c Asymptomatic infection by Plasmodium falciparum is an important obstacle to eliminating malaria. Asymptomatic carriers do not seek treatment for infection, and therefore they become a reservoir for the parasite. For this reason, these carriers pose a real public health risk. The systematic identification and treatment of asymptomatic infections should reduce the parasite reservoir. A large reduction in this pool will lower the chance of transmission of the disease. In this study, we screened a tribal population of 1,040 individuals in the Purulia district of West Bengal by using a dual-antigen rapid diagnostic kit (RDK), microscopy, and species-specific PCR. All positive individuals were treated with artemisinin-based combination therapy (ACT) (artesunate plus sulfadoxine-pyrimethamine) and followed for 42 days. Polymorphisms in candidate genes were screened by DNA sequencing. A significant proportion (8.4%) of the study population was infected with P. falciparum but showed no clinical manifestations. The PCR method was more sensitive in detecting infection than the RDK or microscopy. The efficacy of the ACT was 97%. In the pfcrt gene, the mutation K76T (the mutated amino acid is indicated by bold type) was found in 100% of the cases. In the pfmdr1 gene, the mutations N86Y and Y184F were noted in 55.5% and 11% of the cases, respectively. Six different haplotypes were identified in the pfdhfr-pfdhps genes. Most importantly, the quintuple mutant A 16 I 51 R 59 N 108 I 164 -S 436 G 437 E 540 A 581 A 613 was found in 10% of the isolates, which is potentially important for the development of sulfadoxine-pyrimethamine resistance. A significant proportion of the study population harboring P. falciparum does not seek treatment and therefore serves as a reservoir for the parasite, maintaining the natural cycle. If the National Vector Borne Disease Control Programme (NVBDCP) of India is to eliminate malaria, then this hidden parasite burden needs to be addressed properly. Similar study in other parts of the country could help to determine the magnitude of the problem.

bPlasmodium vivax malaria, though benign, has now become a matter of concern due to recent reports of life-threatening severity and development of parasite resistance to different antimalarial drugs. The magnitude of the problem is still undetermined. The present study was undertaken to determine the in vivo efficacy of chloroquine (CQ) and chloroquine plus primaquine in P. vivax malaria in Kolkata and polymorphisms in the pvmdr1 and pvcrt-o genes. A total of 250 patients with P. vivax monoinfection were recruited and randomized into two groups, A and B; treated with chloroquine and chloroquine plus primaquine, respectively; and followed up for 42 days according to the WHO protocol of 2009. Data were analyzed using per-protocol analyses. T he burden of malaria caused by Plasmodium vivax has been greatly underappreciated in terms of both its clinical spectrum and incidence of disease (1, 2). P. vivax is the most widely distributed cause of malaria in the world; approximately 2.6 billion people are at risk, and 10 countries, including India, are at the highest risk of infection (3,4,5,6).P. vivax infections have been associated with mild symptoms, such as fever, headache, fatigue, chills, and musculoskeletal pain, and, in particular, paroxysms. Recently, however, severe complications, including renal failure, jaundice, acute respiratory distress syndrome, cerebral malaria, seizures, anemia, hyperparasitemia, thrombocytopenia, pulmonary edema, splenic rupture, and death, have been reported in exclusive association with P. vivax (7,8). The situation is further complicated by the emergence of resistance of the parasite to chloroquine (CQ).In most of the world, CQ remains the first-line treatment for patients with vivax malaria. In India, CQ was replaced by artemisinin combination therapy (ACT), a combination of artesunate and sulfadoxine-pyrimethamine, in 2010 for Plasmodium falciparum malaria, but for P. vivax malaria, CQ remains the first-line agent, along with primaquine (PQ) (0.25-mg/kg base) for 14 days under supervision or by detecting the glucose-6-phosphate dehydrogenase (G6PD) level. The first case of P. vivax resistance to CQ was reported in 1989 from Papua New Guinea (9). A higher rate of CQ-resistant P. vivax malaria, which exceeded 50%, was reported from different regions of Indonesia (10,11,12,13,14). Further sporadic cases were subsequently observed in the Philippines, Myanmar, Vietnam, Colombia, Guyana, and Turkey (15). Similar reports are also available from Madagascar (16) and Ethiopia (17). Despite these reports, it remains difficult to estimate the worldwide prevalence of P. vivax resistance to CQ. In India, the first case of CQ-resistant P. vivax malaria was reported from Assam in 1995 (18) and then in Mumbai (19) and Gujarat (20).The molecular mechanisms underlying CQ resistance in P. vivax malaria remain unknown and may involve multigenic loci, but two genes orthologous to the pfmdr1 and pfcrt genes that encode putative transporters, pvmdr1 (21) and pvcrt-o (22), have been suspected as possi...

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