Anaphylaxis

An envenomation or the administration of antivenom can elicit an allergic reaction. In the previously sensitized individual, the antigen (venom, aquatic protein, or animal serum) complexes with immunoglobulin E (IgE) and perhaps with IgG homocytotropic antibodies or activated complement cleavage products attached to the membranes of mast cells and basophils. This induces membrane permeability, which allows degranulation or membrane production of histamine, serotonin, kinins, prostaglandins, platelet-activating factor, eosinophil and neutrophil chemotactic factors, leukotrienes, and other bioactive chemical mediators.⁹

The signs and symptoms of anaphylaxis may occur within minutes of exposure. They include hypotension, bronchospasm, tongue and lip swelling, laryngeal edema, pulmonary edema, seizures, cardiac arrhythmia, pruritus, urticaria, angioedema, rhinitis, conjunctivitis, nausea, vomiting, diarrhea, abdominal pain, gastrointestinal bleeding, and syncope. Most severe allergic reactions occur within 15 to 30 minutes of envenomation, and nearly all occur within 6 hours. Fatalities are often related to airway obstruction or hypotension. Acute elevated pulmonary vascular resistance may contribute to hypotension that results from generalized arterial vasodilation.^10,12

Serum Sickness

The formation of IgG antibodies in response to antigens present in antivenom (prepared in heterologous serum) results in the deposition of immune complexes in many tissue sites, notably in the walls of blood vessels. These complexes induce vascular permeability, activate the complement cascade and chemotactic factors, degranulate mast cells, and trigger the release of proteolytic enzymes. Decreased levels of C₃ and C₄ are accompanied by increased C_3a/C_3a des-arginine, a split product C₃.^69,105 Although immune complexes can be measured by various tests (Raji-cell IgG assay and C_1q-binding assay), levels of immune complexes may not correlate with the clinical presentation.^69,138 Cutaneous venulitis may precede vasculitis. Dermal biopsy of lesional skin may reveal leukocytoclastic vasculitis.

Symptoms are generally present within 8 to 24 days and include fever, arthralgias, malaise, urticaria, lymphadenopathy, urticarial and morbilliform skin rashes, peripheral neuritis, and swollen joints. It is not uncommon for the primary urticarial lesion to be noted at the injection site. Serum sickness is managed with the administration of corticosteroids. An initial loading dose of prednisone (40-60 mg for adults, and 2 to 5 mg/kg, not to exceed 50 mg, for children) should be administered and maintained daily until symptoms markedly resolve. The corticosteroid should be tapered over a 2- to 3-week course to avoid induction of adrenal insufficiency. Aspirin or other nonsteroidal antiinflammatory agents are rarely helpful and may be contraindicated because of circulating immune complex–induced platelet dysfunction.

Life and Habits

There are approximately 5000 species of sponges (phylum Porifera, predominantly of class Desmospongiae), which are supported by horny, but elastic, internal collagenous skeletons of spongin, some forms of which we use as bath sponges. Sponges are without digestive, excretory, respiratory, endocrine, circulatory, and nervous systems. Embedded in the connective tissue matrices and skeletons are spicules of silicon dioxide (silica) or calcium carbonate (calcite), by which some sponges can be definitively identified. In general, sponges are stationary acellular animals that attach to the sea floor or coral beds and may be colonized by other sponges, hydrozoans, mollusks, coelenterates, annelids, crustaceans, echinoderms, fish, and algae. These secondary coelenterate inhabitants are responsible for the dermatitis and local necrotic skin reaction termed sponge diver’s disease (maladie des plongeurs).¹⁸³ In recognition of a medicinal property, the ancient Greeks burned sea sponges and inhaled the vapors for prophylaxis against goiter.⁴⁶ Sponges harbor various biodynamic substances, with possible antineoplastic, antibacterial, growth-stimulating, antihypertensive, neuropharmacologic, psychopharmacologic, and antifungal properties. A number of sponges produce crinotoxins that may be direct dermal irritants, such as subcritine, halitoxin (Haliclona species), p-hydroxybenzaldehyde, and okadaic acid. These may be present in surface or internal secretions. Murine monoclonal antibodies against okadaic acid intended for use in an assay system for the detection of diarrhetic shellfish poisoning have been prepared from the sponge Halichondria okadai.¹⁹⁹ The causative agent of Dogger Bank itch, (2-hydroxyethyl) dimethylsulfoxonium chloride, has been isolated from the marine sponge Theonella aff. mirabilis.²⁰⁵

