Zoobiquity

  As a triggering food for regurgitation, dairy products are preferred by another member of the great ape family. Michael Strober noted, “Yogurt is one of the favorite foods of people with eating disorders. They have this affinity for yogurt.… Ask them to list their favorite food; they’d probably say yogurt.”

  TEN

  The Koala and the Clap

  The Hidden Power of Infection

  When monster wildfires scorched southern Australia in 2009, destroying homes and killing nearly two hundred people, one photograph came to symbolize the epic clash of man against nature and the plight of the vulnerable creatures caught in the middle. It showed a firefighter in bright yellow battle fatigues. With smoke rising around him, he crouched on the charred earth, holding a plastic water bottle to the lips of an exhausted koala. As it drank, the animal gripped the firefighter’s hand with its small paw. The human—face sooty, hair mussed—gazed intently at the animal, a striking image of compassion and interspecies cooperation.

  Around the world, people anxiously followed the story of the koala and the firefighter. At the shelter where the animal’s burns were salved and her paws bandaged, she acquired the nickname Sam. This icon of Australia—pulled from the ashes—became the furry face of resilience overcoming adversity, more phoenix than marsupial.

  But six months later, Sam hit the blogs again. This time, her story didn’t have such a happy ending. In fact, Sam had died. It wasn’t the burns that had killed her. The koala was dead of complications from chlamydia.* She had a sexually transmitted disease (STD). Readers learned that chlamydia is an epidemic of such proportions among the thousands of wild koalas in Australia that it threatens extinction of the iconic animals.

  Chlamydia and koalas. It’s a combination that just seems wrong, like a toddler with a heart attack. Small marsupials are innocent and natural, even cute. STDs, let’s be honest, are not. Even among physicians accustomed to the sights and smells of the human body, STDs hold little appeal. An international survey of physicians once ranked afflictions by their level of prestige. Brain tumors, heart attacks, and leukemia were the top three. Diseases that strike below the belt were dead last.

  And medical advances of the past half century have made it even easier to look away from sexual infections. In developed countries, most of us have the luxury of thinking of STDs as being essentially curable—or, at worst, treatable, chronic diseases requiring daily medication. (Think of antiviral medication for herpes or, in a more extreme case, daily drug cocktails for HIV.) What’s more, pervasive and effective “safe sex” education has given the strong message—true in some cases—that barrier methods and abstinence can make you practically impervious to STDs.

  But for animals, safe sex isn’t a choice. In fact, when you think about it, unprotected sex is the only kind nonhuman animals have. Without access to condoms and abstinence pledges, not to mention antibiotics and vaccines, nonhuman animals have to cope and survive and reproduce somehow, regardless of what infections come their way. When you consider the amount of “unsafe” sex going on, 24/7, in a mere square mile of wilderness, it seems remarkable that animals aren’t 100 percent infected at all times with STDs.

  Veterinarians, like physicians, often give animal STDs scant attention, compared to other health concerns. Wildlife veterinarians don’t regularly count the genital warts on tundra swan penises when they radio-collar them for migration surveys. Nor does yearly population tracking of Yukon caribou end with the females in stirrups and the vet chitchatting while warming up an Arctic-chilled speculum. Even when zoos transport and relocate their animals for breeding, most don’t routinely screen for STDs. Among biologists, the handful of professional academic organizations that might discuss animal STDs are loosely organized and spread thinly throughout the world.

  Like most patients and physicians, I wasn’t exactly clamoring to hear more about STDs. But we all should pay attention, because STDs are remarkably deadly. HIV/AIDS is the world’s sixth biggest cause of death. When you combine those numbers with cancer deaths from sexually spread viruses such as human papilloma virus (HPV) and hepatitis B and C, the mortality climbs even higher. STDs are tenacious, ancient, and lethal, and they continue to outfox human attempts to control them. Perhaps physicians can find help for human STD patients in a place they’ve never thought to look: the genitals of nonhuman animals.

