Advances in Jellyfish Sting Mechanisms and Treatment Strategies

Abstract

Jellyfish stings, as one of the most prevalent forms of marine injury, have increasingly become a subject of concern. Despite their simple morphology and structure, jellyfish possess a complex venom composition that can inflict varying degrees of damage on multiple human physiological systems. Consequently, the clinical symptoms associated with jellyfish stings are highly intricate. Although antivenoms have been developed for certain jellyfish species (e.g., C. fleckeri), specific antivenoms targeting the mechanisms of most jellyfish venoms remain understudied. To effectively prevent, treat, and cure jellyfish stings, we adhere to the principle of knowing their nature and their reasons. It is essential to investigate the emission mechanism of jellyfish nematocysts and the composition of their venom. Understanding these factors is crucial for the development of targeted treatment strategies. This review delves into the venom emission mechanism of jellyfish stinging cells, the symptoms resulting from jellyfish stings, and the comprehensive treatment strategies post-sting. It offers a scientific reference for comprehending jellyfish stings and establishes a theoretical foundation for subsequent research endeavors.

Keywords: biological activity; emission mechanism; jellyfish stings; treatment.

Figure 2

The skin is pathological after jellyfish stings [49]. (A) epidermal necrosis and vesicle formation following a Pelagia noctiluca sting. Pigmented keratinocytes (black arrows), vasodilatation, edema, and erythrocyte extravasation are displayed; (B) fragments of nematocyst tubules are shown in the stratum corneum (black arrow); (C) remains of nematocysts (arrow) following a C. fleckeri sting.

Figure 4

(A). Sika Deer antler protein antagonizes the inflammatory response and oxidative damage induced by jellyfish venom [99]. **** p < 0.001. (B). Troxerutin suppresses the inflammation response and oxidative stress in jellyfish dermatitis by activating the Nrf2/HO-1 signaling pathway [100]. (C). Protective Effects of Epigallocatechin-3-gallate (EGCG) against the Jellyfish Nemopilema nomurai Envenoming [91].

Figure 1

Schematic diagram of the cnidocyte emission process [5]. (A) The cnidocyst in a resting state. The cnidocyst’s cnidae are coiled and not discharged, remaining in a ready-to-fire state; (B) After being stimulated, the osmotic pressure inside the cnidocyst changes, and the pressure inside the cnidocyst rises. The cnidae start to prepare for eversion and discharge; (C) The cnidae start to evert and discharge. The top of the cnidocyst opens, and the cnidae are rapidly ejected outward; (D) The cnidae are completely discharged and penetrate target objects, and venom may be released simultaneously.

Figure 3

Dermoscopy of Pelagia noctiluca jellyfish stings: (A) Tingling for 1 week, 0.1 mm brown spot; (B) Brown spot disappeared at 21 days in same lesion; (C) Brown crusts (black arrows) & red dots (yellow arrows) on pink; (D) “Linear purpura”: linear band of regularly spaced red dots in tabby pattern; (E) “Chinese character” pattern: brown dots joined by light brown granular lines (★), matching linear vesicular disease variant; (F) “Snake ulcer”. Scales & brown dots mark margin, with internal linear purpura; (G) “Round opalescent red area” due to repeated, persistent inflammatory response to sting; [53] (H) RCM shows multiple special structures (arrow) through epidermis, corresponding to cnidocysts; (I) Another RCM slice (frontal epidermis view) displays harpoon structure (cnidocyst) passing through epidermis (arrow) [55].