Cutaneous Reactions to Arthropod Bites
Arthropods are defined by an exoskeleton, segmented body, and jointed appendages. Four of 9 classes of arthropods cause local and systemic reactions associated with their bites: Arachnida, Chilopoda, Diplopoda, and Insecta.
Cutaneous reactions to arthropod bites are inflammatory and/or allergic reactions.
Characterized by an intensely pruritic eruption at the bite sites immediately to minutes to hours to days after the bite, persisting for days to weeks, manifested by solitary or grouped: Urticarial papules; papulovesicles; bullae. Persons are often unaware of having been bitten.
Systemic symptoms may occur, ranging from mild to severe, with death occurring from anaphylactic shock.
Arthropods are vectors of many systemic infections.
Arthropods that Bite, Sting, or Infest
Four of nine classes of arthropods cause local or systemic reactions.
1. Arachnida (four pairs of legs): mites, ticks, spiders, scorpions
a. Acarina. (mites and ticks) Sarcoptes scabiei (scabies). Demodex folliculorum and D. brevis (demodicidosis). Environmental mites. Ticks (Fig. 28-1) that feed on humans and are vectors for disease include blacklegged or Ixodes tick, lone star tick, and dog tick.
Figure 28-1. Comparison of blacklegged, lone star, and dog ticks Blacklegged or Ixodes nymphal ticks transmit Borrelia burgdorferi (Lyme disease) and other infections. Lone star ticks or Amblyomma americanum is the vector for anaplasmosis, tularemia, and Southern tick-associated rash illness. Dog or wood ticks, Dermacentor variabilis, transmit Rocky Mountain spotted fever and tularemia.
b. Araneae. (spiders) Loxosceles reclusa or brown recluse spider. Latrodectus or widow spiders. Tegenaria or hobo spiders cause necrotic arachnidism in Pacific Northwest of United States. Tarantula: Mild inflammatory response to bite and to shed hairs.
c. Scorpionida. Venom contains a neurotoxin that can cause severe local and systemic reactions.
2. Chilopoda or centipedes
3. Diplopoda or millipedes
4. Insecta (three pairs of legs)
a. Anoplura. Phthirius pubis or crab lice. Pediculus capitis or head lice. Pediculus corporis or body lice.
b. Coleoptera. Beetles. Blister beetles contain the chemical cantharidin, which produces a blister when the beetle is crushed on the skin.
c. Diptera. Mosquitoes, black flies (bites produce local reactions as well as black fly fever with fever, headache, nausea, generalized lymphadenitis), midges (punkies, no-see-ums, sand flies), Tabanidae (horseflies, deerflies, clegs, breeze flies, greenheads, mango flies); botflies, Callitroga americana, Dermatobia hominis, phlebotomid sand flies, tsetse flies
d. Hemiptera. Bedbugs, kissing bugs
e. Hymenoptera. Ants, bees, wasps, hornets
f. Lepidoptera. Caterpillars, butterflies, moths
g. Siphonaptera. Fleas, chigoe or sand flea
• Lyme borreliosis, tularemia, bubonic plague
• Scrub typhus, endemic (murine) typhus, spotted fever groups, Q fever
• Human granulocytic anaplasmosis
• Tick-borne meningoencephalitis
• Leishmaniasis, trypanosomiasis (sleeping sickness, Chagas disease).
• Malaria, babesiosis.
• Filariasis, onchocerciasis (river blindness), loiasis
Erythematous macules. occur at bite sites and are usually transient.
Papular urticaria or urticarial papules persistent for >48 h (Fig. 28-2, Fig. 28-3); usually <1 cm; vesicle may for on papule. Large urticarial plaques may occur.
Figure 28-2. Papular urticaria A 21-year-old male awoke with multiple pruritic erythematous papules on exposed of face, neck, forearms, and hands. Bedding was heavily colonized with bedbugs.
Figure 28-3. Papular urticaria A 6-year-old girl with multiple mosquito bites on face.
Bullous Lesions. Tense bullae with clear fluid on a slightly inflamed base (Fig. 28-4); excoriation results in large erosion.
Figure 28-4. Bullous insect bite A 10-year-old child with bullous lesions on the ventral wrist and popular urticarial on the forearm.
Secondary Lesions. Excoriations of urticarial, papular, vesicular lesions common. Painful erosion may be secondarily infected with Staphylococcus aureus. Excoriated or secondarily infected lesions may heal with hyper- or hypopigmentation and/or raised or depressed scars, especially in more darkly pigmented individuals.
Systemic findings may occur associated with toxin or allergy to substance injected during bite. Many varied systemic infections can be injected during bite.
Clinical Variations by Arthropod
Mites. Sarcoptes scabiei causes infestation scabies (see Scabies). Demodex folliculorum and D. brevis live in human hair follicles and sebaceous glands, causing demodicidosis (see Fig. 28-15).
Figure 28-5. Furuncular myiasis A pruritic papule at the site of deposition of a botfly larva, slowly enlarging over several weeks into a domed nodule (resembles a furuncle). The lesion has a central pore through which the posterior end of the larva (inset) intermittently protrudes and thus respires.