  Consider the following: Atlantic bottlenose dolphins sprout cervical and penile warts. Baboons get genital herpes. Copulating whales, donkeys, wildebeests, wild turkeys, and Arctic foxes harbor and transmit warts, herpes, infectious pustular vulvovaginitis, venereal pox, and chlamydia.

  Sexually spread brucellosis, leptospirosis, and trichomoniasis cause repeated miscarriages and reduced milk output in cattle. Pig litters can be decimated by bacterial infections acquired during mating. Venereal diseases in farmed geese cause death as well as drops in egg production. Contagious equine metritis so predictably devastates fertility in mares that every stallion of breeding age imported to the United States is required to go into a minimum three-week quarantine to make sure he’s not a carrier. Dog STDs can cause abortions and birth failures.

  When I first started learning about animal STDs, I was surprised by the range of species they infect. But it wasn’t too hard to picture the mechanics of mouse or horse or elephant sex and imagine the genital contact that could lead to the spread of an infection. What was truly eye-opening to me, however, was that the dark, balmy environments favored by sexually transmitted pathogens aren’t limited to warm-blooded creatures. Dungeness crabs, for example, are vulnerable to a worm that spreads from males to females when they mate. The worms invade the female looking for her cache of eggs. Once they find it, they start feeding, reducing the number of viable crab offspring.

  Even insects carry STDs on their tiny genitals. Two-dot ladybugs, one of the most promiscuous creatures on Earth, can become infected with a sexually spread mite that makes them sterile. A postcoital housefly that lands hungrily on your freshly prepared Dungeness crab chowder may himself harbor a genital fungus, also acquired through copulation. Astonishingly, some of the diseases we humans catch from insects—such as St. Louis encephalitis from mosquitoes and spotted fever from ticks—are actually sexually transmitted among the insects themselves. (If you’ve never pictured what ladybug or tick or housefly sex looks like, you have an illuminating twenty minutes of Internet image searching ahead of you. Most insects do engage in penetrative sex with genital contact—often in the doggy-style position.)

  Indeed, STDs have been found thriving in so many living things, from fish and reptiles to birds and mammals and even plants, it’s safe to say they’re ubiquitous in all sexually active populations. Experts agree that these infections are legion.

  And yet you might be whispering to yourself: So what? Yes, we want to reduce animal suffering. But in terms of human health, why should we give a moment’s thought to diseases of their genitals? To be blunt, since we’re not having sex with these animals, why should we care if some koala catches the clap?

  The answer is as simple as it is unsettling: because pathogens are always looking for new paths, and they don’t differentiate between humans and other animals. For example, rabbit syphilis once spread to trappers in East Yorkshire, who got sores on their hands after handling the animals. There was no sexual contact between the humans and the animals, but the syphilis pathogens didn’t care. They were happy to jump the species barrier and curl into warm moist tissue through cuts on the men’s hands.

  Or think about brucella. In livestock, these nasty bacteria cause spontaneous, late-term miscarriages in females and swollen, bleeding testicles in males. So unforgiving is brucella’s attack on the reproductive system that one of its common strains is called Brucella abortus. But what’s instructive about brucella is how it spreads. Cattle, pigs, and dogs transmit it through sex. So do hares, goats, and sheep. But all these animals can also acquire it nonsexually … by eating it. Under the right conditions, brucella orga
nisms can live for several months on many things that might end up in an animal’s mouth: feed, water, equipment, and clothing, not to mention manure, hay, blood, urine, and milk.

  In a number of animals, the same pathogen has found two different paths of entry into the body—sexual and oral. Through the mouth is the way humans usually acquire brucella infections, too—when they eat contaminated meat, unpasteurized milk, or soft cheeses. Spread this way, from animals to humans, brucellosis is a major public health concern, especially in developing countries, where thousands of cases emerge each year. (In developed countries, it has become mercifully rare, thanks largely to veterinarians who vaccinate animals and monitor the spread of disease.)

  Like livestock, humans can become infected with brucella in more than one way. Like the trappers who contracted syphilis infections by touching sick rabbits, zookeepers in Japan got brucellosis when, during the delivery of an infected baby moose, they came in contact with the placenta and mother’s vaginal secretions.

