eMedicine Specialties > Dermatology > Environmental

Jellyfish Stings

Author: David Cheng, MD, Assistant Professor of Emergency Medicine, Associate Emergency Medicine Residency Director, Associate Medical Director of Emergency Services, University of Arkansas Medical Sciences
Coauthor(s): Judith A Dattaro, MD, FACEP, Assistant Professor of Emergency Medicine in Surgery, Cornell University Medical College; Consulting Staff, Department of Emergency Medicine, Weill-Cornell University Medical Center, New York Presbyterian Hospital; Ramy Yakobi, MD, MBA, Medical Director of Emergency Department, Beth Israel/Kings Highway Division; Lecturer, Physician Assistant School, Cornell School of Medicine; Lecturer, Pre-hospital Management of Patient, Cornell/New York Presbyterian Hospital; Director of Emergency Department, New York Community Hospital
Contributor Information and Disclosures

Updated: Apr 23, 2009

Introduction

Background

With more than 10,000 species in the sea, jellyfish are responsible for the most common human envenomations. More than 100 species are toxic to humans, and contact with toxic jellyfish causes a wide range of conditions, from cutaneous rashes to cardiovascular and respiratory collapse.

Jellyfish are categorized into 4 classes as follows:

• Hydrozoa (Portuguese man-of-war)
• Scyphozoa (true jellyfish; most common)
• Cubozoa (box jellyfish; most toxic)
• Anthozoa (sea anemones and corals)

Jellyfish have a single gastrovascular cavity opening, which is used for digestion and circulation, and a set of tentacles. The tentacles are covered with batteries of specialized stinging cells termed nematocytes (also termed nematocysts). Each nematocyte contains a stinging apparatus known as the nematocyst. This stinging apparatus basically consists of a poison sac with an attached sharp hollow tube armed with barbs.

Detached tentacles found on the beach pose a hazard to humans because they remain capable of envenomation for several weeks.

The following also may be of interest:

• Cutaneous Manifestations Following Exposures to Marine Life
• Stingray Envenomation
• Octopus Envenomation
• Cnidaria Envenomation

Pathophysiology

The stinging process of the nematocyte resembles a jack-in-the-box mechanism. Specifically, mechanical and chemical stimulation of the sensory hairs (ie, cnidocil) surrounding the pressurized nematocyte results in a calcium-mediated bioelectric signal that causes an opening of its lid, allowing the ejection of the nematocyst into the prey to express the venom. This pressurized process has a high internal hydrostatic pressure of 150 atm that causes the ejection to occur within 3 milliseconds, with an acceleration power of 40,000 g and a force of penetration of 20-33 kPa. In addition, the nematocyst is capable of penetrating up to a depth of 0.9 mm. This depth deposits the toxin into the microvasculature of the dermal tissue to be absorbed into the systemic circulation and anchors the tentacles to the prey.¹ Finally, the nematocyte must be replaced because it cannot regenerate the ejected nematocyst. This replacement is done via differentiation of the pluripotent cells.

Nematocysts

The nematocysts' size and arrangement on jellyfish tentacles differ from species to species, much like a fingerprint. This architectural arrangement of warts, ridges, spirals, and terminal swelling may be reflected in the skin pattern left via the sting and helps identify the species involved in the envenomation.

Toxin

Microscopically, nematocysts appear structurally similar from one species to another, but the venom differs in composition. For example, because the box jellyfish feeds on fish larger than its own body, it requires potent venom for rapid paralysis. While the amount of toxin expressed by a single nematocyst is minute, several thousand nematocysts discharging at once have a significant effect.²

Functionally, the toxin causes sodium and calcium ion transport abnormalities, disrupts cellular membranes, releases inflammatory mediators, and acts as a direct toxin on the myocardium, nervous tissue, hepatic tissue, and kidneys.

Specifically, the toxin may contain catecholamines, vasoactive amines (eg, histamine, serotonin), kinins, collagenases, hyaluronidases, proteases, phospholipases, fibrinolysins, dermatoneurotoxins, cardiotoxins, neurotoxins, nephrotoxins, myotoxins, and antigenic proteins.³ The protein component of the toxin tends to be heat labile, nondialyzable, and is degradable by proteolytic agents.

Reaction to venom

Immediate acute reactions to the venom tend to be toxic rather than allergic.⁴ Since pain occurs immediately after exposure, venom injection into different mammals induces similar clinical results, and victims can be stung repeatedly without differences in symptoms. The more rapidly the venom gets into the bloodstream, the higher the venom concentration in blood and the more rapid the onset of systemic symptoms. Delayed reactions to jellyfish stings are related immunologically, as evidenced by persistent immunoglobulin G (IgG) levels, prolonged T-cell response, and cross-reactivity among various jellyfish venom antigens.

