Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 134. Spider and Arthropod Bites

Timothy B. Erickson

Navneet Cheema

HIGH-YIELD FACTS

• Black widow spider bites result in painful muscle spasms, secondary to neurotoxicity, that are responsive to antivenin.

• Brown recluse spider bites result in hematotoxicity and manifest locally as skin necrosis.

• Scorpion stings cause severe localized pain with occasional systemic effects in children.

• Hymenoptera stings from bees and wasps can result in severe anaphylactic reactions and are responsible for more adverse outcomes and fatalities in children than any other arthropods.

• Fire ant stings can cause painful localized skin reactions.

INTRODUCTION

In North America, bites and stings by arthropods occur frequently. Approximately 50,000 bites or stings occur every year with about half of these caused by spiders. There are more than 41,000 species of spiders,1 most of which cannot inflict serious bites to humans.2 The majority of exposures are unnoticed and do not need treatment. There are a few medically relevant spiders that produce toxic venoms, which can lead to local reactions, systemic illnesses, and neurotoxicity.

BLACK WIDOW SPIDERS

image ANATOMY

The Latrodectus genus of spiders includes five primary species found in North America: Latrodectus bishopL. geometricusL. hesperusL. variolus, and L. mactans.2 They live in dimly lit, secluded areas such as woodpiles, barns, and stonewalls. They are present in every US state except Alaska.3 Black widows are described as shiny jet black with a characteristic red hourglass mark on the ventral aspect of the abdomen (Fig. 134-1). The red hourglass is specific to L. mactans, and other species have distinctive ventral markings, such as triangles and spots. There is a seasonal variation in the number of black widow bites, starting to rise in spring, peaking in September, and reaching a nadir in January–February.3

image

FIGURE 134-1. Female black widow spider with egg sac.(www.prevailpest.com)

image PATHOPHYSIOLOGY

Black widows are overall shy, nocturnal, and only bite when their web is disturbed. The female black widow is generally considered poisonous to humans. The male black widow spider, with its smaller jaw and minimal venom, is not significantly poisonous to humans. These spiders use striated muscles to control the amount of venom they inject, and about 15% of bites do not deliver venom.4 The venom’s toxicity is due to the presence of α-latrotoxin. This toxin facilitates exocytosis of synaptic vesicles and the release of the neurotransmitters norepinephrine, γ-aminobutyric acid, and acetylcholine.5 The toxin also causes degeneration of motor end plates, resulting in denervation. The venom destabilizes nerve cell membranes by opening ion channels, causing a massive influx of calcium into the cell, which may lead to hypocalcemia.

image CLINICAL PRESENTATION

Latrodectism is the clinical syndrome that follows a black widow bite. The bite produces a pinprick sensation that often goes unnoticed. Within the first few hours local irritation may develop, including erythema, urticaria, or a characteristic halo-shaped target lesion. These local symptoms may be followed by generalized symptoms of pain and muscle spasms in the chest, abdomen, and lower back. Abdominal rigidity can be quite severe and may even be mistaken as a surgical emergency, especially in children who are often unable to provide a preceding history of a bite.6 According to one study, signs and symptoms in infants were wound erythema, irritability, constant crying, sialorrhea, agitation, and seizures. Elementary aged children and adolescents described pain on the wound site, abdominal and thoracic pain, muscle spasms, and fine tremors.7 About one-third of patients will go on to have systemic symptoms.1 These include hypertension, sweating, salivation, dyspnea with increased broncho-secretions, and convulsions. Less common effects include myocarditis,8 compartment syndrome of the upper extremity,9 and priapism.10Death is rare, with no cases reported in the United States and only two in the worldwide literature from black widow envenomation alone.1113 Symptoms of latrodectism typically last days, but patients can have intermittent muscle weakness and spasms for weeks.

image MANAGEMENT

Local wound care is appropriate, and pain at the bite site may be relieved with early application of ice. Tetanus immunization should be updated, but antibiotics are unnecessary unless there is evidence of a wound infection. Oral and parenteral analgesics, such as morphine, may be used if pain is severe. Muscle spasms may require administration of benzodiazepines.

