BackgroundThe first identified Chikungunya outbreak occurred in Bangladesh in 2008. In late October 2011, a local health official from Dohar Sub-district, Dhaka District, reported an outbreak of undiagnosed fever and joint pain. We investigated the outbreak to confirm the etiology, describe the clinical presentation, and identify associated vectors.MethodologyDuring November 2–21, 2011, we conducted house-to-house surveys to identify suspected cases, defined as any inhabitant of Char Kushai village with fever followed by joint pain in the extremities with onset since August 15, 2011. We collected blood specimens and clinical histories from self-selected suspected cases using a structured questionnaire. Blood samples were tested for IgM antibodies against Chikungunya virus. The village was divided into nine segments and we collected mosquito larvae from water containers in seven randomly selected houses in each segment. We calculated the Breteau index for the village and identified the mosquito species.ResultsThe attack rate was 29% (1105/3840) and 29% of households surveyed had at least one suspected case: 15% had ≥3. The attack rate was 38% (606/1589) in adult women and 25% in adult men (320/1287). Among the 1105 suspected case-patients, 245 self-selected for testing and 80% of those (196/245) had IgM antibodies. In addition to fever and joint pain, 76% (148/196) of confirmed cases had rash and 38%(75/196) had long-lasting joint pain. The village Breteau index was 35 per 100 and 89%(449/504) of hatched mosquitoes were Aedes albopictus.ConclusionThe evidence suggests that this outbreak was due to Chikungunya. The high attack rate suggests that the infection was new to this area, and the increased risk among adult women suggests that risk of transmission may have been higher around households. Chikungunya is an emerging infection in Bangladesh and current surveillance and prevention strategies are insufficient to mount an effective public health response.

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Insect GABA receptors (GABARs) represent important targets for insecticides. Thirteen iminopyridazine GABA analogs were synthesized and evaluated for their antagonism of three cloned insect GABARs. Of the synthesized analogs, 4-[4-cyclobutyl-1,6-dihydro-6-imino-3-(2-naphthyl)pyridazin-1-yl]butyronitrile greatly reduced GABA-activated responses in small brown planthopper (SBP) and common cutworm (CC) GABARs at 100 µM. Removal of the cyclobutyl group did not affect the levels of inhibition in both GABARs, whereas it increased the inhibition levels in housefly (HF) GABARs to afford an analog with an IC 50 of 75.5 µM. 4-[3-(4-Biphenylyl)-1,6-dihydro-6-iminopyridazin-1-yl]butyronitrile and the 3-(2-fluoro-4-biphenylyl) congener exhibited >80% inhibition in SBP and CC GABARs at 100 µM. These analogs showed relatively potent antagonism of HF GABARs, with IC 50 s of 37.9 µM and 42.3 µM, respectively. Ethyl 3-[3-(4-biphenylyl)-1,6-dihydro-6-iminopyridazin-1-yl]propylphosphonate was the most potent inhibitor of GABA-induced currents in HF GABARs, with an IC 50 of 18.8 µM. These findings suggest that the iminopyridazine analogs could be leads for the development of insecticides.

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