Gigitan Serangga

01Pathophysiology

Insect bites and stings produce tissue injury through two broad mechanisms: direct tissue toxicity from venom components and immune-mediated hypersensitivity to venom or salivary proteins.

When a Hymenoptera insect (bee, wasp, hornet, or fire ant) stings, it injects venom containing phospholipase A2, hyaluronidase, and melittin. These components cause local cell membrane disruption, pain, and inflammation. In a non-sensitized individual, this produces a normal local reaction with pain, erythema, and swelling confined to the sting site, resolving within hours.

In sensitized individuals, prior exposure has generated venom-IgE antibodies that are bound to mast cells and basophils. Upon re-exposure, venom antigens crosslink surface IgE, triggering mast cell degranulation and releasing histamine, leukotrienes, prostaglandins, and tryptase. When this degranulation is localized, it produces a large local reaction (swelling >10 cm lasting >24 hours). When it becomes systemic, the result is anaphylaxis: widespread vasodilation, increased vascular permeability, bronchospasm, and cardiovascular collapse. This is the reason why the same patient who tolerated a sting years ago can now present in shock.

Spider bites operate differently. Brown recluse (Loxosceles) venom contains sphingomyelinase D, which activates the complement cascade and causes dermonecrosis through neutrophil-mediated tissue destruction. This explains the characteristic progression from a painless bite to a violaceous plaque and then a necrotic ulcer with an eschar over days. Black widow (Latrodectus) venom contains alpha-latrotoxin, which forces massive acetylcholine and norepinephrine release at neuromuscular junctions, producing severe muscle spasms, rigidity, and autonomic instability rather than local necrosis.

Tick bites are notable because the tick's salivary glands secrete immunosuppressive compounds that allow prolonged feeding. Certain species inject a neurotoxin that blocks acetylcholine release at the neuromuscular junction, causing ascending flaccid paralysis (tick paralysis). This is purely toxin-mediated and reverses with tick removal. Separately, ticks serve as vectors for Borrelia (Lyme disease), Rickettsia (Rocky Mountain Spotted Fever), and other pathogens.

Mosquito, flea, and bedbug bites cause reactions primarily through salivary protein hypersensitivity. The characteristic pruritic papule is a combination of immediate (type I, IgE) and delayed (type IV, T-cell mediated) hypersensitivity, which is why new exposures in travelers may produce exaggerated reactions compared to residents who have developed tolerance.

02Classification and Clinical Manifestation

Reaction Severity Classification (Hymenoptera)

Clinical Manifestation by Arthropod Type

03Diagnostic Workup

The diagnosis of an insect bite or sting is overwhelmingly clinical. The best initial test is a thorough history (what the patient was doing, geographic location, time of day, appearance of the insect) combined with physical examination of the lesion's morphology and distribution. In most cases, no laboratory testing is needed for uncomplicated local reactions.

When anaphylaxis is suspected, draw a serum tryptase level during the acute episode or within 1 to 2 hours of symptom onset. Tryptase is released from mast cells and basophils during degranulation and peaks at 1 to 2 hours, returning to baseline by 6 to 8 hours. An elevated tryptase (>11.4 ng/mL) supports the diagnosis of anaphylaxis. However, a normal tryptase does not rule out anaphylaxis, particularly in food-triggered or mild episodes. In insect sting anaphylaxis, tryptase is more reliably elevated.

For patients who have experienced a systemic allergic reaction to a Hymenoptera sting, the most accurate (confirmatory) test is venom skin prick testing performed 4 to 6 weeks after the event. The delay is critical because testing too early (during the refractory period) can yield false negatives due to temporary depletion of venom-IgE. Skin testing determines whether the patient is a candidate for venom immunotherapy. If skin testing is negative but clinical suspicion remains high, serum venom-IgE (component-resolved diagnostics) is the next step.

For brown recluse spider bites, diagnosis is clinical. There is no widely available confirmatory lab test for loxoscelism. The wound may show characteristic findings of a necrotic ulcer with a "red, white, and blue" color pattern (erythema, ischemia, thrombosis). If the wound is atypical or not healing, a biopsy can help exclude other causes such as pyoderma gangrenosum, necrotizing fasciitis, or cutaneous anthrax. Many suspected brown recluse bites, particularly outside the spider's endemic range (south-central United States), turn out to be staphylococcal abscesses.

For tick bites, the priority is identifying whether tick-borne illness has developed. If erythema migrans is present (an expanding erythematous ring >5 cm with or without central clearing), the diagnosis of Lyme disease is clinical and treatment should not be delayed for serology. If tick paralysis is suspected (ascending flaccid paralysis), the diagnosis is confirmed by finding and removing the embedded tick with subsequent rapid resolution of symptoms within hours.

