Funnel-web spider bite: a systematic review of recorded clinical cases

The document attached has been archived with permission from the editor of the Medical Journal of Australia (09 January 2008). An external link to the publisher’s copy is included.Objective: To investigate species-specific envenoming rates and spectrum of severity of funnel-web spider bites, and the efficacy and adverse effects of funnel-web spider antivenom. Data sources: Cases were identified from a prospective study of spider bite presenting to four major hospitals and three state poisons information centres (1999–2003); museum records of spider specimens since 1926; NSW Poisons Information Centre database; MEDLINE and EMBASE search; clinical toxinology textbooks; the media; and the manufacturer’s reports of antivenom use. Data extraction: Patient age and sex, geographical location, month, expert identification of the spider, clinical effects and management; envenoming was classified as severe, mild–moderate or minor/local effects. Data synthesis: 198 potential funnel-web spider bites were identified: 138 were definite (spider expertly identified to species or genus), and 77 produced severe envenoming. All species-identified severe cases were attributed to one of six species restricted to NSW and southern Queensland. Rates of severe envenoming were: Hadronyche cerberea (75%), H. formidabilis (63%), Atrax robustus (17%), Hadronyche sp. 14 (17%), H. infensa (14%) and H. versuta (11%). Antivenom was used in 75 patients, including 22 children (median dose, 3 ampoules; range, 1–17), with a complete response in 97% of expertly identified cases. Three adverse reactions were reported, all in adults: two early allergic reactions (one mild and one with severe systemic effects requiring adrenaline), and one case of serum sickness. Conclusions: Severe funnel-web spider envenoming is confined to NSW and southern Queensland; tree-dwelling funnel webs (H. cerberea and H. formidabilis) have the highest envenoming rates. Funnel-web spider antivenom appears effective and safe; severe allergic reactions are uncommon.Geoffrey K Isbister, Michael R Gray, Corrine R Balit, Robert J Raven, Barrie J Stokes, Kate Porges, Alan S Tankel, Elizabeth Turner, Julian White and Malcolm McD Fishe

Clinical effects and antivenom dosing in brown snake (Pseudonaja spp.) envenoming - Australian snakebite project (ASP-14)

BACKGROUND: Snakebite is a global health issue and treatment with antivenom continues to be problematic. Brown snakes (genus Pseudonaja) are the most medically important group of Australian snakes and there is controversy over the dose of brown snake antivenom. We aimed to investigate the clinical and laboratory features of definite brown snake (Pseudonaja spp.) envenoming, and determine the dose of antivenom required. METHODS AND FINDING: This was a prospective observational study of definite brown snake envenoming from the Australian Snakebite Project (ASP) based on snake identification or specific enzyme immunoassay for Pseudonaja venom. From January 2004 to January 2012 there were 149 definite brown snake bites [median age 42 y (2-81 y); 100 males]. Systemic envenoming occurred in 136 (88%) cases. All envenomed patients developed venom induced consumption coagulopathy (VICC), with complete VICC in 109 (80%) and partial VICC in 27 (20%). Systemic symptoms occurred in 61 (45%) and mild neurotoxicity in 2 (1%). Myotoxicity did not occur. Severe envenoming occurred in 51 patients (38%) and was characterised by collapse or hypotension (37), thrombotic microangiopathy (15), major haemorrhage (5), cardiac arrest (7) and death (6). The median peak venom concentration in 118 envenomed patients was 1.6 ng/mL (Range: 0.15-210 ng/mL). The median initial antivenom dose was 2 vials (Range: 1-40) in 128 patients receiving antivenom. There was no difference in INR recovery or clinical outcome between patients receiving one or more than one vial of antivenom. Free venom was not detected in 112/115 patients post-antivenom with only low concentrations (0.4 to 0.9 ng/ml) in three patients. CONCLUSIONS: Envenoming by brown snakes causes VICC and over a third of patients had serious complications including major haemorrhage, collapse and microangiopathy. The results of this study support accumulating evidence that giving more than one vial of antivenom is unnecessary in brown snake envenoming.George E. Allen, Simon G. A. Brown, Nicholas A. Buckley, Margaret A. O, Leary, Colin B. Page, Bart J. Currie, Julian White, Geoffrey K. Isbister, for the ASP Investigator

