Neglected tropical diseases have been in the news this week. A big meeting at the World Health Organisation in Geneva has resulted in big pledges from the UK aid progamme and the Bill and Melinda Gates Foundation to banish the scourge affecting around a billion people worldwide.
This is good news, and to be commended. But the focus of many of the announcements has been on drugs and vaccines – the technical solutions to prevention and cure. These are of course vital parts of the solution, but, as we have found in work on ‘sleeping sickness’ in southern Africa, as part of the ESPA-funded Dynamic Drivers of Disease in Africa project, they are not the whole story. Without a wider look at how politics and ecology interact in local situations, opportunities for disease or vector control may be missed, and money wasted.
Over the last few years, a team from the University of Zimbabwe and the Tsetse Control Branch of the Ministry of Agriculture of Zimbabwe has been looking at trypanosomiasis (a disease affecting animals and humans, when it’s called sleeping sickness), and the vector that carries it, the tsetse fly (see picture) in the Zambezi valley. We have been trying to unravel the complex puzzle that connects changing ecologies, disease and livelihood impacts, working as a cross-disciplinary team.
Despite decades of control efforts – from clearance of vegetation to wildlife extermination to aerial spraying of chemicals to baited traps (see this paper), the tsetse fly and trypanosomiasis, affecting both animals and humans, persists. And indeed in the last few years we have seen peaks in both human and animal forms. Not high, but definitely worrying – and devastating for those who are affected.
In our work, we trapped flies along transects, took blood from animals to look for parasites, examined habitat change from satellite imagery and talked to people in the villages. The question we had – why did the disease persist? – was a difficult one to answer. The official maps showed the tsetse ‘belt’ being kept to the south, into the Highveld. Control measures continued to some extent, and official reporting of trypanosomiasis, both animal and human, was highlighting very few cases.
Our tsetse fly surveys in Hurungwe district showed a peak of fly populations along the valley escarpment, with declining numbers of flies caught in our traps as you travel south away from the valley. Cluster traps located near villages and dips also showed a variable pattern. But overall tsetse fly populations (of different species) were low and relatively few were trapped. Why, if people complain about both animal and human trypanosomiasis? The answer came through an analysis of habitat change.
Abandoning very coarse grained images in favour of LANDSAT images with a higher resolution, we found a major shift in vegetation patterns over time, and particularly a noticeable fragmentation of habitat. Maybe the flies were residing in these fragmented habitat patches, and were not being picked up by the standard belt transects? This indeed proved to be the case.
When villagers analysed the satellite image maps of their area with us, they quickly pointed to particular patches where they knew flies were. The Mushangishe gorge, the pools near the Chewore river, the villages along the edge of the hunting area, the Makuti area, and so on. Some more focused trapping, sampling not randomly but purposively according to what people had indicated, showed that flies do still persist, even in heavily populated areas, but just in small patches.
So what about the disease-causing trypanosomes themselves? Analysis of 209 tsetse flies showed that nearly half were carrying trypanosomes following molecular DNA analysis at Edinburgh University. The most prevalent species was T. vivax (in 32% of flies), followed by T. brucei. This pattern was consistent across fly species (G. m. mortisans and G. pallidipes) and sex. Blood sampling of 400 cattle and 222 goats across 19 villages again showed a very heterogeneous pattern of presence, with trypanosomes (T vivax and T. brucei) being found in only four village sites, with presence in cattle ranging from 2-10 per cent. The places where infected animals were found tallied almost exactly with the places where local people had identified tsetse infested habitat patches. Perhaps surprisingly, given the reports of human trypanosomiasis, we found no evidence of T. b. rhodesiense in either fly or livestock samples; although of course this does not mean it is not present.
The puzzle had been (partially) solved. Tsetse flies and so trypanosomiasis (although no human sleeping sickness causing trypanosmes found as yet) persist because of the maintenance of particular habitat patches. Who gets sick (and whose animals) depends on who goes to these sites. Those most likely to get the disease, and those whose animals are the most susceptible, are mostly poor and marginalised people who must make a living on the edge of wildlife areas. They are hired herders or children of school age moving with animals deep into forested areas; they are groups of men going on hunting trips harvesting wild animals as a source of protein; they are women who forage in the forests, or who collect water from streams and rivers; and they are the new in-migrants into the area, offered land to settle and farm in the frontier areas, sometimes in the buffer zones of the national park and hunting areas.
As people put it to us “we are now fighting a guerrilla war against the tsetse”. They don’t exist along a ‘front’, an identifiable belt on a map as in the past, but in particular sites, which only particular people go to. Gender, age, occupation all make a big difference as to who gets potentially exposed. This has important implications for both monitoring (coarse grained satellite imagery, broad transects and random sampling are no use) and response (by the same token, generic, area-wide approaches make little sense). A more targeted approach, identifying particular patches, and particular people at risk is vital.
In addition, disease risk has to be understood through an appreciation of history, politics and social relations. Such people and their animals do not become sick by chance. Disease is often caused by what Paul Farmer calls ‘structural violence’, with disease being “the biological reflection of social fault lines”. Inequality, poverty, dispossession, alienation, lack of rights, and deep neglect by states results in disease impacts that are often not even noticed or recorded. The biological impacts of disease are thus reflected through politics, class, race and gender and changing landscape ecologies.
Tackling a neglected disease like sleeping sickness requires an understanding of ecology, social relations, politics and more. Expensive, magic bullet solutions through drugs or vaccines may not be the only answer – instead much simpler solutions may be on offer, if the social causes of disease are addressed and the ecological dynamics of disease risk understood. It is good that BGMF and DFID have pledged money; let’s hope it is used in an integrated ‘One Health’ approach, where complex solutions are developed for complex, multi-sectoral challenges.
The Dynamic Drivers of Disease in Africa work was supported by ESPA (Ecosystem Services for Poverty Alleviation) programme funded by NERC, ESRC and DFID, and the Zimbabwe study was led by Professor Vupenyu Dzingirai (CASS, UZ), working with William Shereni (Ministry of Agriculture), Learnmore Nyakupinda (Ministry of Agriculture), Lindiwe Mangwanya (UZ), Amon Murwira (UZ), Farai Matawa (UZ), Neil Anderson (Edinburgh University) and Ewan McLeod (Edinburgh University), among others.
This post was adapted from an earlier blog, and was written by Ian Scoones and appeared on Zimbabweland