Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SCORPIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2002

[Epidemiology of scorpion envenomations in the pediatric service of the Agadez hospital center (Niger) in 1999].

In Agadez, northern Niger, envenomations due to scorpion sting is a major public health problem, ranking first among reasons for emergency admission to hospital and inducing significant mortality. In order to provide best medical care, improved knowledge of scorpion sting envenomation was required. From April to September 1999, we carried out a prospective, descriptive survey on the paediatric ward of the departmental hospital of Algadez. All children admitted to the ward for scorpion stings were included. Data was collected by questionnaire. Requested items were age, sex, type of scorpion, sting location, and clinical development. Over the 6 months of the survey, a total of 44 cases of scorpion sting were recorded on the ward. The majority of the cases (52%) were recorded in July. The main types of scorpion identified according to colour were black (18%), yellow (18%), and brown (5%). In 59% of the cases, the type of scorpion was not identified. 6-15 year-old children represented 50% of the cases. The lower limb was the main site of stings (66%). A majority of cases (52%) were admitted fewer than 30 minutes after the sting, and 30% between 30 minutes and 1 hour after the sting. The overall lethality rate was 23% (10/44). All the deaths occurred within 2 hours following the sting. Of all the deaths, 60% (6/10) occurred with 30 minutes after the sting. Our study has shown that scorpion stings remain a significant health problem in the area. As a consequence of our findings, we have introduced a new therapeutic protocol for the early case management.

Adolescent↗
PubMed1981

Further evidence for the involvement of Na+ channels in the release of adrenal catecholamine: the effect of scorpion venom and grayanotoxin I.

1 The effects of venom from the scorpion, Leiurus quinquestriatus, and grayanotoxin I on catecholamine secretion were studied in the perfused adrenal glands of guinea-pig. 2 Scorpion venom (0.1 to 10 micrograms/ml) caused a dose-dependent increase in catecholamine output. The response to the venom was partially inhibited by atropine (0.5 mM) plus hexamethonium (1mM). The dose-response curve was shifted to the right in the presence of these blocking agents. 3 Grayanotoxin I (0.1 to 0.5 mM) caused a dose-dependent increase in catecholamine output which was significantly reduced by atropine (0.5 mM) plus hexamethonium (1 mM). However, when grayanotoxin I (0.1 mM) was applied together with scorpion venom (0.1 micrograms/ml, a concentration which alone, was almost ineffective) the maximum catecholamine output was reached even in the presence of atropine plus hexamethonium. 4 Tetrodotoxin (0.1 or 0.2 microM) reversibly inhibited the secretory response induced by scorpion venom (10 micrograms/ml) and grayanotoxin I (0.1 mM) plus scorpion venom (0.1 micrograms/ml). 5 Scorpion venom and grayanotoxin I plus scorpion venus did not cause catecholamine secretion in the absence of extracellular Na+ or Ca2+ ions. However, the secretory response was restored by reintroduction of Na+ or Ca2+ ions. 6 It is suggested that both scorpion venom and grayanotoxin I activate Na+ channels on the chromaffin cell and result in catecholamine secretion.

Adrenal Glands↗
PubMed2004

Lung compliance, plasma electrolyte levels and acid-base balance are affected by scorpion envenomation in anesthetized rats under mechanical ventilation.

To determine the effects of Tityus serrulatus scorpion toxin on lung compliance and resistance, ionic equilibrium and acid-base balance over time in anesthetized and mechanically ventilated rats, we measured air flow, tracheal and esophageal pressure. Lung volume was obtained by electronic integration of airflow signal. Arterial blood samples were collected through a catheter at baseline (before) and 5, 15, 30 and 60 min after scorpion toxin injection for arterial blood gases, bicarbonate, and alkali reserve levels as well as for, sodium, potassium, magnesium, glucose, lactate, hematocrit, and osmolality analysis. Injection of the gamma fraction of the T. serrulatus scorpion venom in rats under mechanical ventilatory support leads to a continuous decrease in lung compliance secondary to pulmonary edema, but no change in airway resistance. The changes in arterial blood gases characterizing metabolic acidosis were accompanied by an increase in arterial lactate and glucose values, suggesting a scorpion toxin-induced lactic acidosis, in association with poor tissue perfusion (hypotension and low cardiac output). Moreover, scorpion toxin injection resulted in hyperosmolality, hyperkalemia, hypermagnesemia and an increase in hematocrit. The experiments have shown a clinically relevant animal model to study severe scorpion envenoming and may help to better understand the scorpion envenoming syndrome.

