Connecting the Dots: Causes Behind Mysterious Bites, Sensations of Bites, and Skin Disturbances 1

— This article by Jerry Cates was first published on 2 January 2017 and last revised on 15 August 2018. © Bugsinthenews Vol. 19:01(01).

General Anatomy of Human Skin (Source: Note that the skin consists of three major layers: (1) the thin outer layer or epidermis, composed of five strata of skin cells that protect the body from microbial contamination and desiccation; followed by (2) the thicker middle layer, or dermis, that contains hair follicles and the muscles that control their movement, the sebaceous and sweat glands, the blood and lymph vessels, and the nerve endings that sense pain, touch, cold and heat; and finally, (3) the thickest layer underlying the other two, or hypodermis, which is composed mostly of fat cells.

Skin Lesions from Stealth Bites, Witnessed Bites, and Non-Bites…

Lots of different organisms bite humans, and much of the time their bites produce lesions on our skin. Sometimes the bites are witnessed, sometimes not. Most flea bites, and many bites caused by other organisms, are immediately felt at the time the bite event takes place. A flea bite, for example, is usually felt and the offending flea is usually seen where it is biting the skin. Later, when the bite wound itches, turns red, and produces a raised wheal, the bitten person normally remembers what caused the wound.

By comparison, many other organisms bite stealthily. The saliva and other secretions associated with the biting apparatus of bed bugs, some mosquitoes, certain mites, and a host of other bloodsucking organisms include anesthetics that numb the bite wound so the nerves in the host’s skin cannot signal an alarm. Only later, when an itchy bump surfaces, does one become aware that the earlier bite event occurred. At that point, the first thought that comes to most minds is “What bit me?

The natural association between skin lesions and biting events is imprinted on our minds early in life, and is reinforced by a string of life experiences that accumulate as we pass from infancy into adulthood. Most adults presume that any lesion found on their skin whose cause is not immediately obvious resulted from a “bite.” When such lesions occur, and we believe we’ve been bitten by something, we usually take steps to identify the offending organism. If the lesions grow more numerous, and begin showing up on parts of our bodies that others can see, worry is accompanied by shame and embarrassment, which makes us redouble our efforts to catch and exterminate the source of our predicament.

Typical Skin Surface, Elderly Male: Upper Wrist. Source: EntomoBiotics Inc. Archives.

Skin Lesions sans Bites…

Most of the time, if our skin lesions are caused by biting organisms, we do not have to search long to find the culprit. Sometimes, however, even the most diligent of searches, conducted over lengthy periods of time, fails to uncover the cause.

When this happens at least two possibilities exist: either the cause is a biting organism adept at hiding its presence, or the skin lesions are not bites at all. Skin lesions can result from immune reactions to foreign materials. Others can be produced by chemical changes within our bodies. Of course, a wide range of combinations of all these causes — biting organisms, immune reactions, irritants, and a changing endocrine system — can also be present at the same time.

It is healthy to shrug off minor, isolated, and infrequent skin lesions that do not persist, or that do not directly impact one’s life. Transitory bumps, sores, and rashes are the natural result of living in a diverse ecosystem. But, when multiple skin wounds of unknown cause suddenly show up on a person’s body, worry can turn to outright concern, even for those with high thresholds of pain. That concern usually leads the affected person on a diligent, even obsessive, search for the cause behind it. Aiding such individuals in conducting a worthwhile search for answers is the object of this article. We begin by considering a few of the usual cause and effect relationships.

Precipitating Events and Chronic Skin Disturbances…

So, although skin lesions are felt as a three-dimensional phenomena, the fourth dimension — time — plays important roles that are easily overlooked. Complications, when dealing with chronic skin disturbances, can arise from several sources. Some of these potential sources may involve biting organisms; others involve biological or mechanical irritants; still others are confined to issues within the body of the affected individual. When one considers the bewildering combinations of these possibilities that can act together, it is no wonder that we sometimes find it difficult to know the exact cause that produces an individual’s acute and chronic skin disturbances.

Typical Underbed Detritus. magnified 400x. This material consists mostly of synthetic and natural textile fibers, but includes microscopic dust particles of plastic, metallic, and wood chips. Source: EntomoBiotics Inc. Archives.

Once worrisome skin lesions are discovered, the sufferer’s immediate reaction impacts the feel and appearance of those lesions later. Applying salves, lotions, emollients, and sprays advertised to soothe, reduce, or cure skin eruptions, infections, rashes, and irritations can cause more skin problems than they solve. Sometimes those resulting problems take on a life of their own, producing skin issues that have nothing to do with the original lesions, but which the sufferer may think come from the same cause.

Similarly, when certain chemicals and pesticides — even those derived from natural, organic plant-based botanical sources — are applied, misted, or sprayed in a home, workplace, or recreation setting to ameliorate, mitigate, or prevent real or suspected infestations of biting organisms, the chemicals and pesticides themselves can lead to skin problems in persons who live, work, or play there.

Mysterious Bites, Sensations of Bites, and Skin Disturbances

This article is about bites, sensations of bites, and skin disturbances affecting humans for which no immediately discernible cause is evident. They are mysterious because no definite cause is at hand, or because — despite suspicions about the possible or likely cause — scientific evidence is lacking.

The focus of this article is three-fold:

First, we will examine those mysterious bites that occur with regularity, but for which no clear cause is obvious.

Next, we will discuss mysterious skin lesions that often accompany such bites or that occur by themselves, again with regularity, without the accompanying sensation of a bite, but for which — again — no definite cause can be identified.

Finally, we will broaden the scope of inquiry into the causes of such mysterious lesions and sensations, including a wide range of inorganic ones. We are led to do this because, although most of those who suffer from these mysterious events automatically presume the cause to be a biting organism of some kind, in a number of important cases organisms that bite, parasitize, or otherwise harm our bodies are not involved.

Keep in mind that this article is in a state of constant evolution. It is somewhat distressing to me that, as I read it through and make changes and additions from time to time, the flow is not as coherent as it “should” be. There is a reason for that. We are dealing with a complex topic here, one with multiple dimensions that are not easily examined in an objective, clinical manner. Faced with the choice of either publishing this material in rudimentary form right away, or waiting months or years until I could feel fully comfortable with the way it is presented and organized, I chose the former. The reader’s comments, criticisms, and recommendations are eagerly solicited…

Life’s Natural, Usually Invisible Detritus…

Often, in each of the broad categories of skin-related mysteries described above, a number of tantalizing possible causes are evident. These mostly include previously unnoticed white, brown, red or black specks, or minuscule fuzzy objects that appear as eggs or biological larvae to the naked eye.

This natural detritus, though always present but not usually noticed, is what the person suffering from mysterious bites and skin lesions finds after diligently searching for a cause. It is tantalizing because it offers hope that proof of a definite cause is readily at hand.

Yet a microscopic analysis, using a good microscope that provides a crisp, well-focused image of the material under investigation, quickly reveals that collections of this naturally occurring detritus are composed of nothing more than skin flakes, plastic chips, fragments of insect or arachnid body parts, and compact clumps of textile fibers. It might be said that nothing good can come from conducting a thorough, microscopic examination of the places where you live, work, and play. Why? Because you will undoubtably find a whole host of tiny stuff that you may easily, and often mistakenly, come to believe is making you miserable.

