All in good time for Toxoplasma
The parasite behind toxoplasmosis adapts its growth rate to its environment.
Over a billion people worldwide are infected, often for life, by a parasite known as Toxoplasma gondii. Most of the time, the parasites remain in a dormant state and cause no symptoms. However, the parasites can reactivate, which can be fatal for people with weaker immune systems. Currently no drugs can kill the dormant stages of T. gondii.
One of the possible reasons T. gondii is so widespread is because it easily passes from host to host, and resists both detection and treatment. Like many parasites, T. gondii infects multiple hosts during its life cycle: it reproduces sexually in its ‘definitive’ host, the cat, and reproduces asexually in its ‘intermediate’ hosts, which include virtually all warm-blooded animals. Unlike most parasites, all hosts can transmit T. gondii to other hosts, making it a very flexible parasite. However, its closest living relative, Hammondia hammondi, can only be transmitted from a definitive host to an intermediate host, or vice versa. The reason for this difference remains unclear, but comparisons between these species can hopefully help uncover how T. gondii came to be such a promiscuous parasite.
Now, Sokol, Primack et al. report that a dramatic difference between H. hammondiand T. gondii is the ability to adapt to changes in the environment. While H. hammondi grows in a very strict and inflexible way, T. gondii can sense its environment and change its growth rate accordingly. This is important because it would allow T. gondii to grow until the host immune response is activated, at which time T. gondii can then quickly become dormant and hide from these host defences. Sokol, Primack et al. suggest that this unique adaptation may have helped T. gondii to become the globally successful parasite that it is today, and explain why H. hammondi is much less lethal.
It is also possible that T. gondii reactivates after periods of dormancy because it senses changes in its environment. If so, and if scientists can identify the sensors required for this, it may also be possible to target them and effectively block reactivation in infected humans. Comparing T. gondii with H. hammondi may provide a good way to identify these sensors.
To find out more
Read the eLife research paper on which this eLife digest is based:
