Toxoplasma Gondii

Meet toxoplasma gondii. Well actually, you probably don’t want to meet it. Toxoplasma is a parasite that can infect almost all warm blooded animals, humans included. It’s interesting because scientists have found an association between it and neurological disorders, namely schizophrenia. In one study, women with high levels of toxoplasma were more likely to give birth to schizophrenic babies. This is because toxoplasma is thought to affect behavior and neurotransmitter function. In fact, mice infected with this parasite became fearless and were attracted to cats (thus leading to their death) because toxoplasma affects brain regions responsible for fear. Pretty interesting isn’t it?. Check out this Scientific American article for more details.


Neurotoxoplasmosis, also know as cerebral toxoplasmosis, is an opportunistic infection, caused by the parasite Toxoplasma gondii, which typically affects patients with HIV/AIDS, and is the most common cause of cerebral abscess in these patients

Clinical presentation

In immunocompetent patients, acute encephalitis is extremely rare. Even in the immunocompromised symptoms are typically vague and indolent. Development of new neurological symptoms in these patients should raise high suspicion of cerebral toxoplasmosis.


Toxoplasma gondii is an intracellular parasite that infects birds and mammals. It’s definitive host is the cat and other Felidae species. Excretion of oocytes in its faecal content followed by human contaminated uncooked consumption can lead to human infection. In immunocompetent individuals, it primarily causes a subclinical or asymptomatic infection. In immunocompromised individuals (e.g. AIDS patients), toxoplasmosis is the most common cause of a brain abscess.

Visualizing a Parasite Crossing the Blood Brain Barrier

An estimated 30 percent of the world’s population is chronically infected with the parasite Toxoplasma gondii. Most people live with the infection without noticeable effect, but it can be life-threatening for people with suppressed immune systems, such as people on cancer therapies or who have HIV/AIDS. Pregnant women can also pass an infection to their unborn children, putting the babies at risk of severe neurological disease.

It’s known that “Toxo” can affect the brain, even influencing the behavior of its hosts. But scientists have debated exactly how the parasite crosses the blood-brain barrier, a physical obstacle intended to keep pathogens out of the brain.

Now, researchers from the University of Pennsylvania School of Veterinary Medicine and colleagues from across the country have identified how the parasite makes its way in. Using a powerful imaging technique that allowed the scientists to track the presence and movement of parasites in living tissues, the researchers found that Toxoplasma infects the brain’s endothelial cells, which line blood vessels, reproduces inside of them, and then moves on to invade the central nervous system.

“Crossing the blood-brain barrier is a rare event in part because this structure is designed to protect the brain from pathogens,” said Christopher Hunter, the Mindy Halikman Heyer President’s Distinguished Professor at Penn Vet. “And yet it happens and we have now been able to visualize these events. It’s something that no one had seen before.”

By illuminating the pathogen’s path into the brain, the research helps inform what treatment strategies may be most effective at combatting the parasite before it wreaks its worst damage.

The study appears in Nature Microbiology. Hunter was the senior author on the study, which was led by Christoph Konradt, a post-doctoral researcher in Hunter’s laboratory.

A few different theories have been considered to explain how Toxoplasma could enter the brain.

Some believe the parasite squeezes between the barrier cells, while others think the parasite goes directly through a cell. Another idea, “beloved of microbiologists,” Hunter said, is the Trojan horse hypothesis, in which the parasite hitches a ride across the barrier while hidden inside an infected host cell.

Konradt used Penn Vet’s multi-photon microscope, which allows them to peer deep into living tissues without damaging them, to try to witness the parasite’s invasion in action. In these studies, they used mice that had been specially bred to express a fluorescent green protein in their endothelial cells. They then infected the mice with modified Toxoplasma that expressed a red fluorescent protein.

After a week, they saw endothelial cells in the brain that were infected, as well as evidence that the parasite was reproducing inside those cells. Two weeks post-infection, they saw that parasites appeared in the brain tissue adjacent to the endothelial cells.

In additional experiments, they were able to visualize parasites bursting out of infected endothelial cells, thereby introducing the parasite into the brain.

