Scorpion venom may produce throbbing indurated lesions at the site of attack, usually on acral parts. Erythema, purpura, bullae, necrosis, ulcers, lymphadenitis, and systemic symptoms may develop. ⁴

Local necrosis may be produced at the site of spider bites; in some cases, e.g. following the bite of a black widow spider (usually Latrodectus mactans), severe systemic symptoms and even death may result. ¹⁸ The genus Loxosceles (which includes the brown recluse spider Loxosceles reclusa) may produce a local lesion with quite extensive necrosis, hemorrhage, blistering, and ulceration.^{19.20.21.22.23.24. and 25.} This has been called ‘necrotizing arachnidism’.^{26. and 27.} Not all necrotic lesions on exposed areas are spider bites. ²⁸ A chronic pyoderma gangrenosum-like reaction has also been reported.^{29. and 30.} The diagnosis of loxoscelism can be made by swabbing the lesion and using a specific enzyme-linked immunosorbent assay to detect the venom. ³¹ A diagnosis of loxoscelism is rarely based on the identification of the spider. ³² Less severe reactions, such as erythema and edema, are more usual with other species of spiders. ³³ Sometimes spider leg spines may dislodge in the skin producing a mild erythematous response. ³⁴ An excellent review of spider bites has been published by Wong and colleagues. ³⁵

The efficacy of various treatments for the brown recluse spider venom has been trialed using a rabbit model. No change in eschar size was produced by any of the treatments used. ³⁶ Tetracyclines may be useful in treating cutaneous loxoscelism. ³⁷

Ticks are blood-sucking arachnids that attach to many vertebrates. They are important as hosts and transmitters of a wide range of diseases.^{42. and 43.} After the mosquito, they are the second most common vectors of human infectious diseases in the world. ⁴⁴ Their salivary secretions may produce systemic toxemia and their embedded mouthparts may produce a local erythematous lesion or a more persistent granulomatous or nodular response. ⁴⁵ Unusual reactions include panniculitis, ⁴⁶ localized alopecia, ⁴⁷ papular urticaria, bullae, and hemorrhage. There are two major families of ticks, soft ticks (Argasidae) and hard ticks (Ixodidae). More than 90 species of ticks, both hard- and soft-bodied varieties, have been identified in Australia. ⁴⁸ Soft ticks (Ornithodoros species) ⁴⁹ are generally not perceived by the victim, although hard ticks – of which there are several genera, including Ixodes, Amblyomma, and Dermacentor – are eventually noticed because they remain attached for days and slowly engorge with blood. Amblyomma americanus, the lone star tick, is the most common species of this genus found in the United States. ⁴⁴ Attempts to remove the tick may cause the embedded mouthparts to separate and remain in the tissue. Successful removal of all parts of a tick is vital to minimize significant medical consequences. ⁴⁸ Multiple pruritic papules due to the partially burrowed larvae of the lone star tick are rarely reported.^{44. and 50.}

