Venomous snakes and snake venom poisoning in Europe

Introduction The intoxication rate due to venomous snake bites in the population in the Republic of Guinea is 100-150 cases per 100 000 habitants with the mortality rate to 18% and represents a serious problem for public health services of the country. In the same time there is a big lack in antivenin sera supply. Nevertheless, the provision with antivenin serum against snake venom in the country is evidently not enough. Aim of research clinical trials of the efficiency and tolerance of a new polyvalent antivenin sera Inoserp® Panafricain against snake venom in comparison with the used previously serum Antivipmyn® Afrique. Methods There were treated 109 patients with pronounced symptoms of intoxication due to venomous snake bites. In the absence of hemolytic and neurologic symptoms they were intravenously administered the 1 dose (10 ml) of serum or 2 doses in the presence of mentioned symptoms. If situation so requires (in the absence of the positive effect, the occurrence of hemorrhage and neurological symptoms) this serum was re-administered 3, 6, 12 or 24 hours after the first injection. There was noted a status ofpatient and the presence of side effects after the application of this serum. Results All 109 patients have received an average of 1.1 doses (ampules) of serum. 108 patients (99%) recovered without consequences. No case of necrosis was observed. There was noted the 1 fatal case (0.9% of total patients). In 6 (5.5%) patients 10 minutes after administration of the serum there were noted side effects, but shortly they disappeared. The overall mortality rate in our experience was lower than in the testing of the similar serum Antivipmyn® Afrique, especially in patients who have not received antisera against the venom of snakes. Conclusion The efficacy and tolerability of the Inoserp® Panafricain serum were higher as mortality rate (0.9%) and side effects (5.5%) - lower in comparison with the serum Antivipmyn® Afrique. This experience has shown the perspectiveness of the use of serum Inoserp® Panafricain for the treatment of cases bitten by venomous snakes in Guinea.

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Venoms and Isolated Toxins from Snakes of Medical Impact in the Northeast Argentina: State of the Art. Potential Pharmacological Applications

Current Topics in Medicinal Chemistry ◽

10.2174/1568026619666190725094851 ◽

2019 ◽

Vol 19 (22) ◽

pp. 1962-1980 ◽

Cited By ~ 3

Author(s):

María Emilia Garcia Denegri ◽

Soledad Bustillo ◽

Claudia Carolina Gay ◽

Andrea Van De Velde ◽

Gabriela Gomez ◽

...

Keyword(s):

Snake Venom ◽

State Of The Art ◽

Protein Composition ◽

Cross Reaction ◽

Medical Emergency ◽

Venomous Snakes ◽

Snake Envenomations ◽

Pharmacological Application

: Among the ophidians that inhabit the Northeast of Argentina, the genus Bothrops such as B. alternatus and B. diporus species (also known as yararás) and Crotalus durisus terrificus (named cascabel), represent the most studied snake venom for more than thirty years. These two genera of venomous snakes account for the majority of poisonous snake envenomations and therefore, constitute a medical emergency in this region. This review presents a broad description of the compiled knowledge about venomous snakebite: its pathophysiological action, protein composition, isolated toxins, toxin synergism, toxin-antitoxin cross-reaction assays. Properties of some isolated toxins support a potential pharmacological application.

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Herbal antidote to snake venom

Nature India ◽

10.1038/nindia.2015.141 ◽

2015 ◽

Keyword(s):

Snake Venom

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Evaluation of the biochemical and anti-snake venom effects of Calliandra portoricensis extract fractions in wistar rat models

Planta Medica ◽

10.1055/s-0032-1320624 ◽

2012 ◽

Vol 78 (11) ◽

Author(s):

PE Ebong ◽

HP Onyeama ◽

MU Eteng ◽

GO Igile ◽

GE Egbung

Keyword(s):

Snake Venom ◽

Wistar Rat ◽

Rat Models

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Trimucytin: A Collagen-Like Aggregating Inducer Isolated from Trimeresurus mucrosquamatus Snake Venom

Thrombosis and Haemostasis ◽

10.1055/s-0038-1651597 ◽

1993 ◽

Vol 69 (03) ◽

pp. 286-292 ◽

Cited By ~ 13

Author(s):

Che-Ming Teng ◽

Feng-Nien Ko ◽

Inn-Ho Tsai ◽

Man-Ling Hung ◽

Tur-Fu Huang

Keyword(s):