Acid-Base Equilibrium↗
PubMed2002

Identification of BmKAPi, a novel type of scorpion venom peptide with peculiar disulfide bridge pattern from Buthus martensii Karsch.

A novel cDNA sequence encoding a new type of scorpion venom peptide (BmKAPi) was first isolated from the venom gland of Buthus martensii Karsch by cDNA library screening combined with 5'-race. The encoded precursor of BmKAPi consisted of 89 amino acid residues including a signal peptide of 24 residues, a putative mature peptide of 64 residues (BmKAPi) and an extra basic residue at the C-terminus which might be removed in the post-translational processing. BmKAPi is stabilized by five disulfide bridges, whereas all other disulfide-bridged scorpion toxins described are cross-linked by three or four disulfide bridges. It suggested the three-dimensional scaffold of BmKAPi might be different from other scorpion toxins. The amino acid sequence of BmKAPi showed no homology with other scorpion venom peptides, but shared a little similarity with some anticoagulant peptides and proteinase inhibitors isolated from hookworm, honeybee or European frog, respectively. RT-PCR analysis showed that BmKAPi mRNA could be induced by venom extraction suggesting BmKAPi might be a component of scorpion venom. These results suggest that BmKAPi is a new type of scorpion venom peptide different from other described scorpion toxins in structural and functional aspects.

Amino Acid Sequence↗
PubMed2003

An 'Old World' scorpion beta-toxin that recognizes both insect and mammalian sodium channels.

Scorpion toxins that affect sodium channel (NaCh) gating in excitable cells are divided into alpha- and beta-classes. Whereas alpha-toxins have been found in scorpions throughout the world, anti-mammalian beta-toxins have been assigned, thus far, to 'New World' scorpions while anti-insect selective beta-toxins (depressant and excitatory) have been described only in the 'Old World'. This distribution suggested that diversification of beta-toxins into distinct pharmacological groups occurred after the separation of the continents, 150 million years ago. We have characterized a unique toxin, Lqhbeta1, from the 'Old World' scorpion, Leiurus quinquestriatus hebraeus, that resembles in sequence and activity both 'New World'beta-toxins as well as 'Old World' depressant toxins. Lqhbeta1 competes, with apparent high affinity, with anti-insect and anti-mammalian beta-toxins for binding to cockroach and rat brain synaptosomes, respectively. Surprisingly, Lqhbeta1 also competes with an anti-mammalian alpha-toxin on binding to rat brain NaChs. Analysis of Lqhbeta1 effects on rat brain and Drosophila Para NaChs expressed in Xenopus oocytes revealed a shift in the voltage-dependence of activation to more negative membrane potentials and a reduction in sodium peak currents in a manner typifying beta-toxin activity. Moreover, Lqhbeta1 resembles beta-toxins by having a weak effect on cardiac NaChs and a marked effect on rat brain and skeletal muscle NaChs. These multifaceted features suggest that Lqhbeta1 may represent an ancestral beta-toxin group in 'Old World' scorpions that gave rise, after the separation of the continents, to depressant toxins in 'Old World' scorpions and to various beta-toxin subgroups in 'New World' scorpions.

Amino Acid Sequence↗
PubMed1986

Pathogenesis of cardiovascular complications in children following scorpion envenoming.

