Clinical Manifestations

The type of reaction that occurs after an arthropod bite depends on the species of insect and the age group and reactivity of the human host. Arthropods may cause injury to a host by various mechanisms, including mechanical trauma, such as the lacerating bite of a tsetse fly; invasion of host tissues, as in myiasis; contact dermatitis, as seen with repeated exposure to cockroach antigens; granulomatous reaction to retained mouthparts; transmission of systemic disease; injection of irritant cytotoxic or pharmacologically active substances, such as hyaluronidase, proteases, peptidases, and phospholipases in sting venom; and induction of anaphylaxis. Most reactions to arthropod bites depend on antibody formation to antigenic substances in saliva or venom. The type of reaction is determined primarily by the degree of previous exposure to the same or a related species of arthropod. When someone is bitten for the first time, no reaction develops. An immediate petechial reaction is occasionally seen. After repeated bites, sensitivity develops, producing a pruritic papule (Fig. 660-1) approximately 24 hr after the bite. This is the most common reaction seen in young children. With prolonged, repeated exposure, a wheal develops within minutes after a bite, followed 24 hr later by papule formation; this combination of reactions is seen commonly in older children. By adolescence or adulthood, only a wheal may form, unaccompanied by the delayed papular reaction. Thus, adults in the same household as affected children may be unaffected. Ultimately, as a person becomes insensitive to the bite, no reaction occurs at all. This stage of nonreactivity is maintained only as long as the individual continues to be bitten regularly. Individuals in whom papular urticaria develops are in the transitional phase between development of primarily a delayed papular reaction and development of an immediate urticarial reaction.

Figure 660-1 Pruritic papules after bedbug bites.

Arthropod bites may occur as solitary, numerous, or profuse lesions, depending on the feeding habits of the perpetrator. Fleas tend to sample their host several times within a small localized area, whereas mosquitoes tend to attack a host at more randomly scattered sites. Delayed hypersensitivity reactions to insect bites, the predominant lesions in the young and uninitiated, are characterized by firm, persistent papules that may become hyperpigmented and are often excoriated and crusted. Pruritus may be mild or severe, transient or persistent. A central punctum is usually visible but may disappear as the lesion ages or is scratched. The immediate hypersensitivity reaction is characterized by an evanescent, erythematous wheal. If edema is marked, a tiny vesicle may surmount the wheal. Certain beetles produce bullous lesions through the action of cantharidin, and various insects, including beetles and spiders, may cause hemorrhagic nodules and ulcers. Bites on the lower extremities are more likely to be severe or persistent or to become bullous than those located elsewhere. Complications of arthropod bites include development of impetigo, folliculitis, cellulitis, lymphangitis, and severe anaphylactic hypersensitivity reactions, particularly after the bite of certain hymenopterans. The histopathologic changes are variable, depending on the arthropod, the age of the lesion, and the reactivity of the host. Acute urticarial lesions tend to show central vesiculation in which eosinophils are numerous. Papules most commonly show dermal edema and a mixed superficial and deep perivascular inflammatory infiltrate, often including a number of eosinophils. At times, however, the dermal cellular infiltrate is so dense that a lymphoma is suspected. Many young children demonstrate extensive dermal but nonerythematous, nontender edema in response to mosquito bites (“skeeter” syndrome), which must be distinguished from cellulitis (painful, tender, red) and which responds to oral antihistamines. Retained mouthparts may stimulate a foreign body type of granulomatous reaction.

Papular urticaria occurs principally in the first decade of life. It may occur at any time of the year. The most common culprits are species of fleas, mites, bedbugs, gnats, mosquitoes, chiggers, and animal lice. Individuals with papular urticaria have predominantly transitional lesions in various stages of evolution between delayed-onset papules and immediate-onset wheals. The most characteristic lesion is an edematous, red-brown papule (Fig. 660-2). An individual lesion frequently starts as a wheal that, in turn, is replaced by a papule. A given bite may incite an id reaction at distant sites of quiescent bites in the form of erythematous macules, papules, or urticarial plaques. After a season or two, the reaction progresses from a transitional to a primarily immediate hypersensitivity urticarial reaction.

Figure 660-2 Red-brown papules in papular urticaria.

One of the most commonly encountered arthropod bites is that due to human, cat, or dog fleas (family Pulicidae). Eggs, which are generally laid in dusty areas and cracks between floorboards, give rise to larvae that then form cocoons. The cocoon stage can persist for up to 1 yr, and the flea emerges in response to vibrations from footsteps, accounting for the assaults that frequently befall the new owners of a recently reopened dwelling. Adult dog fleas can live without a blood meal for about 60 days. Attacks from fleas are more likely to occur when the fleas do not have access to their usual host; cat or dog fleas are more voracious and problematic when one visits an area frequented by the pet than when the pet is encountered directly. Flea bites tend to be grouped in lines or irregular clusters. Fleas are often not seen on the body of a pet. Diagnosis of flea bites is aided by examination of debris from the animal’s bedding material. The debris is collected by shaking the bedding into a plastic bag and examining the contents for fleas or their eggs, larvae, or feces.

