A probable case of Irukandji syndrome in Thailand
ABSTRACT The Irukandji syndrome is a jellyfish envenomation caused by Carukia barnesi or related jellyfish. In literature, the distribution of "Irukandji-like" syndromes is restricted to Australia. We report a case of probable Irukandji syndrome in Thailand. With this report, we hope to promote awareness to aid sting prevention and stimulate research.
Full-textDOI: · Available from: Kenneth Daniel Winkel, Aug 17, 2015
- SourceAvailable from: Kenneth Daniel Winkel
[Show abstract] [Hide abstract]
- "Irukandji syndrome reported from Broome (Macrokanis et al., 2004) 2005 New species of carybdeids identified: Malo maxima, Carukia shinju, Alatina mordens and Gerongia rifkinae (Gershwin, 2005a; Gershwin 2005b; Gershwin & Alderslade, 2005 ) 2005 Pharmacological analysis of Carukia barnesi venom extracts confirming release of catecholamines (Winkel et al., 2005; Ramasamay et al., 2005) and modulation of neural sodium channel (Winkel et al., 2005). 2006 Irukandji syndrome recognised in South East Asia (de Pender et al., 2006) 2007 Identification of another species of carybdeid: Malo kingi (Gershwin, 2007) 2008 Re-classification of genus of carybdeid: Morbakka fenneri (Gershwin, 2008). Catecholamine release by Alatina nr mordens (Winter et al., 2008). "
ABSTRACT: The Australian carybdeid jellyfish associated with Irukandji syndrome is Carukia barnesi, (Barnes' jellyfish). Other Australian carybdeid jellyfish that may be associated with the syndrome include Carukia shinju, Carybdea xaymacana, Malo maxima, Malo kingi, Alatina mordens, Gerongia rifkinae, and Morbakka fenneri ("Morbakka"). These small jellyfish are difficult to capture and identify. They are located offshore of the coasts of Australian states including Queensland, The Northern Territory, Western Australia and South Australia. The syndromic illness, resulting from a characteristic relatively minor sting, develops after about 30 minutes and consists of severe muscle pains especially of the lower back, muscle cramps, vomiting, sweating, agitation, vasoconstriction, prostration, hypertension and in cases of severe envenomation, acute heart failure. The mechanisms of actions of their toxins are obscure but they appear to include modulation of neuronal sodium channels leading to massive release of endogenous catecholamines (C. barnesi, A. mordens and M. maxima) and thereby to possible stress-induced cardiomyopathy. In addition, pore formation may occur in myocardial cellular membranes (C. xaymacana). In human cases of severe envenomation, systemic hypertension and myocardial dysfunction are associated with membrane leakage of troponin. Clinical management includes parenteral analgesia, antihypertensive therapy, oxygen and mechanical ventilation. No effective first-aid is known. Large knowledge gaps exist in biology of the jellyfish, their distribution, their toxins and mode of actions and in treatment of the Irukandji syndrome.Toxicon 02/2012; 59(6):617-25. DOI:10.1016/j.toxicon.2012.01.006 · 2.58 Impact Factor
[Show abstract] [Hide abstract]
- "The deaths in 2002 of two tourists in Far North Queensland, Australia, highlighted the potential risk and severity of this syndrome (Fenner and Hadok, 2002; Huynh et al., 2003). It is now appreciated to occur elsewhere in the Indo-Pacific and the Caribbean (de Pender et al., 2006; Grady and Burnett, 2003; Pommier et al., 2005; Yoshimoto and Yanagihara, 2002). Only a single species – Carukia barnesi – has been definitively confirmed as a cause of Irukandji syndrome, however many different species have been linked to it (Barnes, 1964; Burnett et al., 1996; Fenner et al., 1985; Gershwin, 2005, 2007; Little et al., 2001, 2006; Little and Seymour, 2003; O'Reilly et al., 2001; Southcott, 1967; Tibballs et al., 2001). "