A bird mite collected from a bathroom fixture in a nursing facility in Round Rock, Texas. The fixture was positioned directly beneath a vent whose exhaust tube was clogged with nesting materials deposited by birds over the previous ten to fifteen years. Mites migrated from the nest to the ventilator cover. When the fan was turned on the assembled mites were blown down, onto whomever was sitting on the commode. Source: EntomoBiotics Inc. archives.

The fact is, being inundated with microscopic detritus, shed by us and other humans, our pets, clothing, furniture, even our electrical and electronic gadgetry, is and has been a fact of life, not only in the modern world, but since time began. The average human sheds many ounces of skin flakes every year, and those skin flakes get distributed throughout all the places where we and other humans live, work, and play.

Carpeting, furniture, clothing, and other sources of textile fibers produce an equal amount of lint that floats in the air and coats exposed surfaces inside our homes. Microscopic plastic and metallic chips left over from the manufacture of our electronic and electrical gadgets also contribute to the detritus that gets scattered throughout the places in which we live, play, and work. When only that and nothing that might be termed “the usual biological suspects” is detected in the course of a thorough microscopic analysis of the detritus collected in such places, the sufferer doesn’t know what to think.

The Usual Biological Suspects

Springtail (Seira bipunctata). Collected in a residence in northwest Austin, Texas. Springtails are sub-microscopic, and some species are coated with microscopic scales that irritate the skin of susceptible individuals. Source: EntomoBiotics Inc. archives.

When the cause of a bite or skin lesion is not immediately obvious, the list of possibilities that comes to mind, or that is revealed in the process of an Internet search, is deceptively short. Bed bugs and mites top the list, followed by fleas, lice, kissing bugs, mosquitoes, no-see-ums, thrips, springtails, spiders, and irritating hairs shed by carpet beetle larvae.

Mature bed bug, from a home in Pflugerville, Texas. Source: EntomoBiotics Inc. archives.

But that’s not the full story. Mites, for example, are represented by a long list of acarid families, genera, and species with remarkably different habits. Tiny springtails are a common inhabitant of many of the ecosystems humans occupy; species diversity is enormous, and though some springtail species possess morphological features such as scales that may irritate human skin, many do not. Though many investigators doubt that springtails are legitimate sources of dermatological lesions, Altschuler (2004) reported finding springtails and fragments of them in skin scrapings from 18 of 20 individuals reporting symptoms of stinging/biting and/or crawling, who had previously diagnosed with delusory parasitosis.

Despite the daunting complexity, however, all of these suspects have one thing in common. A careful investigation by an experienced investigator practically always results in identifying either the causal organism or the presence of conditions conducive to the presence of specific causal organisms that are the most likely culprits.

A rodent mite, one of several species collected from the floor of an Austin, Texas residence, that had migrated from an abandoned rat’s nest underneath the home. The resident was being bitten by the mites, whose bites produced angry red wheals on his skin that could have been misdiagnosed as bed bug bites. Source: EntomoBiotics Inc. archives.

Such investigations are difficult to carry out, and amateurish attempts to do so often lead sufferers astray. Cheap microscopes that produce blurry images, for example, easily turn plain plastic chips and skin flakes into “tiny animals with legs.”

Triatomid kissing bug. Collected at a rural home near Copeland, Texas. These bugs were hiding in the baseboards of the home’s master bedroom, and coming out at night to suck blood from the husband and wife who slept there. Source: EntomoBiotics Inc. archives.

It is not unusual for a client show me a slightly out-of-focus object that, under the client’s personal microscope or magnifying glass, seems to have eight hairy legs.

Yet, when I take that same object, place it on the stage of the laboratory-grade microscope I brought to the client’s location, and bring it into sharp focus, the legs disappear and the object is exposed as an inert piece of detritus.

Professional Forensic Inspections…

A proper investigation into the causes of a sufferer’s symptoms includes inspecting the premises where the person or persons suffering bites or skin lesions lives, works, or plays. It also involves documenting, step-by-step, the events leading to the start of the bites or skin lesions. The investigator must be trained and experienced in entomology, acarology, and arachnology, and equipped with appropriate, laboratory-grade instruments and collection accessories.

Carpet beetle larva (approx. 2mm long) collected from a home in south Austin. Texas. The robust hairs (spicasetae) do not cause irritation, but microscopic hairs (hastisetae, shown in figs. 506 & 507) concentrated at the larva’s posterior and scattered on its body can be highly irritating to susceptible individuals. Source: EntomoBiotics Inc. archives.

Further, the investigator must have high-quality dissecting instruments, uncontaminated specimen collection vials, microscope slides and fixing media, and the accessories related to them, close at hand.

Assembling such materials and maintaining them, and acquiring the necessary training and experience in their use and in the art of forensic investigation, is time-consuming and expensive. For that reason, such investigations cannot be carried out at little or no cost, but must come with a price.

Microscopic hastisetae from the larva of a carpet beetle collected in Lakeway, Texas. The spearpoint tips of the hairs easily get caught in the interstitial spaces between skin cells, then progress deeper into the skin with time. The barbed shafts of the hairs are arranged like tiny umbrellas, such that they point away from the hair tip. Because of this, as the hairs sink deeper into the skin, the tiny umbrella-like structures are forced open, contaminating the wound path with any debris they contain. Since, in those with intact immune systems, infectious pathogens would immediately be attacked and neutralized, contact with hastisetae and their contaminants rarely leads to the production of noticeable lesions or even minor irritation. Stressed individuals, however, with compromised immune systems, are unable to mount the immediate immune response needed to  prevent pathogens from proliferating, though secondary immune responses usually nullify them before long. Thus, small, localized infections often are experienced by such individuals, and may produce skin lesions mimicking bed bug bites. Most individuals who are affected by carpet beetle hastisetae are undergoing unusual levels of stress. Source: EntomoBiotics Inc. archives.

For the sufferer, though, that price is well worth it, provided objectivity is brought to the fore. Finding out what is and is not causing their bites and skin lesions is a crucial first step toward bringing them to a halt. Ineffectually guessing about the cause, and experimenting with an endless stream of worthless remedies in the process, ends up costing many times more in the long run. Furthermore, instead of helping, such ineffectual guessing does nothing to ease the suffer’s misery, and often only makes it worse.

The author has published a separate article entitled “What’s Biting You?” that describes the usual biological suspects in some detail. Please refer to that paper for detailed information on those organisms.

Carpet beetle hastisetae and spicasetae. Note the hastisetae can be quite long, while the more robust spicasetae, which do not irritate the skin, are shorter and have projecting structures that make it difficult to penetrate and progress deep into human skin. The photographs in figs. 506 and 507 were taken through a digital microscope, at the EntomoBiotics Lab, that magnified the hastisetae 750-1000x. Source: EntomoBiotics Inc. archives.

When Forensic Investigations Fail to Detect a Cause…

Forensic inspections alone don’t always succeed in finding a cause. The investigator is not acting as a medical professional and therefore is, by definition, searching for an indirect cause that is external to the sufferer. When a direct cause is involved, one internal to the sufferer, the inspection fails.

As mentioned earlier, this article is about causes behind mysterious bites, sensations of bites, and lesions that even well-conducted forensic investigations often cannot easily detect. Dealing with a witnessed bite, an event caused by an organism that is observed in an act that leads to a skin lesion or another human malady, and with any of the “usual biological suspects” that a forensic investigation detects, is generally uncomplicated.