Two species of follicle mites are found as normal inhabitants of human skin:^{58.59.60.61.62.63.64.65.66.67.68. and 69.} Demodex folliculorum lives mainly in the hair follicles and Demodex brevis in the sebaceous glands. The larger of the two, Demodex folliculorum, measures about 0.4 mm in length. Mites of this species are often aggregated in a follicle, whereas D. brevis is usually solitary. ⁶⁰ The mites have been found in 10% of routine skin biopsies (from all sites), and in 12% of all follicles examined in these same biopsies. ⁶¹ They are common in basal cell carcinomas removed from the eyelids. ⁷⁰ They are not increased in pregnancy. ⁷¹ The face is most often involved, although D. brevis has a wider distribution. ⁶⁷ Genital lesions are rare. ⁷² Although increased numbers of mites are found in sections of rosacea and in subclinical forms of folliculitis, this does not prove a causal relationship.^{73.74. and 75.} It is generally accepted that Demodex mites are not etiologically involved in the usual form of rosacea, although they may possibly play a role in the granulomatous form, in which extrafollicular mites are sometimes seen. Demodex may produce a blepharitis⁶² and so-called ‘rosacea-like’ demodicosis.^{66.76.77.78.79. and 80.} Scalp demodicosis (demodicidosis) mimicking favus has been reported in a child. ⁸¹Demodex has been incriminated as a cause of localized pustular folliculitis of the face,^{63.78.82. and 83.} facial plaques, ⁸⁴ and of a more widespread eruption in patients with an immunosuppressed state.^{85.86.87.88. and 89.} Refractory Demodex folliculitis may also occur in children with leukemia. ⁹⁰ However, mite density is not always increased in immunosuppressed patients.^{80.91. and 92.} They are increased in hemodialysis patients but the increase is not statistically significant. ⁹³ Mite density is increased in patients receiving phototherapy. ⁹⁴ The mites themselves may produce local immunosuppression, allowing them to survive. ⁹⁵ This theory is based on the finding that Demodex mites appear to increase lymphocyte apoptosis in infested skin. ⁹⁵ Recently, a rosacea-like demodicosis was reported as a complication of the use of pimecrolimus for the treatment of seborrheic dermatitis. ⁹⁶ Otophyma is a rare complication of rosaceous lymphedema of the ear associated with Demodex infestation. ⁹⁷

Facial erythema with follicular plugging (pityriasis folliculorum) is another manifestation of Demodex infestation. ⁹⁸ The third clinical form of demodicosis in humans, demodicosis gravis, presents a clinical picture similar to severe granulomatous rosacea. ⁹⁹

Scabies is a contagious disease caused by the mite Sarcoptes scabiei var. hominis. It is acquired particularly under conditions of overcrowding and poor personal hygiene, or during sexual contact.103. ^{and 104.} Scabies was present in 8.8% of the population in a Brazilian slum. ¹⁰⁵ Patients with both minimal disease and only a few mites¹⁰⁶ and exaggerated atypical lesions complicating AIDS^{107.108.109.110.111. and 112.} are now being seen, as are patients with inherited disorders of keratinization¹¹³. The disease tends to appear in epidemics, which have a cyclical character, recurring at intervals of about 30 years and lasting for about 15 years. ¹¹⁴ The reasons for these cyclic fluctuations are not understood. A new cycle probably commenced in 1993, although there are conflicting reports on the date of commencement of this most recent cycle. ¹¹⁵ Infections are more frequent in the cooler months of the year, possibly related to host overcrowding. ¹¹⁶

Three clinical forms are found: papulovesicular lesions, persistent nodules, and Norwegian (crusted) scabies. The usual lesions are papules and papulovesicles which are intensely pruritic. The vesicles are usually found at the end of very fine wavy dark lines, best seen with the help of a hand lens or by applying a small amount of ink to the surface and removing the excess. ¹¹⁷ These lines represent the excreta-soiled burrows in the horny layer in which the female travels to deposit her eggs. Epiluminescence microscopy enhances the diagnosis of scabies; it gives a low number of false-negative results.^{118. and 119.} Amplification of Sarcoptes DNA in the cutaneous scale, using PCR, has been used to confirm inapparent infection. ¹²⁰ The application of cyanoacrylate glue (Super Glue) to the skin, followed by a glass slide which is pressed on the suspect skin site, is a recently described method for mite identification. ¹²¹

The female mite measures up to 0.4 mm in length and rather less in breadth, whereas the adult male, which dies after copulation, is much smaller (Fig. 30.8). The sites most commonly affected are the interdigital skin folds, the palmar surfaces of the hands and fingers, the wrists, the nipples, the inframammary regions, and the male genitals. The vulva is a rare site. ¹²² A more generalized eruption is sometimes seen in infants and young children; ¹²³ misdiagnosis is common in this group.^{124.125. and 126.} In addition to the burrows, there is nearly always a secondary rash of small urticarial papules with no mites, which may result from autosensitization.^{127. and 128.} Bullae, resembling bullous pemphigoid, are rarely seen.^{129.130.131.132. and 133.} The presence of circulating antibodies against BP180 and/or BP230 suggests that scabies may induce true bullous pemphigoid. ¹³⁴

