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Objective to describe the clinical presentation of two canines present in anaphylactic shock secondary to rattlesnake envenomation. In both cases, there was no previous documented previous envenomation event and the initial sensitization required for anaphylactic response is believed to be secondary to Crotalus atrox toxoid vaccine. Case description In the first case, a 12-year-old golden retriever present for collapse, severe hematochezia, and vomiting after first time envenomation from a suspected western diamondback rattlesnake. The patient presented in severe hypovolemic shock and required aggressive fluid therapy, antivenom, anti-emetics, and pain management. The patient made a full recovery within 24 hours. In the second case, an 8-year old English setter presented for acute collapse, vomiting, and facial swelling after suspected first time envenomation from a suspected Prairie rattlesnake. The patient presented in severe hypovolemic shock with cardiac arrhythmias and required aggressive fluid therapy, antivenom, pain control, anti-emetics, and antibiotics. The patient made a full recovery after three days of hospitalization. Both patients had been previously vaccinated with the C. atrox vaccine. Conclusion This case report documents suspected anaphylaxis in two canine patients after first time envenomation by a rattlesnake. Both patients were previously vaccinated by the Crotalus atrox toxoid, which is hypothesized to be the initial inciting trigger.

Snake venom disintegrins inhibit platelet aggregation and have anti-cancer activities. In this study, we report the cloning, expression, and functional activities of a recombinant disintegrin, r-viridistatin 2 (GenBank ID: JQ071899), from the Prairie rattlesnake. r-Viridistatin 2 was tested for anti-invasive and anti-adhesive activities against six different cancer cell lines (human urinary bladder carcinoma (T24), human fibrosarcoma (HT-1080), human skin melanoma (SK-Mel-28), human colorectal adenocarcinoma (CaCo-2), human breast adenocarcinoma (MDA-MB-231) and murine skin melanoma (B16F10)). r-Viridistatin 2 shares 96% and 64% amino acid identity with two other Prairie rattlesnake medium-sized disintegrins, viridin and viridistatin, respectively. r-Viridistatin 2 was able to inhibit adhesion of T24, SK-MEL-28, HT-1080, CaCo-2 and MDA-MB-231 to various extracellular matrix proteins with different affinities. r-Viridistatin 2 decreased the ability of T24 and SK-MEL-28 cells to migrate by 62 and 96% respectively, after 24 h of incubation and the invasion of T24, SK-MEL-28, HT-1080 and MDA-MB-231 cells were inhibited by 80, 85, 65 and 64% respectively, through a reconstituted basement membrane using a modified Boyden chamber. Finally, r-viridistatin 2 effectively inhibited lung colonization of murine melanoma cells in BALB/c mice by 71%, suggesting that r-viridistatin 2 could be a potent anti-cancer agent in vivo.

California ground squirrels (Spermophilus beecheyi) show blood-based defenses to a variety of toxins in the venom of the Northern Pacific rattlesnake (Crotalus oreganus oreganus). In this study we demonstrate the presence of an effective snake venom metalloproteinase inhibitor (SVMPI) in S. beecheyi. The blood sera of California ground squirrels were effective at reducing the metalloproteinase activity of Northern Pacific (C. o. oreganus) and prairie rattlesnake (Crotalus viridis viridis) venoms by over 75%, significantly more than its ability to reduce the activity of western diamondback rattlesnake venom. We used anion exchange and affinity chromatography to isolate this protein from the blood sera of S. beecheyi. This SVMPI had a molecular mass of 108.3 kDa and a pI of 5.1. The IC(50) of this inhibitor against whole venom from C. o. oreganus was determined to be 3.14 × 10(-8) M. Subsequent LC MS/MS analysis of a CNBr/tryptic digest of the inhibitor yielded multiple internal peptide sequences. These sequences showed homology to three other known mammalian plasma proteins: inter-α trypsin inhibitor, and two hibernation-associated proteins, HP25 and HP27. The presence of SVMPI in S. beecheyi blood sera is consistent with the resistance of these animals to venom-induced hemorrhage and tissue damage, and consistent with the protective factors conferring venom resistance in other mammals. However, the variety of SVMPI identified to date from mammalian taxa suggests that different species have converged on neutralization of venom metalloproteinase activity as a key step in venom neutralization.