Food, fowl, grain, straw, harvest, and animal mite bites cause papular urticaria.
Food Mites. Cheese, grain, mold mites can cause mild contact dermatitis: baker’s or grocer’s itch. Straw mites. Bites occur during harvest season causing dermatitis; straw itch. Harvest mite: Chiggers. Bites can cause dermatitis. One species transmits Rickettsia tsutsugamushi, the cause of scrub typhus.
Dermatophagoides species of house dust mites are implicated in the pathogenesis of asthma and atopic dermatitis. Feed on desquamated human skin and other organic detritus, living in bedding, carpets, and furniture. Bodies and excreta may have a role in asthma and other allergies. Affected persons respond with production of IgE antibodies. Fowl mites. Chicken, pigeons, etc. Bites cause papular urticaria on exposed sites. Rat mites cause painful bites and dermatitis and transmit endemic/murine typhus. House mouse mite is the vector for rickettsialpox. Cheyletiella spp. (dog and cat mites) bite pet owners causing pruritic lesions on forearms, chest, and abdomen. Canine sarcoptic mange (S. scabiei var. canis) and feline mange (Notoedres cati) cause a pruritic dermatosis in pet owners.
Ticks. Ticks attach and feed painlessly. Secretions can produce local bite reactions (erythema), febrile illness, and paralysis. Blacklegged or Ixodes tick, lone star tick, and dog tick are vectors for diseases. Erythema migrans (Fig. 25-81), characteristic of primary Lyme disease or borreliosis, occurs at the bite site of an infected Ixodes tick that transmits Borrelia burgdorferi.
Lymphocytoma cutis (Fig. 25-82) also occurs at the site of bite of an infected Ixodes tick.
Spiders. Brown recluse spider bites can result in mild local urticarial reactions to full-thickness skin necrosis. Associated with a maculopapular exanthem, fever, headache, malaise, arthralgia, and nausea/vomiting. Most lesions diagnosed as brown recluse spider bites are bite reactions to other arthropods. Widow spiders inject a neurotoxin (α-latrotoxin) that produces bite site reactions as well as varying degrees of systemic toxicity.
Insects. Pubic lice, head lice, body lice papular urticaria, excoriations, secondary infections (see page 707).
Mosquitoes. Bites usually present as papular urticaria (Fig. 28-2) on exposed sites; reactions can be urticaria, eczematous, or granulomatous.
Black Flies. Anesthetic is injected, resulting in painless initial bite; may subsequently become painful with itching, erythema, and edema. Black fly fever characterized by fever, nausea, and generalized lymphadenitis.
Midges. Bites produce immediate pain with erythema at bite site with 2- to 3-mm papule and vesicles, followed by indurated nodules (up to 1 cm) persisting for many months.
Tabanidae or horse flies. Bites painful with papular urticaria; rarely associated with anaphylaxis.
Dermatobia hominis (human botfly) in tropical regions causes furuncular myiasis, painful lesions that resemble pyogenic granuloma or abscess. Female botfly captures mosquito and attaches its eggs to the mosquito body, and then releases the mosquito. Eggs hatch on mosquito becoming larvae and are deposited on human skin. Larvae use bite site as portal of entry into skin. A pruritic papule develops at the site, slowly enlarging over several weeks into a domed nodule (resembles a furuncle) with a central pore (Fig. 28-5). Larvae drop out after 8 weeks to pupate in soil.
House Flies. Larvae deposited into any exposed skin site (ear, nose, paranasal sinuses, mouth, eye, anus, and vagina) or at any wound site (leg ulcers, ulcerated squamous and basal cell carcinomas, hematomas, umbilical stump) and grow into maggots, which can be seen on surface of wound causing wound myiasis (Fig. 28-6). Maggot debridement therapy is used to selectively debride necrotic wound tissue.
Figure 28-6. Wound myiasis Multiple housefly larvae in a chronic stasis ulcer on the ankle after castellani paint and Unna boot treatment for 1 week. Upon removal, the maggots were visible; and base of the ulcer was red and clean, having been debrided by maggots.
Cimex lectularius or bedbugs bite exposed skin (face, neck, arms, hands) of sleeping humans. Feeding, which takes 5–10 minutes. Papular urticaria (Fig. 28-2) occur at bite sites. Bedbug hides in crevices of walls, mattresses, and furniture. Reddish brown streaks may be seen on mattress; bedbugs defecate old blood meal while ingesting a new meal.
Reduviid or kissing bugs bite usually present as papular urticaria; severe reactions can produce necrosis and ulceration. Subfamily of reduviid bugs transmits Trypanosoma cruzi, the agent of Chagas disease.
Fleas. Papular urticaria at bite site. Dog fleas often live in carpeting and bite exposed lower legs. Secondary changes of excoriation, prurigo nodularis, and S. aureus infection occur.
