Pyrethroid resistance mechanisms in the head louse Pediculus capitis from Israel: implications for control

Citation
J. Hemingway et al., Pyrethroid resistance mechanisms in the head louse Pediculus capitis from Israel: implications for control, MED VET ENT, 13(1), 1999, pp. 89-96
Citations number
28
Categorie Soggetti
Entomology/Pest Control
Journal title
MEDICAL AND VETERINARY ENTOMOLOGY
ISSN journal
0269283X → ACNP
Volume
13
Issue
1
Year of publication
1999
Pages
89 - 96
Database
ISI
SICI code
0269-283X(199902)13:1<89:PRMITH>2.0.ZU;2-T
Abstract
In Israel, the head louse, Pediculus capitis, developed resistance to DDT t hrough the extensive use of this insecticide until the 1980s. In 1991, perm ethrin was introduced for control of DDT resistant P. capitis in Israel, le ading to control failure of this pyrethroid insecticide by 1994. Pyrethroid resistance of P, capitis in Israel extends to phenothrin, which has not be en used for louse control. We identified a glutathione S-transferase(GST)-b ased mechanism of DDT resistance in the Israeli head lice. This GST mechani sm occurred before 1989, while permethrin resistance in P. capitis develope d after 1994, suggesting that the main GST resistance mechanism selected by DDT use does not confer any pyrethroid cross-resistance. Esterase activity levels were equivalent in pyrethroid resistant and susceptible P. capitis field-collected in Israel, and in a susceptible strain of P.humanus, the bo dy louse, indicating no involvement of any esterase-based mechanism in resi stance. A weak monooxygenase-based permethrin metabolism resistance mechani sm was the only factor identified which could account for any of the observ ed pyrethroid resistance in P. capitis. However, the lack of synergism of p henothrin resistance by piperonyl butoxide suggests that a non-oxidative me chanism is also present in the resistant lice. Therefore it seems probable that pyrethroid resistance in Israeli P. capitis is due to a combination of nerve insensitivity (knockdown resistance or 'kdr') and monooxygenase resi stance mechanisms.