Not only do doctors and nurses know how to treat such bites and lesions, but experienced pest management personnel use similar information to devise rational extermination, mitigation, and prevention programs that stop the biting and skin disturbances emanating from them.

But what happens when the cause cannot be identified even after a supposedly thorough investigation has been carried out?

Diagram of the Epidermis (Source:, showing the five strata of cells that make up the outer skin. Note that this diagram is an elucidation of the uppermost layer of the three layers comprising human skin as previously diagrammed in Fig. 1. The uppermost layer of the stratum corneum, shown here as the dark, thin layer at the top of the diagram, is the outer skin. It is this layer that is constantly shed as we live our lives. The average human sheds their outermost layer of epidermis at the rate of 0.001 – 0.003 ounces of skin flakes every hour, roughly 0.024 – 0.072 ounces per day, or 9-27oz/year, which translates to 0.55 – 1.6 pounds of dead skin per year, per person. 

If the bites soon stop and the skin lesions go away quickly, nothing happens. Life goes on, and the bites or the skin lesions are forgotten. Most of us experience a multitude of such “road-bump” events throughout our lives. We roll with the punches, brush ourselves off, and continue undaunted down the path of life on which we presently tread.

On the other hand, what if the bites continue, the skin lesions worsen, and/or more skin lesions develop? Then the sufferer’s life is turned upside down as he or she is subjected to an on-going, arduous, frustrating experience that for most is costly, harrowing, emotionally draining, and physiologically damaging.

The author is often brought in to investigate such cases, usually after months or years have passed since the bites and/or skin lesions commenced. Sometimes the sufferer has been informed by physicians and others in authority that their problem is purely psychological. In other cases they have concluded, have been told by trusted acquaintances, or have found what appears to be authoritative information on the Internet that their suffering is caused by new classes of organisms that scientists don’t yet know about.

Blood Brain Barrier. Source: Stolp HB, Liddelow SA, Sá-Pereira I, Dziegielewska KM and Saunders NR (2013) Immune responses at brain barriers and implications for brain development and neurological function in later life. Front. Integr. Neurosci. 7:61. doi: 10.3389/fnint.2013.00061. Four main interfaces separate the central nervous system and the periphery. (1) the blood-brain barrier proper; (2) the blood-CSF barrier; (3) the outer CSF-brain barrier and the level of the pia arachnoid; and (4) the inner CSF-brain barrier, present only in early development (not present in the adult).

Though it is folly to absolutely rule out the existence of new classes of organisms we have yet to discover, it is just as foolish to ascribe to such organisms the suffering caused by bites and skin lesions of unknown etiology. The fact is, a multitude of possible and likely causes of such suffering is known. Many of those transcend simple interactions between the sufferer and the environment. Even if the cause is not purely psychological, it can be caused, and exacerbated, by unexpected and misinterpreted interactions between a number of natural anatomical structures within the sufferer’s body. The author describes those structures and their interactions later in this article.

Sadly, many of these sufferings could have been brought to a halt early on, had the sufferer and the sufferer’s advisors understood the underlying cause or causes involved. Some, however, are not amenable to the simple resolutions that surround the identification and eradication of limited, specific causes. Multiple causations that interact to present a confusing picture are often involved. In a few of these cases, the cause actually is one or more live biological organisms that previous investigations overlooked. In others, though live biological organisms are implicated, it is not they but the remnants they leave behind after molting or dying, that become problematic. In yet other cases, even though live or remnants of dead organisms may have been involved at the onset, those causes had been resolved earlier, but the continuation of the sufferer’s problems results strictly from the remedies the sufferer or his/her advisors employ in a misguided campaign to bring the bites and lesions to a halt.

Delusory Parasitosis (DP) and Ekbom Syndrome (ES)…

Norepinephrine (from Greek roots meaning “at or alongside the kidneys”): an organic chemical in the catecholamine family, functioning as a hormone and neurotransmitter in the brain and body.

Beyond causes stemming from interactions with actual organisms of one kind or another, in some cases the sufferer is delusional. Such sufferers are victims of what researchers like Nancy Hinkle, PhD, refer to as Delusory Parasitosis. Originally known as “Delusions of Parasitosis,” the term was shortened to its present form by W. G. Waldron in 1962, and is today often described simply by the initials “DP” or by the medical definition known as Ekbom Syndrome (ES). Hinkle has more recently (2010) published a paper on “Ekbom Syndrome: The Challenge of ‘Invisible Bug’ Infestations.


Here we will refer to this malady as DP/ES, but the reader is cautioned against drawing hasty conclusions from what is presented. It is important to point out, before exploring this topic in more detail, that diagnosing DP/ES is a difficult process, and this article is not intended as a guide to such diagnoses. As Hinkle points out, the medical community considers the incidence of DP/ES to be somewhat rare, yet pest control personnel and entomologists encounter clients suffering from what they (including, from all indications, researchers like Nancy Hinkle) assume to be cases of DP/ES on a regular basis. The implication of this disparity is that many suspected cases of DP/ES are misdiagnosed. This author’s own investigatory work bears that out.

Wolfgang Trabert (1995) estimated that at the time he was conducting research on DP/ES there were about 25,000 DP/ES sufferers in the United States. Considering that the U.S. population in 1995 stood at 262,764,948, the incidence rate estimated by Trabert was in the neighborhood of 95 individuals out of every 1 million. Thus, assuming that figure still holds, we could surmise that in a metropolitan area the size of Austin, Texas (calculated as including  Bastrop, Caldwell, Hays, Travis, and Williamson Counties, with a combined total population in 2013 estimated at 2,000,860), we would expect to find — at least in 2013 — about 190 DP/ES sufferers. For one reason or another, many of those with DP/ES will not seek treatment or other forms of professional remediation for their condition. If as many as 10% do, the number of such individuals encountered by pest management personnel would be close to 20.

This author has met a number of individuals who — to one degree or another — fit the mold of the DP/ES sufferer. Some have all the symptoms, but others present with only one or a few. For those with the least number of signs of DP/ES, rational intervention and a sympathetic, informed approach often works wonders, but an unsympathetic, impatient investigator who cannot or will not comprehend what the sufferer is going through, and who is unable to explain to the sufferer how their symptoms may point away from parasitic causes, can do more harm than good.

DP/ES and Recreational Drug Abuse


Many recreational drugs have been known to produce DP/ES in those who abuse them. Methamphetamine, in particular, is known to be associated with the condition. Significant research has been conducted into the association between methamphetamine abuse and DP/ES over the past four decades, to the point that, today, physiologists have a relatively well-developed understanding of the etiology and progression of the associative relationship between them. That relationship, and similar ones that result in outright psychoses, has figured significantly in world history.


Famous cases of amphetamine addiction and less than sane behavior include Nazi Germany’s Adolf Hitler. That tragic figure was a vegetarian tee-totaler who, besides shunning alcohol, refused to drink coffee because of its supposed toxic nature, and was said to not even touch women. Despite this long list of what he considered to be rational, ethically-based restrictions on some of the most significant facets of his life, Hitler had himself injected, almost daily, with methamphetamine by his personal physician, Dr. Theodor Morell. The injections began as early as 1942, and continued afterward until his death in 1945.