In the past, administration of calcium gluconate was considered because of concern for the development of hypocalcemia following black widow envenomation. This practice is currently not advocated, as studies have proven no benefit to the administration of calcium.6

In extreme cases with severe symptoms, Latrodectus antivenom is recommended.14 Currently, only one antivenom is available in the United States, Black Widow Antivenin® (Merck). This is a horse serum-derived product containing IgG antibodies to L. mactans venom. The use of Latrodectus-specific antivenom is restricted to patients with severe envenomation (e.g., hypertensive crisis or intractable pain), no allergic contraindications, and in whom opioids and benzodiazepines are ineffective. Young children15 and elderly patients with severe toxicity should receive antivenom early in the clinical course. There has traditionally been reluctance to use antivenom because of concern for anaphylaxis. Two recent reviews of antivenom use in the United States have demonstrated low rates of adverse reactions.3,11 In the medical literature, there have only been two deaths reported after black widow antivenom administration.6,16 Patients receiving antivenom may experience flu-like symptoms or serum sickness for 1–3 weeks following treatment. This entity is generally self-limited and responsive to antihistamines and steroids.

image DISPOSITION

Any symptomatic pediatric patient who has suffered a bite from a black widow spider should be admitted for observation and pain control. If there is cardiopulmonary compromise or convulsions, the child should be admitted to the intensive care unit for stabilization and antivenom administration.

BROWN RECLUSE SPIDERS

The six species of recluse spiders in North America are Loxosceles arizonicaL. desertaL. deviaL. laetaL. rufescens, and L. reclusa. Of these, L. reclusa is the most common. These spiders are known to be reclusive nocturnal hunters and are more active from April to October.17,18 Their webs are scant and ill defined. Victims typically are bitten on the extremities while rummaging in confined spaces such as a closet or an attic while putting on a shoe or using a blanket that a spider is trapped in.

image ANATOMY

The brown recluse gets its name because of its brown- or fawn-colored body. It is approximately 1–5 cm in length, with a characteristic violin-or fiddle-shaped marking on the dorsal cephalothorax (Fig. 134-2). They have long, slender legs and have six eyes rather than eight, which is the norm for most other spiders, including the black widow.19

image

FIGURE 134-2. Loxosceles reclusa—also known as the brown recluse or “iddle back” spider. ()

image PATHOPHYSIOLOGY

The venom of the recluse spider, per volume, is more potent than that of the rattlesnake and can cause extensive skin necrosis. The venom acts directly on the cell wall, causing immediate injury and cell death. It contains the calcium-dependent enzyme sphingomyelinase D that, along with C-reactive protein, has a direct lytic effect on red blood cells.

Following cell wall damage, intravascular coagulation causes a cascade of clotting abnormalities and local polymorphonuclear leukocyte infiltration, culminating in a necrotic ulcer.

image CLINICAL PRESENTATION

Most brown recluse bites occur in predawn hours and are often painless. The seasonality of brown recluse bites and the geographic area should be strongly considered when making this diagnosis. One study demonstrated that 43/45 brown recluse bites occurred between the months of April and October.17 L. reclusa is primarily found in south central United States.20 The clinical response to loxoscelism ranges from cutaneous irritation (necrotic arachnidism) to a life-threatening systemic reaction. Most signs and symptoms of envenomation are localized to the bite area. The majority (90%) result in nothing more than a local reaction and resolve spontaneously.21 Within a few hours, the patient experiences itching, swelling, erythema, and tenderness over the bite site. Classically, erythema surrounds a dull, blue-gray macule circumscribed by a ring or halo of pallor. The color difference is important in identifying necrotic arachnidism. Gradually, over 3–4 days, the wound forms a necrotic base with a central black eschar. In 7–14 days, the wound develops a full necrotic ulceration.22 Some sources state that the diagnosis of necrotic arachnidism secondary to brown recluse spiders is over reported in many case series due to inadequate documentation and call for stricte, r diagnostic criteria.2325

The systemic reaction, which is much less common than the cutaneous reaction, is associated with a higher morbidity. The reaction rarely correlates with the severity of the cutaneous lesion. Within 24–72 hours following the envenomation, the patient experiences fever, chills, myalgias, and arthralgias. In severe systemic reactions, the patient may suffer coagulopathies, hypotension, jaundice, disseminated intravascular co agulation (DIC), convulsions, renal failure, and hemolytic anemia.26,27 In rare cases, a patient may succumb to the systemic reaction.21

HOBO SPIDER

The Hobo spider (Tegenaria agrestis), originally from Europe and central Asia, now resides in the Pacific Northwest region of the United States and Canada.26 This spider should be included with Loxoscelesspecies when discussing cases of necrotic arachnidism. Similar symptomatology leads many to incorrectly attribute hobo spider bites to that of the brown recluse, which is not indigenous to the northwest United States. This species exhibits an aggressive nature, biting with minor provocation.28 Hobo spiders are brown with gray markings, have a 7–14-mm body length and 27–45-mm leg span (Fig. 134-3). They live in moist, dark environments such as woodpiles or basements.

image

FIGURE 134-3. The Hobo spider (Tegenaria agrestis) can cause a necrotic skin lesion similar to a brown recluse spider. (www.entomology.unl.edu)

image MANAGEMENT

The proper management of envenomation by the brown recluse or hobo spider depends on whether the reaction is local or systemic. It is difficult to predict which type of wound will eventually progress to a disfiguring necrotic ulcer, so appropriate wound care should be done for all suspected brown recluse wounds. Proper care includes wound cleansing, immobilization, and elevation of the affected extremity to reduce pain and swelling. Early application of ice to the bite area will lessen the local wound reaction whereas heat will exacerbate the symptoms. Tetanus immunization should be updated, but antibiotics are only indicated if there is a secondary wound infection. Antihistamines and analgesics prove to be beneficial, especially in children.

