Toxic, harmful, environmental influences threaten human existence. Backyards, parks, and wilderness areas, so inviting and natural, also pose dangers to humans in the form of toxic spider bites or illnesses spread from animals to humans.

In forensic medicine, when causes of morbidity and mortality have to be uncovered, circumstantial

evidence may point to a toxic or infective arthropod bite, and knowledge of the victim’s signs and symptoms and of the suspected culprit determines the course of the investigation.

Patients and doctors alike are known to quickly blame severe ulcers and other consequences of alleged bites on the brown recluse spider; however, incorrect diagnosis and litigation can result from such a presumption (Kunkel, 1985; Vetter, Cushing, Crawford, & Royce, 2003). Yet, warnings against over-diagnosing have led some to under-recognize the spider’s potentially lethal bite, should it actually occur.

Clinically, the causes of skin ulcers are often

unknown and as a consequence, appropriate therapies are delayed (Isbister & Whyte, 2004;

Weenig, Davis, Dahl, & Su, 2002). In assumed

arthropod bites or stings, the dermal and systemic

effects from arachnids and insects of the order hymenoptera (bees, wasps, ants) have to be differentiated. Only a few spider genera inflict

necrotizing lesions (Vetter & Visscher, 1998).

Ticks, also grouped with the arachnids, not only transmit infections, but can secrete toxins of danger to humans. A bite by an Ornithodoros coriaceus (“pajahuello”) of California, a venomous

soft tick, is associated with necrotic lesions resembling those produced by brown spiders, including the brown recluse, genus Loxosceles

(Dooley, 1967; Lewis, 1967; Russell & Waldron,

1967; Vetter & Visscher). Infectious tick bites

can be confused with other arthropod bites before

serological testing is completed. Such confusion

has occurred in cases where Lyme disease is masquerading as a brown recluse (Osterhoudt, Zaoutis, & Zorc, 2002; Rosenstein & Kramer,

1987) or hobo spider bite (Vest, 1993a). Further,

suspected Cheiracanthium spider bites have mimicked African tick-bite fever (Newlands &

Atkinson, 1990).

The skin-tissue damage, which resembles that of a brown recluse spider bite, as well as the systemic effects of being bitten by the hobo spider in the United States, are described below. Note that the spider’s toxicity to humans is not proven (Binford, 2001; Isbister & White, 2004).

The diversity of bite symptoms attributed to this spider (Akre & Myhre, 1991) and the particularly severe systemic reactions (Fisher, Kelly, Krober, Weir, & Jones, 1994; U.S. Department of Health and Human Services, 1996; Vest, 1989, 1993b) known worldwide to stem from agelenids, suggest other possible causes, such as tick exposure.

The Myth of Necrotic Arachnidism

The brown recluse spider bite is often erroneously

linked to cases of dying skin tissue, even in geographical areas of the United States where

the spider is not found, which has hindered or

confused diagnostic accuracy (Russell, 1986;Swanson & Vetter, 2005; Vetter, 2000, 2005;

Vetter & Barger, 2002; Vetter & Bush, 2002a,b; Vetter, Cushing, et al., 2003; Vetter, Edwards,

& James, 2004). The hobo spider also falls victim

to false accusations (Bennett & Vetter, 2004;

Vetter, 2000; Vetter & Isbister, 2004; Vetter, Roe, et al., 2003).

Local infections, skin cancers, plant poisoning

(i.e., poison ivy), Lyme disease, tularemia, pyoderma gangrenosum, and other conditions have

been known to masquerade as necrotizing spider

bites (Bennett & Vetter, 2004; Swanson & Vetter, 2005) or as the tick-borne illness Rocky Mountain spotted fever (Erickson, Hryhorezuk, Lipscomb, Burda, & Greenberg, 1990; Vetter, Cushing, et al., 2003).

