Do you remember the movie “Alien”, in which extra-terrestrials burrowed into flesh of a space ship’s crew members, slowly taking over the control of their behavior, while eating the hosts from the inside?
If you believe such a scenario belongs only in the realm of fantasy, then you are mistaken. The alien stowaway is very close. Crawling, shape-shifting beings may enter our bodies whenever we eat a steak tartare or a rare one. An alien can attack us when we cut meat on the same chopping board we use to prepare other foods. It may enter our bodies by contact with an outdoor cat’s feces, because it is cats that are the final prey of the invisible foe. Parasites, whose behavior is not unlike the aforementioned alien, enter an animal’s GI tract with food, in infected mice and birds. Toxoplasmosis does no harm to cats, even though the aim of this parasite is to enter the feline GI tract, where it can reproduce sexually, produce gametes, fertilize them, and finally create oocysts, which enter human bodies due to insufficient hygiene (e.g. unwashed hands). Petting a cat’s fur poses no danger, however an accidental contact with cat feces does. One does not even need to have a cat at home and clean its litter box, because oocysts can be found, for example, in a sandbox or even on vegetables.
Infection and symptoms in people
Cat is a so-called final host. Us humans, similarly to all the other animals (including those we eat: cows, sheep, pigs, poultry) are intermediate hosts. An infected cat excretes oocysts for merely 3 weeks, however spores can survive in damp soil for up to one and a half years. People usually get infected with toxoplasmosis by eating meat. The symptoms are non-specific, similar to flu: light fever, muscle aches, feeling unwell, and occasionally long-term swelling of lymph nodes.
It is estimated that in the USA, approximately 20% of the population may suffer from toxoplasmosis, especially considering the fact that often the infection is asymptomatic. The infection is the more dangerous, considering a possibility of compromise of immune system due to parasites, which leads to disastrous results.
Alien in control
Toxoplasmosis in this case changes the signals in the central nervous system, which leads to brain disorders including epilepsy. It may also meddle with neural connections.
Researchers form Buffalo have discovered that the parasite uses a neurotransmitter called gamma-Aminobutyric acid, or GABA. By using it, it can proliferate in the brain in the so-called gabaergic neurons, damaging them and changing the enzyme GAD67, on which GABA production is dependent. A secondary deficiency of gamma-Aminobutyric acid leads to epilepsy attacks.
Fear not! Be devoured!
The research shows that Toxoplasma gondii affects risk-taking and other unusual behaviors. For example, rats infected with toxoplasmosis are not afraid of cats, which obviously decreases their chance of survival. The parasite does not want to remain in a random body, therefore it manipulates the behavior of its intermediate host in order to increase the chance of it being devoured by the final host.
Lack of fear is just one of behavioral changes brought about by Toxoplasma gondii. Neurotransmitter changes are also responsible for aggression, depression and schizophrenia. Prof. Prandota, a Polish researcher, suggest that childhood autism may be a result of toxoplasmosis.
Until recently it has been believed that toxoplasmosis is only dangerous to pregnant women, causing fetal defects. We now know, that e.g. ocular toxoplasmosis can lead to loss of vision. The cerebral form is rarely diagnosed, because it causes non-specific changes. There is still a lingering belief in medicine that one can be cured of toxoplasmosis, meaning that if we have IgG antibodies against the parasite, we have fought it off. This may be true only in cats.
In humans, if Toxoplasma gondii enters the body, it remains there permanently. It may either cause symptoms or be asymptomatic, depending on the place it resides. In people with well-functioning immune systems, toxoplasma gondii may end its travels in lymph nodes (nodular form) and create cysts, in which spores wait for a decrease in immunity. In people with weakened immune systems it causes eye or multi-organ infections. A “sleeping” parasite in our bodies may reactivate once favorable conditions occur, for example during a cold or other disease.
Therefore we cannot talk about a “fought off and inactive” toxoplasmosis, we always have to keep in mind that once we are infected, the parasite is here to stay. Transplantologists know this well, since it can be transplanted with e.g. bone marrow.
Toxoplasmosis forms and transmission routes
The host becomes infected via food. The protozoa present in an oocyst leave it in the small intestine, and enter macrophages of the colon of its host, where they multiply by division. Their offspring, called tachyzoites, are able to move: they travel throughout the body, cross the intestinal barrier into blood and lymph, and then into macrophages, where they multiply vigorously. From this place they spread to many organs, such as the central nervous system, eyes, muscles, the heart and the placenta. It is tachyzoites which cause immune response in the host’s body, stopping the multiplication process. Once attacked by the immune system, the tachyzoites morph into spores, called bradyzoites. Clusters of bradyzoites, or tissue cysts, are present in many places, usually the brain, eyes and muscles. Bradyzoites remain active throughout the whole life of the host. At a moment of compromised immunity, they exit their cysts and once again morph into the invasive form – tachyzoites. Bradyzoites multiply very slowly, making them practically invulnerable to antibiotic treatment.
J. M. Fuks et al., GABAergic signaling is linked to a hypermigratory phenotype in dendritic cells infected by Toxoplasma gondii, PLoS Pathog., 8(12):e1003051, 2012 DOI: https://doi.org/ 10.1371/journal.ppat.1003051
G. Kannan and M. V. Pletnikov, Toxoplasma gondii and cognitive deficits in schizophrenia: An animal model perspective, Schizophr. Bull., 38(6):1155–1161, 2012 DOI: https://doi.org/ 10.1093/schbul/sbs079
G. A. McConkey et al., Toxoplasma gondii infection and behavior—location, location, location?, J. Exp. Biol., 216:113–119, 2013 DOI: https://doi.org/ 10.1242/jeb.074153
J. P. Webster et al., Toxoplasma gondii infection, from predation to schizophrenia: Can animal behaviour help us understand human behaviour?, J. Exp. Biol., 216:99–112, 2013 DOI: https://doi.org/ 10.1242/jeb.074716