CHAPTER 137: ECTOPARASITE INFESTATIONS AND ARTHROPOD INJURIES

Ectoparasites include arthropods and creatures from other phyla that infest the skin or hair of animals; the host animals provide them with sustenance and shelter. The ectoparasites may penetrate within or beneath the surface of the host or may attach by mouthparts and specialized claws. These organisms may inflict direct mechanical injury, consume blood or nutrients, induce hypersensitivity reactions, inoculate toxins, transmit pathogens, and incite fear or disgust. Humans are the sole or obligate hosts for many kinds of ectoparasites and serve as facultative or paratenic (accidental) hosts for many others.

Arthropods that are ectoparasitic or otherwise cause injury include insects (such as lice, fleas, bedbugs, wasps, ants, bees, and flies), arachnids (spiders, scorpions, mites, and ticks), millipedes, and centipedes. Certain nematodes (helminths), such as the hookworms (Chap. 131), are ectoparasitic in that they penetrate and migrate through the skin. Infrequently encountered ectoparasites in other phyla include the pentastomes (tongue worms) and leeches.

Arthropods may also cause injury when they attempt to take a blood meal or as they defend themselves by biting, stinging, or exuding venoms. Various arachnids (spiders and scorpions), insects (bees, hornets, wasps, ants, flies, true bugs, caterpillars, and beetles), millipedes, and centipedes produce ill effects during these behaviors. Similarly, certain ectoparasites (e.g., ticks, biting mites, and fleas) that typically infest nonhuman animals can be medically significant. In the United States, lesions caused by arthropod bites and stings are so diverse and variable that it is rarely possible to identify the precise causative organism without a bona fide specimen and taxonomic expertise.

The human itch mite, Sarcoptes scabiei var. hominis, is a common cause of itching dermatosis, infesting ~300 million persons worldwide at any one time. Gravid female mites (~0.3 mm in length) burrow superficially within the stratum corneum, depositing three or fewer eggs per day. Six-legged larvae mature to eight-legged nymphs and then to adults. Gravid adult females emerge to the surface of the skin about 8 days later and then (re)invade the skin of the same or another host. Newly fertilized female mites are transferred from person to person mainly by direct skin-to-skin contact; transfer is facilitated by crowding, poor hygiene, and sex with multiple partners. Generally, these mites die within a day or so in the absence of host contact. Transmission via sharing of contaminated bedding or clothing occurs far less frequently than is often thought. In the United States, scabies may account for up to 5% of visits to dermatologists. Outbreaks occur in preschools, hospitals, nursing homes, and other residential institutions.

The itching and rash associated with scabies derive from a sensitization reaction to the mites and their secretions/excretions. A person’s initial infestation remains asymptomatic for up to 6 weeks before the onset of intense pruritus, but a reinfestation produces a hypersensitivity reaction without delay. Burrows become surrounded by inflammatory infiltrates composed of eosinophils, lymphocytes, and histiocytes, and a generalized hypersensitivity rash later develops in remote sites. Immunity and associated scratching limit most infestations to <15 mites per person. Hyperinfestation with thousands of mites, a condition known as crusted scabies (formerly termed Norwegian scabies), may result from glucocorticoid use, immunodeficiency, and neurologic or psychiatric illnesses that limit the itch and/or the scratch response.

Pruritus typically intensifies at night and after hot showers. Classic burrows are often difficult to find because they are few in number and may be obscured by excoriations. Burrows appear as dark wavy lines in the upper epidermis and are 3–15 mm long. Scabetic lesions are most common on the volar wrists and along the digital web spaces. In males, the penis and scrotum become involved. Small papules and vesicles, often accompanied by eczematous plaques, pustules, or nodules, appear symmetrically at those sites; within intertriginous areas; around the navel and belt line; in the axillae; and on the buttocks and upper thighs. Except in infants, the face, scalp, neck, palms, and soles are usually spared. Crusted scabies often resembles psoriasis: both are characterized by widespread thick keratotic crusts, scaly plaques, and dystrophic nails. Characteristic burrows are not seen in crusted scabies, and patients usually do not itch, although their infestations are highly contagious and have been responsible for outbreaks of classic scabies in hospitals.

Scabies should be considered in patients with pruritus and symmetric superficial, excoriated, papulovesicular skin lesions in characteristic locations, particularly if there is a history of household contact with an infested person. Burrows should be sought and unroofed with a sterile needle or scalpel blade, and the scrapings should be examined microscopically for mites, eggs, and fecal pellets. Examination of skin biopsies (including superficial cyanoacrylate biopsy) or scrapings, dermatoscopic imaging of papulovesicular lesions, and microscopic inspection of clear cellophane tape lifted from lesions also may be diagnostic. In the absence of identifiable mites or eggs, the diagnosis is based on a history of pruritus, a clinical examination, and an epidemiologic link. Diverse kinds of dermatitis from other causes frequently are misdiagnosed as scabies, particularly in presumed “outbreak” situations. Scabies mites of other animals may cause transient irritation, but they do not reside or reproduce in human hosts.