Platelet Aggregation ◽

Snake Venom ◽

Inositol Phosphate ◽

Shape Change ◽

Platelet Activating Factor ◽

Atp Release ◽

Platelet Membrane ◽

Thromboxane B2 ◽

Dependent Manner ◽

Concentration Dependent Manner

SummaryTrimucytin is a potent platelet aggregation inducer isolated from Trimeresurus mucrosquamatus snake venom. Similar to collagen, trimucytin has a run of (Gly-Pro-X) repeats at the N-terminal amino acids sequence. It induced platelet aggregation, ATP release and thromboxane formation in rabbit platelets in a concentration-dependent manner. The aggregation was not due to released ADP since it was not suppressed by creatine phosphate/creatine phosphokinase. It was not either due to thromboxane A2 formation because indomethacin and BW755C did not have any effect on the aggregation even thromboxane B2 formation was completely abolished by indomethacin. Platelet-activating factor (PAF) was not involved in the aggregation since a PAF antagonist, kadsurenone, did not affect. However, RGD-containing peptide triflavin inhibited the aggregation, but not the release of ATP, of platelets induced by trimucytin. Indomethacin, mepacrine, prostaglandin E1 and tetracaine inhibited the thromboxane B2 formation of platelets caused by collagen and trimucytin. Forskolin and sodium nitroprusside inhibited both platelet aggregation and ATP release, but not the shape change induced by trimucytin. In quin-2 loaded platelets, the rise of intracellular calcium concentration caused by trimucytin was decreased by 12-O-tetradecanoyl phorbol-13 acetate, imipramine, TMB-8 and indomethacin. In the absence of extracellular calcium, both collagen and trimucytin caused no thromboxane B2 formation, but still induced ATP release which was completely blocked by R 59022. Inositol phosphate formation in platelets was markedly enhanced by trimucytin and collagen. MAB1988, an antibody against platelet membrane glycoprotein Ia, inhibited trimucytinand collagen-induced platelet aggregation and ATP release. However, trimucytin did not replace the binding of 125I-labeled MAB1988 to platelets. Platelets pre-exposed to trimucytin were resistant to the second challenge with trimucytin itself or collagen. It is concluded that trimucytin may activate collagen receptors on platelet membrane, and cause aggregation and release mainly through phospholipase C-phosphoinositide pathway.

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Impairment of Platelet Aggregation by Echis colorata Venom Mediated by L-Amino Acid Oxidase or H2O2

Thrombosis and Haemostasis ◽

10.1055/s-0038-1657280 ◽

1982 ◽

Vol 48 (03) ◽

pp. 277-282 ◽

Cited By ~ 22

Author(s):

I Nathan ◽

A Dvilansky ◽

T Yirmiyahu ◽

M Aharon ◽

A Livne

Keyword(s):

Hydrogen Peroxide ◽

Amino Acid ◽

Platelet Aggregation ◽

Snake Venom ◽

Oxidase Activity ◽

Enzyme Preparation ◽

Acid Oxidase ◽

Crude Venom ◽

Amino Acid Oxidase ◽

Hemostatic Disorders

SummaryEchis colorata bites cause impairment of platelet aggregation and hemostatic disorders. The mechanism by which the snake venom inhibits platelet aggregation was studied. Upon fractionation, aggregation impairment activity and L-amino acid oxidase activity were similarly separated from the crude venom, unlike other venom enzymes. Preparations of L-amino acid oxidase from E.colorata and from Crotalus adamanteus replaced effectively the crude E.colorata venom in impairment of platelet aggregation. Furthermore, different treatments known to inhibit L-amino acid oxidase reduced in parallel the oxidase activity and the impairment potency of both the venom and the enzyme preparation. H2O2 mimicked characteristically the impairment effects of L-amino acid oxidase and the venom. Catalase completely abolished the impairment effects of the enzyme and the venom. It is concluded that hydrogen peroxide formed by the venom L-amino acid oxidase plays a role in affecting platelet aggregation and thus could contribute to the extended bleeding typical to persons bitten by E.colorata.

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Autoprothrombin C Activity from Prothrombin with Snake Venom or Trypsin

Thrombosis and Haemostasis ◽

10.1055/s-0038-1655440 ◽

1962 ◽

Vol 08 (03) ◽

pp. 425-433 ◽

Cited By ~ 1

Author(s):

Ewa Marciniak ◽

Edmond R Cole ◽

Walter H Seegers

Keyword(s):

Snake Venom ◽

Thrombolytic Agent ◽

Sodium Citrate ◽

Specific Activity ◽

High Specific Activity ◽

Citrate Solution ◽

Clotting Factors ◽

Activation Products ◽

Russell’S Viper ◽

Autoprothrombin C

SummarySuitable conditions were found for the generation of autoprothrombin C from purified prothrombin with the use of Russell’s viper venom or trypsin. DEAE chromatographed prothrombin is structurally altered and has never been found to yield autoprothrombin C and also did not yield it when Russell’s viper venom or trypsin were used. Autoprothrombin C is derived from prothrombin with tissue extract thromboplastin, but not in large amounts with the intrinsic clotting factors. With the latter thrombin and autoprothrombin III are the chief activation products. Autoprothrombin III concentrates were prepared from serum and upon activation with 25% sodium citrate solution or with Russell’s viper venom large amounts of autoprothrombin C were obtained, and this was of high specific activity. Theoretically trypsin is not a thrombolytic agent, but on the contrary should lead to intravascular clotting.

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