Toxoplasmosis
How Your Cat Is Making You Crazy - By
Kathleen McAuliffe
http://www.theatlantic.com/magazine/archive/2012/03/how-your-cat-is-making-you-crazy/8873/
JAROSLAV FLEGR IS NO KOOK. AND YET, FOR YEARS, HE SUSPECTED
HIS MIND HAD BEEN TAKEN OVER BY PARASITES THAT HAD INVADED HIS BRAIN. SO THE
PROLIFIC BIOLOGIST TOOK HIS SCIENCE-FICTION HUNCH INTO THE LAB. WHAT HE’S NOW
DISCOVERING WILL STARTLE YOU. COULD TINY ORGANISMS CARRIED BY HOUSE CATS BE
CREEPING INTO OUR BRAINS, CAUSING EVERYTHING FROM CAR WRECKS TO SCHIZOPHRENIA? A
BIOLOGIST’S SCIENCE- FICTION HUNCH IS GAINING CREDENCE AND SHAPING THE
EMERGING SCIENCE OF MIND- CONTROLLING PARASITES.
NO ONE WOULD accuse Jaroslav Flegr of being a conformist. A
self-described “sloppy dresser,” the 63-year-old Czech scientist has the
contemplative air of someone habitually lost in thought, and his still-youthful,
square-jawed face is framed by frizzy red hair that encircles his head like a
ring of fire.
Certainly Flegr’s thinking is jarringly unconventional.
Starting in the early 1990s, he began to suspect that a single-celled parasite
in the protozoan family was subtly manipulating his personality, causing him to
behave in strange, often self-destructive ways. And if it was messing with his
mind, he reasoned, it was probably doing the same to others.
The parasite, which is excreted by cats in their feces, is
called Toxoplasma gondii (T. gondii or Toxo for short) and is the microbe that
causes toxoplasmosis—the reason pregnant women are told to avoid cats’
litter boxes. Since the 1920s, doctors have recognized that a woman who becomes
infected during pregnancy can transmit the disease to the fetus, in some cases
resulting in severe brain damage or death. T. gondii is also a major threat to
people with weakened immunity: in the early days of the AIDS epidemic, before
good antiretroviral drugs were developed, it was to blame for the dementia that
afflicted many patients at the disease’s end stage. Healthy children and
adults, however, usually experience nothing worse than brief flu-like symptoms
before quickly fighting off the protozoan, which thereafter lies dormant inside
brain cells—or at least that’s the standard medical wisdom.
But if Flegr is right, the “latent” parasite may be
quietly tweaking the connections between our neurons, changing our response to
frightening situations, our trust in others, how outgoing we are, and even our
preference for certain scents. And that’s not all. He also believes that the
organism contributes to car crashes, suicides, and mental disorders such as
schizophrenia. When you add up all the different ways it can harm us, says Flegr,
“Toxoplasma might even kill as many people as malaria, or at least a million
people a year.”
An evolutionary biologist at Charles University in Prague,
Flegr has pursued this theory for decades in relative obscurity. Because he
struggles with English and is not much of a conversationalist even in his native
tongue, he rarely travels to scientific conferences. That “may be one of the
reasons my theory is not better known,” he says. And, he believes, his views
may invite deep-seated opposition. “There is strong psychological resistance
to the possibility that human behavior can be influenced by some stupid
parasite,” he says. “Nobody likes to feel like a puppet. Reviewers [of my
scientific papers] may have been offended.” Another more obvious reason for
resistance, of course, is that Flegr’s notions sound an awful lot like fringe
science, right up there with UFO sightings and claims of dolphins telepathically
communicating with humans.
But after years of being ignored or discounted, Flegr is
starting to gain respectability. Psychedelic as his claims may sound, many
researchers, including such big names in neuroscience as Stanford’s Robert
Sapolsky, think he could well be onto something. Flegr’s “studies are well
conducted, and I can see no reason to doubt them,” Sapolsky tells me. Indeed,
recent findings from Sapolsky’s lab and British groups suggest that the
parasite is capable of extraordinary shenanigans. T. gondii, reports Sapolsky,
can turn a rat’s strong innate aversion to cats into an attraction, luring it
into the jaws of its No. 1 predator. Even more amazing is how it does this: the
organism rewires circuits in parts of the brain that deal with such primal
emotions as fear, anxiety, and sexual arousal. “Overall,” says Sapolsky,
“this is wild, bizarre neurobiology.” Another academic heavyweight who takes
Flegr seriously is the schizophrenia expert E. Fuller Torrey, director of the
Stanley Medical Research Institute, in Maryland. “I admire Jaroslav for doing
[this research],” he says. “It’s obviously not politically correct, in the
sense that not many labs are doing it. He’s done it mostly on his own, with
very little support. I think it bears looking at. I find it completely
credible.”