Chiggers are the larvae of trombiculid (harvest) mites that normally feed on mice in grassy or brush-covered sites in tropical, subtropical, and (less frequently) temperate areas during warm months. They reside on low vegetation and attach themselves to passing mammalian hosts. While feeding, larvae secrete saliva with proteolytic enzymes to create a tube-like invagination in the host’s skin; this stylostome allows the mite to imbibe tissue fluids. The stylostomal saliva is highly antigenic and causes exceptionally pruritic papular, papulovesicular, or papulourticarial lesions (≤2 cm in diameter). In people previously sensitized to salivary antigens, the papules develop within hours of attachment. While attached, mites appear as tiny red vesicles on the skin. Generally, lesions vesicate and develop a hemorrhagic base. Scratching, however, invariably destroys the body of a mite. Itching and burning often persist for weeks. The rash is common on the ankles and areas where clothing obstructs the further wanderings of the mites. Repellents are useful for preventing chigger bites.

Many kinds of mites that are associated with peridomestic birds and rodents are particularly bothersome when they invade homes and bite people. In North America, the northern fowl mite, chicken mite, tropical rat mite, and house mouse mite normally feed on poultry, various songbirds, and small mammals and are abundant in and around their hosts’ nests. After their natural hosts die or leave the nest, these mites frequently invade human habitations. Although the mites are rarely seen because of their small size, their bites can be painful and pruritic. Once confirmed as the cause of irritation, rodent- and bird-associated mites are best eliminated by excluding their hosts, removing the nests, and cleaning and treating the nesting area with appropriate acaricides. Pyemotes and other mites that infest grain, straw, cheese, hay, or other products occasionally produce similar episodes of rash and discomfort and may produce a unique dermatologic “comet sign” lesion—a paisley-shaped urticarial plaque.

Diagnosis of mite-induced dermatitides (including those caused by chiggers) relies on confirmation of the mite’s identity or elicitation of a history of exposure to the mite’s source. Oral antihistamines or topical steroids may suppress mite-induced pruritus temporarily but do not eliminate the mites.

Ticks attach superficially to skin and feed painlessly; blood is their only food. Their salivary secretions are biologically active and can produce local reactions, induce fevers, and cause paralysis in addition to transmitting diverse pathogens. The two main families of ticks are the hard (ixodid) and soft (argasid) ticks. Generally, soft ticks attach for <1 h, leaving red macules after they drop off. Some species in Africa, the western United States, and Mexico produce painful hemorrhagic lesions. Hard ticks are much more common and transmit most of the tick-borne infections that are familiar to physicians and patients. Hard ticks attach to the host and feed for several days or sometimes for >1 week. At the site of hard-tick bites, small areas of induration, often purpuric, develop and may be surrounded by an erythematous rim. A necrotic eschar, called a tâche noire, occasionally develops. Chronic nodules (persistent tick-bite granulomas) can be several centimeters in diameter and may linger for months after the feeding tick has been removed. These granulomas can be treated with injected intralesional glucocorticoids or by surgical excision. Tick-induced fever, unassociated with transmission of any pathogen, is often accompanied by headache, nausea, and malaise but usually resolves ≤36 h after the tick is removed.

Tick paralysis, an acute ascending flaccid paralysis that resembles Guillain-Barré syndrome, is believed to be caused by one or more toxins in tick saliva that block neuromuscular transmission and decrease nerve conduction. This rare complication has followed the bites of more than 60 kinds of ticks, although in the United States dog and wood ticks (Dermacentor species) are most commonly involved. Weakness begins symmetrically in the lower extremities ≤6 days after the tick’s attachment, ascends symmetrically during several days, and may culminate in complete paralysis of the extremities and cranial nerves. Deep tendon reflexes are diminished or absent, but sensory examination and findings on lumbar puncture are typically normal. Removal of the tick generally leads to rapid improvement within a few hours and complete recovery after several days, although the patient’s condition may continue to deteriorate for a full day. Failure to remove the tick may lead to dysarthria, dysphagia, and ultimately death from aspiration or respiratory paralysis. Diagnosis depends on finding the tick, which is often hidden beneath scalp hair. An antiserum to the saliva of Ixodes holocyclus, the usual cause of tick paralysis in Australia, effectively reverses paralysis caused by these ticks.

Removal of hard ticks during the first 36 h of attachment nearly always prevents transmission of the agents of Lyme disease, babesiosis, anaplasmosis, and ehrlichiosis, although several tick-borne viruses may be transmitted more quickly. Ticks should be removed by traction with fine-tipped forceps placed firmly around the tick’s mouthparts. Careful handling (to avoid rupture of ticks) and use of gloves may avert accidental contamination with pathogens contained in tick fluids. Use of occlusive dressings, heat, or other substances (in an attempt to induce the tick to detach) merely delay tick removal. Afterward, the site of attachment should be disinfected. Tick mouthparts sometimes remain in the skin but generally are shed spontaneously within days without excision. Although somewhat controversial, current guidelines from the Centers for Disease Control and Prevention suggest that, rather than awaiting the onset of erythema migrans, the results of tick testing, or seroconversion to antigens diagnostic for Lyme disease, administering prophylaxis with a single oral dose of doxycycline (200 mg) within 72 h of tick removal is appropriate in adult patients with bites thought to be associated with deer ticks (Fig. 137-1) in Lyme disease–endemic areas from Maryland to Maine and in Wisconsin and Minnesota.

