Zoobiquity (34 page)

A mare’s raised tail is also a signal of sexual receptivity. So is something else, familiar to every horse breeder, that’s visible when the tail is up. It’s called vulval “winking.” Caused by the vulva’s contracting and releasing, vulval winking happens when a mare is in heat.

But an under-the-weather, dourine-infected mare, her tail raised and her vulva wet with discharge and perhaps winking with discomfort, may incite randiness in a stallion with her STD-induced false advertising. While the stallion may suffer from the mistake, the pathogen will benefit.

Sometimes the connection between infection and behavior can seem very roundabout. One of the most perplexing endpoints of many STDs is the destruction of their host’s fertility. You would think this would be a terrible ploy, for two reasons. If a population can’t produce offspring, that usually means the end of the line for the bug. Without a new supply of hosts, where are a bug’s descendants to live? And then there’s the other problem: If an animal can’t have offspring, what would drive it to have sex?

But bugs’ success is tied to how much their host
mates
, not to how much
their host
reproduces
. (
The increasing incidence of STDs in people over fifty illustrates how these infections need sexually active hosts … not necessarily fertile ones.) A female animal who is having trouble procreating may in fact try harder—that is, have more sex—than one who is already pregnant. If a pathogen can disrupt the pregnancy cycle by inducing miscarriages or preventing conception, it is likely to enjoy the benefits of increased mating attempts. Is it possible that by hindering reproduction certain STDs are actually driving their hosts to have more sex?

In fact, some veterinary literature supports just that.
An STD of deer and other ungulates, for example, puts the females permanently in heat and thus more receptive to sexual overtures.
When
Brucella abortus
causes a cow to miscarry her calf, it makes her ready for a new breeding cycle—sooner than if she had carried the calf to term. This revelation suggests that subclinical infections (those percolating below the surface but not actively causing symptoms)—or even as-yet-unidentified pathogens—may play a greater role in unexplained human infertility and repeated miscarriage than we currently suspect.

In other words, even low levels of infection might alter sexual function and behavior. STDs are especially good at going deep undercover once they’re inside a body, quietly colonizing it with few overt symptoms. Whether the infections are small and contained or widespread and subclinical, these organisms do affect our bodies and minds in ways that might be unseen to us.

As a medical student at U.C. San Francisco during the height of the AIDS epidemic there, I was instructed to aggressively dispense safe-sex advice. Even if a patient came in with an earache, I brought sex into the conversation. I recommended wearing condoms and avoiding multiple partners. (Remember that quintessential 1984 line “When you sleep with someone, you are sleeping with everyone they’ve ever slept with”?) I counseled patients to question potential mates (“Do you ever have sex with men?” “Do you use IV drugs?”). A veterinarian can’t warn her patient to wear condoms and interview a sex partner before even getting to first base. But one more preventive technique I used to recommend does have an animal correlate. I was trained to advise that potential partners inspect one another’s genitals for sores and lesions before engaging in sex.

An animal version of this has been reported in birds.
It’s called cloacal
pecking
^†
and has been described as a male bird pecking inquisitively at the vaginal opening of a female before mounting her. Some researchers speculate that the fluffy white feathers or prominent “lips” around the cloacal openings of many bird species serve as additional aids for assessing health in a potential partner, since ectoparasites and lesions might show up against the pale background. If soiled by diarrhea or other bodily fluids, these structures would also warn a potential suitor of an unhealthy bird.
^‡

Lab studies also show that postsex cleansing might offer a modest level of protection.
Rats that are prevented from genital grooming after coitus have higher STD rates than their cleaner counterparts.
Many birds preen vigorously after copulation, which some researchers suggest may help do away with bugs trying to hitch a ride on the act.
In humans, genital scrubbing does not protect against viral STDs, but it may be slightly effective against bacterial infections.
A study of Cape ground squirrels in South Africa showed that the ones having the most sex were also the most frequent masturbators; the researcher speculated that it’s a way to flush out the urethra after intercourse in order to protect the animal from sexual infection.