Germany has, historically, nurtured more than its share of pharmacologists. In the early decades of the last century that nation was not just a leading exporter of opiates, including morphine and cocaine, but held a near-worldwide monopoly on the drugs. In 1937 methamphetamine-hydrochloride, later manufactured in pill form and branded and marketed as Pervitin, was patented by Dr. Fritz Hauschild, the head chemist at Temmler Werke GmbH, Berlin. Factory workers were recommended to take Pervetin, in pill and confectionary forms (e.g., Hildebrand chocolates), throughout the day as a means staying awake and getting more work done. College students, doctors, and others seeking to shed the shackles of normal life — “shackles” such as sleep, which today is regarded as a prerequisite to maintaining one’s physiological and psychological health — happily accepted that methamphetamine would give them superhuman stamina and concentration. Soon even the German military “recognized” the “value” of methamphetamine as a means of attenuating anxiety, increasing concentration, and maintaining courage in battle.

The German experiment with methamphetamine during WW-II proved that it does all those things, but only for a time. Then it turns on its users and makes their lives a living hell.


Methamphetamine does one thing well, and a bunch of other things badly: it is unusually capable of passing through the blood-brain barrier where it induces an increase in norephenephrine and serotonin levels in the brain. Thus it elevates mood, making the user euphoric, but at a high cost. Unlike amphetamine, it is neurotoxic, and at high doses induces psychosis, seizures and brain hemorrhages.

Amphetamine has one methyl group, and is known as methylated phenylethylamine. Methamphetamine, with two methyl groups, is known as double methylated phenylethylamine. Methyl groups reduce the polarity of a molecule, and the more methyl groups, the less polar a molecule is the more hydrophobic and lipophilic it becomes. Amphetamine, with one methyl group, is somewhat lipophilic, and is able to slowly permeate the blood-brain barrier; methamphetamine, with two methyl groups, is highly lipophilic, and crosses the blood-brain barrier quickly.


Once inside the brain, methamphetamine retains its molecular structure much longer than amphetamine, producing euphoric effects with a duration several times that of the latter. Then, when it is metabolized, it first is stripped of its extra methyl group, and turns into amphetamine. The user, in the extended euphoric state that methamphetamine induces, can stay awake up to seven or more days at a time. But sleep is necessary for the brain to retain its hold on reality, and it should come as no surprise that methamphetamine abusers often begin to experience hallucinations in which they sense bugs crawling on their skin.

Earlier, above, we briefly touched upon the postulated, but unlikely, existence of organisms science has yet to discover. What about chemicals that mimic neurotransmitters in the brain, chemicals that exist only for short periods of time but are able, in that short time, to produce the sensation of crawling bugs, on the skin? We have only touched the surface of understanding where brain chemistry is concerned in this regard…

The Curious Case of J. R. Traver…

Perhaps the most storied of alleged DP/ES victims was J. R. Traver, a zoologist at the University of Massachusetts, Amherst. In 1951 Traver published a treatise on her research into a mite, which she identified taxonomically as Dermatophagoides scheremetewskyi Bogdanov (sometimes, as in Traver’s treatise, Bogdanov is spelled Bogdanow, but because most references use the former spelling it shall be used here), that she claimed had been infesting her body for the past 17 years.

And thereby hangs a tale…

A tale that, in fact, presented scientists of the day with a perplexing question of monumental import. For most, the answer to that question is now fully settled: Traver was, pure and simple, a victim of DP/ES. To a small number of others, however, DP/ES is either not a full answer, or is no answer at all. This investigator confesses to be caught between these two extremes. To explain why, it is first necessary to provide some important background information.

The genus Dermatophagoides is, as biological genera go, a poorly known genus of cosmopolitan pyroglyphid (i.e, that cause eczema, a rash — pyro = fire — on the skin) house dust mites that live in human habitations. Dust mites feed on organic detritus. They are particularly fond of flakes of shed human skin, and because the average human sheds from 0.5-1.75 grams of skin daily (0.4-1.41 pounds of shed skin annually), occupied human dwellings provide considerable nutriment for them. They flourish in the stable environment of human-occupied homes and, though they perform a service by scavenging spent human skin, they are considered pests because of their causal relationship with asthma and allergies.

This causal relationship stems from the potent digestive chemicals in the house mite’s intestinal tract. These chemicals consist of specialized protease enzymes that enable the mites to break down the proteins composing the human skin flakes they ingest. Inasmuch as they persist in the mite’s feces and contaminate its exoskeleton, these enzymes, when inhaled with ordinary dust particles, naturally begin to break down the proteins composing the mucosa and other cellular structures of the respiratory tracts of the inhaler. As the inhaler’s respiratory tract come under attack, an immune response ensues that produces allergic reactions, including excessive production of mucus, a flooding of the affected area with excessive blood and lymph flows, and others.

The European house dust mite (Dermatophagoides pteronyssinus) and the American house dust mite (Dermatophagoides farinae) are two different species, but are not necessarily confined to Europe or North America. A third species, Euroglyphus maynei, is also widely distributed. Unlike scabies mites or skin follicle mites, none of the species in the genus Dermatophagoides, or in the genus Euroglyphus, is known to burrow under the skin or to thrive within the human body. Thus these house mites have never been confirmed, from a scientific point of view, as parasitic, though Traver claimed that a species in the genus Dermatophagoides parasitized her body and the bodies of two of her close relatives.

The species Traver described, Dermatophagoides scheremetewskyi Bogdanov, is rarely mentioned in today’s scientific literature. It was first reported in 1864 by Bogdanov, in a paper in which he also first described the genus Dermatophagoides. The species D. scheremetewskyi is mentioned cryptically in a number of scattered scientific papers published worldwide since Traver published her treatise and, according to the Global Biodiversity Information Facility (GBIF), it is today considered to be a valid species. However, a number of investigators, including Matthew J. Colloff’ in his 2009 treatise “Dust Mites,” infer the strong possibility that it is synonymous with D. pteronyssinus. In the 1975 edition (and in the 1978 revision) of Walter Ebeling’s authoritative handbook on urban entomology, D. scheremetewskyi was reported as a legitimate pest of humans:

“The problem of the person really having pests is, of course, generally much easier to solve than the problem of the person who has no pests but believes he has. An example of how obscure a real pest problem can be is illustrated by a report by J. R. Traver (1951) on an infestation of mites, Dermatophagoides scheremetewskyi Bogdanov, on her own person, resulting in itching red papules on scalp, eyes, ears, nostrils, shoulders, under the arms, beneath the breasts, on the chest, both upper and lower back, and occasionally around the umbilicus. Other members of her family were likewise infested. The ailment was initially diagnosed by a physician as ”psychoneurotic.” Fortunately, the victim was a zoologist, had access to a microscope, and found the causative agent. Many attempted treatments failed to eradicate the infestation. However, attacks by the implicated mite species are extremely rare.” Source: Ebeling, Walter, 1975. Urban Entomology. University of California, Riverside.

J. R. Traver died in 1974, having never succeeded in curing or ameliorating the self-identified infestation of these mites with which she claimed to be afflicted. Traver’s 1951 treatise has been the subject of numerous studies, positive and negative, including one that was particularly negative, published in 2011 by Matan Shelomi, entitled “Mad Scientist: The Unique Case of a Published Delusion.” Shelomi’s paper builds a case for retraction of Traver’s 1951 treatise based on the generally accepted conclusion that, in Shelomi’s own words, Traver’s “conclusions may be based on data that was unconsciously fabricated by the author’s mind. The paper may merit retraction on the grounds of error or even scientific misconduct ‘by reason of insanity,’ but such a retraction raises the issue of discrimination against the mentally ill.” Note, however, that even Shelomi could not state with certainty that Traver was the victim of a self-induced hoax.