Tunga Penetrans or Chigoe Flea. Papule, nodule, or vesicle (6–8 mm in diameter) with central black dot (tungiasis) produced by posterior part of the flea’s abdominal segments. As eggs mature, papule becomes a white, pea-sized nodule (Fig. 28-7). With severe infestation, nodules and plaques with a honeycombed appearance. Ulceration, inflammation, and secondary infection can occur. Most common on feet, especially under toenails, webspaces, plantar aspect of the feet, sparing weight-bearing areas; in sunbathers, any area of exposed skin.
Figure 28-7. Tungiasis Periungual papule with surrounding erythema on the lateral margin of the fifth toe; the larva is visualized by removing the overlying crust.
Female bee, hornet, or wasp sting producing immediate burning/pain, followed by intense, local, erythematous reaction with swelling and urticaria. Severe systemic reactions occur in individuals who are sensitized, with angioedema/generalized urticaria and/or respiratory insufficiency from laryngeal edema or bronchospasm and/or shock.
Fire and harvester ants produce local skin necrosis and systemic reactions to sting; bite reaction begins as an intense local inflammatory reaction that evolves to a sterile pustule.
Caterpillar/moth contact can produce burning/itching sensation, papular urticaria, irritation due to histamine release, allergic contact dermatitis (Fig. 28-8), and/or systemic reactions. Windborne hairs can cause keratoconjunctivitis.
Figure 28-8. Immunologic IgE-mediated contact urticaria: pine processionary caterpillar Linear edematous papules and vesicles occurred on the exposed arm shortly after exposure to Thaumetopoea pityocampa in a pine forest.
Papular urticaria. Allergic contact dermatitis, especially to plants such as poison ivy or poison oak.
Clinical diagnosis, at times, confirmed by lesional biopsy.
Prevention. Apply insect repellent such as diethyltoluamide (DEET) to skin and permethrin spray to clothing. Use screens, nets, clothing. Treat flea-infested cats and dogs; spray household with insecticides (e.g., malathion, 1–4% dust).
Larvae in Skin. Tungiasis. remove flea with needle, scalpel, or curette; oral thiabendazole (25 mg/kg per day) or albendazole (400 mg/d for 3 days) for heavy infestations.
Furuncular myiasis: suffocate larvae by covering with petrolatum and removing the following day.
Glucocorticoids. Give potent topical glucocorticoids for a short duration for intense pruritis. Oral glucocorticoids can be given for persistent pruritus.
Antimicrobial Agents. Secondary Infection Antibiotic treatment with topical agents. Systemic Infection/Infestation Treat with appropriate antimicrobial agent.
Pediculosis Capitis ICD-9: 132.0 ICD-10: B85.0
Infestation of the scalp by the head louse.
Feeds on scalp and neck and deposits its eggs on hair.
Presence of head lice is associated with few symptoms but much consternation.
Etiology and Epidemiology
Subspecies. Pediculus Humanus Capitis. Sesame seed size, 1–2 mm. Feed every 4–6 h. Move by grasping hairs close to scalp; can crawl up to 23 cm/day. Lice lay nits within 1–2 mm of scalp. Nits are ova within chitinous case. Young lice hatch within 1 week, passing through nymphal stages, growing larger and maturing to adults over a period of 1 week. One female can lay 50–150 ova during a 16-day lifetime. Survive only for a few hours off scalp. Transmission: head-to-head contact; shared hats, caps, brushes, combs; theater seats; pillows. Head louse is not a vector of infectious disease.
Demography. In United States, more common in whites than blacks; claws have adapted to grip cylindrical hair; hair pomade may inhibit infestation. In Africa, pediculosis capitis is relatively uncommon; however, lice easily grip noncylindrical hair. Estimated that 6–12 million persons in the United States are infested annually.
Symptoms. Pruritus of the back and sides of scalp. Scratching and secondary infection associated with occipital and/or cervical lymphadenopathy. Some individuals exhibit obsessivecompulsive disorder or delusions of parasitosis after eradications of lice and nits.
Infestation. Head lice are identified by eye or by microscopy (hand lens or dermatoscope) but are difficult to find. Most patients have a population of <10 head lice. Nits are the oval grayish-white egg capsules (1 mm long) firmly cemented to the hairs (Fig. 28-9); vary in number from only a few to thousands. Nits are deposited by head lice on the hair shaft as it emerges from the follicle. With current infestation, nits are near the scalp; with infestation of long standing, nits may be 10–15 cm from the scalp. In that scalp hair grows 0.5 mm daily, the presence of nits 15 cm from the scalp indicates that the infestation is approximately 9 months old. New viable eggs have a creamy-yellow color; empty eggshells are white. Sites of predilection: Head lice nearly always confined to scalp, especially occipital and postauricular regions. Rarely, head lice infest beard or other hairy sites. Although more common with crab lice, head lice can also infest the eyelashes (pediculosis palpebrarum).
Figure 28-9. Pediculosis capitis: nits (A) Arrows: grayish-white egg capsules (nits) are firmly attached to the hair shafts, visualized with a lens. (B) Magnified, an egg with a developing head louse nymph attached to a hair shaft is seen.
