’s outpatient TB clinic, clearly agitated. The waiting room was packed with people of all ages who chattered loudly, mostly in Spanish, or watched the Puerto Rican soap opera flickering from the television that was secured to the wall by two separate sets of locks and chains. Unfortunately, none of the men, women, and children crammed into the Health Stat 10 waiting room were Brudney’s patients.
As she angrily moved up and down the clinic hallway, avoiding the crowds and gurneys with the skill of an experienced rush-hour driver, Brudney grumbled.
“Clinic’s been open an hour and not one single client is here. We’ll be lucky if two out of the twelve clients that are supposed to be here actually show up for their TB checkups. We’re only open once a week, they can’t get their meds without coming to clinic, but we never get a better than fifty percent turnout,†Brudney said, taking yet another look at her client list. “If they don’t show up, it means they’re not taking their meds. And if they’re not taking their medication, they’re contagious.â€
Her eye caught sight of a particular name—“Joanneâ€â€”and Brudney’s aquiline face screwed up into an expression of disgust.
“This one! Ugh!†Brudney exclaimed. “This one is somebody they should lock up. She’s out there infecting everybody. She’s already been responsible for one outbreak, one where people died. And the strain she’s carrying is multiply drug-resistant. If she showed up right now I wouldn’t even want her in clinic, exposing everyone.
“What the hell would I do with Joanne if she did show up—which, of course, she won’t. If I ordered a mandatory detention on her I’d need a bed here in the hospital. That’s a whole day’s work, a mountain of paperwork, a real nightmare. Then suppose I succeed in getting a bed, who’s going to pay for the twenty-four-hour guard on her? And she’s not going to stay, guard or no guard. What’s security going to do, shoot her? Chain her in shackles in her bed?
“That woman is carrying a mutant TB strain that is virtually untreatable, 50 percent fatal. She’s spreading it all over New York City. And there’s nothing—nothing—I can do about it,†Brudney exclaimed as she snapped Joanne’s chart shut.
Minutes later Vernon, a thirty-three-year-old African-American male, strolled in unannounced. He didn’t have an appointment, but so what—nobody else had shown up. Even an amateur could tell that Vernon had tuberculosis: his six-foot-one frame was down to 149 pounds, his movements were slow, from deep in his lungs came periodic painful coughing fits, and his eyes had that ghostly look that comes with acute illness. Characteristically, Vernon compensated for his illness with a forced kinetic energy that could be mistaken for an amphetamine high.
“You’ve lost more weight, Vernon. You taking your pills?†Brudney asked.
Vernon launched into an earnest, lengthy description of his daily medication routine, insisting that, despite all their side effects and the painful injections involved with one of his four medications, he was taking all fifteen pills and one shot a day, just as instructed. Brudney rolled her eyes, grunted a smirking sound, and let it be known that she’d heard all this before from Vernon.
“I’m not ashamed,†Vernon insisted. “I’m dealing with it. I really am. This time.â€
“Yeah, this time,†Brudney responded. The physician called in a social worker and, in front of Vernon, told the patient’s story. Vernon enthusiastically added details along the way, seemingly proud of his dubious battle with tuberculosis.
In early 1989 Vernon had been hospitalized with what appeared to be pneumonia. Three weeks later the hospital lab returned a different verdict: tuberculosis. There was nothing special at the time about Vernon’s strain of M. tuberculosis; it was garden-variety TB.
So Vernon was released from the hospital and ordered to take two relatively inexpensive, extremely effective drugs every day for six months: isoniazid and rifampin.
“But you screwed up, didn’t you, Vernon?†Brudney said.
Shrugging his shoulders, Vernon said, “I figured anytime I felt bad, I’d just go to the emergency room and get more pills.â€
After a year of sporadic, improper use of the drugs, Vernon’s tuberculosis bacteria mutated, becoming resistant to both drugs. Since he had long disappeared off the City Health Department’s radar screen, investigators were sent out in search of Vernon.
But he had disappeared.
“I move around a lot,†Vernon said, vaguely referring to several emergency homeless shelters and the apartments of friends and relatives.
Then he had suffered a major tuberculosis relapse and in November 1991 ended up back in Lincoln Hospital, spitting up blood. For ninety-four days Vernon struggled at death’s doorstep in Lincoln, his lung mucus coming up clear.
“That’s bad,†Vernon said, though he deferred to Brudney for an explanation. The TB colonies in his lungs had formed a hard, calcified cavity inside of which they thrived, protected from his immune system and from the four powerful drugs that dripped via an intravenous line into his bloodstream all day, every day, for three months.
Since his discharge from Lincoln Hospital in January 1992, Vernon had been having night sweats and felt fatigued. “But I’m alive, and I’m gonna stay that way.â€
“You are, if you take all of your medication,†Brudney scolded.
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