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Effects of the bite: The victim is often not aware of the bite until two to six hours later, unless, and this is rarely the case, he witnesses the spider in the act. The first symptoms after the bite include a stinging sensation with mild to intense pain. The immediate local effects of envenomation are a transient erythema, which produces a dusky or mottled appearance to the skin. Sometimes a blister quickly follows. During the first several hours the dusky hue expands, traveling downward from the site of the bite, along the forces of gravity. The pathologic process is fully established within six hours, and within 24 hours the area where necrosis is taking place is indeed striking. The zone of erythema is replaced by violaceous discoloration, and subsequently an irregular zone of necrosis develops ranging
in measurement from a few centimeters to more than 30cm. Aseptic necrosis proceeds to dry gangrenous slough and black eschar formation. Open ulcers form as the necrotic area breaks away from surrounding healthy tissue. Thus the venom diffuses through subcutaneous tissue until the supply is exhausted. In some cases it extends through the fascia, exposing the underlying muscles. Healing of such ulcerous wounds can require months, and often a sunken scar endures. If the quantity of venom is small, no necrosis occurs and only the local erythema appears.
The venom: Numerous studies have been conducted on the action of the brown recluse spider venom. A wide variety of enzymatic activities have been reported. The venom contains a phospholipase, sphingomyelinase D, and this component is believed to play a role in cell lysis. A study as recent as 1994 reported that the mechanism by which the venom causes necrotic lesions is currently unknown. Certainly, though, envemonation by the brown recluse spider can result in an impressive dermonecrotic lesion. These lesions are remarkable given the fact that the spider injects his victim with only a few tenths of a microliter of venom!
This "ulcer" is formed because the venom of the Brown Recluse (Loxosceles reclusa) is cytotoxic. (Rayor, 1995). It kills the cells in the area around the bite. It typically takes 25 days for the ulcer to appear, however. Typically, the victim first notices that the area around the bite itches. After 2 to 8 hours a papule forms around the bite. This papule turns into a vesicle that often "weeps" a yellowish fluid (Clark 1994) . After 25 days or so, the vesicle will usually rupture and form a black crust. When this black crust comes off, there will be an ulcer that frequently exposes the muscle underneath.
This venom is stored in paired gland sacs and ducts beneath the carapace of the cephalothorax. (Botes et al., 1989) and contains an enzyme called sphingomyelinase D. This enzyme reacts with a protein that occurs in our cells called the "amyloid p component". The significance of this component in everyday life is unknown. However, it is known that the that the sphingomyelinase D causes the amyloid p component to produce excessive amounts of platelets and serotonin. Research suggests that the excessive amounts of platelets interfere with the cells normal activities and cause it to die. (Gates and Rees 1990).
Some patients experience more severe reactions to the spider’s bite. Approximately 10% of the patients who report some degree of skin necropsy develop symptoms ranging from fever and chills to extreme nausea. In very extreme cases, the patients life may be threatened. There are a variety of treatments available to such patients, but none are particularly effective. The most common is to treat the patients with antibiotics to reduce the swelling and to clean the wound on a regular basis. Steroids have been used as a form of treatment, but have been found to be useless in healing the bite. Antihistamines are sometimes used to reduce the swelling and itching. Surgically removing the affected area has been found to provide no clear benefit to the patient. Electric shock therapy has been suggested as a possible method of treatment, but experimental evidence is lacking. (Walker and Hogan 1995). Recently, however, there have been some breakthroughs. A study of fourteen patients treated with hyperbaric oxygen indicates that it may be an effective form of treatment. In addition, an antivenom has developed at Vanderbilt University. Studies suggest that it may be effective in reducing the size of the "ulcer" formed by the spider’s bite if used before the necropsy begins. Unfortunately, it is not yet widely available. (Walker and Hogan, 1995).
Ostomy Wound Manage. 2005 Mar;51(3):59-66.
Brown recluse spider bites: a complex problem wound. A brief review and case study.
Wilson JR, Hagood CO Jr, Prather ID.
Department of Kinesiology, University of Texas at Arlington, Arlington, TX 76019, USA. email@example.com
Brown recluse spiders (Loxosceles reclusa) are responsible for virtually all documented cases of spider bites leading to significant necrosis. The actual spider bite often goes unnoticed for as long as 4 to 6 hours, which makes diagnosis and, therefore, appropriate treatment, difficult. The spider bite generally results in either a necrotic wound or systemic symptoms that can lead to hemolysis. The patient described in this article experienced both complications. Dapsone and hyperbaric oxygen therapy brought the adverse response to the bite under control. The patient was hospitalized for 7 days during treatment for hemolysis and an extensive, necrotic wound. Efforts are underway to develop an assay to provide a definitive diagnosis for the brown recluse spider bite, but none is yet commercially available. Antivenom is scarce; capture of the offending spider appears to be most helpful in the diagnosis and proper treatment of spider bites.
Biochem J. 2005 Jun 1; [Epub ahead of print]
Brown recluse spider (Loxosceles reclusa) venom phospholipase D (PLD) generates lysophosphatidic acid (LPA).
Lee S, Lynch KR.
Envenomation by the brown recluse spider (Loxosceles reclusa) may cause local dermonecrosis and rarely, coagulopathies, kidney failure, and death. A venom phospholipase, sphingomyelinase D (SMaseD), is responsible for the pathological manifestations of envenomation. Recently, the recombinant SMaseD from Loxosceles laeta was demonstrated to hydrolyze lysophosphatidylcholine (LPC) to produce lysophosphatidic acid (LPA) and choline. Therefore, activation of LPA signaling pathways may be involved in some manifestations of Loxosceles envenomation. To begin investigating this idea, we cloned a full-length cDNA encoding Loxosceles reclusa SMaseD. The 305 amino acid sequence of the L. reclusa enzyme is 87%, 85% and 60% identical with those of L. arizonica, L. intermedia and L. laeta, respectively. The recombinant enzyme expressed in bacteria had broad substrate specificity. The lysophospholipids LPC, LPI, LPS, LPG, LBPA (all with various acyl chains), lyso-platelet activating factor (lysoPAF, 16:0), cyclic phosphatidic acid (cPA) and sphingomyelin were hydrolyzed while sphingosylphosphorylcholine (SPC), phosphatidylcholine (PC, 22:6, 20:4, 6:0), oxidized PCs and PAF (16:0) were not hydrolyzed. The PAF analog, edelfosine, inhibited enzyme activity. Recombinant enzyme plus LPC (18:1) induced the migration of A2058 melanoma cells, and this activity was blocked by the LPA receptor antagonist, VPC32183. The recombinant spider enzyme was haemolytic, but this activity was absent in catalytically inactive H37N and H73N mutants. Our results demonstrate that Loxosceles phospholipase D hydrolyzes a wider range of lysophospholipids than previously supposed, and thus the term "SMaseD" is too limited in describing this enzyme.