PubMed HealthSearch

PubMed · 2227687

[Brown spider bite].

Abstract

The diagnosis of bite by the brown recluse spider, Loxosceles reclusus, is rarely based on absolute identification of the insect because the victims are usually bitten while sleeping or dressing. More often, the history, clinical findings and course of the bite lead to the diagnosis. For early confirmation up to 24 hours after the bite, the passive hemagglutination test can be used. For older lesions, the in-vitro lymphocyte transformation test is useful, but is available in only a few medical centers. Treatment of the bite of the brown recluse spider varies from conservative to more active approaches. Resting, local cooling, systemic antibiotics to prevent infection and mild anti-inflammatory drugs may be given. In the more active approach oral corticosteroids are added in the first 72 hours to the antibiotics, especially in massive bites with necrotic centers greater than 2 cm in diameter, or when there is systemic loxoscelism. Recently, good results have been reported with Avlosulfon (dapsone), which is claimed to cure necrotic cutaneous ulcerations, presumably by reducing the activity of polymorphonuclear leukocytes. Other treatments include specific antivenin, (of limited use because it must be administered shortly after the bite), and surgery to prevent spreading of the venom. We describe 3 cases of brown spider bite with typical clinical presentations in adults aged 20-40 years. 2 were treated with corticosteroids and antibiotics and 1 with Avlosulfon and prednisone, all within 72 hours of the bite. 2 recovered completely within a few days, but the third treated with prednisone and antibiotics, developed an ulcer which healed only after several months of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

O Bitterman-Deutsch, R Bergman, R Friedman-Birnbaum. 1990. [Brown spider bite].. https://pubmed.ncbi.nlm.nih.gov/2227687/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Corticosteroids inhibit lymphocyte binding to endothelium and intercellular adhesion: an additional mechanism for their anti-inflammatory and immunosuppressive effect.

Glucocorticosteroids (GCS) are potent anti-inflammatory and immunosuppressive agents widely used in the treatment of many medical conditions, but their mechanism of action is not yet fully understood. Some of the anti-inflammatory effects of GCS have been attributed to the synthesis of lipocortins, whereas the immunosuppressive effects are thought to be mediated through the inhibition of several immune functions through a down-regulation of cytokine gene expression. Another important mechanism of action of GCS may relate to their ability to interfere with the phenomena of adhesion and migration of inflammatory cells. In this study, the direct effects of GCS on lymphocyte adhesion capacity in vitro were investigated. We demonstrate that GCS inhibit lymphocyte adhesion to endothelium through the down-modulation of lymphocyte adhesion molecules. We also provide evidence that GCS inhibit cell aggregate formation induced by TCR ligation, which directly correlates with the down-modulation of LFA-1 and CD2, but not LFA-3 or ICAM-1. Such down-modulation was paralleled by a decrease in the steady state mRNA level of LFA-1 and CD2 gene products, which suggests a direct GCS control of the expression of these genes. Finally, we show that GCS effects are mediated through the GCS receptor, since they can be completely reversed by the GCS-R antagonist RU-486. This study supports the concept that some of the immunosuppressive and anti-inflammatory effects of GCS are likely to be exerted by the inhibition of adhesion-dependent lymphocyte functions.

Adrenal Cortex Hormones

Mechanisms of action of anti-inflammatory medications used for the treatment of osteoarthritis.

Nonsteroidal anti-inflammatory (NSAID) drugs have been used to treat osteoarthritis ever since 1899, when the effects of aspirin were first recognized. Widespread use of these compounds continues despite their recognized potential toxicity, mostly because they are generally effective for palliation of the pain associated with osteoarthritis. The discovery of cyclooxygenase (COX)-1 and COX-2 has sparked interest in development of NSAID that specifically target COX-2, with the hope that such compounds would be associated with a lower incidence of adverse gastrointestinal effects. Other potential methods of avoiding adverse gastrointestinal effects associated with NSAID use include concurrent administration of prostaglandins and use of pure analgesics, such as acetaminophen. The role of nitric oxide in inflammation is an exciting area of research, and addition of nitric oxide-producing moieties to NSAID may prove to be another mechanism of avoiding gastrointestinal toxicity. There is likely to be considerable reward for the development of an NSAID that relieves pain associated with a wide variety of conditions, does not cause gastrointestinal toxicoses, and spares normal cartilage. Whether such a drug exists remains speculative.

Adrenal Cortex Hormones