The brown recluse spider lives inside houses as well as in its surroundings. Inside homes, the arachnid lives in dark places, such as cracks, corners, seldom used clothes, curtains and inside furniture. Yet, it is very common for a spider to get trapped in showers and bathtubs because of their smooth surface, and there have been lots of cases in which spiders bit the legs of a person who was having a bath. Outdoors, the BRS is usually located underneath rocks or within hollow woods. If you live in areas where the BRS lives, you must be careful when manipulating garden objects such as boxes, piles of wood, pots, etc.
In the United States, reports of severe envenomations by brown spiders began to appear in the late 1800s, and today, in endemic areas, brown spiders continue to be of significant clinical concern. Of the 13 species of Loxosceles in the United States, at least 5 have been associated with necrotic arachnidism. Loxosceles reclusus, or the brown recluse spider, is the spider most commonly responsible for this injury. Dermonecrotic arachnidism refers to the local skin and tissue injury noted with this envenomation. Loxoscelism is the term used to describe the systemic clinical syndrome caused by envenomation from the brown spiders.
Brown recluse spider bites can cause significant cutaneous injury with tissue loss and necrosis. Less frequently, more severe reactions develop, including systemic hemolysis, coagulopathy, renal failure, and, rarely, death. Brown recluse venom, like many of the other brown spider venoms, is cytotoxic and hemolytic. It contains at least 8 components, including enzymes such as hyaluronidase, deoxyribonuclease, ribonuclease, alkaline phosphatase, and lipase. Sphingomyelinase D is thought to be the protein component responsible for most of the tissue destruction and hemolysis caused by brown recluse spider envenomation.
The intense inflammatory response mediated by arachidonic acid, prostaglandins, and chemotactic infiltration of neutrophils is amplified further by an intrinsic vascular cascade involving the mediator C-reactive protein and complement activation. These and other factors contribute to the local and systemic reactions of necrotic arachnidism. Although numerous cases of cutaneous and viscerocutaneous reactions have been attributed to spiders of the genus Loxosceles, confirming the identity of the envenomating arachnid is difficult and rarely accomplished.
Although various species of Loxosceles are found throughout the world, L reclusus is found in the United States from the East to the West Coast, with predominance in the south. Recently, reports of persons with “spider bites” presenting to emergency departments have reached near urban legend proportions, prompting many physicians to question the diagnosis of a brown recluse bite in nonendemic areas. The list of conditions that can present in a similar fashion to that of a brown recluse spider envenomation is extensive.
A more likely explanation for this epidemic of spider bites is in fact community-acquired methicillin-resistant Staphylococcus aureus (MRSA) skin infections. Data regarding mortality rates are not reliable because diagnostic tests to detect brown recluse venom in tissue are not readily available. Although deaths have been attributed to presumed brown recluse envenomation, severe outcomes are rare. Typical cases involve only local soft tissue destruction. In South America, the more potent venom of the species Loxosceles laeta is responsible for several deaths each year.
The brown recluse spider, living up to its name, is naturally nonaggressive toward humans and prefers to live in undisturbed attics, woodpiles, and storage sheds. active at night from spring to fall. Brown recluse spiders vary in size and can be up to 2-3 cm in total length. They are most active at night from spring to fall. Characteristic violin-shaped markings on their backs have led brown recluse spiders to also be known as fiddleback spiders. Envenomation from the brown recluse spider elicits minimal initial sensation and frequently goes unnoticed until several hours later when the pain intensifies.
An initial stinging sensation is replaced over 6-8 hours by severe pain and pruritus as local vasospasm causes the tissue to become ischemic. Symptoms of systemic loxoscelism are not related to the extent of local tissue reaction and include the following: Morbilliform rash Fever Chills Nausea Vomiting Joint pain Hemolysis Disseminated intravascular coagulation (DIC) Renal failure Seizures Coma Edema around the ischemic bite site produces the appearance of an erythematous halo around the lesion. The erythematous margin around the site continues to enlarge peripherally, secondary to gravitational spread of the venom into the tissues.
Typically, at 24-72 hours, a single clear or hemorrhagic vesicle develops at the site, which later forms a dark eschar. Necrosis is more significant in the fatty areas of the buttocks, thighs, and abdominal wall. Treatment of brown recluse envenomation is directed by the severity of the injury. General wound management consists of local debridement, elevation, and loose immobilization of the affected area. Because the activity of sphingomyelinase D is temperature dependent, application of local cool compresses is helpful and should be continued until progression of the necrotic process appears to have stopped.
Dapsone, because of its leukocyte inhibiting properties, frequently has been recommended by authorities to treat local lesions. However, because of the potential for adverse effects associated with dapsone use, especially in the setting of G-6-PD deficiency, appropriate caution should be exercised if using this medication. To date, no well-controlled studies have shown dapsone to affect clinical outcome in human brown recluse envenomations; therefore, it is not routinely recommended. Other treatments such as colchicine, steroids, antivenom, nitroglycerin patches, and surgical excision have been reported, but nsufficient data exist to support their clinical use today. Some evidence indicates that hyperbaric oxygen therapy is beneficial in an animal model for reducing skin lesion size, but controlled human studies of this technique have not been performed. Patients exhibiting signs of systemic toxicity should be admitted and evaluated for evidence of coagulopathy, hemolysis, hemoglobinuria, renal failure, or further progression of systemic illness. Urinalysis can provide early evidence of systemic involvement, and can be performed easily at the bedside in all patients.