Treatment

Treatment is directed at alleviation of pruritus by oral antihistamines and cool compresses. Potent topical corticosteroids are helpful. Topical antihistamines are potent immunologic sensitizers and have no role in the treatment of insect bite reactions. A short course of systemic steroids may be helpful if many severe reactions occur, particularly around the eyes. Insect repellents containing diethyltoluamide (DEET) may afford moderate protection against mosquitoes, fleas, flies, chiggers, and ticks but are relatively ineffective against wasps, bees, and hornets. DEET must be applied to exposed skin and clothing to be effective. The most effective protection against mosquitoes, the human body louse, and other blood-feeding arthropods is use of DEET and permethrin-impregnated clothing. These measures are not effective, however, against the phlebotomine sand fly, which transmits leishmaniasis.

An effort should be made to identify and eradicate the etiologic agent. Pets should be carefully inspected. Crawl spaces, eaves, and other sites of the house or outbuildings frequented by animals and birds should be decontaminated, and baseboard crevices, mattresses, rugs, furniture, and animal sleeping quarters should be decontaminated. Agents that are effective for ridding the home of fleas include lindane, pyrethroids, and organic thiocyanates. Flea-infested pets may be treated with powders containing rotenone, pyrethroids, Malathion, or methoxychlor.

Etiology and Pathogenesis

An adult female mite measures approximately 0.4 mm in length, has 4 sets of legs, and has a hemispheric body marked by transverse corrugations, brown spines, and bristles on the dorsal surface. A male mite is approximately half her size and is similar in configuration. After impregnation on the skin surface, a gravid female exudes a keratolytic substance and burrows into the stratum corneum, often forming a shallow well within 30 min. She gradually extends this tract by 0.5-5 mm/24 hr along the boundary with the stratum granulosum. She deposits 10- 25 oval eggs and numerous brown fecal pellets (scybala) daily. When egg laying is completed, in 4-5 wk, she dies within the burrow. The eggs hatch in 3-5 days, releasing larvae that move to the skin surface to molt into nymphs. Maturity is achieved in about 2-3 wk. Mating occurs, and the gravid female invades the skin to complete the life cycle.

Clinical Manifestations

In an immunocompetent host, scabies is frequently heralded by intense pruritus, particularly at night. The first sign of the infestation often consists of 1- to 2-mm red papules, some of which are excoriated, crusted, or scaling. Threadlike burrows are the classic lesion of scabies (Fig. 660-3) but may not be seen in infants. In infants, bullae and pustules are relatively common. The eruption may also include wheals, papules, vesicles, and a superimposed eczematous dermatitis (Fig. 660-4). The palms, soles, and scalp are often affected. In older children and adolescents, the clinical pattern is similar to that in adults, in whom preferred sites are the interdigital spaces, wrist flexors, anterior axillary folds, ankles, buttocks, umbilicus and belt line, groin, genitals in men, and areolas in women. The head, neck, palms, and soles are generally spared. Red-brown nodules, most often located in covered areas such as the axillae, groin, and genitals, predominate in the less common variant called nodular scabies. Additional clues include facial sparing, affected family members, poor response to topical antibiotics, and transient response to topical steroids. Untreated, scabies may lead to eczematous dermatitis, impetigo, ecthyma, folliculitis, furunculosis, cellulitis, lymphangitis, and id reaction. Glomerulonephritis has developed in children from streptococcal impetiginization of scabies lesions. In some tropical areas, scabies is the predominant underlying cause of pyoderma. A latent period of about 1 mo follows an initial infestation. Thus, itching may be absent and lesions may be relatively inapparent in contacts who are asymptomatic carriers. On re-infestation, however, reactions to mite antigens are noted within hours.

Figure 660-3 Classic scabies burrow.

Figure 660-4 A, Diffuse scabies on an infant. The face is clear. The lesions are most numerous around the axillae, chest, and abdomen. B, Scabies. Infestation of the palms and soles is common in infants. The vesicular lesions have all ruptured.

(From Habif TP, editor: Clinical dermatology, ed 4, Philadelphia, 2004, Mosby, pp 502–503.)

Differential Diagnosis

Differential diagnosis of scabies can often be made clinically but is confirmed by microscopic identification of mites (Fig. 660-5A), ova, and scybala (Fig. 660-5B) in epithelial debris. Scrapings most often test positive when obtained from burrows or fresh papules. A reliable method is application of a drop of mineral oil on the selected lesion, scraping of it with a No. 15 blade, and transferring the oil and scrapings to a glass slide.