Nymphs and adults of all three kinds of human lice feed at least once a day, ingesting human blood exclusively. Head lice (Pediculus capitis) infest mainly the hair of the scalp, body lice (Pediculus humanus) the clothing, and crab or pubic lice (Pthirus pubis) mainly the hair of the pubis. The saliva of lice produces a pruritic morbilliform or urticarial rash in some sensitized persons. Female head and pubic lice cement their eggs (nits) firmly to hair, whereas female body lice cement their eggs to clothing, particularly to threads along clothing seams. After ~10 days of development within the egg, a nymph hatches. Empty eggs may remain affixed for months thereafter.

In North America, head lice infest ~1% of elementary school-age children. Head lice are transmitted mainly by direct head-to-head contact rather than by fomites such as shared headgear, bed linens, hairbrushes, and other grooming implements. Chronic infestations by head lice tend to be asymptomatic. Pruritus, due mainly to hypersensitivity to the louse’s saliva, generally is transient and mild. Head lice removed from a person succumb to desiccation and starvation within ~1 day. Head lice are not known to serve as a natural vector for any pathogens.

Body lice remain on clothing except when feeding and generally succumb in ≤2 days if separated from their host. In most Western countries, body lice are generally found on a small proportion of indigent persons but may become increasingly prevalent after upheaval associated with natural or human-caused disasters, when homeless victims are in close contact with infested individuals with whom they share accommodations. Body lice are acquired by direct contact or by sharing of infested clothing and bedding. These lice are vectors for the agents of louse-borne (epidemic) typhus (Chap. 83), louse-borne relapsing fever (Chap. 81), and trench fever (Chap. 69). Pruritic lesions from their bites are particularly common around the neckline. Chronic infestations result in a postinflammatory hyperpigmentation and thickening of skin known as vagabond’s disease.

The crab or pubic louse is transmitted mainly by sexual contact. These lice occur predominantly on pubic hair and less frequently on axillary or facial hair, including the eyelashes. Children and adults may acquire pubic lice by sexual or close nonsexual contact. Intensely pruritic, bluish macules ~3 mm in diameter (maculae ceruleae) develop at the site of bites. Blepharitis commonly accompanies infestations of the eyelashes.

Pediculiasis is often suspected upon the detection of nits firmly cemented to hairs or in clothing. Many bona fide nits, however, are dead or hatched relics of prior infestation, and pseudo-nits are frequently misconstrued to be signs of a louse infestation. Confirmation of a louse infestation, therefore, best relies on the discovery of a live louse.

Myiasis refers to infestations by several kinds of fly larvae (maggots) that invade living or necrotic tissues or body cavities and produce different clinical syndromes, depending on the species of fly.

In forested parts of Central and South America, larvae of the human botfly (Dermatobia hominis) produce furuncular (boil-like) papules or subcutaneous nodules ≤3 cm in diameter. A gravid adult female botfly captures a mosquito or another bloodsucking insect and deposits her eggs on its abdomen. When the carrier insect attacks a human or bovine host several days later, the warmth and moisture of the host’s skin stimulate the eggs to hatch. The emerging larvae promptly penetrate intact skin. After 6–12 weeks of development, mature larvae emerge from the skin and drop to the ground to pupate and then become adults.

The African tumbu fly (Cordylobia anthropophaga) deposits its eggs on damp sand or leaf litter or on drying laundry, particularly that contaminated by urine or sweat. Larvae hatch from eggs upon contact with a host’s body and penetrate the skin, producing boil-like lesions from which mature larvae emerge ~9 days later. Furuncular myiasis is suggested by uncomfortable lesions with a central breathing pore that emits bubbles when submerged in water. A sensation of movement under the patient’s skin may cause severe emotional distress.

Larvae that cause furuncular myiasis may be induced to emerge if the air pore is coated with petrolatum or another occlusive substance. Removal may be facilitated by injection of a local anesthetic into the surrounding tissue, but surgical excision is sometimes necessary because upward-pointing spines of some species hold the larvae firmly in place.

Other fly larvae cause nonfuruncular myiasis. For example, larvae of the horse botfly (Gasterophilus intestinalis) emerge from eggs deposited on the horse’s flanks and may come into contact with and infest human beings. After penetrating human skin, these larvae rarely mature but instead may migrate for weeks in the dermis. The resulting pruritic and serpiginous eruption resembles cutaneous larva migrans caused by canine or feline hookworms (Chap. 131). Larvae of rabbit and rodent botflies (Cuterebra species) occasionally cause dermal or tracheopulmonary myiasis.