04Management and Treatment

Anaphylaxis is the highest-yield management scenario on the exam. The single most important intervention is intramuscular epinephrine, given into the mid-outer thigh. The adult dose is 0.3 to 0.5 mg of 1:1,000 (1 mg/mL) concentration. In children, the dose is 0.01 mg/kg up to a maximum of 0.3 mg. This can be repeated every 5 to 15 minutes if symptoms persist. Epinephrine must never be delayed for any other intervention. IV fluids (normal saline 1 to 2 L bolus) address distributive shock. H1 blockers (diphenhydramine 25 to 50 mg IV) and H2 blockers (ranitidine 50 mg IV or famotidine 20 mg IV) are adjunctive for urticaria and are never substitutes for epinephrine. Corticosteroids (methylprednisolone 125 mg IV) help prevent biphasic anaphylaxis but take hours to work and have no role in acute stabilization. After recovery, every patient must be observed for at least 4 to 6 hours (some guidelines recommend up to 24 hours for severe episodes) because biphasic reactions can occur. Upon discharge, prescribe an epinephrine auto-injector and refer to an allergist for venom skin testing and immunotherapy.

Venom immunotherapy (VIT) is indicated for all patients who have experienced a systemic reaction to a Hymenoptera sting and have positive venom testing. It is the only intervention that meaningfully reduces the recurrence risk of anaphylaxis (from approximately 60% per subsequent sting to less than 5%). The standard protocol involves weekly subcutaneous injections with escalating doses during the buildup phase (8 to 16 weeks), followed by monthly maintenance injections for 3 to 5 years. Patients with very severe prior reactions, mast cell disorders, or elevated baseline tryptase may need indefinite therapy.

For brown recluse bites, the cornerstone is conservative wound care. Early surgical excision is contraindicated because it worsens outcomes and delays healing. The necrotic area should be allowed to demarcate fully before any debridement is attempted, typically at 6 to 8 weeks. Antibiotics are not indicated prophylactically but should be started if signs of secondary bacterial infection develop (expanding erythema, warmth, purulent drainage, fever). Dapsone has been used historically for its anti-neutrophil properties, but clinical evidence supporting its use is weak and it carries a risk of hemolytic anemia, particularly in patients with G6PD deficiency.

For black widow bites, the primary goal is symptomatic relief of severe muscle spasms. IV benzodiazepines (diazepam 5 to 10 mg) or opioid analgesics are first-line. IV calcium gluconate was historically recommended but has shown limited benefit in clinical practice. Latrodectus antivenom is reserved for severe envenomation with uncontrolled hypertension, respiratory compromise, or refractory pain. It carries a risk of serum sickness and anaphylaxis and requires careful risk-benefit analysis.

Tick paralysis is unique because the treatment is simply removing the tick. Once the source of the neurotoxin is eliminated, neurologic function begins returning within hours. If the tick is not found and removed, however, the paralysis can progress to involve the respiratory muscles and become fatal. The key exam teaching point is that tick paralysis mimics Guillain-Barre syndrome, but the presence of an embedded tick and rapid improvement after removal distinguishes the two.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on insect bite questions is by hesitating on epinephrine for anaphylaxis. The vignette will describe a patient with urticaria, throat tightness, or hypotension after an insect sting, and the answer choices will include diphenhydramine, IV corticosteroids, and IM epinephrine. Students who pick antihistamines or steroids as the "next best step" are wrong every time. Epinephrine is always the first intervention in anaphylaxis, regardless of the trigger. Nothing else reverses bronchospasm and vasodilation quickly enough.

A second trap is the "spider bite that is really MRSA." Exam writers love presenting a patient with a painful, red, swollen lesion on an extremity who says "I think a spider bit me." If the patient lives outside the brown recluse's geographic range (south-central US), or if the lesion is fluctuant with purulent drainage, the correct answer is incision and drainage for a staphylococcal abscess, not wound care for loxoscelism.

Another high-yield distractor is confusing tick paralysis with Guillain-Barre syndrome. Both present with ascending flaccid paralysis and areflexia. The critical discriminator is the clinical context: a child who was playing outdoors, with a tick found on the scalp, whose weakness rapidly reverses after tick removal. GBS does not reverse with any single physical intervention, and the CSF shows elevated protein.

Students also get tripped up on the timing of venom allergy testing. Ordering skin prick testing immediately after anaphylaxis will produce a false negative because of the refractory period. The correct timing is 4 to 6 weeks after the event, which allows IgE levels to replenish.

Finally, remember that large local reactions (even dramatic ones with swelling of an entire limb) carry a low risk of progression to future anaphylaxis (about 5 to 10%). These patients do not routinely require venom immunotherapy. VIT is reserved for patients with documented systemic (anaphylactic) reactions and confirmed venom sensitization. The core competency being tested here is the ability to stratify allergic reaction severity and match it to the appropriate level of intervention.