The researchers also wanted to revisit the Trojan horse hypothesis, to see if, as had been proposed, infected monocytes, a type of immune cell, might be responsible for carrying the parasite into the brain. To test this, the team infected monocytes with a form of Toxo, labeled red, that can’t reproduce, then introduced those cells into mice. If the monocytes were indeed acting as a Trojan horse, the scientists would expect to see the parasite breach the blood-brain barrier. But they only saw infected cells within blood vessels, and these cells were not able to cross the blood brain barrier.

To further illuminate the mechanism by which Toxo infects and disseminates through the body, the researchers looked specifically at levels of free parasites, that is, parasites that had not already infected or become engulfed by a host cell.

They were surprised to see that a significant portion, around a third of the mouse’s total parasite load, existed as free parasites in the blood.

“I think we expected to see a small number of parasites outside cells, because they have to come out to move from cell to cell,” Konradt said. “But I don’t think anyone had fully appreciated the sheer number of parasites that are free and able to infect other cells in the vasculature.”

This presence of free parasites was, however, transient. By 10 days after infection, most mice had no free parasites in their blood.

“From a treatment perspective,” Hunter said, “that means if a pregnant woman gets infected for the first time, there is a fairly short period of time when the parasite can cross the placenta and affect the fetus. That tells us that targeting these stages in the blood during this narrow window could be effective at preventing congenital transmission.”

As a final test to see whether parasites could directly access the brain from the blood, the researchers infected mice with a mixture of normal parasites and mutants that was unable to reproduce, each labeled in different colors. They then showed that only the normal, reproducing parasite made its way into the functional brain tissue.

“This shows that the parasite has to replicate in order to spread from the blood into other tissues,” Konradt said. “That could mean a drug that blocks replication could be effective at preventing dissemination.”

The team’s findings suggest that the current theories about how Toxoplasma crosses the blood-brain barrier are probably not the main way the brain is infected. Rather, parasites move directly from the blood into endothelial cells, where they replicate, cause the cell to burst and then infect neighboring brain cells.

Beyond its implications for Toxoplasma infections, the research may give insights into how other viral, bacterial and parasitic pathogens may move from the blood into the brain.

“Toxo is a really nice model for studying vascular immunity in general,” Konradt said.

A great example of the interconnectedness of life forms on this planet and what happens when natural barriers are breached.

Cat Parasite Spreads to Arctic Beluga Whales - Potential Public Health Issue

Prof Michael Grigg at the University of British Columbia in Vancouver said tests on hundreds of beluga whales in the Beaufort Sea, on the edge of the Arctic, revealed that 14% of the creatures harboured the Toxoplasma gondii infection. The tests are the first to show the infection has reached the region.

The most likely cause of the outbreak was infected cat faeces washing into waterways and on to the sea, where fish and other marine organisms became contaminated and ultimately eaten by the whales.

The rise in pet cats among the Inuit and a warming climate which helps the pathogen survive until it finds a host could be to blame for the emergence of the infection, Grigg told the American Association for the Advancement of Science meeting in Chicago.

“Ice is a major eco-barrier for pathogens. What we are seeing with the big thaw is the liberation of pathogens gaining access to vulnerable new hosts and wreaking havoc,” he added.

A Beluga whale swimming under ice at the Arctic Circle dive center in the White Sea, northern Russia. Photograph: Franco Banfi/Barcroft Media
How Your Cat Is Making You Crazy - The Atlantic

A tiny parasite called Toxoplasma gondii might be driving people crazy. That’s what Jaroslav Flegr believes, anyway. For years he has pursued the odd, yet increasingly realistic theory that this brain-dwelling parasite could be infecting humans via household cats and affecting the way they behave. Toxo literally changes the way you produce dopamine, a key neurotransmitter.

It’s not “crazy cat lady” syndrome, per se, but if Toxo can drive rats so nuts that they walk right into the jaws of a cat, could it influence things like extroversion and schizophrenia in humans?

There is strong psychological resistance to the possibility that human behavior can be influenced by some stupid parasite. Nobody likes to feel like a puppet.

Read more about his work and how Toxo affects the brain at The Atlantic.

Bonus feature: A Radiolab segment about Toxo from 2009.

