New research reveals how toxoplasmosis alters the brain
Scientists have shown how the toxoplasmosis parasite hides away in the brain, altering synapses and potentially causing depression, schizophrenia and autism.
Mice infected with toxoplasmosis parasites behave strangely: They lose their natural fear of cats. Presented with the smell of cat urine, they even seem attracted to the deadly predator, scientists have found.
Up to half of all adults are infected with toxoplasma pathogens. But mostly, the parasite goes unnoticed.
Toxoplasmosis is dangerous to people with a weakened immune system or unborn children whose mothers are infected during pregnancy. But for most of us, the most we might suffer is a brief bout of flu-like symptoms with fever, fatigue, muscle pain and diarrhea.
Once you're infected, however, the parasite often sticks around in muscle or brain tissue for the rest of your life — what doctors call a "hidden infection."
And, just as it makes a timid rodent dangerously brave, research suggests it may change the way unwitting human carriers behave, too. Toxoplasmosis has been linked to schizophrenia, depression, autism and even an increased risk of being involved in traffic accidents.
Now, new research is revealing just how the parasite might change the way the brain works.
The parasite alters the molecular composition of synapses, which are responsible for signal-processing in the brain, according to the research published in the Journal of Neuroinflammation.
"Toxoplasma gondii is absorbed by humans via digestion, enters the bloodstream and also migrates into the brain to get into nerve cells for the rest of one's life," said Karl-Heinz Smalla of the Special Laboratory for Molecular Biology Techniques at LIN.
In cooperation with the Helmholtz Center for Infection Research, the team was able to prove that the infection alters the quantities of 300 synaptic proteins in the brains of infected mice.
In particular, the animals had significantly fewer proteins in the vicinity of glutamate-releasing excitatory synapses. At the same time, proteins involved in immune responses were up.
"Malfunctions of glutamatergic synapses are associated with depression, schizophrenia and autism. Components of the immune response also show links to these diseases," said Ildiko Rita Dunay, an immunologist who worked on the study.
"This suggests that immune reactions may cause changes in the synapse that may lead to neuropsychiatric disorders," she added.
Treatment at hand
The good news is, sulfadiazine, an antibiotic used to treat toxoplasmosis infections, restored the infected mice's brain metabolism to normal.
"All investigated proteins responsible for the glutamatergic signal transmission were back to normal. The inflammatory activity also decreased measurably," said Björn Schott of the team in Magdeburg.
And hopefully, the rodent's aversion to ending up as lunch was back, too.
Close to ending a parasitic disease
In 1986, there were an estimated 3.6 million cases of Guinea worm disease per year in 21 countries in Africa and Asia. Today, the parasitic disease is close to eradication. In 2017, there were only 30 cases in Chad and Ethiopia. In the first three months of 2018, there were only 3 human cases in one country, Chad.
Former US President Jimmy Carter's foundation in 1986 led an international campaign against Guinea worm. Nearly 80 million cases have been averted due to the campaign. Guinea worm would be the first human parasitic disease to be eradicated and only the second disease after smallpox to be eliminated. It would also be the first disease to be eradicated without the use of a vaccine or medicine.
The life cycle of the parasite begins when humans drink unfiltered water from ponds or stagnant water sources containing microscopic copepods (water fleas) infected with larvae. Once ingested, the copepods die and release the larvae into the digestive tract, where they mature and mate. Males die but females grow to about 60-100 centimeters (2-3 feet) long and as wide as a spaghetti noodle.
The female worm usually exits from the leg or foot after about one year inside the body. The blister is painful. Attempts to clean or sooth the pain of the blister in ponds or other water sources lead to the release of millions of immature larvae into the water. Copepods then consume first-stage larvae. The larvae develop in the copepods until they are again consumed by humans.
There is no drug or treatment for Guinea worm. The worm is usually removed a couple centimeters per day over the course of weeks using gauze or a stick. The process is debilitating and can lead to secondary bacterial infections. The disease prevents people from taking care of themselves, working, attending school or farming for extended periods.
Guinea worm has largely been stopped through community programs to educate and change behavior. Simple education such as teaching people to drink filtered water and preventing infected people from entering water have limited the spread of the disease.
Only 30 cases in 2017
Guinea worm disease remains endemic in South Sudan, Mali, Chad and Ethiopia. In 2017, there were only 30 isolated cases in 20 villages in two countries, Chad and Ethiopia.
Infected dogs were first discovered in Chad in 2012, raising concern about animal transmission even though they are not the natural host of Guinea worm. Dogs in fishing villages in Chad are believed to have acquired the disease by eating raw fish and guts carrying Guinea worm larvae. Interventions and education with locals have brought down infection rates since the problem developed.