Scorpion envenoming is known to produce serious complications in children, and the complications differ with different species seen in the world. Peripheral failure, hypotension, myocarditis and seizures are the serious complications related to scorpion envenoming. The pathogenesis of cardiovascular complications caused by the Buthotus (Buthus) tamulus species is likely to be related to the direct effect of the venom on the myocardium rather than to catecholamine-induced hypoxia, as reported earlier. A scorpion sting is a common event both in urban and rural areas and the complications are more severe in children than in adults. Though several species have been identified throughout the world, stings by the Buthotus tamulus species are most commonly seen in southern states of India. Many complications have been reported related to the venom of different species of scorpion but the pathogenesis of cardiovascular complications seems to differ with different species. Most of the published reports suggest that hypotension and myocarditis were frequently observed following scorpion stings, whereas, in our children, peripheral failure and hypotension are the complications observed initially. Myocarditis and other serious complications are observed only during follow-up. The complications and lethal effects of scorpion venom seen in our earlier study indicated that in children cardiovascular complications were seen more frequently than neurological or haematological complications. The aim of the present study is to identify the frequency and nature of the cardiovascular complications and the pathogenesis of myocarditis following scorpion envenoming.

Cardiovascular Diseases↗
PubMed2004

Epidemiology of scorpion envenomations in Texas.

About 90 scorpion species occur in the US, and scorpion stings accounted for over 15,600 calls to poison centers in the US in 2002. However, epidemiologic information on scorpion envenomations in the US, and Texas in particular, is limited. This study investigated the relationship between epidemiological factors and the scorpion stings reported to the Texas poison centers. Cases consisted of all human exposure calls of scorpion stings to Texas poison centers during 1998-2003; there were 11,545 total cases. The reported scorpion envenomation penetrance increased during 1998-2002. Among cases with a known patient age, 10.9% were < 6 y of age, 21.7% were age 6-19 y and 67.3% were > 19 y of age. Females accounted for 55.8% of the cases and males for 44.2% of the cases. Scorpion stings were most frequently reported in May and June with envenomation penetrance lowest in northeast Texas and highest in west Texas. The exposure site was the patient's own residence for 93.9% of the cases. The management site was not a health care facility for 95.8% of cases, and there were minor effects in 88.4% of cases with a known clinical outcome.

Adolescent↗
PubMed2006

Bilateral cerebellar infarction: a rare complication of scorpion sting.

INTRODUCTION: Complications following scorpion sting are common in India and can be fatal. Stroke following scorpion sting is a rare complication and can occur by various mechanisms such as hypertension, hypotension, DIC, myocarditis and venom-induced vasculitis. We present a rare case of extensive cerebellar infarction following scorpion sting, which has rarely been reported in medical literature. OBJECTIVES: To study the clinical profile of two patients presenting with an acute onset of cerebellar symptoms following a scorpion sting. To evaluate the possible causes of the stroke and to study the relation of their symptoms to the scorpion sting. METHODS: Two young women presented with a history of acute onset of dysarthria, ataxia and incoordination following scorpion sting. They did not have any known risk factors for stroke. They had cerebellar type of dysarthria and cerebellar signs on both sides along with incoordination. A CT-scan of the brain showed bilateral extensive cerebellar infarctions. They were investigated for other causes of stroke without any positive results. With treatment the patients made a gradual but complete recovery. CONCLUSION: Since there was no evidence of hypertension, hypotension, myocarditis or disseminated intravascular coagulation, we can conclude that the patients had suffered a thrombotic stroke caused by the vasculotoxic action of the scorpion venom.

Acute Disease↗
PubMed1975

Prejunctional effects of a purified toxin from the scorpion Tityus serrulatus: release of 3H-noradrenaline and enhancement of transmitter overflow elicited by nerve stimulation.

The effects of a purified fraction of the venom of the Brazilian scorpion, Tityus serrulatus, were studied in isolated guinea-pig atria previously labelled with 3H-noradrenaline. Exposure to 0.3 and 1.0 mug/ml of the scorpion toxin resulted in a long lasting positive chronotropic effect which was concentration-dependent. The increase in atrial rate coincided with an enhancement in spontaneous outflow of radioactivity. The increase in outflow of radioactive products elicited by exposure to 1.0 mug/ml of the scorpion toxin was approximately 3-fold. 3H-noradrenaline accounted for 60% of the total increase in outflow of radioactivity elicited by the scorpion toxin and the 3H-deaminated glycol (3,4-dihydroxyphenyl-glycol) represented the main metabolite formed, accounting for approximately 35% of the total release. 20 min after exposure to 1.0 mug/ml of the scorpion toxin the overflow of the labelled transmitter elicited by accelerans nerve stimulation (4 Hz, during 60 sec. supramaximal voltage) was increased 8-fold. This effect of the scorpion toxin appears to be unrelated to inhibition of neuronal uptake, block of alpha-adrenoceptors or stimulation of beta-adrenoceptors. Consequently, in addition to releasing noradrenaline, the scorpion toxin enhances transmitter overflow elicited by nerve stimulation through a prejunctional effect which appears to reflect a nove mechanism of action.

