Zoobiquity (33 page)

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.

Hydrophobia, or fear of water, is a classic symptom of rabies infection. So is aerophobia (fear of moving air) and, as the disease progresses, an uncontrollable urge to bite. These seemingly random behaviors stem from changes the virus causes in the central nervous system of its host. And they may have a fortuitous side effect for the virus itself. The actions may actually help it transmit itself into a new victim. Because the rabies virus is spread through saliva, causing an urge to bite, for example, would be a useful microbial “strategy.” So far, however, infectious disease veterinarians haven’t found adaptive purposes for causing a fear of water or moving air.

Or consider
Enterobius vermicularis
, a.k.a. pinworms. This common childhood infection alters human behavior by drawing hands away from more productive activities, like homework and setting the table, and redirects them into ferocious anal scratching. This scratching serves two purposes for
E. vermicularis
: It helps burst the gravid females’ bodies, releasing the ten thousand eggs they each carry. And it helps those freshly exposed eggs burrow under the child’s fingernails, where they wait patiently for the next thumb suck or nail bite to permit them entry into the host’s mouth and, from there, his GI tract, where they reproduce.

Or take
Toxoplasma gondii
. Infection with this protozoan has an unusual effect on rodents: it makes them lose their fear of cats. From the rodent’s perspective, of course, this is terrible. It makes them easy prey. But from the toxo’s point of view, it could not be more clever. That’s because the only place on Earth that
Toxoplasma gondii
can reproduce is inside a cat’s intestine. By making rodents fearless, the parasite practically
gift-wraps and delivers itself to the cats’ claws and jaws … and from there to guaranteed reproduction.

Humans are “dead-end” hosts for toxo, meaning it can’t reproduce in us. But the parasites can still enter our bodies when we eat or touch infected meat, soil, or cat feces. Once inside our brains, the toxo can “encyst,” essentially lying dormant and waiting to get back into a cat. The pathogen doesn’t know whether it’s in a mouse or a mail carrier, a rat or a receptionist. But it continues to produce chemicals and help itself to nutrients in our blood and tissues. In fact, many of us have these encysted toxo infections. And, incredibly, this microorganism may affect our behavior as individuals.
Exposure to toxo in the womb may be a contributing factor in developing the often devastating human disease of schizophrenia.

“Brainworms” and
other parasites have been shown to spark killing sprees within ant colonies and make crickets and grasshoppers suicidal. One wasp creates a bodyguard for its offspring by infecting a hapless caterpillar which then fights off the wasp’s stinkbug predators with powerful swings of its caterpillar head. While toxo, pinworms, and rabies aren’t STDs, certain sexually spread ailments work their own microbial puppetry on their hosts. Two STDs—HIV and syphilis—notoriously produce extreme behaviors in people with end-stage infections. HIV dementia compromises judgment and memory. The egomania, impulsivity, and disinhibition that characterize advanced syphilis may have not only propelled the infamous sexual appetites of known syphilitics Al Capone, Napoleon Bonaparte, and Idi Amin but facilitated their power grabs as well. And while patients in the late stages of syphilis are no longer contagious and can’t spread the disease, there are diseases where the behavior caused will promote infection.

And this is another way we can learn from animal STDs. Many microbes depend on sex for their transmission. It makes sense that they might induce subtle sex-friendly behaviors, if they could.

But how would a crafty STD microbe get people jumping into the sack with each other? Maybe it would improve the males’ pickup lines … or confuse normal signaling so that rejections got misinterpreted as come-ons. Maybe it would make the females more alluring. Or increase libido or lower inhibitions to lead to more sex.

This may indeed be exactly what goes on in a range of animals infected by STDs. Male
Gryllodes sigillatus
crickets attract females with intricate
symphonies of sound, produced by rubbing their hind legs together. Crickets infected with a certain parasite sing slightly differently than uninfected crickets—but the change seems to increase the
males’ attractiveness and bring more females their way.

When infected with the sexually transmitted virus Hz-2V, female corn earworm moths start producing excessive amounts of sex pheromones—some two to three times as much as their uninfected sisters and peers. The extra come-hither perfume is believed to attract more male moths—thus aiding the spread of the virus. Intriguingly, these infected females also demonstrate a kind of lepidopteral “no means yes” behavior. Apparently unaware of how politically incorrect it is, they appear to further excite their mates through acts of resistance.

Sexually acquired infection can spur some animals into assertive sex-seeking behaviors.
Male swamp milkweed beetles infected with a sexually transmitted mite aggressively move in on nearby mating pairs, busting up the action and pushing aside the other male. When no females are in the vicinity, these infected males approach and attempt to mate with other males.

STDs may even change the “behavior” of plants. Like all living things, plants need to reproduce. For flowering plants, this means getting the sperm-laden pollen from male flowers to the eggs of female flowers. One way floral “sex” is accomplished is by the peripatetic flights and landings of birds, bees, and bats, which carry the pollen from flower to flower when they feed on the blossoms’ nectar.

However, the pollen of many flowers teems with microscopic fungi, viruses, and worms … all seeking to be transmitted into new hosts. When animal pollinators ascend from a bloom—legs and bellies sticky with what is essentially flower semen—these minute pathogens are often along for the ride. When the bee or hummingbird visits the next flower, it deposits pollen … along with a load of these flower STDs.

What’s really interesting is that these diseases can make plants, for lack of a better word, promiscuous.
The white campion flower, for example, is susceptible to a fungus aptly named “anther smut.”
A Duke University botanical disease ecologist, Peter Thrall, found that plants infected with anther smut tended to produce larger floral displays. Uninfected plants had punier bunches of flowers. With their big, ostentatious blooms, the flower hussies received (and could accommodate) more visits from more pollinating suitors. By forcing the plant to produce bigger, showier flowers,
the fungus was biologically changing its host in a way that made it more attractive to pollinating creatures. This directly benefited the fungus.

A similar “strategy” may be used by the trypanosome that causes an equine disease called dourine. Infected horses, mules, and zebras suffer fever, genital swelling, lack of coordination, paralysis, and even death. Although it’s now extremely rare in North America and Europe, dourine once ravaged the cavalries of the Austro-Hungarian Empire and swept across the horse populations of southern Russia and northern Africa. In Canada in the early twentieth century, dourine decimated Indian pony herds.

Dourine spreads when animals mate.
Intriguingly, scientists and veterinarians report anecdotally that when dourine is present in a group, the libido of stallions seems to increase.

How this works may be very similar to how anther smut influences the “behavior” of flowers. Full-blown dourine wreaks physical havoc on the animal … but the early signs of infection are more subtle. A mare may seem perfectly healthy except for a minor vaginal discharge that reveals itself as a wetness around her tail. Mares infected with dourine often keep their tails slightly raised, presumably to ease discomfort from the increased wetness.