Certain flies are attracted to blood and pus, laying their eggs on open or draining sores. Newly hatched larvae enter wounds or diseased skin. Larvae of several types of green bottle flies (Lucilia/Phaenicia species) usually remain superficial and confined to necrotic tissue. Specially raised, sterile “surgical maggots” are sometimes used intentionally for wound debridement. Larvae of screwworm flies, Cochliomyia, and the flesh fly invade viable tissues more deeply and produce large suppurating lesions. Larvae that infest wounds also may enter body cavities such as the mouth, nose, ears, sinuses, anus, vagina, and lower urinary tract, particularly in unconscious or otherwise debilitated patients. The consequences range from harmless colonization to destruction of the nose, meningitis, and deafness. Treatment involves removal of maggots and debridement of tissue.

The maggots responsible for furuncular and wound myiasis also may cause ophthalmomyiasis. Sequelae include nodules in the eyelid, retinal detachment, and destruction of the globe. Most instances in which maggots are found in human feces result from deposition of eggs or larvae by flies on recently passed stools, not from an intestinal maggot infestation.

Pentastomids (tongue worms) inhabit the respiratory passages of reptiles and carnivorous mammals. Human infestation by Linguatula serrata is common in the Middle East and results from the consumption of encysted larval stages in raw liver or lymph nodes of sheep and goats, which are true intermediate hosts for the tongue worms. Larvae migrate to the nasopharynx and produce an acute self-limiting syndrome—known as halzoun or marrara—characterized by pain and itching of the throat and ears, coughing, hoarseness, dysphagia, and dyspnea. Severe edema may cause obstruction that requires tracheostomy. In addition, ocular invasion has been described. Diagnostic larvae measuring ≤10 mm in length appear in copious nasal discharge or vomitus. Individuals become infected with another type of tongue worm, Armillifer armillatus, by consuming its eggs in contaminated food or drink or after handling the definitive host, the African python. Larvae encyst in various organs but rarely cause symptoms. Cysts may require surgical removal as they enlarge during molting, but they usually are encountered as an incidental finding at autopsy. Parasite-induced lesions may be misinterpreted as a malignancy, with the correct diagnosis confirmed histopathologically. Cutaneous larva migrans–type syndromes of other pentastomes have been reported from Southeast Asia and Central America.

Medically important leeches are annelid worms that attach to their hosts with chitinous cutting jaws and draw blood through muscular suckers. The medicinal leech (Hirudo medicinalis) is still used occasionally for medical purposes to reduce venous congestion in surgical flaps or replanted body parts. This practice has been complicated by intractable bleeding, wound infections, myonecrosis, and sepsis due to Aeromonas hydrophila, which colonizes the gullets of commercially available leeches.

Ubiquitous aquatic leeches that parasitize fish, frogs, and turtles readily attach to the skin of human beings and avidly suck blood. More notorious are arboreal land leeches that live among moist vegetation of tropical rain forests. Attachment is usually painless, and the leeches will detach themselves when satiated with a blood meal. Hirudin, a powerful anticoagulant secreted by the leech, causes continued bleeding after the leech has detached. Healing of a leech-bite wound is slow, and bacterial infections are not uncommon. Several kinds of aquatic leeches in Africa, Asia, and southern Europe can enter the mouth, nose, and genitourinary tract and attach to mucosal surfaces at sites as deep as the esophagus and trachea. Externally attached leeches generally drop off after they have engorged, but removal is hastened by gentle scraping aside of the anterior and posterior suckers the leech uses for attachment and feeding. Some authorities dispute the wisdom of removing leeches with alcohol, salt, vinegar, insect repellent, a flame or heated instrument, or applications of other noxious substances. Internally attached leeches may detach on exposure to gargled saline or may be removed by forceps.

Of the more than 30,000 recognized species of spiders, only ~100 defend themselves aggressively and have fangs sufficiently long to penetrate human skin. The venom that some spiders use to immobilize and digest their prey can cause necrosis of skin and systemic toxicity. Whereas the bites of most spiders are painful but not harmful, envenomations by recluse or fiddleback spiders (Loxosceles species) and widow spiders (Latrodectus species) may be life-threatening. Identification of the offending spider is important because specific treatments exist for bites of widow spiders and because injuries attributed to spiders are frequently due to other causes. Except in cases where the patient actually observes a spider immediately associated with the bite or fleeing from the site, lesions reported as spider-bite reactions are most often due to other injuries or to infections with bacteria such as methicillin-resistant Staphylococcus aureus (MRSA).

Recluse spider bites and necrotic arachnidism

Brown recluse spiders live mainly in the south-central United States and have close relatives in Central and South America, Africa, and the Middle East. Bites by brown recluse spiders usually cause only minor injuries, with edema and erythema. Envenomation, however, occasionally causes severe necrosis of skin and subcutaneous tissue and more rarely causes systemic hemolysis. These spiders are not aggressive toward humans and will bite only if threatened or pressed against the skin. They hide under rocks and logs or in caves and animal burrows. They invade homes and seek dark and undisturbed hiding spots in closets, in folds of clothing, or under furniture and rubbish in storage rooms, garages, and attics. Despite their impressive abundance in some homes, these spiders rarely bite humans. Bites tend to occur while the victim is dressing and are sustained primarily on the hands, arms, neck, and lower abdomen.

