An in vivo comparison of the efficacy of CSL box jellyfish antivenom with antibodies raised against nematocyst-derived Chironex fleckeri venom.

Although CSL box jellyfish antivenom (AV) remains the primary treatment for Chironex fleckeri envenoming, there has been considerable debate regarding its clinical effectiveness. Animal studies have shown that AV is largely ineffective in preventing C. fleckeri-induced cardiovascular collapse. This study examined the effectiveness of CSL box jellyfish AV (ovine IgG), raised against 'milked' venom, and polyclonal rabbit IgG antibodies (Ab) raised against nematocyst-derived venom. A venom dose of 30microg/kg, i.v., which causes an initial presser response (34+/-5mmHg; n=7) followed by cardiovascular collapse, was used in all experiments. A bolus dose of AV (3000U/kg, i.v.) or Ab (12mg; i.e. an equivalent protein 'load' to 3000U/kg AV), administered 15min prior to a bolus dose of venom, did not significantly attenuate the effects of venom. The venom response was also not significantly attenuated when AV (3000U/kg) was given as a bolus dose 10-60min prior to venom infusion. However, when the venom was incubated with either AV (3000U/kg) or Ab (12mg) for 3h prior to infusion, the effect of the venom was almost abolished. The results of this study demonstrate that antibodies raised against both 'milked' and nematocyst-derived venom are able to neutralise the cardiovascular collapse produced by the venom. However, large amounts of AV are required and must be preincubated with the venom to be protective. This indicates a very rapid action of the toxin(s) and that AV is unlikely to be clinically effective because it cannot be administered early enough.

Envenoming by the rough-scaled snake (Tropidechis carinatus): a series of confirmed cases.

OBJECTIVE: To describe demographic, geographical and clinical features of envenoming by the rough-scaled snake (RSS) (Tropidechis carinatus). DESIGN, SETTING AND PARTICIPANTS: Prospective cohort study of RSS snakebite victims, recruited between January 2004 and December 2008, as part of the Australian Snakebite Project. RSS envenoming cases were confirmed by snake identification and/or venom-specific enzyme immunoassay. MAIN OUTCOME MEASURES: Clinical and laboratory features of envenoming. RESULTS: There were 24 confirmed cases of RSS envenoming, nearly all occurring in coastal areas between northern New South Wales and south-eastern Queensland. Twenty-three patients had local bite-site effects and 17 had at least three non-specific systemic effects (eg, nausea, headache). All 24 had venom-induced consumption coagulopathy (VICC), and 19 had an international normalised ratio>3.0. Six had bleeding from the bite site or intravenous cannula site, 10 had blood detected on urinalysis, and one had a major intra-abdominal haemorrhage. Mild neurotoxicity developed in two patients, and one patient developed myotoxicity with generalised myalgia, myoglobinuria and a peak creatine kinase level of 59 700 IU/L. Twenty-three patients were treated with antivenom (21 with tiger snake antivenom, two with polyvalent antivenom). Free venom was undetectable in 19 of 20 blood samples taken after antivenom administration. CONCLUSION: RSS envenoming occurs predominantly in coastal areas of northern NSW and southern Queensland, and within this range, most envenoming is due to the RSS rather than tiger snakes. Clinically it is characterised by VICC, with mild neurotoxicity and myotoxicity in some cases. Tiger snake antivenom appears to be effective against RSS envenoming.