Early excision of ulcers and steroid injections are not recommended since studies have demonstrated that wound healing is slowed, and scarring is more severe as a result of those practices. Some complications of early surgical intervention include recurrent wound breakdown as well as long-term distal extremity dysfunction. Delayed excision of ulcers after the necrotic process has subsided (usually within 8 weeks), followed by secondary closure with skin grafting, is the preferred way of dealing with necrotic ulcers due to brown recluse bites. With appropriate wound care, most bite wounds heal well with a 10–15% occurrence of major scarring.

Historically, the use of the polymorphonuclear leukocyte inhibitor, dapsone, was advocated to diminish scarring and subsequent surgical complications. Its use, however, has not proven effective in any large study with human or animal models.29 Because of the potential for dapsone to induce methemoglobinemia and hemolytic anemia in children with G6PD deficiency, administration in pediatric patients is generally not advised. Another suggested method of treating expanding wound necrosis due to brown recluse spider bites is hyperbaric oxygen treatment. However, results with such treatment have been mixed, and little evidence exists to support its use.21,29

Systemic effects of brown recluse spider bites are rare but can be life threatening and should be treated aggressively. Although not proven in clinical trials, glucocorticoids may provide a protective effect on the RBC membrane, thus slowing hemolysis. The patient must be monitored closely for the development of DIC. Transfusion of RBCs and platelets may be necessary. Urine alkalinization with bicarbonate may lessen renal damage if the patient is experiencing acute hemolysis. Although it is not commercially available in the United States, there is ongoing research with brown recluse antivenom.30 However, there is little evidence to support its efficacy, particularly against local effects.31

image DISPOSITION

Patients with a rapidly expanding lesion or necrotic area with evidence of hemolysis should be hospitalized. Patients who are asymptotic following a period of observation in the emergency department and have normal baseline laboratory values may be discharged home with close outpatient follow-up for wound care within 24–48 hours.

TARANTULAS

Tarantulas are widely feared because they are the largest of all spiders (Fig. 134-4). Found predominantly in the deserts of the western United States, but spotted even as far east as the Mississippi River Valley, these large, hairy spiders are relatively harmless. They are extremely shy and bite only when vigorously provoked or roughly handled. Their bites usually cause minimal pain and surrounding edema with little or no necrosis and no serious systemic effects. While tarantula bites are usually of little consequence in humans, they can be more severe in household animals, especially canines. Treatment of bites includes local wound care and tetanus prophylaxis. Involved limbs should be raised and immobilized, and medication can be given to alleviate pain. If needed, the patient can be treated with antihistamines and topical glucocorticoids. The growing trade of these arachnids as exotic pets should prompt the clinician to inquire about this as a possible cause for an unusual skin lesion.32

image

FIGURE 134-4. Common tarantulas are extremely shy and bite only when vigorously provoked or roughly handled. (www.userbars.be)

More concerning than tarantula bites is exposure to the hairs on their abdomen. These hairs can be flicked off in large numbers as a defense mechanism and are capable of producing urticaria and pruritus that may persist for several weeks. The hairs may also get into the eyes and cause keratoconjuctivitis or ophthalmia nodosa, a nodular, granulomatous lesion in the eye.33 Patients with these complaints after exposure to a tarantula should be immediately referred to an ophthalmologist. Without appropriate care, these eye lesions may progress to keratitis, uveitis, retinitis, and even orbital cellulitis.