Was Traver suffering from DP/ES? To this author the jury is still out, though the weight of the evidence available today is heavy in favor of that diagnosis. The author has nothing but the highest regard for Nancy Hinkle, and finds her research, which seems to suggest that Traver was such a victim, to be persuasive. Still, some doubt remains, scant though it may be. Both of Hinkle’s papers on DP/ES, which are linked to above, are highly recommended reading by anyone who is suffering from bites and skin lesions of unknown etiology, as well as by physicians treating such individuals, and by pest management professionals who are servicing the homes, places of work and recreation used by such individuals.

It is instructive to acknowledge the difficulties we in America face, today, when attempting to pursue a genuinely objective investigation of Traver’s condition. One impediment is the fact that, when she first concluded she was infested by the dust mite she identified, air conditioning was not available in most homes. For that reason, dust mites were much more prevalent then than now. Dust mites require a relative humidity above 65-70% to thrive, and in most modern air conditioned homes the relative humidity falls considerably below that figure all year long. For that reason, dust mites of all species are, in modern American homes, a rarity today.

The questionable treatise by J. R. Traver, also linked to above, may be instructive for yet another reason: if, as Hinkle, Shelomi, and a host of others authoritatively assert, Traver was suffering from DP/ES, her treatise provides insight into the mind of the DP/ES sufferer. Traver was highly educated. She was also capable of articulating her ironclad convictions so persuasively to physicians, entomologists, and others in academia and the medical community, that few of those she sought out for help could or would diagnose her condition as anything other than that which she, herself, had concluded it to be.

However — and, to this author, this is the most crucial point of all — besides her condition itself, Traver also describes in great detail the methods, procedures, and medications (including a list of clearly dangerous pesticides and drugs known to produce secondary physiological and neurological conditions) that she used to treat that condition. Whether her condition commenced with an infestation by the cited mite, or from the emanations of a troubled mind, those descriptions provide strong evidence pointing away from biological causes for the continuation of her skin conditions. Instead they point toward a variety of possible non-biological causes for them, DP/ES being but one of several.

Objectivity: Avoiding Confirmation Bias…

Charles Dickens illustrated confirmation bias in his novel, David Copperfield, in the person of the fictional character Uriah Heep. Heep, one of the main antagonists in the novel, made frequent references to his own ‘umbleness, and displayed what has been described aptly as a cloying humility. He was demonstrably insincere, attentive and obedient to the point of servility, and today his name is synonymous with being a sycophant (a bootlicker who flatters powerful people to secure their approval). The above ink and wash drawing was made by the British illustrator Fred Barnard, in the 1870’s. It is now in the public domain, in its country of origin and in other countries and areas where the copyright term is the author’s life plus 100 years or less.

This author discovered the power of the written word while very young, and as a child read with great interest how, in times past, scientists of antiquity were reviled for thinking and proposing ideas contrary to the accepted norm. Galileo was one of those, and he suffered greatly for his heretical views, views that later were found scientifically correct.

In every age new ideas that go against the grain are treated much as were those of Galileo, and today is no different. Centuries from now scientists of the future will look back on the “scholarly” work we have done and smirk with contempt. We know so little. But like those who came before, we delude ourselves into thinking we have most of “it” figured out. Yes, delusions do not discriminate, but afflict even the best among us (including even you and me), and the chief instrument of our delusory state is what is known as confirmation bias.

Confirmation bias describes the tendency to search for, interpret, favor, and recall information in a way that confirms one’s preexisting beliefs or hypotheses. Rather than weigh all the evidence equally (which would be the objective thing to do), we give disproportionately less consideration to alternative possibilities. Those suffering from confirmation bias are generally unconscious practitioners of systematic errors of inductive reasoning, and the malady is not limited to a few but is widespread in today’s culture, just as it was widespread in the cultures of history. For example, people display this bias when they collect or remember information selectively, or when they interpret that information in a biased way.

The effect is more pronounced when emotionally charged issues and deeply entrenched beliefs are involved, and is particularly evident when interpretations of ambiguous evidence — which, from an objective standpoint, should be examined with a jaundiced eye — are introduced without caveat in support of existing positions. Examples include situations in which attitudes become polarized, so that disagreements become more extreme even though the different parties are exposed to the same evidence. Beliefs can persevere even after the evidence for them is shown to be false. It is common for investigators to irrationally assign a greater relevance to information that is encountered early in the research project, and less relevance to that encountered later. Analysts are strangely prone to perceive associations between two events or situations when, on objective analysis, no such association exists.

Experiments in the 1960s confirmed the tendency, within even the most hallowed halls of academia, to conduct research in a way that confirmed existing beliefs and norms. It is folly to ignore this clear and well-documented tendency to test ideas in a one-sided way that focuses on a singular possibility while ignoring the alternatives, yet it is deceptively easy to fall into that trap. We are speaking here of the curious way the human mind works, and how what may appear to be firm conclusions are strongly, though often unconsciously, biased by preconceptions.

The reasons why this happens are varied, but perhaps the most important stems from the tendency for researchers to give more weight to the societal costs of being “wrong,” i.e., being thought as such, whether in actuality or not, than to the objective costs of investigating in a neutral, scientific way and, in the process, possibly producing results contrary to those being obtained by others, particularly others held in high esteem. In other words, nobody wants to be embarrassed within their scientific community, and the easiest way to avoid embarrassment is to go along with prevailing opinions, even if one has to spin the data under examination in the process.

What is not factored in, of course, is the cost that confirmation biases incur on the pace of scientific progress. Some beliefs are so closely held as to make their holders refuse to consider alternatives. Such attitudes contribute to overconfidence, leading even otherwise serious scientists to maintain or strengthen those beliefs despite being confronted with a mountain of contrary evidence.

This explains why the author is reluctant to arrive at firm conclusions on anything that remains yet in question, even if the questions appear to be on shaky ground. Hinkle rightly points out, in both her papers cited above, that even when many of the signs and symptoms of DP/ES are present, there may be genuine non-psychological causes involved. She then goes on to say that, even when psychological issues impinge, they may not be the only issues, nor the most important ones. It is incumbent on the investigator to conduct a thorough and objective analysis of every case. Unfortunately, such analyses are time-consuming and require the use of expensive investigatory instruments, and few field entomologists, and even fewer pest managers are sufficiently equipped, have the time required, or even the inclination needed, to invest in such projects.

Why Bites and Skin Lesions are so Discomfiting…

The mere sensation of a “bite,” even if the sensation is brief and slight and the immediate cause of the sensation cannot be discerned, is naturally upsetting to most sentient human beings. Similarly, discovering a disturbed area on the skin, especially upon awakening from sleep or on removing an article of clothing, is alarming.

We typically react to such experiences with varying degrees of emotion, trepidation, and genuine concern. We do so because past experiences and our grasp of the wealth of scientific knowledge at our fingertips tells us the “bite” we felt or the disturbed area on our skin we’ve found is likely not the end of it.

