Identifying transmission cycles at the human-animal interface: the role of animal reservoirs in maintaining gambiense human african trypanosomiasis

PLoS Comput Biol. 2013;9(1):e1002855. doi: 10.1371/journal.pcbi.1002855. Epub 2013 Jan 17.

Abstract

Many infections can be transmitted between animals and humans. The epidemiological roles of different species can vary from important reservoirs to dead-end hosts. Here, we present a method to identify transmission cycles in different combinations of species from field data. We used this method to synthesise epidemiological and ecological data from Bipindi, Cameroon, a historical focus of gambiense Human African Trypanosomiasis (HAT, sleeping sickness), a disease that has often been considered to be maintained mainly by humans. We estimated the basic reproduction number [Formula: see text] of gambiense HAT in Bipindi and evaluated the potential for transmission in the absence of human cases. We found that under the assumption of random mixing between vectors and hosts, gambiense HAT could not be maintained in this focus without the contribution of animals. This result remains robust under extensive sensitivity analysis. When using the distributions of species among habitats to estimate the amount of mixing between those species, we found indications for an independent transmission cycle in wild animals. Stochastic simulation of the system confirmed that unless vectors moved between species very rarely, reintroduction would usually occur shortly after elimination of the infection from human populations. This suggests that elimination strategies may have to be reconsidered as targeting human cases alone would be insufficient for control, and reintroduction from animal reservoirs would remain a threat. Our approach is broadly applicable and could reveal animal reservoirs critical to the control of other infectious diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Disease Reservoirs*
  • Disease Vectors*
  • Ecosystem
  • Humans
  • Models, Theoretical
  • Trypanosoma brucei gambiense / isolation & purification*
  • Trypanosomiasis, African / parasitology
  • Trypanosomiasis, African / transmission*

Grants and funding

SF was supported by EU FP7 funded integrated project EPIWORK (grant agreement number 231807). HN was supported by the JST PRESTO program. FC was supported by an AXA Research Fund Post-Doctoral Fellowship. This work was also assisted through participation in the Mathematical Modeling of Wildlife Zoonoses Investigative Workshop at the National Institute for Mathematical and Biological Synthesis, sponsored by the National Science Foundation, the U.S. Department of Homeland Security, and the U.S. Department of Agriculture through NSF Award #EF-0832858, with additional support from The University of Tennessee, Knoxville. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.