Master equation approach to the conjugate pairing rule of Lyapunov spectra for many-particle thermostatted systems

The master equation approach to Lyapunov spectra for many-particle systems is applied to non-equilibrium thermostatted systems to discuss the conjugate pairing rule. We consider iso-kinetic thermostatted systems with a shear flow sustained by an external restriction, in which particle interactions are expressed as a Gaussian white randomness. Positive Lyapunov exponents are calculated by using the Fokker-Planck equation to describe the tangent vector dynamics. We introduce another Fokker-Planck equation to describe the time-reversed tangent vector dynamics, which allows us to calculate the negative Lyapunov exponents. Using the Lyapunov exponents provided by these two Fokker-Planck equations we show the conjugate pairing rule is satisfied for thermostatted systems with a shear flow in the thermodynamic limit. We also give an explicit form to connect the Lyapunov exponents with the time-correlation of the interaction matrix in a thermostatted system with a color field.Comment: 10 page

Structure and neurotoxicity of novel amyloids derived from the BRI gene

Abstract A number of human neurodegenerative diseases involve aggregated amyloid proteins in the brain, e.g. Alzheimer's disease (β-amyloid) and Parkinson's disease (α-synuclein). Other examples are rare familial dementias which involve the BRI gene. In a British family, mutation of the termination codon extends the reading frame of BRI to yield a furin-processed 34-residue peptide (Abri; British dementia peptide), 11 residues longer than the wild-type (WT). In a Danish family, a ten-base insertion also yields a 34-residue peptide (Adan; Danish dementia peptide). To explore the roles of Abri and Adan in neurodegeneration, we synthesized Abri and Adan in oxidized and reduced forms and generated transgenic mice colonies expressing the WT and mutated forms of BRI. We have generated transgenic mice colonies bearing the genes coding for WT-BRI, Adan and Abri under the control of the Thy1 promoter. Whereas WT-BRI transgenic mice express full-length WT-BRI protein in their brains, Adan protein is fully processed to small peptides. FBD (familial British dementia) and FDD (familial Danish dementia) are rare autosomal dominant neurodegenerative disorders that share features of AD (Alzheimer's disease), including amyloid plaques surrounded by astrocytes and microglia, neurofibrillary tangles, neuronal loss and progressive dementi

A game-based corpus for analysing the interplay between game context and player experience

Recognizing players’ affective state while playing video games has been the focus of many recent research studies. In this paper we describe the process that has been followed to build a corpus based on game events and recorded video sessions from human players while playing Super Mario Bros. We present different types of information that have been extracted from game context, player preferences and perception of the game, as well as user features, automatically extracted from video recordings. We run a number of initial experiments to analyse players’ behavior while playing video games as a case study of the possible use of the corpus.peer-reviewe

The impact of a standardised intramuscular sedation protocol for acute behavioural disturbance in the emergency department

Background: Acute behavioural disturbance (ABD) is an increasing problem in emergency departments. This study aimed to determine the impact of a structured intramuscular (IM) sedation protocol on the duration of ABD in the emergency department. Methods: A historical control study was undertaken comparing 58 patients who required physical restraint and parenteral sedation with the structured IM sedation protocol, to 73 historical controls treated predominantly by intravenous sedation, according to individual clinician preference. The primary outcome was the duration of the ABD defined as the time security staff were required. Secondary outcomes were the requirement for additional sedation, drug related-adverse effects and patient and staff injuries. Results: The median duration of the ABD in patients with the new sedation protocol was 21 minutes (IQR: 15 to 35 minutes; Range: 5 to 78 minutes) compared to a median duration of 30 minutes (IQR: 15 to 50 minutes; Range: 5 to 135 minutes) in the historical controls which was significantly different (p = 0.03). With IM sedation only 27 of 58 patients (47%; 95% CI: 34% to 60%) required further sedation compared to 64 of 73 historical controls (88%; 95%CI: 77% to 94%). There were six (10%) drug-related adverse events with the new IM protocol [oxygen desaturation (5), oxygen desaturation/airway obstruction (1)] compared to 10 (14%) in the historical controls [oxygen desaturation (5), hypoventilation (4) and aspiration (1)]. Injuries to staff occurred with three patients using the new sedation protocol and in seven of the historical controls. Two patients were injured during the new protocol and two of the historical controls. Conclusion: The use of a standardised IM sedation protocol was simple, more effective and as safe for management of ABD compared to predominantly intravenous sedation