Oh, maybe we’ll go for days without another “bite.” Maybe the bump, wheal, or rash we’ve found will disappear within minutes, or hours, or a few days without leading to something worse. Or maybe not. There may be more to come. Maybe a lot more. And, yes, some of the possibilities are, to say the least, ugly.

We typically interpret a “bite” to mean that we have been attacked by a foreign organism. We know that most environments are loaded with a broad range of biters of one kind or another. We also know, from experience or from perusing the media du jour, that most of those biters are fitted with a minuscule but gruesome apparatus capable of injecting bad stuff into our bodies.

Really bad stuff…

How bad? Well, stuff like venom, viruses, bacteria, and parasites. Some of that bad stuff can, in fact, kill people. Others can produce virulent diseases that can lead to an early grave, and chronic ones lasting a long, tortuous lifetime. Between those extremes and “nothing to worry about” lies a huge gulf, and even when near the “nothing to worry about” side, practically all that bad stuff still makes life less pleasant. Therefore, one naturally reasons, it would be foolish not to recognize the risks that come with bites and skin disturbances.

The Human Skin and How It Recognizes Pressure, Touch, Heat, Cold, and Pain…

The largest internal organ in the human body is the liver (unless one views largeness in terms of surface area rather than volume, and considers the gastrointestinal tract to be an internal organ). But this article isn’t about internal organs, so we will leave discussions on the liver to others. Our interest is in the body’s largest organ over all, which happens to be the skin, particularly if you consider the gastrointestinal tract an extension of the skin. The human skin, particularly that portion which covers our outer body, is the organ we use to interact, immediately and directly, with the outside world. The world outside our body tells us about itself by touching us, and our skin uses that touch, from the outside world, to communicate to our brain the nature of the outside world with which we are in direct contact. It does so by activating a number of specialized sensors: Meissner’s corpuscles, Pacinian corpuscles, Merkel disks, and Ruffini endings.

Meissner’s and Pacinian corpuscles adapt rapidly, and quickly stop firing in response to a constant stimulus. Merkel disks and Ruffini endings, on the other hand, adapt slowly and do not stop firing as long as a stimulus is present. A pencil held in one hand will cause the holder’s Meissner’s corpuscles, Pacinian corpuscles, Merkel’s disks, and Ruffini’s endings to fire the moment it is picked up. If the pen is held still, though, the Meissner’s and Pacinian corpuscles immediately stop firing, while the Merkel’s disks and Ruffini endings will continue to fire as long as the pencil is held.

Pain and temperature sensing does not require the use of specialized nerve receptors. Instead, free nerve endings throughout skin, muscle, bone, and connective tissue manage to perceive changes in temperature and pain peptides indirectly. Although the sensation of pain results whenever a free nerve ending is damaged, the sensation of pain mostly results when certain substances are released by damaged tissues. Free nerve endings have receptors for these substances, which include prostaglandins, histamine, and substance P. When those receptors are activated the free nerve endings signal the brain that the affected tissue has been damaged.

Free Nerve Endings

Fig. 1100. Details of Skin Structure (Source: unknown) showing major sensory organs in the various skin layers.

In figure 3 (click on the image to get a larger view of it) we see a diagram of the sensory organs within the skin that allow us to discern the nature of the outside world impinging upon us at any given time. One of the most important of these sensory organs is a scattering of free nerve ends.

Free nerve endings, which happen to be the most common type of nerve endings in the body, resemble the fine roots of plants. They penetrate the dermis layer of the skin, and terminate in the stratum granulosum. They are able to detect temperature, touch, pressure, stretch, or pain.

Root Hair Plexus, and Arrector Pili Muscle

Fig. 1101. Free Nerve Endings (Source: staff. “Blausen gallery 2014”).

One very important group of free nerve endings in the human skin forms a plexus (from a Latin root meaning “braid”; in human anatomy the term refers to a branching network of vessels or nerves, and  as used here refers specifically to a network of nerve axons in the skin) around our skin’s hair follicles. Each root hair plexus forms a network around the hair follicle, and sends and receives nerve impulses to and from the brain when the hair moves.

Notice that another structure, located in the same area and attached to each hair, is a muscle known as the arrector pili. Each arrector pili muscle is composed of a bundle of smooth muscle fibers that attach to several hair follicles at once. The hair follicles attached to a given arrector pili muscle are known as a follicular unit; each arrector pili muscle is innervated by the sympathetic branch of the autonomic nervous system.

The autonomic nervous system is involuntary. We don’t consciously control how it operates. Instead, it gets its instructions from the portion of the brain known as the hypothalamus, which controls a host of body organs (like the beating of our hearts, and the contraction and relaxation of our diaphragms) and keeps us going without the need of conscious action on our part.

When, for example, stresses such as cold air are sensed by the root hair plexus, the hypothalamus tells the arrector pili to contract. The hairs to which the contracting arrector pili is attached then become erect, giving us what we call “goose bumps,” conveniently trapping the air closest to the skin so that body heat is conserved. But coldness is not the only thing that causes the arrector pili to contract. Fear produces the same result, and the reaction, being involuntary, takes place unexpectedly.

Imagine the huge number of arrector pili muscles in the skin, all being managed and instructed, individually, by the hypothalamus. Like any computer, the sensory inputs to the hypothalamus can become overwhelmed, particularly when the body is under unusual levels of stress. One result can be that part of the autonomic nervous system won’t know what other parts of the system are doing.

Whenever the arrector pili contracts, other sensitive nerve endings nearby — nerve endings that are not associated with the arrector pili but that are associated with the huge number of root hair plexuses — report back to the brain that the hair has moved. If, when this happens, the brain is so preoccupied by other stressors that it cannot associate the two events in a direct cause-and-effect relationship, the result may be a “feeling” that something foreign is crawling on the skin.

Meissner’s (Tactile) Corpuscles

Meissner’s Corpuscle. (Source: Drawn by Henry Vandyke Carter, now in public domain). Papilla of the hand. Magnified 350 times.
A. Side view of a papilla of the hand.
a. Cortical layer.
b. Tactile corpuscle.
c. Small nerve of the papilla, with neurolemma.
d. Its two nervous fibers running with spiral coils around the tactile corpuscle.
e. Apparent termination of one of these fibers.
B. A tactile papilla seen from above so as to show its transverse section.
a. Cortical layer.
b. Nerve fiber.
c. Outer layer of the tactile body, with nuclei.
d. Clear interior substance.

The root hair plexus isn’t the only sensory organ in the skin that can fool the brain into thinking something external to a person’s body has intruded when the source of the stimulus is within the body itself. Meissner’s (tactile) corpuscles, Pacinian (lamellar) corpuscles, Merkel’s disks or cells, and Ruffini endings (also known as Ruffini Corpuscles or Bulbous Corpuscles) also are capable of psychophysical tomfoolery of one kind or another.

Meissner’s corpuscle is a relatively large sensory organ found scattered over our bodies. It is a highly adaptive nerve ending that senses light touch, and has its highest sensitivity when exposed to vibrations between 10 and 50 Hertz. Arrays of Meissner’s corpuscles are most concentrated in thick, hairless skin, in areas especially sensitive to light touch, such as the fingers and lips, just beneath the epidermis within the dermal papillae.

