Ectoparasites are arthropods or helminths that infest the skin or hair of other animals, from which they derive sustenance and shelter. They may penetrate beneath the surface of the host or attach superficially by their mouthparts and specialized claws. These organisms damage their hosts by inflicting direct injury, eliciting a hypersensitivity reaction, inoculating toxins or pathogens, and inciting fear. The main medically important ectoparasites are arachnids (including mites and ticks), insects (including lice, fleas, bedbugs, and flies), pentastomes (tongue worms), and leeches. Arthropods also may harm humans through brief encounters during which they take a blood meal or attempt to defend themselves by biting, stinging, or exuding venoms. Various arachnids (spiders, scorpions), insects (bees, hornets, wasps, ants, flies, bugs, caterpillars, and beetles), millipedes, and centipedes produce ill effects in these manners, as do certain ectoparasites of animals, including ticks, biting mites, and fleas. In the United States, more people die each year from arthropod stings than from the bites of poisonous snakes. Lesions resulting from the bites and stings of arthropods are so diverse and variable that it is rarely possible to identify precisely what kind of insect or tick is involved without a bona fide specimen and entomologic expertise.
The human itch mite, Sarcoptes scabiei, is a common cause of itching dermatosis, infesting ∼300 million persons worldwide. Gravid female mites that measure ∼0.3 mm in length burrow superficially beneath the stratum corneum, depositing three or fewer eggs per day. Nymphs mature in ∼2 weeks and then emerge as adults to the surface of the skin, where they mate and (re)invade the skin of the same or another host. Transfer of newly fertilized female mites from person to person occurs mainly by intimate contact and is facilitated by crowding, poor hygiene, and multiple sexual partners. Generally, these mites die within a day or so in the absence of host contact. Transmission via sharing of contaminated bedding or clothing therefore occurs infrequently. In the United States, scabies may account for up to 5% of visits to dermatologists. Outbreaks occur in nursing homes, mental institutions, and hospitals.
The itching and rash associated with scabies derive from a sensitization reaction directed against the excreta that the mite deposits in its burrow. An initial infestation remains asymptomatic for up to 6 weeks, and a reinfestation produces a hypersensitivity reaction without delay. Burrows become surrounded by infiltrates 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 or Norwegian scabies, may result from glucocorticoid use, immunodeficiency, and neurologic and psychiatric illnesses that limit itching and scratching.
Intense itching worsens at night and after a hot shower. Typical burrows may be difficult to find because they are few in number and may be obscured by excoriations. Burrows appear as dark wavy lines in the epidermis and measure up to 15 mm. Lesions occur most frequently on the volar wrists, between the fingers, on the elbows, and on the penis. Small papules and vesicles, often accompanied by eczematous plaques, pustules, or nodules, are distributed symmetrically in those sites and in skinfolds under the breasts and around the navel, axillae, belt line, buttocks, upper thighs, and scrotum. Except in infants, the face, scalp, neck, palms, and soles are spared. Crusted scabies resembles psoriasis in its typical widespread erythema, thick keratotic crusts, scaling, 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 polymorphic skin lesions in characteristic locations, particularly if there is a history of household contact with an affected person. Burrows should be sought and unroofed with a sterile needle or scalpel blade, and the scrapings should be examined microscopically for the mite, its eggs, and its fecal pellets. Biopsies (including superficial cyanoacrylate biopsy), scrapings, and dermascopic imaging of papulovesicular lesions as well as microscopic inspection of clear adhesive tape lifted from lesions also may be diagnostic. In the absence of identifiable mites or mite products, the diagnosis is based on clinical presentation and history. Diverse kinds of dermatitis due to other causes frequently are misdiagnosed as scabies.
Permethrin cream (5%) is less toxic than 1% lindane preparations and is effective against lindane-tolerant infestations. Scabicides are applied thinly but thoroughly behind the ears and from the neck down after bathing and are removed 8 h later with soap and water. Successful treatment of crusted scabies requires preapplication of a keratolytic agent such as 6% salicylic acid and then of scabicides to the scalp, face, and ears. Repeated treatments or the sequential use of several agents may be necessary. Ivermectin has not been approved by the U.S. Food and Drug Administration (FDA) for use against any form of scabies, but a single oral dose (200 μg/kg) effectively treats scabies in otherwise healthy persons; patients with crusted scabies may require two doses separated by an interval of 1–2 weeks.