Frequency

United States

Jellyfish stings occur most commonly during the summer along coastal regions. As the coastal population grows and more tourists come to the beaches, the frequency of jellyfish sting is likely to increase. One investigator reported 500,000 annual envenomations in the Chesapeake Bay area and 200,000 annually along the Florida coast.

International

Jellyfish stings occur in tropical oceans, especially between latitudes 30° south to 45° north, because of a high natural concentration of coelenterates. This is especially true of the east coast of Australia during the warm summer months between November and May.

Mortality/Morbidity

Jellyfish stings usually are mild, except those caused by species in the South Pacific, such as the box jellyfish or Portuguese man-of-war. Exact mortality and morbidity is not known because of underreporting and the lack of an international jellyfish sting registry. However, an epidemiology study of 118 cases of jellyfish stings from the Texas gulf coast showed 0.8% had no effect, 80.5% had minor effects, and 18.6% had moderate effects.⁵

• Box jellyfish venom has a median lethal dose of 40 mcg/kg, which makes it the most potent marine toxin. The venom may kill a person weighing 70 kg within 3 minutes and is responsible for a mortality rate of 20%. Box jellyfish venom has caused 72 deaths secondary to respiratory paralysis, neuromuscular paralysis drowning, and cardiovascular collapse.⁶
• The sting of the Portuguese man-of-war is more painful than a common jellyfish sting. It has been described as feeling like being struck by a lightning bolt, and some victims dread it more than a shark bite. This sting has been responsible for 2 reported deaths.
• The Arctic jellyfish is the largest, with tentacles reaching 200 ft, allowing the jellyfish to sweep an area slightly larger than a basketball court.

Race

No racial predilection exists. Any differences in individual reactions to jellyfish are a reflection of immune status rather than race.

Sex

• Men are more likely to be stung than women because they are more likely to participate in water activities such as surfing, sailing, saltwater fishing, and scuba diving.
• Lower body weight makes women more susceptible than men to the same amount of jellyfish venom.

Age

• Children are most susceptible to the effects of toxins because of their large surface area–to–volume ratio and lower body weight.
• Older adults are more susceptible than younger adults because of their decreased physiologic reserves and concurrent debilitation.

Clinical

History

For patients presenting with jellyfish stings, it is essential to ascertain (1) the time of envenomation, (2) the nature of the incident, (3) a description of the coelenterate, and (4) local and systemic symptoms.

• Toxicity and variations of symptoms depend on several factors.
  • Patient age and health
  • Patient body weight relative to the toxin amount
  • Patient surface area involved in the sting (any sting >50% of limb area is associated with severe envenomation)
  • Thickness of the skin at contact points (calloused palms and soles are most resistant)
  • Site of envenomation (proximity to head and torso results in quicker venom absorption into central circulation)
  • Species of the jellyfish
  • Maturity of the jellyfish
  • Venom potency
  • Number of nematocysts discharged
• Hot water sensation with skin tingling or stinging may be reported at the body site where the jellyfish originally made contact, secondary to pain and stinging after the release of thousands of nematocysts at the site.
• Jellyfish stings are suggested in patients who experience an unexplained near drowning or collapse in water secondary to incapacitating muscle spasms or loss of consciousness. Interestingly, an Australian jellyfish sting epidemiology study showed 17% stings occurred while entering the water and 83% occurred in water 1 m or less deep.
• Precipitant environmental factors are as follows:
  • Lower than average rainfall in last 7 days
  • Onshore winds greater than 15 km/h
  • Summer temperatures warmer than average

Physical

Variations in reactions to the sting appear to be related to the specific toxicity of the venom. Venom deposited intravascularly causes quicker onset of symptoms and signs. Physical findings of envenomation can be classified as local effects, systemic effects, delayed effects, or specific jellyfish syndromes.⁷