Initially, the bite is painless or may produce a stinging sensation. Within the next few hours, the site becomes painful and pruritic, with central induration surrounded by a pale ischemic zone that itself is encircled by a zone of erythema. In most cases, the lesion resolves without treatment in just a few days. In severe cases, the erythema spreads, and the center of the lesion becomes hemorrhagic or necrotic with an overlying bulla. A black eschar forms and sloughs several weeks later, leaving an ulcer that eventually may create a depressed scar. Healing usually takes place in ≤6 months but may take as long as 3 years if adipose tissue is involved. Local complications include injury to nerves and secondary bacterial infection. Fever, chills, weakness, headache, nausea, vomiting, myalgia, arthralgia, maculopapular rash, and leukocytosis may develop ≤72 h after the bite. Reports of deaths attributed to bites of North American brown recluse spiders have not been verified.

TREATMENT

Widow spider bites

The black widow spider, common in the southeastern United States, measures ≤1 cm in body length and 5 cm in leg span and is shiny black with a red hourglass marking on the ventral abdomen. Other dangerous Latrodectus species occur elsewhere in temperate and subtropical parts of the world. The bites of the female widow spiders are notorious for their potent neurotoxins.

Widow spiders spin their webs under stones, logs, plants, or rock piles and in dark spaces in barns, garages, and outhouses. Bites are most common in the summer and early autumn and occur when a web is disturbed or a spider is trapped or provoked. The initial bite is perceived as a sharp pinprick or may go unnoticed. Fang-puncture marks are uncommon. The venom that is injected does not produce local necrosis, and some persons experience no other symptoms. α-Latrotoxin, the most active component of the venom, binds irreversibly to presynaptic nerve terminals and causes release and eventual depletion of acetylcholine, norepinephrine, and other neurotransmitters from those terminals. Painful cramps may spread within 60 min from the bite site to large muscles of the extremities and trunk. Extreme rigidity of the abdominal muscles and excruciating pain may suggest peritonitis, but the abdomen is not tender on palpation and surgery is not warranted. The pain begins to subside during the first 12 h but may recur during several days or weeks before resolving spontaneously. A wide range of other neurologic sequelae may include salivation, diaphoresis, vomiting, hypertension, tachycardia, labored breathing, anxiety, headache, weakness, fasciculations, paresthesia, hyperreflexia, urinary retention, uterine contractions, and premature labor. Rhabdomyolysis and renal failure have been reported, and respiratory arrest, cerebral hemorrhage, or cardiac failure may end fatally, especially in very young, elderly, or debilitated persons.

Tarantulas and other spiders

Tarantulas are hairy spiders of which 30 species are found in the United States, mainly in the Southwest. The tarantulas that have become popular household pets are usually imported from Central or South America. Tarantulas bite only when threatened and usually cause no more harm than a bee sting, but on occasion the venom causes deep pain and swelling. Several species of tarantulas are covered with urticating hairs that are brushed off in the thousands when a threatened spider rubs its hind legs across its dorsal abdomen. These hairs can penetrate human skin and produce pruritic papules that may persist for weeks. Failure to wear gloves or to wash the hands after handling the Chilean Rose tarantula, a popular pet spider, has resulted in transfer of hairs to the eye with subsequent devastating ocular inflammation. Treatment of bites includes local washing and elevation of the bitten area, tetanus prophylaxis, and analgesic administration. Antihistamines and topical or systemic glucocorticoids are given for exposure to urticating hairs.

Atrax robustus, a funnel-web spider of Australia, and Phoneutria species, the South American banana spiders, are among the most dangerous spiders in the world because of their aggressive behavior and potent neurotoxins. Envenomation by A. robustus causes a rapidly progressive neuromotor syndrome that can be fatal within 2 h. The bite of a banana spider causes severe local pain followed by profound systemic symptoms and respiratory paralysis that can lead to death within 2–6 h. Specific antivenoms for use after bites by each of these spiders are available. Yellow sac spiders (Cheiracanthium species) are common in homes worldwide. Their bites, though painful, generally lead to only minor erythema, edema, and pruritus.

Scorpions are arachnids that feed on ground-dwelling arthropods and small lizards. They paralyze their prey and defend themselves by injecting venom from a stinger on the tip of the tail. Painful but relatively harmless scorpion stings need to be distinguished from the potentially lethal envenomations that are produced by ~30 of the ~1000 known species and that cause more than 5000 deaths worldwide each year. Scorpions are nocturnal and remain hidden during the day in crevices or burrows or under wood, loose bark, or rocks. They occasionally enter houses and tents and may hide in shoes, clothing, or bedding. Scorpions sting humans only when threatened.