Although effectively treated scabies infestations become noninfectious within a day, itching and rash due to hypersensitivity to the dead mites and their excreted and secreted products frequently persist for weeks or months. Unnecessary re-treatment with topical agents may provoke contact dermatitis. Antihistamines, salicylates, and calamine lotion relieve itching during treatment, and topical glucocorticoids are useful for pruritus that lingers after effective treatment. To prevent reinfestations, bedding and clothing should be washed and/or dried on high heat or heat-pressed, and close contacts, even if asymptomatic, should be treated simultaneously.
Chiggers and Other Biting Mites
Chiggers are the larvae of trombiculid (harvest) mites that normally feed on mice in grassy or brush-covered sites in the tropics and subtropics and less frequently in temperate areas during warm months. They wait for hosts on low vegetation and attach themselves to passing animals or humans. The larva pierces the skin of its host and produces a secreted tubelike structure (stylostome) in the dermis through which it imbibes tissue fluids. The stylostome is highly antigenic and causes an exceptionally pruritic papular, papulovesicular, or papulourticarial lesion (≤2 cm in diameter) that develops within hours of attachment in persons previously sensitized to mite antigen. Feeding mites appear as tiny red vesicles adjacent to hair follicles. Scratching invariably destroys the body of a mite. Generally, lesions vesiculate and develop a hemorrhagic base. Itching and burning 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.
Diverse mites associated with birds and rodents can be particularly bothersome when they invade homes and bite human inhabitants. In North America, the northern fowl mite, the chicken mite, the tropical rat mite, and the house mouse mite normally feed on poultry, various songbirds, and small mammals and are abundant in and near their hosts' nests. These mites invade homes after their natural hosts die or leave their nests. Although the mites often are not seen because of their small size, their bites can be painful and pruritic. Painful bitelike sensations associated only with certain rooms of a home may be due to biting mites. Rodent- and bird-associated mites are best eliminated by excluding hosts, removing 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.
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. Antihistamines or topical steroids effectively reduce mite-induced pruritus.
Tick Bites and Tick Paralysis
Ticks attach and feed painlessly; blood is their only food. Their secretions produce local reactions, a febrile illness, or paralysis and transmit diverse pathogens. Generally, soft ticks attach for <1 h and may produce erythematous macular lesions ≤3 cm in diameter. Some species in Africa, the western United States, and Mexico produce painful hemorrhagic lesions. In contrast, hard ticks attach and feed for several days or sometimes for >1 week. At the site of hard-tick bites, small areas of induration with surrounding erythema and occasionally necrotic ulcers develop. Chronic nodules (tick granulomas) reach several centimeters in diameter and may require surgical excision. Tick-induced fever, associated with headache, nausea, and malaise, usually resolves ≤36 h after the tick is removed.
Tick paralysis, an acute ascending flaccid paralysis, is believed to be caused by one or more toxins in tick saliva that produce neuromuscular block, decreased nerve conduction, and sometimes hypertension. Throughout the world, this rare complication has followed the bites of >60 kinds of ticks; in the United States, dog and wood ticks are most commonly involved. Weakness begins in the lower extremities ≤6 days after the tick's attachment and ascends symmetrically over several days to result in complete paralysis of the extremities and cranial nerves. Deep tendon reflexes are diminished or lacking altogether, but sensory examination and findings on lumbar puncture are typically normal. Removal of the tick generally results in improvement within a few hours and complete recovery after several days, although the patient's condition may continue to deteriorate for up to 1 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 hair. An antiserum to the saliva of Ixodes holocyclus, the usual cause of tick paralysis in Australia, effectively reverses paralysis caused by these ticks.
Ticks should be removed by firm traction with fine-tipped forceps placed near the point of attachment. Use of occlusive dressings, heat, or other substances merely delays tick removal. The site of attachment should be disinfected. Tick mouthparts remaining in the skin generally are shed within days without excision. Removal of ticks during the first 36 h of attachment nearly always prevents transmission of the agents of Lyme disease, babesiosis, anaplasmosis, and ehrlichiosis. Gentle handling (to avoid rupture of ticks) and use of gloves may avert accidental contamination with tick fluids containing pathogens. Rather than awaiting results of tick testing or seroconversion to Lyme disease, adult patients with bites thought to be associated with deer ticks (Fig. 397-1) in Lyme disease–endemic areas from Maryland to Maine and in Wisconsin and Minnesota may be treated presumptively with a single oral dose of doxycycline (200 mg) within 72 h of tick removal.