Prairie rattlesnake (Crotalus viridis viridis) venom was separated using liquid column chromatography. The fractions were tested for biological activity in mice and for immunological reactivity against polyvalent (Crotalidae) antivenom and a monovalent antivenom to the crude venom. Several of the basic fractions and most of the non-basic fractions had hemorrhagic activity. Six of eight basic fractions had direct myotoxic activity, two of the basic fractions. Monovalent antivenom formed multiple precipitin bands with almost all of the fractions. These results clearly demonstrate that most of the venom components are antigenic and immunogenic. Immunodiffusion using the monovalent antivenom demonstrated that C. v. viridis venom contains many antigens common to 10 other crotaline venoms. One of the hemorrhagic components was present in five of the other venoms tested, one of the direct myotoxic components was present in three other venoms, and one of the lethal components was common to two other venoms. Another highly active hemorrhagic component was common to all of the venoms tested except that of Trimeresurus flavoviridis.

Antiserum to myotoxin a was tested for its ability to prevent local myonecrosis induced by myotoxin a and C. v. viridis venom. Antiserum was injected i.v. either 5 min before or immediately, 15 min, 30 min, 1 hr or 3 hr after i.m. injection of toxin or venom. A light microscopic method was used to measure the effects of myotoxin a, i.e. vacuolation index, and whole venom, i.e. myonecrosis index. The results show that antimyotoxin a serum neutralizes the myotoxicity of a sublethal amount of myotoxin a if injected 5 min before or immediately after toxin, but not if injected 15 min after the toxin. Its neutralizing ability for crude C. v. viridis venom was considerably better, neutralizing a dose of 0.75 μg/g even if injection of antiserum was delayed for 30 min after venom injection. Thus, antimyotoxin a serum might be useful in treating myonecrosis resulting from prairie rattlesnake (C. v. viridis) venom poisoning.

C. L. Ownby and T. R. Colberg . Classification of myonecrosis induced by snake venoms: venoms from the prairie rattlesnake (Crotalus viridis viridis), western diamondback rattlesnake (Crotalus atrox) and the Indian cobra (Naja naja naja). Toxicon26, 459 – 474, 1988. — The pathogenesis of myonecrosis induced by three different snake venoms was studied by light microscopic examination of skeletal muscle tissue taken at time periods ranging from 0.25 hr to 4 weeks after an intramuscular injection of the venom into mice. It was possible to identify different types of myonecrosis based on the abnormal morphologic states of the damaged cells. The types of myonecrosis observed correlated with the types of components present in the venom injected. Venoms containing direct acting toxins such as myotoxin a or phospholipase A2 induced specific types of myonecrosis. Also, venoms containing hemorrhagic toxins produced a type of myonecrosis similar to that induced by pure hemorrhagic toxins. The pathogenesis of each type of myonecrosis could be divided into the same four phases based on the pathologic states of the affected cells and the time after injection. During the ‘early phase’ (0.25 – 3 hr) affected muscle cells were in several different pathologic states reflecting the types of components present in the venom injected. During the ‘intermediate phase’ (6 – 24 hr) the pathologic state of the damaged cells had changed and depending on the venom new states might be present. By the ‘late phase’ (48 – 96 hr) all damaged cells have reached a common pathologic state of necrosis. The ‘final phase’ (1 – 4 weeks) is characterized by regeneration (partial or complete) of muscle cells. Although the number of different types of myonecrosis depended on the type of venom injected, i.e. Naja naja naja venom produced only two different types whereas Crotalus atrox venom produced at least four different types, cells of each type of myonecrosis progressed through the same four phases. In studies of the myotoxicity of snake venoms it is important to examine tissues taken during the early and intermediate phases to obtain accurate and useful information on the types of myonecrosis caused by the venom.