What’s more, many experts think T. gondii may be far from
the only microscopic puppeteer capable of pulling our strings. “My guess is
that there are scads more examples of this going on in mammals, with parasites
we’ve never even heard of,” says Sapolsky.
Familiar to most of us, of course, is the rabies virus. On
the verge of killing a dog, bat, or other warm-blooded host, it stirs the animal
into a rage while simultaneously migrating from the nervous system to the
creature’s saliva, ensuring that when the host bites, the virus will live on
in a new carrier. But aside from rabies, stories of parasites commandeering the
behavior of large-brained mammals are rare. The far more common victims of
parasitic mind control—at least the ones we know about—are fish,
crustaceans, and legions of insects, according to Janice Moore, a behavioral
biologist at Colorado State University. “Flies, ants, caterpillars, wasps, you
name it—there are truckloads of them behaving weirdly as a result of
parasites,” she says.
Flegr himself traces his life’s work to another master of
mind control. Almost 30 years ago, as he was reading a book by the British
evolutionary biologist Richard Dawkins, Flegr was captivated by a passage
describing how a flatworm turns an ant into its slave by invading the ant’s
nervous system. A drop in temperature normally causes ants to head underground,
but the infected insect instead climbs to the top of a blade of grass and clamps
down on it, becoming easy prey for a grazing sheep. “Its mandibles actually
become locked in that position, so there’s nothing the ant can do except hang
there in the air,” says Flegr. The sheep grazes on the grass and eats the ant;
the worm gains entrance into the ungulate’s gut, which is exactly where it
needs to be in order to complete—as the Lion King song goes—the circle of
life. “It was the first I learned about this kind of manipulation, so it made
a big impression on me,” Flegr says.
After he read the book, Flegr began to make a connection
that, he readily admits, others might find crazy: his behavior, he noticed,
shared similarities with that of the reckless ant. For example, he says, he
thought nothing of crossing the street in the middle of dense traffic, “and if
cars honked at me, I didn’t jump out of the way.” He also made no effort to
hide his scorn for the Communists who ruled Czechoslovakia for most of his early
adulthood. “It was very risky to openly speak your mind at that time,” he
says. “I was lucky I wasn’t imprisoned.” And during a research stint in
eastern Turkey, when the strife-torn region frequently erupted in gunfire, he
recalls being “very calm.” In contrast, he says, “my colleagues were
terrified. I wondered what was wrong with myself.”
His bewilderment continued until 1990, when he joined the
biology faculty of Charles University. As it happened, the 650-year-old
institution had long been a world leader in documenting the health effects of T.
gondii, as well as developing methods for detecting the parasite. In fact, just
as Flegr was arriving, his colleagues were searching for infected individuals on
whom to test their improved diagnostic kits, which is how he came to be asked
one day to roll up his sleeve and donate blood. He discovered that he had the
parasite—and just possibly, he thought, the key to his baffling
self-destructive streak.
He delved into T. gondii’s life cycle. After an infected
cat defecates, Flegr learned, the parasite is typically picked up from the soil
by scavenging or grazing animals—notably rodents, pigs, and cattle—all of
which then harbor it in their brain and other body tissues. Humans, on the other
hand, are exposed not only by coming into contact with litter boxes, but also,
he found, by drinking water contaminated with cat feces, eating unwashed
vegetables, or, especially in Europe, by consuming raw or undercooked meat.
Hence the French, according to Flegr, with their love of steak prepared saignant—literally,
“bleeding”—can have infection rates as high as 55 percent. (Americans will
be happy to hear that the parasite resides in far fewer of them, though a still
substantial portion: 10 to 20 percent.) Once inside an animal or human host, the
parasite then needs to get back into the cat, the only place where it can
sexually reproduce—and this is when, Flegr believed, behavioral manipulation
might come into play.