Figure 397-1 Deer ticks (Ixodes scapularis, black-legged ticks) on a U.S. penny: larva (below ear), nymph (right), adult male (above), and adult female (left).
Louse Infestation (Pediculiasis and Pthiriasis)
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 an irritating maculopapular or urticarial rash in certain sensitized persons. Female head and pubic lice cement their eggs firmly to hair, and female body lice cement their eggs to clothing. A nymph hatches after ∼10 days of development. The empty egg (nit) 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 (shared headgear, grooming implements, bedding). 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 unimportant as vectors of pathogenic agents.
Body lice remain on clothing except when feeding and generally succumb in ≤2 days if separated from their host. These lice mainly infest disaster victims or indigent people who are in close contact with other infested individuals. Body lice are acquired by direct contact or by sharing of clothing and bedding. These lice are vectors for the agents of louse-borne typhus (Chap. 174), louse-borne relapsing fever (Chap. 172), and trench fever (Chap. 160). Pruritic lesions from their bites are particularly common around the neckline. Chronic infestations result in a postinflammatory hyperpigmentation and thickening of skin known as vagabonds' disease.
The crab or pubic louse is transmitted mainly by sexual contact. These lice occur mainly on pubic hair and less frequently on hair of the axillae and the face, including the eyelashes. Children and adults may acquire pubic lice by sexual or close nonsexual contact. Intensely pruritic lesions and blue macules ∼3 mm in diameter (maculae ceruleae) develop at the site of bites. Blepharitis commonly accompanies infestations of the eyelashes.
Pediculiasis may be suspected upon the detection of nits on hairs or in clothing, but confirmation should be based on discovery of a live louse.
Treatment: Louse Infestation
Generally, treatment is warranted only if live lice are discovered. The presence of nits alone is evidence of former—not current—infestation. Mechanical removal of lice and their eggs by means of a fine-toothed louse or nit comb (Fig. 397-2) often fails to eliminate infestations. Treatment of newly identified active infestations generally relies on a 10-min application of ∼1% permethrin or pyrethrins, with a second application 10 days later. Lice persisting after this treatment may be resistant to pyrethroids (see below). Chronic infestations may be treated for ≤12 h with 0.5% malathion. Lindane is applied for just 4 min but seems less effective and may pose a greater risk of adverse reactions, particularly when misused. Resistance of head lice to permethrin, malathion, and lindane has been reported. Newer pediculicides contain benzyl alcohol, dimethicone, or spinosad. Although children infested by head lice are frequently isolated or excluded from school, this practice increasingly is seen as unjustified.
Figure 397-2 Adult female human head louse (Pediculus capitis) on a nit (louse-egg) comb.
Body lice usually are eliminated by bathing and by changing to laundered clothes. Application of topical pediculicides from head to foot may be necessary for hirsute patients. Clothes and bedding are effectively deloused by heating in a clothes dryer at ≥55°C (131°F) for 30 min or by heat-pressing. Emergency mass delousing of persons and clothing may be warranted during periods of civil strife and after natural disasters to reduce the risk of pathogen transmission by body lice.
Pubic louse infestations are treated with topical pediculicides except for eyelid infestations (pthiriasis palpebrum), which generally respond to a coating of petrolatum applied for 3–4 days.
Myiasis (Fly Infestation)
Myiasis refers to infestations by diverse kinds of fly larvae (maggots) that invade living or necrotic tissue 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 boil-like subcutaneous nodules ≤3 cm in diameter. The adult female 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 surface stimulate the larvae to hatch. The larvae promptly penetrate intact skin. After 6–12 weeks of development, mature larvae emerge from the skin and drop to the ground. The African tumbu fly Cordylobia anthropophaga deposits its eggs on sand or drying laundry contaminated with urine or sweat. Larvae hatch on contact with the body, penetrate the skin, and produce boils from which they 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 lead to severe emotional distress. Botfly larvae 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 often necessary because upward-pointing spines of some species hold the larva firmly in place.
