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Long-lasting insecticidal nets (LLINs) and indoor residual spraying of insecticide (IRS) are the primary vector control interventions used to prevent malaria in Africa. Although both interventions are effective in some settings, high-quality evidence is rarely available to evaluate their effectiveness following deployment by a national malaria control program. In Uganda, we measured changes in key malaria indicators following universal LLIN distribution in three sites, with the addition of IRS at one of these sites.
Methods and Findings
Comprehensive malaria surveillance was conducted from October 1, 2011, to March 31, 2016, in three sub-counties with relatively low (Walukuba), moderate (Kihihi), and high transmission (Nagongera). Between 2013 and 2014, universal LLIN distribution campaigns were conducted in all sites, and in December 2014, IRS with the carbamate bendiocarb was initiated in Nagongera. High-quality surveillance evaluated malaria metrics and mosquito exposure before and after interventions through (a) enhanced health-facility-based surveillance to estimate malaria test positivity rate (TPR), expressed as the number testing positive for malaria/number tested for malaria (number of children tested for malaria: Walukuba = 42,833, Kihihi = 28,790, and Nagongera = 38,690); (b) cohort studies to estimate the incidence of malaria, expressed as the number of episodes per person-year [PPY] at risk (number of children observed: Walukuba = 340, Kihihi = 380, and Nagongera = 361); and (c) entomology surveys to estimate household-level human biting rate (HBR), expressed as the number of female Anopheles mosquitoes collected per house-night of collection (number of households observed: Walukuba = 117, Kihihi = 107, and Nagongera = 107). The LLIN distribution campaign substantially increased LLIN coverage levels at the three sites to between 65.0% and 95.5% of households with at least one LLIN. In Walukuba, over the 28-mo post-intervention period, universal LLIN distribution was associated with no change in the incidence of malaria (0.39 episodes PPY pre-intervention versus 0.20 post-intervention; adjusted rate ratio [aRR] = 1.02, 95% CI 0.36-2.91, p = 0.97) and non-significant reductions in the TPR (26.5% pre-intervention versus 26.2% post-intervention; aRR = 0.70, 95% CI 0.46-1.06, p = 0.09) and HBR (1.07 mosquitoes per house-night pre-intervention versus 0.71 post-intervention; aRR = 0.41, 95% CI 0.14-1.18, p = 0.10). In Kihihi, over the 21-mo post-intervention period, universal LLIN distribution was associated with a reduction in the incidence of malaria (1.77 pre-intervention versus 1.89 post-intervention; aRR = 0.65, 95% CI 0.43-0.98, p = 0.04) but no significant change in the TPR (49.3% pre-intervention versus 45.9% post-intervention; aRR = 0.83, 95% 0.58-1.18, p = 0.30) or HBR (4.06 pre-intervention versus 2.44 post-intervention; aRR = 0.71, 95% CI 0.30-1.64, p = 0.40). In Nagongera, over the 12-mo post-intervention period, universal LLIN distribution was associated with a reduction in the TPR (45.3% pre-intervention versus 36.5% post-intervention; aRR = 0.82, 95% CI 0.76-0.88, p < 0.001) but no significant change in the incidence of malaria (2.82 pre-intervention versus 3.28 post-intervention; aRR = 1.10, 95% 0.76-1.59, p = 0.60) or HBR (41.04 pre-intervention versus 20.15 post-intervention; aRR = 0.87, 95% CI 0.31-2.47, p = 0.80). The addition of three rounds of IRS at ~6-mo intervals in Nagongera was followed by clear decreases in all outcomes: incidence of malaria (3.25 pre-intervention versus 0.63 post-intervention; aRR = 0.13, 95% CI 0.07-0.27, p < 0.001), TPR (37.8% pre-intervention versus 15.0% post-intervention; aRR = 0.54, 95% CI 0.49-0.60, p < 0.001), and HBR (18.71 pre-intervention versus 3.23 post-intervention; aRR = 0.29, 95% CI 0.17-0.50, p < 0.001). High levels of pyrethroid resistance were documented at all three study sites. Limitations of the study included the observational study design, the lack of contemporaneous control groups, and that the interventions were implemented under programmatic conditions. Conclusions Universal distribution of LLINs at three sites with varying transmission intensity was associated with modest declines in the burden of malaria for some indicators, but the addition of IRS at the highest transmission site was associated with a marked decline in the burden of malaria for all indicators. In highly endemic areas of Africa with widespread pyrethroid resistance, IRS using alternative insecticide formulations may be needed to achieve substantial gains in malaria control.
