How does flea medication work? - briefly
«Flea medication» contains adulticides—often neonicotinoids or pyrethrins—that disrupt the flea’s nervous system, causing swift death, and may add insect‑growth regulators that block egg and larval development. The compounds distribute across the pet’s skin and coat, reaching parasites through direct contact and ingestion during grooming.
How does flea medication work? - in detail
Flea control products fall into two principal categories: compounds that kill adult insects and agents that interrupt the life cycle. Adulticidal chemicals act on the nervous system, causing rapid paralysis and death. Common neurotoxins include:
- pyrethroids, which bind to voltage‑gated sodium channels and maintain them in an open state, leading to uncontrolled nerve firing;
- neonicotinoids, which stimulate nicotinic acetylcholine receptors, producing overstimulation and eventual collapse;
- organophosphates and carbamates, which inhibit acetylcholinesterase, resulting in accumulation of acetylcholine and continuous nerve impulse transmission.
Insect growth regulators (IGRs) target immature stages. They mimic or block hormones essential for metamorphosis, preventing larvae from developing into viable adults. Typical IGRs such as methoprene and pyriproxyfen interfere with the synthesis of juvenile hormone, causing malformed or non‑viable offspring.
Delivery systems ensure the active ingredient reaches the host and the parasite. Topical spot‑on formulations spread across the skin’s lipid layer, providing a reservoir that contacts fleas during grooming. Oral tablets distribute systemically through the bloodstream; when a flea feeds, it ingests the drug, resulting in internal exposure. Collars release low‑dose vapors over weeks, maintaining a protective zone. Sprays and powders apply directly to the animal’s coat for immediate contact.
Pharmacokinetic properties influence efficacy. After application, the compound penetrates the epidermis, enters the circulatory system, and distributes to sebaceous glands or blood plasma. Metabolic breakdown in the liver and excretion via urine or feces determine the duration of activity. Formulations with long‑acting carriers, such as polymeric matrices, extend the therapeutic window.
Resistance development arises from repeated exposure to a single mode of action. Rotating products with different active ingredients or combining adulticides with IGRs reduces selection pressure on flea populations, preserving effectiveness. Continuous monitoring of field efficacy guides adjustments in treatment protocols.