Animals↗
PubMed2003

A canine study of immunotherapy in scorpion envenomation.

OBJECTIVE: To evaluate the effects of scorpion venom and antivenom in experimental envenomation. DESIGN: Prospective, controlled animal study. SETTING: University research laboratory SUBJECTS: Twenty-nine anesthetized and ventilated dogs. INTERVENTIONS: The first group of animals had venom alone (0.05 mg/kg). Animals from the second group had simultaneous administration of 10 ml of scorpion antivenom (SAV). In the third and fourth groups, 10 ml and 40 ml SAV, respectively, were injected 10 min following venom. MEASUREMENTS AND RESULTS: Hemodynamic parameters using right heart catheter were recorded and dosage of catecholamines, neuropeptide Y (NPY), endothelin-1, and atrial natriuretic peptide (ANP) were performed at baseline and during 60 min following envenomation. In the control group, at 5 min, there was a sharp increase in pulmonary artery occluded pressure (PAOP, from 2 mmHg to 23 mmHg), mean arterial pressure (MAP, from 125 mmHg to 212 mmHg) and systemic vascular resistance (SVR, from 2450 dyn sec(-1 )m(5) to 5775 dyn sec(-1 )m(5), P<0.05 for all). Heart rate, cardiac output, and stroke volume decreased. There was a 40-fold increase in epinephrine and norepinephrine plasma concentrations. Circulating NPY and ANP dosages increased too. PAOP and MAP decreased thereafter to reach baseline levels. Simultaneous administration of SAV with venom totally offset the hallmarks of scorpion envenomation. Delayed administration of SAV at any dosage failed to alter the features of scorpion envenomation. CONCLUSION: While simultaneous administration of SAV and scorpion venom is effective in preventing scorpion envenomation-related manifestations, delayed administration of SAV, either at standard or elevated dosages, failed to alter any of the scorpion envenomation features.

Animals↗
PubMed2003

Atypical relaxation by scorpion venom in the lamb urethral smooth muscle involves both NO-dependent and -independent responses.

The sustained depolarisation induced by alpha-toxins from scorpion venom (20 microg/ml(-1)) was used to test the hypothesis that an endogenous, photo-sensitive, nitrocompound could act as a stable nitrergic transmitter in the sheep (lamb) urethra. Scorpion venom-treatment effectively abolished neurogenic responses to electrical field stimulation, but it did not modify the spontaneous urethral photorelaxation. On the other hand, scorpion venom induced an atypical relaxation in noradrenaline-contracted preparations, which could be reverted, but not prevented, by tetrodotoxin (TTX, 1 microM). However, after TTX-pretreatment, relaxations elicited by scorpion venom were significantly delayed and slowed down, and similar responses were obtained in the presence of ouabain (10 microM), low sodium medium, or after the inhibition of the NO-cGMP pathway. Although the involvement of K(+) and Cl(-) channels can be ruled out since both charybdotoxin (300 nM) and chlorotoxin (50 nM) did not elicit any urethral relaxation nor modified the scorpion venom-induced one. However, a slow Ca(2+) channel seems to be involved. GVIA omega-conotoxin (1 microM), but not MVIIC omega-conotoxin (1 microM), significantly inhibited both EFS- and scorpion venom-induced relaxations and almost abolished the partial relaxation that was resistant to NO synthase inhibition. On the other hand, the presence of L-cis-diltiazem (0.3 mM), a selective inhibitor of cyclic nucleotide gated channels (CNGCs), also delayed and slowed down relaxation induced by scorpion venom, as well as abolish its reversal by TTX. L-cis-diltiazem pre-treatment induced a progressive decay in urethral relaxation brought about by electrical field stimulation only when repetitive, long duration stimulation protocols were used. Taken together, our results do not support the hypothesis of the endogenous, photo-sensitive, urethral nitrocompound as reflecting a stable nitrergic transmitter instead of NO. However, they suggest the involvement of both a NO-cGMP-dependent and TTX-sensitive component and a NO-independent response, mediated by GVIA omega-conotoxin-sensitive Ca(2+) channels, in the neurogenic relaxation of the urethral muscle. In addition, the likely involvement of CNGCs as an additional component of the cGMP signalling mechanism is suggested.

