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Introduction Understanding human mobility’s role in malaria transmission is critical to successful control and elimination. However, common approaches to measuring mobility are ill-equipped for remote regions such as the Amazon. This study develops a network survey to quantify the effect of community connectivity and mobility on malaria transmission.Methods We measure community connectivity across the study area using a respondent driven sampling design among key informants who are at least 18 years of age. 45 initial communities will be selected: 10 in Brazil, 10 in Ecuador and 25 in Peru. Participants will be recruited in each initial node and administered a survey to obtain data on each community’s mobility patterns. Survey responses will be ranked and the 2–3 most connected communities will then be selected and surveyed. This process will be repeated for a third round of data collection. Community network matrices will be linked with each country’s malaria surveillance system to test the effects of mobility on disease risk.Ethics and dissemination This study protocol has been approved by the institutional review boards of Duke University (USA), Universidad San Francisco de Quito (Ecuador), Universidad Peruana Cayetano Heredia (Peru) and Universidade Federal Minas Gerais (Brazil). Results will be disseminated in communities by the end of the study.

[This corrects the article DOI: 10.1371/journal.pone.0287412.].

Malaria transmission is influenced by climate and land use/land cover change (LULC). This study examines the impact of climate and LULC on malaria risk in the Ecuadorian Amazon. Weekly malaria surveillance data between 2008 and 2019 from Ecuador's Ministry of Public Health were combined with hydrometeorological and LULC data. Cross-correlation analyses identified time lags. Bayesian spatiotemporal models estimated annual LULC rates of change (ARC) by census area and assessed the effects on Plasmodium vivax and Plasmodium falciparum incidence. ARC for the five land cover classes (forest, agriculture, urban, shrub vegetation, water) ranged from -1 to 4% with agriculture increasing across areas. Forest and shrub vegetation ARC were significantly associated with both Plasmodium vivax and Plasmodium falciparum. Temperature and terrestrial water content showed consistent negative relationships with both species. Precipitation had varying effects on Plasmodium vivax (null) and Plasmodium falciparum (increase) incidence. Shrubs and forest expansion, increased temperature, and terrestrial water content reduced malaria incidence, while increased precipitation had varying effects. Relationships between malaria, LULC, and climate are complex, influencing risk profiles. These findings aid decision-making and guide further research in the region.

Artisanal and small-scale gold mining (ASGM) is the largest global anthropogenic mercury (Hg) source and is widespread in the Peruvian Amazon. Consuming Hg-laden foods exposes people to this potent neurotoxin. While numerous studies have examined fish Hg content near ASGM, Hg accumulation in other commonly consumed animal-and plant-based foods from terrestrial environments is often overlooked. In this study, we aim to address understudied dietary Hg exposures. To understand Hg exposure from food staples in the Peruvian Amazon, we measured total and methyl Hg in local crops, fish, chicken meat, chicken feathers, and eggs from ASGM-impacted and upstream (reference) communities. Diet surveys were used to estimate probable weekly Hg intake from each food. Fish and chicken stable carbon and nitrogen isotope signatures were analyzed to evaluate trophic magnification. Though few crops exceeded food safety recommendations, rice methyl Hg proportions were high (84%). Trophic level was an expected key predictor of fish Hg content. 81% (17 of 21) of local carnivorous fish exceeded WHO and EPA recommendations. Compared to upstream communities, mining-impacted communities demonstrated elevated total Hg in crops (1.55 (interquartile ranges (IQR): 0.60–3.03) μ g kg ^−1 upstream versus 3.38 (IQR: 1.62–11.58) in mining areas), chicken meats (2.69 (IQR: BDL–9.96) μ g kg ^−1 versus 19.68 (IQR: 6.33–48.1)), and feathers (91.20 (IQR: 39.19–216.13) μ g kg ^−1 versus 329.99 (IQR: 173.22–464.99)). Chicken meats from mining areas exhibited over double the methyl Hg concentrations of those upstream. Methyl Hg fractions in chicken muscle tissue averaged 93%. Egg whites and livers exceeded Hg recommendations most frequently. Proximity to mining, but not trophic position, was a predictor of chicken Hg content. Our results demonstrate that terrestrial and aquatic foods can accumulate Hg from mining activity, introducing additional human Hg exposure routes. However, locally sourced carnivorous fish was the largest contributor to an estimated three-fold exceedance of the provisional tolerable weekly Hg intake.

