In the top floor of the Faculty of Science of Charles University in Prague, one room is filled with the soft thud thud thud of restless shifting feet. Opposite a table laden with biscuits and soft drinks, students listening to techno music through clunky headphones dance on plastic mats, following instructions that flash up on laptops in front of them. This strangely silent disco looks like any group of graduates letting off steam, but this isn’t the rec room, it’s the lab.
For the past 20 years, Professor Jaroslav Flegr has been designing games for his students to play, from simple reaction tests to the Dance Dance Revolution marathon currently underway. The light-hearted challenges underlie a more serious question: is a common brain parasite dimming the cognitive powers of his students? The parasite in question is Toxoplasma gondii, a small protozoan with great ambitions. Although it takes cats as its definitive host, and can only complete its life cycle there, T. gondii practices a startling promiscuity when it comes to secondary hosts. The parasite is typically spread by rodents, which ingest spores deposited in cat droppings, but T. gondii’s scattergun approach means that it can be found in almost any warm-blooded animal, from dogs to dolphins, and notably all of our major livestock – cattle, pigs, sheep, goats. And, of course, humans. It’s a major success story of the single-celled kingdom, cropping up across the planet at an extraordinarily high prevalence: depending on where in the world you’re reading this, your chances of harbouring T. gondii are between 30 and 80 per cent.
The parasite’s ability to cause serious and even fatal birth defects in mammals meant that for a long time T. gondii was primarily a concern to farmers and expectant mothers. For everyone else, T. gondii was something you’d eventually expose yourself to, most likely through eating undercooked meat, that would produce mild flu-like symptoms before dying or lying dormant in your muscle and nervous tissue. Unless you became acutely immunocompromised (at which point T. gondii wakes up and begins eating big holes in your brain), you’d carry the bug for the rest of your life without any noticeable effect. Well, that was the idea at least.
You see, T. gondii has a very interesting trick. It can produce dopamine. Not for itself, of course; the protozoan has no mind of its own that would need a neurotransmitter. But its hosts do. And dopamine is the skeleton key that T. gondii uses to unlock the mammalian brain. Rats, as it happens, have a longstanding animosity toward cats, which is a problem for any T. gondii hoping to make the leap up the food chain. So the microbe sets about reprogramming the rodent brain, making it braver, more intrepid, willing it to take risks. The rats’ instinctual fear of the smell of cats, stamped millennia-deep in the rodent brain, is papered over. So too its cautious neophobia. And this new cavalier attitude ends up putting the rat in the jaws of a passing cat, and the parasite into the gut of its definitive host.
Professor Flegr wondered if T. gondii might attempt the same transformation on humans. After all, how different do a rat and a human look from the inside? It’s all blood and bone and dopamine to a parasite. From previous research, Flegr knew that humans exposed to T. gondii showed diminished reaction times. He visited local hospitals and took blood samples from those who had been involved in traffic accidents, in particular those who had been at fault in traffic accidents where alcohol wasn’t a factor. He found that they were almost three times as likely to test seropositive for Toxoplasma than the general population. The link implied that the effects of exposure to T. gondii – a change in risk perception, and a slowing of reflexes, were both strong enough to increase the chances of an accident and yet subtle enough that the victim was not aware of their altered state of mind. It appeared to be a very real and very serious effect of T. gondii infection. Road traffic accidents claim the lives of some two million people worldwide every year; a parasite with even a small hand in that would still be responsible for thousands of deaths annually.
Like a suspect in the dock, Toxoplasma has the means, the motive and the opportunity to inflict brain damage and behavioural changes. Flegr found women exposed to the parasite became more outgoing and sociable, while men expressed greater insecurity. Researchers have also implicated the parasite in illnesses such as schizophrenia. The idea that an infectious agent might be at the root of mental illness is not a new one – in fact, T. gondii came under suspicion over a 100 years ago, in an editorial published by Scientific American. However, this coincided with the arrival of an exciting new science from Vienna called psychoanalysis, which held that repressed desires were at the seat of most mental disturbance, and the idea of contagious insanity seemed terribly unfashionable by contrast. It was only after the great waves that Freud cast had died down to ripples that people once again began to entertain the idea of an infectious agent responsible for diseases of the mind. Acute toxoplasmosis is known to cause severe psychological disturbances in some patients, giving rise to auditory and visual hallucinations, disorganized speech and delusions. Might this damage also manifest itself as long-term mental disorders, or even subtle but significant changes in behaviour?
After visiting Professor Flegr, I had to wonder, how many other infectious diseases produce similar effects in us? The sheer prevalence of T. gondii, coupled with its habit of infecting non-target species, lends it the status of something approaching an environmental hazard. Just as fog obscures the land, allowing travellers to wander lost, T. gondii stretches over the human landscape, a kind of mental fog that blurs our perceptions of the real world. The question is: why aren’t our brains better at fighting this kind of deception?
Of course, Toxoplasma is not the only parasite to have evolved an extraordinary ability to adapt a host’s behaviour. Examples abound through the animal kingdom – Carl Zimmer dedicated an entire chapter to behavioural manipulation in his bestseller Parasite Rex. The larvae of the Hymenopimecis wasp convince the spider they latch onto to abandon its normal web architecture and instead follow a set of blueprints of the insect’s own devising. The result is a sturdy, well anchored cocoon in which the larvae can safely undergo its transformation into an adult wasp. Closer to home, the Plasmodium protist responsible for malaria is a parasite of mosquitoes as much as one of mankind. After infecting a mosquito, it suppresses the insect’s feeding behaviour until it is ready to be passed on through the animal’s salivary glands. Every blood meal carries the risk of being swatted; the protist wants to make sure each one counts. In relationships such as these, where the parasite’s dictated behaviour acts as a direct threat to survival of the host, should we expect their brain to evolve in response just as their bodies have? Should a mosquito not grow a mental shell as impenetrable as its physical one? Instead of physically defeating the parasite, might a host develop tolerance or immunity to the parasite’s behavioural tweaks, incorporating redundancy and error-checking in its behavioural loops like a robust piece of software? I put the question to Professor Robert Poulin at the University of Otago, New Zealand. “I’ve been asking myself the same question for years,” he replied. “Why don’t hosts put up a better fight against manipulation? Whatever the actual mechanism, I am not aware of any case of a host actively resisting. Animals have numerous adaptations to avoid parasites, or eliminate them if they succeed at infecting the host; if the parasite gets through these, however, it wins.”
Part of the problem is the difficulty in identifying what this kind of resistance would look like, whether it be the upregulation of certain genes or a shift in brain chemistry in response to parasitic infection. These are events playing out in a vague stage somewhere between psychology and physiology, and require an understanding of the physical foundations of behaviour that we perhaps do not have yet. But it seems unlikely that we have arrived at this point without the effects of behavioural manipulation leaving some kind of mark in the architecture of our brain. Like the students dancing in Flegr’s loft to music no one else can hear, the patterns of behaviour in our brains may be choreographed to some invisible, long silent orchestra.
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