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      Confronting the neglected problem of snake bite envenoming: the need for a global partnership.

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          Abstract

          Envenoming resulting from snake bites is an important public health hazard in many regions of the world, yet public health authorities have given little attention to the problem.

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          Snake-bites: appraisal of the global situation.

          J Chippaux (1998)
          The true global incidence of envenomations and their severity remain largely misunderstood, except for a few countries where these accidents are rare or are correctly reported. Nevertheless, this information is essential for drawing up guidelines for dealing with snake-bites, to plan drug supplies, particularly antivenin, and to train medical staff on snake-bite treatments. Since the comprehensive review by Swaroop & Grab in 1954 no global survey has been carried out on snake-bite epidemiology. The present article is an attempt to draw the attention of health authorities to snake envenomations and urges them to prepare therapeutic protocols adapted to their needs.
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            Skeletal muscle degeneration induced by venom phospholipases A2: insights into the mechanisms of local and systemic myotoxicity.

            José María Gutiérrez, Charlotte Ownby (2003)
            Local and systemic skeletal muscle degeneration is a common consequence of envenomations due to snakebites and mass bee attacks. Phospholipases A2 (PLA2) are important myotoxic components in these venoms, inducing a similar pattern of degenerative events in muscle cells. Myotoxic PLA2s bind to acceptors in the plasma membrane, which might be lipids or proteins and which may differ in their affinity for the PLA2s. Upon binding, myotoxic PLA2s disrupt the integrity of the plasma membrane by catalytically dependent or independent mechanisms, provoking a pronounced Ca2+ influx which, in turn, initiates a complex series of degenerative events associated with hypercontraction, activation of calpains and cytosolic Ca(2+)-dependent PLA2s, and mitochondrial Ca2+ overload. Cell culture models of cytotoxicity indicate that some myotoxic PLA2s affect differentiated myotubes in a rather selective fashion, whereas others display a broad cytolytic effect. A model is presented to explain the difference between PLA2s that induce predominantly local myonecrosis and those inducing both local and systemic myotoxicity. The former bind not only to muscle cells, but also to other cell types, thereby precluding a systemic distribution of these PLA2s and their action on distant muscles. In contrast, PLA2s that bind muscle cells in a more selective way are not sequestered by non-specific interactions with other cells and, consequently, are systemically distributed and reach muscle cells in other locations.
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              Snake venom metalloproteinases: their role in the pathogenesis of local tissue damage.

              J Gutiérrez, A Rucavado (2000)
              The biochemical characteristics of hemorrhagic metalloproteinases isolated from snake venoms are reviewed, together with their role in the pathogenesis of the local tissue damage characteristic of crotaline and viperine snake envenomations. Venom metalloproteinases differ in their domain structure. Some enzymes comprise only the metalloproteinase domain, others have disintegrin-like and high cysteine domains and others present, besides these domains, an additional lectin-like subunit. All of them are zinc-dependent enzymes with highly similar zinc binding environments. Some metalloproteinases induce hemorrhage by directly affecting mostly capillary blood vessels. It is suggested that hemorrhagic enzymes cleave, in a highly selective fashion, key peptide bonds of basement membrane components, thereby affecting the interaction between basement membrane and endothelial cells. As a consequence, these cells undergo a series of morphological and functional alterations in vivo, probably associated with biophysical hemodynamic factors such as tangential fluid shear stress. Eventually, gaps are formed in endothelial cells through which extravasation occurs. In addition to hemorrhage, venom metalloproteinases induce skeletal muscle damage, myonecrosis, which seems to be secondary to the ischemia that ensues in muscle tissue as a consequence of bleeding and reduced perfusion. Microvessel disruption by metalloproteinases also impairs skeletal muscle regeneration, being therefore responsible of fibrosis and permanent tissue loss after snakebites. Moreover, venom metalloproteinases participate in the degradation of extracellular matrix components and play a relevant role in the prominent local inflammatory response that characterizes snakebite envenomations, since they induce edema, activate endogenous matrix metalloproteinases (MMPs) and are capable of releasing TNF-alpha from its membrane-bound precursor. Owing to their protagonic role in the pathogenesis of local tissue damage, snake venom metalloproteinases constitute relevant targets for natural and synthetic inhibitors which may complement antivenoms in the neutralization of these effects.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): PLoS Med
                Title: PLoS medicine
                Publisher: Public Library of Science (PLoS)
                ISSN (Electronic): 1549-1676
                ISSN (Print): 1549-1277
                Publication date (Electronic): Jun 2006
                Volume: 3
                Issue: 6
                Affiliations
                [1 ] Instituto Clodomiro Picado, Facultad de Microbiología, Universidad de Costa Rica, San José, Costa Rica. jgutierr@icp.ucr.ac.cr
                Article
                Publisher Item ID: 05-PLME-ND-0753R1
                DOI: 10.1371/journal.pmed.0030150
                PMC ID: 1472552
                PubMed ID: 16729843
                SO-VID: 72182ee2-a92b-416d-8321-0bc0cebe2478
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