SCORPIONS

Epidemiologically, scorpions are the most significant of all arachnid envenomations, potentially resulting in adult morbidity and pediatric mortality.31 Worldwide, scorpions are responsible for thousands of deaths annually.34,35 In the United States, there have been no reported deaths from scorpion stings in more than 25 years. Nevertheless, they remain a public health concern throughout the South and Southwest. Despite a steady decline in the number of deaths from scorpion stings over the past 20 years in Mexico, children younger than 5 years and the elderly remain the most vulnerable patient populations.36

image ANATOMY

The scorpion has a pair of anterior legs with pinchers, a segmented body, and a long, mobile tail equipped with a stinger (Fig. 134-5). While members of the genera HadrurusVejovis, and Uroctonus are capable of inflicting painful wounds, only the southwestern desert scorpion (Centruroides exilicauda, formerly C. sculpturatus) poses a serious health threat in the United States. Also called bark scorpions because they cling to the bottom of fallen brush and trees, they are brownish in color, vary in length from 1 to 6 cm and are most active at night. The chitin shell of this scorpion will fluoresce under an ultraviolet or Wood’s lamp, aiding in identification.

image

FIGURE 134-5. The bark scorpion or Centruroides exilicauda has a pair of anterior legs with pinchers, a segmented body, and a long, mobile tail equipped with a stinger. (www.museum.utep.edu)

image PATHOPHYSIOLOGY

Centruroides venoms cause spontaneous depolarization of both the sympathetic and parasympathetic nervous systems.

image CLINICAL PRESENTATION

Unless the scorpion is identified, the diagnosis is based on clinical symptoms. Most victims will have only local pain, tenderness, and tingling; however, young children and those who suffer more serious envenomations may manifest the venom effects of overstimulation of the sympathetic, parasympathetic, and central nervous systems. Elevation of all the vital signs usually occurs within an hour of envenomation, and tachydysrhythmias may develop during this time. Dysconjugate, “roving” eye movements are very common in children, along with other neurological findings including muscle fasciculations, weakness, agitation, and opisthotonos. Less common findings are ataxia, respiratory distress, and seizures.

image MANAGEMENT

The treatment of Centruroides envenomations is supportive. Cool compresses and analgesics are used for the local symptoms and pain. Wound care and tetanus prophylaxis are indicated. Tachydysrhythmias and hypertension may be treated with intravenous β-blockers, such as esmolol or labetalol. Benzodiazepines may be helpful for agitation and muscle spasms. Advanced life support and airway control are essential for more severe envenomations. A clinical score predicting the need for hospitalization in scorpion stings has been described.37

In the United States, Centruroides-specific antivenom, an immune F(ab)2 equine injection (Anascorp), was approved for severe envenomations by the FDA in 2011.38 Scorpion antivenom directed against different species has been produced for research or clinical use in several other countries.39 As with all animal-derived antivenoms, both immediate and delayed allergic reactions including serum sickness are possible.40 For this reason, Centruroides-specific antivenom should be reserved for cases of severe systemic toxicity. Although investigations outside the United States have found no benefit in routine administration of antivenom for scorpion stings, one to two vials of antivenom, in cases of severe toxicity, can lead to rapid resolution of symptoms.28

Consultation with a toxicologist experienced in scorpion envenomation is recommended before using antivenom.

HYMENOPTERA

The order hymenoptera includes bees, vespids (hornets and wasps), and fire ants. These insects cause one-third of all reported envenomations in the United States and an estimated 50–150 annual deaths. While hymenoptera venoms possess intrinsic toxicity, it is their ability to sensitize the victim and cause subsequent anaphylactic reactions that makes them so lethal.

image BEES AND VESPIDS

Honeybees (Apis mellifera) are fuzzy insects with alternating black and tan body stripes. Not intrinsically aggressive, they usually sting defensively when stepped on. Like that of other hymenoptera, the honeybee’s stinger is a modified ovipositor (only females’ sting) that is connected to a venom sac. Since honeybees lose their barbed stinger after stinging and die, they generally only sting in defense when provoked.

Africanized honeybees, or “killer bees,” (Apis mellifera scutellata) (Fig. 134-6) are now found in Texas, Arizona, California, and most of the temperate southeastern and southwestern states.41 In the 1950s, African bees were imported into Brazil for breeding experiments designed to improve honey production and disease resistance. Many escaped and subsequently mated with previously imported European honeybees.42 These hybrids have since migrated northward along the coasts and temperate regions of the continent. Although the toxicity of their venom is equal to that of their native counterpart, they are far more aggressive. A hive can respond to a perceived threat with more than 10 times the number of bees than its typical native North American counterpart. Massive numbers of stings from an attack of Africanized bees can result in multisystem damage and death from severe venom toxicity. Most patients of massive envenomation suffer acute tubular necrosis or renal involvement with myoglobinuria.43 In swarms, these bees can overwhelm and kill even healthy nonallergic victims.44

image

FIGURE 134-6. Africanized honeybees, or “killer bees” (Apis mellifera scutellata), are dangerous because they sting in large swarms. (www.uni.uiuc.edu).

