Venomous: How Earth's Deadliest Creatures Mastered Biochemistry by Christie Wilcox

Author:Christie Wilcox [Wilcox, Christie]
Language: eng
Format: epub, azw3
ISBN: 9780374712211
Publisher: Farrar, Straus and Giroux
Published: 2016-08-09T06:00:00+00:00

Chip Cochran moving a large red rattlesnake out of its enclosure at Loma Linda University

(Photograph by Christie Wilcox)

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Every year, millions of people show up at their doctors’ offices with what they assume are spider bites that have opened up into large, leaking wounds. Most don’t actually know their attacker. (If you study these things, it’s not hard to guess which group of spiders is responsible if a verified spider bite festers into a gaping sore. The recluse spiders, including the brown recluse, Loxosceles reclusa, are known for two things: their shy nature—hence the name—and their potent necrotic venom. The lesions and other symptoms that result from their bites are medically referred to as loxoscelism—don’t Google it … trust me.)

The wound from a recluse spider starts innocently enough: just a small pair of holes where the spider’s venom-laden chelicerae (or mouthparts) pierced the skin. The capillaries around the site begin to constrict and slow blood flow, then fall apart. Within three hours, white blood cells have migrated to the wound, infiltrating the tissues where the venom was injected. The skin swells and becomes itchy and inflamed. In the center of the forming lesion the skin appears blue surrounded by a ring of white (from a lack of blood), then red—a bull’s-eye of tissue death. Death hurts. Slowly, areas that were once red turn purple, then black, as the flesh dies. In some cases the dead area forms a hard ulcer that later falls off, exposing raw flesh. The process is described in the medical literature as liquefication—“liquefactive necrosis.”

Though recluse bite wounds can become large and disfiguring, they usually heal on their own with time. Occasionally, skin grafts are necessary. Loxoscelism can also be systemic; in up to 16 percent of cases, the gangrenous wound can be accompanied by fever, nausea, vomiting, weakness, anemia, coma, and, only in the rarest of cases, death.

Western medicine was completely unaware of these spiders’ potent bites until the late nineteenth century, when the first necrotic lesions were described from bites in Tennessee and Kansas. By the mid-twentieth century, we knew that members of the genus Loxosceles were to blame, and soon, reports of the terrible wounds that could result from their bites became commonplace. But even now, there is no consensus on the best treatment for loxoscelism. What we do know is that the tissue loss is due largely to a single component of their venom, an enzyme called sphingomyelinase D. Removing this protein from the venom reduces the dermonecrotic activity by 90 to 97 percent. Sphingomyelinase D’s main action is to chop up sphingomyelin, a lipid commonly found in your cell membranes. The exact pathways that follow upon this lipid cleavage aren’t well understood, but the end result is clear: massive activation of the immune system.

We like to think of our immune system as our body’s guardsmen protecting us from trespassers and unsavory folk who have no business being there. Unfortunately, our various immune cells are more like mercenaries: they willingly fight our battles, but given the right incentive, they can easily switch sides.

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