Skin Lesions. Bite reactions: papular urticaria on the neck. Reactions related to immune sensitivity/tolerance. Secondary lesions: Eczema, excoriation, lichen simplex chronicus on occipital scalp and neck secondary to chronic scratching/rubbing. Secondary infection with S. aureus of eczema or excoriations; may extend onto neck, forehead, face, ears. Posterior occipital lymphadenopathy.
Small White Hair “Beads” Hair casts (inner root sheath remnants), hair lacquer, hair gels, dandruff (epidermal scales), piedra.
Scalp Pruritus. Atopic dermatitis, impetigo, lichen simplex chronicus.
No Infestation. Delusions of parasitosis.
Microscopy. Nits 0.5-mm oval, whitish eggs (Fig. 28-9B). Nonviable nits show an absence of an embryo or operculum. Louse. Insect with six legs, 1–2 mm in length, wingless, translucent grayish-white body that is red when engorged with blood.
Clinical findings, confirmed by detection of lice. Louse comb increases chances of finding lice. Nits alone are not diagnostic of active infestation. Nits within 4 mm of scalp suggest active infestation.
Topically Applied Insecticides. Permethrin, malathion, pyrethrin, piperonyl, butoxide.
Systemic. Oral ivermectin (200 mg/kg).
Pediculosis Corporis ICD-9: 132.1 ICD-10:B85.1
Body lice reside and lay eggs in clothing. Occur in poor socioeconomic conditions.
Lice leave clothing to feed on human host. Body louse survives more than a few hours away from the human host.
Body lice are vectors of many systemic infections.
Epidemiology and Etiology
Etiologic Agent. Pediculus Humanus Humanus. Larger than head louse: 2–4 mm; otherwise indistinguishable. Life span 18 days. Female lays 270–300 ova. Nits: ova within chitinous case. Nits incubate for 8–10 days; nymphs mature to adults in 14 days.
Habitat: live in seams of clothing; can survive without blood meal for up to 3 days. Attaches to body hairs to feed. Risk factors for infestation include poverty, war, natural disasters, indigence, homelessness, and refugee-camp populations.
Body Lice as Vectors of Disease. Body lice transmit many infectious agents while feeding. Bartonella quintana causes trench fever and endocarditis. Rickettsia prowazekii causes epidemic typhus. Brill–Zinsser disease (louse-borne relapsing fever) is recrudescence of epidemic typhus fever.
Infestation. Lice and nits are found in clothing seams (Fig. 28-10). Lice grab on to body hairs to feed.
Figure 28-10. Pediculosis corporis A 60-year-old homeless male. Multiple lesions secondary to excoriations, prurigo nodularis, and lichen simplex chronicus. Lice and nits are seen in the seams of clothing (inset).
Reactions to Bites. Bite reactions such as popular urticarial (Fig. 28-10) are similar to those of head lice. Changes secondary to rubbing and scratching include excoriations, eczema, lichen simplex, infection with S. aureus, and postinflammatory hyperpigmentation (Fig. 28-10). Scabies, pediculosis capitis, and Pulex irritans (the human flea) can coexist.
Atopic dermatitis, contact dermatitis, scabies, adverse cutaneous drug reaction.
Lice and eggs are found in clothing seams.
Decontamination of Clothing and Bedding. Hygiene measures.
Delousing. Pyrethrin, permethrin, malathion.
Pediculosis Pubis ICD-9: 132.2 ICD-10: B85.2
In infestation of hair-bearing regions by the crab or pubic lice.
Most commonly inhabit the pubic area; hairy parts of the chest and axillae; upper eyelashes.
Manifested clinically by mild-to-moderate pruritus, papular urticaria, and excoriations.
Etiology and Epidemiology
Phthirius pubis, the crab or pubic louse. Size 0.8–1.2 mm. First pair of legs vestigial; other two clawed (Fig. 28-11). Life span 14 days. Female lays 25 ova. Nits incubate for 7 days; nymphs mature over 14 days. Mobility: adults can crawl 10 cm/day. Prefer a humid environment; tend not to wander. Infestation most common in young males. Transmission during close physical contact: sharing bed. May coexist with another sexually transmitted diseases.
Figure 28-11. Crab louse Adult female with an egg developing within her body.
Often Asymptomatic. Mild-to-moderate pruritus for months. With excoriation and secondary infection, lesions may become tender and be associated with enlarged regional.
Infestation. Lice appear as 1- to 2-mm, brownishgray specks (Fig. 28-12, Fig. 28-13) in hairy areas involved. Remain stationary for days; mouth parts embedded in skin; claws grasping a hair on either side. Usually few in number. Nits attached to hair appear as tiny white-gray specks (Fig. 28-13). Few to numerous. Eggs at hair–skin junction indicate active infestation. Infestation most common in pubic and axillary areas; also, perineum, thighs, lower legs, trunk, periumbilical. In children, eyelashes (Fig. 28-13) and eyebrows may be infested without pubic involvement. Maculae cerulea most common on lower abdominal wall, buttocks, and upper thighs.
Figure 28-12. Crab louse Crab louse (arrow) on the skin in the pubic region.
Figure 28-13. Crab lice in eyelashes A 10-year-old child. Crab lice (arrows) and nits on the upper eyelashes of a child; this was the only site of infestation.
