Skin Invading Mites

Representatives of only two families of mites typically invade human skin or associated dermal structures and glands. They are the Demodicidae, or follicle mites, and the Sarcoptidae, or scabies mites. Whereas only a relatively small number of humans infested with follicle mites develop clinical problems, most individuals who become infested with the human scabies mite experience an annoying, often severe, dermatitis.

Demodicidae

Members of this family are called follicle mites. They are extremely tiny, elongate, annulate mites with very short, stout, three-segmented legs (Fig. 23.17). They lack body setae and possess a pair of tiny, needle-like cheiicerae which are used to pierce dermal cells, on which the mites feed. Their minute size and strong reduction of most of the external features represent adaptations for living in the close confines of hair follicles and associated ducts and glands.

Two species of Demodex infest humans, Demodex fol-liculorum (Fig. 23,17) occurs primarily in hair follicles, whereas D. brevis is generally found in the sebaceous glands that open via ducts into the hair follicles. Both species may infest the same host, appearing together in samples taken from a given individual. Adults of the two

FIGURE 23.17 Human follicle mire, Demodex foiliculorum (Demodicidae) (A) Female, ventral view, (B) male, dorsal view. (From Hirst, 1919.)

Dog Demodex Life Cycle
FIGURE 23.18 Life cycle of human follicle mite, Demodex follictdo-rum (Demodicidae). (Modified from Nutting, 1984.)

species closely resemble one another but can be distinguished based on the general body shape and relative size of the males and females. D. folliculorum females have elongate bodies that are gently tapered from the podosoma to the slender, rounded caudal end. D. bre-vis females have bodies that are usually widened posterior to the podosoma and terminate in a more broadly rounded caudum. The eggs are also distinctive, being spindle-shaped in D. folliculorum and oval in D. brevis.

The entire life cycle of D. folliculorum (Fig. 23.18) and D. brevis is spent on their human host. The mites feed by piercing host cells with their styletiform chelicerae and drawing the cell contents into the esophagus with a pumping action of the pharynx. They are highly host-specific and can survive only on humans. Transfer of mites from one individual to another is presumed to occur primarily between mothers and infants during the intimacy associated with facial contact and nursing. Adults of both sexes are readily transferred between hosts at these times. The fact that 90—100% of all humans apparently harbor follicle mites attests to the success with which such transfers are accomplished.

Human follicle mites tend to occur primarily in the regions of the forehead, eyelids, and nose. They also can occur in the eyebrows, the Meibomian glands of the eyelids, perioral mucosa, ear canal, chest, nipples, and other parts of the body (Nutting et aL, 1989). In most cases they cause no apparent harm and go virtually unnoticed. Only under unusual circumstances, which remain largely unexplained, do they cause clinical problems that warrant medical attention. Such cases involving dermal reactions to Demodex mites are called demodicosis. It does not appear that any specific pathogens are involved, although secondary bactcrial infections can aggravate the condition.

In addition to differences in one's body chemistry and immunological responses, certain hormones affect population levels of Demodex mites and the development of demodicosis. Populations tend to build as the host matures, leveling off in the middle age groups. Substances such as diethylstilbestrol tend to inhibit mite populations, whereas progesterone and testosterone may promote an increase. The long-term use of topically applied corticosteroids has been correlated with an increased incidence of demodicosis, suggesting a possible link between hormonal levels and the development of inflammatory reactions induced by follicle mites. Cases of human demodicosis can be categorized into five clinical forms: demodex folliculitis, demodex blepharitis, pityriasis folliculorum, demodex granuloma, and human demodectic mange.

Demodex folliculitis occurs most commonly on the face, but also on the forearms and chest, It typically causes rosacea-like skin lesions, initially appearing as red follicular papules and tiny pustules. This is the most difficult Demodex infestation to diagnose because it is almost indistinguishable clinically from other skin problems such as acne cosmetica, corticosteroid telangiectasia (dilated blood vessels within the skin that have a tortuous appearance), and rosacea. In some cases it may complicate or aggravate preexisting skin conditions. Confirmation of demodicosis is therefore dependent on demonstrating the presence of the mites, all stages of which can be found in the pustule contents.

Demodex blepharitis, also known as ocular demodicosis, is an inflammation of the hair follicles of the eyelids associated with high populations of demodicid mites. The patient's eyelids typically itch or burn, become reddened, and are often characterized by accumulations of waxy or gelatinous debris at the base of the eyelashes. The presence of mites can usually be detected by plucking affected lashes and examining them under a microscope.

