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Title: MODE OF ACTION OF LUFENURON ON CUTICLE OF LARVAL CAT FLEAS, CTENOCEPHALIDESFELIS (BOUCHE) (SIPHONAPTERA:PULICIDAE)

Author
item DEAN, SUSAN - TEXAS A&M UNIVERSITY
item MEOLA, ROGER - TEXAS A&M UNIVERSITY
item Meola, Shirlee
item SITTERTZ-BHATKAR, HELGA - TEXAS A&M UNIVERSITY
item SCHENKER, RUFOLF - CIBA-GEIGY LTD.

Submitted to: Journal of Medical Entomology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/18/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary: Blood-sucking insects that attack farm animals and domestic pets are very serious problems. In most cases, the use of appropriate pesticides is the most effective way to control these parasites. One of the most effective pesticides for use in flea control is a compound known as lufenuron. Animals can be safely fed low doses of lufenuron and it is taken up by the blood stream and then kills fleas as they suck the treated animal's blood. We have done studies that better define how lufenuron actually affects the fleas and have shown that fleas which have fed on lufenuron-treated animals lay eggs that do not hatch as well as those of normal fleas. Also, the flea larvae that do hatch out of eggs from lufenuron-treated fleas tend to die shortly after hatching because their outside skin (the cuticle) does not form properly. These studies are important because they describe how an important pesticide works to kill a blood-sucking insect. The information obtained will also be useful in ongoing efforts to develop eve more effective and safer chemicals to control insect parasites that attack livestock and other domestic animals.

Technical Abstract: When adult cat fleas, Ctenocephalides felis, were fed lufenuron in blood at concentrations of 0.5, 0.25, or 0.125 ppm, egg hatch was 4, 15 or 64%, respectively. In contrast, percent hatch of eggs from adults fed lufenuron at concentrations of 0.025, 0.08, or 0.125 ppm did not differ significantly from the control. However, many larvae from the 0.08 ppm group and higher concentrations died during the first instar. Microscopic examination of these larvae revealed that they died from desiccation caused by bleeding from tears in the cuticle or the inability to complete the molt to the next instar. Electron micrographs showed that lufenuron often disrupted formation of new endocuticle resulting in the deposition of an amorphous mass of randomly oriented chitin microfibrils. Other larvae formed normal endocuticle but were unable to digest the old cuticle or produce new endocuticle during apolysis. Failure of the larva to form endocuticle was ultimately caused by degeneration of the epidermal cells and a reduction i the number of cytoplasmic organelles which inhibited chitin synthesis.