Updated: Nov 10, 2009
The fire ant is a wingless member of the order Hymenoptera, which includes wasps and bees. It is a potentially lethal environmental hazard in the United States, infesting more than 310 million acres of land. Fire ants are resistant to control efforts and can overwhelm an environment. They damage farm equipment, electrical systems, irrigation systems, and land. They build mounds in sunny, open areas (eg, lawns, playgrounds, parks, golf courses) and aggressively attack anyone who disrupts their mound.
Each year, fire ants sting more than one half of the population in endemic areas of the Southeast. They cause a variety of medical problems, including increasing numbers of hypersensitivity reactions, secondary infections, neurologic complications, and even death.
The fire ant uses its mandibles to grasp its victim. It arches its body and drives an abdominal stinger into the skin to release venom. If not quickly removed, it then pivots around its mandibles and inflicts further stings in a circular pattern.
The stinger is a modified ovipositor that consists of a dorsal stylet and 2 ventrolateral lancets. These structures surround the venom canal, which connects to the venom sac. A pair of coiled glands produces the venom that discharges into the venom sac.
The venom also contains several allergenic proteins, measuring about 1.5% by dry weight. Four major allergenic proteins exist; Soli 1-4 induce immunoglobulin E (IgE) responses, including anaphylaxis, in patients who are allergic. Antigenic similarity exists between these proteins and bee and wasp venoms.
Many patients have venom-specific IgE-mediated wheal and flare reactions that develop over hours into pruritic edematous, indurated, and erythematous lesions that persist for up to 72 hours. These lesions may involve an entire extremity. They histologically resemble late-phase mast cell–dependent reactions and show an infiltrate of eosinophils, neutrophils, and fibrin deposition. Large, local reactions rarely can cause edematous tissue compression, leading to vascular compromise of an extremity.
Because most fire ant stings are not severe enough to cause the victim to seek medical attention, estimating the frequency of stings is difficult; however, annually, more than one half of the population in endemic areas is stung, and the incidence appears to be increasing.
Fire ants are becoming an increasingly important public health concern in the United States. More than 80 fatalities have been reported from fire ant-induced anaphylaxis.
Fire ant stings may occur in people of any race. No race has been shown to have an increased risk of being stung or to have a higher predisposition to complications.
Fire ants sting both males and females without discrimination.
Fire ants sting people of all ages, but children are overrepresented, probably because of greater environmental exposure.
Physical findings from fire ant bites and stings can be subdivided into local and systemic reactions.
The fire ant prefers open, sunny areas, such as pastures, parks, lawns, playgrounds, golf courses, and fields. Colonies also occur in or around buildings. Mound building increases considerably during warm months of the year when soil is moist. Concentrations in some areas exceed 200 mounds per acre. Several risk factors have been identified:
| Acneiform Eruptions | Folliculitis |
| Acropustulosis of Infancy | Herpes Simplex |
| Bedbug Bites | Herpes Zoster |
| Black Widow Spider Bite | Insect Bites |
| Brown Recluse Spider Bite | Linear IgA Dermatosis |
| Bullous Disease of Diabetes | Psoriasis, Pustular |
| Candidiasis, Cutaneous | Seabather's Eruption |
| Cellulitis | Subcorneal Pustular Dermatosis |
| Chickenpox | Transient Neonatal Pustular Melanosis |
| Cutaneous Larva Migrans | Urticaria, Cholinergic |
| Drug-Induced Bullous Disorders | |
| Eosinophilic Pustular Folliculitis | |
| Erythema Toxicum Neonatorum |
Local reaction (infection, punctures, foreign bodies, various other dermatoses)
Toxic reaction (chemical exposure/ingestion, intravenous drug abuse, environmental, plants)
Allergic reaction (medications, illicit drugs, foods, topical products, environmental, plants, chemicals)
The histologic findings depend on the stage of evolution of the lesion. In early lesions, a perivascular infiltrate of lymphocytes, neutrophils, and eosinophils is found within the dermis. Later, an intraepidermal vesicle or pustule (containing mostly neutrophils) is usually present, often with a central focus of epidermal necrosis. Dermal edema is often present. Compared with other arthropod assaults, fire ant stings are far more pustular, with more neutrophils and fewer eosinophils.
An allergist/immunologist consultation for evaluation and possible skin or in vitro testing for fire ant hypersensitivity is appropriate for any patient who has a systemic reaction to a fire ant sting. Consultation should be considered if the patient meets 1 of the following criteria:
No dietary changes are recommended; however, patients should have nothing by mouth if experiencing a severe systemic reaction.
No restriction in activity is required; however, rest is recommended in severe cases to possibly slow the spread of the reaction.
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
These agents are for mild-to-severe reactions.
For symptomatic relief of symptoms caused by release of histamine in allergic reactions.
