william a. donahue, jr., ph.d. sumiko de la vega sierra research laboratories, modesto, ca nebraska...
TRANSCRIPT
Bed Bug Resistance to Insecticides
William A. Donahue, Jr., Ph.D.Sumiko De La Vega
Sierra Research Laboratories, Modesto, CA
Nebraska Urban Pest Management ConferenceFebruary 12-13, 2013
RESISTANCE
The ability of a significant portion of a pest population to survive a pesticide at rates that once killed most individuals of that population.
A genetic change in response to selection.
A natural process controlled by genetics and expressed in specific biochemical processes.
TYPES OF RESISTANCE
Metabolic – changes in detoxification (enzyme) system within the arthropod.
Target Site Insensitivity - receptors
Reduced Penetration - arthropod cuticle or plant surfaces (leaves)
Behavioral - avoidance
REASONS FOR RESISTANCE
High Intensity Cropping Systems – Agriculture
Food Production Animal Operations Disease Vector Control Programs Urban Pest Control Programs Commodity Treatments
Routine pest control relying primarily on chemical control, often a single pesticide or class of pesticides.
Insecticide ResistanceBed Bugs
1930’s – 40’s: DDT insecticide of choice 1952-1956 DDT resistance wide spread 1950’s: Malathion insecticide of choice 1960-2000: Low incidence of bed bugs world
wide 1990’s: Pyrethroids insecticides of choice
Why Does Resistance Develop?
Resistance is quick to develop to compounds with high effective kill, long residual and are highly selective at a single biochemical target site.
Why? High Selection Pressure within the Population!
Introduction Resistance – The genetically acquired ability of an
organism to survive a pesticide application at doses that once killed most individuals of the same species.
Baseline dose response Field-collection and colony start-up
Diff. rates of reproduction, length of time until obtaining usable numbers
Objectives
Evaluate the insecticide susceptibility of specific populations of bed bugs Compare dose response bioassays of selected
populations Establish discriminating dose bioassays
The SRL Strains Tested “Harlan/Ft. Dix” – susceptible laboratory strain in colony since
1973, obtained 2008 “Earl” –pyrethroid-susceptible field strain, collected in Modesto,
Stanislaus County, CA, 2007 “Cincinnati” –field strain, collected in Cincinnati, Hamilton
County, OH, 2007, pyrethroid- resistant upon initial testing “James” – pyrethroid-susceptible field strain collected in
Modesto, Stanislaus County, CA, 2009 “Jersey” – moderately pyrethroid-resistant field strain collected
in Jersey City, Hudson County, NJ, 2010 “Wolverine” –moderately pyrethroid-resistant field strain
collected in Modesto, Stanislaus County, CA, 2010 “Stockton 2” – highly pyrethroid-resistant field strain collected in
Stockton, San Joaquin County, CA, 2011
© Sierra Research Laboratories, 2012 © Sierra Research Laboratories, 2012
LD and Discriminating Dose LT Tests
© Sierra Research Laboratories, 2010
Formulated Permethrin LD evaluations – in 2008, 2010, and 2012
Permethrin technical – 0.05% Deltamethrin technical – 0.05% Imidacloprid technical – 0.05% Propoxur technical – 0.5%
LD and LT Evaluations – Materials and Methods
1 mL test substance applied inside a wax outline of a 10 cm circle on a glass panel
10 bed bugs per replicate, mixed sex ratio, confined with a 100 x 15 mm Petri dish lid
Mortality: 5, 15, 30, 45, 60 min, 2, 4, 6, and 24, 48, 72, 96, and 120 hr.
Initial Permethrin Dose Response Test, 2008
•Harlan strain• 100% mortality at 24 hours at all rates -
0.0005%, 0.005%, 0.05%, and 0.5%
•Cincinnati strain• Maximum % mortality was 20.0% at the
0.5% rate (approximately 10x label rate!)
