Citation

Hogan CJ, Barbaro KC, Winkel KD. Ann. Emerg. Med. 2004; 44(6): 608-624.

Affiliation

Department of Emergency Medicine, Medical College of Virginia, USA; Laboratory of Immunopathology, Butantan Institute, Sao Paulo, Brazil; Australian Venom Research Unit, University of Melbourne, Australia

Copyright

(Copyright © 2004, American College of Emergency Physicians, Publisher Elsevier Publishing)

DOI

10.1016/S0196064404013149

PMID

15573037

Abstract

Loxosceles spiders have a worldwide distribution and are considered one of the most medically important groups of spiders. Envenomation (loxoscelism) can result in dermonecrosis and, less commonly, a systemic illness that can be fatal. The mechanism of venom action is multifactorial and incompletely understood. The characteristic dermonecrotic lesion results from the direct effects of the venom on the cellular and basal membrane components, as well as the extracellular matrix. The initial interaction between the venom and tissues causes complement activation, migration of polymorphic neutrophils, liberation of proteolytic enzymes, cytokine and chemokine release, platelet aggregation, and blood flow alterations that result in edema and ischemia, with development of necrosis. There is no definitive treatment for loxoscelism. However, animal model studies suggest the potential value of specific antivenom to decrease lesion size and limit systemic illness even when such administration is delayed.