In about 7% of patients, particularly children and young adults, reddish-brown pruritic nodules develop with a predilection for the lower trunk, scrotum, and thighs. ¹¹⁴ These lesions may persist for a year, despite treatment. Mites are rarely found, and this form (persistent nodular scabies) is thought to represent a delayed hypersensitivity reaction similar to that found following some other arthropod bites.

Norwegian (crusted) scabies is a rare contagious form consisting of widespread crusted and secondarily infected hyperkeratotic lesions, found in the mentally and physically debilitated,^{135.136. and 137.} as well as in immunosuppressed patients.^{112.138.139.140.141.142.143.144.145.146. and 147.} This form has also been reported in an otherwise healthy pregnant woman, ¹⁴⁸ and in a healthy infant. ¹⁴⁹ Norwegian scabies also occurs in patients with epidermolysis bullosa,^{150. and 151.} and in neurological disorders with sensory impairment. ¹⁵² There is an extremely heavy infestation with mites. Longitudinal nail splitting has been reported as a consequence of crusted scabies. ¹⁵³

Human infestation with varieties of Sarcoptes scabiei of animal origin is not uncommon. ¹⁵⁴ They produce a self-limiting disease without the presence of burrows.^{155. and 156.} These animal variants are morphologically indistinguishable from the human variant of Sarcoptes scabiei.

The conventional antiscabetics have poor compliance; however, ivermectin, an oral scabicide, is proving a useful substitute.^{157.158. and 159.} Tea tree oil, derived from Melaleuca alternifolia, has recently been found to possess acaricidal activity in vitro. ¹⁶⁰

Several species of Cheyletiella, a mite found on dogs, rabbits, and cats, can produce an intensely pruritic dermatitis in humans.184.^{185. and 186.} In animals it produces so-called ‘walking dandruff’. There are erythematous papules and papulovesicles, sometimes grouped, with a predilection for the chest, abdomen, and proximal extremities. ¹⁸⁷ Involved areas usually correspond to the sites of close physical contact with the infested pet. ¹⁸⁸ The mite is almost never found on humans, and the diagnosis may be confirmed by examining fur brushings of the patient’s pet for the mite.^{189. and 190.} This condition is no longer thought to be synonymous with so-called ‘itchy red bump’ disease (papular dermatitis), a papular pruritic disorder of uncertain histogenesis which was originally reported from Florida, USA (see p. 113).^{184. and 191.} Delayed hypersensitivity mechanisms are thought to play a role in the pathogenesis of the eruption. ¹⁹²

Five other families of mites have been incriminated in the production of cutaneous lesions: Tyroglyphoidea (food mites), Pyemotidae (predacious or grain itch mites), Dermanyssidae (parasitoid or rat mites), Trombiculidae (trombiculid or harvest mites, chiggers), and Tydeidae (sawdust mite).^{4.5.185. and 194.}

Food mites and predacious mites produce erythematous papules, papulovesicles, or urticaria in workers handling certain foods and grain. The lesions may be mistaken for scabies, but there are no burrows. ⁴⁵ The genera involved include Glycophagus (grocery mite), Acarus (cheese mite), Tyrophagus (copra mite), Pyemotes (grain itch mite), and Tyroglyphus.^{45.155. and 195.} The house dust mite Dermatophagoides pteronyssinus and related species are widely distributed in bedding and clothing, and may play a role in producing or exacerbating chronic dermatitis.^{196. and 197.}

The parasitoid mites may produce papular urticaria in people employed in grain stores or living in places harboring rats.^{198. and 199.} Pet rabbits may be infected by the mite Listrophorus gibbus, which can produce a papular urticaria in the handler. ²⁰⁰ Various birds, including pet gerbils, may harbor mites from the family Dermanyssidae.^{201.202.203. and 204.} The term ‘gamasoidosis’ has been used to describe the human skin disease caused by mites from birds and other animals. ²⁰¹

The trombiculid mites may produce a severe dermatitis with minute, intensely pruritic red elevations. ²⁰⁵ They have a predilection for the lower legs, groin, and waistline.