Skin Lesions. Papular urticaria (small erythematous papules) at sites of feeding, especially periumbilical (Fig. 28-14). Changes secondary to rubbing lichenification and excoriations. Secondary S. aureus infection. Maculae ceruleae (taches bleues) are slate-gray or bluish-gray macules 0.5–1 cm in diameter, nonblanching. With eyelid infestation, serous crusts may be present along with lice and nits; occasionally, edema of eyelids with severe infestation.
Figure 28-14. Crab lice infestation: papular urticaria A 25-year-old with pruritus. Multiple inflammatory papules at sites of crab lice bites on the abdomen and the inner aspects of the thighs.
With secondary impetiginization, regional lymphadenopathy.
Atopic dermatitis, seborrheic dermatitis, tinea cruris, molluscum contagiosum, scabies. These disorders may coexist with crab louse infestation.
Demonstration of live adult lice, nymphs, or nits in pubic area to diagnose active infestation.
Treatment is usually effective. Reinfestation can occur. Retreatment may be necessary if lice are found or if eggs are observed at hair–skin junction.
Pediculosis. See p. 705. Decontaminate bedding and clothing. Treat sex partners.
Demodicidosis ICD-9: 133.8 ICD-10: B88.0
Demodex species are human face mites, part of the human cutaneous microbiome. D. folliculorum resides in hair follicles; D. brevis, infundibulum of sebaceous glands. Mites do not invade tissue. Site of habitation usually symptomatic. In some cases causes an inflammatory reaction (demodicidosis) that occurs with lesions resembling rosacea, suppurative folliculitis, or perioral dermatitis (Fig. 28-15).
Treatment. Topical metronidazole, permethrin; in severe cases oral ivermectin 200 mg/kg.
Figure 28-15. Demodicidosis A 18-year-old female noted facial rash the day after competing in a triathlon. (A) Tender red papules on the face. (B) Microscopic examination of curetting of papule demonstrates Demodex mite. Lesions resolved with oral ivermectin.
Scabies ICD-9: 133.0 ICD-10: B86
Superficial epidermal infestation by the mite S. scabiei var. hominis. Transmission: Usually spread by skin-to-skin contact and fomites. Chronic undiagnosed scabies is the basis for the colloquial expression, “the 7-year itch.”
Clinical Manifestation. Pruritus often with minimal cutaneous findings. Burrows under stratum corneum.
Scabetic Nodules. Eczematous dermatitis. Hyperinfestation (crusted or hyperkeratotic or Norwegian scabies).
Diagnosis easily missed and should be considered in a patient of any age with persistent generalized severe pruritus.
Etiology and Epidemiology
Etiologic Agent. S. scabiei var. hominis. Obligate human parasite. Mites of all developmental stages burrow into epidermis shortly after contact, no deeper than stratum granulosum; deposit feces in tunnels (Fig. 28-16). Female life span 4–6 weeks; lays 40–50 eggs. Lays 3 eggs per day in burrows; eggs hatch in 4 days. Burrow 2–3 mm daily, usually at night, and lay eggs during the day. Hatched larvae migrate to skin surface and mature into adults. Males and females copulate. Gravid female burrows back under stratum corneum; male falls off. In classic scabies, approximately 10 females per patient are present. With hyperinfestation, > 1 million mites may be present. Estimated at 300 million cases/year worldwide.
Figure 28-16. Burrow with Sarcoptes scabiei (female), eggs, and feces Female mite at the end of a burrow with seven eggs and smaller fecal particles obtained from a papule on the webspace of the hand.
Demography. Major public health problem in many less-developed countries. In some areas of South and Central America, prevalence is about 100%. In Bangladesh, the number of children with scabies exceeds that of children with diarrheal and upper-respiratory disease. In countries where human T cell leukemia/lymphoma virus (HTLV-I) disease is common, hyperinfestation scabies is a marker of this infection. Transmission by skin-to-skin contact and fomites. Mites can remain alive for >2 days on clothing or in bedding. Persons with hyperinfestation shed many mites into their environment daily and pose a high risk of infecting those around them.
Hypersensitivity of both immediate and delayed types occurs in the development of lesions other than burrows. During first infestation, pruritus occurs after sensitization to S. scabiei has occurred, usually within 4–6 weeks. After reinfestation, pruritus may occur within 24 h. With hyperinfestation, persons are often immunocompromised or have neurologic disorders.
Patients are often aware of similar symptoms in family members or sexual partners. Pruritus is intense, widespread, usually sparing head and neck. Itching often interferes with or prevents sleep. Pruritus may be absent with hyperinfestation. Rash ranges from no rash to generalized erythroderma. Patients with atopic diathesis scratch, producing eczematous dermatitis. Some individuals experience pruritus for many months with no rash. Tenderness of lesions suggests secondary bacterial infection.
(1) Lesions occurring at the sites of mite infestation, (2) cutaneous manifestations of hypersensitivity to mites, (3) lesions secondary to chronic rubbing and scratching, (4) secondary infection, (5) hyperinfestation, and (6) variants of scabies in special hosts: those with an atopic diathesis, nodular scabies, scabies in infants/small children, scabies in the elderly.