Animals↗
PubMed1976

Stimulation of sodium and calcium uptake by scorpion toxin in chick embryo heart cells.

Scorpion toxins, the basic miniproteins of scorpion venom, stimulated the passive uptake of Na+ and Ca2+ in chick embryo heart cells. Half-maximum stimulation was obtained for 20-30 nM Na+ and 40-50 nM Ca2+. Scorpion toxin-activated Na+ and Ca2+ uptakes were fully inhibited by tetrodotoxin, a specific inhibitor of the action potential Na+ ionophore in excitable membranes. Half-maximum inhibition was obtained with the same concentration of tetrodotoxin (10 nM) for both Na+ and Ca2+. Scorpion toxin-stimulated Ca2+ uptake was dependent on extracellular Na+ concentration and was not inhibited by Ca2+ channel blocking drugs which are inactive on heart cell action potential. Thus, in heart cells scorpion toxin affects the passive Ca2+ transport, which is coupled to passive Na+ ionphore. Other results suggest that (1) tetrodotoxin and scorpion toxin bind to different sites of the sarcolemma and (2) binding of scorpion toxin to its specific sites may unmask latent tetrodotoxin - sensitive fast channels.

Animals↗
PubMed1993

Utilization of aspirin, quinine and verapamil in the prevention and treatment of scorpion venom intoxication.

Aside from serotherapy, the treatment of scorpion venom intoxication is symptomatic. The aim of this study was to compare the efficacy of drugs usually used in scorpion venom intoxications (atropine, propranolol) to that of other compounds, chosen in light of the pathophysiology of scorpion venom intoxication: dipyridamole, doxapram, quinine formate, lysine-acetyl-salicylate, valproate and verapamil. Using mice, the parameters evaluated were the preventive and therapeutic effects of drugs during experimental venom intoxication by Androctonus australis Hector and one of its toxins AaH 1, and by Buthus occitanus and Tityus serrulatus tunetanus on the other hand. It was found that although most of the drugs used could prolong the survival of the animals, the administration of verapamil and more so that of aspirin or quinine formate led to a 50 to 100% loss of venom and toxin toxicity, depending on the drug and the origin of the venom. In the case of propranolol, doxapram, atropine, dipyridamole and valproate, no or little protection were observed. If these results are confirmed in humans, the systematic use of these drugs could be a simple means for treating scorpion venom intoxication. The problem of scorpion venom intoxication poses a health problem both in the North African Maghreb and in the Americas. As a result of considerable information campaigns, the number of scorpion venom intoxications in Tunisia has dropped from 3000 in 1967 to 1000 per year in the 1980s. Serotherapy has reduced mortality to 0.35%, most deaths occurring in underweight children. In light of the large number of countries in which there is a risk of scorpion venom intoxication in the summertime, however, its prevention and treatment remain a major problem.

Animals↗
PubMed2006

Scorpion venom increases mRNA expression of lung cytokines.