Physiologically they are encapsulated unmyelinated nerve endings, made up of flattened supportive cells, arranged as horizontal lamellae surrounded by a connective tissue capsule. Neurologically they are sensitive to shape and textural changes in exploratory and discriminatory touch. They can only signal that something is touching the skin.

Pacinian (lamellar) Corpuscles

Pacinian (Lamellar) Corpuscle. (Source: Henry Vandyke Carter – Henry Gray (1918) Anatomy of the Human Body; Gray’s Anatomy, Plate 935; now in public domain)

Pacinian, also known as lamellar, corpuscles are larger and fewer in number than Meissner’s corpuscles, rapidly adapt to change, and are especially sensitivity to vibration (optimally those at 250 Hz, ) and pressure. They respond to sudden disturbances, particularly the rhythmic variety. They detect surface texture and enable the brain to sense pressure changes.

Physiologically, Pacinian corpuscles are oval cylinders some 1 mm long, fully wrapped in connective tissue; the interiors of each corpuscle are arranged into 20 to 60 concentric page-shapped lamellae, with each “page” comprising an axon membrane that is separated from the adjacent membranes by a gelatinous insulator. Neurologically, each corpuscle is sensitive to being deformed, whereupon pressure-sensitive sodium ion channels in the axon membranes are opened that, on leaking sufficient sodium ions, causes the corpuscle to “fire,” or transmit, a receptor signal to the brain. The transmitted signal is not binary, but analog, in that the frequency of transmitted impulses from the corpuscle indicates the severity of the potentiating deformity.

Merkel’s disks (Merkel nerve endings, or Merkel cells)

Merkel’s Disks (Source: Anatomy & Physiology, Connexions Web).

Merkel’s disks, cells, or nerve endings (as they are variously described in the scientific literature) are large, myelinated nerve endings that reside in the basal epidermis and hair follicles. They are mechanorecepters that, unlike Meissner’s and Pacinian corpuscles, adapt slowly to stimuli. In human physiology, they provide the brain with information relating to pressure, position, and deep static touch, and thus serve to detect and analyze shapes and edges.

Physiologically, Merkel cells are somewhat rigid, and are not encapsulated. The cell structure involved consists of an enlarged nerve terminal intimately associated with a nerve ending, and forms what is termed a Merkel cel-neurite complex. Merkel cells and Meissner’s corpuscles are found in superficial skin layers, and are clustered beneath the ridges making up our fingerprints. Merkel nerve endings in hairy skin cluster in specialized structures referred to as touch domes or hair disks.

Neurologically, one afferent nerve fiber is capable of innervating up to 90 such endings, wherein each Merkel cell stores neuropeptides which, on being released to the nerve ending associated with it in response to pressure, causes the complex to “fire” and send a signal to the brain. Signal transmission is most rapid when the skin is stimulated by point objects that concentrate pressure in a small portion of the skin, and is reduced when pressure is applied with flat or curved objects. Pressure from rounded, i.e., convex, objects produce the slowest signal transmission of all. Of all human skin mechanoreceptors, Merkel cells are most sensitive to low-frequency vibrations (5-15 Hz). They are often sensitive to tissue displacements of less than 1 μm.

Ruffini endings, Ruffini Corpuscles, or Bulbous Corpuscles

Ruffini Endings (Source: Henry Vandyke Carter – Henry Gray (1918) Anatomy of the Human Body, Gray’s Anatomy, Plate 937; now in public domain).

This mechanoreceptor, variously referred to as Ruffini endings, Ruffini corpuscles or Bulbous corpuscle, is a slowly adapting mechanoreceptor located in the deep layers of human cutaneous tissue, where they register mechanical joint deformation as a function of angular change, with a resolution of 2.75 degrees. Ruffini endings are now recognized as the primary mechanoreceptor in periodontal ligaments, the group of specialized connective tissue fibers that attach teeth to the alveolar bone.

Physiologically, Ruffini endings are enlarged, spindle-shaped, elongated, encapsulated dendritic nerve endings.

Neurologically, it is sensitive to skin stretch, responds to sustained pressure, shows little adaptation, and contributes to the kinesthetic sense and control of finger position and movement. Thus it is found in high densities around the fingernails where it enables the brain to monitor slippage of objects along the surface of the skin. This, in turn, allows the brain to modulate one’s grip on an object.

The Bottom Line…

Though this article has covered a wide range of subjects, it has a point. To that point we now seek to come. It has several elements, and those elements will be elucidated here over time. Be patient, please, as I work to make sense out of this complex subject.

First, it is a mistake to rule out the presence of biological causes for skin conditions, even when a biological organism cannot immediately be found. Though psychological issues are now well-known and respected causes of such conditions, a number of biological causes that are difficult to diagnose are also known to exist, and those causes can manifest in individuals who have many if not all the other signs and symptoms of ES/DP.

It is never wise to refer to a wheal of unknown etiology as a “bite.” Instead, such conditions should be categorized, thought of, and spoken of as “skin lesions,” because calling them bites presupposes a fact not in evidence. Skin lesions that occur as the result of an unwitnessed event cannot, as a rule, be diagnosed as having a specific cause without further investigation. The cause is just as likely to be the result of chemical changes in the victim’s body as from a spider, mite, or other biting organism.

Second, though, the person afflicted with a skin condition of unknown cause is wise to not jump to the conclusion that the cause is biological without further investigation by a professional, experienced investigator. Other possible causes should be ruled out first. Among these are the presence of unusual emotional stressors caused by, for example, the loss of a loved one, divorce, legal and financial issues, mid-term or semester exams or similar tests, onset or cessation of menses, etc. Such stresses are not only emotional but physiological as well. We are not the same person we were yesterday. Our body changes as we age, to a degree we only faintly fathom. With those physiological changes come expressions of hormonal actions and reactions that ripple throughout our bodies, and sometimes the reactions result in skin lesions.

Third, and perhaps most important, the presence of a mild, transitory, or infrequent skin condition that produces one or a small number of skin lesions of short duration is not something that one should necessarily become alarmed about. In fact, most of the time no alarm at all is warranted, and in no case is excessive alarm justified. Life is not conducted linearly, but has its turns, bumps, and twists. Some of those result in skin issues that are temporary, while some are more lasting. Few, in the vast majority of cases, are life-threatening. Take time to consult with one or more professionals. Study for yourself, too, but use authoritative sources, particularly sources that are associated with a recognized medical or academic community, and avoid those that push a sensational agenda.

Most important, as you are patient with me as I work to flesh out this paper, be patient with yourself and those with whom you seek counsel. Don’t assume your condition will worsen, and if it does take a turn for the worst, don’t assume it will continue to grow worse over time.