Larvae of the horse botfly Gasterophilus intestinalis do not mature after penetrating human skin but migrate for weeks in the epidermis. The resulting pruritic and serpiginous eruption resembles cutaneous larva migrans caused by hookworms (Chap. 216). Horseback riders become infested when eggs deposited on the flank of the horse hatch against their bare legs. The larvae of the cattle botfly invade more deeply and produce boil-like swellings, and larvae of rabbit and rodent Cuterebra occasionally cause dermal or tracheopulmonary myiasis.
Certain flies are attracted to blood and pus, and their newly hatched larvae enter wounds or diseased skin. Larvae of the green bottle fly usually remain superficial and confined to necrotic tissue, but specially prepared "surgical maggots" sometimes are used intentionally for wound debridement. Larvae of screwworm flies and the flesh fly invade viable tissue more deeply and produce large suppurating lesions. Larvae that infest wounds also may infest 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 larviposition by flesh flies on recently passed stools.
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 ingestion of encysted larval stages in raw liver or lymph nodes of sheep and goats—the intermediate hosts. Larvae migrate to the nasopharynx and produce an acute self-limiting syndrome known as Halzoun or Marrara, which is characterized by pain and itching of the throat and ears, coughing, hoarseness, dysphagia, and dyspnea. Severe edema may cause obstruction that necessitates tracheostomy; ocular invasion has been described. Diagnostic larvae measuring ≤10 mm in length appear in copious nasal discharge or vomitus. Individuals become infected with Armillifer armillatus by ingesting 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 occasionally 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 by histopathologic findings. Cutaneous larva migrans syndromes due to 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 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 humans and avidly suck blood. More notorious are the land leeches that live among moist vegetation of tropical rain forests. Attachment is usually painless. Hirudinin, a powerful anticoagulant secreted by the leech, causes continued bleeding after the leech has detached. Healing of the wound is slow, and bacterial infections are not uncommon. Several kinds of aquatic leeches in Africa, Asia, and southern Europe can enter through 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 and traction or by application of alcohol, salt, vinegar, insect repellent, or a flame or heated instrument to the leech. Internally attached leeches may detach on exposure to gargled saline or may be removed by forceps.
Of the >30,000 recognized species of spiders, only ∼100 defend themselves aggressively and have fangs sufficiently long to penetrate human skin. The venom that 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 fiddle spiders (Loxosceles species) and widow spiders (Latrodectus species) may be life-threatening. Identification of the offending spider should be attempted both because specific treatments exist for bites of widow and brown recluse 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 to be due to spider bites are most often due to other injuries or to infections with bacteria such as methicillin-resistant Staphylococcus aureus.
Recluse Spider Bites and Necrotic Arachnidism
Brown recluse spiders occur mainly in the southern and midwestern United States, and their close relatives are found in the Americas, Africa, and the Middle East. Most bites by the brown recluse spider result in only minor injury with edema and erythema. Envenomation, however, may cause severe necrosis of skin and subcutaneous tissue and systemic hemolysis. These spiders are not aggressive toward human beings and 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 only infrequently bite humans. Bites tend to occur while the victim is dressing and are sustained primarily on the arms, neck, and lower abdomen.
The venoms of these spiders contain an esterase, alkaline phosphatase, proteases, and other enzymes that produce tissue necrosis and hemolysis. Sphingomyelinase D, the most important dermonecrotic factor, binds cell membranes and promotes chemotaxis of neutrophils, leading to vascular thrombosis and an Arthus-like reaction. Initially, the bite is painless or produces a stinging sensation. Within the next few hours, the site becomes painful and pruritic, with central induration surrounded by a pale zone of ischemia and 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 and necrotic with an overlying bulla. A black eschar forms and sloughs several weeks later, leaving an ulcer that eventually may result in 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 infection. Fever, chills, weakness, headache, nausea, vomiting, myalgia, arthralgia, maculopapular rash, and leukocytosis may develop ≤72 h after the bite. In rare instances, acute complications such as hemolytic anemia, hemoglobinuria, and renal failure are fatal.
