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Objectives: This study explored the health problems of inhabitants of small South Pacific Islands under the influence of climate change, focusing on three communities in the Solomon Islands., Design: Cross-sectional study of the Solomon Islands' populations., Setting: A field survey was conducted in Taro Island, a small, urbanised island with a whole-community relocation plan; Manuopo community of Reef Islands, a small remote island on an atoll environment and Sasamungga, an intermediately urbanised community on a larger island. The Sasamungga community was used for comparison., Participants: Each community's participants were recruited through local health authorities, and 113, 155 and 116 adults (aged 18+ years) from Taro, Manuopo and Sasamungga, respectively, participated voluntarily., Methods: Each participant's body height, weight and body mass index were measured. A drop of blood was sampled for malaria testing; glycated haemoglobin and C reactive protein levels, measured from another drop of blood, were markers for diabetes and inflammation, respectively. The Primary Care Screening Questionnaire for Depression measured depressive mental states., Primary and Secondary Outcome Measures: Regarding health status, the dependent variables-communicable diseases, non-communicable diseases and mental state-and independent variables-differences in communities and socioeconomic status-were measured through health check-ups and interviews of individual participants., Results: Taro Island inhabitants had a higher risk of obesity (OR 1.13, 95% CI 1.02 to 1.27, p=0.0189), and Manuopo inhabitants had a higher risk of depression (1.25, 95% CI 1.08 to 1.44, p=0.0026) than Sasamungga inhabitants. Manuopo inhabitants recognised more serious problems of food security, livelihood, place to live and other aspects of daily living than other communities' inhabitants., Conclusions: The three small island communities' observation identified different health problems: the urbanised community and remote community had a high risk of non-communicable diseases and mental disorders, respectively. These health problems should be monitored continuously during future climate-related changes., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: In Plasmodium falciparum, resistance to chloroquine (CQ) is conferred by a K to T mutation at amino acid position 76 (K76T) in the P. falciparum CQ transporter (PfCRT). To date, at least 15 pfcrt genotypes, which are represented by combinations of five amino acids at positions 72-76, have been described in field isolates from various endemic regions. To identify novel mutant pfcrt genotypes and to reveal the genetic relatedness of pfcrt genotypes, a large-scale survey over a wide geographic area was performed., Methods: Sequences for exon 2 in pfcrt, including known polymorphic sites at amino acid positions 72, 74, 75 and 76, were obtained from 256 P. falciparum isolates collected from eight endemic countries in Asia (Bangladesh, Cambodia, Lao P.D.R., the Philippines and Thailand), Melanesia (Papua New Guinea and Vanuatu) and Africa (Ghana). A haplotype network was constructed based on six microsatellite markers located -29 kb to 24 kb from pfcrt in order to examine the genetic relatedness among mutant pfcrt genotypes., Results: In addition to wild type (CVMNK at positions 72-76), four mutant pfcrt were identified; CVIET, CVIDT, SVMNT and CVMNT (mutated amino acids underlined). Haplotype network revealed that there were only three mutant pfcrt lineages, originating in Indochina, Philippines and Melanesia. Importantly, the Indochina lineage contained two mutant pfcrt genotypes, CVIET (n = 95) and CVIDT (n = 14), indicating that CVIDT shares a common origin with CVIET. Similarly, one major haplotype in the Melanesian lineage contained two pfcrt genotypes; SVMNT (n = 71) and CVMNT (n = 3). In Africa, all mutant pfcrt genotypes were the CVIET of the Indochina lineage, probably resulting from the intercontinental migration of CQ resistance from Southeast Asia., Conclusions: The number of CQ-mutant lineages observed in this study was identical to that found in previous studies. This supports the hypothesis that the emergence of novel CQ resistance is rare. However, in the mutant pfcrt genotypes, amino acid changes at positions 72, 74 and 75 appear to have recently been generated at least several times, producing distinct pfcrt mutant genotypes. The occurrence of new mutations flanking K76T may yield stronger resistance to CQ and/or a higher fitness than the original pfcrt mutant.

Pyrimethamine resistance in Plasmodium falciparum has previously been shown to have emerged once in Southeast Asia, from where it spread to Africa. Pyrimethamine resistance in this parasite is known to be conferred by mutations in the gene encoding dihydrofolate reductase (dhfr). We have analyzed polymorphisms in dhfr as well as microsatellite haplotypes flanking this gene in a total of 285 isolates from different regions of Melanesia (Papua New Guinea, Vanuatu, and the Solomon Islands) and Southeast Asia (Thailand and Cambodia). Nearly all isolates (92%) in Melanesia were shown to carry a dhfr double mutation (CNRNI [underlining indicates the mutation]) at positions 50, 51, 59, 108, and 164, whereas 98% of Southeast Asian isolates were either triple (CIRNI) or quadruple (CIRNL) mutants. Microsatellite analysis revealed two distinct lineages of dhfr double mutants in Melanesia. One lineage had the same microsatellite haplotype as that previously reported for Southeast Asia and Africa, suggesting the spread of this allele to Melanesia from Southeast Asia. The other lineage had a unique, previously undescribed microsatellite haplotype, indicative of the de novo emergence of pyrimethamine resistance in Melanesia.

Tumour necrosis factor-alpha (TNF-alpha) is one of the key cytokines that influence the pathology of microbial infections. The genetic susceptibility to severe forms of falciparum malaria is differentially associated with TNF-alpha promoter gene polymorphisms (TNFP alleles). In a previous study, we identified a TNFP-allele characterized by a C to T transition at position -857 (TNFP-D allele) as a marker for susceptibility to cerebral malaria in Myanmar. The frequencies of TNFP alleles on six islands of Vanuatu, Melanesia (South-west Pacific) were estimated to investigate whether malaria selection pressure on this susceptibility marker has influenced its prevalence. Within the archipelago of Vanuatu there is a decreasing cline of parasite incidence from North to South. Of the four alleles of the TNFP gene detected in Vanuatu, the TNFP-D allele frequencies were inversely correlated with the parasite incidence of islands; TNFP-D varied from 0.55 on the island with the lowest parasite incidence to 0.26 on the island with the highest parasite incidence (r = -0.855, P = 0.03). We also observed a significant correlation between the frequencies of alpha-thalassaemia alleles, thought to protect against malaria and parasite incidence in the same populations. These data are consistent with a previously reported correspondence between the frequencies of glucose 6-phosphate dehydrogenase (G6PD) deficiency and parasite incidences on the islands of Vanuatu (Kaneko et al. 1998) and indicate that the degree of malaria endemicity has influenced the allele frequencies of at least three loci that confer both susceptibility (TNFP-D) and protection (alpha-thalassaemias and G6PD deficiency).