Where Leprosy Lurks

As we step up the drug battle against AIDS, a new threat lies waiting for us in armadillos and monkeys.

By Gordon Grice|Wednesday, November 01, 2000


In the Oklahoma Panhandle, where I grew up, if you keep your eyes peeled for the road-killed and the road-living, you soon begin to notice patterns: Tarantulas cross the road mostly in November, just before a freeze, or on misty 50-degree days in the spring. A hirsute kind of caterpillar tends to cross in early autumn, when it's still hot. Most of the animals I see on the road are in extreme circumstances— either dying to mate, like the box turtles I spot every summer, or simply dying. I find them fascinating even in their misfortune. We are bound to other animals by ties we hardly suspect— by the highways that link our cities and incise their habitats, by seasonal desires, even by the tiny parasitic lives hidden inside us all.

Armadillos not only carry leprosy, but They also have been expanding their range in america for more than a century

—photographed at Louisiana State University

It was on a stretch of Highway 51, in north central Oklahoma, that I witnessed the worst road apocalypse I have ever seen. It was an August morning, and I was on my way to college in the town of Stillwater, when I began to notice hundreds of bronze carcasses littering the road and the right-of-way. The day was hot, and many of the carcasses had bloated, their legs jutting out at 45-degree angles. One in particular caught my eye—a car tire had halved it as neatly as a ripe watermelon. When I pulled over for a closer look I could see the animals’ squinted eyes, the blond tufts protruding between their plates of armor, the metallic tails curled on the asphalt. They were surprisingly heavy: When I nudged one with my boot, it hardly budged.

  

But I didn’t put my hands on it. This was in the early 1980s, when armadillos seemed, for a time, almost as great a threat to us as we are to them. A few years earlier, researchers had discovered leprosy among wild armadillos in Louisiana. More recently, five people in Texas had contracted leprosy, and the common factor in their backgrounds was close contact with armadillos. If leprosy was new to the armadillo population, there was no way to know how fast it might spread among armadillos—or even into the human population.

Ironically, two factors that help make armadillos vulnerable on the road have also made them seem like threats to us. First, the animals have been expanding their range to the north for more than a century, coming into ever more frequent contact with North American highways. Second, armadillos are indiscriminate feeders, eager for the easy meat of a roadside kill, and they love the grubs and maggots that go with it. If the meat happens to be another armadillo—or even a human corpse, Southern folklore claims—they don’t object. Such grave robbing, it has been thought, can spread leprosy.

As it turned out, the possibility of an armadillo-fueled epidemic was extremely remote. But just as a straight highway can prove to be a veritable cloverleaf of intersecting ecosystems, the story of American leprosy is more convoluted than it seems—an object lesson in the complexity of the natural world. It winds its way through human history and the landscape itself, hinting at the connections between disparate organisms. It begins with an ancient disfiguring disease and ends with the new one of AIDS, and the players along the way include not just armadillos but mangabey monkeys. Just when it seems ready to be relegated to history, this oldest and slowest of diseases reappears, threatening an epidemic once again.

Leprosy, also known as Hansen’s disease, attacks 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 damaged 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 oldest hard evidence of leprosy can be seen in the skulls of four Egyptians from the second century B.C., whose faces seem to have eroded before death. But detailed descriptions of symptoms in various documents push our known contacts with leprosy back even further, to about 600 B.C. Beyond that, the vagueness of historical descriptions becomes a problem. There are accounts of a leprosylike 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 as 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 described figuratively. If the biblical references are to a literal skin-mottling disease, some commentators find smallpox a more likely candidate.

Certainly, leprosy has peeked into human history at odd junctures, as when the soldiers of Alexander the Great conquered the East and brought back the disease, as well as silks and spices. Europeans came back from the Crusades infected—a public relations problem for the church, because the Crusades were supposed to be a holy war, and leprosy appeared to place God on the other side. For a few centuries, leper colonies could be found throughout Europe, but the Black Death eventually killed most lepers and thus broke the chain of transmission.