Of the 40 or so scorpion species in the United States, only bark scorpions—e.g., Centruroides sculpturatus (C. exilicauda) in the Southwest—produce venom that is potentially lethal to humans. This venom contains neurotoxins that cause sodium channels to remain open. Such envenomations usually are associated with little swelling, but prominent pain, paresthesia, and hyperesthesia can be accentuated by tapping on the affected area (the tap test). These symptoms soon spread to other locations; dysfunction of cranial nerves and hyperexcitability of skeletal muscles develop within hours. Patients present with restlessness, blurred vision, abnormal eye movements, profuse salivation, lacrimation, rhinorrhea, slurred speech, difficulty in handling secretions, diaphoresis, nausea, and vomiting. Muscle twitching, jerking, and shaking may be mistaken for a seizure. Complications include tachycardia, arrhythmias, hypertension, hyperthermia, rhabdomyolysis, and acidosis. Symptoms progress to maximal severity in ~5 h and subside within a day or two, although pain and paresthesia can last for weeks. Fatal respiratory arrest is most common among young children and the elderly.

Envenomations by Leiurus quinquestriatus in the Middle East and North Africa, by Mesobuthus tamulus in India, by Androctonus species along the Mediterranean littoral and in North Africa and the Middle East, and by Tityus serrulatus in Brazil cause massive release of endogenous catecholamines with hypertensive crises, arrhythmias, pulmonary edema, and myocardial damage. Acute pancreatitis occurs with stings of Tityus trinitatis in Trinidad, and central nervous toxicity complicates stings of Parabuthus and Buthotus scorpions of South Africa. Tissue necrosis and hemolysis may follow stings of the Iranian Hemiscorpius lepturus.

Stings of most other species cause immediate sharp local pain followed by edema, ecchymosis, and a burning sensation. Symptoms typically resolve within a few hours, and skin does not slough. Allergic reactions to the venom sometimes develop.

Insects that sting in defense or to subdue their prey belong to the order Hymenoptera, which includes bees, wasps, hornets, yellow jackets, and ants. Their venoms contain a wide array of amines, peptides, and enzymes that cause local and systemic reactions. Although the toxic effect of multiple stings can be fatal to a human, nearly all of the ≥100 deaths due to hymenopteran stings in the United States each year result from allergic reactions.

Bee and wasp stings

The stinger of the honeybee (Apis mellifera) is unique in being barbed. When a bee stings a foe, its stinging apparatus and attached venom sac tear loose from its body. Muscular contraction of the venom sac continues to inject venom into the skin. Other kinds of bees, ants, and wasps have smooth stinging mechanisms and can sting numerous times in succession. Honeybees, bumblebees, and social wasps generally attack only when a colony is disturbed. Africanized honeybees (now present in South and Central America and the southern and western United States) respond to minimal intrusions more aggressively. Whereas the sting of an Africanized bee contains less venom than that of its non-Africanized relatives, victims tend to sustain far more stings and therefore to receive a far greater overall volume of venom. Most patients who report having sustained a “bee sting,” however, are more likely to have encountered stinging wasps instead.

The venoms of different species of hymenopterans are biochemically and immunologically distinct. Direct toxic effects are mediated by mixtures of low-molecular-weight compounds such as serotonin, ­histamine, acetylcholine, and several kinins. Polypeptide toxins in honeybee venom include mellitin that damages cell membranes, mast cell–degranulating protein that causes histamine release, the neurotoxin apamin, and the anti-inflammatory compound adolapin. Enzymes in venom include hyaluronidase and phospholipases. There appears to be little cross-sensitization between the venoms of honeybees and wasps.

Uncomplicated hymenopteran stings cause immediate pain, a wheal-and-flare reaction, and local edema, all of which usually subside in a few hours. Multiple stings can lead to vomiting, diarrhea, generalized edema, dyspnea, hypotension, and non-anaphylactic circulatory collapse. Rhabdomyolysis and intravascular hemolysis may cause renal failure. Death from the direct (nonallergic) effects of venom has followed stings of several hundred honeybees. Stings to the tongue or mouth may induce life-threatening edema of the upper airways.

Large local reactions accompanied by erythema, edema, warmth, and tenderness that spread ≥10 cm around the sting site over 1–2 days are not uncommon. These reactions may resemble bacterial cellulitis but are caused by hypersensitivity rather than by secondary infection. Such reactions tend to recur on subsequent exposure but are seldom accompanied by anaphylaxis and are not prevented by venom immunotherapy.

An estimated 0.4–4.0% of the U.S. population exhibits clinical immediate-type hypersensitivity to hymenopteran stings, and 15% may have asymptomatic sensitization manifested by positive skin tests. Persons who experience severe allergic reactions are likely to have similar reactions after subsequent stings by the same or closely related species. Occasionally, persons who have had mild reactions earlier in life will experience more serious reactions to subsequent stings. Mild anaphylactic reactions from insect stings, as from other causes, consist of nausea, abdominal cramping, generalized urticaria, flushing, and angioedema. Serious reactions, including upper airway edema, bronchospasm, hypotension, and shock, may be rapidly fatal. Severe reactions usually begin within 10 min of the sting and only rarely develop after 5 h.