Intraepidermal Burrows. Skin-colored ridges, 0.5–1 cm in length (Figs. 28-15, 28-17), either linear or serpiginous, with minute vesicle or papule at end of tunnel. Each infesting female mite produces one burrow. Mites are about 0.5 mm in length. Burrows average 5 mm in length but may be up to 10 cm. Distribution: Areas with few or no hair follicles, usually where stratum corneum is thin and soft, i.e., interdigital webs of hands, wrists, shaft of penis, elbows, feet, buttocks, axillae > (Fig. 28-18). In infants, infestation may occur on head and neck.
Figure 28-17. Scabies with burrows Papules and burrows in typical location on the finger web. Burrows are tan or skin-colored ridges with linear configuration with a minute vesicle or papule at the end of the burrow; they are often difficult to define.
Figure 28-18. Scabies: Predilection sites Burrows are most easy to identify on the webspace of the hands, wrists, lateral aspects of the palms. Scabietic nodules occur uncommonly, arising on the genitalia, especially the penis and scrotum, waist, axillae, and areolae.
Scabies with nodules 5–20 mm in diameter, red, pink, tan, or brown in color, smooth (Fig. 28-19); burrow sometimes seen on the surface of a very early lesion. Distribution: Scrotum, penis, axillae, waist, buttocks, areolae (Fig. 28-20). Resolve with postinflammatory hyperpigmentation. May be more apparent after treatment, as eczematous eruption resolves.
Figure 28-19. Scabies with nodules Red-brown papules and nodules on the penis and scrotum; these lesions are pathognomonic for scabies, occurring at sites of infestation in some individuals.
Figure 28-20. Scabies with nodules A 60-year-old female with reddish brown nodules on L-breast persisting after treatment with ivermectin.
Scabies with Hyperinfestation (formerly called Norwegian Scabies). May begin as ordinary scabies. In others, clinical appearance is of chronic eczema, psoriasiform dermatitis, seborrheic dermatitis, or erythroderma. Lesions often markedly hyperkeratotic and/or crusted (Figs. 28-21, 28-22). Warty dermatosis of hands/feet with nail bed hyperkeratosis. Erythematous scaling eruption on face, neck, scalp, and trunk. Affected persons have a characteristic odor. Distribution: Generalized (even involving head and neck in adults) or localized. In patients with neurologic deficit, hyperinfestation may occur only in affected limb. May be localized only to scalp, face, finger, toe-nail bed, or sole.
Figure 28-21. Scabies with hyperinfestation A 42-year-old Hispanic female with HTLV-I infection. Pruritus was minimal. Skin was hyperkeratotic and had a odor. Hundreds of burrows were seen on the back in Fig. 28-16.
Figure 28-22. Scabies with hyperinfestation A 79-year-old male with hyperkeratotic scabies for 4 years. The patient had been treated in his home with topical antiscabetic agents and oral ivermectin as well as extensive decontamination of his home on multiple occasions. Confluent hyperkeratotic plaques are seen on the back, buttocks, and legs. As many as five scabetic mites were seen on one microscope field (see inset).
“Id” or autosensitization-type reactions characterized by widespread small urticarial edematous papules mainly on anterior trunk, thighs, buttocks, and forearms.
Secondary Changes. Excoriations, lichen simplex chronicus, prurigo nodules. Postinflammatory hyper- and hypopigmentation in more deeply pigmented individuals. Bullous scabies can mimic bullous pemphigoid. Secondary infection by S. aureus.
Pruritus, localized or generalized, rash delusions of parasitosis, adverse cutaneous drug reaction, atopic dermatitis, allergic contact dermatitis, metabolic pruritus.
Nodular scabies. urticaria pigmentosa (in young child), papular urticaria (insect bites), prurigo nodularis, pseudolymphoma.
Scabetic Hyperinfestation. Psoriasis, eczematous dermatitis, seborrheic dermatitis, erythroderma.
Microscopy. Highest yield in identifying a mite is in typical burrows on the finger webs, flexor aspects of wrists, and penis. A drop of mineral oil is placed over a burrow, and the burrow is scraped off with a curette or no. 15 scalpel blade and placed on a microscope slide. Three findings are diagnostic of scabies: S. scabiei mites, eggs, and fecal pellets (scybala) (Fig. 28-23).
Figure 28-23. Scabies with multiple burrows A 42-year-old woman with HTLV-I infection and scabies with hyperinfestation (see Fig. 28-22). Multiple dark linear lesions on the back. Each of these lesions in an intraepidermal burrow created by a scabetic mite.
Dermatopathology. Scabietic burrow: located within stratum corneum; female mite with eggs situated in blind end of burrow. Spongiosis (epidermal edema) near mite with vesicle formation common. Dermis shows infiltrate with eosinophils. Nodules: dense chronic inflammatory infiltrate with eosinophils. In some cases, persistent arthropod reaction resembling lymphoma with atypical mononuclear cells. Hyperinfestation: thickened stratum corneum riddled with innumerable mites.
