BackgroundPolymorphisms within the PfATP6 gene have been indicated as potential molecular markers for artemisinin efficacy. Since 2004, the use of artemisinin combination therapy (ACT) was introduced as first-line treatment of the uncomplicated malaria cases in Suriname. The aim of this research was to determine changes in Suriname in the status of the polymorphic markers in the PfATP6 gene before and after the adoption of the ACT-regimen, particularly of the S769N mutation, which was reported to be associated with in vitro Artemether resistance in the neighboring country French Guiana.MethodsThe PfATP6 gene from Plasmodium falciparum parasites in Suriname was investigated in 28 samples using PCR amplification and restriction enzyme analysis, to assess and determine the prevalence of potentially interesting single nucleotide polymorphisms. The polymorphisms [L263E; A623E; S769N], which may be associated with the artemisinin resistant phenotype were characterized in parasites from three endemic regions before and after the adoption of the ACT-regimen. In addition, the status of these molecular markers was compared in paired P. falciparum isolates from patients with recurring malaria after controlled ACT.ResultsAll the investigated samples exhibit the wild-type genotype at all three positions; L263, A623, S769.ConclusionAll investigated isolates before and after the adoption of the ACT-regimen and independent of endemic region harbored the wild-type genotype for the three investigated polymorphisms. The study revealed that decreased artemisinin susceptibility could occur independent from PfATP6 mutations, challenging the assumption that artemisinin resistance is associated with these mutations in the PfATP6 gene.

Abstract. The aim of this translational study was to show the use of molecular surveillance for polymorphisms and copy number as a monitoring tool to track the emergence and dynamics of Plasmodium falciparum drug resistance. A molecular baseline for Suriname was established in 2005, with P. falciparum chloroquine resistance transporter (pfcrt) and P. falciparum multidrug resistance (pfmdr1) markers and copy number in 40 samples. The baseline results revealed the existence of a uniformly distributed mutated genotype corresponding with the fully mefloquine-sensitive 7G8-like genotype (Y184F, S1034C, N1042D, and D1246Y) and a fixed pfmdr1 N86 haplotype. All samples harbored the pivotal pfcrtK76T mutation, showing that chloroquine reintroduction should not yet be contemplated in Suriname. After 5 years, 40 samples were assessed to trace temporal changes in the status of pfmdr1 polymorphisms and copy number and showed minor genetic alterations in the pfmdr1 gene and no significant changes in copy number, thus providing scientific support for prolongation of the current drug policy in Suriname.

Amplification of the pfmdr1 gene is associated with clinical failures and reduced in vivo and in vitro sensitivity to both mefloquine and artemether-lumefantrine in South-East Asia.

Background Suriname has accomplished a steep decline in malaria burden, even reaching elimination levels. Plasmodium serology data are not available for Suriname and even extremely scarce within the region, therefore malaria serology testing was introduced, country customized cut-off values were determined and a study was performed to explore the antibody status for Plasmodium falciparum, Plasmodium vivax and Plasmodium malariae. Methods A cross-sectional survey was conducted between July 2017 and March 2018 in two areas of the interior with different malaria settings: Stoelmanseiland, representing Maroon villages and Benzdorp, a gold mining area, with mostly Brazilian miners. Dried blood spots (DBS) were collected (n = 197) and antibody presence against seven Plasmodium antigens was detected using a multiplex bead-based, IgG antibody assay. Demographic information was gathered through a questionnaire. Country customized cut-off values were generated from a Surinamese malaria-naïve reference population (n = 50). Results Serological analysis for the reference population revealed cut-off values ranging from 14 MFI for LSA-1 to 177 MFI for PmMSP-119. Seroprevalence against any of the three MSP-119 antibodies was similar in both regions and surpassed 75%. Single seropositivity against PfMSP-119 antibodies was higher in Stoelmanseiland (27.0%) than Benzdorp (9.3%), in line with the historical malaria burden of Stoelmanseiland, while the reverse was observed for PvMSP-119 antibodies. Despite sporadic reports of P. malariae infections, PmMSP-119 antibody presence was 39.6%. A more detailed examination of P. falciparum serology data displayed a higher seroprevalence in villagers (90.7%) than in Brazilians (64.6%) and a highly diverse antigenic response with 22 distinct antibody combinations. Conclusions The results on the malaria antibody signature of Maroon villagers and Brazilian miners living in Suriname displayed a high Plasmodium seroprevalence, especially for P. falciparum in villagers, still reflecting the historical malaria burden. The seroprevalence data for both regions and the observed combinations of P. falciparum antibodies provided a valuable dataset from a historically important region to the international malaria serology knowledge. First insight in malaria serology data for Suriname indicated that the use of other target groups and assessment of age-dependent seroprevalence are required to successfully use malaria serology as tool in the national elimination strategy.