Stinging ants

Stinging fire ants are an important medical problem in the United States. Imported fire ants (Solenopsis species) infest southern states from Texas to North Carolina, with colonies now established in California, New Mexico, Arizona, and Virginia. Slight disturbances of their mound nests have provoked massive outpourings of ants and as many as 10,000 stings on a single person. Elderly and immobile persons are at high risk for attacks when fire ants invade dwellings.

Fire ants attach to skin with powerful mandibles and rotate their bodies while repeatedly injecting venom with posteriorly situated stingers. The alkaloid venom consists of cytotoxic and hemolytic piperidines and several proteins with enzymatic activity. The initial wheal-and-flare reaction, burning, and itching resolve in ~30 min, and a sterile pustule develops within 24 h. The pustule ulcerates over the next 48 h and then heals in ≥1 week. Large areas of erythema and edema lasting several days are not uncommon and in extreme cases may compress nerves and blood vessels. Anaphylaxis occurs in fewer than 2% of victims; seizures and mononeuritis have been reported. Stings are treated with ice packs, topical glucocorticoids, and oral antihistamines. Pustules should be cleansed and then covered with bandages and antibiotic ointment to prevent bacterial infection. Epinephrine administration and supportive measures are indicated for anaphylactic reactions. Fire ant whole-body extracts are available for skin testing and immunotherapy, which appears to lower the rate of anaphylactic reactions.

European fire (red) ants (Myrmica rubra) have recently become public health pests in the northeastern United States and southern Canada. The western United States is home to harvester ants (Pogonomyrmex species). The painful local reaction that follows harvester ant stings often extends to lymph nodes and may be accompanied by anaphylaxis. The bullet or conga ant (Paraponera clavata) of South America is known locally as hormiga veinticuatro (“24-hour ant”), a designation that refers to the 24 h of throbbing, excruciating pain following a sting that delivers the potent paralyzing neurotoxin poneratoxin.

In the process of feeding on vertebrate blood and tissue fluids, adults of certain flies inflict painful bites, produce local allergic reactions, and may transmit pathogenic agents. Bites of mosquitoes, tiny “no-see-um” (ceratopogonid) midges, and phlebotomine sand flies typically produce a wheal and a pruritic papule. Small humpbacked black flies (simuliids) lacerate skin, resulting in a lesion with serosanguineous discharge that is often painful and pruritic. Regional lymphadenopathy, fever, or anaphylaxis occasionally ensues. The widely distributed deerflies and horseflies as well as the tsetse flies of Africa are stout flies measuring ≤25 mm in length that attack during the day and produce large and painful bleeding punctures. Houseflies (Musca domestica) do not consume blood but use rasping mouthparts to scarify skin and feed upon tissue fluids and salt. Beyond direct injury from bites of any kind of fly, risks include transmission of diverse pathogens and secondary infection of the lesion.

Common human-biting fleas include the dog and cat fleas (Ctenocephalides species) and the rat flea (Xenopsylla cheopis), which infest their respective hosts and the hosts’ nests and resting sites. Sensitized persons develop erythematous pruritic papules (papular urticaria) and occasionally vesicles and bacterial superinfection at the site of the bite. Symptom-based treatment consists of antihistamines, topical glucocorticoids, and topical antipruritic agents.

Flea infestations are eliminated by removal and treatment of animal nests, frequent cleaning of pet bedding, and application of contact and systemic insecticides to pets and the dwelling. Flea infestations in the home may be abated or prevented if pets are regularly treated with veterinary antiparasitic agents and insect growth regulators.

Tunga penetrans, like other fleas, is a wingless, laterally flattened insect that feeds on blood. Also known as the chigoe flea, sand flea, or jigger (not to be confused with the chigger), it occurs in tropical regions of Africa and the Americas. Adult female chigoes live in sandy soil and burrow under the skin, usually between toes, under nails, or on the soles of bare feet. Gravid chigoes engorge on the host’s blood and grow from pinpoint to pea size during a 2-week interval. They produce lesions that resemble a white pustule with a central black depression and that may be pruritic or painful. Occasional complications include tetanus, bacterial infections, and autoamputation of toes (ainhum). Tungiasis is treated by removal of the intact flea with a sterile needle or scalpel, tetanus vaccination, and topical application of antibiotics.

Several true bugs of the family Reduviidae inflict bites that produce allergic reactions and are sometimes painful. The cone-nose bugs, so called because of their elongated heads, include the assassin and wheel bugs, which feed on other insects and bite vertebrates only in self-defense, and the kissing bugs, which routinely feed on vertebrate blood. The bites of the night-feeding kissing bugs are painless. Reactions to such bites depend on prior sensitization and include tender and pruritic papules, vesicular or bullous lesions, extensive urticaria, fever, lymphadenopathy, and (rarely) anaphylaxis. Bug bites are treated with topical antipruritics or oral antihistamines. Persons with anaphylactic reactions to reduviid bites should keep an epinephrine kit available. Some reduviids transmit Trypanosoma cruzi, the agent of New World trypanosomiasis (also called Chagas disease) (Chap. 127).

