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Black widow spider (Latrodectus mactans) envenomation is found throughout both the temperate and tropical latitudes, and is one of the leading causes of death from arthropod envenomations worldwide. The venom is highly neurotoxic, affecting the presynaptic motor endplate to allow massive noradrenaline (norepinephrine) and acetylcholine release into synapses causing excessive stimulation and fatigue of the motor end plate and muscle. Clinically, patients develop a bite site lesion and pain, abdominal pain and tenderness, and lower extremity pain and weakness within minutes to hours of envenomation. Symptoms progress over several hours, then subside over 2 to 3 days. The recommended treatment of 'common' envenomation is calcium gluconate 10% intravenously, titrated to relief of symptoms; antivenin, although effective, may cause hypersensitivity and serum sickness reactions, and should be restricted to life-threatening envenomations only. Brown recluse spider (Loxosceles reclusa) envenomations are seen in the Americas and in Europe, and are endemic to the south and central United States. The venom contains at least 8 enzymes, consisting of various lysins (facilitating venom spread) and sphingomyelinase D, which causes cell membrane injury and lysis, thrombosis, local ischaemia, and chemotaxis. Local envenomations begin as pain and itching that progresses to vesiculation with violaceous necrosis and surrounding erythema, and ultimately ulcer formation. Systemic envenomations may be life threatening, and present with fever, constitutional symptoms, petechial eruptions, thrombocytopenia, and haemolysis with haemoglobinuric renal failure. Treatment of local envenomations is conservative (local wound care, cryotherapy, elevation, tetanus prophylaxis, and close follow-up); systemic envenomation requires supportive care and treatment of arising complications, corticosteroids to stabilise red blood cell membranes, and support of renal function. Dapsone 100mg daily has emerged as a promising therapeutic agent in both animal studies and clinical trials. Over 650 species of scorpions are known to cause envenomation (mostly in children under 10 years); they are endemic mostly in arid and tropical areas. Different venoms and clinical presentations are seen across the different species. Most commonly, an inflammatory local reaction occurs with envenomation, which is treated with wound debridement and cleaning, tetanus prophylaxis, and antihistamines. Occasionally the venom is allergenic, and the resultant allergic reaction is treated in a standard fashion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute arthropod envenomation. Incidence, clinical features and management. 266 28

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.
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PMID:Brown recluse spider bites: a complex problem wound. A brief review and case study. 1598

The venom from spiders of the genus Loxosceles, the most famous being Loxosceles recluse (the most brown recluse spider) can cause serious poisoning. These spiders inhabit the south and south central states from Georgia through Texas and north to southern Wisconsin. They are commonly called violin spiders because of the violin-shaped marking on the dorsum of the cephalothorax. Many dermonecrotic lesions are incorrectly diagnosed as Brown recluse bites, as up to 50% of the diagnoses are in geographic regions of the country which do not have Loxosceles spiders. Sphingomyelinase D is the primary venom dermonecrotic factor. The toxin depletes serum hemolytic complement, prolongs the activated partial thromboplastin time and depletes clotting factors VIII, IX, XI, and XII. The venom induces rapid coagulation and occlusion of small capillaries, causing subsequent tissue necrosis. A classic "bulls eye" lesion develops, an erythematous area inside of which is a pale ischemic region that develops a dark necrotic center as the lesion matures. Healing is slow, and these ulcers may persist for months leaving a deep scar. Systemic signs occur less commonly but can be life threatening. The most prevalent sign is a hemolytic anemia with significant hemoglobinuria. There is no specific antidote. Dapsone a leukocyte inhibitor has been shown to be effective in treating dermal lesions in animal models. Conservative therapy includes several cleanings daily with Burrow's solution and hydrogen peroxide. Systemic signs of Loxosceles envenomation are potentially fatal and should be aggressively addressed. Hospitalization and intravenous fluid therapy may be needed to maintain adequate hydration and to protect renal function.
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PMID:Brown spider envenomation. 1726 4

Ocular cicatricial pemphigoid is a particular form of mucous membrane pemphigoid and it is characterized by a chronic bilateral conjunctivitis with relapsing-remitting periods. Without therapy 75% of the cases develop visual loss due to major ocular complications (e.g. severe dry-eye syndrome, corneal erosions, corneal keratinization, entropion, symblepharon). Pathogenesis remains uncertain and probably linked to an autoimmune type II hypersensitivity response in patients with a genetic predisposition and exposure to different environmental triggers. With a worldwide distribution, no racial predilection and an estimated incidence that largely varies from 1/10,000-1/60,000, ocular cicatricial pemphigoid predominantly affects women aged ~60 years. Conjunctival biopsy with direct immunofluorescence is the gold standard in diagnosis confirmation, but up to 40% of the patients have a negative biopsy result that does not rule out the diagnosis. The skin and many other mucous membranes (e.g. oral, trachea, esophagus, pharynx, larynx, urethra, vagina and anus) may be involved. The disease grading relies on Foster staging system (based on clinical signs) and Mondino and Brown system (based on the inferior fornix depth loss). The differential diagnosis includes atopy, allergies, trauma, chemical burns, radiation, neoplasia, infectious, inflammatory and autoimmune etiologies. The main goals of the treatment are to stop disease progression, to relieve symptoms and to prevent complications. With long-term systemic therapy 90% of the cases can be efficiently controlled. While Dapsone is the first-line treatment in mild to moderate disease in patients without G6PD deficiency, more severe cases require immunosuppressant therapy with azathioprine, mycophenolate mofetil, methotrexate or cyclosporine. Cyclophosphamide, biologics (etanercept or rituximab) and intravenous immunoglobulin therapy are usually reserved for recalcitrant disease and unsatisfactory results to conventional therapy. Dry eye syndrome requires constant lubricating medication and topical steroids, cyclosporine-A and tacrolimus. Surgery should be planed only in quiescent phase as minor conjunctival trauma can significantly worsen the disease.
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PMID:Ocular cicatricial pemphigoid (Review). 3290 66