The pathophysiology of a spider bite is due to the effect of its venom. A spider envenomation occurs whenever a spider injects venom into the skin. Not all spider bites inject venom – a dry bite, and the amount of venom injected can vary based on the type of spider and the circumstances of the encounter. The mechanical injury from a spider bite is not a serious concern for humans. Some spider bites do leave a large enough wound that infection may be a concern. However, it is generally the toxicity of spider venom that poses the most risk to human beings; several spiders are known to have venom that can cause injury to humans in the amounts that a spider will typically inject when biting. Only a small percentage of species have bites that pose a danger to people. Many spiders do not have mouthparts capable of penetrating human skin. While venoms are by definition toxic substances, most spiders do not have venom that is toxic to humans (in the quantities delivered) to require medical attention. Of those that do, fatal outcomes are rare. Spider venoms work on one of two fundamental principles; they are either neurotoxic (impairing the nervous system) or necrotic (dissolving tissues surrounding the bite). In some cases, the venom targets vital organs and systems.
Neurotoxic venom Spiders paralyze prey with neurotoxic venom of some sort. A few have a venom that cross reacts with mammalian nervous system, though the specific manner in which the nervous system is attacked varies from spider to spider.
Widow spider venom contains components known as latrotoxins, which cause the massive release of the neurotransmitters causing muscle contractions, sweating, and gooseflesh. This can affect the body in several ways, including causing painful abdominal cramps The atracotoxins of Australian funnel-web spiders work by opening sodium channels, causing excessive neural activity including strange sensations (paresthesias), muscle contractions, unstable blood pressure (hypertension or hypotension). The venom may cause fluid to accumulate in the lungs (pulmonary edema) that can be fatal. The venom of Brazilian wandering spiders is also a potent neurotoxin, which attacks multiple types of ion channels. Principally generating severe pain that travels up the limb, autonomic effects, including painful erections, occur with moderate envenomation. With severe envenomation heart and lung failure can result in death. In addition, the venom contains high levels of serotonin, making an envenomation by this species particularly painful.
Necrotic venom Spiders known to have necrotic venom occur most notoriously in the family Sicariidae, which includes both the recluse spiders and the six-eyed sand spiders in the genus Hexophthalma and Sicarius. Spiders in this family possess a known dermonecrotic agent sphingomyelinase D, which is otherwise found only in a few pathogenic bacteria. Bites by spiders in this family can produce symptoms ranging from minor localized effects, to severe dermonecrotic lesions, up to and including severe systemic reactions including renal failure, and in some cases, death. Even in the absence of systemic effects, serious bites from sicariid spiders may form a necrotising ulcer that destroys soft tissue and may take months and very rarely years to heal, leaving deep scars. The damaged tissue may become gangrenous and eventually slough away. Initially there may be no pain from a bite, but over time the wound may grow to 10 inches (25 cm) in extreme cases. Bites usually become painful and itchy within two to eight hours, pain and other local effects worsen 12 to 36 hours after the bite, and then necrosis will develop over the next few days. Systemic effects are unusual but include mild nausea, vomiting, fever, rashes, and muscle and joint pain. Rarely, more severe symptoms occur including red blood cell destruction (hemolysis), low platelets (thrombocytopenia), and loss of clotting factors (disseminated intravascular coagulation). Children may be more susceptible to systemic loxoscelism effects. Deaths have been reported for both the brown recluse and the related South American species Loxosceles laeta and Loxosceles intermedia related to hemolysis and the injury that results to the kidney. Deaths attributed to brown recluse where no brown recluse live, highlight misdiagnosis and misconception Numerous other spiders have been associated with necrotic bites. The white tailed spider (Lampona spp.) had been suspected in necrotic lesions for decades only to be exonerated by the first extensive review. An early report Sac spider causing necrosis has been frequently referenced. Recent surveys doubt the incidence of necrosis. Necrosis from Hobo spider, a member grass spider family Agelenidae, bite is under the same debate and doubt.
Differential diagnosis The skin manifestations of recluse venom are thought to arise from Sphingomyelinase D. The enzyme acts on cell membranes. The action is therefore limited as the venom can only spread through a set area. The originally red swollen area becomes a dry black ulcer. Skin infections, in particular the widespread methicillin-resistant Staphylococcal aureus, remain swollen and red. Pus forms and the lesion often drains. It can continue to spread and expand as the bacteria grow. Other skin lesions and infections are much more common than spider bites. Physicians have reported brown recluse spider bites where no brown recluse exist. Ed: in 100 pictures retrieved online only 3 were consistent with Sphingomyelinase pathophysiology.
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