Treatment: Recluse Spider Bites
Initial management includes RICE (rest, ice, compression, elevation). Analgesics, antihistamines, antibiotics, and tetanus prophylaxis should be administered if indicated. Debridement and later skin grafting may be necessary after signs of acute inflammation have subsided, but immediate surgical excision of the wound is detrimental. Patients should be monitored closely for signs of hemolysis, renal failure, and other systemic complications.
The black widow, which is best known and most abundant 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 the web is disturbed or when the spider is trapped or provoked. The initial bite goes unnoticed or is perceived as a sharp pinprick. 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 nerves and causes release and eventual depletion of acetylcholine, norepinephrine, and other neurotransmitters from presynaptic 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. The pain begins to subside during the first 12 h but may recur during several days or weeks before resolving spontaneously. Other features 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.
Treatment: Widow Spider Bites
Treatment consists of RICE and tetanus prophylaxis. Hypertension that does not respond to analgesics and antispasmodics (e.g., benzodiazepines or methocarbamol) requires specific antihypertensive medication. The efficacy of antivenom is controversial. Because of the risk of anaphylaxis and serum sickness, antivenom should be reserved for severe cases involving respiratory arrest, uncontrollable hypertension, seizures, or pregnancy.
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 species. Tarantulas bite only when threatened and cause no more harm than a bee sting, but the venom occasionally provokes deep pain and swelling. Tarantulas of several species 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 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 and 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 envenomation by each of these spiders are available. Yellow sac spiders (Cheiracanthium) 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, which they paralyze 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 >5000 deaths worldwide each year. Scorpions feed at night and remain hidden during the day in crevices or burrows or under wood, loose bark, or rocks on the ground. They seek cool spots under buildings and often enter houses, where they hide in shoes, clothing, or bedding or enter bathtubs and sinks in search of water. Scorpions sting human beings only when disturbed.
Of the 40 or so scorpion species in the United States, only the bark scorpion (Centruroides sculpturatus or C. exilicauda) produces venom that can be lethal. This venom contains neurotoxins that cause sodium channels to remain open and neurons to fire repetitively. 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.
Treatment: Scorpion Stings
Identification of the offending scorpion aids in planning therapy. Stings of nonlethal species require at most ice packs, analgesics, or antihistamines. Because most victims experience only local discomfort, they can be managed at home with instructions to return to the emergency department if signs of cranial-nerve or neuromuscular dysfunction develop. Aggressive supportive care and judicious use of antivenom can reduce or eliminate deaths from more severe envenomations. Keeping the patient calm and applying pressure dressings and cold packs to the sting site are measures that decrease the absorption of venom. A continuous IV infusion of midazolam controls the agitation, flailing, and involuntary muscle movements produced by scorpion stings. Close monitoring during treatment with this drug and other sedatives or narcotics is necessary for persons with neuromuscular symptoms because of the risk of respiratory arrest. Hypertension and pulmonary edema respond to nifedipine, nitroprusside, hydralazine, or prazosin, and bradyarrhythmias can be controlled with atropine.
Commercially prepared antivenoms are available in several countries for some of the most dangerous species. A C. sculpturatus antivenom (not yet approved by the FDA) is available as an investigational drug only in Arizona. IV administration of antivenom rapidly reverses cranial-nerve dysfunction and muscular symptoms but does not affect pain and paresthesia. The benefit of scorpion antivenom has not been established in controlled trials.
Insects that sting to defend their colonies or 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, nearly all of the ≥100 deaths due to hymenopteran stings in the United States each year result from allergic reactions.
Honeybees often lose their stinging apparatus and the attached venom sac in the act of stinging and subsequently die, whereas other bees, ants, and vespids can sting numerous times in succession. The familiar honeybees (Apis mellifera) and bumblebees (Bombus and other genera) generally attack only when a colony is disturbed. Africanized honeybees, however, respond to minimal intrusions more aggressively. Since their introduction into Brazil in 1957, these "killer bees" have spread through South and Central America to the southern and western United States.
In bees and wasps, venom is produced in glands at the posterior end of the abdomen and is expelled rapidly by contraction of muscles of the venom sac, which has a capacity of up to 0.1 mL. 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, and acetylcholine and several kinins. Polypeptide toxins in honeybee venom include mellitin, which damages cell membranes; mast cell–degranulating protein, which causes histamine release; apamin, a neurotoxin; and adolapin, which has anti-inflammatory activity. Enzymes in venom include hyaluronidase, which allows the spread of other venom components, and phospholipases, which may be among the major venom allergens. There appears to be little cross-sensitization between honeybee and wasp venoms.
