The Book of Deadly Animals makes its debut in the United Kingdom November 3. To celebrate, I'm running here some expanded versions of tales I told in the book. If you read the magazine version of this story, you've only seen about half of it; I've revisited this one to add more information and more of my first-hand experience with the animals. This is the director's cut.
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.