Facial diplegia, pharyngeal paralysis, and ophthalmoplegia after a timber rattlesnake envenomation.

The timber rattlesnake, also known as Crotalus horridus, is well known to cause significant injury from toxins stored within its venom. During envenomation, toxic systemic effects immediately begin to cause damage to many organ systems including cardiovascular, hematologic, musculoskeletal, respiratory, and neurologic. One defining characteristic of the timber rattlesnake is a specific neurotoxin called crotoxin, or the "canebrake toxin," which is a potent ß-neurotoxin affecting presynaptic nerves that can cause paralysis by inhibiting appropriate neuromuscular transmission. We present an unusual case of an 8-year-old boy bitten twice on his calf by a timber rattlesnake, who presented with a life-threatening envenomation and suffered multisystem organ failure as well as a prominent presynaptic neurotoxicity resulting in facial diplegia, pharyngeal paralysis, and ophthalmoplegia.

Detoxification of the crotoxin complex by gamma radiation.

1. Crotoxin, the major neurotoxin of the South American rattlesnake venom (2 mg protein/ml in 0.85% NaCl) was irradiated with a Co-60 gamma source at a dose rate of 1100 Gy/h and at doses of 250, 500, 1000, 1500 and 2000 Gy. 2. Irradiated crotoxin was analyzed for free SH-groups, protein concentration, electrophoretic profile (SDS-PAGE), 50% lethal dose (LD50) in mice, and antigenicity against crotalic antiserum by diffusion immunoassay. 3. Irradiation led to the formation of protein aggregates and solubility was reduced at doses of 1000 Gy or higher. 4. The LD50 increased about 2-fold for 1000 Gy and 3.5-fold for 1500 Gy. However, the antigenic response was not changed as judged by the capacity of irradiated protein receiving up to 1000 Gy to react with anti-Crotalus durissus terrificus venom horse serum. 5. The dose of 1000 Gy cleaved 0.95 disulfide bridges/mol and 1500 Gy cleaved 1.42 bridges/mol, indicating the importance of disulfide bond integrity for toxicity.