ABSTRACT: The in vitro cardiac and vascular pharmacology of Malo maxima, a newly described jellyfish suspected of causing Irukandji syndrome in the Broome region of Western Australia, was investigated in rat tissues. In left atria, M. maxima crude venom extract (CVE; 1-100μg/mL) caused concentration-dependent inotropic responses which were unaffected by atropine (1μM), but significantly attenuated by tetrodotoxin (TTX; 0.1μM), propranolol (1μM), Mg(2+) (6mM) or calcitonin gene-related peptide antagonist (CGRP(8-37); 1μM). CVE caused no change in right atrial rate until 100μg/mL, which elicited bradycardia. This was unaffected by atropine, TTX, propranolol or CGRP(8-37). In the presence of Mg(2+), CVE 30-100μg/mL caused tachycardia. In small mesenteric arteries CVE caused concentration-dependent contractions (pEC(50) 1.03±0.07μg/mL) that were unaffected by prazosin (0.3μM), ω-conotoxin GVIA (0.1μM) or Mg(2+) (6mM). There was a 2-fold increase in sensitivity in the presence of CGRP(8-37) (3μM). TTX (0.1μM), box jellyfish Chironex fleckeri antivenom (92.6U/mL) and benextramine (3μM) decreased sensitivity by 2.6, 1.9 and 2.1-fold, respectively. CVE-induced maximum contractions were attenuated by C. fleckeri antivenom (-22%) or benextramine (-49%). M. maxima CVE appears to activate the sympathetic, but not parasympathetic, nervous system and to stimulate sensory nerve CGRP release in left atria and resistance arteries. These effects are consistent with the catecholamine excess thought to cause Irukandji syndrome, with additional actions of CGRP release.Toxicology Letters 03/2011; 201(3):221-9. DOI:10.1016/j.toxlet.2011.01.003 · 3.36 Impact Factor
[Show abstract] [Hide abstract]
- "Other carybdeid species have also been implicated in causing Irukandji or milder Irukandji-like syndromes (e.g. Burnett et al., 1996b; Grady and Burnett, 2003; Huynh et al., 2003; Gershwin, 2005a, 2007; Little et al., 2006; de Pender et al., 2006; Winter et al., 2008) and occasional fatalities have been reported (Fenner and Hadok, 2002). The chirodropid, C. fleckeri, is considered to be the most dangerous jellyfish to humans in the world (Wiltshire et al., 2000) and whilst the vast majority of human envenoming by C. fleckeri are not lethal, w70 fatalities have been reported in Australia alone (Fenner and Harrison, 2000; Ramasamy et al., 2004). "
ABSTRACT: Class Cubozoa includes several species of box jellyfish that are harmful to humans. The venoms of box jellyfish are stored and discharged by nematocysts and contain a variety of bioactive proteins that are cytolytic, cytotoxic, inflammatory or lethal. Although cubozoan venoms generally share similar biological activities, the diverse range and severity of effects caused by different species indicate that their venoms vary in protein composition, activity and potency. To date, few individual venom proteins have been thoroughly characterised, however, accumulating evidence suggests that cubozoan jellyfish produce at least one group of homologous bioactive proteins that are labile, basic, haemolytic and similar in molecular mass (42-46 kDa). The novel box jellyfish toxins are also potentially lethal and the cause of cutaneous pain, inflammation and necrosis, similar to that observed in envenomed humans. Secondary structure analysis and remote protein homology predictions suggest that the box jellyfish toxins may act as alpha-pore-forming toxins. However, more research is required to elucidate their structures and investigate their mechanism(s) of action. The biological, biochemical and molecular characteristics of cubozoan venoms and their bioactive protein components are reviewed, with particular focus on cubozoan cytolysins and the newly emerging family of box jellyfish toxins.Toxicon 03/2009; 54(8):1162-73. DOI:10.1016/j.toxicon.2009.02.006 · 2.58 Impact Factor