What's Causing Florida's Leprosy Cases?: "Leprosy-causing bacteria continue to infect people in the southern United States, including in Florida, where nine people have been diagnosed with the disease so far this year."
This news item reminded me of the piece I did a few years ago, about similar cases of leprosy in Louisiana. In both cases, the vector of the disease is armadillos. In Louisiana, people caught the disease by eating the armadillos. Here's my original report, which first appeared in Discover.
Dr. Richard Truman and I dressed in gowns, disposable booties, masks, and rubber gloves. Then we opened a door and stepped into an odor Truman had warned me about. It was something like a diaper pail and quite a bit like sour milk. I was glad for the mask.
The room was full of cement runs – walls about four feet high, forming rectangular pens about six by three feet. The cement floors were littered with sawdust. The dishes for food and water were just like those one might provide for a dog or cat—in fact, the food included cat chow—but the residents here were nine-banded armadillos. An ordinary plastic kitchen trash can lay in each run to serve as a burrow.
Truman, a tall, soft-spoken man whose silver hair didn’t match his youthful face, asked a lab assistant to roust one armadillo from its sawdust. The animal looked like an inverted bronze gravy boat with a head and tail. The assistant gripped it at the back of the neck and the back of the tail—pretty much the only option if you want to avoid an armadillo’s impressive digging claws. Truman let me hold the thing. Excluding the tail, it was about the size of a football, but heavier than your average cat. It wriggled and flexed, kicking with all four feet. Its pink belly was studded with protuberances from which tufts of hair sprouted. These structures, Truman said, have a sensory function.
After that brief hands-on encounter, Truman asked the assistant to put the armadillo back. They’re sensitive animals, poorly suited to captivity, and too much human handling can prove fatal for them. I was, in fact, allowed to see only the healthy armadillos at Louisiana State University, home to the Laboratory Research Branch of the G. W. Long Hansen’s Disease Center, and those only with strict sanitary controls. The ones with leprosy were strictly off-limits—I was more dangerous to them as a source of secondary infections than they were to me.
I was there to learn about two mysterious organisms, both poorly understood even after centuries of contact with people. One, of course, is the armadillo; the other is Mycobacterium leprae, the microorganism responsible for leprosy. Truman and other researchers are using the former to study the latter. What they’ve discovered so far is a lesson in the complexity of the natural world.
The symptoms of leprosy, also known as Hansen’s disease, start in the nerves. Patches of skin lose feeling. For some people, that’s as far as it goes. For others, things get much worse. Grainy, ulcerating lesions appear on the hands, feet, and back, and, in men, the testicles. Nerves degenerate, causing the glands that oil the skin to stop working. The skin cracks, leaving the extremities vulnerable to secondary infections. People lose fingers and toes—not because of the disease itself, but because they don’t notice that they’re too close to a fire or that rats are nibbling at them. The dead nerves create an array of odd postures—the claw-hand, the staring eye that cannot be closed. The respiratory system is invaded; a slimy discharge issues from the nose. The eyes succumb to infection and eventually to blindness. The disease progresses slowly, the first lesion following the actual infection by three years or more, the worst manifestations developing years after that. But these horrific symptoms occur in only a tiny minority of those infected, and most people are not susceptible to infection at all. “M. leprae is almost the perfect parasite,” Truman said, because it so rarely destroys its host, and then only very slowly.
The skulls of four Egyptians from the second century BCE have curious deformities. Certain parts of the face seem to have eroded before death. These skulls are the oldest hard evidence of leprosy, one of the oldest human diseases. Detailed descriptions of symptoms in various documents push our known contacts with leprosy back even further, to about 600 BCE. Beyond that, the vagueness of historical descriptions becomes a problem. There are accounts of a leprosy-like disease invading Egypt from the Sudan during the reign of Ramses II. The disease mentioned with such horror in the Bible may not be the same thing as modern leprosy—its symptoms are only vaguely alluded to, and sometimes it seems not even to be a disease as we understand the idea, but sin figuratively described. If the biblical references are to a literal skin-mottling disease, some commentators find smallpox a more likely candidate.
