Sunday, 24 February 2008

spider bites



Spider Bites

Envenomation of animals by spiders is relatively uncommon and

difficult to recognize. It may be suspected on clinical signs, but

confirmatory evidence is rare. Spiders of medical importance in the

USA do not inflict particularly painful bites, so it is unusual for a

spider bite to be suspected until clinical signs appear. It is also

unlikely that the offending spider will remain in close proximity to

the victim for the time (30 min to 6 hr) required for signs to

develop. Almost all spiders are venomous, but few possess the

attributes necessary to cause clinical envenomation in mammals--mouth

parts of sufficient size to allow penetration of the skin and toxin of

sufficient quantity or potency to result in morbidity.

The spiders in the USA that are capable of causing clinical

envenomation belong to 2 groups--widow spiders ( Latrodectus spp ) and

brown spiders (mostly Loxosceles spp ).

Widow Spiders:

Widow spiders usually bite only when accidental skin contact occurs.

The most common species is the black widow, Latrodectus mactans ,

characterized by a red hourglass shape on the ventral abdomen. In the

western states, the western black widow, L hesperus , predominates,

while the brown widow, L bishopi , is found in the south, and the red

widow, L geometricus , is found in Florida.

Latrodectus venom is one of the most potent biologic toxins. The most

important of its 5 or 6 components is a neurotoxin that causes release

of the neurotransmitters norepinephrine and acetylcholine at synaptic

junctions, which continues until the neurotransmitters are depleted.

The resulting severe, painful cramping of all large muscle groups

accounts for most of the clinical signs.

Unless there is a history of a widow spider bite, diagnosis must be

based on clinical signs, which include restlessness with apparent

anxiety or apprehension; rapid, shallow, irregular respiration; shock;

abdominal rigidity or tenderness; and painful muscle rigidity,

sometimes accompanied by intermittent relaxation (which may progress

to clonus and eventually to respiratory paralysis). Partial paresis

also has been described.

An antivenin (equine origin) is commercially available but is usually

reserved for confirmed bites of high-risk individuals (very young or

very old). Symptomatic treatment is usually sufficient but may require

a combination of therapeutic agents. Calcium gluconate IV (10 mL of a

10% solution is the usual human dose) is reportedly helpful.

Meperidine hydrochloride or morphine, also given IV, provides relief

from pain and produces muscle relaxation. Muscle relaxants and

diazepam are also beneficial. Tetanus antitoxin also should be

administered. Recovery may be prolonged; weakness and even partial

paralysis may persist for several days.

Brown Spiders:

There are at least 10 species of Loxosceles spiders in the USA, but

the brown recluse spider, L reclusa , is the most common, and

envenomation by it is typical. These spiders have a violin-shaped

marking on the cephalothorax, although it may be indistinct or absent

in some species. In the northwestern USA, the unrelated spider

Tegenaria agrestis reportedly causes a clinically indistinguishable

dermonecrosis in humans and presumably in other animals. Brown recluse

spider venom has vasoconstrictive, thrombotic, hemolytic, and

necrotizing properties. It contains several enzymes, including a

phospholipase (sphingomylinase D) that attacks cell membranes.

Pathogenetic mechanisms of the characteristic dermal necrosis are

poorly understood, but activation of complement, chemotaxis, and

accumulations of neutrophils affect (or amplify) the process.

A history of a bite by a "fiddleback" brown spider is useful but rare.

A presumptive diagnosis may be based on the presence of a discrete,

erythematous, intensely pruritic skin lesion that may have irregular

ecchymoses. Within 4-8 hr, a vesicle develops at the bite wound, and

sometimes a blanched zone circumscribes the erythematous area,

imparting a "bull's-eye" appearance to the lesion. The central area

sometimes appears pale or cyanotic. The vesicle may degenerate to an

ulcer that, unless treated in a timely manner, may enlarge and extend

to underlying tissues, including muscle. Sometimes, a pustule follows

the vesicle and, on its breakdown, a black eschar remains. The final

tissue defect may be extensive and indolent and require months to

heal. However, medical authorities claim that not all brown recluse

spider bites result in severe, localized dermal necrosis.

Systemic signs sometimes accompany brown recluse spider envenomation

and may not appear for 3-4 days after the bite. Hemolysis,

thrombocytopenia, and disseminated intravascular coagulation are more

likely to occur in cases with severe dermal necrosis. Fever, vomiting,

edema, hemoglobinuria, hemolytic anemia, renal failure, and shock may

result from systemic loxoscelism.

In known bites, early treatment can be successful, but unfortunately,

many cases are not recognized until cutaneous necrosis has become

extensive; treatment at that stage is less rewarding but is still of

value. Immediate application of cold packs is beneficial, and if

administered early, corticosteroids protect against cutaneous necrosis

by stabilizing cell membranes and suppressing chemotaxis.

Corticosteroids also tend to protect against systemic involvement.

Radical excision has been advocated, but its value is questionable.

Dapsone, an inhibitor of leukocyte function, which is frequently used

in the treatment of leprosy, is currently considered the drug of

choice for brown recluse spider bites. In humans, it is administered


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