Many Homeless suffer from these bites. There are two types of bites: Ingestive (festering) and Defensive (hardened)
By Doc
From numerous websites
The truth behind hobo spider bites has been especially hard to determine. Hobo venom produces symptoms similar to those caused by brown recluse venom. When the brown recluse was first identified as dangerous in the 1950s, doctors in the Pacific Northwest began to attribute certain lesions to them. But the brown recluse lives in the Midwest and the South, with a few close relatives in the Southwest; no member of its genus is regularly found in the northern United States.
VENOMOUS AMERICAN ARACHNIDS
The United States has five groups of spiders that can cause serious injury. The black widow and yellow sac spider are found throughout the country, although the latter’s range has yet to be mapped precisely. The hobo spider has expanded its range in the Pacific Northwest, while the brown recluse is found in the South and lower Midwest. Other recluses are found in the Southwest. (Legend: Purple, black widow; yellow, yellow sac; red, hobo spider; green, brown recluse; blue, other recluses)
he late 1970s and early 1980s this mystery came to the attention of toxinologist Darwin Vest, an autodidact whose work on cobras, rattlesnakes, and other venomous creatures had won him respect. While working at Washington State University in Pullman, Vest learned that the local zoology department often received queries about necrotic arachnidism—flesh-killing lesions apparently caused by spider bites. Vest looked into the cases of 75 patients in the Pacific Northwest. He blamed most of the injuries on insect bites, cigarette burns, and other causes. But that left 22 cases. Vest and his team surveyed the homes of these patients, collecting thousands of specimens by hand and with sticky traps. None of the homes yielded brown recluses, but 16 of them revealed healthy populations of hobo spiders. Sometimes a single sticky trap would fill with hoboes in a week’s time.
The presence of hoboes in such numbers was suggestive, but it proved nothing. The average home in any temperate region is likely to host several dozen species of spiders. So Vest decided to bring hobo spiders, and several other suspect species, into the lab for tests. He and his team milked live spiders, using a mild anesthetic and micropipettes, under a dissecting microscope, working carefully so that the spiders could be released unharmed. The spiders were so small that the capillary action of the pipettes was often enough to draw venom from the fangs. When that didn’t work, the researchers sometimes resorted to mild electric shock, using a nine-volt battery to make the venom glands contract and prompt the release of a droplet or two. Since each spider produced only a minuscule amount, the researchers had to milk a great many to obtain a workable sample. Their result: The hobo spider venom produced necrotic lesions in rabbits. To confirm this result, Vest shaved the backs of rabbits and held a hobo spider down on each bald patch, forcing a bite. The lesions that formed were similar to those found in human victims.
SPIDER’S MILK
Researchers at Lewis and Clark College in Portland, Oregon, draw the venom from an immature female hobo spider using electrical stimulation. The venom is drawn into a thin glass tube (bottom right). Female hoboes produce more venom than males. But the venom of the males is more toxic.
The hobo spider is now widely recognized as dangerous. The Centers for Disease Control lists it as such, as do medical textbooks and publications like the The Journal of the American Medical Association. Doctors know the signs of hobo venom—a blistering wound ringed with yellow, like the moon in a halo of smog, often accompanied by headaches and, in rare cases, disturbed thinking.
But skeptics remain. In 1998 evolutionary biologist Greta Binford of Lewis and Clark College and some of her colleagues at the University of Michigan tried to replicate Vest’s experiment. When they injected hobo spider venom into rabbits, however, the rabbits developed nothing worse than a red bump. Like several other prominent skeptics, Binford notes that the hobo spider is rarely caught in the act of biting and then taken to a competent specialist for identification. Its appearance is unremarkable, so its supposed victims can’t be expected to distinguish it from dozens of other spiders. In Europe the hobo has never been implicated in human injuries, although its venom is nearly identical to that of North American hoboes.
In four of the cases that Darwin Vest investigated, a hobo spider was captured or crushed near the victim. But Vest noted that one of these victims—the 42-year-old woman mentioned at the beginning of this story—had a history of phlebitis, a circulatory problem. According to Rick Vetter, an arachnologist at the University of California at Riverside, phlebitis sometimes causes necrotic lesions. Vetter also notes that the Australian white-tailed spider, once widely accepted by doctors as a source of necrotic arachnidism, has recently been exonerated. Researchers studied 130 cases of confirmed white-tailed spider bites and found not a single necrosis. Vetter would like to see hobo bites subjected to a similarly rigorous study. He points out that a mistaken diagnosis can have serious consequences: Certain skin cancers, for instance, look like necrotic arachnidism and can be fatal if left untreated.
Even if hobo spiders are responsible for the lesions, their bites may not always be venomous. It has long been known that black widow spiders, like some venomous snakes, can deliver “dry bites” to warn off larger animals without wasting venom on them. Typically, these are followed by a dose of venom if the harassment persists. Vest’s sister, Rebecca, who worked with him in his investigations, reports that hoboes often give dry bites. Widows vary in their toxicity with age, health, and gender, and these factors seem to come into play with hobo spiders as well. For example, male hoboes pack a more potent venom than females. It is typically the male hobo, wandering away from its web in search of a mate at the end of summer, that bites people.