But it’s certain that genuine leprosy has peeked into human history at odd junctures, as when the soldiers of Alexander the Great conquered the East and brought back silks, spices, and the disease. Europeans came back from the crusades infected—a public relations problem for the Church, since the crusades were supposed to be a holy war, and leprosy appeared to place God on the other side. For a few centuries, lepers’ homes existed throughout Europe. Leprosy’s decline as a major health problem on that continent coincided with the Black Death, which tended to kill the inmates of lepers’ homes and thus break the mysterious chain of transmission for the older disease. But elsewhere in the world, leprosy has never lost its hold. Half a million new cases appear annually, and the total number of people afflicted is at least ten million. India and Brazil currently have especially severe leprosy problems, but the disease occurs virtually everywhere in the world, including about 6000 cases currently in the United States.
The notion that leprosy is contagious has been around for at least 2500 years, but a competing hypothesis blamed heredity. It made some sense: relatives of lepers proved more likely than others to become lepers themselves. Western science dropped the hereditary theory in the 1880s, when a missionary named Father Damien, who had a well-documented and leprosy-free family background, was revealed to have caught the disease while working with lepers on Molokai. By that time, a Norwegian doctor named Armauer Hansen had discovered Mycobacterium leprae, the organism that causes the disease. The nasal secretions of people with severe cases carry enormous quantities of M. leprae, and many physicians and researchers assume that the microbe infects new victims through the respiratory system or through open wounds. Hansen immediately recognized the importance of cultivating M. leprae for study, but he found he couldn’t keep the bacterium alive in a dish. Even now, no one has succeeded in cultivating it outside a warm body. “It starts to die as soon as it’s out of the tissue,” said James Krahenbuhl, Truman’s colleague at the G. W. Long Hansen’s Disease Center. Hansen tried to infect rabbits with M. leprae, but it didn’t take.
In 1956, Chapman H. Binford, having noted that leprosy attacks the coolest areas of the human body, suggested that lab animals might be susceptible to infection in their cooler regions. By 1960, C. C. Sheppard had successfully inoculated the footpads of mice. Soon mouse footpads and hamster ears were yielding fresh supplies of M. leprae, though never in the quantities needed for effective leprosy research. The fresh cadavers of infected humans remained the best source for the microbes.
Then the team of Wally Kirchheimer and Eleanor Storrs noticed that armadillos are cool all over. At 30-35 degrees Celsius, armadillos run several degrees cooler than typical mammals. The animal’s armor probably has something to do with its low temperature; it certainly makes the armadillo a poor regulator of body temperature, as mammals go.
My personal acquaintance with armadillos began at a freak show in the Oklahoma Panhandle in the early 1970s. The show’s exhibits included a five-legged sheep, a three-legged chicken, a hairless Mexican “Elephant-dog,” and, at the curtained end of the tent, to be seen only after payment of an extra dollar, a pickled, two-headed human baby (“Born to live,” a taped voice kept saying, and when I asked my mother what that meant, she said we’d talk about it later, but we never have). And a Living Dinosaur.
Contrary to its billing, the Living Dinosaur was not actually alive. Its desiccated carcass was glued to a felt-covered board. A placard explained that this creature had existed “when dinosaurs ruled the earth” and had survived to the present day. The placard didn’t make clear that the thing itself was not a dinosaur, despite its resemblance to a miniature triceratops. It was, in fact, an armadillo. A huge taxonomic blunder had been compounded with the slip of an era.
Nowadays, when armadillo knick-knacks litter eBay and caricatures of the animal have promoted everything from Lone Star beer to the professional baseball team of Amarillo, Texas, the “Living Dinosaur” fraud would fool nobody. But in the early 1970s, armadillos were unknown in the Oklahoma Panhandle and most of the rest of the country, though they had long been familiar to people in south Texas, Louisiana, and Florida. Since crossing the Rio Grande into the United States in the 1870s, armadillos have colonized most of the Southeast, their progress having only recently come to an apparent halt at the Rockies in the West and around the southern tip of Indiana in the north, where cold has barred them from further progress.
During the 1970s armadillos also colonized the consciousness of the American public, so that soon everybody seemed to know what one looked like. In the early 1980s I ventured downstate to attend college at Stillwater, Oklahoma. On my first trip there, though I no longer found armadillos exotic, I nonetheless found myself startled at the sight of several hundred dead ones. They littered the road and the right of way. The day was hot, and many of the carcasses had bloated, their legs jutting at forty-five degree angles. One in particular caught my eye: a car tire had halved it as neatly as a ripe watermelon.
