Spider Bites: Introduction - The Merck Veterinary Manual

Spider Bites: Introduction

Envenomation of animals by spiders is relatively uncommon and difficult to recognize. It may be suspected on clinical signs, but confirmatory evidence is rare. Spiders of medical importance in the USA do not inflict particularly painful bites, so it is unusual for a spider bite to be suspected until clinical signs appear. It is also unlikely that the offending spider will remain in close proximity to the victim for the time (30 min to 6 hr) required for signs to develop. Almost all spiders are venomous, but few possess the attributes necessary to cause clinical envenomation in mammals—mouth parts of sufficient size to allow penetration of the skin and toxin of sufficient quantity or potency to result in morbidity.

The spiders in the USA that are capable of causing clinical envenomation belong to 2 groups—widow spiders ( Latrodectus spp ) and brown spiders (mostly Loxosceles spp ).

Widow Spiders:

Widow spiders usually bite only when accidental skin contact occurs. The most common species is the black widow, Latrodectus mactans , characterized by a red hourglass shape on the ventral abdomen. In the western states, the western black widow, L hesperus , predominates, while the brown widow, L bishopi , is found in the south, and the red widow, L geometricus , is found in Florida.

Latrodectus venom is one of the most potent biologic toxins. The most important of its 5 or 6 components is a neurotoxin that causes release of the neurotransmitters norepinephrine and acetylcholine at synaptic junctions, which continues until the neurotransmitters are depleted. The resulting severe, painful cramping of all large muscle groups accounts for most of the clinical signs.

Unless there is a history of a widow spider bite, diagnosis must be based on clinical signs, which include restlessness with apparent anxiety or apprehension; rapid, shallow, irregular respiration; shock; abdominal rigidity or tenderness; and painful muscle rigidity, sometimes accompanied by intermittent relaxation (which may progress to clonus and eventually to respiratory paralysis). Partial paresis also has been described.

An antivenin (equine origin) is commercially available but is usually reserved for confirmed bites of high-risk individuals (very young or very old). Symptomatic treatment is usually sufficient but may require a combination of therapeutic agents. Calcium gluconate IV (10 mL of a 10% solution is the usual human dose) is reportedly helpful. Meperidine hydrochloride or morphine, also given IV, provides relief from pain and produces muscle relaxation. Muscle relaxants and diazepam are also beneficial. Tetanus antitoxin also should be administered. Recovery may be prolonged; weakness and even partial paralysis may persist for several days.

Brown Spiders:

There are at least 10 species of Loxosceles spiders in the USA, but the brown recluse spider, L reclusa , is the most common, and envenomation by it is typical. These spiders have a violin-shaped marking on the cephalothorax, although it may be indistinct or absent in some species. In the northwestern USA, the unrelated spider Tegenaria agrestis reportedly causes a clinically indistinguishable dermonecrosis in humans and presumably in other animals. Brown recluse spider venom has vasoconstrictive, thrombotic, hemolytic, and necrotizing properties. It contains several enzymes, including a phospholipase (sphingomylinase D) that attacks cell membranes. Pathogenetic mechanisms of the characteristic dermal necrosis are poorly understood, but activation of complement, chemotaxis, and accumulations of neutrophils affect (or amplify) the process.

A history of a bite by a “fiddleback” brown spider is useful but rare. A presumptive diagnosis may be based on the presence of a discrete, erythematous, intensely pruritic skin lesion that may have irregular ecchymoses. Within 4-8 hr, a vesicle develops at the bite wound, and sometimes a blanched zone circumscribes the erythematous area, imparting a “bull’s-eye” appearance to the lesion. The central area sometimes appears pale or cyanotic. The vesicle may degenerate to an ulcer that, unless treated in a timely manner, may enlarge and extend to underlying tissues, including muscle. Sometimes, a pustule follows the vesicle and, on its breakdown, a black eschar remains. The final tissue defect may be extensive and indolent and require months to heal. However, medical authorities claim that not all brown recluse spider bites result in severe, localized dermal necrosis.

Systemic signs sometimes accompany brown recluse spider envenomation and may not appear for 3-4 days after the bite. Hemolysis, thrombocytopenia, and disseminated intravascular coagulation are more likely to occur in cases with severe dermal necrosis. Fever, vomiting, edema, hemoglobinuria, hemolytic anemia, renal failure, and shock may result from systemic loxoscelism.

In known bites, early treatment can be successful, but unfortunately, many cases are not recognized until cutaneous necrosis has become extensive; treatment at that stage is less rewarding but is still of value. Immediate application of cold packs is beneficial, and if administered early, corticosteroids protect against cutaneous necrosis by stabilizing cell membranes and suppressing chemotaxis. Corticosteroids also tend to protect against systemic involvement. Radical excision has been advocated, but its value is questionable. Dapsone, an inhibitor of leukocyte function, which is frequently used in the treatment of leprosy, is currently considered the drug of choice for brown recluse spider bites. In humans, it is administered at 100 mg, bid for 14-25 days. Broad-spectrum antibiotics are useful in preventing secondary infection, and tetanus immunoprophylaxis should be considered.