The cosmopolitan bedbugs (Cimex species) hide in crevices of mattresses, bed frames and other furniture, walls, and picture frames and under loose wallpaper. Bedbug populations have resurged, recently attaining levels and spreading to an extent not encountered since the mid-twentieth century. These bugs are now a common pest in homes, dormitories, and hotels; on cruise ships; and even in medical facilities. Generally, the bugs hide during the day and take blood meals at night. Their bite is painless, but minutes to days later, sensitized persons develop erythema, itching, and wheals around a central hemorrhagic punctum. Bedbugs are not known to transmit pathogens.

The fangs of centipedes of the genus Scolopendra can penetrate human skin and deliver a venom that produces intense burning pain, swelling, erythema, and sterile lymphangitis. Dizziness, nausea, and anxiety are described occasionally, and rhabdomyolysis and renal failure have been reported. Treatment includes washing of the site, application of cold dressings, oral analgesic administration or local lidocaine infiltration, and tetanus prophylaxis.

Millipedes are docile and do not bite, but some secrete defensive fluids that may burn and discolor human skin. Affected skin turns brown overnight and may blister and exfoliate. Secretions in the eye cause intense pain and inflammation that can result in corneal ulcers and even blindness. Management includes irrigation with copious amounts of water or saline, use of analgesics, and local care of denuded skin.

Caterpillars of several moth species are covered with hairs or spines that produce mechanical irritation and may contain or be coated with venom. Contact with these caterpillars or their hairs may lead to lepidopterism or caterpillar envenomation. The response typically consists of an immediate burning sensation followed by local swelling and erythema and occasionally by regional lymphadenopathy, nausea, vomiting, and headache. A rare reaction to a South American caterpillar, Lonomia obliqua, can cause disseminated coagulopathy and fatal hemorrhagic shock. In the United States, dermatitis is most often associated with caterpillars of the io, puss, saddleback, and brown-tail moths. Even contact with detached hairs of other caterpillars, such as gypsy moth larvae, can later produce a pruritic urticarial or papular rash called erucism. Spines may be deposited on tree trunks or drying laundry or may be airborne and cause irritation of the eyes and upper airways. Treatment of caterpillar stings consists of repeated application of adhesive or cellophane tape to remove the hairs, which can then be identified microscopically. Local ice packs, topical glucocorticoids, and oral antihistamines relieve symptoms.

Several families of beetles have independently developed the ability to produce chemically unrelated vesicating toxins. When disturbed, blister beetles (family Meloidae) extrude cantharidin, a low-molecular-weight toxin that produces thin-walled blisters (≤5 cm in diameter) 2–5 h after contact. The blisters are not painful or pruritic unless broken and resolve without treatment in ≤10 days. Nephritis may follow unusually heavy cantharidin exposure. Contact occurs when individuals sit on the ground, work in the garden, or deliberately handle the beetles. The hemolymph of certain rove beetles (Staphylinidae) contains pederin, a potent vesicant. When these beetles are crushed or brushed against the skin, the released fluid causes painful, red, flaccid bullae. These beetles occur worldwide but are most numerous and problematic in parts of Africa (where they are called “Nairobi fly”) and southwestern Asia. Ocular lesions may develop after impact with flying beetles at night or unintentional transfer of the vesicant on the fingers. Treatment is rarely necessary, although ruptured blisters should be kept clean and bandaged.

Larvae of common carpet beetles are adorned with dense arrays of ornate hairs called hastisetae. Contact with these larvae or their setae results in delayed dermal reactions in sensitized individuals. The lesions are commonly mistaken as bites of bedbugs.

The groundless conviction that one is infested with arthropods or other parasites (Ekbom’s syndrome, delusory parasitosis, delusions of parasitosis, and perhaps Morgellons syndrome) is extremely difficult to treat and, unfortunately, is not uncommon. Patients describe uncomfortable sensations of something moving in or on their skin. Excoriations and self-induced ulcerations typically accompany the pruritus, dysesthesias, and imaginary insect bites. Patients often believe that some invisible or as yet undescribed creatures are infesting their skin, clothing, homes, or environment in general. Frequently, patients submit as evidence of infestation specimens that consist of plant-feeding and nonbiting peridomestic arthropods, pieces of skin, vegetable matter, lint, and other inanimate detritus. When evaluating a patient with possible delusional parasitosis, it is imperative to rule out true infestations and bites by arthropods, endocrinopathies, sensory disorders due to neuropathies, opiate and other drug use, environmental irritants (e.g., fiberglass threads), and other causes of tingling or prickling sensations. Frequently, such patients repeatedly seek medical consultations, resist alternative explanations for their symptoms, and exacerbate their discomfort by self-treatment. Long-term pharmacotherapy with pimozide or other psychotropic agents has been more helpful than psychotherapy in treating this disorder. Patients with delusional parasitosis often develop the unshakeable conviction that they are infested by a previously unknown pathogen, while their personal lives, family support, and employment collapse around them.

Acknowledgment

The substantial contributions of Andrew Spielman and James H. Maguire to this chapter in previous editions are gratefully acknowledged.