Human African trypanosomiasis – sleeping sickness – is a potentially fatal disease, which currently affects ~3,500 people in sub-Saharan Africa. The disease is caused by parasites called African trypanosomes and is spread by tsetse flies. Controlling these biting insects, combined with surveillance and treatment, reduces the impact of outbreaks of the disease and the World Health Organisation (WHO) hopes to eliminate sleeping sickness by 2020. A new paper suggests that this target might be overambitious.
Detection of trypanosomes in the skin is not well documented, although there are descriptions of cutaneous symptoms associated with African trypanosomiasis. This paper reports the investigation of a possible anatomical reservoir in the skin and provides evidence of T.b. brucei, (a causative agent of animal trypanosomiasis) and the human-infective trypanosome, T.b. gambiense, invading the extravascular tissue of the skin (including but not restricted to the adipose tissue) and undergoing onward transmission despite undetected vascular parasitaemia. It also provides evidence of localisation of trypanosomes within the skin of undiagnosed humans. The presence of a significant transmissible population of T. brucei in this anatomical compartment is likely to impact future control and elimination strategies for both animal and human trypanosomiases.
The skin is a significant but overlooked anatomical reservoir for vector-borne African trypanosomes. eLife 2016; 5: e17716 doi: 10.7554/eLife.17716
The role of mammalian skin in harbouring and transmitting arthropod-borne protozoan parasites has been overlooked for decades as these pathogens have been regarded primarily as blood-dwelling organisms. Intriguingly, infections with low or undetected blood parasites are common, particularly in the case of Human African Trypanosomiasis caused by Trypanosoma brucei gambiense. We hypothesise, therefore, the skin represents an anatomic reservoir of infection. Here we definitively show that substantial quantities of trypanosomes exist within the skin following experimental infection, which can be transmitted to the tsetse vector, even in the absence of detectable parasitaemia. Importantly, we demonstrate the presence of extravascular parasites in human skin biopsies from undiagnosed individuals. The identification of this novel reservoir requires a re-evaluation of current diagnostic methods and control policies. More broadly, our results indicate that transmission is a key evolutionary force driving parasite extravasation that could further result in tissue invasion-dependent pathology.