The parasite T. gondii, seen here, may be changing
connections between our neurones, altering how we act and feel. (Dennis Kunkel
Microscropy, Inc./Visuals Unlimited/Corbis Images)
Researchers had already observed a few peculiarities about
rodents with T. gondii that bolstered Flegr’s theory. The infected rodents
were much more active in running wheels than uninfected rodents were, suggesting
that they would be more-attractive targets for cats, which are drawn to
fast-moving objects. They also were less wary of predators in exposed spaces.
Little, however, was known about how the latent infection might influence
humans, because we and other large mammals were widely presumed to be accidental
hosts, or, as scientists are fond of putting it, a “dead end” for the
parasite. But even if we were never part of the parasite’s life cycle, Flegr
reasoned, mammals from mouse to man share the vast majority of their genes, so
we might, in a case of mistaken identity, still be vulnerable to manipulations
by the parasite.
In the Soviet-stunted economy, animal studies were way
beyond Flegr’s research budget. But fortunately for him, 30 to 40 percent of
Czechs had the latent form of the disease, so plenty of students were available
“to serve as very cheap experimental animals.” He began by giving them and
their parasite-free peers standardized personality tests—an inexpensive, if
somewhat crude, method of measuring differences between the groups. In addition,
he used a computer-based test to assess the reaction times of participants, who
were instructed to press a button as soon as a white square popped up anywhere
against the dark background of the monitor.
The subjects who tested positive for the parasite had
significantly delayed reaction times. Flegr was especially surprised to learn,
though, that the protozoan appeared to cause many sex-specific changes in
personality. Compared with uninfected men, males who had the parasite were more
introverted, suspicious, oblivious to other people’s opinions of them, and
inclined to disregard rules. Infected women, on the other hand, presented in
exactly the opposite way: they were more outgoing, trusting, image-conscious,
and rule-abiding than uninfected women.
The findings were so bizarre that Flegr initially assumed
his data must be flawed. So he tested other groups—civilian and military
populations. Again, the same results. Then, in search of more corroborating
evidence, he brought subjects in for further observation and a battery of tests,
in which they were rated by someone ignorant of their infection status. To
assess whether participants valued the opinions of others, the rater judged how
well dressed they appeared to be. As a measure of gregariousness, participants
were asked about the number of friends they’d interacted with over the past
two weeks. To test whether they were prone to being suspicious, they were asked,
among other things, to drink an unidentified liquid.
The results meshed well with the questionnaire findings.
Compared with uninfected people of the same sex, infected men were more likely
to wear rumpled old clothes; infected women tended to be more meticulously
attired, many showing up for the study in expensive, designer-brand clothing.
Infected men tended to have fewer friends, while infected women tended to have
more. And when it came to downing the mystery fluid, reports Flegr, “the
infected males were much more hesitant than uninfected men. They wanted to know
why they had to do it. Would it harm them?” In contrast, the infected women
were the most trusting of all subjects. “They just did what they were told,”
he says.
Why men and women reacted so differently to the parasite
still mystified him. After consulting the psychological literature, he started
to suspect that heightened anxiety might be the common denominator underlying
their responses. When under emotional strain, he read, women seek solace through
social bonding and nurturing. In the lingo of psychologists, they’re inclined
to “tend and befriend.” Anxious men, on the other hand, typically respond by
withdrawing and becoming hostile or antisocial. Perhaps he was looking at flip
sides of the same coin.
Closer inspection of Flegr’s reaction-time results
revealed that infected subjects became less attentive and slowed down a minute
or so into the test. This suggested to him that Toxoplasma might have an adverse
impact on driving, where constant vigilance and fast reflexes are critical. He
launched two major epidemiological studies in the Czech Republic, one of men and
women in the general population and another of mostly male drivers in the
military. Those who tested positive for the parasite, both studies showed, were
about two and a half times as likely to be in a traffic accident as their
uninfected peers.
WHEN I MET Flegr for the first time, last September, at his
office on the third floor of Charles University’s Biological Sciences
building, I was expecting something of a wild man. But once you get past the
riotous red hair, his style is understated. Thin and slight of build, he’s
soft-spoken, precise with his facts, and—true to his Toxo status—clad in old
sneakers, faded bell-bottom jeans, and a loose-fitting button-up shirt. As our
conversation proceeds, I discover that his latest findings have become—to
quote Alice in Wonderland—“curiouser and curiouser,” which may explain why
his forehead has the deep ruts of a chronic worrier, or someone perpetually
perplexed.