• Mild envenomation
  • Local skin contact reactions
    • Tenderness, burning, and pruritus, which may spread centrally and differ in intensity depending on the species involved
    • Local soft tissue edema and angioedema
    • Erythematous papules and blisters in a whiplike pattern with desquamation within 1-8 weeks. The induction of granulomatous inflammation at the site is a rare but reported sequela.⁸
    • Ischemic changes distal from localized arterial vasospasm underlying the sting site
    • Thrombophlebitis of the vessel underlying the sting site
    • Local neurapraxia occurring adjacent to sting site from immunologic reaction to toxin or to toxin-induced alteration of the nerve's ionic permeability
    • Tender regional lymphadenopathy
    • Distant skin site reactions secondary to a hypersensitive response to the antigenic component of the venom
• Ophthalmologic contact reactions^9,10
  • Conjunctival hyperemia with chemosis
  • Punctate epithelial keratosa
  • Corneal stromal inflammatory edema
  • Anterior chamber inflammation
  • Iritis
  • Mydriasis secondary to sphincter myotoxicity
  • Ophthalmic sequelae, including corneal ulcer with scarring, lens opacification, and elevated intraocular pressure (32-48 mmHg) secondary to obstruction of trabecular meshwork with inflammatory debris
• Moderate or severe envenomation implies the appearance of systemic symptoms following the initial localized reaction.
  • Cardiovascular
    • Peripheral and coronary vasospasm
    • Dilated cardiomyopathy
    • Hypokinetic cardiac failure (hyperkinetic failure in Irukandji syndrome)
    • Arrhythmia from toxin-induced damage to Purkinje fibers
    • Cardiovascular collapse or arrest, usually indicating a larger amount of envenomation than in respiratory arrest
  • Respiratory
    • Laryngeal edema
    • Bronchospasm
    • Pulmonary edema/acute respiratory distress syndrome
    • Hypoxia and acidosis from intercostal muscle spasm and pain
    • Respiratory failure and arrest
  • Neurologic
    • Autonomic dysfunction from alteration of sodium and calcium ion transport
    • Spastic paralysis
    • Headache, agitation, and neuropsychiatric disturbances
    • Ataxia
    • Cerebral edema
    • Seizures
    • Stupor or coma
  • Gastrointestinal
    • Nausea and vomiting
    • Abdominal muscle rigidity and pain
    • Hypersalivation and dysphagia
    • Hepatic inflammatory necrosis from direct toxin injury to hepatocytes
    • Renal failure from toxin-induced glomerulonephritis or RBC hemolysis
  • Musculoskeletal
    • Incapacitating muscle spasm of limb and torso
    • Reactive arthritis
    • Rhabdomyolysis
  • Hematologic/immunologic
    • Hemolysis
    • Hypersensitive reaction (anaphylaxis is rare) to jellyfish venom
  • Long-term or delayed reactions^11,12,13,14
    • Keloids
    • Pigmented striae
    • Lichenification from persistent rubbing
    • Granuloma
    • Ulceration and necrosis
    • Gangrene
    • Fat atrophy
    • Scarring and contractures
    • Recurrent reactions without repeated exposure occurring at the original sting site secondary to sequestered, intracutaneous, antigen-induced, immunologic reaction (may be more severe than original reaction)
• Specific jellyfish envenomations
  • Seabather eruption¹⁵
    • Intensely pruritic eruption develops under swimwear, occurring minutes to 12 hours after exposure to the larvae of the thimble jellyfish (Linuche unguiculata).
    • Itching is worse at night and tends to prevent the patient from sleeping.
    • Erythematous macules and papules last for 2-14 days and resolve spontaneously.
• Irukandji syndrome^16,17
  • Delayed, severe, systemic symptoms occur 10-40 minutes (mean of 30 min) after the initial sting by Carukia barnesi. The latent period results from traveling of the venom in the lymphatic system into the central circulatory system.
  • The sting frequently is not visible or may resemble small insect bites.
  • Systemic symptoms mimic an autonomic-excess picture, with abdominal muscle rigidity, vomiting, profuse sweating, and excessive shaking. This is followed by pyrexia, tachyarrhythmias, hypertensive crisis, and hyperkinetic cardiogenic shock with pulmonary edema and elevated troponin I levels and echocardiographic ventricular dysfunction.
• Box jellyfish envenomation
  • Pathognomonic frosted-looking lesions develop in a transverse crosshatched pattern 8-10 mm wide. Secondary blistering occurs.
  • Lesions occur within 6 hours of the sting and superficial ulceration or necrosis follows in another 12-18 hours.
  • Immediate, intense, localized pain occurs with incapacitating muscular spasm resulting in death by drowning.
  • The pain and spasms spread centrally as the venom travels to the central circulatory system, inducing parasympathetic overstimulation and respiratory-cardiac arrest. Most fatalities occur within 20 minutes of the envenomation; according to animal studies, approximately 5-10 mcg/kg of venom is required to induce cardiac arrest.

Causes

• Injury occurs as a result of accidental exposure to jellyfish tentacles. Jellyfish move slowly and are nonaggressive.
• Bathers, waders, and divers are at risk of contacting these creatures in seawater with strong currents or poor visibility.
• The curious are at risk because of careless or unknowledgeable handling of jellyfish.

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