0.01% 0.05% 0.50%0.0%
20.0%
40.0%
60.0%
80.0%
100.0%
Cincinnati
Linear (Cincinnati)
Harlan
Linear (Har-lan)
Earl
Linear (Earl )
James
Linear (James)
Wolverine
Linear (Wolverine)
Permethrin Concentration
Linear Regression of the Mortality of Laboratory and Field Strains of Cimex lectularius 24 Hours After Initial Exposure to Selected
Concentrations of Permethrin, 2010
Avg
. % M
orta
lity
Permethrin Dose Response Test – Establishing Baselines For New Field Strains and Re-evaluating Existing
Strains, 2010
Permethrin Lethal Time Tests Repeated Over a Span of Two Years
Against “Earl” susceptible field strain
5 min 15 min
30 min
1 hr 2 hr 4 hr 6 hr 24 hr0
0.1
0.2
0.3
0.4
0.5
0.6
0.7
0.8
0.9
1
Mortality of Earl Strain Bed Bugs Exposed to 0.05% Permethrin on Glass Panels
Permethrin formulation 27-Jul-10Permethrin technical 17-Jan-12Permethrin formulation 6-Mar-12
Avg %
Mort
ality
5 min 15 min
30 min
1 hr 2 hr 4 hr 6 hr 24 hr0.0%
10.0%
20.0%
30.0%
40.0%
50.0%
60.0%
70.0%
80.0%
90.0%
100.0%
Mortality of Cincinnati Strain Bed Bugs Exposed to 0.05% Permethrin on Glass
Panels
Permethrin technical 5-Jun-08Permethrin formulation 27-Jul-10Permethrin technical 17-Jan-12Permethrin formulation 6-Mar-12
Avg %
Mort
ality
Permethrin Lethal Time Tests Repeated Over a Span of Four Years Against “Cincinnati” Resistant Field Strain
Permethrin Technical – 0.05%
5 min 15 min 30 min 45 min 1 hr 2 hr 4 hr 24 hr 48 hr 72 hr 96 hr 120 hr0.0
20.0
40.0
60.0
80.0
100.0
Mortality of Bed Bugs Exposed to Glass Panels Treated With 0.05% Technical Permethrin, 2012
Harlan
Earl
Cincinnati
James
Jersey
Wolverine
Stockton 2
UTC
Avg %
Mort
ality
Deltamethrin Technical – 0.05%
5 min 15 min 30 min 45 min 1 hr 2 hr 4 hr 24 hr 48 hr 72 hr 96 hr 120 hr0.0
20.0
40.0
60.0
80.0
100.0
Mortality of Bed Bugs Exposed to Glass Panels Treated With 0.05% Technical Deltamethrin,
2012
Harlan
Earl
Cincinnati
James
Jersey
Wolverine
Stockton 2
UTC
Avg %
Mort
ality
Imidacloprid Technical – 0.05%
5 min 15 min 30 min 45 min 1 hr 2 hr 4 hr 24 hr 48 hr 72 hr 96 hr 120 hr0.0
20.0
40.0
60.0
80.0
100.0
Knockdown and >24 Hour Mortality of Bed Bugs Exposed to Glass Panels Treated With 0.05%
Technical Imidacloprid , 2012
Harlan
Earl
Cincinnati
James
Jersey
Wolverine
Stockton 2
UTC
Avg %
Mort
ality
Propoxur Technical – 0.5%
5 min 15 min 30 min 45 min 1 hr 2 hr 4 hr 24 hr 48 hr 72 hr 96 hr 120 hr0.0
20.0
40.0
60.0
80.0
100.0
Knockdown and >24 Hour Mortality of Bed Bugs Exposed to Glass Panels Treated With 0.5%
Technical Propoxur, 2012
Harlan
Earl
Cincinnati
James
Jersey
Wolverine
Stockton 2
UTC
Avg %
Mort
ality
How Can We Slow Down Resistance?
Resistance is slow to develop with inefficient, short residual compounds because selection pressure is low!
Select compounds that interfere with multiple biochemical or physiological systems.
Mixtures like Botanical Insecticides, Synergists, IGR’s
Refugia – A source of susceptible individuals (genetic) within a population – Don’t Kill ‘em All!
Integrated Pest Management – Ecology in Action!
Conclusion
Discriminating dose – important in evaluating a newly-collected field strain or assisting PMPs in selecting treatments
Full Dose Response – difficult to run on new populations
Genetic shifts in populations associated with resistance – need to re-evaluate colonies over time