He’s published some data, he tells me, that suggest
infected males might have elevated testosterone levels. Possibly for that
reason, women shown photos of these men rate them as more masculine than
pictures of uninfected men. “I want to investigate this more closely to see if
it’s true,” he says. “Also, it could be women find infected men more
attractive. That’s something else we hope to test.”
Meanwhile, two Turkish studies have replicated his studies
linking Toxoplasma to traffic accidents. With up to one-third of the world
infected with the parasite, Flegr now calculates that T. gondii is a likely
factor in several hundred thousand road deaths each year. In addition,
reanalysis of his personality-questionnaire data revealed that, just like him,
many other people who have the latent infection feel intrepid in dangerous
situations. “Maybe,” he says, “that’s another reason they get into
traffic accidents. They don’t have a normal fear response.”
It’s almost impossible to hear about Flegr’s research
without wondering whether you’re infected—especially if, like me, you’re a
cat owner, favor very rare meat, and identify even a little bit with your Toxo
sex stereotype. So before coming to Prague, I’d gotten tested for the
parasite, but I didn’t yet know the results. It seemed a good time to see what
his intuition would tell me. “Can you guess from observing someone whether
they have the parasite—myself, for example?,” I ask.
“No,” he says, “the parasite’s effects on
personality are very subtle.” If, as a woman, you were introverted before
being infected, he says, the parasite won’t turn you into a raving extrovert.
It might just make you a little less introverted. “I’m very typical of
Toxoplasma males,” he continues. “But I don’t know whether my personality
traits have anything to do with the infection. It’s impossible to say for any
one individual. You usually need about 50 people who are infected and 50 who are
not, in order to see a statistically significant difference. The vast majority
of people will have no idea they’re infected.”
Still, he concedes, the parasite could be very bad news for
a small percentage of people—and not just those who might be at greater risk
for car accidents. Many schizophrenia patients show shrinkage in parts of their
cerebral cortex, and Flegr thinks the protozoan may be to blame for that. He
hands me a recently published paper on the topic that he co-authored with
colleagues at Charles University, including a psychiatrist named Jiri Horacek.
Twelve of 44 schizophrenia patients who underwent MRI scans, the team found, had
reduced gray matter in the brain—and the decrease occurred almost exclusively
in those who tested positive for T. gondii. After reading the abstract, I must
look stunned, because Flegr smiles and says, “Jiri had the same response. I
don’t think he believed it could be true.” When I later speak with Horacek,
he admits to having been skeptical about Flegr’s theory at the outset. When
they merged the MRI results with the infection data, however, he went from being
a doubter to being a believer. “I was amazed at how pronounced the effect
was,” he says. “To me that suggests the parasite may trigger schizophrenia
in genetically susceptible people.”
One might be tempted to dismiss the bulk of Flegr’s work
as hokum—the fanciful imaginings of a lone, eccentric scholar—were it not
for the pioneering research of Joanne Webster, a parasitologist at Imperial
College London. Just as Flegr was embarking on his human trials, Webster, then a
freshly minted Ph.D., was launching studies of Toxo-infected rodents, reasoning,
just as Flegr did, that as hosts of the parasite, they would be likely targets
for behavioral manipulation.
She quickly confirmed, as previous researchers had shown,
that infected rats were more active and less cautious in areas where predators
lurk. But then, in a simple, elegant experiment, she and her colleagues
demonstrated that the parasite did something much more remarkable. They treated
one corner of each rat’s enclosure with the animal’s own odor, a second with
water, a third with cat urine, and the last corner with the urine of a rabbit, a
creature that does not prey on rodents. “We thought the parasite might reduce
the rats’ aversion to cat odor,” she told me. “Not only did it do that,
but it actually increased their attraction. They spent more time in the
cat-treated areas.” She and other scientists repeated the experiment with the
urine of dogs and minks, which also prey on rodents. The effect was so specific
to cat urine, she says, that “we call it ‘fatal feline attraction.’”
She began tagging the parasite with fluorescent markers and
tracking its progress in the rats’ bodies. Given the surgically precise way
the microbe alters behavior, Webster anticipated that it would end up in
localized regions of the brain. But the results defied expectations. “We were
quite surprised to find the cysts—the parasite’s dormant form—all over the
brain in what otherwise appeared to be a happy, healthy rat,” she says.