This mini-apocalypse points to two interesting armadillo behaviors. One is a defensive tactic: when threatened, an armadillo springs straight up. This move is effective against most predators, but suicidal against cars. The other behavior is dietary: armadillos eat carrion, including dead armadillos, and the grubs and maggots they find therein. So a highway strewn with kindred carcasses apparently strikes an armadillo as an irresistible feast.
The armadillo family tree includes a number of interesting branches, including about twenty extant species in South America. Some of them look like opossums that have tumbled through a dryer’s fluff cycle. Among their ancestors are an extinct North American species that weighed five or six hundred pounds. Their nearest relatives are the anteaters and sloths, with which they share some extra flexibility in the spine and a lack of well-developed, specialized teeth. The only armadillo found in the United States in modern times is the nine-banded species, so called because accordion folds in the middle of its back join the shell-like sections fore and aft. The armor is made of ossified skin. It’s not hard like a tortoise’s shell; it’s more like stiff leather. The head and limbs sport plates of this armor as well.
Its unusual architecture causes the armadillo to copulate in the missionary position. Its young are normally identical quadruplets all wrapped in the same placenta, though occasionally it produces eight or twelve identical young. The fertilized armadillo egg can lie in its mother’s reproductive tract for up to three years, bathed in nourishing fluids, before implanting. Some female armadillos, having mated only once, give birth to separate litters in successive years.
The armadillo’s oddities don’t stop there. It can gulp air until its digestive tract balloons, making its heavy body light enough to swim. Alternatively, it can stay deflated and walk underwater, holding its breath for as long as six minutes. It doesn’t roll into a ball when attacked, as some of its southern relatives do, but it can plug a burrow entrance with its armored back and thrust its claws into the dirt so that it’s almost impossible to remove. One authority claims a person can induce an armadillo to relax its grip by inserting a finger into its rectum, but I have not personally verified this fact.
One fact I have verified is that armadillos are don’t do well in captivity. When I was in college my dorm competed in an armadillo race. It was, if memory serves, part of a festival involving a pie-in-the-face auction and other such revelry. My dorm-mates and I went into the country a week or so before the event to capture our entrant. We went at night and took flashlights. A few miles out of town, we could actually hear the animals crashing around in a wash where people had dumped their trash. When a flashlight beam caught one, it paused, then turned with surprising grace and fled. It ran faster than I had expected, its pill-bug body scooting along like a drop of water sliding down a window pane, but its erratic course allowed us to catch up. The guy who grabbed it uttered increasingly vile profanity as the armadillo bruised his gut with stiff kicks. A flashlight beam showed the claws drawing a flurry of down from the guy’s vest.
Once we had the armadillo back to the dorm, it stayed in our rooms. Whoever had it would go sleepless, because the thing wandered around all night, knocking over furniture and smacking into walls. We fed it an assortment of leftovers smuggled from the cafeteria; it particularly liked cantaloupe. We won the race by default because no one else bothered to catch an armadillo. Afterwards, we let ours go. No one had intentionally mistreated it, but its tail had somehow become ringed with wicked black wounds.
Though we didn’t mean to be, we were cruel to capture the armadillo. We didn’t know that captive armadillos may sleep around the clock, like human victims of depression, or refuse food and water. The males may dehydrate themselves by zealously scent-marking their cages with urine. The captives may suffer from boils or constipation. If several are caged together, they lick each other’s wounds, keeping them open and weeping. Sometimes the licking turns to cannibalism. And they seldom breed in captivity, so armadillo colonies like the one at LSU have to be replenished with frequent new captures. Truman regularly sends his graduate students into the woods near Baton Rouge for more armadillos.
Such were the problems Storrs and Kirchheimer had to overcome in 1968, when they attempted to inoculate armadillos with M. leprae. Not only did the armadillos get leprosy, they got it more thoroughly than any human being ever had. Organs that remain untouched in the worst human cases were loaded with bacilli in the armadillos. With their twelve-year life-spans—much longer than those of mice and rabbits—the armadillos lived long enough to develop full-blown cases. This complete susceptibility is the reason armadillos remain the animal of choice for leprosy research. It comes down to numbers: an armadillo yields one million times more of the M. leprae bacilli than a mouse footpad.