Crop Updates 2000 - Cereals part 1

This session covers eleven papers from different authors: PLENARY PAPERS 1. New Wheat for a Secure, Sustainable Future, Timothy G. Reeves, Sanjaya Rajaram, Maarten van Ginkel, Richard Trethowan, Hans-Joachim Braun, and Kelly Cassaday, International Maize and Wheat Improvement Centre (CIMMYT) 2. Managing Cereal Rusts - a National Perspective, R.A. McIntosh, University of Sydney Plant Breeding Institute, New South Wales 3. Managing Cereal Rusts in 2000 - a regional imperative, R. Loughman, Agriculture Western Australia 4. Is nutrition the answer to wheat after canola problems?Ross Brennan1, Bill Bowden1, Mike Bolland1, Zed Rengel2 and David Isbister2 1 Agriculture Western Australia 2University of Western Australia 5. Improved Sandplain Cropping Systems by Controlled Traffic, Dr Paul Blackwell, Agriculture Western Australia 6. Raised bed farming for improved cropping of waterlogged soils, Derk Bakker, Greg Hamilton, David Houlbrooke, Cliff Spann and Doug Rowe, Agriculture Western Australia 7. Banded Urea increased wheat yields, Patrick Gethin, Stephen Loss, Frank Boetel, and Tim O’Dea, CSBP futurefarm 8. Flexi N is as effective as Urea on wheat and canola, Frank Boetel, Stephen Loss, Patrick Gethin, and Tim O’Dea CSBP futurefarm 9. Why potassium may reduce cereal leaf disease, Noeleen Edwards, Agriculture Western Australia 10, Trace elements, Wayne Pluske CSBP futurefarm, and Ross BrennanAgriculture Western Australia 11. Historical Nutrient Balance at Paddock and Whole Farm scales for typical wheatbelt farms in the Dowerin - Wongan Hills area, M.T.F. Wong, K. Wittwer and H. Zhang Precision Agriculture Research Group, CSIRO Land and Wate

Death adder envenoming causes neurotoxicity not reversed by antivenom - Australian snakebite project (ASP-16)

BACKGROUND: Death adders (Acanthophis spp) are found in Australia, Papua New Guinea and parts of eastern Indonesia. This study aimed to investigate the clinical syndrome of death adder envenoming and response to antivenom treatment. METHODOLOGY/PRINCIPAL FINDINGS: Definite death adder bites were recruited from the Australian Snakebite Project (ASP) as defined by expert identification or detection of death adder venom in blood. Clinical effects and laboratory results were collected prospectively, including the time course of neurotoxicity and response to treatment. Enzyme immunoassay was used to measure venom concentrations. Twenty nine patients had definite death adder bites; median age 45 yr (5-74 yr); 25 were male. Envenoming occurred in 14 patients. Two further patients had allergic reactions without envenoming, both snake handlers with previous death adder bites. Of 14 envenomed patients, 12 developed neurotoxicity characterised by ptosis (12), diplopia (9), bulbar weakness (7), intercostal muscle weakness (2) and limb weakness (2). Intubation and mechanical ventilation were required for two patients for 17 and 83 hours. The median time to onset of neurotoxicity was 4 hours (0.5-15.5 hr). One patient bitten by a northern death adder developed myotoxicity and one patient only developed systemic symptoms without neurotoxicity. No patient developed venom induced consumption coagulopathy. Antivenom was administered to 13 patients, all receiving one vial initially. The median time for resolution of neurotoxicity post-antivenom was 21 hours (5-168). The median peak venom concentration in 13 envenomed patients with blood samples was 22 ng/mL (4.4-245 ng/mL). In eight patients where post-antivenom bloods were available, no venom was detected after one vial of antivenom. CONCLUSIONS/SIGNIFICANCE: Death adder envenoming is characterised by neurotoxicity, which is mild in most cases. One vial of death adder antivenom was sufficient to bind all circulating venom. The persistent neurological effects despite antivenom, suggests that neurotoxicity is not reversed by antivenom.Christopher I. Johnston, Margaret A. O, Leary, Simon G. A. Brown, Bart J. Currie, Lambros Halkidis, Richard Whitaker, Benjamin Close, Geoffrey K. Isbister, for the ASP investigator