A 30 y/o healthy male presents to the emergency department 5 hours after being bitten on the hand by a spider while moving boxes in a basement.

The site of the bite is edematous, erythematous, painful, and ulcerated. He finds more of the same spiders behind the boxes and takes a picture of one…

It’s a brown recluse spider! These spiders are characterized by a gray-orange or red-brown color and are 6-20 mm long. They have a violin-shaped mark on the dorsum of the cephalothorax and three sets of eyes arranged in a semi-circle. Their legs are up to five times as long as their body.

Recluse spiders prefer to live in dark, secluded areas. They are not aggressive but will defend themselves if they feel threatened or trapped against the skin.

Loxosceles is the genus name of the recluse spider. Loxosceles has a worldwide distribute. Over 100 species have been identified within the genus.

The scientific name for the brown recluse spider is Loxosceles recluse.

Within the United States, recluse spiders are mainly found in the southeast and southwest. However, L. reufescens has been introduced into several buildings in New York City recently. Additionally, brown recluse spider bites have been identified in New York City by the New York City Poison Center Toxicology Fellowship Program (picture).

Recluse spiders are quite resilient. They can survive without food or water for up to six months. They can also tolerate a wide range of temperatures, 46.4F to 100.4 F (8-43C).

There are three main clinical presentations of recluse spider bites.

In the mildest and most common presentation, patients present with a small, stinging or painless, erythematous papule. It becomes firm and then heals. Unlike the other clinical presentations, it is not associated with a urticarial response. Most of these symptoms resolve spontaneously on their own and patients do not need to seek medical help.

The second type of clinical presentation is characterized by a cytotoxic reaction.

It may be painless but is usually very painful. The site of the bite blisters, bleeds, and ulcerates within 2-8 hours. The pain subsides over 6-8 hours but is replaced by aching and intense itching caused by local vasospasm.

In 24-48 hours, the lesion expands and demarcates an area of central hemorrhagic vesiculation. Afterwards, it develops violaceous necrosis and is surrounded by ischemic blanching of the skin.

Central necrosis develops between 48-96 hours.

An eschar begins to form between 5-7 days. The wound endurates and the eschar falls off after 7 days; this leaves an ulcer that heals by secondary intention.

Fatty areas experience local areas of necrosis that are much greater than less fatty areas. The larger the lesion, the longer it takes to heal. Lesions over 30 cm can require months to heal.

The third type of clinical presentation is characterized by systemic involvement and is the most dangerous, requiring extensive medical support; however, it is much less likely to occur.

Systemic involvement has no relation to cutaneous involvement. A patient may have a small cutaneous wound but experience a great systemic response, or vice versa.

Systemic reaction to recluse spider envenomation occurs 24-72 hours after the bite. Patients can experience fever, chills, weakness, nausea, vomiting, and arthralgias. More importantly, hemolytic anemia can occur, as well as methemaglobinemia, thrombocytopenia, DIC, acute kidney injury, tubular necrosis, and death. Hemolytic anemia with hemoglobinuria begins within 1 day and resolves in 1 weeks time.

Recluse spider venom contains hundreds of proteins that have been identified by gel electrophoresis. They include alkaline phosphotase, collagenase, deoxyribonuclease, esterase, ribonuclease, lipase, proteases, and more. The two major components are hyaluronidase and sphingomyelinase-D.

Although we don’t understand the mechanism of action of most of the proteins, we have an idea of how the major ones contribute to the clinical presentation.

Hyaluronidase acts as a “spreading factor.” It helps facilitate the penetration and spread of venom into tissue. It does not actually induce lesion development.

Sphingomyelinase-D is the factor that causes necrosis, RBC hemolysis, and platelets to release serotonin. This triggers a chain reaction that releases inflammatory mediators, such as thromboxanes, leukotrienes, prostaglandins, and neutrophils, which in turn cause thrombosis, tissue ischemia, and skin loss. Collections of PMNs cause intravascular clotting that lead to occlusion of the vessel and, eventually, necrosis.

Sphingomyelinase-D has been detected in the venom of various species of Loxosceles throughout the world; it is assumed that all species have venom capable of dermonecrosis.

There are several aspects of treatment of recluse spider envenomation.

Almost every patient presenting with a bite will require analgesia and, perhaps, anxiolytics. In mild cases, simple wound care may be all that is necessary. Thoroughly cleaning the wound, providing tetanus prophylaxis, applying cool compresses, and elevating and immobilizing the affected extremity is generally all that is required for treatment.

More extensive wounds will require debridement of necrotic tissue after erythema has subsided to better define the margins of the central eschar. Several weeks after the bite, surgical debridement may be required, as well as measures to help close the wound.

One case series reported that curettage of the necrotic tissue improved wound healing, presumably by removing remaining lytic enzyme activity on the surrounding tissue.

Wound vacuum assisted closure, in one case series, showed that wounds healed more quickly when compared to standard treatment.

Patients with a systemic response to envenomation need to be hospitalized and closely monitored. In the case of severe hemolysis, transfusion should be considered. If hemoglobinuria occurs, IVFs should be increased and efforts taken, such as through urinary alkalization, to prevent acute kidney injury. CBC, platelet count, PT, PTT, fibrin split products, and fibrinogen should be monitored for coagulopathy.

Antivenom for recluse spider bites does not exist in the United States. Mexico has an approved antivenom, but more research needs to be done to determine effectiveness and safety before approval in the US.

The last thing to watch for in envenomation is secondary bacterial infection. Clostridium perfringens has been found in Loxosceles venom and fangs, which suggests that the bacteria can be inoculated with the venom. Other infections involving skin flora, such as with S. aureus, are also possible. Some physicians choose to treat patients prophylactically, while others watch for signs of infection before starting antibiotics.

References:

Berger RS: The unremarkable brown recluse spider bite. JAMA 1973; 225: pp. 109

Boyer L, Binford G, Degan J. "Spider Bites." Wilderness Medicine, 6e. Philadelphia, PA: Elsevier, 2012. n.pag.AccessPharmacy.Web.20Sep.2015..

Hahn, In-Hei. "Arthropods." Goldfrank's Toxicologic Emergencies, 10e. Eds. Robert S. Hoffman, et al. New York, NY: McGraw-Hill, 2015. n. pag.AccessPharmacy. Web. 20 Sep. 2015..

Miller MJ, Gomez HF, Snider RJ, et al: Detection of Loxosceles venom in lesional hair shafts and skin: Application of a specific immunoassay to identify dermonecrotic arachnidism. Am J Emerg Med 2000; 18: pp. 626

Monteiro CLB, Rubel R, Cogo LL, et al: Isolation and identification of Clostridium perfringens in the venom and fangs of Loxosceles intermedia (brown spider): enhancement of the dermonecrotic lesion in loxoscelism. Toxicon 2002; 40: pp. 409

Truett AP, and King LE: Sphingomyelinase D: A pathogenic agent produced by bacteria and arthropods. Adv Lipid Res 1993; 26: pp. 275