How does benzyl benzoate kill a scabies mite? - briefly
Benzyl benzoate penetrates the mite’s cuticle, disrupting cellular membranes and causing rapid desiccation and death. Its lipophilic properties also interfere with respiratory and nervous functions, leading to paralysis.
How does benzyl benzoate kill a scabies mite? - in detail
Benzyl benzoate acts as a potent topical acaricide through several complementary mechanisms that culminate in rapid mite mortality. Its high lipophilicity enables rapid penetration of the arthropod cuticle, allowing the compound to reach internal tissues within minutes of application. Once inside, the following processes occur:
- Disruption of membrane integrity: the ester interferes with the lipid matrix of the cuticle and cell membranes, causing loss of selective permeability and subsequent desiccation.
- Interference with neural transmission: benzyl benzoate inhibits acetylcholinesterase activity, leading to accumulation of acetylcholine at synaptic junctions, uncontrolled nerve firing, paralysis, and eventual loss of coordinated movement.
- Mitochondrial dysfunction: the compound uncouples oxidative phosphorylation, reducing ATP production and inducing energetic collapse in the mite’s cells.
- Egg lethality: exposure of ova to the agent prevents embryogenesis by impairing chorion formation and halting metabolic processes essential for development.
The combined effect of membrane breakdown, neurotoxic paralysis, and metabolic inhibition produces swift immobilization followed by death of both adult mites and their eggs. Clinical formulations typically contain 25 % benzyl benzoate in a carrier oil, applied to the entire body surface and left in contact for several hours to ensure complete penetration and eradication of the infestation.