The most common hornets in the United States are the yellow jackets (Vespula pensylvanica). They are usually seen around garbage cans, beverage containers, and various foods. They are extremely aggressive and sting with little provocation. Wasps (Polistes annularis, the paper wasp) have thin, smooth bodies and a formidable sting. They build their nests in the eaves of buildings. These vespids are carnivorous and able to use their smooth stingers multiple times, unlike honeybees, which lose their stingers after a single sting.45,46

image PATHOPHYSIOLOGY

Hymenoptera venoms contain enzymes that directly affect vascular tone and permeability. Although their enzymes are similar, there is little immunologic cross-reactivity between bee and vespid venoms. While a bee sting may not sensitize a person to yellow jacket venom, a yellow jacket sting would more likely sensitize one to wasp venom.47 Four possible reactions are seen after hymenoptera stings: a local reaction, toxic reaction, systemic anaphylaxis, and a less common delayed-type hypersensitivity reaction.28,48

Local reactions are the most common reactions resulting from the vasoactive effects of the venom and are generally mild. The most common response includes pain, mild erythema, edema, and pruritus at the sting site. There are no systemic signs or symptoms, but a severe local reaction may involve one or more contiguous joints. Local reactions occurring in the mouth or throat can produce swelling that may lead to upper airway obstruction, especially in younger children.

Toxic reactions may occur when a patient suffers from multiple stings. Africanized bees are notorious for such attacks, but an aggressive native hive may elicit a similar response. The essential lethal dose is approximately 20 stings/kg in most mammals.45 Symptoms of a toxic reaction may resemble anaphylaxis, but gastrointestinal manifestations (nausea, vomiting, and diarrhea) and sensations of light-headedness and syncope may also occur. Headache, fever, drowsiness, involuntary muscle spasms, edema without urticaria, and convulsions may ensue. Although urticaria and bronchospasm are not always present, severe envenomations may lead to respiratory insufficiency and arrest. Hepatic failure, rhabdomyolysis, and DIC have been reported in both adult and pediatric victims. Toxic reactions are believed to occur from a direct multisystem effect of the venom.

Anaphylactic reactions are generalized systemic allergic reactions that may occur after envenomation. Generalized systemic reactions to hymenoptera venom are thought to occur from an immunoglobulin E-mediated mechanism, leading to the release of pharmacologically active mediators within mast cells and basophils. Symptoms are often mild, but severe reactions can lead to death within minutes. Unlike the toxic reaction, there is no correlation between systemic allergic reactions and the number of stings. The majority of allergic reactions occur within the first 10–15 minutes and nearly all occur within 6 hours. Fatalities that occur within the first hour of the sting usually result from airway obstruction or hypotension. Initial symptoms typically consist of ocular pruritus, facial flushing, and generalized urticaria. Symptoms may intensify rapidly with chest or throat constriction, wheezing, dyspnea, abdominal cramping, diarrhea, vomiting, vertigo, fever, laryngeal stridor, syncope, and shock.

Delayed reactions, appearing 1–2 weeks after a sting, consist of serum sickness-like signs and symptoms of fever, malaise, headache, urticaria, lymphadenopathy, and polyarthritis. This reaction is believed to be immune complex mediated.48

image MANAGEMENT

If present, the embedded stinger should be removed manually. Previous sources recommended cautiously scraping the stinger off with lateral pressure, rather than grasping it, in order to avoid compression of the venom sac resulting in further release of venom. However, recent studies have demonstrated that this is erroneous because the venom has likely been completely released within seconds of envenomation.49Treatment is symptomatic, with ice or cold compresses and an antihistamine. In more severe local reactions, there is a more sustained inflammatory response, and the swelling may spread to the entire extremity and persist for several days. A short course of prednisone (1 mg/kg/day for 5 days) may decrease the duration of symptoms.

Toxic reactions reflect the effects of multiple stings, usually 25–50 stings or more. Gastrointestinal symptoms are the principal features; urticaria and bronchospasm are not usually present. Treatment is supportive.

Systemic reactions occur in approximately 1% of hymenoptera stings. They range from mild, non–life-threatening cutaneous reactions to classic anaphylactic shock. In all but the mildest of systemic reactions, the mainstay of treatment is epinephrine. Epinephrine counteracts the bronchospastic and vasodilatory effects of histamine. Epinephrine can be given as a subcutaneous injection (0.01 mL/kg of 1:1000 solution; not to exceed 0.3 mL). In more severe reactions, the intravenous or endotracheal route is preferred (0.1 mL/kg of 1:10,000 solution). The dose may be repeated at 15-minute intervals as needed. Early intubation is indicated if there is evidence of severe laryngeal edema or stridor because airway obstruction is the leading cause of death in anaphylaxis. Antihistamines should be given early but not as a substitute for epinephrine. An H2-receptor blocker (e.g., cimetidine or ranitidine), in addition to an H1-receptor blocker (diphenhydramine), may aid in inhibiting the vasodilatory effects of histamine. Adjunctive therapy for bronchospasm might include inhaled β2-agonists (e.g., albuterol). When hypotension is present, vigorous isotonic fluid resuscitation should be instituted. Glucocorticoids should be given for their anti-inflammatory effects as well as their effect in preventing the late-phase response.