Measures of Malaria Burden after Long-Lasting Insecticidal Net Distribution and Indoor Residual Spraying at Three Sites in Uganda: A Prospective Observational Study
Agaba Katureebe, 1 Kate Zinszer, 2 Emmanuel Arinaitwe, 1 John Rek, 1 Elijah Kakande, 1 Katia Charland, 3 Ruth Kigozi, 1 , 4 Maxwell Kilama, 1 Joaniter Nankabirwa, 1 , 5 Adoke Yeka, 1 , 4 Henry Mawejje, 1 Arthur Mpimbaza, 4 , 6 Henry Katamba, 7 Martin J. Donnelly, 8 Philip J. Rosenthal, 9 Chris Drakeley, 10 Steve W. Lindsay, 11 Sarah G. Staedke, 10 David L. Smith, 12 Bryan Greenhouse, 9 Moses R. Kamya, 1 , 5 and Grant Dorsey 9 ,*
According to the Developmental Origin of Health and Disease (DOHaD) concept, maternal obesity and accelerated growth in neonates predispose offspring to white adipose tissue (WAT) accumulation. In rodents, adipogenesis mainly develops during lactation. The mechanisms underlying the phenomenon known as developmental programming remain elusive. We previously reported that adult rat offspring from high-fat diet-fed dams (called HF) exhibited hypertrophic adipocyte, hyperleptinemia and increased leptin mRNA levels in a depot-specific manner. We hypothesized that leptin upregulation occurs via epigenetic malprogramming, which takes place early during development of WAT.
As a first step, we identified in silico two potential enhancers located upstream and downstream of the leptin transcription start site that exhibit strong dynamic epigenomic remodeling during adipocyte differentiation. We then focused on epigenetic modifications (methylation, hydroxymethylation, and histone modifications) of the promoter and the two potential enhancers regulating leptin gene expression in perirenal (pWAT) and inguinal (iWAT) fat pads of HF offspring during lactation (postnatal days 12 (PND12) and 21 (PND21)) and in adulthood.
PND12 is an active period for epigenomic remodeling in both deposits especially in the upstream enhancer, consistent with leptin gene induction during adipogenesis. Unlike iWAT, some of these epigenetic marks were still observable in pWAT of weaned HF offspring. Retained marks were only visible in pWAT of 9-month-old HF rats that showed a persistent “expandable” phenotype.
Consistent with the DOHaD hypothesis, persistent epigenetic remodeling occurs at regulatory regions especially within intergenic sequences, linked to higher leptin gene expression in adult HF offspring in a depot-specific manner.
Perinatal programming, Adipose tissue, Epigenetic mechanisms, Developmental origin of health and disease, Gene expression, Fat expansion
Maternal obesity programs increased leptin gene expression in rat male offspring via epigenetic modifications in a depot-specific manner
Simon Lecoutre,1 Frederik Oger,1 Charlene Pourpe,1 Laura Butruille,1 Lucie Marousez,1 Anne Dickes-Coopman,1 Christine Laborie,1 Celine Guinez,1 Jean Lesage,1 Didier Vieau,1 Claudine Junien,2,3 Delphine Eberle,1 Anne Gabory,2 Jerôme Eeckhoute,4 and Christophe Breton1,∗
The present study represents an introduction to the revision of Pheidole Westwood, 1839 from Madagascar. Sixteen species groups are established, of which eleven are revised below, and illustrated identification keys to species groups and species of groups revised in this monograph are presented. Two species are raised to species level: Pheidole petax Forel, 1895 stat. nov., and P. scabrata Forel, 1895 stat. nov. We also redescribe worker castes and designate lectotypes for P. annemariae Forel, 1918, P. nemoralis Forel, 1892, P. petax Forel, 1895, P. ensifera Forel, 1897, P. longispinosa Forel, 1891, and P. scabrata Forel, 1895. The following 46 new species are described: Pheidole aelloeasp. nov., P. alasp. nov., P. andapasp. nov., P. ankeranasp. nov., P. avaratrasp. nov., P. bemarahaensissp. nov., P. bemarivoensissp. nov., P. binarasp. nov., P. boriborasp. nov., P. brevipilosasp. nov., P. curvistriatasp. nov., P. diakritossp. nov., P. ehazoarasp. nov., P. ferrugineasp. nov., P. fisakasp. nov., P. fitaratasp. nov., P. glabrasp. nov., P. goavanasp. nov., P. lamperossp. nov., P. longipilosasp. nov., P. luteasp. nov., P. madinikasp. nov., P. mahaboensissp. nov., P. maizinasp. nov., P. makaensissp. nov., P. makirovanasp. nov., P. manantenensissp. nov., P. mantadiasp. nov., P. marieannaesp. nov., P. masoalasp. nov., P. mavesatrasp. nov., P. miramilasp. nov., P. moramanaensissp. nov., P. navoatrensissp. nov., P. ocypodeasp. nov., P. parvioculasp. nov., P. podargeasp. nov., P. praegrandissp. nov., P. ranohirensissp. nov., P. rugocephalasp. nov., P. rugofitaratasp. nov., P. typhlossp. nov., P. vatovavensissp. nov., P. voasarasp. nov., P. vohemarensissp. nov., and P. zavamanirasp. nov. At present, there are 69 valid species and subspecies of Pheidole known from Madagascar, but this number is expected to increase significantly with upcoming taxonomic revisions of the species groups not revised in this study.
endemic species, Malagasy region, Myrmicinae , taxonomy
Pheidole Westwood, 1839 (Hymenoptera, Formicidae) of Madagascar - an introduction and a taxonomic revision of eleven species groups
Sebastian Salatacorresponding author1 and Brian L. Fisher1
2020 Jan 20.