(Image caption: GLT-1, a glutamate transporter, soaks up glutamate (a neurotransmitter) released by neurons and converts it back into a safer substance. Credit: Wilson lab, UC Riverside)

Researchers Unpack How Toxoplasma Infection Is Linked to Neurodegenerative Disease

Toxoplasma gondii, a protozoan parasite about five microns long, infects a third of the world’s population. Ingested via undercooked meat or unwashed vegetables, the parasite infects 15-30 percent of the US population. In France and Brazil, up to 80 percent of the population has the infection.

Particularly dangerous during pregnancy – infection in pregnant women can cause serious congenital defects and even death of the fetus – this chronic infection has two components: the unicellular parasite, and inflammation of tissues it causes.

Working on mice (like all mammals, a natural host for this parasite), a University of California, Riverside team of biomedical scientists reports in the journal PLOS Pathogens that Toxoplasma infection leads to a disruption of neurotransmitters in the brain and postulates that it triggers neurological disease in those already predisposed to such a disease.

They note that Toxoplasma infection leads to a significant increase in glutamate – the primary and most important neurotransmitter in the brain, which transmits excitatory signals between neurons. This glutamate increase is “extracellular,” meaning outside the cell, and is strictly controlled by specialized cells in the central nervous system (brain and spinal cord), called astrocytes. Glutamate buildup is seen in traumatic brain injury as well as highly pathological and neurodegenerating diseases such as epilepsy, multiple sclerosis and amyotrophic lateral sclerosis (ALS).

One role astrocytes play is to remove extracellular glutamate, lest it increase to pathological levels that could damage neurons. This is primarily achieved using a glutamate transporter, called GLT-1, tasked with regulating extracellular glutamate. GLT-1 soaks up glutamate released by neurons and converts it back into the safer substance glutamine, which can then be used by cells for energy.

“When a neuron fires it releases glutamate into the space between itself and a nearby neuron,” explained lead researcher Emma H. Wilson, an associate professor in the Division of Biomedical Sciences in the School of Medicine, who has worked on toxoplasmosis for more than 15 years. “The nearby neuron detects this glutamate which triggers a firing of the neuron. If the glutamate isn’t cleared by GLT-1 then the neurons can’t fire properly the next time and they start to die.”

Wilson and her team found that during toxoplasma infection, astrocytes swell and are not able to regulate extracellular glutamate concentrations. Further, GLT-1 is not expressed properly. This leads to a buildup of the glutamate released from neurons and the neurons misfire.

“These results suggest that in contrast to assuming chronic Toxoplasma infection as quiescent and benign, we should be aware of the potential risk to normal neurological pathways and changes in brain chemistry,” Wilson said.

When the researchers treated the infected mice with ceftriaxone, an antibiotic known to produce beneficial results in mouse models of ALS as well as neuroprotection in a variety of central nervous system injuries, they found that GLT-1 was upregulated. This restoration of GLT-1 expression significantly reduced extracellular glutamate from pathological to normal concentrations, returning neuronal function to a normal state.

“We have shown for the first time the direct disruption of a major neurotransmitter in the brain resulting from this infection,” Wilson said. “More direct and mechanistic research needs to be performed to understand the realities of this very common pathogen.”

Next, Wilson and her colleagues will research what initiates the downregulation of GLT-1 during chronic Toxoplasma infection.

“Despite the importance of this transporter to maintaining glutamate homeostasis, there is little understanding of the mechanism that governs its expression,” Wilson said. “We’d like to know how cells, including peripheral immune cells, control the parasite in the brain. Toxoplasma infection results in the lifelong presence of parasitic cysts within the neurons in the brain. We’d like to further develop a project focused on killing the cysts, which is where the parasite hides from the immune response for the rest of the infected person’s life. Getting rid of the cyst removes the threat of reactivation of the parasite and the risk of encephalitis while also allowing us to minimize chronic inflammation in the brain.”

Mysteriously, the parasite that causes toxoplasmosis can sexually reproduce only in cats. Asexually, it can replicate and live in any mammalian cell that has a nucleus. Indeed, the parasite has been found in every mammal ever tested.