A delayed serum sickness-like reaction may appear 10–14 days following the initial sting. This immune complex disorder may be treated with a short course of prednisone.

Venom immunotherapy desensitization is very effective in preventing further systemic reactions, with 95–100% protection after 3 months of treatment. Referral to an allergist is indicated for any child who has experienced life-threatening respiratory symptoms or hypotension. Children less than 16 years old who have only urticaria or angioedema do not require venom immunotherapy. Only 10% of these children will have systemic reactions with subsequent stings.49

Essential to the treatment of any systemic reaction is the prevention of future reactions. Patients who have had a systemic reaction should be instructed to wear protective clothing and avoid hymenoptera-infested habitats. Portable epinephrine kits (Epi-Pen and Epi-Pen Jr) are available. They should be prescribed prior to the patient leaving the emergency department. The patient should be urged to carry the kit at all times and to use epinephrine for any systemic symptoms. Even if symptoms are mild, the patient should seek emergency care. The patient should also be instructed to wear a medical alert tag.

IMPORTED FIRE ANTS

Five known species of fire ants belonging to the genus Solenopsis are found in the United States. Two of the species were imported into the United States, the red fire ant (Solenopsis invicta) and the black fire ant (Solenopsis richteri), of which S. invicta is the predominant species (Fig. 134-7). They were “imported” aboard ships from South America during World War II and subsequently spread throughout the Southeast. They are presently found in 13 southern states, from Florida to Texas; their geographic range apparently limited by soil, temperature, and moisture.50

image

FIGURE 134-7. Fire ants (Solenopsis) are social insects that tend to attack in swarms, inflicting multiple stings. (www.sbs.utexas.edu)

Solenopsis invicta are 2–5 mm in size and red in color. They live in colonies and build large mounds, up to 3 ft. in diameter, which are interconnected by underground tunnels up to 100-ft. long. These mounds are found most commonly in yards, playgrounds, and open fields.51 Fire ants are aggressive insects with no natural enemies. They are social insects and tend to attack in swarms, with multiple stings the norm. In endemic areas, nearly 50% of the exposed population is stung each year. Stings are more common among children and occur most frequently on their ankles and feet during the summer months.

image PATHOPHYSIOLOGY

Bee and wasp venoms are made of proteins. Conversely, fire ant venoms are 95% alkaloids.45 Fire ants sting in a two-phase process. The ant first bites the victim with powerful mandibles, then, if undisturbed, will arch the body and swivel around the attached mandibles to sting the victim repeatedly with the stinger. This produces a characteristic circular pattern of papules/stings around two central punctures. Fierce fire ant attacks ensue in response to an alarming pheromone released by an individual or group of ants.

Fire ant venoms produce a sharp, burning sensation; hence the name. The venoms have cytotoxic, bactericidal, insecticidal, and hemolytic properties. They also activate the complement pathway and promote histamine release. Fire ant venoms are immunogenic and result in sensitization of the sting victim creating the risk of future anaphylaxis.

image CLINICAL PRESENTATION

Clinical manifestations reflect the venom’s effects and are predominantly local dermatologic reactions. The initial bites and stings cause burning pain associated with circular wheals or papules around the central hemorrhagic punctures. The wheal-and-flare reactions resolve within 1 hour, but then develop into sterile pustules within 24 hours. The pustules slough off over 48–72 hours, leaving shallow ulcerated lesions. The pustules are intensely pruritic and often become contaminated after the victim scratches the lesions. Secondary infections are usually minor but may cause considerable morbidity.

Between 15 and 50% of victims develop more severe local reactions, characterized by an exaggerated wheal-and-flare response, followed by the development of erythema, edema, and induration >5 cm in diameter. These lesions are intensely pruritic, may resemble cellulitis, and persist for 24–72 hours.51

image MANAGEMENT

Topical glucocorticoid ointments, local anesthetic creams, and oral antihistamines may be useful for the itching associated with these reactions. No intervention has been shown to prevent or resolve the pustules. Treatment consists of local conservative measures including application of ice or cool compresses for symptomatic relief and gentle, frequent cleansing of the affected areas to prevent secondary infections.

Anaphylactic reactions have been estimated to occur after as many as 1% of fire ant stings. Anaphylaxis may occur several hours after a sting and is known to occur more frequently in children than in adults.

