Scabies and Lice: Killing the Parasite on the Skin

The mite: a burrow, an egg, and a sensitising visitor

Scabies is not an infection you catch from the air — it is an animal you catch by contact. The culprit is Sarcoptes scabiei, a mite invisible to the naked eye. A fertilised female is transferred by prolonged skin-to-skin contact — which is why scabies runs through households, sexual partners, and care homes rather than passing on a casual handshake. She burrows into the stratum corneum, the dead outer layer, and tunnels forward a fraction of a millimetre a day, laying eggs behind her. The eggs hatch, the young mature, and the cycle repeats. Crucially, the whole drama plays out in the surface layer of skin — the mite never goes deep. That is exactly why a topical drug that coats the skin can reach and kill every mite; and it is why you must apply it everywhere, not just where it itches.

Why the itch is an allergy, not a bite

Here is the single most important idea in the whole topic. The maddening itch of scabies is not the mite biting you. It is a delayed (type IV) hypersensitivity reaction — the same cell-mediated immunology as the Contact Dermatitis chapter — mounted against the mite, its saliva, its eggs and its faeces left behind in the burrows. This has two consequences students constantly get wrong. First, in a person's very first infestation the itch takes weeks to appear, because the immune system has to become sensitised before it can react — the mites are multiplying silently for a month before the patient feels anything. Second, and clinically vital: because the reaction is against mite debris, not living mites, the itch persists for one to two weeks after successful treatment while the immune system slowly clears the antigen. The mites are dead; the allergy has not yet caught up.

First-line therapy: permethrin and the sodium-channel trap

The workhorse of scabies treatment is a synthetic cousin of a chrysanthemum flower toxin. Permethrin 5% cream is first-line almost everywhere. It is a pyrethroid — a synthetic analogue of the natural pyrethrins from chrysanthemum flowers. Its mechanism is elegant and selective: it binds the arthropod's voltage-gated sodium channels and holds them open. Normally a nerve fires by opening these channels briefly and then closing them; permethrin jams them ajar, so the neuron cannot repolarise and reset. The result is repetitive firing, then paralysis and death of the mite. It is selective for parasites over humans for two reasons — arthropod sodium channels are far more sensitive to pyrethroids than mammalian ones, and human skin rapidly metabolises the drug — which is why permethrin has an excellent safety record and is the preferred agent in children and pregnancy. Apply it to the whole body from the neck down (in infants and the elderly, include the scalp and face), leave it on overnight, wash it off, and repeat after about a week to catch mites that hatched from eggs the first dose missed.

Oral ivermectin: paralysing the parasite from the inside

When scabies is too widespread to smear with cream, when a topical course has failed, or when you must treat an entire institution at once, the answer is a tablet: ivermectin. It works on a channel humans essentially do not have exposed to it. Ivermectin is an agonist at the parasite's glutamate-gated chloride channels, found in invertebrate nerve and muscle. Opening these channels floods the cell with chloride, hyperpolarising it into silence — the parasite is paralysed and dies. Mammals have no glutamate-gated chloride channels in the periphery; the structurally related GABA channels that could be affected sit behind the blood–brain barrier, which ivermectin normally cannot cross. That anatomical firewall is the basis of its wide safety margin. Ivermectin is the same molecule met systemically in the Antiparasitics chapter — where it is the drug that tamed onchocerciasis (river blindness) and lymphatic filariasis — and topically in the Rosacea article, where it is used against Demodex mites. One drug, three very different dermatological and tropical roles.

The principles that actually cure: everyone, everything, at once

A perfectly chosen scabicide fails routinely — because of what happens around the patient, not to them. Treating scabies is as much a public-health task as a pharmacological one, and three principles decide success. First, treat all close contacts simultaneously — the whole household and any sexual partners — even those with no itch yet, because a newly infested contact is silently incubating mites and will re-seed the patient after the sensitisation lag. Treating the index patient alone guarantees a ping-pong re-infestation. Second, decontaminate the environment: mites survive only a couple of days off the body, so bedding, towels and worn clothing are machine-washed hot and dried hot, or sealed in a bag for about 72 hours to let any stragglers die. Third, continue the itch treatment after the mite is dead — the emollients, topical steroid and antihistamine discussed above — so the patient does not mistake the lingering hypersensitivity for treatment failure. Miss any one of these and the cream will be blamed for a failure it did not cause.

Crusted (Norwegian) scabies: the hyper-infested exception

Ordinary scabies is a sparse infestation — a healthy person harbours only ten or twenty mites, kept in check by an immune response that, ironically, is also what causes the itch. Crusted scabies (also called Norwegian scabies) is the terrifying opposite. In someone whose cell-mediated immunity is blunted — advanced HIV, high-dose corticosteroids or other immunosuppression, or frailty — the mites are not contained and multiply into the thousands or millions, building thick, hyperkeratotic, warty crusts teeming with parasites. Two features make it a clinical emergency of sorts. It is intensely contagious — those crusts shed mite-laden scale, causing institutional outbreaks from a single case — and, paradoxically, it may barely itch, because the very immune weakness that permitted the explosion also mutes the hypersensitivity that would normally drive scratching. Treatment escalates accordingly: combined therapy with repeated oral ivermectin plus a topical scabicide (and a keratolytic to break down the crusts so the drug can penetrate), often over weeks. This is the setting where ivermectin's oral reach becomes indispensable.

Lice: the same drugs, and the rise of the physical agents

Three lice, three sites, but one pharmacological story — and a growing resistance problem. Lice are insects that live on us rather than in us. Head lice (Pediculus humanus capitis) infest the scalp — overwhelmingly a childhood affair, spread by head-to-head contact, and no reflection of hygiene. Pubic lice (Phthirus pubis, the "crab" louse) cling to coarse pubic hair and spread through sexual contact, so their discovery warrants a check for other sexually transmitted infections. Body lice (Pediculus humanus corporis) are the exception — they live in the seams of clothing rather than on the skin, are a disease of poverty, overcrowding and displacement, and, unlike the others, can transmit systemic infections such as typhus. For all of them the classic drugs are the familiar insecticides: permethrin and malathion, killing by the same sodium-channel and cholinesterase mechanisms. But head lice have evolved widespread resistance to these neurotoxic insecticides, and this has driven a real shift in practice: physical, occlusive agents such as dimeticone are now often preferred. Dimeticone is a silicone oil that works mechanically — it coats the louse and blocks its breathing spiracles, and disrupts its ability to manage water, so it suffocates or dies of physiological stress. Because there is no biochemical target, there is essentially nothing for the insect to evolve resistance against. Wet-combing — systematically dragging a fine-toothed comb through conditioned wet hair to physically remove lice and eggs — is the effective drug-free alternative, especially useful in the very young and in pregnancy.