Rodent borne diseases in Thailand : targeting rodent carriers and risky habitats

Background: Comparative analysis, which aims at investigating ecological and evolutionary patterns among species, may help at targeting reservoirs of zoonotic diseases particularly in countries presenting high biodiversity. Here, we developed a simple method to target rodent reservoirs using published studies screening microparasite infections. Methods: We compiled surveys of microparasites investigated in rodents trapped in Thailand. The data comprise a total of 17,358 rodents from 18 species that have been investigated for a total of 10 microparasites (viruses, bacteria and protozoans). We used residual variation of microparasite richness controlled for both rodent sample size and pathogens’ screening effort to identify major rodent reservoirs and potential risky habitats. Results: Microparasite species richness was positively related to rodent sample size and pathogens’ screening effort. The investigation of the residual variations of microparasite species richness showed that several rodent species harboured more pathogens than expected by the regression model. Similarly, higher pathogen richness than expected was observed in rodents living in non-flooded lands, forests and paddy fields. Conclusion: Our results suggest to target some rodent species that are not commonly investigated for pathogen screening or surveillance such as R. adamanensis or B. savilei, and that non-flooded lands and forests should be more taken into caution, whereas much surveys focused on paddy rice fields and households

Environmental factors and public health policy associated with human and rodent infection by leptospirosis: a land cover-based study in Nan province, Thailand

International audienceLeptospirosis incidence has increased markedly since 1995 in Thailand, with the eastern and northern parts being the most affected regions, particularly during flooding events. Here, we attempt to overview the evolution of human prevalence during the past decade and identify the environmental factors that correlate with the incidence of leptospirosis and the clinical incidence in humans. We used an extensive survey of Leptospira infection in rodents conducted in 2008 and 2009 and the human incidence of the disease from 2003 to 2012 in 168 villages of two districts of Nan province in Northern Thailand. Using an ad-hoc developed land-use cover implemented in a geographical information system we showed that humans and rodents were not infected in the same environment/habitat in the land-use cover. High village prevalence was observed in open habitat near rivers for the whole decade, or in 2008–2009 mostly in rice fields prone to flooding, whereas infected rodents (2008–2009) were observed in patchy habitat with high forest cover, mostly situated on sloping ground areas. We also investigated the potential effects of public health campaigns conducted after the dramatic flood event of 2006. We showed that, before 2006, human incidence in villages was explained by the population size of the village according to the environmental source of infection of this disease, while as a result of the campaigns, human incidence in villages after 2006 appeared independent of their population size. This study confirms the role of the environment and particularly land use, in the transmission of bacteria, emphasized by the effects of the provincial public health campaigns on the epidemiological pattern of incidence, and questions the role of rodents as reservoirs

Dichloroacetate for lactic acidosis in severe malaria: a pharmacokinetic and pharmacodynamic assessment.

Lactic acidosis and hypoglycemia are potentially lethal complications of falciparum malaria. We have evaluated the pharmacokinetics and pharmacodynamics of dichloroacetate ([DCA], 46 mg/kg infused over 30 minutes), a stimulant of pyruvate dehydrogenase and a potential treatment for lactic acidosis, in 13 patients with severe malaria and compared the physiological and metabolic responses with those of a control group of patients (n = 32) of equivalent disease severity. The mean +/- SD peak postinfusion level of DCA was 78 +/- 23 mg/L, the total apparent volume of distribution was 0.75 +/- 0.35 L/kg, and systemic clearance was 0.32 +/- 0.16 L/kg/h. Geometric mean (range) venous lactate concentrations in control and DCA recipients before treatment were 4.5 (2.1 to 19.5) and 5.5 (2 to 15.4) mmol/L, respectively (P > .1). A single DCA infusion decreased lactate concentrations from baseline by a mean of 27% after 2 hours, 40% after 4 hours, and 41% after 8 hours, compared with decreases of 5%, 6%, and 16%, respectively, in controls (P = .032). These changes were preceded by rapid and marked decreases in pyruvate concentrations. Arterial pH increased from 7.328 to 7.374 (n = 10, P < .02) 2 hours after the infusion. Hypoglycemia was prevented by infusing glucose at 3 mg/kg/min. There was no clinical, electrocardiographic, or laboratory evidence of toxicity. These results suggest that DCA should be investigated further as an adjunctive therapy for severe malaria