## 1 Introduction  
Ciguatera fish poisoning (CP) is a seafood-borne illness that is endemic to many tropical and subtropical regions of the world [1; 2; 3; 4; 5; 6; 7]. It is caused by the ingestion of a range of fish species that are generally associated with coral reefs from all oceans and seas, especially between the latitudes of 35\({}^{\circ}\) N and 35\({}^{\circ}\) S. Ciguatera can be also caused by the consumption of marine invertebrates such as sea urchins [8], lobsters and cotopuses [9; 10], giant clams [10; 11], and sea stars [12]. Authorities and researchers have published rapid fish identification guides with colour photographs to enable the general public to identify fishes in the region that may pose a risk of ciguatera [13; 14; 15]. Despite these precautions, ciguatera risk remains poorly managed, with exposure to potentially ciguatoxic fishes growing as the international fish trade increases [7; 16; 17]. Some countries or regions use reporting systems, for example, the surveillance system of the Centers for Disease Control and Prevention (CDC, Atlanta, GE, USA) and the Ciguawatch online site from the Louis Malarde Institute in French Polynesia [18], to track reported cases. In the EU, the Rapid Alert System for Food and Feed (RASFF, European Union) issues alerts to food safety agencies and consumers regarding ciguatera. In humans, CP is characterized by a polymorphic syndrome with more than 175 symptoms reported by the Food and Agriculture Organization of the United Nations (FAO) and the World Health Organization (WHO) Expert Meeting on Ciguatera Poisoning [19]. Within 24 h following toxic fish consumption, CP usually begins with gastrointestinal symptoms including vomiting, diarrhea, abdominal pain, and nausea, followed by general and neurological effects including cold allodynia, paresthesia in the extremities, a metallic taste, the sensation of loose teeth, pruritus, myalgia, arthalgia, headache, and dizziness [2; 3; 5; 7; 16; 20; 21; 22; 23]. In the Pacific Ocean, acute neurological forms predominate [2; 5; 16; 24], whereas in the Caribbean, gastrointestinal symptoms are more frequently reported during the early phase of the illness, again followed by neurological signs [2; 3; 25; 26]. Additional hallucinatory symptoms are frequently observed in the Indian Ocean [27]. In more severe cases, cardiovascular symptoms may also occur, with bradycardia and/or hypotension predominating [25; 26; 28], especially in hospitalized cases [25]. While gastrointestinal and cardiovascular symptoms remain for 1-2 days and 3-4 days, respectively, peripheral neurological symptoms and generalized malaise, weakness, fatigue, and headaches can last for weeks, months, or even years [2; 3]. Some ciguatera-specific symptoms (pruritus and cold allodynia), can be exacerbated by alcohol ingestion, and may reappear even in asymptomatic patients after eating non-toxic seafood, caffeine, nuts, chicken, and pork [2; 3]. CP-related toxins (CTXs) are closely related structural congeners with a polyether backbone similar to brevetoxins. CTXs are classified based on their geographic origin into Pacific Ocean ciguatoroxins (P-CTXs) [29; 30; 31; 32; 33; 34], Caribbean Sea ciguatoroxins (C-CTXs) [3; 35; 36; 37; 38; 39; 40; 41; 42; 43], and Indian Ocean ciguatoroxins (I-CTXs) [44; 45; 46; 47]. I-CTX-1 and -2 have the same molecular weight of 1140.6 Da as C-CTX-1 and -2 and are [PERSON] related, but they do not co-elute, and there are no structures available for I-CTX due to poor chromatographic recoveries [44; 45; 46; 47][PERSON] Although CP has been known for centuries [48; 49], it was only in the late 1950s that several groups of researchers initiated multidisciplinary work to identify the cause of CP and the nature of the causative toxins [50]. These included [PERSON] et al. in Hawaii [51; 52]), [PERSON] et al. in Japan [53], [PERSON] and [PERSON] in Hawaii [54], and [PERSON] in Miami [55; 56].