Pediculosis, which has been known for over 10 000 years, is caused by three types of lice, each having a separate microenvironment. ²⁰⁶ The head louse (Pediculus humanus capitis) infests the hairs of the scalp. It is an increasing problem in many urban communities, ¹⁰⁵ with outbreaks particularly in schools,^{207.208.209.210.211. and 212.} although the incidence is declining in some communities. ²¹³ Recent work suggests that fomite transmission is an important source of infestation.^{214.215. and 216.} In some parts of the world, including the United States, Canada, and Australia, public health authorities have adopted a ‘no nit’ policy which results in the immediate dismissal from school of any child found to have lice or eggs (nits) in their hair. As not all nits are viable, and not all children with them have concurrent lice, it has been suggested that the ‘no nit’ policy be replaced with other programs. ²¹⁷ As the nit sheath is similar in composition to hair, eradication programs will need to take note of this fact. ²¹⁸ Bug buster kits (fine-toothed combs) are favored in some regions over the use of pediculicides, such as malathion and permethrin.^{219.220.221.222. and 223.} In a comparative trial malathion was found to be superior to permethrin for the treatment of head lice. ²²⁴ There is an emerging resistance to pediculicides in some parts of the world. ²²⁵ New pediculicides are being trialed. ²²⁶

The pubic louse (Phthirus pubis) infests pubic and axillary hair in particular, although there may be colonization of any heavy growth of hair on the trunk and limbs. ²²⁷ Occasionally the eyebrows are infested, and very rarely the scalp.^{228.229.230. and 231.} It is more common in the cooler months. ²³² The HIV status of the patient does not appear to influence the severity of the infestation. Both the pubic louse and the head louse cement their eggs to hair, forming the minute gritty projection that is known as a nit. Multiple bluish spots (maculae ceruleae) may be found, particularly on the trunk, in persons infested with the pubic louse. ²³³

The body louse (Pediculus humanus corporis) divides its existence between the host and the host’s clothing, in the seams of which it deposits its eggs.

The lice are blood-suckers but the amount consumed is minimal. ²³⁴ The injected saliva may produce an allergic reaction. This hypersensitivity rash, or pediculid, may mimic a viral exanthem. ²⁰⁶ The resulting itching may lead to excoriation or secondary bacterial infection.

Bedbugs (Cimicidae) are found usually in dirty and dilapidated housing, associated with unwashed bedlinen. ²³⁶ They may also infest wooden seating in public transport. They are notoriously difficult to eliminate. ²³⁷

The common bedbug (Cimex lectularius) can produce pruritic, urticarial, vesicular, and even bullous lesions.^{238. and 239.} Anaphylactic reactions and persistent nodular lesions are rare. ²⁴⁰ The distribution of the lesions is influenced by the method of infestation and the wearing of bedclothes. ²³⁷ At least six other species may rarely parasitize humans. ²⁴¹

