Toxicity and histopathology of the growth regulator pyriproxyfen to adults and eggs of the cat flea (Siphonaptera:Pulicidae).
Adult cat fleas, Ctenocephalides felis (Bouché), exposed continuously to pyriproxyfen died within 8-10 d. Microscopic examination of 7-d-old adults indicated death was caused by histopathological damage to fat body, Malpighian tubules, midgut epithelia, salivary gland cells, and other internal tissues. Fleas were killed by pyriproxyfen regardless of whether they were held as unfed adults on treated filter paper or as feeding adults on treated dog hair. In addition to these toxic effects on adults, pyriproxyfen also induced formation of large autophagic vacuoles in maturing oocytes leading to partial reabsorption of yolk, degeneration of the nucleus, and lysis of the follicular epithelium. Consequently, most of the eggs laid by treated fleas lacked a nucleus, had a poorly formed chorion, and were ruptured during ovulation. These laboratory results suggest that continuous exposure of fleas to pyriproxyfen on a host animal could prevent deposition of viable eggs and eventually kill adults, thereby controlling all stages of flea development.[1]References
- Toxicity and histopathology of the growth regulator pyriproxyfen to adults and eggs of the cat flea (Siphonaptera:Pulicidae). Meola, R., Pullen, S., Meola, S. J. Med. Entomol. (1996) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