  1. Altschuler, Deborah Z. 2004. Collembola (Springtails) (Arthropoda: Hexapoda: Entognatha) found in scrapings from individuals diagnosed with delusory parasitosis. J. New York Entomol. Soc. 112(1):87–95.
  2. Aw, DCW, et al. 2004. Delusional Parasitosis: Case of 8 Patients and Review of the Literature. Ann Acad Med Singapore, 33:89-94.
  3. Aydede, Murat. 2016. Pain: Perception or Introspection? Department of Philosophy, University of British Columbia.
  4. Berrios, G. E. 1982. Tactile Hallucinations: Conceptual and Historical Aspects. Journal of Neurology, Neurosurgery, and Psychiatry 45:285-293
  5. Bhatia, Manjeet, et al. 2000. Delusional Parasitosis: A Clinical Profile. International Journal of Psychiatry, Vol. 30:1.
  6. Bochkov, André V., et al. 2009. In Memorium of Alexander Fain, 1912-2009. Acarina 17 (2): 243–244.
  7. Brown. Sam. 1930. How Your Senses fool you. Modern Mechanics, July 1930.
  8. Doucet, Yanne, et al. 2013. The Touch Dome Defines an Epidermal Niche Specialized for Mechanosensory Signaling. Cell Reports 3, 1759–1765
  9. Ebeling, Walter. 1975. Delusory Parasitosis and “Cable Mite” Dermatitis. Ch. 14, Urban Entomology.
  10. Fain, Alan. 2002. Nociceptors and the Perception of Pain. University of Connecticut Health Center 263 Farmington Ave. Farmington, CT.
  11. Fain, Alexander. 1967. Le genre Dermatophagoides Bogdanow 1864. Son importance dans les allergies respiratoires et cutane ́es chez l’homme (Psoroptidae: Sarcoptiformes). Acarologia 9: 179–225.
  12. Falcon, Delialah. 2016. Delusional Parasitosis (Ekbom’s Syndrome).
  13. Fogel, Alan. 2012. Emotional and Physical Pain Activate Similar Brain Regions: Where does emotion hurt in the body? Psychology Today, Apr 19, 2012.
  14. Ghesquier, Daniel. 1999. A Gallic Affair: The case of the missing Itch-Mite in French Medicine in the early Nineteenth Century. Medical History 43:26-54.
  15. Gohar, Ofra. 2005. Contribution of Ion Channels in Pain Sensation. Modulator, No.19.
  16. Hinkle, Nancy C. 2000. Delusory Parasitosis. American Entomologist, V. 46, No. 1
  17. Hinkle, Nancy C. 2010. Ekbom Syndrome: The Challenge of “Invisible Bug” Infestations.  Annu. Rev. Entomol. 2010. 55:77–94.
  18. Hobson, Anthony R., and Qasim Aziz. 2003. Central Nervous System Processing of Human Visceral Pain in Health and Disease. Physiology, Vol. 18 no. 3, 109-114.
  19. Hong, Dennis. 2013. 5 Mind-Blowing Ways Your Senses Lie to You Every Day. Cracked, June 2013.
  20. Kim, Chuleung, et al. 2002. Delusional Parasitosis as ‘Folie à Deux’. J. Korean Med. Sci. 2003:18
  21. Klimov, Pavel B., and Barry M. O’Connor. 2009. Improved tRNA prediction in the American house dust mite reveals widespread occurrence of extremely short minimal tRNAs in acariform mites. BMC Genomics 10:598
  22. Krimm, Robin F. 2004. NT3 Expressed in Skin Causes Enhancement of SA1 Sensory Neurons That Leads to Postnatal Enhancement of Merkel Cells. THE JOURNAL OF COMPARATIVE NEUROLOGY 471:352–360.
  23. Lepping, Peter, et al. 2007. Antipsychotic treatment of primary delusional parasitosis: Systematic review. bjp.bp.106.029660
  24. Lester, Roy. 1943. Deceive Your Senses. Mechanix Illustrated, November 1943.
  25. Lewy, Jonathan. 2008. The Drug Policy of the Third Reich. Social History of Alcohol and Drugs, Vol. 22, No. 2
  26. Maeda, T., et al. 1999. Ruffini Ending as the Primary Mechanoreceptor in the Periodontal Ligament: Its Morphology, Cytochemical Features, Regenertion, and Development. Critical Review, Oral Biological Medicine: 10(3)
  27. McClenathan, Jane. 2013. Serotonin Keeps You Sad and Sleepy. WR150, Science Writing for the Public.
  28. McParland, Joanna. 2016. People may feel more pain if they carry a sense of grievance. The Conversation, Aug. 16, 2016,
  29. Munde,Prashant Balasaheb, et al. 2013. Pathophysiology of Merkel Cell. J Oral Maxillofac Pathol. 17(3)
  30. Nguyen, Thai. 2014. Hacking Into Your Happy Chemicals: Dopamine, Serotonin, Endorphins, and Oxytocin. The Huffington Post.
  31. Ribiero, José M. C.  Ribeiro, et al. 2012. An Insight into the Sialomes of Bloodsucking Heteroptera. Psyche, Volume 2012 (2012), Article ID 470436.
  32. Pollan, Michael. 2013. THE INTELLIGENT PLANT: Scientists debate a new way of understanding flora. The New Yorker, A Reporter At Large, December 23 & 30, 2013 Issue.
  33. Richards, Sabrina. 2012. Pleasant to the Touch: Scientists hope an understanding of nerve fibers responsive only to gentle touch will give insight into the role the sense plays in social bonding. Scientist: September 1, 2012.
  34. Skott, Annika. 1978. Delusions of infestation : Dermatozoenwahn – Ekbom’s syndrome. University of Gothenburg, Doctoral Thesis.
  35. Shelomi, Matan. Mad Scientist: The Unique Case of a Published Delusion. Science and Engineering Ethics, June 2013, Volume 19, Issue 2, pp 381–388
  36. Trabert, Wolfgang. 1995. 100 Years of Delusions of Parasitosis: Meta-analysis of 1223 Case Reports. Psychopathology 28:238–46
  37. Traver, Jay R. 1951. Unusual Scalp Dermatitis in Humans Caused by the Mite, Dermatophagoides (Acarina, epidermoptidae). Proceedings of the Entomological Society of Washington, Vol. 53, February, 1951, No. 1.
  38. Walton, Shelly F., and Bart J. Currie. 2007. Problems in Diagnosing Scabies, a Global Disease in Human and Animal Populations. CLINICAL MICROBIOLOGY REVIEWS, Vol. 20, No. 2
  39. Weir, Kirsten. 2012. The pain of social rejection: As far as the brain is concerned, a broken heart may not be so different from a broken arm. American Psychological Association, Vol 43, No. 4.
  40. Wilson, J. Walter, and Hiram E. Miller. 1946. Delusion of Parasitosis (Acarophobia). Arch Derm Syphilol. 1946;54(1):39-56.
  41. Woo, Seung-Hyun, et al. 2014. Piezo2 is required for Merkel-cell mechanotransduction. Nature 509, 622–626.
  42. Wright, Margaret C. et al. Unipotent, Atoh1+ progenitors maintain the Merkel cell population in embryonic and adult mice. Journal of Cell Biology, No. 367.
  43. Wykoff, Randolf F. 1987. Delusions of Parasitosis, a Review. Review of Infectious Diseases, V. 9:3
  44. Xiao, Ying, et al. 2015. Neural Hedgehog signaling maintains stem cell renewal in the sensory touch dome epithelium. PNAS Volume 112, No. 23.
  45. Xiao, Ying, et al. 2016. A Cascade of Wnt, Eda, and Shh Signaling Is Essential for Touch Dome Merkel Cell Development. PLOS Genetics.

— Questions? Comments? Corrections? e-mail You may also leave a comment in the space provided below.

One comment on “Connecting the Dots: Causes Behind Mysterious Bites, Sensations of Bites, and Skin Disturbances

  1. Reply Mesothelioma prognosis Sep 13,2017 6:32 am

    Thanks a lot for posting, your post is very useful

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