Background Plasmodium vivax malaria remains a major public health burden in Myanmar. Resistance to chloroquine (CQ), the first-line treatment for P. vivax, has been reported in the country and has potential to undermine local control efforts.MethodsPatients over 6 years of age with uncomplicated P. vivax mono-infection were enrolled into clinical efficacy studies in Myawaddy in 2014 and Kawthoung in 2012. Study participants received a standard dose of CQ (25 mg/kg over 3 days) followed by weekly review until day 28. Pvmdr1 copy number (CN) and microsatellite diversity were assessed on samples from the patients enrolled in the clinical study and additional cross-sectional surveys undertaken in Myawaddy and Shwegyin in 2012.ResultsA total of 85 patients were enrolled in the CQ clinical studies, 25 in Myawaddy and 60 in Kawthoung. One patient in Myawaddy (1.2%) had an early treatment failure and two patients (2.3%) in Kawthoung presented with late treatment failures on day 28. The day 28 efficacy was 92.0% (95% CI 71.6–97.9) in Myawaddy and 98.3% (95% CI 88.7–99.8) in Kawthoung. By day 2, 92.2% (23/25) in Myawaddy and 85.0% (51/60) in Kawthoung were aparasitaemic. Genotyping and pvmdr1 CN assessment was undertaken on 43, 52 and 46 clinical isolates from Myawaddy, Kawthoung and Shwegyin respectively. Pvmdr1 amplification was observed in 3.2% (1/31) of isolates in Myawaddy, 0% (0/49) in Kawthoung and 2.5% (1/40) in Shwegyin. Diversity was high in all sites (H E 0.855–0.876), with low inter-population differentiation (F ST 0.016–0.026, P < 0.05).ConclusionsTreatment failures after chloroquine were observed following chloroquine monotherapy, with pvmdr1 amplification present in both Myawaddy and Shwegyin. The results emphasize the importance of ongoing P. vivax drug resistance surveillance in Myanmar, particularly given the potential connectivity between parasite population at different sites.Electronic supplementary materialThe online version of this article (doi:10.1186/s12936-017-1912-y) contains supplementary material, which is available to authorized users.

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Background Achieving the elimination of soil-transmitted helminth (STH) infections requires a sufficient understanding of the current epidemiological status of STH endemicity. We aimed to examine the status of STH in Myanmar – a country with the eighth highest STH prevalence in the world, 10 years after instigation of the national deworming programme. Methods In August 2016 we screened for STH infections using Kato Katz (KK) microscopy and real-time PCR (qPCR) in schoolchildren from the Bago Region township of Phyu, a STH sentinel site in Myanmar. Ten schools were randomly selected, and one stool sample each from a total of 264 students was examined. Prevalence and intensity of infection were calculated for each STH. Results High prevalence of STH was identified in the study area with 78.8% of the schoolchildren infected with at least one STH by qPCR, and 33.3% by KK. The most prevalent STH was Trichuris trichiura, diagnosed by both KK (26.1%) and qPCR (67.1%), followed by Ascaris lumbricoides (15.5% KK; 54.9% qPCR). No hookworm infections were identified by KK; however, the qPCR analysis showed a high prevalence of Ancylostoma sp. infection (29.6%) with few Necator americanus (1.1%) infections. Conclusions Despite bi-annual deworming of schoolchildren in the fourth-grade and below, STH prevalence remains stubbornly high. These results informed the expansion of the Myanmar National STH control programme to include all school-aged children by the Ministry of Health and Sports in 2017, however further expansion to the whole community should be considered along with improving sanitation and hygiene measures. This would be augmented by rigorous monitoring and evaluation, including national prevalence surveys.

Chronic obstructive pulmonary disease (COPD) is a major cause of mortality worldwide, and pulmonary epithelial cell apoptosis is regarded as one of the most important factors in its pathogenesis. Here we examined the molecular mechanisms of apoptosis caused by cigarette smoke (CS). In the normal bronchial epithelium cell line BEAS-2B, a CS extract markedly induced apoptosis together with transient early growth response 1 (EGR1) protein expression, which is activated over time via the aryl hydrocarbon receptor (AHR). The CS extract induced apoptosis and decreased cell count of BEAS-2B cells and was significantly reversed by knockdown of either EGR1 or AHR. In vivo, the CS extract caused alveolar wall destruction, mimicking COPD, 1 week after intrathoracic injection. Bronchoalveolar lavage fluid (BALF) from the CS extract-treated mice contained massive numbers of apoptotic epithelial cells. Furthermore, it was found that aminoanthracene induced EGR1 expression and cell apoptosis. By contrast, the AHR antagonist stemregenin 1 (SR1) restored apoptosis upon CS treatment. These results suggest that aryl hydrocarbons, such as aminoanthracene, induce EGR1 expression via the AHR, resulting in cell apoptosis and that this can be prevented by administration of an antagonist of AHR.