Previous studies have demonstrated that scorpion toxins increase the serum levels of IL-1, IL-6, INF-gamma, and GM-CSF in patients with severe shock and pulmonary edema. Moreover, it has been shown that experimental models of scorpion envenomation presented an increase in serum levels of IL-1, IL-6, IFN-gamma and nitric oxide. Thus, it is possible that the cytokine release may contribute to the onset and maintenance of the pulmonary edema induced by scorpion venom. This study was designed to investigate whether inflammatory and non-inflammatory cytokines, contribute to the pulmonary injury induced by infusion of Tityus serrulatus scorpion toxin in rats. We show that scorpion venom not only increases the expression of mRNA pulmonary inflammatory cytokines but also non-inflammatory cytokines as well. Moreover, the expression of IL-1alpha, IL-1beta and IL-6 mRNA was shown to be higher among the remaining detectable cytokines. The findings of this study provide additional insight towards the understanding of the pathophysiology of the pulmonary edema induced by scorpion venom. The increased level of pulmonary cytokines observed during the pulmonary edema may be responsible for the exacerbation and maintenance of the inflammatory response to scorpion venom in the lungs.

Animals↗
PubMed2006

Indian black scorpion (Heterometrus bengalensis Koch) venom induced antiproliferative and apoptogenic activity against human leukemic cell lines U937 and K562.

Venoms are rich source of several bioactive compounds that possess therapeutic potentials. The different constituents of scorpion venom can modulate cell proliferation, cell growth and cell cycle. In the present communication, the cytotoxic activity of Indian black scorpion (Heterometrus bengalensis) venom was explored on human leukemic U937 and K562 cells. Scorpion venom induced U937 and K562 cell growth inhibition and the IC(50) value calculated to be 41.5 microg/ml (U937) and 88.3 microg/ml (K562). The scorpion venom showed characteristic features of apoptosis such as membrane blebbing, chromatin condensation and DNA degradation in both the cells as evidenced by confocal, fluorescence, scanning electron microscopy. Scorpion venom (IC(50) dose, 48 h) induced DNA fragmentation as evidenced by comet formation. Flow-cytometric assay revealed a significant amount of apoptotic cells (early and late) due to scorpion venom treatment. The venom induced cell cycle arrest was observed with maximum cell accumulation at sub-G(1) phase. Thus, the Indian scorpion (H. bengalensis) venom possessed antiproliferative, cytotoxic and apoptogenic activity against human leukemic cells.

Animals↗
PubMed1997

Lung oedema induced by Tityus serrulatus scorpion venom in the rat.

The effects of drugs were investigated on the induction of acute lung oedema by scorpion Tityus serrulatus venom in male Wistar rats (200-230 g) anaesthetized with sodium pentobarbital (40 mg/kg, i.p.). Intravenous (i.v.) injection of scorpion venom (0.5 mg/kg) into 12 rats induced arterial hypertension and severe lung oedema, whereas i.v. injection of scorpion venom into 16 rats previously injected with commercial heparin induced arterial hypertension, but only a slight lung oedema. It is suggested that the inhibitory effect of commercial heparin on the genesis of lung oedema may be due to a decrease in vascular permeability in the lungs. Previous i.v. injection of aprotinin did not prevent the arterial hypertension and the lung oedema induced by scorpion venom. Previous injections of platelet-activating factor antagonists (BN-52021 and WEB-2170) or of an inhibitor of lipo- and cyclooxygenase (Nordihydroguaiaretic acid) did not prevent the arterial hypertension induced by scorpion venom, but decreased the magnitude of the lung oedema elicited by the venom. Previous injections of inhibitors of 5-lipoxygenase (MK-886) or cyclooxygenase (aspirin or indomethacin) significantly decreased the magnitude of the lung oedema induced by scorpion venom. It is concluded that the release of vascular permeability factors, such as platelet-activating factors, leukotrienes, and prostaglandins may play a role in the induction of acute lung oedema by scorpion venom in rats.

Animals↗
PubMed2003

Scorpion envenomations in young children in central Arizona.

