Abstract
ABSTRACT.Dracunculus medinensis, also known as the African Guinea worm, is the causative agent of dracunculiasis and the focus of the global Guinea Worm Eradication Program (GWEP). Transmission of D. medinensis to humans occurs primarily by drinking water containing cyclopoid copepods infected with third-stage D. medinensis larvae. A common intervention to interrupt transmission and decrease the number of copepods in infected water bodies is the application of the organophosphate larvicide Abate® (temephos). However, the use of alternative compounds to help decrease copepod populations would be beneficial to the GWEP. We compared the immobilization of copepods by three compounds: Abate, Natular® (spinosad), and diflubenzuron. Our results confirm that neither diflubenzuron nor Natular immobilized copepods as quickly or as effectively as Abate. However, doubling or tripling the suggested concentration of Natular resulted in immobilization rates similar to Abate over 72 hours of continuous exposure. Further research on the possible effects of higher concentrations of Natular on the environment and nontarget organisms is necessary to determine whether this compound can be used safely to control the copepod population.
Highlights
Dracunculiasis (Guinea worm disease) is a neglected tropical disease that historically caused significant morbidity in people living in previously endemic communities
This disease is caused by infection with the parasitic nematode, Dracunculus medinensis,[1,2,3,4] which is transmitted to definitive hosts when cyclopoid copepod intermediate hosts infected with third-stage guinea worm larvae (L3s) are ingested from contaminated drinking water.[2,4]
Abate was introduced as a mosquito larvicide, but is effective for controlling D. medinensis transmission because of its high toxicity to copepods and low toxicity to mammals when used in small doses at application sites.[7,8]
Summary
Dracunculiasis (Guinea worm disease) is a neglected tropical disease that historically caused significant morbidity in people living in previously endemic communities. This disease is caused by infection with the parasitic nematode, Dracunculus medinensis,[1,2,3,4] which is transmitted to definitive hosts when cyclopoid copepod intermediate hosts infected with third-stage guinea worm larvae (L3s) are ingested from contaminated drinking water.[2,4] The global Guinea Worm Eradication Program (GWEP), started by the CDC in 1980 and led by The Carter Center since 1986, has been extremely successful in reducing the number of human cases by . Abate was introduced as a mosquito larvicide, but is effective for controlling D. medinensis transmission because of its high toxicity to copepods and low toxicity to mammals when used in small doses at application sites.[7,8] Abate inhibits cholinesterase production and after 12 hours of exposure at the field approved application rate of 1 mg/L, cholinesterase levels in copepods begin to reduce and they lose their ability to feed and swim normally.[7]
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