A recent study showed that simply
looking at a photograph
of a sick person caused some people’s immune systems to surge. Indeed, animals may have other ways of visually sizing up the health of a mate.
For example, in males, red pigmentation—whether in a grouse’s comb, a house finch’s feathers, or a guppy’s skin—may indicate underlying fitness. These animals’ bodies cannot create the color red on their own. To impart the bright tint, they have to be healthy enough to source and eat lots of red-pigmented carotenoids, found in fruit or shellfish. Conveniently for any females who might be speed-dating with these males, parasites can interfere with the absorption of these pigments. Animals with paler features are in effect advertising their inferior health status.

But if the thought of colonies of invisible organisms invading your body and controlling your behavior has you reaching for the doxycycline,
think again. Our best response to the microbial arms race is not necessarily a scorched-earth campaign.

In the 1980s, a British scientist shook up the world of microbiology by asking an outrageous question:
Can we be too clean?
David Strachan was pondering whether hay fever might be related to hygiene and household size.
A few years later, a German scientist, Erika von Mutius, was investigating childhood asthma. She was vexed by data that consistently showed that it was most prevalent not in lower-income, more polluted East Germany but, rather, in wealthier, cleaner-living West Germany. The so-called hygiene hypothesis started to circulate, postulating that there are serious consequences to wiping out too many of the microorganisms that have colonized us and our planet for so long. Overusing pesticides, antibacterial agents, and antibiotics, it suggests, kill “good” pathogens along with harmful ones. Plain old better housekeeping and even overly thorough food inspections, the theory goes, create microorganic dead zones. These sterile environments deprive our immune systems, honed over hundreds of millions of years, of necessary daily battles against invaders. And when deprived of external organisms to fight, they sometimes launch an internal attack. An idle immune system will sometimes start attacking itself.

The hygiene hypothesis, while still a matter of debate, is now being used to explain more than just asthma, allergies, and other respiratory diseases. Upsurges in gastrointestinal disorders, cardiovascular disease, autoimmune disorders, and even some cancers are being traced to it, too. However, no one has really looked at the genital environment—and whether it, too, can suffer from being “too clean.”

This leads to an intriguing thought. Are some of the pathogens associated with sexual activity beneficial?
Most animals have multiple sexual partners—which means that sperm from many different males must duke it out inside vaginas, uteruses, and fallopian tubes to win the conception derby. Conception is not some genteel, quiet pastime; it’s a fierce and unforgiving team sport. The swimmers that win sometimes have assists from microscopic wingmen—the
sperm-enhancing microorganisms
that live in semen and may be transferred from penis to vagina to penis to vagina. The sexual act may propel the package of semen, but it is then up to the ejected sperm and its microbiological posse to obstruct
and destroy competing sperm. Some of these pathogens aid their sperm’s motility, while others act as blockers and killers of competing males’ spermatozoa. And if that isn’t enough, these teams must also successfully negotiate the vagina’s own mix of receptive and defensive microflora.

This means the microorganisms inhabiting an animal’s urethra or vagina might make the difference between conceiving and not. Or, when there are multiple male partners, determine which of these males’ sperm wins the ultimate prize: fertilization, the chance for his DNA to advance to the next round.
^§

This made me wonder whether striving for an aseptic genital environment could, in fact, be harmful (beyond the well-known risk of a yeast infection after antibiotic therapy). The human immune system fully matures between the ages of eleven and twenty-five—just when sexual activity is moving into full gear, bringing with it a barrage of new, unfamiliar microorganisms. The hygiene hypothesis demonstrates the risks of underexposure to pathogens of the respiratory and GI systems. Might there be a genital version of the hygiene hypothesis? Could a “just right” mix of microorganisms in your genitals improve your chances for conception or help select the highest-quality sperm for your soon-to-be-conceived child? Might there be a place for a probiotic product to aid conception—similar to the products that improve digestion in the gut microbiome? Or maybe there’s an intriguing flip side: Could studying sperm-killing micropathogens in animals lead to new contraceptives?

It’s important to stress that, given the threats STDs pose to human health, this is not an argument for unsafe sex. Condoms save lives. Physicians and educators must resoundingly continue to emphasize the absolute necessity of safe-sex practices. But physicians should join veterinarians in considering the long-term ecological perspective of therapies and remain open-minded about unlikely or unexpected consequences of intervention.

As Janis Antonovics, a disease biologist at the University of Virginia, told me, “
There is no imperative to cure disease in natural populations. Disease is natural!” Doctors first and foremost have a responsibility to treat individual patients. But ecologists like Antonovics take the
pathogen’s-eye view of infection. As he explained it to me, every time we perturb a system, by extermination or prevention, there is always a repercussion. An individual may see an immediate benefit from a round of antibiotics, but invariably, necessarily, killing off those organisms causes some unintended side effect, either immediately or down the line. Sometimes it comes back in a more virulent form. Infection (and all the viruses and worms and bacteria and other organisms that create it) is a complex, interconnected, multidimensional web. Tugging out one strand alters the architecture of the entire network.

If Sam the koala had been born a few years later, she might have benefited from the kindness of not just the firefighter but also a biologist named Peter Timms.
Timms, along with his colleagues at the Queensland University of Technology, has been developing a vaccine for koala chlamydia. Early trials of the vaccine have cut infection rates slightly and blunted the virulence of the disease. Timms hopes his research will someday not only save koalas but also inform a human chlamydia vaccine.

It’s hard to imagine anyone in Australia objecting to vaccinating their national symbol against a disease that causes blindness, infertility, and death. It hardly seems the koalas’ fault that the disease that’s wiping them out happens to spread via sex. But the development of human vaccines against STDs from chlamydia to HPV to HIV has been hindered by some groups that believe offering protection against these diseases is the same thing as actively encouraging the “immoral behavior” that spreads them.

But here’s where a zoobiquitous perspective helps. Looking at these diseases in animals allows us to see infection as infection—independent of the route of introduction. While thinking about a human with chlamydia may make us grimace or blush, koalas with chlamydia likely make us feel sympathetic, or at least impassive. Most of us don’t judge the koala for its sexuality. Decreasing the stigma of STDs can improve treatment.

An evolutionary approach could inspire clinical solutions. As we’ve seen, studying the history of infections may give epidemiologists a head start in identifying those bugs that are getting ready to jump transmission pathways. Maybe there are “good” microorganisms that spread sexually and maintain genital health, the way certain “good” microorganisms maintain intestinal health.

Finally, studying STDs in animals can enlighten us in ways that extend beyond our consideration of the illness, infertility, and death these pathogens can cause. Sexually acquired infections have played an oceanic, though microscopic, role in evolutionary biology. Sam the koala may have succumbed to chlamydia, but not all her sexual partners met with the same fate. In fact, despite their unprotected sexual free-for-all, a small percentage of koalas never became infected. Something enabled them to resist the infection … and that something is genetic variation. Every time egg and sperm meet, a new and unique combination of genetic material is created. Every once in a while, the mix is such that the creature that possesses it gains an infection-resistant advantage.
This is why, although HIV is complex and deadly to most humans, infectious disease researchers have discovered that about 1 percent of humans (primarily Swedes) seem to be immune to it.
^‖

In populations of clones—those with identical genetics—a single species of virus, bacterium, fungus, or worm can wipe out the whole group. But when individuals within a group each possess a slightly different genetic makeup, chances increase dramatically that some will survive. And nothing provides diversity as predictably and effectively as one particular act: sexual reproduction.

And herein lies a central irony with insights for evolutionary biologists, infectious disease specialists, and sexually active humans. Today we protect ourselves against sex. But over the course of evolution, it has been sex itself that protected us.