INTRODUCTION: Centruroides sculpturatus, also known as Centruroides exilicauda or bark scorpion, is the only scorpion native to the United States whose venom produces a potentially life-threatening illness, particularly in children. OBJECTIVES: To describe the distribution of the severity grades following scorpion envenomations, the onset of clinical signs and symptoms, the time to deterioration, and side effects of antivenom treatment in children < or = 2 yrs of age. METHODS: Prospective case-series with the following inclusion criteria of presumed scorpion envenomation, witnessed scorpion or signs and symptoms consistent with envenomation, patient age < or = 2 yrs, and the call was received by the poison center. After data were entered prospectively, a reviewer who was blinded as to the purpose of the study reviewed the charts. A second reviewer examined 10% of the charts for accuracy in coding. Envenomation severity grades were based on a previously described scorpion grading scale and were correlated with admission rates, clinical deterioration, and outcomes. Descriptive statistics (STATA & EXCEL) were used. RESULTS: Of the 491 charts, 483 (98%) had adequate information available. The mean age was 20.8 [range 2-24] months with 133 patients (27.5%) presenting to an emergency department (ED), 86 patients (17.8%) received antivenom, and 25 patients (5.2%) were admitted. The p-value for kappa and the 95% confidence interval (CI) for interobserver reliability kappa score was 0.69 with CI (0.44-0.95). The grade distributions were Grade I = 343 cases (71%), Grade II = 8 cases (1.7%), Grade III = 49 cases (10.1%), and Grade IV = 83 cases (17.2%). The mean time to advancement of grade was 14 min (95% CI [10.97,17.06], 99% CI [10.04,18.03]) and the median time was < 1 min (range 0-140 min). Twenty-five patients (5.2%) were admitted, of which 13 were Grade III and 12 were Grade IV. Three patients (0.6% of total), all Grade IV envenomations, were intubated (95% CI [0.0021-0.0181] or an upper limit of 8.7 patients). Antivenom was administered to 86 patients (17.8%). The mean time of abatement of symptoms following antivenom was 31 [95% CI 10-82] min vs. 22.2 h [95% CI 12-46]. There was one acute reaction (rash) to antivenom administration and 49 cases (57%) of serum sickness. CONCLUSIONS: Clinical progression following scorpion envenomation in children < or = 2 yrs old occurred on average within 14 min of envenomation with onset almost immediately. Serum sickness occurred in 57% of toddlers receiving antivenom and typically lasted less than 3 days. Admissions were less common among patients receiving antivenom.

Antivenins↗
PubMed1980

Binding of scorpion toxin to sodium channels in vitro and its modification by beta-bungarotoxin.

1. Binding of a purified scorpion toxin to membrane fragments isolated from electroplaque of an electric eel Electrophorus electricus was studied using a radio-iodinated toxin.2. A scorpion toxin was purified from the venom of Leiurus quinquestriatus and iodinated with (125)I in a lactoperoxidase-catalysed reaction. Monoiodinated toxin, isolated by an ion exchange chromatography, retarded the inactivation kinetics of Na current to a similar extent as the native toxin, indicating that radioiodination did not appreciably affect physiological and binding properties of the native toxin.3. Analyses of binding properties by Scatchard plots showed the presence of two classes of binding sites (with low and high affinities) in the membrane preparation from eel electroplaque; similar preparation from an electric skate, of which the electroplaque is known to be devoid of Na channels, possessed only the low affinity sites.4. The number of high affinity sites in the eel preparation was 41.8 +/- 10.5 p-mole/g tissue; the value was within the range reported for tetrodotoxin binding to similar preparations (15-148 p-mole/g tissue).5. A variety of cations (Na(+), Mn(2+) and La(3+)) inhibited the high affinity scorpion toxin binding, as indicated for the toxin binding to Na channels by a previous electrophysiological study. K(D) value in the presence of 120 mM-Na(+) (approx. 8 nM) agreed reasonably with that (approx. 10nM) reported for the scorpion toxin binding to excitable neuroblastoma cells or synaptic nerve ending particles under conditions where membrane potential was depolarized by the addition of 135 mM-KCl.6. Pretreatment of the eel membrane preparation with beta-bungarotoxin (7-44 ng/ml.) in the presence of Ca ions (10-200 muM) resulted in a substantial loss of high affinity binding of scorpion toxin. When phospholipase A(2) activity of the beta-toxin was inactivated by a chemical modification with p-bromophenacyl bromide, the inhibitory action of the beta-bungarotoxin was abolished.7. It is concluded that a high affinity binding of scorpion toxin to the eel electroplaque membrane fragments represents the binding to Na channels in vitro, and that phospholipase A(2) activity of beta-bungarotoxin interferes with the binding of scorpion toxin to Na channels.

Animals↗