[LINK] O/T Toxoplasma gondii

[stephen at melbpc.org.au]

How Your Cat Is Making You Crazy

BY Kathleen McAuliffe, Atlantic Magazine
http://www.theatlantic.com/magazine/archive/2012/03/how-your-cat-is-
making-you-crazy/308873/  (and)
http://www.heraldsun.com.au/news/the-other-side/cat-poo-contains-a-common-
bug-that-may-be-controlling-your-mind/story-e6frfhk6-1226532097725


No one would accuse Jaroslav Flegr of being a conformist. A self-
described “sloppy dresser,” the 53-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. 

Consider Polysphincta gutfreundi, a parasitic wasp that grabs hold of an 
orb spider and attaches a tiny egg to its belly. A wormlike larva emerges 
from the egg, and then releases chemicals that prompt the spider to 
abandon weaving its familiar spiral web and instead spin its silk thread 
into a special pattern that will hold the cocoon in which the larva 
matures. The “possessed” spider even crochets a specific geometric design 
in the net, camouflaging the cocoon from the wasp’s predators. 

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. 
 
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. 

Human-genome studies, both scientists believe, are also in keeping with 
that finding—and might explain why schizophrenia runs in families. The 
most replicated result from that line of investigation, they say, 
suggests that the genes most commonly associated with schizophrenia 
relate to the immune system and how it reacts to infectious agents. So in 
many cases where the disease appears to be hereditary, they theorize, 
what may in fact be passed down is an aberrant or deficient immune 
response to invaders like T. gondii. 

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

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