Snakebite Publications (4695)
The development cohort consisted of 879 patients with snakebite who presented to the Ngwelezane Hospital Emergency Department from December 2008 to December 2013. Factors predictive of ATI and the optimal cut-off score for predicting an ATI were identified. These factors were then used to develop a standard scoring system. The score was then tested prospectively for accuracy in a new validation cohort consisting of 100 patients admitted for snakebite to our unit from 1 December 2014 to 31 March 2015. Accuracy of the score was determined.
Of 879 snakebite admissions, 146 in the development cohort and 40 of 100 in the development validation cohort reached the primary endpoint of an ATI. Six risk predictors for ATI were identified from the development cohort: age <14 years (odds ratio (OR) 2.13), delay to admission >7 hours (OR 4.63), white cell count >10 × 109/L (OR 3.15), platelets <92 × 109/L (OR 2.35), haemoglobin <7.1 g/dL (OR 5.68), international normalised ratio >1.2 (OR 2.25). Each risk predictor was assigned a score of 1; receiver operating characteristic curve analysis returned a value of >4 out of 6 as the optimal cut-off for prediction of an ATI (area under the curve 0.804; 95% confidence interval 0.758 - 0.84). Testing of the score on the validation cohort produced a specificity of 96.6% and a sensitivity of 22.5%. The positive predictive value and negative predictive value were 81.8% and 65.2%, respectively.
Our results show that the identified score is a useful adjunct to clinical assessment in managing snakebite. Its value is greatest when used in those patients who fall in the mild to moderate clinical category. Until our severity score has been validated (or modified) for use across SA, we propose to name it the Zululand Severity Score; a true SA Severity Score may follow.
Patients with suspected Russell's viper bites and coagulopathy were randomly allocated (1:1) high-dose antivenom (20 vials) or low-dose antivenom (10 vials) plus 4U FFP. The primary outcome was the proportion of patients with an international normalized ratio (INR)<2, 6h post-antivenom. Secondary outcomes included anaphylaxis, major haemorrhage, death and clotting factor recovery.
From 214 eligible patients, 141 were randomized; 71 to high-dose antivenom, 70 to low-dose antivenom/FFP; five had no post-antivenom bloods. The groups were similar except for a delay of 1h in antivenom administration for FFP patients. 6h post-antivenom 23/69 (33%) patients allocated high-dose antivenom had an INR<2 compared with 28/67 (42%) allocated low-dose antivenom/FFP [absolute difference 8%;95%Confidence Interval:-8% to 25%]. 15 patients allocated FFP did not receive it. Severe anaphylaxis occurred equally frequently in each group. One patient given FFP developed transfusion related acute lung injury. Three deaths occurred in low-dose/FFP patients including one intracranial haemorrhage. There was no difference in recovery rates of INR or fibrinogen, but more rapid initial recovery of factor V and X in FFP patients.
FFP post-antivenom in Russell's viper bites didn't hasten recovery of coagulopathy. Low-dose antivenom/FFP did not worsen VICC, suggesting low-dose antivenom is sufficient. This article is protected by copyright. All rights reserved.
The extraction process was carried out on fresh and dried leaves at 28 to 30°C with liquid-to-solid ratio of 10 mL/g for 72 hrs. The extracts were collected intermittently analysed using mathematical Peleg's model and RP-HPLC. The highest amount of flavonoids was used to evaluate the inhibitory concentration (IC50) via 2D cell culture of A549. Based on the results obtained, the predicted maximum extract density was observed at 29.20 ± 14.54 hrs of extraction (texhaustive). However, the exhaustive time of extraction to acquire maximum flavonoids content exhibited approximately 10 hrs earlier. Therefore, 18 hrs of extraction time was chosen to acquire high content of flavonoids. The best antiproliferative effect (IC50) on A549 cell line was observed at 138.82 ± 0.60 µg/mL. In conclusion, the flavonoids content in Clinacanthus nutans water extract possesses potential antiproliferative properties against A549, suggesting an alternative approach for cancer treatment.
palaestinae monovalent (equine) immunoglobulin G antivenom used in two pediatric emergency departments. In particular, we wanted to assess the need for repeated antivenom administration and the rate of adverse antivenom effects in children.
A retrospective chart review was performed for all children admitted with definite or probable signs of V. palaestinae envenomation to Chaim Sheba Medical Center and Kaplan Medical Center between 1 March 2008 and 1 March 2014. Extracted data included: age, location of bite, time to hospital arrival, time to antivenom administration if indicated, outcomes, and complications of the envenomation and adverse effects to the antivenom.
57 patients met inclusion criteria; they ranged from 1 to 17 years in age and median age was 9.5 years. Clinical manifestations were evident in 55 (96.4%) of victims: 18 presented with minimal local signs and 37 showed marked progressive, local features (rapidly progressing edema) and signs of systemic envenomation: tachycardia (20), vomiting (17), abdominal pain (11) and hypotension (6). Two patients developed compartment syndrome and underwent surgical decompression (both received only a loading dose of antivenom with no subsequent maintenance dose). One patient developed thrombocytopenia and three patients presented with mild coagulopathy. Antivenom was administered to 25 (42%) children. Indications for antivenom administration included moderate to severe local signs (19 patients) and systemic signs (6 patients). None of these patients developed adverse reactions, serum sickness, or other side effects to the antivenom. One patient received a single additional 30mL dose of antivenom, due to hypotension and syncope, with good response.
In children, 50 ml dosing of V. palaestinae antivenom is efficacious and safe for the treatment of systemic and progressive local manifestations of envenomation by V. palaestinae.
