After a distressing episode involving my elderly mother and a nursing home, I've been reading up on scabies. It seems that in healthy people, the immune system limits the mite population to around 10 of the creatures at any one time; elderly and immunocompromised people can be infested by many more - thousands, even millions of mites (shudder).

So my question is, given that the mites burrow in the top, dead, layer of the skin, how does the immune system detect them and suppress them at all? Conversely, if the immune system can limit the mite population so effectively, why doesn't it wipe them out entirely?

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    $\begingroup$ Welcome to Biology.SE! I think this is a very good question and made some edits to clarify it. Please feel free to further edit! $\endgroup$ Commented May 12, 2017 at 11:17
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    $\begingroup$ @Alex Thanks. I have only reverted the 'S' in the question, b/c I believe 'scabies' isn't a plural - same as eg 'measles' $\endgroup$
    – peterG
    Commented May 12, 2017 at 13:02
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    $\begingroup$ Did you do any reaearch, say, into the immunology of susceptibility and resistance to scabies? If so, what did you find? On this site, some attempt to answer the question, even if the research doesn't help, is expected and appreciated. (Btw, I never heard that number. And from the numbers of healthy people I've had to treat for scabies - and having suffered a bad infection myself in early adolescence [an unforgettible experience] - I'd say the immune system is not all that great at suppressing the infection.) $\endgroup$ Commented May 12, 2017 at 18:12
  • $\begingroup$ @anongoodnurse As in my OP, my research consisted of googling 'scabies', the results of which led me to those figures. (eg Wikipedia suggests a number as high as 2 million mites for encrusted scabies.) I don't really have access to anything more specialised, which is why I posed the question on here. $\endgroup$
    – peterG
    Commented May 12, 2017 at 19:13
  • $\begingroup$ while it seems that you're getting answers here, it's likely that SE Medical Sciences is a more appropriate forum for this question. $\endgroup$ Commented Jul 11, 2021 at 19:12

2 Answers 2


Found from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3535073/

In addition to being a physical barrier, the skin is an immunological barrier63. The skin immune response is vital in wounding and infection and also modulates the commensal microbiota that colonizes the skin. Keratinocytes continuously sample the microbiota colonizing the skin surface through pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), mannose receptors and the NOD-like receptors. These receptors recognize pathogen-associated molecular patterns (PAMPs) including flagellin and nucleic acids, as well as lipopolysaccharide from Gram-negative bacteria, mannan and zymosin from fungal cell walls, and peptidoglycan and lipoteichoic acid from Gram-positive bacteria. The activation of keratinocyte PRRs by PAMPs immediately initiates the innate immune response, resulting in the secretion of antimicrobial peptides (AMPs), cytokines and chemokines. Beyond effecting an adaptive immune response, AMPs also directly kill bacteria, fungi and enveloped viruses64. Therefore, there is a constant interplay among keratinocytes, immune cells and microorganisms that is modulated by AMPs, cytokines, chemokines and microbial peptides.

While mites certainly are not fungal, viral, or bacterial, you can extrapolate the mechanisms required to prevent mite infestation being similar to those referenced above. Hope this helps!


This is an excellent question. We mostly hear about parasites being attacked by white blood cells, but mites are obviously too large to be phagocytosed, and furthermore the white blood cells are in the mite's stomach by the time they come into contact with the mite. Yet, mites are usually too small for us to see, so we can't crush them like we crush fleas. I know that aphids are eaten by other insects, but they are macroscopic, and I don't have any macroscopic insects on my skin. At the same time, when people get sick they start to be at risk for mite infestations. Also, sometimes one individual who is asymptomatic will give a mite infection to another individual, through close contact, which then causes a visible immune reaction in the victim: small red bumps indicating the locations of bites. This suggests that the immune system might be involved.