Storrs and Kirchheimer published their results in 1971 and 1972. Besides armadillos and mice, several other mammals had proved, or soon would prove, susceptible to injections of M. leprae—rats, hedgehogs, ground squirrels. But scientists had always believed people were the only natural host for the microbe. That’s why they were shocked by a 1975 report of leprosy in wild armadillos.
Several factors combined to make the situation seem like a horror story. The wild leprous armadillos had turned up in Louisiana, not too far from the site of experiments by Storrs, Kirchheimer, and others. The obvious inference was that experimental animals might have escaped, or at least that the carcasses of lab animals might have been cannibalized by wild armadillos. If leprosy was new to the armadillo population, there was no way to know how fast it might spread between armadillos—or even into the human population.
At roughly the same time, the armadillo’s conquest of the United States was fast becoming familiar to the average American. Newspapers reported the leprosy connection, creating the latest version of the deadly animal invasion story that seems to crop up with a different cast of characters every few years (black widow spiders, killer bees, and fire ants have all figured in similar scare-stories). Finger-pointing among a few biologists didn’t help matters.
Armadillos dig for insects and carrion compulsively, and that trait had already given them a folkloric reputation as grave-robbers in parts of the south. The possibility of armadillos having contracted leprosy from human corpses was an alternative to blaming the scientists—though not an attractive one, since either scenario left open the possibility that people might be in for a wave of disease. Of course, scientists who worked with leprosy realized that its threat was minor. Not only does the disease progress slowly, but it is frequently re-introduced to the United States by human immigrants without spreading widely. These points were not always mentioned in the press.
Other developments complicated the story. Chimpanzees came down with leprosy in 1977, as did sooty mangabey monkeys in 1981. In both cases, the primates were lab animals, but not the subjects of leprosy experiments. These discoveries, which suggested that leprosy might occur naturally in any number of nonhuman species, lent credence to the idea that armadillos might have carried the disease long before the species was used in leprosy research. Whether wild primates get the disease outside labs is still hotly debated; skeptics think humans infected a few chimps and mangabeys somewhere in the process of capture or lab work. To add another layer of mystery, no one has yet observed leprosy transmitted between armadillos in captivity, but cage-mates of infected primates have come down with the disease.
In 1983, researchers reported leprosy in five people in Texas who had frequently handled armadillos. It was impossible to prove that armadillos were the source of the infection, since even now no one is certain of the disease’s route of transmission, but the implication couldn’t be ignored. Since then, armadillos have been implicated in a number of other human cases. Why so many people would be handling armadillos puzzled me, since my only hands-on experience had been the ridiculous armadillo race. Truman resolved my confusion: “People do eat quite a lot of armadillo.”
Truman and his colleagues finally put the question of scientific culpability to rest in 1986. They tested blood samples which had been drawn from armadillos in the early 1960s and kept frozen in a wildlife sera collection at Louisiana State ever since. Truman’s group found some of these samples contained definitive evidence of M. leprae. Since the samples predated the 1968 clinical work, Storrs and Kirchheimer and later leprosy researchers were off the hook. They couldn’t have provided the first contact between M. leprae and wild armadillos.
But if scientists weren’t to blame, who was? Leprosy is un-American; even today, Native Americans don’t seem to get it. Truman and company looked into the distribution of the disease in the U.S. In both armadillos and people, the disease occurs most frequently in moist, low-lying areas. So far, this generalization has held true for people on several continents. So perhaps M. leprae is hiding in some natural reservoir that occurs in such moist areas. It’s already been established that the microbe can survive for several weeks in soil, but no one knows whether it typically does so.
Truman’s survey could hypothetically have revealed an origin point from which the disease was spreading. In fact, leprosy turned out not to follow such a pattern. No point of origin showed up. The even distribution led Truman’s group to deduce that leprosy has been here a long time, in both humans and armadillos—maybe centuries. We’ll probably never know when M. leprae arrived in America. Columbus’s invasion marks the earliest possible date. And after the disease arrived, it was only a matter of time until a cold and hungry mammal raided the wrong grave.