BackgroundAt present, malaria cases in Suriname occur predominantly in migrants and people living and/or working in areas with gold mining operations. A molecular survey was performed in Plasmodium falciparum isolates originating from persons from gold mining areas to assess the extent and role of mining areas as reservoirs of malaria resistance in Suriname.MethodsThe status of 14 putative resistance-associated single nucleotide polymorphisms in the pfdhfr, pfcrt, pfmdr1, and pfATP6 genes was assessed for 28 samples from gold miners diagnosed with P. falciparum malaria using polymerase chain reaction amplification and restriction fragment length polymorphism analysis, and the results were compared with earlier data from nonmining villagers.ResultsIsolates from miners showed a high degree of homogeneity, with a fixed pfdhfr Ile51/Asn108, pfmdr1 Phe184/Asp1042/Tyr1246, and pfcrt Thr76 mutant genotype, while an exclusively wild-type genotype was observed for pfmdr1 Asn86 and pfdhfr Ala16, Cys59, and Ile164, and for the pfATP6 positions Leu263/Ala623/Ser769. Small variations were observed for pfmdr1 S1034C. No statistically significant difference could be detected in allele frequencies between mining and nonmining villagers.ConclusionDespite the increased risk of malaria infection in individuals working/living in gold mining areas, we did not detect an increase in mutation frequency at the 14 analyzed single nucleotide polymorphisms. Therefore, mining areas in Suriname cannot yet be considered as reservoirs for malaria resistance.

Please cite this paper as: Adhin et al. (2012) Trends of Influenza infection in Suriname. Influenza and Other Respiratory Viruses DOI: 10.1111/irv.12037.The trends of influenza infection in Suriname were assessed from February 2010 through February 2011. Testing of 393 patients with symptoms of acute respiratory infection (ARI) revealed 15·3% Influenza B and 18·6% could be identified as influenza A positive, consisting of 56% influenza A(H1N1)pdm09 and 44% seasonal A(H3N2). Influenza infection occurred throughout the year, and all three influenza types affected young children as the primary population. The annual incidence of A(H1N1)pdm09 was 6·88 per 100 000 inhabitants [CI] 4·87–9·45. The spread of influenza could neither be linked to tourist flow from the Netherlands nor to contact rates related to school schedules.

Herpes simplex virus (HSV) infection of the corneal stroma is the most prominent cause of scar formation impairing visual acuity and HSV keratitis is the leading cause of corneal opacity throughout the world. Suriname lacked test systems for microbial causes of ocular disease, therefore a polymerase chain reaction-based Herpes virus assay was introduced, enabling prompt recognition, and timely treatment, preventing progressive eye damage. The incidence and epidemiology of Herpes simplex virus type 1 (HSV-1), type 2 (HSV-2), and varicella zoster virus (VZV) in ocular disease in Suriname was assessed. In a cross-sectional prospective study, ocular swabs were collected from 91 patients with a presumptive α-Herpes virus ocular infection attending the Academic Hospital between November 2008 and August 2010 and were tested by a PCR-based α-Herpes virus assay. Alpha-Herpes virus ophthalmic infections were caused predominantly by HSV-1 with a prevalence of 31%. The prevalences of VZV, HSV-2, and a mixed HSV-1/HSV-2 infection were 4%, 3%, and 2%, respectively. The first reported annual incidence of herpetic induced ocular disease in Suriname was estimated at 11.4 per 100,000 person-years (95% CI, 4.8-18.1). No clear age, ethnic or gender dependent difference in incidence was observed. The information obtained on α-Herpes virus positive ocular infections and the distribution of subtypes provided the first insight in the South American situation of α-Herpes virus induced ocular disease.

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