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<< Bites and Stings Snakes, Spiders, and Scorpions in the United States

Part II. Spiders: Epidemiology, Etiology, And Pathophysiology

Epidemiology

The two main species of spiders that account for virtually all of the medically significant spider bites in the United States are the Black Widow Spider (Latrodectus spp.) and the Brown Recluse Spider (Loxosceles spp.)



Loxosceles

The brown recluse spider, as its name implies, is known to be reclusive. Most species of Loxosceles reside in the southern and western United States. The bites have the capacity to be significantly harmful, but life-threatening envenomation is rare.32 Other recluse spider species are distributed further to the southwest. However, these species cause less necrotizing wounds. In 2005, there were 2236 brown recluse spider exposures called in to U.S. poison centers, with 464 victims being less than 19 years of age. 1016 victims were evaluated at a health care facility, and 14 envenomations were considered life-threatening. No deaths from Loxosceles envenomations were reported.5 Brown recluse spider bites are most prevalent during the summer time but may occur from spring to autumn.

Latrodectus

In the past 20 years, more than 40,000 presumed black widow spider bites have been reported to the American Association of Poison Control Centers. Death is rarely reported. Most of the fatality reports are from Africa and Europe, and even these are unusual.5,51,52

Etiology

Latrodectus

Black widow spiders are found throughout most of North America. They prefer warm, dark, and dry places either outdoors (such as woodpiles), or indoors (such as basements and garages). People are usually bitten when they disturb the spider, often when they approach the web or otherwise encroach on the spider. The female black widow spider is larger (8-10 mm) than the male and has a characteristic red hourglass-shaped mark on the undersurface of the abdomen. The male black widow spider is smaller, does not have the hourglass mark, and is not capable of envenomating humans due to its inability to penetrate the skin.33,53

Loxosceles

Brown recluse spiders are often found in the house because they thrive in the dark environments of attics, basements, and boxes. The spider has a  brown violin shaped mark on the dorsum of the cephalothorax (hence the common nickname "fiddleback spider"), three pairs of eyes arranged in a semicircle on top of the head, and legs that are five times as long as the body. Brown recluse spiders are 6 - 20 mm long and usually gray to reddish brown.32,34

Pathophysiology

Latrodectus

Black widow spider venom is a complex mixture of six recognized toxins which induce symptoms by stimulating the release of peripheral and central nervous system neurotransmitters.54

The venom lacks cytotoxic agents so there is little to no local tissue injury and tenderness. The most important human neurotoxin, α-latrotoxin, acts at the pre-synaptic membrane of the neuromuscular junction, opening cation channels, and decreasing reuptake of acetylcholine which results in severe muscle cramping. It can also trigger release of dopamine, norepinephrine, glutamate, γ-aminobutyric acid, and other neuropeptides.6

Latrodectism has been recognized as a clinical syndrome for the last two centuries. The syndrome consists of abdominal pain and spasms with lesser involvement of the muscles of the flank, thighs, and chest. Other less common findings include intercostal muscle pain and spasm producing dyspnea, hypertension, hyperreflexia, fever, diaphoresis, headache, anxiety, nausea, vomiting, urinary retention, and priapism. This clinical syndrome has also been referred to as the hypertoxic myopathic syndrome of latrodectism. Death is fortunately rare and occurs as a sequel to cardiovascular failure, especially in children.54

Loxoceles

Loxosceles venom contains many cytotoxic enzymes which aid the brown recluse spider in the capture and digestion of its prey. The enzymes include alkaline phosphatase, 5-ribonucleotide phosphohydrolase, esterase, hyaluronidase, and, most importantly, sphingomyelinase D. Sphingomyelinase D interacts with plasma membranes of cells, leading to hemolysis, platelet aggregation, and thrombosis. Other inflammatory mediators are released, such as prostaglandins, leukotrienes, and thromboxanes, resulting in further tissue injury and dermatonecrosis.30

Cutaneous lesions caused by Loxosceles species vary from mild erythema to extensive dermatonecrosis. The initial bite may be painless and early vesicle or bullae formation may occur up to three hours after the bite. The wound increases in size over the next 12 - 24 hours and develops central hemorrhagic vesicles and violaceous necrosis. The surrounding skin can display blanching and ischemia, with a surrounding rim of erythema and induration often described as "red, white, and blue." Eschar formation follows necrosis and occurs five to seven days after the bite. The ulcer can continue to expand for up to six weeks, with the eschar eventually falling off after 7 - 14 days. The resulting denuded area heals by secondary intention. Fatty areas of the body, such as thighs and buttocks, are more susceptible to the necrosis caused by Loxosceles venom. The size of the dermatonecrosis can be quite large, up to 30 centimeters in diameter.55-57

Systemic loxoscelism is rare but occurs with a higher incidence and mortality in pediatric and immunocompromised patients.57,58 Systemic symptoms begin 24 - 72 hours after envenomation, and range from mild flu-like symptoms of fever, chills, arthralgias, malaise, vomiting, and a generalized pruritic rash to severe symptoms of hemolytic anemia, thrombocytopenia, leukocytosis, disseminated intravascular coagulation, renal failure, pulmonary edema, shock, convulsions, and possibly death. A purpuric morbilliform eruption lasting 24 - 48 hours may occur, often on the trunk and extremities. Systemic toxicity is unlikely to develop if it has not occurred within 72 hours of envenomation.55,57

Systemic loxoscelism may be caused by distribution of venom away from the local site of envenomation. Systemic effects have been attributed to the capacity of sphingomyelinase D to alter the plasma membranes of red blood cells, platelets, and endothelial cells resulting in hemolysis, platelet aggregation, and thrombosis. It is also postulated that the venom itself may set into motion a cascade of effects which lead to systemic loxoscelism via the release of interleukins and other mediators.57


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Last Modified: 05/26/2017
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