Clinical Aspects

Two general syndromes, with variations, are induced by contact with sponges. The first is a pruritic dermatitis similar to plant-induced allergic dermatitis, although the dermatopathic agent has not been identified. Rarely, erythema multiforme or an anaphylactoid reaction may be present. A typical offender is the friable Hawaiian (Figure 80-1) or West Indian fire sponge (Tedania ignis), a brilliant yellow-vermilion-orange (Figure 80-2) or reddish-brown organism with a crumb-of-bread appearance found off the Hawaiian Islands and the Florida Keys.^171,180 Other “fire sponges” have a similar appearance (Figure 80-3, online). This sponge grows in thick branches, which extend from a larger base and are easily broken off. Other culprits include Fibula (or Neofibularia) nolitangere, the poison bun sponge (Figure 80-4) (and the related sponge Neofibularia mordens), and Microciona prolifera, the red moss sponge (found in the northeastern United States).⁹⁸ F. nolitangere is found in deeper water and grows in clusters, with holes (oscula) large enough to admit a diver’s finger. It is brown (Figure 80-5) and bready in texture, so it may crumble in the hands.

FIGURE 80-1 Pacific fire sponge.

(From Norbert Wu, with permission. http://www.norbertwu.com.)

FIGURE 80-2 Atlantic fire sponge.

(Courtesy Dee Scarr.)

FIGURE 80-4 Poison bun sponge Neofibularia nolitangere.

(Courtesy Dee Scarr.)

FIGURE 80-5 Crumb-of-bread appearance of poison bun sponge.

(Courtesy Dee Scarr.)

FIGURE 80-3 Fire sponge.

(Courtesy Vidal Haddad Jr.)

Within a few hours after skin contact, but sometimes within 10 to 20 minutes, the reactions appear. They are characterized by itching and burning, which may progress to local joint swelling, soft tissue edema, vesiculation, and stiffness, particularly if small pieces of broken sponge are retained in the skin near the interphalangeal or metacarpophalangeal joint. Most victims of sponge-induced dermatitis have hand involvement, because they handled the sponges without proper gloves. In addition, abraded skin, such as that which has been scraped on stony coral, may allow more rapid or greater absorption of toxins.¹⁶⁴ When the sponge is penetrated, torn, or crumbled, the skin is exposed to the toxic substances. Untreated, mild reactions subside within 3 to 7 days. When large skin areas are involved, the victim may complain of fever, chills, malaise, dizziness, nausea, muscle cramps, and formication. Bullae induced by contact with M. prolifera may become purulent. Systemic erythema multiforme, dyshidrotic eczema, or an anaphylactoid reaction may develop 1 to 2 weeks after a severe exposure.²²⁶ The skin may become mottled or purpuric, occasionally after a delay of up to 10 days.¹⁸⁰

The second syndrome is an irritant dermatitis and follows penetration of small spicules of silica or calcium carbonate into the skin. Most sponges have spicules; toxic sponges may possess crinotoxins that enter microtraumatic lesions caused by the spicules.

In severe cases, surface desquamation of the skin may follow in 10 days to 2 months. No medical intervention can retard this process. Recurrent eczema and persistent arthralgias are rare complications.

Treatment

Because distinguishing clinically between the allergic and spicule-induced reactions is usually impossible, it is reasonable to treat for both. The skin should be gently dried. Spicules should be removed, if possible, using adhesive tape, a thin layer of rubber cement, or a facial peel. As soon as possible, dilute (5%) acetic acid (vinegar) soaks for 10 to 30 minutes 3 or 4 times a day should be applied to all affected areas.^180,184,225 Isopropyl alcohol (40% to 70%) is a reasonable second choice. Although topical steroid preparations may help relieve the secondary inflammation, they are of no value as an initial decontaminant. If they precede the vinegar soak, they may worsen the primary reaction. Delayed primary therapy or inadequate decontamination can result in the persistence of bullae, which may become purulent and require months to heal.

Erythema multiforme or dyshidrotic eczema may require administration of a systemic glucocorticoid, beginning with a moderately high dose (prednisone, 60 to 100 mg) tapered over 2 to 3 weeks. Anecdotal remedies for the management of sponge envenomation that have been suggested without demonstration of efficacy include antiseptic dressings, broad-spectrum antibiotics, methdilazine, tripelennamine, phenobarbital, diphenhydramine, promethazine, and topical carbolic oil or zinc oxide cream.¹⁸⁰

After the initial decontamination, a mild emollient cream or steroid preparation may be applied to the skin. If the allergic component is severe, particularly if there is weeping, crusting, and vesiculation, a systemic glucocorticoid (prednisone, 60 to 100 mg, tapered over 2 weeks) may be beneficial, as might a potent topical steroid preparation. Severe itching may be controlled with an antihistamine.