Nonetheless, the cysts were most abundant in a part of the brain that deals with
pleasure (in human terms, we’re talking sex, drugs, and rock and roll) and in
another area that’s involved in fear and anxiety (post-traumatic stress
disorder affects this region of the brain). Perhaps, she thought, T. gondii uses
a scattershot approach, disseminating cysts far and wide, enabling a few of them
to zero in on the right targets.
To gain more clarity on the matter, she sought the aid of
the parasitologist Glenn McConkey, whose team at the University of Leeds was
probing the protozoan’s genome for signs of what it might be doing. The
approach brought to light a striking talent of the parasite: it has two genes
that allow it to crank up production of the neurotransmitter dopamine in the
host brain. “We never cease to be amazed by the sophistication of these
parasites,” Webster says.
Their findings, reported last summer, created immediate
buzz. Dopamine is a critical signaling molecule involved in fear, pleasure, and
attention. Furthermore, the neurotransmitter is known to be jacked up in people
with schizophrenia—another one of those strange observations about the
disease, like its tendency to erode gray matter, that have long puzzled medical
researchers. Antipsychotic medicine designed to quell schizophrenic delusions
apparently blocks the action of dopamine, which had suggested to Webster that
what it might really be doing is thwarting the parasite. Scientists had already
shown that adding the medicine to a petri dish where T. gondii is happily
dividing will stunt the organism’s growth. So Webster decided to feed the
antipsychotic drug to newly infected rats to see how they reacted. Lo and
behold, they didn’t develop fatal feline attraction. Suddenly, attributing
behavioral changes to the microbe seemed much more plausible.
As the scientific community digested the British team’s
dopamine discoveries, Robert Sapolsky’s lab at Stanford announced still more
attention-grabbing news. The neuroscientist and his colleagues found that T.
gondii disconnects fear circuits in the brain, which might help to explain why
infected rats lose their aversion to cat odor. Just as startling, reports
Sapolsky, the parasite simultaneously is “able to hijack some of the circuitry
related to sexual arousal” in the male rat—probably, he theorizes, by
boosting dopamine levels in the reward-processing part of the brain. So when the
animal catches a whiff of cat scent, the fear center fails to fully light up, as
it would in a normal rat, and instead the area governing sexual pleasure begins
to glow. “In other words,” he says, “Toxo makes cat odor smell sexy to
male rats.”
The neurobiologist Ajai Vyas, after working with Sapolsky
on this study as a postdoctoral student, decided to inspect infected rats’
testicles for signs of cysts. Sure enough, he found them there—as well as in
the animals’ semen. And when the rat copulates, Vyas discovered, the protozoan
moves into the female’s womb, typically infecting 60 percent of her pups,
before traveling on up to her own brain—creating still more vehicles for
ferrying the parasite back into the belly of a cat.
Could T. gondii be a sexually transmitted disease in humans
too? “That’s what we hope to find out,” says Vyas, who now works at
Nanyang Technological University, in Singapore. The researchers also discovered
that infected male rats suddenly become much more attractive to females.
“It’s a very strong effect,” says Vyas. “Seventy-five percent of the
females would rather spend time with the infected male.”
After I return from Prague, Flegr informs me that he’s
just had a paper accepted for publication that, he claims, “proves fatal
feline attraction in humans.” By that he means that infected men like the
smell of cat pee—or at least they rank its scent much more favorably than
uninfected men do. Displaying the characteristic sex differences that define
many Toxo traits, infected women have the reverse response, ranking the scent
even more offensive than do women free of the parasite. The sniff test was done
blind and also included urine collected from a dog, horse, hyena, and tiger.
Infection did not affect how subjects rated these other samples.
“Is it possible cat urine may be an aphrodisiac for
infected men?,” I ask. “Yes. It’s possible. Why not?” says Flegr. I
think he’s smiling at the other end of the phone line, but I’m not sure,
which leaves me wondering whether I’ve stumbled onto a topic ripe for a
Saturday Night Live skit, or a matter worthy of medical concern. When I ask
Sapolsky about Flegr’s most recent research, he says the effects Flegr is
reporting “are incredibly cool. However, I’m not too worried, in that the
effects on humans are not gigantic. If you want to reduce serious car accidents,
and you had to choose between curing people of Toxo infections versus getting
people not to drive drunk or while texting, go for the latter in terms of
impact.”