One theory is that we are looking for something like a mobile bacterium, which could live inside human white blood cells. Normally the bacterium would be dormant, but when white blood cells are ingested by a flea or a mite, the bacterium would start reproducing and releasing chemicals to counteract digestion by the parasite. Eventually the bacterium, if clever enough, would release enough chemicals to kill the mite that ingested it. However, mites have short lifespans and therefore evolve much more quickly than humans do. Unless your body can upgrade its defenses at the same pace, it will fall behind and mites will evolve resistance to the bacteria and its chemicals. The bacteria could evolve within the body, but we have no way to measure their fitness until after they are swallowed by the mite. So how could your immune system keep track of which bacteria are still effective against your mites? How does it know which bacteria should multiply and be deployed against future mites, and which ones are no longer useful?

From an information theoretic standpoint, in order for coevolution to occur, there needs to be some way for the bacterium to get back to the original host after living inside the mite. One way to accomplish this is if the bacteria kill mites by crawling up their throats and blocking them. Then when the mites try to feed a second time, some of the bacteria will get regurgitated back into the blood of the host, where it could be scavenged and returned to the lymph nodes for selection and review by the immune system.

Such a bacterium exists. Let's give it an alias: Bacterium X. Bacterium X blocks the throats of many kinds of fleas, as is well known. It can live inside white blood cells, usually being dormant in lymph nodes. Mites are observed to feed poorly on mice that are infected with Bacterium X, although they feed well on healthy mice. Fleas can transmit Bacterium X to new hosts both before and after they become blocked. Blockage in susceptible fleas leads to death by starvation. The bacteria is endemic in rodents worldwide, and normally harmless. However, when a pandemic strain emerges then it can be exceptionally virulent, producing lethal bacteremia in both human and rodent hosts. The Bacterium X disease condition is often characterized by swelling of the lymph nodes where the bacterium resides. Presumably, some of the high infectivity of pathogenic strains of Bacterium X could be due to its role as an endosymbiont, and the immune system's consequent eagerness to scavenge it from the environment so that co-evolution may happen.

The relationship of Bacterium X with mites is not well studied, perhaps partly because mites haven't been observed to transmit it between rodents, as fleas do. But many of X's traits in mites could be expected to generalize from its behavior in fleas; for example, smaller-sized species of flea are more susceptible to blockage, suggesting that mites, which are smaller than fleas, should be even more vulnerable to attack by Bacterium X.

I haven't given the actual name of Bacterium X because I wanted others to have the chance to figure it out. However, it is known that human white blood cells can contain multiple species of bacteria capable of killing fleas, in addition to the particular one I described. For me, an interesting question here is whether these bacteria are doing this on purpose, and if so, how the body keeps them evolving so that it can win the biological arms race against mites. However, I have trouble finding actual discussion of these ideas in the scientific literature. It seems possible that we have a tendency to want to view inter-species interactions as primarily hostile or pathological rather than potentially cooperative. Perhaps there is some other reason why evidences of symbiosis seems to go unremarked-upon, even when they seem fairly apparent: an ability for a bacterium to reproduce inside human and rodent macrophages, for example, or to kill a common insect parasite...

  • $\begingroup$ "mites are usually too small for us to see, so we can't crush them like we crush fleas." Ah, you raise an interesting point - has anyone really tried ? I had scabies once, it was truly horrid and I scratched till I bled, which didn't stop the itching. Problem is that dead mites are just as provocative to the immune system as live ones. But I wonder if you could kill them by skin pressure before they proliferate ? I think they are probably evolved to survive pressure, but who knows ? $\endgroup$ Commented Jun 2, 2020 at 17:57
  • $\begingroup$ @JimmyWiddle Thanks for sharing. Yeah, if mites are anything like fleas ... fleas are almost indestructible. You said "I scratched till I bled" - maybe that is another way to encourage contact between skin parasites and the immune system. Mother always said "don't scratch, that will only make it worse", but I suspected this of being bad advice. $\endgroup$ Commented Jun 3, 2020 at 0:36

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