Immunotherapy may be appropriate for persons with severe hypersensitivity to fire ant venom or those who have had a previous anaphylactic reaction to a fire ant sting. The efficacy of immunotherapy has been variable, but it has been reported to provide as high as 98% protection.50,52

REFERENCES

1. Isbister GK, Fan HW. Spider bite. Lancet. 2011;378:2039.

2. Diaz JH, Leblanc KE. Common spider bites. Am Fam Physician. 2007;75:869.

3. Monte AA, Bucher-Bartelson B, Heard KJ. A US perspective of symptomatic Latrodectus spp. envenomation and treatment: a National Poison Data System review. Ann Pharmacother. 2011;45:1491.

4. Peterson ME. Black widow spider envenomation. Clin Tech Small Anim Pract. 2006;21:187.

5. Rash LD, Hodgson WC. Pharmacology and biochemistry of spider venoms. Toxicon. 2002;40:225.

6. Clark RF, Wethern-Kestner S, Vance MV, Gerkin R. Clinical presentation and treatment of black widow spider envenomation: a review of 163 cases. Ann Emerg Med. 1992;21:782.

7. Sotelo-Cruz N, Hurtado-Valenzuela JG, Gomez-Rivera N. Poisoning caused by Latrodectus mactans (Black Widow) spider bite among children. Clinical features and therapy. Gac Med Mex. 2006;142:103.

8. Dendane T, Abidi K, Madani N, et al. Reversible myocarditis after black widow spider envenomation. Case Report Med. 2012;2012:794540.

9. Cohen J, Bush S. Case report: compartment syndrome after a suspected black widow spider bite. Ann Emerg Med. 2005;45:414.

10. Hoover NG, Fortenberry JD. Use of antivenin to treat priapism after a black widow spider bite. Pediatrics. 2004;114:e128.

11. Nordt SP, Clark RF, Lee A, Berk K, Lee Cantrell F. Examination of adverse events following black widow antivenom use in California. Clin Toxicol (Phila). 2012;50:70.

12. Gonzalez Valverde FM, Gomez Ramos MJ, Menarguez Pina F, Vázquez Rojas JL. Fatal latrodectism in an elderly man. Med Clin (Barc). 2001;117:319.

13. Pneumatikos IA, Galiatsou E, Goe D, Kitsakos A, Nakos G, Vougiouklakis TG. Acute fatal toxic myocarditis after black widow spider envenomation. Ann Emerg Med. 2003;41:158.

14. Clark RF. The safety and efficacy of antivenin Latrodectus mactans. J Toxicol Clin Toxicol. 2001;39:125.

15. Reeves JA, Allison EJ Jr, Goodman PE. Black widow spider bite in a child. Am J Emerg Med. 1996;14:469.

16. Murphy CM, Hong JJ, Beuhler MC. Anaphylaxis with Latrodectus antivenin resulting in cardiac arrest. J Med Toxicol. 2011;7:317.

17. Rader RK, Stoecker WV, Malters JM, Marr MT, Dyer JA. Seasonality of brown recluse populations is reflected by numbers of brown recluse envenomations. Toxicon. 2012;60:1.

18. Vetter RS. Seasonality of brown recluse spiders, Loxosceles reclusa, submitted by the general public: implications for physicians regarding loxoscelism diagnoses. Toxicon. 2011;58:623.

19. Erickson T, Hryhorczuk DO, Lipscomb J, Burda A, Greenberg B. Brown recluse spider bites in an urban wilderness. J Wilderness Med. 1990;258.

20. Saupe EE, Papes M, Selden PA, Vetter RS. Tracking a medically important spider: climate change, ecological niche modeling, and the brown recluse (Loxosceles reclusa). PLoS One. 2011;6:e17731.

21. Tutrone WD, Green KM, Norris T, Weinberg JM, Clarke D. Brown recluse spider envenomation: dermatologic application of hyperbaric oxygen therapy. J Drugs Dermatol. 2005;4:424.

22. Swanson DL, Vetter RS. Bites of brown recluse spiders and suspected necrotic arachnidism. N Engl J Med. 2005;352:700.

23. Furbee RB, Kao LW, Ibrahim D. Brown recluse spider envenomation. Clin Lab Med. 2006;26:211.

24. Osterhoudt KC. Diagnosis of brown recluse spider bites in absence of spiders. Clin Pediatr (Phila). 2004;43:407; author reply 407.

25. Vetter RS, Swanson DL: Of spiders and zebras: publication of inadequately documented loxoscelism case reports. J Am Acad Dermatol. 2007;56:1063.