In the past this was not a concern, but due to the current shortage in Viperfav™ and European viper venom antiserum availability, V. a. ammodytes venomous bites have recently been treated with ViperaTAb(®), which is a pharmaceutical formulation containing a monospecific ovine Fab fragments against the venom of V. berus.
To evaluate ViperaTAb(®) in V. a. ammodytes envenomations.
This is a prospective case series of three consecutive patients envenomed by V. a. ammodytes snakebite treated with ViperaTAb(®). V. ammodytes venom, neurotoxic ammodytoxins, and Fab fragment levels were determined in serum samples and a pharmacokinetic analysis of the antivenom Fab fragments was carried out.
Three patients bitten by V. a. ammodytes with extensive local swelling, neurological symptoms and recurrent thrombocytopenia were treated with ViperaTAb(®). V. ammodytes venom was detected in serum of all three patients. Ammodytoxins were detected in the serum of only the most severely envenomed patient who developed neurological symptoms. In the presented moderate cases, a dose of 8 mL of ViperaTAb(®) reduced swelling and improved systemic effects, such as thrombocytopenia. However, this dose of ViperaTAb(®) was not effective in the most severely envenomed patient with the highest serum values of V. ammodytes venom. In this case ViperaTAb(®) did not stop local swelling and it had no effect on neurological signs. ViperaTAb(®)'s systemic clearance, distribution and elimination half-lives were 4.3-13.4 mL/h/kg, 1.2-3.2 h and 14.1-55.4 h, respectively.
In patients envenomed by V. a. ammodytes venom, ViperaTAb(®) reduces moderate swelling and temporarily improves systemic effects, except neurological symptoms. ViperaTAb(®) application induces a decrement of V. ammodytes venom level in the blood, but did not affect serum concentration of neurotoxic ammodytoxins in the one patient with measurable concentrations.
Here we show that D. russelli and E. carinatus venoms induce strong oxidative stress that persists even after antivenom administration in mice model. Additionally, antivenoms also induce oxidative stress. Polyvalent antivenom induces more oxidative stress than monovalent antivenom. Strikingly, antivenom and melatonin together not only inhibits venom and antivenom induced oxidative stress but also significantly reduces the neutralizing antivenom dose. This study provides a therapeutic potential for enhancing the existing snakebite therapy. The combined treatment of antivenom+melatonin would prevent the upsurge of oxidative stress, minimize the antivenom load. Thus the investigation offers immense scope for physicians and toxinologists to reinvestigate, design new strategies and think beyond the conventional mode of antivenom therapy.
The first and last fatal reports envenoming by B. ceylonicus was in 1993. After over two decades, we report two confirmed cases of B. ceylonicus bites-one a dry bite and the other with signs and symptoms of moderate envenoming. The envenoming occurred at night while the victim was asleep, causing tightness in the chest and dyspnoea on waking up, followed by neuromuscular paralysis that did not cause respiratory failure and complete recovery was observed three days following the bite.
Two major snake venom metalloproteinases (SVMPs): RVV-X and Daborhagin were purified from Myanmar Russell's viper venom using a new purification strategy. Using the Next Generation Sequencing (NGS) approach to explore the Myanmar RV venom gland transcriptome, mRNAs of novel tripeptide SVMP inhibitors (SVMPIs) were discovered. Two novel endogenous tripeptides, pERW and pEKW were identified and isolated from the crude venom. Both purified SVMPs showed caseinolytic activity. Additionally, RVV-X displayed specific proteolytic activity towards gelatin and Daborhagin showed potent fibrinogenolytic activity. These activities were inhibited by metal chelators. Notably, the synthetic peptide inhibitors, pERW and pEKW, completely inhibit the gelatinolytic and fibrinogenolytic activities of respective SVMPs at 5 mM concentration. These complete inhibitory effects suggest that these tripeptides deserve further study for development of a therapeutic candidate for Russell's viper envenomation.
A total of 216 field force members participated in this study; Results: A total of 10.3% had experienced snakebites and 86.4% rated their demands for knowledge about snakebite as "high". No significant correlation between the actual and perceived snakebite knowledge status was detected (κ = 0.0237, p = 0.3852). Ineffective and harmful traditional first-aid methods, such as the application of tourniquets, sucking the venom out of the wound, and making local incisions, were used by more than three quarters of the respondents. However, pressure immobilization bandages were applied by only 17.3% of members. The proportion of responses for each question was not significantly different among the respondents when considering separate demographic groups; Conclusions: Snakebite knowledge among Chinese field force members is inadequate and in some cases misleading, when focusing on manifestation, prevention, and first-aid. A pragmatic, intensive educational scheme should be undertaken in at-risk populations.
In many Viperidae venoms, a subset of the basic Asp49-PLA2s displays some functional and structural characteristics of PLA2-like proteins and group within the same phylogenetic clade, but their myotoxic mechanism is still largely unknown. In the present study, we have crystallized and solved the structure of myotoxin I (MT-I), a basic myotoxic Asp49-PLA2 isolated from Bothrops asper venom. The structure presents a dimeric conformation that is compatible with that of previous dimers found for basic myotoxic Asp49-PLA2s and Lys49-PLA2s and has been confirmed by other biophysical and bioinformatics techniques. This arrangement suggests a possible cooperative action between both monomers to exert myotoxicity via two different sites forming a putative membrane-docking site (MDoS) and a putative membrane disruption site (MDiS). This mechanism would resemble that proposed for Lys49-PLA2s, but the sites involved appear to be situated in a different region. Thus, as both sites are close to one another, they form a "myotoxic cluster", which is also found in two other basic myotoxic Asp49-PLA2s from Viperidae venoms. Such arrangement may represent a novel structural strategy for the mechanism of muscle damage exerted by the group of basic, Asp49-PLA2s found in viperid snake venoms.