Under My Skin: After infection, sleeping sickness parasite subpopulation grows in host skin

Under My Skin: After infection, sleeping sickness parasite subpopulation grows in host skin

The tsetse fly, which spreads the sleeping sickness parasite

The tsetse fly, which spreads the sleeping sickness parasite

Trypanosomiasis, also known as sleeping sickness, is endemic in the African continent. Humans contract the parasitic disease when bitten by an infected tsetse fly. However, little was previously known about early infection after transmission of the parasites via fly bite.

Guy Caljon, recently appointed as research professor at the University of Antwerp and formerly at the Institute of Tropical Medicine Antwerp, and his colleagues investigated what happens after a tsetse fly bite transfers trypanosome parasites to a mammalian host.

In the lab, tsetse flies infected with fluorescently-tagged trypanosomes were allowed to bite and infect mice, and the researchers studied how the parasites spread and multiplied. As reported in their PLOS Pathogens paper, Caljon and colleagues discovered a subpopulation of infectious parasites that remained and multiplied in the inner layer of skin near the fly bite site, which might reinfect tsetse flies to help transmit sleeping sickness to more hosts.
To learn more about Caljon and his research, I interviewed him via email.

Guy CaljonWhen did you become interested in parasitology, and what made you study trypanosomes in particular?

GC: As a biologist, my interest in parasitology was fueled by courses at Vrije Universiteit Brussel. I was particularly fascinated by the various ingenious strategies that trypanosomes use to cope with the host’s immune system, culminating in the neglected tropical disease for which unfortunately no effective vaccines are yet available. At the Institute of Tropical Medicine Antwerp, I had the opportunity to include the tsetse fly vector in my research which allowed me to study the natural route of African trypanosome infection. I am excited by the challenge of understanding the highly complex interactions between the vector, the parasite and the host.

You decided to study the very early stages of host infection by trypanosomes – why? And why was it important to infect the mice via a tsetse fly bite, rather than by needle injection?


GC: The early stages of infection are crucial for trypanosomes to survive at the biting site micro-environment and to transform into a stage that is able to continue life in their host. We have tried to mimic tsetse fly-mediated infections with needle injection, but we rapidly came to the conclusion that only a real infective bite reflects the natural situation. The role of tsetse flies in this process goes beyond acting as flying syringes.

One of your findings was that it took just seven parasites in the infectious metacyclic stage to infect 50% of exposed mice. What are the implications of this finding?

GC: This result was surprising, given that a previous study using bloodstream-stage parasites revealed a much lower infectivity, with the dermis appearing refractory to infection with low doses of bloodstream-stage trypanosomes. Our findings with metacyclic parasites from the tsetse fly salivary glands illustrate that this form is particularly capable of initiating infections in the skin. This unique feature of metacyclic parasites is partly responsible for the transmission success of trypanosomes.

Trypanosoma brucei parasites (blue) interacting with a fat cell (grey) in the ear dermis of an infected mouse.

Trypanosoma brucei parasites (blue) interacting with a fat cell (grey) in the ear dermis of an infected mouse.

You discovered a parasite population residing at the tsetse fly bite site in the mouse ear. Why is this significant?

GC: There is a lot to learn about this dermal population and its interaction with the skin micro-environment. It could serve as a parasite reservoir, given that the fly bite site might represent the best place for reacquisition by other tsetse flies. We observed that the dermal parasite burden results in elevated skin surface temperatures, which might potentially trigger tsetse feeding at those locations. It remains to be seen whether the dermis can also be a parasite sanctuary, where parasites are less exposed to the host immune system and the effects of drugs.

What do you see as the next steps in studying early host infection by trypanosomes, and where do you hope this work might lead?

GC: We will need to understand how metacyclic parasites are so infective despite the stringency of the intradermal route. Another enigma is the contribution made by the intradermal population at the bite site to the progression of host infection and to reacquisition by tsetse flies. Nonetheless, I believe that the early dermal stage of parasitic infection offers a window of opportunity for intervention. A thorough analysis of early parasitological and immunological events shaping successful infection should provide a solid scientific basis for designing transmission blocking strategies.


Research Article: Caljon G, Van Reet N, De Trez C, Vermeersch M, Pérez-Morga D, Van Den Abbeele J (2016) The Dermis as a Delivery Site of Trypanosoma brucei for Tsetse Flies. PLoS Pathog 12(7): e1005744. doi:10.1371/journal.ppat.1005744

Images Credits: Michael Wunderli, Flickr; Guy Caljon; Caljon et al. (2016)


Beth works at PLOS as Journal Media Manager. She read Natural Sciences, specializing in Pathology, at the University of Cambridge before joining PLOS in 2013. She feels fortunate to be able to read and write about the exciting new research published by PLOS.

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