In fact, Sapolsky thinks that Toxo’s inventiveness might
even offer us some benefits. If we can figure out how the parasite makes animals
less fearful, he says, it might give us insights into how to devise treatments
for people plagued by social-anxiety disorder, phobias, PTSD, and the like.
“But frankly,” he adds, “this mostly falls into the ‘Get a load of this,
can you believe what nature has come up with?’ category.”
Webster is more circumspect, if not downright troubled.
“I don’t want to cause any panic,” she tells me. “In the vast majority
of people, there will be no ill effects, and those who are affected will mostly
demonstrate subtle shifts of behavior. But in a small number of cases, [Toxo
infection] may be linked to schizophrenia and other disturbances associated with
altered dopamine levels—for example, obsessive-compulsive disorder,
attention-deficit hyperactivity disorder, and mood disorders. The rat may live
two or three years, while humans can be infected for many decades, which is why
we may be seeing these severe side effects in people. We should be cautious of
dismissing such a prevalent parasite.”
The psychiatrist E. Fuller Torrey agrees—though he came
to this viewpoint from a completely different angle than either Webster or Flegr.
His opinion stems from decades of research into the root causes of
schizophrenia. “Textbooks today still make silly statements that schizophrenia
has always been around, it’s about the same incidence all over the world, and
it’s existed since time immemorial,” he says. “The epidemiology literature
contradicts that completely.” In fact, he says, schizophrenia did not rise in
prevalence until the latter half of the 18th century, when for the first time
people in Paris and London started keeping cats as pets. The so-called cat craze
began among “poets and left-wing avant-garde Greenwich Village types,” says
Torrey, but the trend spread rapidly—and coinciding with that development, the
incidence of schizophrenia soared.
Since the 1950s, he notes, about 70 epidemiology studies
have explored a link between schizophrenia and T. gondii. When he and his
colleague Robert Yolken, a neurovirologist at Johns Hopkins University, surveyed
a subset of these papers that met rigorous scientific standards, their
conclusion complemented the Prague group’s discovery that schizophrenic
patients with Toxo are missing gray matter in their brains. Torrey and Yolken
found that the mental illness is two to three times as common in people who have
the parasite as in controls from the same region.
Epstein-Barr virus, mumps, rubella, and other infectious
agents, they point out, have also been linked to schizophrenia—and there are
probably more as yet unidentified triggers, including many that have nothing to
do with pathogens. But for now, they say, Toxo remains the strongest
environmental factor implicated in the disorder. “If I had to guess,” says
Torrey, “I’d say 75 percent of cases of schizophrenia are associated with
infectious agents, and Toxo would be involved in a significant subset of
those.”
Just as worrisome, says Torrey, the parasite may also
increase the risk of suicide. In a 2011 study of 20 European countries, the
national suicide rate among women increased in direct proportion to the
prevalence of the latent Toxo infection in each nation’s female population.
According to Teodor Postolache, a psychiatrist and the director of the Mood and
Anxiety Program at the University of Maryland School of Medicine, a flurry of
other studies, several conducted by his own team, offers further support of T.
gondii’s link to higher rates of suicidal behavior. These include
investigations of general populations as well as groups made up of patients with
bipolar disorder, severe depression, and schizophrenia, and in places as diverse
as Turkey, Germany, and the Baltimore/Washington area. Exactly how the parasite
may push vulnerable people over the edge is yet to be determined. Postolache
theorizes that what disrupts mood and the ability to control violent impulses
may not be the organism per se, but rather neurochemical changes associated with
the body’s immune response to it. “As far-fetched as these ideas may
sound,” says Postolache, “the American Foundation for Suicide Prevention was
willing to put money behind this research.”
GIVEN ALL THE nasty science swirling around this parasite,
is it time for cat lovers to switch their allegiance to other animals?
Even Flegr would advise against that. Indoor cats pose no
threat, he says, because they don’t carry the parasite. As for outdoor cats,
they shed the parasite for only three weeks of their life, typically when
they’re young and have just begun hunting. During that brief period, Flegr
simply recommends taking care to keep kitchen counters and tables wiped clean.
