How does carbofos act on bedbugs? - briefly
Carbofos, an organophosphate insecticide, inhibits acetylcholinesterase in bedbugs, causing excess acetylcholine, continuous nerve firing, paralysis, and death. The toxin acts quickly after the insects contact or ingest treated surfaces.
How does carbofos act on bedbugs? - in detail
Carbofos is an organophosphate compound that interferes with the nervous system of Cimex lectularius. After contact or ingestion, the insect absorbs the chemical through the cuticle and the digestive tract. The molecule binds to the active site of acetylcholinesterase (AChE), an enzyme responsible for hydrolyzing the neurotransmitter acetylcholine at cholinergic synapses. By phosphorylating the serine residue in the enzyme’s catalytic center, carbofos renders AChE inactive, causing acetylcholine to accumulate in the synaptic cleft.
The excess neurotransmitter continuously stimulates nicotinic and muscarinic receptors, producing uncontrolled nerve impulses. Observable effects include rapid tremor, loss of coordination, hyperexcitation of the ventral nerve cord, paralysis of the leg muscles, and eventual respiratory failure due to loss of control over the tracheal system. Lethal concentrations for bedbugs are typically in the low microgram per insect range; sub‑lethal doses can impair feeding behavior and reduce reproductive output.
Resistance can develop through several mechanisms. Mutations in the AChE gene that reduce binding affinity for organophosphates, up‑regulation of detoxifying enzymes such as cytochrome P450 mono‑oxygenases, and enhanced cuticular thickness all diminish carbofos efficacy. Monitoring for these traits is essential when planning control programs.
Application formats influence the speed and extent of action. Direct spray onto harborages delivers immediate contact toxicity, while impregnated fabrics provide prolonged exposure as insects crawl across treated surfaces. Residual activity depends on formulation stability, ambient temperature, and humidity; higher temperatures accelerate degradation, whereas low humidity slows absorption through the cuticle.
Safety considerations include avoidance of human exposure, as the same AChE inhibition mechanism affects mammals. Personal protective equipment and adherence to label rates minimize risk. Proper disposal of unused product and contaminated materials prevents environmental contamination and non‑target toxicity.