Post-infection, a competent immune system is needed to prevent parasite reactivation and encephalitis. Infected people with compromised immune systems need to be on prophylactic drugs for life. Otherwise they are at risk of cyst reactivation and death. The parasite lives in areas of the brain that have the potential to disrupt certain behaviors such as risk-seeking (infected mice will run toward cat urine instead of away from it).

The parasite is not as latent or dormant as researchers once thought. Cases of congenital infection and retinal toxoplasmosis are on the rise (the brain and retina are closely linked). People who have schizophrenia are more likely to be infected with Toxoplasma. Infection shows some correlation with Alzheimer’s disease, Parkinson’s disease and epilepsy.

Nevertheless, Wilson notes that infection is no cause for major worry.

“We have been living with this parasite for a long time,” she said. “It does not want to kill its host and lose its home. The best way to prevent infection is to cook your meat and wash your hands and vegetables. And if you are pregnant, don’t change the cat litter.”

Does a common parasite play a role in rage disorder?

Individuals with a psychiatric disorder involving recurrent bouts of extreme, impulsive anger—road rage, for example—are more than twice as likely to have been exposed to a common parasite than healthy individuals with no psychiatric diagnosis.                                

In a study involving 358 adult subjects, a team led by researchers from the University of Chicago found that toxoplasmosis, a relatively harmless parasitic infection carried by an estimated 30 percent of all humans, is associated with intermittent explosive disorder and increased aggression.

The findings are published in the Journal of Clinical Psychiatry on March 23, 2016.

“Our work suggests that latent infection with the toxoplasma gondii parasite may change brain chemistry in a fashion that increases the risk of aggressive behavior,” said senior study author Emil Coccaro, MD, Ellen. C. Manning Professor and Chair of Psychiatry and Behavioral Neuroscience at the University of Chicago.

More information:Emil F. Coccaro et al. Toxoplasma gondii Infection, The Journal of Clinical Psychiatry (2016). DOI: 10.4088/JCP.14m09621 ,

Scanning electron micrograph of the protozoan parasite Toxoplasma gondii, tissue cyst in brain of an infected mouse. Credit: David Ferguson    

Toxoplasma gondii's life cycle is one of the most interesting fixtures of parasitology and biology as a whole.  The definitive or reproductive host for the parasite is the common housecat, but the life cycle necessitates transmission through the barn mouse.  Research shows that gondii’s eggs are present in a large proportion of cat’s litter boxes, which the barn mouse then interacts with via foraging behavior.  The oocysts themselves are highly resistant to weather, temperature, rupture, etc, so they spread to anything that can be contaminated, namely soil, water, food, trash, etc.  When the mouse ingests the egg, the parasite grows, and studies dictate an attraction to cat urine is promoted in the infected rodent.  The definitive host, the cat, then ingests the mouse, infecting its intestinal track with the parasite, where Toxoplasma can reproduce.  Some evolutionary theorists believe this demonstrates an “extended phenotype” which creates a linkage among these species as an adaptation by the Toxoplasma parasite which does not typically transfer directly from cat to cat.

Some human studies indicate a correlative relationship between Toxoplasma infection and mental illness or behavioral changes, but these are both controversial and purely correlative.  No causal mechanism has been discovered for the behavioral changes in humans or mice.

Pregnant women are directed by the CDC to avoid cleaning cat litter boxes because Toxoplasma gondii infection is easily transmissible through the prenatal membrane, and prenatal infection is highly correlated with blindness and mental illness in the baby later in life.

What a sweet story, right?

Sweet Valentine

By Peter Bradley, University of California, Los Angeles

Four intracellular Toxoplasma gondii parasites are shown undergoing cellular division by an internal budding process known as endodyogeny. Staining with a T. gondii surface antigen provided heart-shaped images (shot on Valentine’s Day). The definitive host of these parasites is the cat, but they infect many warm-blooded animals, including humans. While toxoplasmosis is typically a minor disease, T. gondii can cause severe central nervous system disorders of immunocompromised individuals—such as those with AIDS, organ transplants, and lymphoma—as well as birth defects in congenitally infected neonates. Eating undercooked meat and ingesting food or water contaminated with cat feces are the most common routes of infection for humans.