Clinical findings, confirmed, if possible, by microscopy (identification of mites, eggs, or mite feces).
Pruritus often persists up to several weeks after successful eradication of mite infestation, understandable in that the pruritus is a hypersensitivity phenomenon to mite antigen(s). If reinfestation occurs, pruritus becomes symptomatic within a few days. Delusions of parasitosis can occur in individuals who have been successfully treated for scabies or have never had scabies. Hyperinfestation: May be impossible to eradicate; recurrence more likely to relapse than reinfestation. Nodules: In treated patients, 80% resolve in 3 months but may persist up to 1 year.
Principles of Treatment. Treat infested individuals and close physical contacts (including sexual partners) at the same time, whether or not symptoms are present. Application should be to all skin sites.
Recommended Regimens. Permethrin 5% Cream applied to all areas of the body. Lindane (g-Benzene Hexachloride) 1% lotion or cream applied thinly to all areas of the body from the neck down; wash off thoroughly after 8 h. Note: Lindane should not be used after a bath or shower, or by patients with extensive dermatitis, pregnant or lactating women, or children younger than 2 years. Mite resistance to lindane exists. Low cost makes lindane a key alternative in many countries.
Alternative Regimens. Topical. Crotamiton 10%, sulfur 2–10% in petrolatum, benzyl benzoate 10% and 25%, benzyl benzoate with sulfiram, malathion 0.5%, sulfram 25%, ivermectin 0.8%.
Systemic. Oral ivermectin, 200 μg/kg; single dose reported very effective in 15–30 days. Two to three doses, separated by 1–2 weeks, usually required for heavy infestation or in immunocompromised individuals. May effectively eradicate epidemic or endemic scabies in institutions such as nursing homes, hospitals, and refugee camps. Not approved by U.S. Food and Drug Administration or European Drug Agency. Do not use in infants, young children or pregnant/lactating women.
Crusted Scabies. Oral ivermectin combined with topical scalicides (not ivermectin). Decontamination of environment.
Postscabietic Itching. Generalized itching that persists a week or more is probably caused by hypersensitivity to remaining dead mites and mite products. For severe, persistent pruritus, especially in indivuduals with history of atopic disorders, a 14-day tapered course of prednisone (70 mg on day 1) is indicated.
Secondary Bacterial Infection. Treat with mupirocin ointment or systemic antimicrobial agent.
Scabietic Nodules. Intralesional triamcinolone, 5–10 mg/ml into each lesion, is effective; repeat every 2 weeks if necessary.
Cutaneous Larva Migrans ICD-9: 126.9 ICD-10: B76
Creeping Eruption. Cutaneous infestation following percutaneous penetration and epidermal migration of hookworm larvae.
Etiologic Agents. Cutaneous larva migrans: Hookworms larvae of Ancylostoma braziliense in United States. Ova of hookworms are deposited in sand and soil in warm shady areas, hatching into larvae that penetrate human skin. Humans are aberrant, dead-end hosts who acquire the parasite from environment contaminated with animal feces. Larvae penetrate human skin, migrating within the epidermis up to several centimeters a day. Most larvae are unable to develop further or invade deeper tissues and die after days or months. Larva currens: Strongyloides stercoralis; filariform larvae can penetrate skin (usually on buttocks), producing lesions similar to larva migrans.
Cutaneous Larva Migrans. Serpiginous, thin, linear, raised, tunnel-like lesion 2–3 mm wide containing serous fluid (Fig. 28-24). Several or many lesions may be present, depending on the number of penetrating larvae. Larvae move a few to many millimeters daily, confined to an area of several centimeters in diameter. Infestation most commonly occurs on the feet, lower legs, and buttocks.
Figure 28-24. Cutaneous larva migrans A serpiginous, linear, raised, tunnel-like erythematous lesion outlining the path of migration of the larva.
Larva Currens (Cutaneous Strongyloidiasis). A distinctive form of larva migrans. Papules, urticaria, papulovesicles at the site of larval penetration (Fig. 28-25). Associated with intense pruritus. Occurs on buttocks, thighs, back, shoulders, and abdomen. Pruritus and eruption disappear when larvae enter blood vessels and migrate to intestinal mucosa.
Figure 28-25. Larva currens Multiple, pruritic, serpiginous, inflammatory lines on the buttocks at sites of penetration of S. stercoralis larvae.
Migratory lesions from other parasites, photoallergic contact dermatitis, jellyfish sting, epidermal dermatophytosis.
Dermatopathology. Parasite seen on biopsy specimens from advancing point of the lesion.
Self-limited; humans are “dead-end” hosts. Most larvae die and the lesions resolve within 2–8 weeks.
Topical Agents. Thiabendazole, ivermectin, albendazole are effective.
Systemic Agents. Thiabendazole, orally 50 mg/kg per day in two doses (maximum 3 g/d) for 2–5 days; ivermectin, 6 mg twice daily, albendazole, 400 mg/d for 3 days; highly effective.
Removal of Parasite. Do not attempt; parasite not in visible lesions.