Worldwide, half a million new cases of leprosy are discovered annually, and the total number of people afflicted is at least 10 million.

            —photographed at Summit hospital, Baton Rouge, LA.

In the United States, as in most of present-day Europe, leprosy doesn’t seem to perpetuate itself; it simply dies out. Although the United States has as many as 6,000 lepers—most of them in Louisiana and Texas—only 35 to 50 new cases are diagnosed each year, most of them recent immigrants. But elsewhere in the world, the disease has never lost its hold. Half a million new cases are discovered annually, and the total number of people afflicted is at least 10 million. India and Brazil have severe leprosy problems, but the disease occurs almost everywhere in the world.

Why leprosy continues to spread in some areas without getting a foothold in others has been a mystery, as indeed has its route of transmission. For a time, the disease was considered hereditary, because relatives of lepers are more likely than others to catch the disease. But Western science dropped that theory in the 1870s, when a missionary named Father Damien, who had a well-documented and leprosy-free family background, caught the disease while working with lepers on the Hawaiian island of Molokai.

For at least 2,500 years, most people have assumed that leprosy is contagious. In 1873 that hypothesis was bolstered when a Norwegian doctor named Armauer Hansen discovered Mycobacterium leprae, the bacterium 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. But no one has proved this, or any other, transmission hypothesis. Even among people in close contact with lepers, only a fraction seems to contract the disease, even in endemic areas. The disease progresses slowly: The first lesion is thought to follow the actual infection by three years or more; the worst manifestations develop years after that. The most 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,” notes microbiologist Richard Truman of the National Hansen’s Disease Programs Laboratory, because it so rarely destroys its host.

To truly untangle the mystery of the disease, scientists must cultivate M. leprae for study. But as Hansen himself first discovered, the bacterium can’t be kept alive in a dish. In fact, no one has yet succeeded in cultivating it outside a warm body. “It starts to die as soon as it’s out of the tissue,” says Truman’s colleague James Krahenbuhl. As a result, much of the history of leprosy research has been devoted to finding suitable hosts to propagate the bacterium. For decades, the fresh tissues of infected humans were the only good source of the microbe. Hansen tried to infect rabbits, but it didn’t take. It was another century before someone thought of using armadillos.

Richard Truman and I don gowns, disposable booties, masks, and rubber gloves. Then we open a door and step into an odor Truman had warned me about. It’s something like a diaper pail and quite a bit like sour milk. I’m grateful for the mask. The room, which is part of the center’s lab, is full of cement runs—walls about four feet high, forming rectangular pens about six by three feet. The cement floors are littered with a sawdust-like material. The dishes for food and water are just like those one might provide for a dog or cat—in fact, the food includes cat chow—but the residents here are nine-banded armadillos. An ordinary plastic kitchen trash can lies in each run to serve as a burrow.

Truman, a tall, soft-spoken man whose silver hair doesn’t seem to match his youthful face, asks a lab assistant to roust one armadillo from its sawdust. The animal looks like an inverted bronze gravy boat with a head and a tail. The assistant grips 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 lets me hold the thing. Excluding the tail, it’s about the size of a football, but heavier than your average cat. It wriggles and flexes, kicking with all four feet. Its pink belly is studded with protuberances that sprout tufts of hair. These structures, Truman points out, have a sensory function.






For a history of Hansen's disease, see: fortyandeight.org/thestar/br_hist_hansen.htm.

For a summary of current leprosy research issues, see the Leprosy Research Support Web site at www.cvmbs.colostate.edu/microbiology/leprosy/globalleprosy3.html.


Leprosy is almost the perfect parasite. it rarely destroys its host, But it can create odd disfigurements: the mutilated ear, the eye that cannot be closed

—photographed at summit hospital, Baton Rouge, LA. 

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