26. Necrotic arachnidism–Pacific Northwest, 1988-1996. MMWR Morb Mortal Wkly Rep. 1996;45:433.

27. Elbahlawan LM, Stidham GL, Bugnitz MC, Storgion SA, Quasney MW. Severe systemic reaction to Loxosceles reclusa spider bites in a pediatric population. Pediatr Emerg Care. 2005;21:177.

28. Tong TSA, Clark RF. Arthropod bites and stings. In: Erickson TB, ed. Pediatric Toxicology: Diagnosis and Management of the Poisoned Child. New York: McGraw-Hill; 2005:624.

29. Phillips S, Kohn M, Baker D, et al. Therapy of brown spider envenomation: a controlled trial of hyperbaric oxygen, dapsone, and cyproheptadine. Ann Emerg Med. 1995;25:363.

30. de Roodt AR, Estevez-Ramirez J, Litwin S, Magaña P, Olvera A, Alagón A. Toxicity of two North American Loxosceles (brown recluse spiders) venoms and their neutralization by antivenoms. Clin Toxicol (Phila). 2007;45:678.

31. Isbister GK, Graudins A, White J, et al. Antivenom treatment in arachnidism. J Toxicol Clin Toxicol. 2003;41:291.

32. Saucier JR. Arachnid envenomation. Emerg Med Clin North Am. 2004;22:405.

33. Belyea DA, Tuman DC, Ward TP, Babonis TR. The red eye revisited: ophthalmia nodosa due to tarantula hairs. South Med J. 1998;91:565.

34. Bucaretchi F, Baracat EC, Nogueira RJ, et al. A comparative study of severe scorpion envenomation in children caused by Tityus bahiensis and Tityus serrulatus. Rev Inst Med Trop Sao Paulo. 1995;37:331.

35. Das S, Nalini P, Ananthakrishnan S, Sethuraman KR, Balachander J, Srinivasan S. Cardiac involvement and scorpion envenomation in children. J Trop Pediatr. 1995;41:338.

36. Celis A, Gaxiola-Robles R, Sevilla-Godinez E, Orozco Valerio Mde J, Armas J. Trends in mortality from scorpion stings in Mexico, 1979-2003. Rev Panam Salud Publica. 2007;21:373.

37. Quan D, LoVecchio F. A clinical score predicting the need for hospitalization in scorpion envenomation. Am J Emerg Med. 2007;25: 856.

38. Quan D. North American poisonous bites and stings. Crit Care Clin. 2012;28:633.

39. Abroug F, ElAtrous S, Nouira S, Haguiga H, Touzi N, Bouchoucha S. Serotherapy in scorpion envenomation: a randomised controlled trial. Lancet. 1999;354:906.

40. LoVecchio F, Welch S, Klemens J, Curry SC, Thomas R. Incidence of immediate and delayed hypersensitivity to Centruroides antivenom. Ann Emerg Med. 1999;34:615.

41. Kim KT, Oguro J. Update on the status of Africanized honey bees in the western states. West J Med. 1999;170:220.

42. Whitfield CW, Behura SK, Berlocher SH, et al. Thrice out of Africa: ancient and recent expansions of the honey bee, Apis mellifera. Science. 2006;314:642.

43. Bourgain C, Pauti MD, Fillastre JP, et al. Massive poisoning by African bee stings. Presse Med. 1998;27:1099.

44. Bledsoe BE. Unwelcome visitors: is EMS ready for fire ants and killer bees. EMS Mag. 2007;36:68.

45. Fitzgerald KT, Flood AA. Hymenoptera stings. Clin Tech Small Anim Pract. 2006;21:194.

46. Vetter RS, Visscher PK, Camazine S. Mass envenomations by honey bees and wasps. West J Med. 1999. 170:223.

47. Hamilton RG. Diagnosis of Hymenoptera venom sensitivity. Curr Opin Allergy Clin Immunol. 2002;2:347.

48. Lazoglu AH, Boglioli LR, Taff ML, Rosenbluth M, Macris NT. Serum sickness reaction following multiple insect stings. Ann Allergy Asthma Immunol. 1995;75:522.

49. Erickson T. North American arthropod envenomation and parasitism. In: Auerbach PS, ed. Wilderness Medicine. Philadelphia: Mosby Elsevier; 2007:2316.

50. Rhoades R. Stinging ants. Curr Opin Allergy Clin Immunol. 2001;1:343.

51. Kemp SF, deShazo RD, Moffitt JE, Williams DF, Buhner WA 2nd. Expanding habitat of the imported fire ant (Solenopsis invicta): a public health concern. J Allergy Clin Immunol. 2000;105:683.

52. Cohen PR. Imported fire ant stings: clinical manifestations and treatment. Pediatr Dermatol. 1992;9:44.