Insect Growth Disruptors in the Control of Cochliomyia hominivorax larvae (Diptera, Calliphoridae)
Myiasis; benzoylphenylureas; juvenile hormone analogs, bioassay
In Brazil, Cochliomyia hominivorax is the main causative species of primary myiasis in livestock, companion animals, and humans, highlighting its social and economic relevance to animal and public health. Chemical control remains one of the primary management strategies, and insect growth disruptors (IGDs) represent promising alternatives due to their interference with the insect life cycle. Larvae of C. hominivorax obtained from a laboratory colony (CEUA 8634020223) were used to evaluate susceptibility to different IGDs (diflubenzuron, fluazuron, teflubenzuron, triflumuron, and pyriproxyfen). Toxicological analyses were conducted through stage-specific bioassays for each larval instar, considering the physiological and behavioral characteristics of each phase. LC₅₀ values were estimated using Probit analysis in RStudio software. For first-instar larvae (L1), the compounds were incorporated into the larval diet at concentrations of 0.001; 0.005; 0.01; 0.05; 0.1; 0.5; 1; 25; 50; and 100 µg·mL⁻¹, characterizing a bioassay based on combined ingestion and contact exposure. The experimental design consisted of 12 groups with six replicates and ten larvae per replicate (n = 720), in addition to a control group and a solvent group (16% acetone with two drops of Tween 80). Pupation inhibition and adult emergence inhibition were evaluated. LC₅₀ values for pupation inhibition, in ascending order, were 0.01, 0.07, 0.15, 3.82, and 5.14 µg·mL⁻¹ for diflubenzuron, triflumuron, fluazuron, teflubenzuron, and pyriproxyfen, respectively. For emergence inhibition, LC₅₀ values in ascending order were 0.01, 0.03, 0.05, 0.06, and 0.10 µg·mL⁻¹, corresponding to diflubenzuron, triflumuron, teflubenzuron, pyriproxyfen, and fluazuron. For third-instar larvae (L3), at the pre-pupal stage, bioassays were conducted exclusively as contact tests. Whatman No. 1 filter paper discs were impregnated with 470 µL of the active compound solutions and placed in Petri dishes, in sextuplicate, at concentrations of 5; 10; 25; 50; 75; 100; 150; 250; 500; and 1000 µg·mL⁻¹, with ten larvae per replicate (n = 720). For pyriproxyfen, additional concentrations of 0.01; 0.05; 0.1; and 0.5 µg·mL⁻¹ were also evaluated (n = 1020), along with control and solvent (analytical grade acetone) groups. For emergence inhibition in L3, LC₅₀ values were 924.6 µg·mL⁻¹ for diflubenzuron, 329.5 µg·mL⁻¹ for teflubenzuron, 47.2 µg·mL⁻¹ for triflumuron, and 0.4 µg·mL⁻¹ for pyriproxyfen. LC₅₀ estimation for fluazuron was not possible under the bioassay conditions employed. The integration of both methodologies demonstrates that IGD efficacy depends on both the larval instar and the route of exposure, reinforcing their strategic potential in the integrated management of this species.