(He practices what he preaches: he and his wife have two school-age children,
and two outdoor cats that have free roam of their home.) Much more important for
preventing exposure, he says, is to scrub vegetables thoroughly and avoid
drinking water that has not been properly purified, especially in the developing
world, where infection rates can reach 95 percent in some places. Also, he
advises eating meat on the well-done side—or, if that’s not to your taste,
freezing it before cooking, to kill the cysts.
As concerns about the latent infection mount, however,
experts have begun thinking about more-aggressive steps to counter the
parasite’s spread. Inoculating cats or livestock against T. gondii might be
one way to interrupt its life cycle, offers Johns Hopkins’ Robert Yolken.
Moving beyond prevention to treatment is a taller order. Once the parasite
becomes deeply ensconced in brain cells, routing it out of the body is virtually
impossible: the thick-walled cysts are impregnable to antibiotics. Because T.
gondii and the malaria protozoan are related, however, Yolken and other
researchers are looking among antimalarial agents for more-effective drugs to
attack the cysts. But for now, medicine has no therapy to offer people who want
to rid themselves of the latent infection; and until solid proof exists that
Toxo is as dangerous as some scientists now fear, pharmaceutical companies
don’t have much incentive to develop anti-Toxo drugs.
Yolken hopes that will change. “To explain where we are
in Toxo research today,” he says, “the analogy I always give is the ulcer
bacteria. We first needed to find ways of treating the organism and showing that
the disease went away when you did that. We will have to show that when we very
effectively treat Toxoplasma, some portion of psychiatric illness goes away.”
But T. gondii is just one of an untold number of infectious
agents that prey on us. And if the rest of the animal kingdom is anything to go
by, says Colorado State University’s Janice Moore, plenty of them may be
capable of tinkering with our minds. For example, she and Chris Reiber, a
biomedical anthropologist at Binghamton University, in New York, strongly
suspected that the flu virus might boost our desire to socialize. Why? Because
it spreads through close physical contact, often before symptoms
emerge—meaning that it must find a new host quickly. To explore this hunch,
Moore and Reiber tracked 36 subjects who received a flu vaccine, reasoning that
it contains many of the same chemical components as the live virus and would
thus cause the subjects’ immune systems to react as if they’d encountered
the real pathogen.
The difference in the subjects’ behavior before and after
vaccination was pronounced: the flu shot had the effect of nearly doubling the
number of people with whom the participants came in close contact during the
brief window when the live virus was maximally contagious. “People who had
very limited or simple social lives were suddenly deciding that they needed to
go out to bars or parties, or invite a bunch of people over,” says Reiber.
“This happened with lots of our subjects. It wasn’t just one or two
outliers.”
Reiber has her eye trained on other human pathogens that
she thinks may well be playing similar games, if only science could prove it.
For example, she says, many people at the end stages of AIDS and syphilis
express an intense craving for sex. So, too, do individuals at the beginning of
a herpes outbreak. These may just be anecdotal accounts, she concedes, but based
on her own findings, she wouldn’t be surprised if these urges come from the
pathogen making known its will to survive.
“We’ve found all kinds of excuses for why we do the
things we do,” observes Moore. “‘My genes made me do it.’ ‘My parents
are to blame.’ I’m afraid we may have reached the point where parasites may
have to be added to the laundry list of excuses.”
She has a point. In fact, I’ve been wondering whether T.
gondii might in some small way be contributing to my extreme extroversion—why
I can’t resist striking up conversations everywhere I go, even when I’m
short of time or with strangers I’ll never see again. Then it occurs to me
that cysts in my brain might be behind my seesaw moods or even my splurges on
expensive clothes. Maybe, I think with mounting conviction, the real me would
have displayed better self-control, had I not been forced to swim upstream
against the will of an insidious parasite. With my feline pal Pixie on my lap
(for the record, she’s an outdoor cat), I call to get the results of my Toxo
test. Negative. I don’t have the latent infection.
I call to tell Flegr the good news. Even though I’m
relieved, I know my voice sounds flat. “It’s strange to admit,” I say,
“but I think I’m a little disappointed.” He laughs. “People who have
cats often feel that way, because they think the parasite explains why they
behave this way or that,” he says. “But,” I protest, “you thought the
same way.” Then it hits me. I may have dodged T. gondii, but given our knack
for fooling ourselves—plus all those parasites out there that may also be
playing tricks on our minds—can anyone really know who’s running the show?