25-50 mg PO qid for local reactions
25-50 mg IV/IM for urticaria, wheezing, and angioedema
<2 years: Not established
2-6 years: 6.25-12.5 mg PO q4-6h
6-12 years: 12.5-25 mg PO q4-6h
>12 years: 25-50 mg PO q4-6h
Potentiates effect of CNS depressants; because of alcohol content, do not give syr dosage form to patient taking medications that can cause disulfiramlike reactions; concomitant alkaloids present in belladonna, antidepressants with strong anticholinergic effects (eg, amitriptyline, trimipramine, amoxapine, doxepin, imipramine, nortriptyline, maprotiline), or phenothiazines with strong anticholinergic effects (eg, chlorpromazine, triflupromazine, thioridazine) and antihistamines may increase possibility of adynamic ileus, urinary retention, or chronic glaucoma (more prominent in elderly patients)
Documented hypersensitivity; acute asthma; newborns; breastfeeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction; elderly more susceptible to side effects; caution in history of bronchial asthma, cardiovascular disease or hypertension; may cause excitation in young children
These agents relieve pain and reduce inflammation.
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
400 mg PO q4-6h prn
4-10 mg/kg PO q6-8h prn
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI tract bleeding or perforation; high risk of bleeding; renal insufficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Class D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli. A short course may be used for severe local reactions.
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Many dosing regimens have been used.
20 mg PO qd for 5 d
Not established
Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI tract disease
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur
This agent is used for anaphylaxis reactions.
DOC for treating anaphylactoid reactions. Has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects of epinephrine include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
0.1-0.5 mg IM/SC q10-15min (1:1000 solution)
Autoinjector: 0.3 mg IM (0.3 mL of 1:1000 sol); may repeat if severe anaphylaxis persists
Injectable sol: 0.2 to 1 mg SC
Neonates: 0.01-0.03 mg/kg IV/ET q3-5min prn
Infants/children: 0.01 mg/kg IM once; alternatively, 0.15 to 0.3 mg IM depending on body weight; 0.01 mg/kg may be appropriate for patients weighing <30 kg
Alpha-blockers antagonize vasoconstriction; antihistamines may potentiate adverse cardiac effects; beta-blockers antagonize effects; cyclopropane may increase risk of arrhythmias; digoxin may increase risk of arrhythmias; ergot alkaloids increase risk of severe hypertension; halothane may increase risk of arrhythmias; TCAs may potentiate adverse cardiac effects; thyroid hormones may potentiate adverse cardiac effects; concurrent administration with chlorpromazine may result in decrease in blood pressure with reflex tachycardia
Chlorpromazine may reduce effect by approximately 50%; coadministration with MAOI including linezolid may cause clinically significant hypertensive effects; concurrent use of guanethidine and direct-acting sympathomimetic amines (eg, epinephrine, methoxamine, norepinephrine, phenylephrine) can result in severe hypertension
Documented hypersensitivity; cardiac arrhythmias or angle-closure glaucoma; local anesthesia in areas such as fingers or toes because vasoconstriction may produce sloughing of tissue; during labor (may delay second stage of labor); cardiac dilatation and coronary insufficiency (injection); concurrent use with cyclopropane or halogenated hydrocarbon anesthetic
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in elderly persons, prostatic hypertrophy, hypertension, cardiovascular disease, diabetes mellitus, hyperthyroidism, and cerebrovascular insufficiency; rapid IV infusions may cause death from cerebrovascular hemorrhage or cardiac arrhythmias
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fire ant bites, imported fire ants, fire ant bite treatment, fire ant bite symptoms, Solenopsis invicta, S invicta, , , , , , , , , Hymenoptera, hypersensitivity reactions, Soli 1-4, anaphylaxis, anaphylactic reaction, fire ant-induced anaphylaxis
James P Ralston, MD, President, Dermatology Center of McKinney
James P Ralston, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, and Texas Medical Association
Disclosure: Nothing to disclose.
Ronald P Rapini, MD, Josey Professor and Chair, Department of Dermatology, Professor of Pathology, University of Texas Medical School at Houston and MD Anderson Cancer Center
Ronald P Rapini, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Society for Investigative Dermatology, Southern Medical Association, and Texas Medical Association
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Daniel J Hogan, MD, Clinical Professor of Internal Medicine (Dermatology), NOVA Southeastern University; Investigator, Hill Top Research, Florida Research Center
Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association
Disclosure: Nothing to disclose.
Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
Jeffrey J Miller, MD, Associate Professor of Dermatology, Penn State University College of Medicine; Staff Dermatologist, Penn State Milton S Hershey Medical Center
Jeffrey J Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, Association of Professors of Dermatology, North American Hair Research Society, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
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Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School
Jonathan Adler, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
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