Necrotic arachnidism, when diagnosed without

substantiated proof of a spider bite and when obscuring other reasonable causes, has been viewed as a modern myth (Isbister, 2004; Kunkel, 1985; Vetter, 2004; Vetter & Bush, 2002a; White, 1999). The alleged skin-tissue death caused by the Brazilian wolf spider (a Lycosa species), the Australian white-tail spider (a Lampona species), and the hobo spider of northwestern Pacific regions provides examples of the myth (Isbister, 2004; Vetter, 2004; Vetter & Bush, 2002a). Verified envenomation case studies have shown that the Brazilian wolf spider (Ribeiro, Jorge, Piesco, & De Andrade Nishioka, 1990) and the white-tail spider (Isbister & Gray, 2003) do not cause necrosis. In alternative medicine, prevailing historical myths about wolf spiders regarding their alleged neurotoxic (Richardson-Boedler, 2001) and severe necrotic effects (Richardson-Boedler, 2002) have been discredited.

For the purposes of clinical descriptions and

the establishment of diagnostic guidelines, only

verified cases of spider bites, when the culprit

species are identified, are acceptable (Anderson,

1991; Bennett & Vetter, 2004; Binford, 2001;

Isbister, 2002; Isbister & White, 2004; Vetter

& Bush, 2002a, b; Vetter & Isbister, 2004).

Documentation, study, and comparison of case

data of probable envenomation enhance understanding of whether and what other etiologies

may be involved.

Agelenidae Family

Tegenaria agrestis, or the Hobo spider, of the

Agelenidae family, came to the United States

from Europe in the early 1900s and was first collected in 1930 in Seattle, Washington (Exline,

1936). The species has become established in the

Pacific Northwest and bordering regions: Oregon,

Washington, Idaho, northern Utah, western

Montana, western Wyoming, Colorado (isolated

populations), and southern British Columbia(Vetter, Roe, et al., 2003). These regions do not overlap with the geographical regions endemic for spiders in the Loxosceles genus, though recently, as reported by Vetter (2005), a specimen of Loxosceles rufescens was submitted from Colorado.

Of the genus Cheiracanthium in the Agelenidae

family, rarely associated with dermal necrosis,

C. mildei and C. inclusum occur in the Pacific

Northwest, as well (Akre and Myhre, 1991). Yet,

Vest (1987b) has noted that Cheiracanthium spiders

were only rarely found in areas infested with T. agrestis spiders, and where necrotic a rachnidism had occurred, victims did not report painful bites, as are caused by Cheiracanthium spiders.

Symptoms of Probable T. agrestis (Hobo Spider)

Envenomation

Despite decades of cohabitation with T. agrestis,

only a few suspected bites between the 1980s

and 1990s have been documented, casting doubt

on the spider’s implication (Vetter & Isbister,

2004), though the bites generally occurred in or

around dwellings where T. agrestis spiders were

found (Fisher et al., 1994; Sadler, Force, Solbrig, & Sommer, 2001; U.S. Department of Health

and Human Services, 1996; Vest, 1987b). Local

and systemic reactions typically include absence

of strong pain; formation of a skin inflammation,

with small central area of induration (a hardened mass or formation); and blistering at the bite site (15–35 hours post-bite). A day later, symptoms include sloughing of blistering skin

and serumal oozing, followed by eschar formation

(observed in dried lesions) and development of sub-scab necrosis (Fisher et al.; Vest, 1987b).

Local edema may occur (Akre & Myrhe, 1991; Vest, 1987b), and lesions may be oblong or elliptical

due to gravitational drift (Vest, 1987b).

The necrosis has been observed to be severe in

fatty areas, and healing has taken up to 2 or 3

years (Vest, 1993b).

Local reactions that diverge from the typical

course have been attributed to the T. agrestis

bite. These reactions include both local edema

spreading to the affected limb or part (Akre &

Myhre, 1991; U.S. Department of Health and Human Services, 1996) and delayed onset of edema (within weeks or months post-bite) (Akre & Myhre).

Systemic symptoms, such as headache, nausea,

influenza-like aches and pains (including

arthralgia), weakness, and dizziness/mental confusion, may occur on the day of the bite or on

the first or second day post-bite, possibly persisting for several days (Akre & Myhre, 1991;

Vest, 1987b). Fever has occurred during the days

following the bite (Akre & Myhre) and up to 7

days post-bite (U.S. Department of Health and

Human Services, 1996).

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