Abstract

Carukia barnesi was the first in an expanding list of cubozoan jellyfish whose sting was identified as causing Irukandji syndrome. Nematocysts present on both the bell and tentacles are known to produce localised stings, though their individual roles in Irukandji syndrome have remained speculative. This research examines differences through venom profiling and pulse wave Doppler in a murine model. The latter demonstrates marked measurable differences in cardiac parameters. The venom from tentacles (CBVt) resulted in cardiac decompensation and death in all mice at a mean of 40 min (95% CL: ± 11 min), whereas the venom from the bell (CBVb) did not produce any cardiac dysfunction nor death in mice at 60 min post-exposure. This difference is pronounced, and we propose that bell exposure is unlikely to be causative in severe Irukandji syndrome. To date, all previously published cubozoan venom research utilised parenterally administered venom in their animal models, with many acknowledging their questionable applicability to real-world envenomation. Our model used live cubozoans on anaesthetised mice to simulate normal envenomation mechanics and actual expressed venoms. Consequently, we provide validity to the parenteral methodology used by previous cubozoan venom research.

Highlights

  • Carukia barnesi was the first of many cubozoan jellyfish known to cause Irukandji syndrome [1,2]

  • We propose that severe Irukandji syndrome is caused by venom from C. barnesi tentacles alone

  • There were distinct differences in protein profiles of the venom extracted from the bell and tentacles of the C. barnesi (Figure 3)

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Summary

Introduction

Carukia barnesi was the first of many cubozoan jellyfish known to cause Irukandji syndrome [1,2]. While Huynh et al [3] showed that it was the principal causative animal in victims demonstrating Irukandji syndrome in Cairns, Australia, other regions of the tropical and subtropical world have identified other jellyfish species. The toxic mechanisms involved remain largely speculative, including the general view that the venom is unlikely to have a direct acting cardiac toxin and instead acts to promote the release of endogenous catecholamines through which the symptoms and signs can be explained. This is indirectly supported by in vivo and in vitro research [6,7,8,9]

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