Pityriasisfolliculorum is an uncommon form of demodicosis which is clinically recognized as dry, scaly skin with brownish or grayish hyperpigmentation and associated pruritus. The condition is often intensified by scratching or shaving, resulting in erythema, excoriation, mottling, and what has been described as a nutmeg-like roughening of the affected skin. It usually occurs on the face and neck in both young and older adults.

Demodex granuloma results when follicle mites rupture out of blocked hair follicles into subcutaneous tissues. There they can elicit a response by lymphocytes and histiocytes to form granulomas.

Human demodectic mange is the term applied to the remaining form of human demodicosis in which transient infestations of humans by Demodex spp, are contracted from other host species. The most common source is dogs and usually involves intimate contact, such as sleeping with a pet. Patches of papules and vesicles develop, accompanied by a burning or itching sensation. Commonly affected areas include the chin, neck, chest, forearms, stomach, and thighs, reflecting the skin surfaces most likely to come into contact when handling household pets.

A positive diagnosis of demodicosis is made by confirming the presence of large numbers of Demodex mites directly associated with the affected areas of skin, The mites can be seen by microscopic examination of skin scrapings, pustule contents, cellular debris from hair follicles, and plucking eyelashes in the case of demodex blepharitis. Adhesive cellophane tape, applied to infested areas of the skin, can be used to recover demodicid mites near the follicular orifices or moving on the surface of the skin. A follicular biopsy also can be helpful, in which a quick-setting cyanoacryiate polymer is used to extract the contents of sebaceous follicles (Mills and Kligman, 1983). Various stages of the mites, including eggs, are usually evident.

Cases of human demodicosis can be effectively treated by daily washing of the affected skin with mild alkaline or sulfur soap, followed by application of a mild sulfur lotion sold for this purpose. Other compounds, such as gamma benzene hexachloride (lindane), metronidazole, and physostigmine ophthalmic ointment in blepharitis cases, also are effective. When properly treated, cases often are resolved in 2-3 weeks but may take as long as 2 months. This is not to say that the mites are eliminated; their numbers simply are reduced to lower levels that do not cause pathogenesis. Regular daily washing of the face and eyelids with alkaline soap helps to suppress Demodex populations and reduces the risk of developing demodicosis. The use of mascara also seems to retard mite increases. On the other hand, the regular use of medicated creams, skin moisturizers, and topical applications of corticosteroids tend to promote Demodex numbers, leading to heavier infestations and increased prospects of related skin problems.

For further information on Demodex species and their medical importance, see Desch and Nutting (1972), Nutting (1976a,b,c), English and Nutting (1981), Rufli and Mumculoglu (1981), Franklin and Underwood (1986), and Burns (1992).

Sarcoptidae

The only mites in this family that commonly infest humans are members of the genus Sarcoptes, generally referred to as scabies mites. They represent a taxonomic complex of varieties or physiological types of the single species Sarcoptes scabiei.

Mites Dorsal View
FIGURE 23.19 Human scabies mite, Sarcoptes scabiei (Sarcoptidae), female, dorsal view. (From Hirst, 1922.)

Human scabies mite (Sarcoptes scabiei)

The form which typically infests people is called the human scabies mite, or human itch mite, S. scabiei var. hominis. This mite is cosmopolitan in distribution and infests human populations of all races as an obligate parasite that lives in the skin. The adults are small (females 350-450 /xm, males 180-240 ¿¿m in length) and rounded in shape, with tiny pointed, triangular spines on their dorsal surface that assist them in burrowing (Fig. 23.19). These spines are more numerous and conspicuous in females than in males. The legs are short, with legs 1 and 2 of the female and legs 1—3 of the male each bearing a terminal sucker. The two hind pairs of legs of the female and the last pair of legs in the male lack a sucker and instead terminate in long setae or bristles.

The adult mites can crawl quite rapidly on the surface of the skin, with females traveling up to 2.5 cm/min. Upon finding a suitable site, the female uses her che-licerae and first two pairs of legs to burrow into the skin, disappearing beneath the surface in about 1 hr. There she waits in this temporary pit, or shallow burrow, for a wandering male to find her, following which mating takes place. The fertilized female then emerges on the skin surface and searches for a site in which to excavate a permanent burrow. She penetrates the skin once again and makes her way down through the stratum corneum, or horny layer of the skin, to its lower boundary with the underlying stratum granulo-sum. There she excavates a horizontal burrow within the stratum corneum where she will spend the rest of her life, commonly 30 days or more. During this time she continues to extend the length of her burrow by 0.5 mm/day or more, commonly reaching a total length of 1 cm or more. As viewed from the skin surface, fresh burrows appear as tiny, grayish, sinuous lines, with the adult female discernible as a whitish speck at the end of the tunnel.