Various aquatic microorganisms can cause softtissue infections after exposure.
Bacteria. Aeromonas hydrophila, Edwardsiella tarda, Erysipelothrix rhusiopathiae, Mycobacterium marinum, Pfiesteria piscicida, Pseudomonas species, Streptococcus iniae, Vibrio vulnificus, and other Vibrio species,
Alga. Prototheca wickerhamii.
Localized Cutaneous Infestations. Cercarial dermatitis and seabather’s eruption can occur after exposure to microscopic marine animals.
Cnidaria (jellyfish) and echinoderms (sea urchins, starfish) can cause envenomation.
Schistosome Cercarial Dermatitis
ICD-9: 120.3 ICD-10: B65.3
Swimmer’s itch, clam digger’s itch, schistosome dermatitis, sedge pool itch.
Acute pruritic papular eruption at the sites of cutaneous penetration by Schistosoma cercariae larvae of schistosomes whose usual hosts are birds and small mammals.
Schistosomes implicated: Trichobilharzia, Gigantobilharzia, Ornithobilharzia, Microbilharzia, Schistosomatium.
Exposure can be to fresh, brackish, or saltwater. Eggs produced by adult schistosomes living in animals are shed with animal feces into the environment; on reaching water, schistosome eggs hatch, releasing fully developed larvae (miracidia). Snails are the appropriate hosts for miracidia, from which they emerge as cercariae. These must penetrate the skin of a vertebrate host to continue development.
Transmission. Humans are dead-end hosts. Cercariae penetrate human skin, elicit an inflammatory response, and die without invading other tissues. Occurs worldwide in areas with fresh and saltwater inhabited by appropriate molluscan hosts. Acquired by skin exposure to fresh/saltwater infested by cercariae.
Pruritus and rash begin within hours after exposure. A pruritic macular, papular, papulovesicular, and/or urticarial eruption develops at exposed sites with marked pruritus (Fig. 28-26), sparing parts of the body covered by clothing. (In contrast, seabather’s eruption occurs on areas of the body covered by swimsuits.) Papular urticaria occurs at each site of penetration in previously sensitized individuals. In highly sensitized persons, lesions may progress to eczematous plaques, urticarial wheals, and/or vesicles, reaching a peak 2–3 days after exposure. Schistosomes capable of causing invasive disease in humans (Schistosoma mansoni, S. haematobium, S. japonicum) may cause a similar skin eruption shortly after penetration as well as late visceral complications.
Figure 28-26. Schistosome cercarial dermatitis A highly pruritic papulovesicular eruption on the knees acquired after the patient waded through a slow-flowing creek.
Lesions usually resolve within a week.
Topical and/or systemic glucocorticoids may be indicated in more severe cases.
Seabather’s Eruption ICD-9: 692.9
Etiology. Caused by exposure to two marine animals: Larvae of the thimble jellyfish, Linuche unguiculata, in waters off the coast of Florida and in the Caribbean. Planula larvae of the sea anemone, Edwardsiella lineata, Long Island, NY.
Pathogenesis nematocysts of coelenterate larvae sting the skin of hairy areas or under swimwear, presumably causing an allergic reaction. Some affected individuals recall a stinging or prickling sensation while in the water.
Lesions present clinically as inflammatory papules 4–24 h after exposure (Fig. 28-27). A monomorphous eruption of erythematous papules or papulovesicles is seen most commonly: vesicles, pustules, and papular urticaria, which may progress to crusted erosions. In comparison with cercarial dermatitis, which occurs on exposed sites, seabather’s eruption occurs at sites covered by bathing apparel while bathing in saltwater.
Figure 28-27. Seabather’s eruption This papulovesicular rash appeared on a swimmer while on vacation in the Caribbean. During swimming, the patient experienced slight stinging in the regions covered by her bikini; later that evening she noticed the eruption. The rash is characteristically confined to the areas covered by the swimwear.
On average, lesions persist for 1–2 weeks. In sensitized individuals, the eruption can become progressively more severe with repeated exposures and may be associated with systemic symptoms.
Topical or systemic glucocorticoids provide symptomatic relief.
Cnidaria Envenomations ICD-9: 989.5 ICD-10: T63.6
Etiology. There are >10,000 Cnideria spp. that are swimming medusa or sessile polyps which inject toxin/venom that has local and systemic effects. Members of the Cnidaria phylum that can affect humans are jellyfish, Portuguese man-of-war, sea anemones, and fire “coral.”
Pathogenesis. Cnidarian stings elicit toxic rather than allergic reactions. Ranging from mild, self-limited irritations to extremely painful and serious injuries.
Pruritic, burning, and painful papules in linear arrangement (Figs. 28-28, 28-29).
Stings from box jellyfish can be fatal.
Wet dressings, topical corticosteroids.
Figure 28-28. Jellyfish envenomation Pruritic and painful papules in a linear arrangement on the leg, appearing after contact with jellyfish.
Figure 28-29. Fire coral envenomation A 47-year-old female with painful palms that occurred after contact with fire coral. The palms and palmar fingers are red and edematous at sites of envenomation.