Related narrative: Brown Recluse Spider Bite
Ten thousand spider bites are reported in the United States yearly. Most spiders produce venom which incapacitates prey and is not a defensive mechanism. Human envenomation is usually an incidental result of disturbing the spider. Few spiders have fangs robust enough to penetrate human skin or venom toxic enough to cause necrosis. The common names of the 7 spider families endemic to the US that are a potential threat to humans are the brown recluse/fiddle back, hobo, wolf, fishing, green lynx, running and jumping spiders. Only the first two have venom potent enough to cause death in humans. Black widow bites cause erythema and edema, but not skin necrosis.
Spider bite is rarely suspected as the cause of lesions; it is even more unusual that the spider brought in for positive identification. Spider bites are most commonly single and on an extremity (95%) in one series. Confidence in the diagnosis is graded as putative, presumptive, probable or documented based on whether the spider is endemic to the area, whether the lesion, symptoms and course are typical, and of course if the spider is positively identified by a qualified authority.
The brown recluse (loxosceles reclusa) spider causes the majority of severe bites in the United states. The greatest concentration is found in the Midwest. Five of the 13 loxosceles species are capable of producing skin necrosis. The brown recluse is a relatively large spider (~1 cm body, 5 cm leg span). The female is slightly larger and more venomous. It is light brown in color with a darker violin shaped marking on the dorsal cephalothorax (see photo). It has three pairs of eyes. It favors dry, dirty, undisturbed environments such as attics and storage areas (cardboard boxes) indoors and barns and woodpiles (particularly vertically stacked boards) outdoors. The spider bites when threatened or trapped (as in clothing). It is not aggressive and retreats in the face of light and noise. The peak incidence of bites is summer with a second spike in the fall when stored winter clothing is put on.
All brown recluse bites cause erythema. If skin necrosis ensues, the bite is by definition graded as moderate to severe. The initial bite is usually painless or experienced as a pinch. The typical course is painless vesicle formation with erythema peripherally and cyanosis centrally in the first 3 hours. Pain and pruritis ensue in the first 12 hours. In the first 24 hours the lesion may progress to bulla formation, hemorrhage and the characteristic peripheral erythema from vasodilatation surrounding an ischemic area with a central thrombotic area, producing the red white and blue components described in the literature. In the first three days the lesion may demarcate and become edematous, and systemic effects may become evident in severe cases (10-15%). In the first week, the lesion becomes indurated, an eschar develops, and the erythema decreases. The eschar eventually separates leaving an ulcer which usually reaches maximum size and then undergoes gradual healing (up to 4 months duration).
There are several enzymes (alkaline phosphatase, hyaluronidase, esterase) in brown recluse venom which immobilize prey. The major toxic component is sphingomyelinase D2 (SMD) which may persist at the site for up to 120 hours. SMD is a phospholipase which acts on the cell membrane of red blood cells, platelets and endothelial cells, causing hemorrhage, coagulation and platelet aggregation. Severe systemic reaction may include refractory headache, fever, nausea, hemolysis (resulting in anemia, hemoglobinuria and renal failure), thrombocytopenia, disseminated intravascular coagulation (DIC, rarely), and pulmonary edema (from destruction of sphingomyelin in surfactant). Degradation of nerve sheath myelin causes pain and may result in lingering anesthesia, hyper- or hypoesthesia. Skin necrosis results from neutrophilic activation, intravascular degranulation (release of lytic enzymes) causing endothelial damage and leading to thrombosis and tissue necrosis. Children and patients with comorbid conditions and increased susceptibility may suffer more severe systemic effects.
Standard treatment of all spider bites consists of rest, iced compression (heat exacerbates the course), and elevation (acronym RICE). Antibiotic prophylaxis is given against secondary infection, which can progress to nectotizing fasciitis (see necrotizing fasciitis). Tetanus booster is given if indicated. Analgesia is given as appropriate. Supportive therapy, including vigorous hydration is given for systemic complications. A short course of systemic steroids may be beneficial in the face of significant hemolysis (reported ranges 20-95%), to stabilize the RBC membrane. Steroids have no effect on dermal necrosis. Dapsone is sometimes cautiously used for severe cases to inhibit neutrophil function and reduce local inflammation, but the side effect of methemoglobinemia can be significant, and the drug is contraindicated in patients with G6PD deficiency. Antivenin is not commercially available in the United States.
Early surgery is not indicated in most cases, as it seems to worsen the course. Gentle excision of defined eschar may be beneficial late in the course (6-10 weeks) when inflammation has receded. Secondary infection may require drainage. The hobo spider (see photo) is brown with a herringbone stripe pattern and its bite also feels like a minor pinprick. It produces erythema, induration and local and distal numbness and tingling within 15 min. By 36 hours vesicle formation occurs and there may be serosanguinous drainage. The most common systemic effect is severe, refractory headache starting from 30 min to 10 hours post-bite, and lasting up to a week. It may be associated with visual disturbances, visual and auditory hallucinations, nausea, weakness, lethargy and paresis. There is a 15% incidence of hemolysis and thrombocytopenia.
Townsend: Sabiston Textbook of Surgery, 16th ed., WB Saunders, 2001, pp 369, 370.
Sams, HH et al, Necrotic arachnidism, J Am Acad Dermatol 2001;44(4):561-73.
Sams HH et al, Nineteen documented cases of Loxoscles reclusa envenomation, J Am Acad Dermatol 2001;44(4):603-8.
Majeski J, Necrotizing fasciitis developing from a brown recluse spider bite, Am Surg, 67(2)Feb 2001: 188-90.
University of Nebraska Cooperative Extension in Lancaster County