Gulf War Illness (GWI) is a major health problem for approximately 250,000 Gulf War (GW) veterans, but the etiology of GWI is unclear. We hypothesized that mitochondrial dysfunction is an important contributor to GWI, based on the similarity of some GWI symptoms to those occurring in some mitochondrial diseases; the plausibility that certain pollutants to which GW veterans were exposed affect mitochondria; mitochondrial effects observed in studies in laboratory models of GWI; and previous evidence of mitochondrial outcomes in studies in GW veterans. A primary role of mitochondria is generation of energy via oxidative phosphorylation. However, direct assessment of mitochondrial respiration, reflecting oxidative phosphorylation, has not been carried out in veterans with GWI. In this case-control observational study, we tested multiple measures of mitochondrial function and integrity in a cohort of 114 GW veterans, 80 with and 34 without GWI as assessed by the Kansas definition. In circulating white blood cells, we analyzed multiple measures of mitochondrial respiration and extracellular acidification, a proxy for non-aerobic energy generation; mitochondrial DNA (mtDNA) copy number; mtDNA damage; and nuclear DNA damage. We also collected detailed survey data on demographics; deployment; self-reported exposure to pesticides, pyridostigmine bromide, and chemical and biological warfare agents; and current biometrics, health and activity levels. We observed a 9% increase in mtDNA content in blood in veterans with GWI, but did not detect differences in DNA damage. Basal and ATP-linked oxygen consumption were respectively 42% and 47% higher in veterans without GWI, after adjustment for mtDNA amount. We did not find evidence for a compensatory increase in anaerobic energy generation: extracellular acidification was also lower in GWI (12% lower at baseline). A subset of 27 and 26 veterans returned for second and third visits, allowing us to measure stability of mitochondrial parameters over time. mtDNA CN, mtDNA damage, ATP-linked OCR, and spare respiratory capacity were moderately replicable over time, with intraclass correlation coefficients of 0.43, 0.44, 0.50, and 0.57, respectively. Other measures showed higher visit-to-visit variability. Many measurements showed lower replicability over time among veterans with GWI compared to veterans without GWI. Finally, we found a strong association between recalled exposure to pesticides, pyridostigmine bromide, and chemical and biological warfare agents and GWI (p < 0.01, p < 0.01, and p < 0.0001, respectively). Our results demonstrate decreased mitochondrial respiratory function as well as decreased glycolytic activity, both of which are consistent with decreased energy availability, in peripheral blood mononuclear cells in veterans with GWI.

IntroductionThe Taenia solium tapeworm is responsible for cysticercosis, a neglected tropical disease presenting as larvae in the body of a host following taenia egg ingestion. Neurocysticercosis (NCC), the name of the disease when it affects the human central nervous system, is a major cause of epilepsy in developing countries, and can also cause intracranial hypertension, hydrocephalus and death. Simulation models can help identify the most cost-effective interventions before their implementation. Modelling NCC should enable the comparison of a broad range of interventions, from treatment of human taeniasis (presence of an adult taenia worm in the human intestine) to NCC mitigation. It also allows a focus on the actual impact of the disease, rather than using proxies as is the case for other models.MethodsThis agent-based model is the first model that simulates human NCC and associated pathologies. It uses the output of another model, CystiAgent, which simulates the evolution of pig cysticercosis and human taeniasis, adding human and cyst agents, including a model of cyst location and stage, human symptoms, and treatment. CystiHuman also accounts for delays in the appearance of NCC-related symptoms. It comprises three modules detailing cyst development, seizure probability and timing, and intracranial hypertension/hydrocephalus, respectively. It has been implemented in Java MASON and calibrated in three endemic villages in Peru, then applied to another village (Rica Playa) to compare simulation results with field data in that village.Results and discussionDespite limitations in available field data, parameter values found through calibration are plausible and simulated outcomes in Rica Playa are close to actual values for NCC prevalence and the way it increases with age and cases with single lesions. Initial simulations further suggest that short-term interventions followed by a rapid increase in taeniasis prevalence back to original levels may have limited impacts on NCC prevalence.

Abstract Background Models can be used to study and predict the impact of interventions aimed at controlling the spread of infectious agents, such as Taenia solium, a zoonotic parasite whose larval stage causes epilepsy and economic loss in many rural areas of the developing nations. To enhance the credibility of model estimates, calibration against observed data is necessary. However, this process may lead to a paradoxical dependence of model parameters on location-specific data, thus limiting the model’s geographic transferability. Methods In this study, we adopted a non-local model calibration approach to assess whether it can improve the spatial transferability of CystiAgent, our agent-based model of local-scale T. solium transmission. The calibration dataset for CystiAgent consisted of cross-sectional data on human taeniasis, pig cysticercosis and pig serology collected in eight villages in Northwest Peru. After calibration, the model was transferred to a second group of 21 destination villages in the same area without recalibrating its parameters. Model outputs were compared to pig serology data collected over a period of 2 years in the destination villages during a trial of T. solium control interventions, based on mass and spatially targeted human and pig treatments. Results Considering the uncertainties associated with empirical data, the model produced simulated pre-intervention pig seroprevalences that were successfully validated against data collected in 81% of destination villages. Furthermore, the model outputs were able to reproduce validated pig seroincidence values in 76% of destination villages when compared to the data obtained after the interventions. The results demonstrate that the CystiAgent model, when calibrated using a non-local approach, can be successfully transferred without requiring additional calibration. Conclusions This feature allows the model to simulate both baseline pre-intervention transmission conditions and the outcomes of control interventions across villages that form geographically homogeneous regions, providing a basis for developing large-scale models representing T. solium transmission at a regional level. Graphical Abstract