Myiasis is the infestation of live human tissues by the larvae of flies in the order Diptera.^{242.243.244. and 245.} It is said to be the fourth most common travel-associated skin disease.^{246. and 247.} In Central and South America dermal myiasis is usually caused by the ‘human botfly’, Dermatobia hominis.^{248.249.250.251.252.253.254. and 255.} In West and Central Africa the tumbu fly (Cordylobia anthropophaga) is involved.^{256.257.258.259.260.261. and 262.} In one study of a rural community in the Niger Delta, 36% of 150 women, and 20% of 75 infants studied were infected by C. anthropophaga. ²⁶³ Other flies, some of them of restricted geographical distribution, can produce myiasis, including species of Parasarcophaga, ²⁶⁴Psychoda, ²⁶⁵Gasterophilus, Hypoderma,^{266. and 267.} Cuterebra,^{268.269.270.271. and 272.} Cochliomyia,^{273.274. and 275.} Chrysomya, ²⁷⁶ and Wohlfahrtia.^{4. and 277.} The larvae of the common housefly Musca domestica may rarely infest the skin of debilitated and extremely neglected patients.278. ^{and 279.} The eggs may be transmitted to humans by another insect, such as the mosquito in the case of Dermatobia hominis, or the larvae may burrow into the skin of a suitable host after hatching on the ground or on clothing, as with the tumbu fly. ²⁸⁰ In contrast to botfly larvae that are larger and have abdominal hooklets anchoring them under the skin, the tumbu larvae do not have anchoring hooklets and they can be extruded by squeezing the skin. ²⁸⁰

The larva completes its molts in from about 2 weeks to 3 months or longer, depending on the species. It then works its way out of the skin and falls to the ground, where pupation occurs. This may be noted by the patient.

The lesions have a predilection for exposed surfaces such as the feet and forearms. ²⁸¹ The scalp is uncommonly involved, while penile involvement is very rare.^{261.282. and 283.} Lesions have a furuncle-like presentation which culminates in ulceration.^{246.284. and 285.} Sometimes there are plaques with draining sinuses. ²⁸⁶ Tissue destruction may result when sites such as the nose are involved. ²⁷⁵ Large inflammatory nodules have been reported in a person with HIV infection. ²⁸⁷ There may be throbbing pain as the lesion enlarges. Ultrasound and dermoscopy can be used to confirm the clinical diagnosis.^{288. and 289.}

Myiasis has been proposed as a risk factor for prion diseases in humans. ²⁹⁰ Prion rods have been identified in both fly larvae and pupae. ²⁹⁰

Treatment may involve three processes: occlusion to deprive the larva of oxygen, removal of the larva by squeezing or a surgical technique, and the use of larvicides such as ivermectin. ²⁴⁵

Tungiasis is produced by infestation of the skin by the pregnant female sandflea Tunga penetrans. ²⁹⁵ It occurs in Central and South America, tropical Africa, and Pakistan.^{296.297.298.299. and 300.} In one community in Nigeria, 45% of the population were found to be infested with this parasite, and the median parasite load was six. ³⁰¹ Close to one hundred parasites have been detected in a patient with Klippel–Trenaunay syndrome. ³⁰² International travel has resulted in its occurrence in many countries.^{303.304.305.306.307.308. and 309.} As the flea is a poor jumper, lesions are usually found on the feet. ³⁰¹ Penetration into the dermis by the flea produces characteristic single or multiple white papules, and eventually nodules about 1 cm in diameter. ³¹⁰ Lesions have a central black dot and erythematous margins. The black region corresponds to the posterior portion of the flea. ³¹¹ Dermoscopy can be used to confirm the diagnosis.^{312.313. and 314.} On entering the skin the female tunga is about 0.1 cm in diameter, but this increases to 0.6 cm or more as the 150–200 eggs within the abdomen of the gravid female mature. Once the ova have been shed through an opening in the skin and the tunga has died, the nodule usually becomes frankly ulcerated.

A second species of Tunga, T. trimamillata, has been reported in humans from Ecuador. ³¹¹ Its preferential hosts are goats, pigs, and cattle.

Surgical removal of the sandflea is the treatment of choice. Topical ivermectin, thiabendazole, and metrifonate have been used. Oral ivermectin is also effective. ³¹⁵

Species within the order Diptera may be responsible for cutaneous lesions other than myiasis. These insects include mosquitoes, gnats, and midges. Mosquitoes may cause urticarial and even bullous lesions in occasional sensitized hosts. They may also cause a life-threatening disorder in patients with Epstein–Barr virus infection (see below).317. ^{and 318.} The biting gnats and midges may give urticarial wheals or pruritic papules. ³¹⁹ Papular urticaria is a common reaction to fleas. Large persistent lesions may develop in patients infected with HIV. ³²⁰ A related phenomenon is the development of exuberant lesions in patients with hematological disorders, particularly chronic lymphocytic leukemia (see below).

