Wild animals may be a key contributor to the continuing spread of African sleeping sickness, new research published in PLOS Computational Biology shows. The West African form of the disease, also known as Gambiense Human African trypanosomiasis, affects around 10,000 people in Africa every year and is deadly if left untreated.
The disease is caused by a brain-invading parasite transmitted by bites of the tsetse fly, and gets its name from the hallmark symptoms of drowsiness and altered sleeping patterns that affect late-stage patients, along with other physical and neurological manifestations including manic episodes and hallucinations that eventually lead to coma and death.
Despite numerous previous studies showing that animals can be infected with the parasite, the prevailing view has been that the disease persisted in its traditional areas almost only because of human-to-human transmission. A new study, from an international team of researchers led by the London School of Hygiene & Tropical Medicine, challenges this assumption by using a mathematical model to show that the disease not only can persist in an area even when there are no human cases, but probably requires the presence of infected wild animals to maintain the chain of transmission. The authors' model was based on data collected in active screening campaigns between November 1998 and February 1999 in the Bipindi area of Cameroon. One of the species in the data group was the White-eyelid mangabey, pictured below.
The research provides an attractive explanation for why sleeping sickness survives in places which have undergone intensive efforts to find and treat infected people in the community. It suggests that efforts to eliminate the disease must factor in the wild animal populations.
"This research suggests that targeting human populations alone, the main current control strategy, might not be enough to control the disease," says Sebastian Funk, the lead author of the study. "Maintenance of transmission in wild animal populations could explain the reappearance of sleeping sickness in humans after years without cases."
Dr. Sebastian Funk
Ecology and Evolutionary Biology
106A Guyot Hall
Princeton, NJ 08544
Phone: +44 7726 026766
Financial disclosure: 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.
Competing interests: The authors have declared that no competing interests exist. Citation: Funk S, Nishiura H, Heesterbeek H, Edmunds WJ, Checchi F (2013) Identifying Transmission Cycles at the Human-Animal Interface: The Role of Animal Reservoirs in Maintaining Gambiense Human African Trypanosomiasis. PLoS Comput Biol 9(1): e1002855. doi:10.1371/journal.pcbi.1002855
Please add this link to the freely available article in online versions of your report (the link will go live when the embargo ends): http://www.ploscompbiol.org/doi/10.1371/journal.pcbi.1002855
This press release refers to an upcoming article in PLOS Computational Biology. The release is provided by journal staff, or by the article authors and/or their institutions. Any opinions expressed in this release or article are the personal views of the journal staff and/or article contributors, and do not necessarily represent the views or policies of PLOS. PLOS expressly disclaims any and all warranties and liability in connection with the information found in the releases and articles and your use of such information.
PLOS Journals publish under a Creative Commons Attribution License, which permits free reuse of all materials published with the article, so long as the work is cited (e.g., Brinkworth RSA, O'Carroll DC (2009) Robust Models for Optic Flow Coding in Natural Scenes Inspired by Insect Biology. PLOS Comput Biol 5(11): e1000555. doi:10.1371/journal.pcbi.1000555). No prior permission is required from the authors or publisher. For queries about the license, please contact the relative journal contact indicated here: http://www.PLOS.org/about/media-inquiries/embargo-policy/
About PLOS Computational Biology
PLOS Computational Biology features works of exceptional significance that further our understanding of living systems at all scales through the application of computational methods. All works published in PLOS Computational Biology are open access. Everything is immediately available subject only to the condition that the original authorship and source are properly attributed. Copyright is retained.
PLOS is a non-profit organization of scientists and physicians committed to making the world's scientific and medical literature a freely available public resource. For more information, visit http://www.PLOS.org.
Everything published by PLOS Computational Biology is open access, allowing anyone to download, reuse, reprint, modify, distribute, and/or copy articles, so long as the original authors and source are cited. Please mention PLOS Computational Biology in your report and use the link(s) below to take readers straight to the online articles. Thank you.
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.