  And although they’re rare, reports do exist of brucella’s spreading from human to human—through blood, milk, and bone marrow … as well as through sexual intercourse.

  Same pathogen. Different paths. Could classifying a condition as “sexually transmitted” be limiting how we consider and understand these infections? After all, bugs are bugs, no matter how they get in. Streptococcus A, the common human pathogen that causes strep throat, scarlet fever, and rheumatic heart disease already exploits several routes into the body. Its most common path is respiratory. One person coughs or sneezes droplets containing the bacteria, and another person inhales or picks them up from doorknobs or silverware. But Strep A can, through oral-genital contact, cause penile inflammation and purulent discharge. You can get salmonella from sex with an infected person or by licking raw cookie dough off your finger—either way you’ll be down for the count with 104-degree fever, hideous diarrhea, and exhaustion. Hepatitis A, as well, can be picked up during a sexual encounter or by eating at a restaurant where the chef didn’t heed the hand-washing instruction sign in the bathroom. No matter which portal it uses to enter your body, the pathogen will give you the same gruesome symptoms: fever, exhaustion, and a complexion the color of Grey Poupon. You might even need a liver transplant.

  Studying STDs in animals reminds us that, like all living things, pathogens are constantly evolving. Species suited to one region of the body can change over time, developing new areas in which to live and thrive. Take Trichomonas vaginalis. Nowadays, “trich” is one of the least glamorous but most common STDs. In women it causes a fishy-smelling, frothy, yellow-green vaginal discharge. Men infected with trich usually have a slight irritation or burning in the penis, but no other symptoms. But contemporary T. vag wasn’t always a lowly genital dweller. Ancient, ancestral T. vaginalis resided in the digestive tracts of termites. This made it, essentially, a gastrointestinal bug. Changes over trillions of generations (and millions of years), however, allowed it to expand beyond termites and guts into the bodily crannies of many different animals. Eventually a version found its way to human vaginas (and fifteen minutes of microbial celebrity in 2007 when it was featured as Science magazine’s “cover bug”).

  Today, cousins of T. vaginalis (descendants of that ancient termite-dwelling ancestor) don’t limit themselves to human penises and vaginas. Other species of trich have found suitable homes in various parts of human and animal bodies. T. tenax, for example, thrives in the dark, moist crevices of rotting teeth. T. foetus causes chronic diarrhea in cats and ravages the fertility of cows. T. gallinae is practically endemic in the mouths of many birds—voracious raptors and peace-loving doves alike.

  T. gallinae (or its close cousin) has, in fact, been colonizing the ancestral birds of Earth for a very long time. Recent research on Sue, the T. rex famously on display in Chicago’s Field Museum, reveals that she may have died of a raging Trichomonas infection that bored holes through her jaw and ultimately left her unable to chew and swallow her food.

  Her infection wasn’t sexually transmitted, but it shows how, over millions of generations, these microorganisms have deftly adapted to new environments. Like a large family conglomerate where one son controls the real estate holdings, another textiles, and another medical devices, trich has differentiated so that each species specializes and thrives in a specific body region. But regardless of their portal of entry or favorite locale, they are all members of the same genus: Trichomonas. So whether it’s swabbed from the cervix of a college freshman or collected from the upper esophagus of a carnivorous hawk, under the microscope trich is trich. Again, similar pathogen, different paths.

  Gut infection today, genital infection tomorrow. The family albums of ancient pathogens show the evidence of their many migrations around the landscape of our bodies. For example, several hundred years ago, syphilis underwent a major evolution. The pathogen found a new path. Before it discovered its current preference for the human genital tract, the ancestors of the current syphilis microbe caused a horrible skin condition called yaws. It was a disease largely of children, and it spread by skin-to-skin contact. (Yaws still exists, mostly in undeveloped, tropical regions.) But sometime in the last thousand years, yaws somehow found its way into adult genitourinary tracts. Once it discovered the sex superhighway, it morphed into what we now call an STD. But the corkscrew-shaped spirochete that causes it retains the genealogy of its yaws forebear, which was basically a skin disease.

