British paper written in WW2 about scabies mite lifecycle based on experiments on volunteers.
Experiments on a couple dozen subjects (involving practices such as placing different counts of mites at different life stages on people, and having people use mite-infested bedding) suggests that infestation transmission is primarily through fertilized adult females moving from one person to another -- even moving a bunch of unfertilized mature adults of both sexes from one person to another usually doesn't result in an infestation
The natural mechanisms by which humans fight scabies infestations are as follows:
The faster time-to-reaction to second-time scabies infestations (a day or so to produce a rash in a second infestation vs a month for a primary infestation) contributes to a type of partial immunity to scabies. The experience of getting scabies a second time is still extremely unpleasant. Also, even if the patient is unable to completely kill all the mites on his own (in a first or second infestation), the number of mites goes down a lot (from 15 or so in a full-blown primary case to low single digits) so it's hard for a second-time-infested patient, or someone who's had scabies for several months and has been scratching/has lots of dead skin, to pass on the infestation.
The article also talks about antibodies contributing to partial immunity. I don't really get how antibodies work. The article discusses antibodies as facilitating the itch-rash reaction. It describes antibodies as causign people to develop a rash in response to injected ground up dead mites. Is that how antibodies work against parasites? For viruses and bacteria, antibodies usually mess with the microbes' chemical pathways, right? That'd be equivalent to being poisonous to parasites? Maybe this has something to do with scale? Mites are like 0.3 mm long. Or maybe something like this: inflamed skin that has lots of mite-specific antibodies in it tastes/smells bad to mites?
Scabies is usually transmitted by intimate personal contact.
The young, newly fertilized adult female Sarcoptes is the stage usually responsible for transmission.
Patients with a high parasite rate (over 100 adult female mites) are much more likely to spread scabies than those with few parasites.
The distribution of the parasites in clinical scabies gives no clue to the original sites of infection.
When a volunteer is infected for the first time he gives no reaction for about a month. During this period he may be quite unaware that the parasites are burrowing in his cuticle.
After a month the patient becomes sensitized, itching and other symptoms develop.
In a first infection the mites increase in numbers far less rapidly than is theoretically possible. A parasite rate of about 25 may be reached in 50 days and of up to 500 in 100 days; after this the number of mites decreases rapidly.
The second time an individual has scabies he itches at the sites of infection within 24 hr. His mite population seldom rises to a fraction of the height reached in his first infection.
Reinfection of cured cases is much more difficult than infection for the first time.
Sarcoptes causes antibody function in man. This causes a partial immunity.
The mechanism of immunity is due to three reactions: (a) scratching by the host which removes the parasites mechanically; (b) oedema renders the cuticle unsuitable for colonization and causes the mites to vacate their burrows; (c) scratching produces sepsis which is fatal to Sarcoptes.
The partial immunity obtained may account for fluctuations in the incidence of the disease.