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Characterization of a Sodium Channel Mutation
in Permethrin-Resistant Rhipicephalus sanguineus
(Acari: Ixodidae)
Nicholas S.G. Tucker,
1,2
Phillip E. Kaufman,
1
Emma N. I. Weeks,
1
Jessica Rowland,
3
Jason Tidwell,
4
and Robert J. Miller
4
1
Entomology and Nematology Dept., University of Florida, Gainesville, FL 32611 (nicktu@ufl.edu; pkaufman@ufl.edu;
eniweeks@ufl.edu),
2
Corresponding author, e-mail: nicholas.s.g.tucker@gmail.com,
3
Environmental and Global Heath Dept.,
University of Florida, Gainesville, FL 32611 (jekableka@gmail.com), and
4
Cattle Fever Tick Research Laboratory, U.S. Department
of Agriculture-Agricultural Research Service (USDA-ARS), Edinburg, TX 78541 (jason.tidwell@ars.usda.gov;
Robert.Miller@ARS.USDA.GOV)
Subject Editor: Guiyun Yan
Received 2 December 2016; Editorial decision 1 June 2017
Abstract
The brown dog tick, Rhipicephalus sanguineus (Latrielle) sensu lato, is an important ectoparasite of dogs and
occasionally humans, capable of transmitting several pathogens, such as Rickettsia and Ehrlichia, which are of
veterinary and medical importance. The brown dog tick is distributed worldwide and has an affinity for human
habitations in much of its range. In some populations, lack of integrated pest management plans and overuse
of pyrethroid pesticides and other sodium channel inhibitors has resulted in high levels of resistance to per-
methrin. Recently, a highly conserved region of the R. sanguineus sodium channel was sequenced, indicating
that a single nucleotide polymorphism of thymine to cytosine on domain III segment VI of the sodium channel
could confer resistance. A molecular assay targeting a point mutation in the sodium channel was developed
and optimized to separate ticks expressing permethrin resistance from those from a susceptible colony.
Thereafter, multiple field-collected phenotypically permethrin-resistant populations were evaluated using this
molecular assay to determine genotype. As confirmed by DNA sequencing, a point mutation was present at a
high rate in phenotypically resistant tick populations that was not present in the susceptible strain. These data
suggest an additional permethrin resistance mechanism to metabolic resistance, which has been reported for
this tick species, and confirm its association with phenotypic resistance. The results of this study further empha-
size the need to preserve acaricide chemistry through rotation of active ingredients used to control
ectoparasites.
Key words: brown dog tick, acaricide resistance, point mutation, integrated pest management, target site insensitivity
The brown dog tick, Rhipicephalus sanguineus Latreille sensu lato, is
a three-host tick, but is highly restricted in its preferred host, the do-
mestic dog. It is perhaps this close association that has led the brown
dog tick to be the only tick known to complete its lifecycle indoors,
particularly in temperate climates (Dantas-Torres 2008). This synan-
thropic adaptation has allowed for increased exposure to acaricides
used both in the environment (residence or kennel) and on the canine
host when compared to exophilic tick species. Brown dog ticks spend
greater than 95% of their life span in the environment, and dogs serve
as the primary dispersal mechanism of this species (Dantas-Torres
2010). Thus, exchange of ticks among locations is largely restricted
to dog visitations to common areas, such as veterinary clinics, or
when uninfested dogs visit infested homes or vice versa. This
restricted genetic exchange along with long-lasting or prophylactic
use of acaricides with a similar mode of action provides tremendous
opportunity for selection of pesticide resistant populations. Acaricide
resistance in R. sanguineus has been observed in several North
America populations (Miller et al. 2001; Eiden et al. 2015a, b), and
samples from around the world are currently being tested in the
Veterinary Entomology Laboratory at the University of Florida.
Brown dog ticks are not unique in their expression of pesticide
resistance. Worldwide, over 440 instances of arthropods expressing
resistance to one or more pesticides have been recorded (Roush and
Tabashnik 1990). Physiological pesticide resistance can occur
through metabolic detoxification, reduced cuticular penetration,
and target site insensitivity. A point mutation conferring target site
Vector Control, Pest Management, Resistance, Repellents
Journal of Medical Entomology, 54(6), 2017, 1633–1638
doi: 10.1093/jme/tjx127
Advance Access Publication Date: 13 July 2017
Research article
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