Sources: 1 2 3 4

Ummmmmm …

Cats in the United States release about 2.6 billion pounds (1.2 million metric tons) of feces into the environment every year. Cat dung carries the parasite Toxoplasma gondii, a single-celled organism that creates infectious agents called oocysts. These oocysts can infect pregnant women, causing congenital problems in the baby such as deafness, seizures, eye damage and mental retardation. The parasite also infects people with compromised immune systems, such as those with HIV/AIDS.

After reviewing past studies on the parasite, a team of researchers believes the Toxoplasma parasite may be a significant public health problem, infecting people who are otherwise healthy. Other studies have even linked the parasite to schizophrenia, depression, suicidal behavior and lower school achievement in children.

… mmmmmmmmmmm

Toxoplasma infection permanently shifts balance in cat-and-mouse game

The toxoplasma parasite can be deadly, causing spontaneous abortion in pregnant women or killing immune-compromised patients, but it has even stranger effects in mice.

Infected mice lose their fear of cats, which is good for both cats and the parasite, because the cat gets an easy meal and the parasite gets into the cat’s intestinal tract, the only place it can sexually reproduce and continue its cycle of infection.

New research by graduate student Wendy Ingram at the University of California, Berkeley, reveals a scary twist to this scenario: the parasite’s effect seem to be permanent. The fearless behavior in mice persists long after the mouse recovers from the flu-like symptoms of toxoplasmosis, and for months after the parasitic infection is cleared from the body, according to research published today (Sept. 18) in the journal PLoS ONE.

“Even when the parasite is cleared and it’s no longer in the brains of the animals, some kind of permanent long-term behavior change has occurred, even though we don’t know what the actual mechanism is,” Ingram said. She speculated that the parasite could damage the smell center of the brain so that the odor of cat urine can’t be detected. The parasite could also directly alter neurons involved in memory and learning, or it could trigger a damaging host response, as in many human autoimmune diseases.

Ingram became interested in the protozoan parasite, Toxoplasma gondii, after reading about its behavior-altering effects in mice and rats and possible implications for its common host, the domesticated cat, and even humans. One-third of people around the world have been infected with toxoplasma and probably have dormant cysts in their brains. Kept in check by the body’s immune system, these cysts sometimes revive in immune-compromised people, leading to death, and some preliminary studies suggest that chronic infection may be linked to schizophrenia or suicidal behavior.

Pregnant women are already warned to steer clear of kitty litter, since the parasite is passed through cat feces and can cause blindness or death in the fetus. One main source of spread is undercooked pork, Ingram said.

With the help of Michael Eisen and Ellen Robey, UC Berkeley professors of molecular and cell biology, Ingram set out three years ago to discover how toxoplasma affects mice’s hard-wired fear of cats. She tested mice by seeing whether they avoided bobcat urine, which is normal behavior, versus rabbit urine, to which mice don’t react. While earlier studies showed that mice lose their fear of bobcat urine for a few weeks after infection, Ingram showed that the three most common strains of Toxoplasma gondii make mice less fearful of cats for at least four months.

Using a genetically altered strain of toxoplasma that is not able to form cysts and thus is unable to cause chronic infections in the brain, she demonstrated that the effect persisted for four months even after the mice completely cleared the microbe from their bodies. She is now looking at how the mouse immune system attacks the parasite to see whether the host’s response to the infection is the culprit.

“This would seem to refute – or at least make less likely – models in which the behavior effects are the result of direct physical action of parasites on specific parts of the brain,” Eisen wrote in a blog post about the research.

“The idea that this parasite knows more about our brains than we do, and has the ability to exert desired change in complicated rodent behavior, is absolutely fascinating,” Ingram said. “Toxoplasma has done a phenomenal job of figuring out mammalian brains in order to enhance its transmission through a complicated life cycle.”

Researchers Unpack How Toxoplasma Infection Is Linked to Neurodegenerative Disease

Working on mice (like all mammals, a natural host for this parasite), a University of California, Riverside team of biomedical scientists reports in the journal PLOS Pathogens that Toxoplasma infection leads to a disruption of neurotransmitters in the brain and postulates that it triggers neurological disease in those already predisposed to such a disease.

