Armadillos and Leprosy (Part 1 of 3)

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, disposablebooties, masks, and rubber gloves.  Thenwe opened a door and stepped into an odor Truman had warned me about.  It was something like a diaper pail and quitea bit like sour milk.  I was glad for themask.
The room was full of cement runs – walls about four feethigh, forming rectangular pens about six by three feet.  The cement floors were littered withsawdust.  The dishes for food and waterwere just like those one might provide for a dog or cat—in fact, the foodincluded cat chow—but the residents here were nine-banded armadillos.  An ordinary plastic kitchen trash can lay ineach run to serve as a burrow.
Truman, a tall, soft-spoken man whose silver hair didn't matchhis youthful face, asked a lab assistant to roust one armadillo from itssawdust.  The animal looked like aninverted bronze gravy boat with a head and tail.  The assistant gripped it at the back of theneck and the back of the tail—pretty much the only option if you want to avoidan armadillo's impressive digging claws. Truman let me hold the thing. Excluding the tail, it was about the size of a football, but heavierthan your average cat.  It wriggled andflexed, kicking with all four feet.  Itspink belly was studded with protuberances from which tufts of hair sprouted.  These structures, Truman said, have a sensoryfunction.
After that brief hands-on encounter, Truman asked theassistant to put the armadillo back. They're sensitive animals, poorly suited to captivity, and too muchhuman handling can prove fatal for them. I was, in fact, allowed to see only the healthy armadillos at LouisianaState University, home to the Laboratory Research Branch of the G. W. LongHansen's Disease Center, and those only with strict sanitary controls.  The ones with leprosy were strictlyoff-limits—I was more dangerous to them as a source of secondary infectionsthan they were to me.
I was there to learn about two mysterious organisms, bothpoorly understood even after centuries of contact with people.  One, of course, is the armadillo; the otheris Mycobacterium leprae, the microorganism responsible for leprosy.  Truman and other researchers are using theformer to study the latter.  What they'vediscovered 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 skinlose feeling.  For some people, that's asfar as it goes.  For others, things getmuch worse.  Grainy, ulcerating lesionsappear on the hands, feet, and back, and, in men, the testicles.  Nerves degenerate, causing the glands thatoil the skin to stop working.  The skincracks, leaving the extremities vulnerable to secondary infections.  People lose fingers and toes—not because ofthe disease itself, but because they don't notice that they're too close to afire or that rats are nibbling at them. The dead nerves create an array of odd postures—the claw-hand, thestaring eye that cannot be closed.  Therespiratory system is invaded; a slimy discharge issues from the nose.  The eyes succumb to infection and eventuallyto blindness.  The disease progressesslowly, 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 atiny minority of those infected, and most people are not susceptible to infectionat all.  "M. leprae is almost the perfectparasite," Truman said, because it so rarely destroys its host, and then onlyvery slowly.
The skulls of four Egyptians from the second century BCEhave curious deformities.  Certain partsof the face seem to have eroded before death. These skulls are the oldest hard evidence of leprosy, one of the oldesthuman diseases.  Detailed descriptions ofsymptoms in various documents push our known contacts with leprosy back evenfurther, to about 600 BCE.  Beyond that,the vagueness of historical descriptions becomes a problem.  There are accounts of a leprosy-like diseaseinvading Egypt from the Sudan during the reign of Ramses II.  The disease mentioned with such horror in theBible may not be the same thing as modern leprosy—its symptoms are only vaguelyalluded to, and sometimes it seems not even to be a disease as we understandthe idea, but sin figuratively described. If the biblical references are to a literal skin-mottling disease, somecommentators find smallpox a more likely candidate.
But it's certain that genuine leprosy has peeked intohuman history at odd junctures, as when the soldiers of Alexander the Greatconquered the East and brought back silks, spices, and the disease.  Europeans came back from the crusadesinfected—a public relations problem for the Church, since the crusades weresupposed to be a holy war, and leprosy appeared to place God on the otherside.  For a few centuries, lepers' homesexisted throughout Europe.  Leprosy'sdecline as a major health problem on that continent coincided with the BlackDeath, which tended to kill the inmates of lepers' homes and thus break themysterious chain of transmission for the older disease.  But elsewhere in the world, leprosy has neverlost its hold.  Half a million new casesappear annually, and the total number of people afflicted is at least tenmillion. India and Brazil currently have especially severe leprosy problems,but the disease occurs virtually everywhere in the world, including about 6000cases currently in the United States.
The notion that leprosy is contagious has been around forat least 2500 years, but a competing hypothesis blamed heredity.  It made some sense: relatives of lepers provedmore likely than others to become lepers themselves. Western science dropped thehereditary theory in the 1880s, when a missionary named Father Damien, who hada well-documented and leprosy-free family background, was revealed to havecaught the disease while working with lepers on Molokai. By that time, aNorwegian doctor named Armauer Hansen had discovered Mycobacterium leprae, theorganism that causes the disease. The nasal secretions of people with severecases carry enormous quantities of M. leprae, and many physicians andresearchers assume that the microbe infects new victims through the respiratorysystem or through open wounds. Hansen immediately recognized the importance ofcultivating M. leprae for study, but he found he couldn't keep the bacteriumalive in a dish.  Even now, no one hassucceeded in cultivating it outside a warm body.  "It starts to die as soon as it's out of thetissue," said James Krahenbuhl, Truman's colleague at the G. W. Long Hansen'sDisease Center.  Hansen tried to infectrabbits with M. leprae, but it didn't take.
In 1956, Chapman H. Binford, having noted that leprosyattacks the coolest areas of the human body, suggested that lab animals mightbe susceptible to infection in their cooler regions.  By 1960, C. C. Sheppard had successfullyinoculated the footpads of mice.  Soonmouse 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 humansremained the best source for the microbes.
Then the team of Wally Kirchheimer and Eleanor Storrsnoticed that armadillos are cool all over. At 30-35 degrees Celsius, armadillos run several degrees cooler thantypical mammals.  The animal's armorprobably has something to do with its low temperature; it certainly makes thearmadillo a poor regulator of body temperature, as mammals go.
to be continued tomorrow


THE BOOK OF DEADLY ANIMALS

A different version of this story originally appeared in Discover.