Within a few hours, the female begins laying eggs in the burrow, producing two to three each day thereafter. The eggs hatch in 3-4 days. The resultant larvae often remain in the burrow for about a day before actively crawling out of the burrow onto the surface of the skin. There they excavate shallow burrows in which they molt to nymphs about 3 days later. The nymphs in turn either remain on the skin surface or dig just beneath the surface, where they molt to adults in 3—4 days. The developmental time from egg to adult typically takes about 10 days for males and 14 days for females.

Although the temporary burrows made by the larvae, nymphs, and virgin females may occur on many parts of the body, the more permanent burrows made by fertilized females tend to be in very characteristic locations. The most frequent sites are folds of the skin about the wrists and in the sides of, or webbing between, the fingers. Other common sites are the elbows, feet, and ankles; axillae; buttocks; penis; scrotum; and, for women, breasts. The location of burrows in infants and young children differs somewhat from that of adults, commonly involving the palms, sides and soles of the feet, and areas about the head and neck. In addition to the rash and discomfort directiy associated with the burrows, rashes often occur on other parts of the body and do not correspond with the distribution of the adult female mites. These other rashes are believed to be caused, in part, by the shallow burrowing of the immature stages of S. scabiei and temporary burrows made by unfertilized females. Unlike adults, children often develop rashes on the face, chest, and back.

The most common means of transmission is by direct contact between individuals when the mites are crawling on the skin surface. However, transmission also can occur via bed linen, clothing, and other fabrics from infested hosts. The mites are able to survive 2—3 days at room temperatures when the relative humidity is more than 30%. The higher the relative humidity, the higher the survival rate. Larvae of S. scabiei can hatch from eggs deposited off the host and infest fomites up to 7 days. However, transmission by fomites generally is not of major importance in temperate regions. S. scabiei from infested horses reportedly has been transmitted to humans via saddle blankets, harnesses, and grooming utensils.

Scabies victims usually experience intense itching, especially at night. The itching typically is out of proportion to the visible signs of the infestation and tends to be aggravated by heat, warm baths, and removal of clothing. The pruritus and rash are attributed to antigens associated with the mite bodies, secretions, and fecal material deposited in the burrows. They stimulate the host's cellmediated immune response, contributing to the development of acquired immunity to subsequent infestations by S. scabiei following initial exposure. This suggests the possibility of vaccines being developed to protect human and other hosts against natural infestations of scabies mites (Arlian et al., 1994a,b). The antigenic nature of the cuticular components of the mites, their secretions, and excretory products helps to explain the persistence of the rash and other clinical signs long after the mites themselves have been killed by acaricidal treatments.

Cases of human scabies occur in a number of clinical forms. The most common type is papular scabies characterized by erythematous papules that erupt as a generalized pruritic rash on various parts of the body. The accompanying itching usually leads to scratching and excoriation of the affected areas, contributing to an eczema-like condition. Vigorously scratched lesions may become secondarily infected with pyogenic, or pus-forming, bacteria, causing an acute, inflammatory, destructive skin condition called pyoderma. In some individuals, tiny vesicles develop in the epidermis in response to burrowing mites. If they become enlarged enough to form macro vesicles, or bullae, they cause what is known as bullous scabies. In other cases, the patient may develop urticarial scabies in which a histamine-like vascular reaction produces wheals or hives that may be intensely itchy and can obscure the primary cause of the problem.

In a small number of individuals, S. scabiei may burrow deeper into the skin, penetrating the dermis and inducing infiltration of lymphocytes. This can lead to the formation of firm, reddish brown, pruritic masses and a condition called nodular scabies. The nodules tend to occur most commonly at the elbows, axillary region, groin, and male genitalia, where they may persist for months or even a year or more despite treatment. Mites seldom are recovered from nodules that are more than a month old. Cases ultimately resolve with or without therapy.

One of the more distinctive, yet rare, clinical types of the disease is crusted scabies, also called hyperkeratotic scabies or Norwegian scabies. It is characterized by dry, scaly,

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