They note that Toxoplasma infection leads to a significant increase in glutamate – the primary and most important neurotransmitter in the brain, which transmits excitatory signals between neurons. This glutamate increase is “extracellular,” meaning outside the cell, and is strictly controlled by specialized cells in the central nervous system (brain and spinal cord), called astrocytes. Glutamate buildup is seen in traumatic brain injury as well as highly pathological and neurodegenerating diseases such as epilepsy, multiple sclerosis and amyotrophic lateral sclerosis (ALS).

Clément N. David, Elma S. Frias, Jenny I. Szu, Philip A. Vieira, Jacqueline A. Hubbard, Jonathan Lovelace, Marena Michael, Danielle Worth, Kathryn E. McGovern, Iryna M. Ethell, B. Glenn Stanley, Edward Korzus, Todd A. Fiacco, Devin K. Binder, Emma H. Wilson. GLT-1-Dependent Disruption of CNS Glutamate Homeostasis and Neuronal Function by the Protozoan Parasite Toxoplasma gondii. PLOS Pathogens, 09 Jun 2016 DOI: 10.1371/journal.ppat.1005643

GLT-1, a glutamate transporter, soaks up glutamate (a neurotransmitter) released by neurons and converts it back into a safer substance. Credit: Wilson lab, UC Riverside.


Is ‘crazy cat lady syndrome’ real?

Can cats really turn women into crazy cat ladies? Some scientists think it’s possible.

Toxoplasma gondii

Toxoplasma gondii. 7 syllables sure to strike fear in to any pregnant woman’s heart. I thought I’d do a little post today to summarise what toxoplasma actually is and how it affects us and the animals around us.

Toxoplasma gondii is a single celled parasite known as a protozoa. It has a complex lifecycle involving felines as its only final host. It does, however, have a vast array of ‘intermediate hosts’ thought to include virtually all warm blooded animals. It’s a very successful parasite infecting animals and humans worldwide. In France, 84% of people are thought to be infected.

Its lifecycle is as follows:

  • A cat becomes infected through consuming the raw meat of infected prey
  • The parasite infects the epithelial cells of the cat’s gut, sexually reproducing in these cells
  • Sexual reproduction produces oocysts which are shed in the cat’s faeces. The time period from consumption to shedding is around 3-10 days. Shedding only occurs for a few weeks before the cat’s immune system fights off the parasite, resulting in a persistent but non-shedding infection that can remain for life. After one infection it is highly unlikely the cat will get infected and shed again due to its raised immune response, however immunosuppression can result in subsequent shedding
  • These oocysts develop in the environment and after 1-5 days are developed enough to infect an intermediate host
  • Intermediate host ingests the oocysts through consumption of an item or fluid infected with cat faeces. Intestinal enzymes break down the oocyst wall releasing the parasite in to the gut
  • Acute asexual multiplication occurs in the intermediate host cells and the parasite is spread around the body in the blood
  • After around 2 weeks the host develops immunity but the infection enters a chronic phase as slow-growing forms of the parasite are ‘walled off’ into what is known as a cyst, protected from the immune system. These can remain infectious for months to years and can revert to the acute form if the host’s immune system becomes depressed (FIV, AIDs, canine distemper). They are often found in the brain and muscle.
  • This cyst-infected meat is consumed by the cat and the whole cycle begins again

Cats can also get infected by consuming oocysts from other cats, however they are a lot less susceptible to this than other intermediate hosts so a large number of oocysts would need to be consumed. To make it even more confusing, intermediate hosts can get infected via carnivorism/ scavenging when they consume meat infected with cysts (e.g. a human eating undercooked, infected pork). As well as this, transplacental transmission can occur in some host species during the acute phase of the infection (however this is not seen in dogs or cats). This creates a complex web of infection. The cysts are killed when meat is cooked.