Uncomplicated stings cause immediate pain, a wheal-and-flare reaction, and local edema and swelling that subside in a few hours. Stings from accidentally swallowed insects may induce life-threatening edema of the upper airways. Multiple stings can lead to vomiting, diarrhea, generalized edema, dyspnea, hypotension, and collapse. Rhabdomyolysis and intravascular hemolysis may cause renal failure. Death from the direct effects of venom has followed 300–500 honeybee stings.
Large local reactions that spread ≥10 cm around the sting site over 24–48 h are not uncommon. These reactions may resemble cellulitis but are caused by hypersensitivity rather than 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 insect 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; occasionally, adults who have had mild reactions later experience serious reactions. 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.
Treatment: Bee and Wasp Stings
Honeybee stingers embedded in the skin should be removed as promptly as possible to limit the quantity of venom delivered. The stinger and venom sac may be scraped off with a blade or a fingernail or grasped with forceps. The site should be cleansed and disinfected and ice packs applied to slow the spread of venom. Elevation of the affected site and administration of analgesics, oral antihistamines, and topical calamine lotion relieve symptoms. Large local reactions may require a short course of oral therapy with glucocorticoids. Patients with numerous stings should be monitored for 24 h for evidence of renal failure or coagulopathy.
Anaphylaxis is treated with subcutaneous (SC) injection of 0.3–0.5 mL of epinephrine hydrochloride in a 1:1000 dilution; treatment is repeated every 20–30 min as necessary. IV epinephrine (2–5 mL of a 1:10,000 solution administered by slow push) is indicated for profound shock. A tourniquet may slow the spread of venom. Parenteral antihistamines, fluid resuscitation, bronchodilators, oxygen, intubation, and vasopressors may be required. Patients should be observed for 24 h for recurrent anaphylaxis.
Persons with a history of allergy to insect stings should carry a sting kit with a preloaded syringe containing epinephrine for self-administration. These patients should seek medical attention immediately after using the kit.
Repeated injections of purified venom produce a blocking IgG antibody response to venom and reduce the incidence of recurrent anaphylaxis. Honeybee, wasp, yellow jacket, and mixed vespid venoms are commercially available for desensitization and for skin testing. Results of skin tests and venom-specific radioallergosorbent tests aid in the selection of patients for immunotherapy and guide the design of such treatment.
Stinging fire ants are an important medical problem in the United States. Imported fire ants infest southern states from Texas to North Carolina, with colonies 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 ≤2% of persons, and seizures and mononeuritis have been reported. Stings are treated with ice packs, topical glucocorticoids, and oral antihistamines. Covering pustules with bandages and antibiotic ointment may prevent bacterial infection. Epinephrine and supportive measures are indicated for anaphylactic reactions. Whole-body extracts are available for skin testing and immunotherapy, which appears to lower the rate of anaphylactic reactions.
The western United States is home to harvester ants. The painful local reaction that follows harvester ant stings often extends to lymph nodes and may be accompanied by anaphylaxis.
Dipteran (Fly and Mosquito) Bites
In the process of feeding on vertebrate blood, adults of certain fly species inflict painful bites, produce local allergic reactions, or transmit pathogenic agents. Bites of mosquitoes, tiny "no-see-um" midges, and phlebotomine sand flies typically produce a wheal and a pruritic papule. Nodular lesions at the site of midge bites may last for months. Bites of small humpbacked black flies (simuliids) leave a bleeding laceration and a painful and pruritic sore that are slow to heal; regional lymphadenopathy, fever, or anaphylaxis occasionally ensues. The widely distributed deer and horse flies 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.
Treatment: Fly and Mosquito Bites
Treatment of fly bites is symptom-based. Topical application of antipruritic agents, glucocorticoids, or antiseptic lotions may relieve itching and pain. Allergic reactions may require oral antihistamines. Antibiotics may be necessary for the treatment of large bite wounds that become secondarily infected.
