The Effect of Socioeconomic Factors and Indoor Residual Spraying on Malaria in Mangaluru, India: A Case-Control Study.

India faces 0.5 million malaria cases annually, including half of all malaria cases worldwide. This case-control study assessed socioeconomic determinants of urban malaria in coastal Mangaluru, Karnataka, southwestern India.

MiRNA-146a Polymorphism Was Not Associated with Malaria in Southern India.

Micro-RNAs (miRNAs) play a crucial role in immune regulation, and a common miRNA-146a polymorphism (rs2910164) increased the odds of falciparum malaria in pregnant African women. Here, we examined whether this association holds true in a different population, that is, 449 mainly male and adult malaria patients and 666 community controls in southwestern India. malaria (67%) predominated over falciparum malaria (11%) and mixed species infections (22%).

Duffy antigen receptor for chemokines gene polymorphisms and malaria in Mangaluru, India.

Background: Duffy blood group antigens serve as receptors for Plasmodium vivax invasion into erythrocytes, and they are determined by polymorphisms of the Duffy antigen receptor for chemokines (DARC), also known as Fy glycoprotein (FY). Duffy negativity, i.e.

Characterization of Polymorphisms in Isolates from Mangaluru, India.

India accounts for approximately half of the global cases, but information as to the presence of chloroquine (CQ) resistance is scarce. In an observational study in Mangaluru, south-western India, of 116 vivax malaria patients analyzed, 89.5% (102/114) had cleared parasitemia on days two or three of CQ treatment.

Molecular Evidence for Resistance to Sulfadoxine-Pyrimethamine but Absence of Mutations in Mangaluru, Southwestern India.

In most of India, sulfadoxine-pyrimethamine (SP) artesunate serves as first-line treatment for uncomplicated falciparum malaria. In 112 clinical isolates from Mangaluru, southwestern India, we sequenced molecular markers associated with resistance to SP, lumefantrine, and artemisinin (, , , and ). The double mutation 59R-108N combined with the 437G mutation occurred in 39.