Toxoplasmosis is most often asymptomatic, with flu-like symptoms possible during the acute phase. It can be fatal in immunosuppressed individuals, however this is rare. You may have heard the parasite’s name mentioned in relation to sheep. If a non-immune ewe is infected during pregnancy it can cause foetal death, reabsorption, abortion, mummified foetuses, still births and weak lambs, depending on when in pregnancy the ewe was infected. In cases of abortion, you can see tiny white spots on the placenta and foetal tissue. Diagnosis can be confirmed through stained impression smears or serological examination of the foetal fluid or blood from the ewe. Prevention in sheep includes a vaccine which primes the immune system to the parasite. Sheep are often infected from eating infected hay or concentrates, so keeping cats away from these can help reduce infection rates.

Toxoplasma is also a favourite in the press, who claim that it ‘controls our brains’ and causes abortions and deformities. Like in sheep, infection of a non-immune, pregnant mother can indeed cause deformities in her child. Does this mean we should all kill off our cats when expecting? Definitely not, and I’ll explain why.

As I stated earlier, infected cats will only shed for 2-3 weeks in their entire lifetime, unless immunologically supressed. To become infected by your cat, you would need to have never been infected before yourself (because if you have, your immune system is primed and ready to fight it off), your cat would have to be in the shedding phase and you’d have to ingest oocytes (that take 1-5 days to become infective, so changing the litter box daily can hugely reduce this risk).  If worried, a blood test to see if you’ve been previously exposed and a blood test in your cat to see if they’ve been previously exposed may put your mind at rest. Indoor cats are less likely to become infected if their only food is tinned or dried. Humans are much more likely to be exposed to the infection through handling and eating undercooked infected meat, soil infected with cat faeces and unwashed vegetables. If you’re a vet in the making and have been on a lambing placement, you may well have been asked if you’re pregnant. This is because being in contact with aborted material from sheep with toxoplasmosis is another way to contract the infection.

As for the ‘mind control’, it has been found that mice infected with toxoplasma are attracted to the smell of cat urine and a lot less frightened of cats than those without infection. This is an incredibly clever mechanism and probably one of the reasons the parasite is so wide-spread. In humans, when analysing the number of people who are involved in car accidents, it was found that a significantly high proportion were infected with toxoplasma gondii. It has been suggested that the parasite is responsible for making people more reckless and argumentative. Toxoplasma cysts in the brain could definitely be responsible for parts of your personality, however conclusions at the moment suggest that although the infection may have some effect, the brain and concept of ‘personality’ are so complex and involve so many factors that its overall influence seems negligible.  

I hope this made sense, it’s quite confusing to explain! I’ve drawn a quick diagram to try and demonstrate the different scenarios in which we could become infected. Enjoy!


Ever feel like your kitty takes charge of your brain?

TOXOPLASMA, a new painting by Martin Hsu

Inspired by Radiolab’s episode on Toxoplasma Gondii, a potentially mind controlling parasite gifted from your cat to you. Listen here

Toxoplasma original painting created for the ZOMBIE show at Last Rites Gallery in New York.

Enjoy the kitties,

‘Hijacking’ and hibernating parasite could alter behaviour

Melbourne researchers have discovered how a common parasite hijacks host cells and stockpiles food so it can lie dormant for decades, possibly changing its host’s behaviour or personality in the process.

The findings could lead to a vaccine to protect pregnant women from Toxoplasma infection, which carries a serious risk of miscarriage or birth defects, as well as drugs to clear chronic infections in people with compromised immune systems, such as cancer patients.

Toxoplasma is a common parasite transmitted by cats and found in raw meat. Around 30 per cent of the population is infected. The research projects were led by Dr Chris Tonkin, Dr Justin Boddey, Dr Alex Uboldi, Mr James McCoy and Mr Michael Coffey from the Walter and Eliza Hall Institute.

Dr Tonkin said Toxoplasma required a human host cell – such as a brain cell (neuron) – to live in. The research team discovered how the parasite hijacks the host cell to enable its own growth and survival, hibernating for decades by creating its own food reserve.

“Toxoplasma infection leads to massive changes in the host cell to prevent immune attack and enable it to acquire a steady nutrient supply,” Dr Tonkin said. “The parasite achieves this by sending proteins into the host cell that manipulate the host’s own cellular pathways, enabling it to grow and reproduce.”

