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Almost all of the 40,000 species of spiders are venomous. However, the fangs of most species are too short or too fragile to penetrate the skin. Serious systemic reactions most frequently occur with bites from
Brown spiders are present in the Midwest and south central US, not in the coastal and Canadian border states, except when imported through clothing or luggage. Black widow spiders are present throughout the US. Distribution of the brown widow recently spread from Florida to all of the Gulf Coast states. Several other venomous spider species (eg, Pamphobeteus,
Cupiennius,
Phoneutria) are not native to the US but may be imported on produce or other materials or through commercial trade in spiders as novelty pets. Spider bites cause < 3 deaths/yr in the US, usually in children.
Only a few spider venoms have been studied in detail. Of greatest significance are those having necrotizing venom components (in brown and some house spiders) and neurotoxic venom components (in widow spiders). Sphingomyelinase D is the protein component that seems to be responsible for most of the tissue destruction and hemolysis caused by brown spider envenomations. The most toxic component of widow spider venom seems to be a peptide, α-latrotoxin, that affects neuromuscular transmission.
Symptoms and Signs
Brown spider bites are most common in the US. Some bites are painless initially, but pain, which can be severe and involve the entire extremity, develops within 30 to 60 min in all cases. The bite area becomes erythematous and ecchymotic and may be pruritic. Generalized pruritus may also be present. A central bleb forms at the bite site, often surrounded by an irregular ecchymotic area (bull's eye lesion). The lesion may mimic pyoderma gangrenosum. The central bleb becomes larger, fills with blood, ruptures, and leaves an ulcer. A black eschar forms over the ulcer and eventually sloughs.
Most bites leave minimal residual scarring but some can leave a large tissue defect, which may involve muscle. Loxoscelism, a venom-induced systemic syndrome, may not be detected until 24 to 72 h after the bite and is uncommon but more prevalent in children and adolescents. Systemic effects (eg, fever, chills, nausea, vomiting, arthralgias, myalgias, generalized rash, seizures, hypotension, disseminated intravascular coagulation, thrombocytopenia, hemolysis, renal failure) are responsible for all reported fatalities.
Widow spider bites usually cause an immediate, sharp, stinging sensation. The pain may be described as dull and numbing and may be disproportionate to the clinical signs. Within 1 h after envenomation, there may be progression to persistent local pain, diaphoresis, erythema, and piloerection at the bite site. Sometimes remote and/or systemic symptoms develop.
Widow spider envenomations are graded as mild, moderate, or severe.
Latrodectism, a systemic syndrome caused by neurotoxic venom components, manifests as restlessness, anxiety, sweating, headache, dizziness, nausea, vomiting, hypertension, salivation, weakness, diffuse erythematous rash, pruritus, ptosis, eyelid and extremity edema, respiratory distress, increased skin temperature over the affected area, and cramping pain and muscular rigidity in the abdomen, shoulders, chest, and back. Abdominal pain may be severe and mimic acute surgical abdomen, rabies, or tetanus. Symptoms tend to resolve over 1 to 3 days, but residual spasms, paresthesias, agitation, and weakness can last weeks to months.
Tarantula bites are extremely rare and nonvenomous with North or South American ("new world") tarantulas. However, agitation of the spider may cause it to throw needle-like hairs. The hairs act as foreign bodies in skin or eyes and can trigger mast cell degranulation and an anaphylactoid reaction (eg, urticaria, angioedema, bronchospasm, hypotension) in sensitized people, usually pet owners who handle the spider daily. Tarantula species native to non-American continents ("old-world" tarantulas) are occasionally kept as pets. They are more aggressive then new world tarantulas, lack needle-like hairs, and can be venomous. All tarantula bites are treated supportively.
Diagnosis
Spider bites are often falsely suspected by patients. Diagnosis is typically suspected based on history and physical signs, but confirmation is rare because it requires witnessed biting, identification of the spider (the spider is rarely recovered intact), and exclusion of other causes. In nonendemic areas, a brown spider bite should not be diagnosed without identifying the spider. Many patients incorrectly attribute much more common methicillin-resistant Staphylococcus aureus (MRSA) skin infections to brown recluse spiders bites. Such infections should be excluded, as should other conditions that mimic spider bites (see Table 4: Bites and Stings: Disorders That Mimic Spider Bites ). Severe cases of latrodectism should be distinguished from acute abdomen, rabies, or tetanus.
Spiders are identified by location and markings. Widow spiders live outdoors in protected spaces (eg, rock piles, firewood cords, hay bales, outhouses) and have a red or orange hourglass marking on the ventral abdomen. Brown spiders live indoors or in protected spaces (eg, in barns, attics, and wood piles; behind furniture; under baseboards) and have a fiddle- or violin-like marking on the dorsal cephalothorax, ranging from the eyes to the abdomen. This marking may be difficult to recognize even in the intact spider.
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Table 4
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| Disorders That Mimic Spider Bites |
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Category
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Examples
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Insect bites
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Ant bites
Bedbug bites
Flea bites
Fly bites
Reduviid (eg, assassin, wheel, kissing) bug bites
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Other arachnid bites
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Mite bites
Tick bites
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Skin disorders
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Erythema chronicum migrans
Erythema nodosum
Leukocytoclastic vasculitis
Sporotrichosis
Toxic epidermal necrolysis
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Infections
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Chronic herpes simplex
Cutaneous anthrax
Disseminated gonococcal infection
Methicillin-resistant Staphylococcus aureus
Septic emboli in endocarditis or IV drug use
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Trauma
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Self-inflicted injuries
Subcutaneous drug injection
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Treatment
Treatment common to all spider bites includes wound cleaning, ice to reduce pain, extremity elevation, tetanus prophylaxis, and observation. Most local reactions respond to these measures alone.
For brown spider bites, limiting intervention to standard wound care and measures that minimize infection risk is usually most prudent:
No intervention has been proved to reduce morbidity or improve outcome after a brown spider bite. Commonly touted or poorly studied treatment options are controversial or potentially harmful. Dapsone (eg, 100 mg po once/day until inflammation subsides) is often considered for ulcers > 2 cm, but its benefit is unproved and dose-related hemolysis almost always develops; agranulocytosis, aplastic anemia, and methemoglobinemia have been documented. Tetracycline has been suggested to prevent the dermonecrosis caused by brown spider envenomation but efficacy is unproven. Corticosteroids, colchicine, nitroglycerin, electric shock therapy, and surgical excision are of no value.
For widow spider bites, medical attention is necessary if symptoms are moderate or severe; initial treatment is parenteral opioids and benzodiazepines. Myalgias and muscle spasms resulting from widow spider bites respond poorly to muscle relaxants and Ca salts.
Symptomatic envenomation is initially treated supportively. Equine-derived antivenom is available, and a new F(ab)2 antivenom is currently being studied. Because death from widow spider envenomation is rare, antivenom treatment has historically been reserved for patients at extremes of age and those with comorbid medical conditions. But because symptoms may persist for weeks or months, antivenom is being used more broadly, for example, if envenomation is severe or sometimes moderate. Antivenom is most effective when used early, but can be effective up to 36 h after the bite. Clinical response is usually dramatic. The dose for children and adults is 1 vial (6000 units) IV in 50 mL of normal saline, usually over 15 min. Although the manufacturer recommends skin testing before administering the antivenom, testing does not always predict adverse reactions such as acute anaphylaxis and is not often done.
Key Points
Last full review/revision February 2013 by Robert A. Barish, MD, MBA; Thomas Arnold, MD
Content last modified March 2013
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