Common human-biting fleas include the dog and cat fleas (Ctenocephalides species) and the rat flea (Xenopsylla cheopis), which inhabit the nests and resting sites of their hosts. Sensitized persons develop erythematous pruritic papules, urticaria, and occasionally vesicles and bacterial superinfection at the site of the bite. Treatment consists of antihistamines and antipruritics.
Flea infestations are eliminated by frequent cleaning of nesting sites and of the host's bedding and by application of contact insecticides. Flea infestations in the home may abate if pets are 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, it occurs in tropical regions of Africa and the Americas. Adults live in sandy soil and burrow under the skin between toes, under nails, or on the soles of bare feet. Chigoes engorge on blood and grow from pinpoint to pea size during a 2-week period. The lesions they produce resemble a white pustule with a central black depression and may be pruritic or painful. Occasional complications include tetanus, bacterial infections, and autoamputation of toes. Tungiasis is treated by removal of the intact flea with a sterile needle or scalpel, tetanus vaccination, and topical application of antibiotics.
Hemipteran (True Bug) Bites
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 nocturnally feeding kissing bugs are painless. Reactions to such bites depend on prior sensitization and include tender and pruritic papules, vesicular or bullous lesions, giant urticaria, fever, lymphadenopathy, and anaphylaxis. Bug bites are treated with topical antipruritics or oral antihistamines. Persons with anaphylactic reactions to reduviid bites should keep an epinephrine kit available. The cosmopolitan bedbugs (Cimex species) hide in crevices of mattresses, bed frames and other furniture, walls, and picture frames and under loose wallpaper. Bedbugs have become resurgent, recently attaining populations and spreading to an extent not encountered since the mid-twentieth century. These bugs are now a fairly common nuisance in homes, dormitories, and hotels and on cruise ships. The bugs hide during the day and take their blood meal at night. Their bite is painless, but sensitized persons develop erythema, itching, and wheals around a central hemorrhagic punctum. Bedbugs are not known to transmit pathogens.
Centipede Bites and Millipede Dermatitis
The fangs of centipedes of the genus Scolopendra can penetrate human skin and deliver a venom that produces intense burning pain, swelling, erythema, and lymphangitis. Dizziness, nausea, and anxiety occasionally are described, 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, unlike centipedes, do not bite, but some secrete defensive fluids that 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 may lead to corneal ulceration and blindness. Management includes irrigation with copious amounts of water or saline, use of analgesics, and local care of denuded skin.
Caterpillar Stings and Dermatitis
The surface of caterpillars of several moth species is covered with hairs or spines that produce mechanical irritation and may contain or be coated with venom. Contact with these caterpillars causes an immediate burning sensation followed by local swelling and erythema and occasionally by regional lymphadenopathy, nausea, vomiting, and headache; shock, seizures, and coagulopathy are rare complications. In the United States, dermatitis most often is associated with io, puss, saddleback, and brown-tail moths. Contact with even detached hairs of other caterpillars, such as gypsy moth larvae, can later produce a pruritic urticarial or papular rash. Spines may be deposited on tree trunks and 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 steroids, and oral antihistamines relieve symptoms.
When disturbed, blister beetles extrude cantharidin, a low-molecular-weight toxin that produces thin-walled blisters measuring ≤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 contains paederin, a potent vesicant. When these beetles are crushed or brushed against the skin, the released fluid may provoke erythematous and bullous lesions. These beetles occur worldwide but are most numerous and problematic in parts of Africa and Asia. Ocular lesions are common from impacts with the flying beetles at night or transfer of the vesicant on the fingers. Treatment is rarely necessary, although ruptured blisters should be kept clean and bandaged.
The groundless conviction that one is infested with arthropods or other parasites is an extremely difficult disorder to treat and unfortunately is not rare. Patients report infestations of their skin, clothing, or homes and describe sensations of something moving in or on their skin. Excoriations often accompany reports of pruritus or insect bites. Frequently, patients submit as evidence of infestation specimens that consist of plant-feeding and nonbiting peridomestic arthropods, pieces of skin, vegetable matter, or inanimate objects. It is imperative to rule out true infestations and bites by arthropods, endocrinopathies, neuropathies, drug use, environmental irritants (e.g., fragments or threads of glass insulation), 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. Pharmacotherapy with pimozide or other psychotropic agents has been more helpful than psychotherapy in treating this disorder.