World Malaria Day 2015 highlighted the progress made in the development of new methods of prevention (vaccines and insecticides) and treatment (single dose drugs) of the disease. However, increasing drug and insecticide resistance threatens the successes made with existing methods. Insecticide resistance has decreased the efficacy of the most commonly used insecticide class of pyrethroids. This decreased efficacy has increased mosquito survival, which is a prelude to rising incidence of malaria and fatalities. Despite intensive research efforts, new insecticides will not reach the market for at least 5 years. Elimination of malaria is not possible without effective mosquito control. Therefore, to combat the threat of resistance, key stakeholders need to rapidly embrace a multifaceted approach including a reduction in the cost of bringing new resistance management methods to market and the streamlining of associated development, policy, and implementation pathways to counter this looming public health catastrophe.

Insecticide-treated nets (ITNs) for malaria control are widespread but coverage remains inadequate. We developed a Bayesian model using data from 102 national surveys, triangulated against delivery data and distribution reports, to generate year-by-year estimates of four ITN coverage indicators. We explored the impact of two potential 'inefficiencies': uneven net distribution among households and rapid rates of net loss from households. We estimated that, in 2013, 21% (17%–26%) of ITNs were over-allocated and this has worsened over time as overall net provision has increased. We estimated that rates of ITN loss from households are more rapid than previously thought, with 50% lost after 23 (20–28) months. We predict that the current estimate of 920 million additional ITNs required to achieve universal coverage would in reality yield a lower level of coverage (77% population access). By improving efficiency, however, the 920 million ITNs could yield population access as high as 95%.DOI: http://dx.doi.org/10.7554/eLife.09672.001

Thermotherapy is an effective, comparatively well-tolerated, and rapid treatment for CL, and it should be considered as an alternative to antimony treatment.

Experimental huts in Côte d'Ivoire were used to evaluate the pyrethroid alphacypermethrin, the non-ester pyrethroid etofenprox, the organophosphate pirimiphos-methyl and the carbamate carbosulfan on bednets against pyrethroidresistant Anopheles gambiae Giles. To test for selection for the resistance gene by the treated nets, A. gambiae collected live or dead from the huts were kept and analysed for the presence of the kdr gene using a new polymerase chain reaction followed by sequence-specific oligonucleotide probing (PCR-SSOP) for kdrgenotyping. Deliberately holed bednets freshly treated with pirimiphos-methyl or carbosulfan caused over 90% kill of A. gambiae s.s. and Culex spp. However, the mortality with alpha-cypermethrin or etofenprox treated nets was similar to that with untreated nets. Bloodfeeding of A. gambiae s.s. on the sleepers under the nets was only significantly reduced by alpha-cypermethrin and carbosulfan. Tests of the residual activity of the bednets after seven months showed that pirimiphosmethyl had lost its efficacy while carbosulfan still performed well. Once again the pyrethroid treated nets gave similar results to the untreated nets. Selection for the kdr-allele by alpha-cypermethrin and etofenprox, but not by carbosulfan, was indicated by PCR-SSOP genotyping of mosquitoes. Thus carbamates such as carbosulfan, or organophosphates of longer persistence than pirimiphos-methyl and of low mammalian toxicity, would seem to be a promising alternative to be used on bednets, particularly in areas of pyrethroid resistance.

Background In East Africa, visceral leishmaniasis (VL) is endemic in parts of Sudan, Ethiopia, Somalia, Kenya and Uganda. It is caused by Leishmania donovani and transmitted by the sandfly vector Phlebotomus martini. In the Pokot focus, reaching from western Kenya into eastern Uganda, formulation of a prevention strategy has been hindered by the lack of knowledge on VL risk factors as well as by lack of support from health sector donors. The present study was conducted to establish the necessary evidence-base and to stimulate interest in supporting the control of this neglected tropical disease in Uganda and Kenya.Methods A case-control study was carried out from June to December 2006. Cases were recruited at Amudat hospital, Nakapiripirit district, Uganda, after clinical and parasitological confirmation of symptomatic VL infection. Controls were individuals that tested negative using a rK39 antigen-based dipstick, which were recruited at random from the same communities as the cases. Data were analysed using conditional logistic regression. ResultsNinty-three cases and 226 controls were recruited into the study. Multivariate analysis identified low socio-economic status and treating livestock with insecticide as risk factors for VL. Sleeping near animals, owning a mosquito net and knowing about VL symptoms were associated with a reduced risk of VL.Conclusions VL affects the poorest of the poor of the Pokot tribe. Distribution of insecticide-treated mosquito nets combined with dissemination of culturally appropriate behaviour-change education is likely to be an effective prevention strategy.

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Effective malaria control requires information on both the geographical distribution of malaria risk and the effectiveness of malaria interventions. The current standard for estimating malaria infection and impact indicators are household cluster surveys, but their complexity and expense preclude frequent and decentralized monitoring. This paper reviews the historical experience and current rationale for the use of schools and school children as a complementary, inexpensive framework for planning, monitoring and evaluating malaria control in Africa. Consideration is given to (i) the selection of schools; (ii) diagnosis of infection in schools; (iii) the representativeness of schools as a proxy of the communities they serve; and (iv) the increasing need to evaluate interventions delivered through schools. Finally, areas requiring further investigation are highlighted.

BackgroundVivax malaria remains a major cause of morbidity in the subtropics. To undermine the stability of the disease, drugs are required that prevent relapse and provide reservoir reduction. A 14-day course of primaquine (PQ) is effective but cannot safely be used in routine practice because of its interaction with glucose-6-phosphate dehydrogenase (G6PD) deficiency for which testing is seldom available. Safe and effective use of PQ without the need for G6PD testing would be ideal. The efficacy and safety of an 8-week, once weekly PQ regimen was compared with current standard treatment (chloroquine alone) and a 14-day PQ regimen.Methods and Principal Findings200 microscopically confirmed Plasmodium vivax patients were randomly assigned to either once weekly 8-week PQ (0.75mg/kg/week), once weekly 8-week placebo, or 14-day PQ (0.5mg/kg/day) in North West Frontier Province, Pakistan. All patients were treated with a standard chloroquine dose and tested for G6PD deficiency. Deficient patients were assigned to the 8-week PQ group. Failure was defined as any subsequent episode of vivax malaria over 11 months of observation. There were 22/71 (31.0%) failures in the placebo group and 1/55 (1.8%) and 4/75 (5.1%) failures in the 14-day and 8-week PQ groups, respectively. Adjusted odds ratios were: for 8-week PQ vs. placebo-0.05 (95%CI: 0.01-0.2, p<0.001) and for 14-day PQ vs. placebo-0.01 (95%CI: 0.002-0.1, p<0.001). Restricted analysis allowing for a post-treatment prophylactic effect confirmed that the 8-week regimen was superior to current treatment. Only one G6PD deficient patient presented. There were no serious adverse events.ConclusionsA practical radical treatment for vivax malaria is essential for control and elimination of the disease. The 8-week PQ course is more effective at preventing relapse than current treatment with chloroquine alone. Widespread use of the 8-week regimen could make an important contribution to reservoir reduction or regional elimination where G6PD testing is not available.Trial RegistrationClinicalTrials.gov NCT00158587