ABSTRACT
Head lice, Pediculis capitis De Geer, populations were investigated for permethrin and malathion resistance after initial establishment of a discriminating dose of topical application bioassay with body lice, Pediculus humanus L. For both insecticides, approximately 2 times the lethal dose (LD)95 at 4 h was selected, 2 ng of permethrin and 100 ng of malathion per head louse, respectively. Head lice were collected from heads of infested children in Denmark at 33 primary schools, one kindergarten, and seven boarding schools. The lice were collected by combing of dry hair, with a fine-toothed antilouse comb attached to a vacuum cleaner. A resistance survey covers head lice collected from 208 of 1,441 persons combed. The frequency of permethrin- and malathion-resistant head lice is high in Danish head lice populations. In 17 of 24 samples tested for permethrin resistance, all head lice survived the discriminating dose. Six samples had between 3 and 25% dead head lice, whereas one sample had 60% mortality. In nine of 25 samples tested for malathion resistance, all head lice survived the discriminating dose. Seven samples had <25% dead head lice, and four samples had a mortality of 50% or more at the discriminating dose. The connection between permethrin resistance and kdr-like mutations is confirmed by our findings. The frequency of the double mutation T929I-L932 F in the voltage-sensitive sodium channel gene associated with permethrin resistance was 0.95 in Danish head lice populations.
Subject(s)
Insecticide Resistance , Malathion , Pediculus , Permethrin , Adolescent , Adult , Animals , Child , Child, Preschool , Denmark , Humans , Insecticide Resistance/genetics , Lice Infestations/drug therapy , Malathion/administration & dosage , Mutation , Pediculus/genetics , Permethrin/administration & dosage , Sodium Channels/geneticsABSTRACT
The toxicity of fipronil to insecticide-susceptible houseflies and the cross-resistance potential of fipronil were determined for six insecticide-resistant laboratory housefly strains by topical application and feeding bioassay. The insecticide-resistant strains represented different levels and patterns of resistance to pyrethroids, organophosphates, carbamates and organochlorines. Five strains were almost susceptible to fipronil in feeding bioassay with resistance factors at LC50 between 0.36 and 3.0. Four of these strains were almost susceptible to topically applied fipronil (resistance factors at LD50 were 0.55, 0.83, 3.3 and 2.5, respectively), whereas one strain was 13-fold resistant to topically applied fipronil. A highly gamma-HCH-resistant strain, 17e, was 430-fold resistant to fipronil in topical application bioassay and 23-fold resistant in feeding bioassay at LD50/LC50. We also tested the toxicity of fipronil in a feeding bioassay and gamma-HCH in topical application bioassay on thirteen housefly field populations. Eleven of the field populations had resistance factors for fipronil ranging from 0.98 to 2.4 at LC50, whereas two populations were 4.0- and 4.6-fold resistant to fipronil. The resistance level to gamma-HCH at LD50 in the field populations ranged from 1.8- to 8.1-fold. The two strains showing fipronil resistance were 3.4- and 8.1-fold resistant to gamma-HCH. Fipronil and gamma-HCH toxicities were positively correlated in the field populations. Biochemical assays of esterase, glutathione S-transferase and cytochrome P450 monooxygenase indicated that the low fipronil resistance observed in laboratory and field strains could be caused by elevated detoxification or be due to a target-site resistance mechanism with cross-resistance to gamma-HCH.