Figure 660-5 A, Human scabies mite obtained from scraping. B, Scabies ova and scybala.

The differential diagnosis depends on the types of lesions present. Burrows are virtually pathognomonic for human scabies. Papulovesicular lesions are confused with papular urticaria, canine scabies, chickenpox, viral exanthems, drug eruptions, dermatitis herpetiformis, and folliculitis. Eczematous lesions may mimic atopic dermatitis and seborrheic dermatitis, and the less common bullous disorders of childhood may be suspected in infants with predominantly bullous lesions. Nodular scabies is frequently misdiagnosed as urticaria pigmentosa and Langerhans cell histiocytosis. The histopathologic appearance of nodular scabies, consisting of a deep, dense, perivascular infiltrate of lymphocytes, histiocytes, plasma cells, and atypical mononuclear cells, may mimic malignant lymphoid neoplasms.

Treatment

The treatment of choice for scabies is permethrin 5% cream (Elimite) applied to the entire body from the neck down, with particular attention to intensely involved areas, which is also standard therapy. Scabies is frequently found above the neck in infants, necessitating treatment of the scalp. The medication is left on the skin for 8-12 hr. If necessary, it may be reapplied in 1 wk for another 8- to 12-hr period. Additional therapies may include lindane 1% lotion or cream and oral ivermectin.

Transmission of mites is unlikely more than 24 hr after treatment. Pruritus, which is due to hypersensitivity to mite antigens, may persist for a number of days and may be alleviated by a topical corticosteroid preparation. If pruritus persists for >2 wk after treatment and new lesions are occurring, the patient should be reexamined for mites. Nodules are extremely resistant to treatment and may take several months to resolve. The entire family should be treated, as should caretakers of the infested child. Clothing, bed linens, and towels should be thoroughly laundered.

Norwegian Scabies

The Norwegian variant of human scabies is highly contagious and occurs mainly in individuals who are mentally and physically debilitated, particularly those who are institutionalized and those with Down syndrome; in patients with poor cutaneous sensation (leprosy, spina bifida); in patients who have severe systemic illness (leukemia, diabetes); and in immunosuppressed patients (HIV infection). Affected individuals are infested by myriad mites that inhabit the crusts and exfoliating scales of the skin and scalp. The nails may become thickened and dystrophic. The subungual debris is densely populated by mites. The infestation is often accompanied by generalized lymphadenopathy and eosinophilia. There is massive orthokeratosis and parakeratosis with numerous interspersed mites, psoriasiform epidermal hyperplasia, foci of spongiosis, and neutrophilic abscesses. Norwegian scabies is thought to represent a deficient host immune response to the organism. Management is difficult, requiring scrupulous isolation measures, removal of the thick scales, and repeated but careful applications of permethrin 5% cream. Ivermectin (200-250 µg/kg) has been used successfully as single-dose therapy in refractory cases, particularly in HIV-infected patients. A second dose may be needed a week later. The U.S. Food and Drug Administration (FDA) has not approved this agent for treatment of scabies.

Canine Scabies

Canine scabies is caused by S. scabiei var. canis, the dog mite that is associated with mange. The eruption in humans, which is most frequently acquired by cuddling an infested puppy, consists of tiny papules, vesicles, wheals, and excoriated eczematous plaques. Burrows are not present because the mite infrequently inhabits human stratum corneum. The rash is pruritic and has a predilection for the arms, chest, and abdomen, the usual sites of contact with dogs. Onset is sudden and usually follows exposure by 1-10 days, possibly resulting from development of a hypersensitivity reaction to mite antigens. Recovery of mites or ova from scrapings of human skin is rare. The disease is self-limited because humans are not a suitable host. Bathing and changing clothes are generally sufficient. Removal or treatment of the infested animal is necessary. Symptomatic therapy for itching is helpful. In rare cases in which mites are demonstrated in scrapings from an affected child, they can be eradicated by the same measures applicable to human scabies.

Other Types of Scabies

Other mites that occasionally bite humans include the chigger or harvest mite (Eutrombicula alfreddugesi), which prefers to live on grass, shrubs, vines, and stems of grain. Larvae have hooked mouthparts, which allow the chigger to attach to the skin, but not to burrow, to obtain a blood meal, most commonly on the lower legs. Avian mites may affect those who come into close contact with chickens or pet gerbils. Humans may occasionally be assaulted by avian mites that have infested a nest outside a window, an attic, heating vents, or an air conditioner. The dermatitis is variable, including grouped papules, wheals, and vesicular lesions on the wrists, neck, breasts, umbilicus, and anterior axillary folds. A prolonged investigation is often undertaken before the cause and source of the dermatitis are discovered.