  If the same pathogen can be transmitted in any number of ways, and if it can mutate from being a gastrointestinal dweller to a urethral specialist and then change again to become a throat denizen, why do we fixate on sex as the pathway? After all, many organisms can infect us using different routes.

  This is a point that physicians—and veterinarians—sometimes overlook. And it’s a reason to pay attention to animal STDs. Because pathogens don’t discriminate between the warm, moist, nutritious environments they choose to call home, and because they frequently mutate, the animal STDs of today can become the human food-borne illnesses of tomorrow. Given chance encounters with human genitals and time to evolve there, those food-borne illnesses can then mutate into the next human STDs.

  This is not just an idle theory. It’s exactly what happened in the case of the deadliest STD currently stalking our planet. It is now generally believed that HIV evolved from SIV (simian immunodeficiency virus), a pathogen of chimpanzees, gorillas, and other primates. Sex and mother’s milk are major transmission routes for SIV within primate populations. Assuming that people were not having sex with chimpanzees or hiring gorillas as their wet nurses, how did SIV jump to humans?

  The answer is: the same way brucella infects humans. Through ingestion. The theory is that, by eating the meat of infected monkeys and apes, or getting their blood or other fluids on their hands and faces, hunters in western Africa became unwitting reservoirs of SIV sometime over the last few decades or centuries. Over many years and through many hosts, SIV mutated into HIV and then exploited the same path it had used in the nonhuman primates: sex. What started as an animal disease evolved into a human version we could give to one another. But, of course, sex is not the only way HIV spreads. It can also travel through blood, breast milk, and, on rare occasions, transplantation of infected tissues and organs. Given the way pathogens exploit many routes of entry into a host, it’s possible that if another animal were to preferentially feed on humans infected with HIV, the virus could jump into that species and eventually become tailored for sexual spread in that population, too.

  But animals—including humans—have not sat idly by as these wily microscopic invaders have launched assaults on our mucous membranes and vulnerable bodily portals. We’ve evolved fierce infection-fighting arsenals. White blood cells. Antibodies. Fever. Viscous mucous. Thick skin. And, intriguingly, our defenses are not just physical. Animals have also evolved ways of behaving that can reduce the risk of infection. Coughing, sneezing, scratching—even grooming behaviors, like picking, rubbing,
and combing—all have an antiparasite benefit at their core. And there are the things we humans do even more deliberately: Washing our hands. Vaccination. Sterilizing dishes. Wearing condoms.

  Some behavioral responses protect us once a pathogen has entered our airspace or breached a battlement. But bacteria, viruses, fungi, and worms don’t even have to enter our bodies in order to influence our actions. Consider the following automatic behaviors: recoiling from a runny-nosed child in the elevator. Sniffing the opened carton of milk before we pour it onto our cereal. Backing out of a public restroom to avoid grabbing the doorknob. Our behavioral strategies—and immune responses—can be activated by just thinking about parasitic infection. (Here, I’ll show you: Bed bugs. Head lice. Pinkeye. Are you having a reaction?)

  Among these reactions are some truly bizarre behaviors that seem to have nothing to do with fighting disease. And, it turns out, they don’t. That’s because the infections themselves may be steering our actions. Although that may sound like the preposterous premise of a zombie movie, these tiny creatures’ ability to influence the behavior of larger animals such as ourselves comes from a billion-year-old game of escalating, coevolutionary cat-and-mouse.

  One of the strangest things I’ve ever seen was a video of a human rabies patient trying to take a drink of water. This patient did not look sick. He was not foaming at the mouth, the way he would have been in a movie. He was not growling like a mad dog or writhing on the gurney with crazy eyes. The man looked perfectly calm and normal. Until a nurse handed him a cup of water. Suddenly, his hands started to tremble. He tried to bring the cup to his lips but couldn’t. His head thrashed from side to side as the liquid approached his mouth. It looked as though someone were using a remote control to direct his movements.