Except for a couple of specific circumstances – notably pregnancy – the world’s most common parasite in humans, Toxoplasma gondii, is thought to induce few symptoms and no serious effects.
However, research from 32 scientists at 16 institutions, linking parasite proteins with small non-coding human RNA molecules known as microRNA, and comparing outcomes for various diseases between infected and non-infected people, suggests we have severely underestimated the situation.
Around the world, more than two billion people carry the parasite. The most common route of infection involves one of its primary reservoirs, the domestic cat. Parasite eggs find their way into humans – and many other animals – via contact with cat faeces.
Such contact does not need to be direct. T. gondii eggs are extremely resilient and can survive dormant for many months in open environments – these frequently include vegetable patches and fields, where cats may defecate into the soil, from which the eggs are transferred to harvested plants.
The parasite, once hatched, lodges in the brain.
Until now, the primary danger recognized for T. gondii infection was to unborn children. If a woman contracts the parasite shortly before or during pregnancy, the foetus can sustain severe brain or eye damage.
In other cases, though, the infection was thought to be largely asymptomatic, except in around 20% of cases where mild flu-like symptoms are known.
The latest work, led by Rima McLeod of the Toxoplasmosis Centre at the University of Chicago, US, indicates that infection can seriously affect human health, but in very subtle ways.
Using a database comprising details of 246 people who sustained infection in the womb, the team looked for parasite-generated biomarkers and analysed their probable health impact.
The results showed a surprising confluence between certain markers and brain disease. Segments of human microRNA associated with infection, and proteins expressed by the parasite, were found not only in children with severe toxoplasmosis, but also in adults with Parkinson’s and Alzheimer’s disease.
There was also evidence that T.gondii proteins interfered with the signaling function of gamma-Aminobutyric acid, which plays in a role in dampening epilepsy.
“We suspect it involves multiple factors,” says McLeod.
“At the core is alignment of characteristics of the parasite itself, the genes it expresses in the infected brain, susceptibility genes that could limit the host’s ability to prevent infection, and genes that control susceptibility to other diseases present in the human host.”
When it infects other species, T. gondii is known to facilitate its own life cycle by affecting behaviour in its host.
For instance, it causes rats and mice to lose their innate fear of the smell of cat urine, thus placing them in greater danger of being eaten. This process facilitates the transfer of the parasite into a fresh host.
In humans, T.gondii infection has been associated with less hazardous behavior changes, such as decreased reaction times and loss of concentration.
McLeod and colleagues, however, also found that the parasite altered the function of 12 different types of olfactory receptor in the brain – indicating that it is also capable of driving our own species to dismiss urine-based signals of predator danger.
All up, the research implicated T. gondii in modifying the functions of 1178 human genes, many of them associated with various cancers.
“This study is a paradigm shifter,” says co-author Dennis Steinler at Tufts University. “We now have to insert infectious disease into the equation of neurodegenerative diseases, epilepsy and neural cancers.”
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