People vary considerably in their reactions to venom. I have been bitten by brown recluses a number of times. Though the stinging sensation that developed after a short delay made it clear that I’d received venom, I never developed a sore or any systemic symptoms, and the same is true of most bite victims. The whole experience was less painful than a mosquito bite—and, taking into account the possibility of mosquito-borne disease, less dangerous. It may be that hobo venom is similarly selective. After all, its function is to subdue insects. It would be comforting to think that a few hundred million years of evolution have put considerable distance between us and our insect kin, but only some of us are immune to insect-killing venoms.
Although hundreds of medically significant cases are diagnosed as spider bites in the Pacific Northwest each year, hard evidence is elusive. Rod Crawford, curator of arachnids at the Burke Museum of the University of Washington, notes that a handful of human deaths have been attributed to the hobo spider but that even a physician’s diagnosis is shaky evidence in the absence of the culprit. Like the recluse before it, the hobo has become what Binford calls “a medical dumping ground”—a default diagnosis when a better one can’t be found.
Agelenids are remarkably tolerant of one another, as spiders go. I have seen a spindly male living on the fringes of a female’s web, suffering no abuse from its larger mate. Perhaps he was helping to guard the eggs. I have seen, too, a bed of wandering Jew covered with 20 or so funnel webs, the inhabitants apparently unconcerned about the proximity of neighbors. But I’ve also seen what happens when two come into conflict: a flurry of legs, then the sudden collapse of one spider, which folds up in the grasp of its enemy. The effect is something like a child’s hand crushed in an adult’s.
As it happens, this tendency for some agelenids to eat others may help explain why the hobo has apparently harmed people in North America but not in Europe. Darwin Vest, who considered pesticides an irresponsible way to control spiders, examined the question of what predators might naturally control hobo populations. The most effective predators proved to be other spider species, like the false black widow (Steatoda grossa) and the American house spider (Achaearanea tepidariorum). Most effective of all was the giant house spider, an agelenid with a leg span as broad as a human palm.
The giant is so closely related to the hobo that the two may interbreed, and it not only preys on the smaller species but also competes with it for food. Vest suspected it was the giant that kept the hobo out of European houses all along. In the past 25 years, the giant house spider has established itself in the Pacific Northwest. Rebecca Vest reports that hobo populations in southern Idaho have shrunk noticeably in that same period. It may be that the hobo, though equally venomous wherever it turns up, simply has fewer chances to bite in Europe. And perhaps the same situation will eventually prevail here as the giant house spider, an unrecognized ally long ago suspected of spreading the Black Death, expands its range across America.
HOBO SPIDER POISONING (TEGENARISM)
Spider venom poisoning constitutes a disease state characterized by a set of signs (observable physical or objective evidence of disease) and symptoms (complaints that the bite victim relays to the physician, etc.), which lead to the diagnosis of spider envenomation. Traditionally, disease states induced by spider bite have been assigned specific names, according to the genus of spider which causes the poisoning. For example, poisoning by the widow spiders (genus Latrodectus) is termed latrodectism, while poisoning by the recluse spiders (genus Loxosceles) is known as loxoscelism; thus, poisoning caused by the hobo spider, Tegenaria agrestis, may be properly termed tegenarism. While not all species in any given spider genus may induce significant poisoning, and while signs and symptoms may differ from species to species in a genus, this nomenclature has proven useful in categorizing different types of spider envenomation.
Hobo spider poisoning (tegenarism) does not invariably develop following a bite by a hobo spider. A large percentage (perhaps 50% or more) of defensive bites by the hobo are “dry”, and no venom is injected when the spider bites (see A Word About Bites and Stings for more on this). Hobo spiders, like many other venomous creatures, are more likely to incorporate venom in a food getting bite than in a defensive bite. Typically, defensive bites by the hobo spider are lightning fast, the spider opening its scissor-like fangs, closing them together into the tissue of the victim, and then withdrawing rapidly. Very often the bite itself is painless, although this varies depending upon the circumstance and location of the bite, and upon the psychological state of the victim. Most spider bites are single, not in rows or patches like those of some parasitic arthropods; multiple bites do occasionally occur, such as when the spider is trapped between skin and clothing, and cannot escape.
When envenomation does occur from the bite of a hobo spider, local and/or systemic manifestations may appear. The severity of these phenomena are dependent to a degree on the age and sex of the biting spider: In laboratory experiments the venom of the male hobo spider produces more severe effects than that of the female, and evidence exists suggesting that the venom of subadults may be more toxic than that of adults. The local effects, which appear following most hobo spider envenomations, represent a type of necrotic arachnidism, which is almost identical to the local effects produced by brown recluse spider, Loxosceles reclusa, poisoning. Typically, immediately following envenomation, a large (several cm.) area of redness (erythema) forms around the bite site: This usually disappears within a few hours, leaving a small reddish induration (hardened area), which is not dissimilar to the classical “mosquito bite”. Within 24 to 48 hours blistering may occur at the bite site. Within an a additional 24 hours these blisters may rupture, leaving an open ulceration. Within a few days of ulceration, if left uncovered, eschar or “scab” formation begins to develop over the lesion, and by three weeks post-bite this becomes pronounced, giving the lesion a “target and bulls-eye” appearance. Following this, the “scab” is sloughed and the lesion generally heals, leaving a scar, within 45 days of the original bite. In some instances, particularly when the bite is delivered in an area of fatty tissue, such local lesions may become deep and extensive, and may not heal for two to three years, as exemplified in the photo below.
