We investigated the association between socioeconomic position (SEP), its determinants, and malaria in children in a rural, high-transmission setting in Uganda. Households with greater agricultural success had higher SEP. In turn, households and children of higher SEP were exposed to a 29 % lower HBR and had 48 % lower odds of malaria infection than the poorest. Finally, there was evidence that the association between SEP and malaria infection was explained partly by house type and food security. Our findings concur with observations elsewhere in sub-Saharan Africa (SSA) that the odds of malaria infection are on average doubled in children with the lowest SEP (as measured by household wealth index scores or parent’s educational status or occupation) compared to children with the highest SEP within the same community [3]. Socioeconomic factors may be as influencial in malaria transmission today in Uganda as they were historically in North America and Europe [4].
To our knowledge, the present study is the first to use mediation analysis to explore the causal pathways by which poverty may cause malaria. First, the analysis suggests that house type may explain part of the association between SEP and malaria infection risk, consistent with previous observations that well-built housing, with closed eaves and modern wall and roof materials, is associated with lower malaria risk through reduced mosquito house entry [11, 16]. Second, we observed that food security may also mediate the poverty-malaria association. While findings on the relationship between nutrition and malaria are inconsistent [20], there is evidence that undernutrition may be associated with greater susceptibility to malaria infection and progression to severe disease [10] and that protein-energy malnutrition is associated with greater malaria morbidity and mortality [21]. Indeed, a previous study in our study district found that stunting (an indicator of chronic malnutrition) was associated with a higher incidence of clinical malaria in children [22]. Conversely, it is possible that our measure of food security was more of a proxy for SEP than nutritional status [23].
Identifying factors potentially mediating between SEP and malaria provides evidence of a biologically plausible mechanism for causality, yet the mediation analysis was subject to a number of limitations. First, house quality and food security together accounted for less than half of the association between poverty and malaria infection risk, suggesting that other mediators remain unaccounted for. While treatment-seeking behaviour was excluded from the mediation analysis, wealthier households sought treatment for fever more promptly than poorer households, so this variable merits future evaluation as a potential mediator. Additional potential mediators may include distance of households to the village periphery, housing density and, given the local clustering of wealthier households, malaria risk in neighbouring households. Education level, while considered an indicator of SEP [15], arguably could also lie on the mediation pathway. Therefore our conceptual framework and analysis were not exhaustive and provide only a preliminary exploration of the complex relationships linking poverty and malaria. Second, the assumptions underlying the mediation analysis may not have been fully met. For example, the costs of malaria can worsen poverty, resulting in reverse causality [7, 8], and the relationship between SEP and malaria may be confounded by environmental factors such as distance to larval habitats (alternatively, location might be on the causal pathway between SEP and malaria). While we aimed to omit from the wealth index variables directly associated with malaria [15], some of the included assets may have been associated with both SEP and house type (e.g. sofa ownership or toilet access). Third, we did not observe any association between SEP and incidence of clinical malaria and the interpretation of this finding is unclear.
To identify potential cross-over between development interventions and malaria control, we sought to understand better the heterogeneity in SEP in the study area. Overall we found that SEP was associated with increased odds of malaria infection. In turn, SEP was associated with relative agricultural success, consistent with agriculture being a major livelihood source in Nagongera as in much of rural Africa [18, 24]. We also observed that wealthier households had larger farms and were overall more successful in agriculture than poorer households. Of course, wealthier households may invest more in agriculture and other enterprises, improving their overall productivity. Yet it is also feasible that agricultural productivity limits household wealth and that land access constrains productivity in Nagongera, since there is extensive land fragmentation stemming from the division of land over generations, which is likely to continue as the Ugandan population expands from 39 million in 2015 to an estimated 102 million in 2050 [25]. Elsewhere in SSA, rural poverty has been linked to lower vegetation index scores, remoteness and poor soil fertility [26]. While the conclusions that may be drawn from our observational study are limited, our findings highlight the importance of understanding malaria transmission within the wider social and ecological landscape.
By examining the relationship between poverty and malaria, practical steps towards multisectoral intervention may be identified. First, there may be overlap between poverty reduction and malaria control [3]. If this is the case, interventions such as Farmer Field Schools (a group-based education approach) might be targeted in areas where agriculture is an important livelihood source to increase production and marketing capacity while incorporating training in Integrated Pest and Vector Management [27]. If land access constrains productivity, diversification into non-agricultural activities may be necessary, alongside interventions to improve productivity and market access among remaining farmers. Second, since house quality is associated with malaria risk, malaria control progammes could work with other sectors to scale-up ‘healthy’ housing [28]. Possible strategies may include microfinance initiatives, education and the use of model houses to encourage good house design, or collaboration with other ministries and the private sector [29]. Third, should good nutrition be protective against malaria, nutrition-sensistive interventions – including those related to agriculture and food security – may be complementary to malaria control.
Our study has a number of limitations. First, the mediation analysis was based on untestable assumptions (Additional file 3). Should these assumptions not hold, this would limit confidence in house quality and food security being mediators of the SEP-malaria relationship and in their associated mediating effects. Throughout our analysis, we assume that SEP affects malaria risk, yet reverse causality from malaria risk to SEP and agricultural productivity is highly probable [7, 8, 30]. Second, the conceptual framework was not an exhaustive representation and we were unable to investigate all causal pathways linking SEP and malaria, nor all potential determinants of poverty. Third, the wealth index is an imperfect metric and its representation of underlying SEP is influenced by the variables included in the index [15]. Fourth, our spatial analysis modelled few variables relevant to malaria. Finally, we studied only one population at one time point, so the findings require future validation in this and other settings. Despite the methodological challenges, it is hoped that our analysis offers a preliminary insight into the complex relationship between poverty and malaria, providing a framework for future interdisciplinary research.