Dr Boddey said some of these proteins might even influence the behaviour of the host. “There is a fascinating association between Toxoplasma infection and psychiatric diseases including schizophrenia and bipolar disorder. It is now possible to test whether proteins sent from the hibernating parasite into a host neuron disrupt normal brain function and contribute to development of these diseases,” he said.

Once Toxoplasma parasites establish infection, they can lie dormant in our bodies for the rest of our lives. In people with suppressed immune systems, such as cancer patients, the parasite can reactivate and cause neurological damage and even death.

Dr Tonkin said the teams had identified pathways that allow the parasite to establish chronic infections, unveiling potential avenues for treatment that clear the dormant parasite.

“We discovered that, similar to animals preparing for hibernation, Toxoplasma parasites stockpile large amounts of starch when they become dormant,” he said. “By identifying and disabling the switch that drives starch storage, we found that we could kill the dormant parasites, preventing them from establishing a chronic infection.”

Dr Tonkin said the finding could lead to a drug to clear chronic Toxoplasma infections, or even a vaccine to prevent infection in at-risk people, such as pregnant women.

“Cats are one of the primary transmitters of Toxoplasma parasites,” Dr Tonkin said. “If the parasites are transmitted to pregnant women, for example through contact with kitty litter, there is a substantial risk of miscarriage or birth defects.

“We hope to use our discoveries to develop a vaccine that stops cats transmitting the parasite, to prevent these potentially catastrophic consequences.”

Dr Boddey said it had long been a mystery how the Toxoplasma parasite transported proteins into the host. “Our study showed that the parasite includes a signature on the exported proteins that ‘earmark’ them for transport into the host cell,” he said. “Blocking transport makes the parasite much less dangerous in infection models, suggesting this may also be a new way of treating Toxoplasma infections.”

The research findings were published in the journal Cell Host & Microbe and in the journal eLife.

Toxoplasma gondii parasite may alter signaling in the brain

It’s creepy, it’s crawly, and it infects 20 percent of people in the United States. Fortunately, most people who carry the Toxoplasma gondii parasite don’t develop the symptoms of the disease it can cause. Only a small fraction of people, typically with compromised immune systems, develop toxoplasmosis.                                

Toxoplasmosis can lead to abnormal brain function, including seizures, by changing signaling in the diseased central nervous system.  

In a study using a rodent model, scientists from the Virginia Tech Carilion Research Institute and the University at Buffalo found that the parasite-induced infection alters neural pathways specifically related to the neurotransmitter gamma-Aminobutyric acid, better known as GABA.

The researchers recently published their results in the American Society for Microbiology’s open-access journal, mBio.

Justin M. Brooks et al.   Infections Alter GABAergic Synapses and Signaling in the Central Nervous System , mBio (2015). DOI: 10.1128/mBio.01428-15

Inhibitory nerve terminals, such as GABA, are shown in red. The right image demonstrates how a Toxoplasma infection alters the inhibitory nerve terminals, compared to the healthy tissue sample in the left image.    


For some reason, toxoplasmosis has been coming up in both Psych classes I’m taking. So I’m going to unravel the secrets behind it a little bit, because it is quite interesting. 

First of all, we start with a little paraside called Toxoplasma gondii. 

This lil dude loves the host body of kitty cats. Toxoplasma gondii will live in the cat and continue living on in the cat poop. Thus if a pregnant woman is carelessly cleaning out her cat’s litter box, she runs the risk of contracting the parasite. It will cause an infection and devastate her unborn child’s immune system (enlarged liver/spleen, eye damage, hearing loss, jaundice, low birth weight, central nervous system deficiencies).

Here’s the crazier part about Toxoplasma gondii.

If a rat contracts the parasite, it Toxoplasma gondii will commandeer the rat’s nervous system. The rat will suddenly be enamored by cats - it will CHASE cats and walk right into the jaws of the predator. The rat is DEAD MEAT. This is an evolutionary FAIL. But for the parasite, this is an amazing evolutionary advantage! Once the cat eats the infected rat, Toxoplasma gondii increases its chances of reproducing with other members of its species potentially living in the cat.

These drastic behavioral changes prompt questions of consciousness related to control of things that are seemingly habitual or instinctual.