Beetles (order Coleoptera) can produce slowly forming blisters, necrotizing lesions, or papular urticaria.^{321.322. and 323.} The best known blister beetle is Lytta vesicatoria (the Spanish fly), an insect endemic to southern Europe. ³²⁴ The blisters are produced by cantharidin, a substance found in certain beetles. ³²⁵ Other families of beetle have a different vesicating toxin in their coelomic fluid, known as pederin, which is released when the beetle is accidentally crushed on the skin. ³²⁶ Recently, an outbreak of over 250 cases of a vesicular dermatitis was reported from Australia. ³²⁴ It was caused by the genus Paederus (rove beetles). ³²⁴ Other outbreaks have been reported from Sri Lanka, ³²⁷ South India, ³²⁸ and Iran. ³²⁹

Some species of moths and butterflies (order Lepidoptera) have larvae (caterpillars) with surface hairs (setae) that may produce urtication on entering the skin. The setae, which contain an urticating toxin (thaumetopoein), may be airborne, producing disease in unsuspecting hosts.^{330. and 331.} Erythematous macules and papules and urticarial wheals may be seen.^{332.333. and 334.} Incidentally, there are more than 165 000 species in the order Lepidoptera, but only 150 are medically important. ³³⁵

Moths of the genus Hylesia (found particularly in South America) may produce an intensely pruritic urticarial rash within a few minutes to several hours after contact with the abdominal hairs of the adult female moth. ³³⁶

Small erythematous papules may result from the bite of the thrip, a tiny insect in the order Thysanoptera. ³³⁷ They are often misdiagnosed as mosquito bites. They may also produce itching without visible lesions. ³³⁸ Psocids, very small insects of the order Psocoptera, very rarely cause infestations of humans. ³³⁹ One such genus, Liposcelis, is found in old, moldy books and called ‘booklice’. They may cause mild pruritus. ³³⁹ One case of infestation associated with onychomycosis has been reported. ³⁴⁰

Severe urticarial edema and even anaphylaxis may follow the stings of species within the order Hymenoptera (bees, wasps, ants, and hornets) in some susceptible individuals.^{3.341.342. and 343.}

There was a recent review on the cutaneous side effects of insect repellents. ³⁴⁴ Despite the widespread use of repellents, complications, such as an irritant contact dermatitis, are quite uncommon. ³⁴⁴

Exuberant papular and vesiculobullous lesions may develop in patients with leukemia, particularly chronic lymphocytic leukemia, apparently as an exaggerated response to arthropod bites.^{351.352. and 353.} A similar reaction has been reported in association with mantle cell lymphoma.^{354. and 355.} Patients usually do not recall being bitten. The reaction may precede the diagnosis of the hematological disorder. Lesions may persist for many years. ³⁵² Immunodeficiency may play a role in their pathogenesis, as similar lesions have been reported in HIV infection (see above). It has been suggested that the term eosinophilic dermatosis of myeloproliferative disease is more appropriate.^{356. and 357.}

Dapsone has been used successfully in the management. ³⁵⁸

The triad of hypersensitivity to mosquito bites, chronic Epstein–Barr virus infection, and natural killer cell leukemia/lymphoma has been reported in recent years, mainly in Japanese children.^{317.359.360. and 361.} Some patients may not express the triad; patients with natural killer cell lymphocytosis have been reported with mosquito hypersensitivity. ³¹⁸ Death from the hemophagocytic syndrome may occur. ³¹⁷ Hypersensitivity to mosquito bites, presenting as a hydroa vacciniforme-like eruption in patients with lymphoma, is a closely related phenomenon. ³⁶² Such patients may not have chronic Epstein–Barr virus infection (EBV). ³⁶²