A house fly strain, ALHF, was collected from a poultry farm in Alabama afte
r a control failure with permethrin, and further selected in the laboratory
with permethrin for five generations. The level of resistance to permethri
n in ALHF was increased rapidly front an initial 260-fold to 1,800-fold aft
er selection. Incomplete suppression of permethrin resistance by piperonyl
butoxide (PBO) and S,S,S,-tributylphosphorotrithioate (DEF) reveals that P4
50 monooxygenase- and hydrolase-mediated detoxication, and one or more addi
tional mechanisms are involved in resistance to permethrin. The ALHF strain
showed a great ability to develop resistance or cross-resistance to differ
ent insecticides within and outside the pyrethloid group including some rel
atively new insecticides. Resistance to beta-cypermethrin, cypermethrin, de
ltamethrin, and propoxur (2,400-4,200-, 10,000-, and >290-fold, respectivel
y, compared, with a susceptible strain, aabys) in ALHF house flies was part
ially or mostly suppressed Ly PBO and DEF, indicating that P450 monooxygena
ses and hydrolases are involved in resistance to these insecticides. Partia
l reduction in resistance with PBO and DEF implies that multiresistance mec
hanisms are responsible for resistance. Fifteen- and more than fourfold res
istance and cross-resistance to chlorpyrifos and imidacloprid, respectively
, were not effected Ly PBO or DEF, indicating that P450 monooxygenases and
hydrolases are not involved in resistance to these two insecticides. Forty-
nine-fold cross-resistance to fipronil was mostly suppressed Ly PBO and DEF
, revealing that monooxygenases are a major mechanism of cross-resistance t
o fipronil. Multiresistance mechanisms in the ALHF house fly strain, howeve
r, do not confer cross-resistance to spinosad, a novel insecticide derived
from tie bacterium Saccharopolysora spinosa. Thus, we propose that spinosad
be used as a potential insecticide against house fly pests, especially res
istant flies.