Sarcoptes scabiei nervous system

The Sarcoptes scabiei nervous system is the primary physiological target for pharmacological intervention against scabies, a contagious skin infestation caused by the itch mite (Heukelbach & Feldmeier, 2006). This system comprises various molecular components, including voltage-gated sodium channels, glutamate-gated chloride channels (GluCls), and gamma-aminobutyric acid (GABA) receptors, which coordinate the mite's movement, feeding, and reproduction (Arlian & Morgan, 2017). Therapeutic agents like ivermectin and permethrin exploit physiological differences between the mite and the human host to induce paralysis and death of the parasite (Mounsey et al., 2008). Specifically, ivermectin targets GluCls—which are absent in vertebrates—while permethrin targets sodium channels with higher affinity for the mite's isoforms (Pasay et al., 2008). Resistance to these treatments is an increasing global concern, driven by mutations in these nervous system targets, such as kdr-like mutations in sodium channels (Mounsey et al., 2009). Understanding the molecular architecture of the mite's nervous system is crucial for developing next-generation scabicides to combat resistant strains.

Other names

Scabies mite nervous systemAcarine nervous systemSarcoptes scabiei var. hominis nervous system

Drugs targeting the Sarcoptes scabiei nervous system primarily act by disrupting ion channel function, leading to paralysis and death of the mite. Ivermectin acts as an agonist at glutamate-gated chloride channels (GluCls), causing an influx of chloride ions and hyperpolarization of nerve and muscle cells. Permethrin binds to voltage-gated sodium channels, slowing their inactivation and causing prolonged depolarization. Lindane and other organochlorines inhibit GABA-gated chloride channels, leading to hyperexcitability and seizures in the parasite.