Because Clostridium tetani has been cultured from sea sponges, sponges should not be used to pack wounds. Proper antitetanus immunization should be part of sponge dermatitis therapy. Frequent follow-up wound checks are important because significant infections sometimes develop.⁹⁹ Infected wounds should be cultured and managed with antibiotics (see Chapter 79). If sponge poisoning induces an anaphylactoid reaction, standard resuscitation using epinephrine, bronchodilators, corticosteroids, and antihistamines should be undertaken.²²⁶

As mentioned previously, sponge diver’s disease is not caused by any toxin produced by the sponge but rather is a stinging syndrome related to contact with the tentacles of the small coelenterate anemone Sagartia rosea (family Sagartiidae) or anemones from the genus Actinia (family Actiniidae) that attach to the base of the sponge. Treatment should include that for coelenterate envenomation (see below).

Prevention

All divers and net handlers should wear proper gloves. Sponges should not be broken, crumbled, or crushed with bare hands. If the victim brings a specimen, the physician should take care to document its appearance. Dried sponges may remain toxic.

Morphology, Venom, and Venom Apparatus

Cnidarians are carnivorous predators that feed on other fish, crustaceans, and mollusks. They are radially symmetric animals of simple structure (95% water) and exist in two predominant life forms—either sedentary, asexual polyps (hydroids) or free-swimming and sexual medusae. They are the lowest form of life organized into different layers.¹⁶⁴ Generally, the polyps are sac-like creatures attached to the substrate at the caudal (aboral) end, with a single orifice or mouth at the upper end surrounded by stinging tentacles (dactylozooids). This form predominates in the hydrozoans and anthozoans. The medusa is a bell-shaped creature, with a floating gelatinous umbrella from which hang an elongated tubular mouth and marginal nematocyst-bearing tentacles. This form predominates in the scyphozoans and is also found in the hydrozoans.

Cnidocytes (include nematocytes, spirocytes, and ptychocytes) are mature living cells that encapsulate the nonliving intracytoplasmic capsules called cnidae (or cnidocysts: include nematocysts, spirocysts, and ptychocysts), within which are found the stinging apparatus. Cnidae are secreted by the Golgi apparatus of cells (cnidoblasts: include nematoblasts, spiroblasts, and pychoblasts) specialized for this function. Nematocysts are initially found in differentiating clusters. After differentiation into the different types of capsules, the clusters break up to allow single nematocytes to migrate to tentacles, where they become mounted in specialized tentacle epithelial cells, called battery cells.¹⁹¹ The nematocytes are located on the outer epithelial surfaces of the tentacles (Figure 80-6) or near the mouth and are triggered by contact with the victim’s body surface. The nematocyst is contained within the cnidoblast, to which is attached a single pointed “trigger,” or cnidocil. The undischarged nematocyst (3 to 100 µm in diameter) varies in shape and is under high osmotic pressure created during capsule morphogenesis by synthesis of poly-γ-glutamate in the capsule matrix. Minicollagen networks determine the structure of the nematocyst wall.⁴³ The nematocyst contains a hollow, sharply pointed, coiled, or folded “thread” tubule (nema) (Figure 80-7). This tubule may attain lengths of 200 to 850 µm and is sufficiently hardy to penetrate a surgical glove. The tubule is initially formed outside the capsule and then invaginates within the wall, so that in the undischarged state, the toxin is located in the folds and invaginations of the tubule’s membrane. This membrane hardens via disulfide bond isomerization to form bridges between minicollagen peptides as the capsule attains its final size.¹⁹¹

FIGURE 80-6 Unfired nematocysts on a Physalia tentacle.

(Courtesy Peter Parks.)

FIGURE 80-7 Nematocyst before discharge.

The tubule is lined with hollow barbs, which help it penetrate and anchor into the victim. In the undischarged state, the barbs occupy the lumen of the twisted and folded tubule. When the cnidocil is stimulated, either by physical contact or by a chemoreceptor mechanism, it causes the opening of a trapdoor (operculum) in the cnidoblast, and the venom-bearing tubule is everted (Figure 80-8) within 3 µsec. This exocytosis has been hypothesized to occur because of osmotic swelling of the capsular matrix caused by high concentration of poly-γ-glutamate, influx of water (leading to a hydrostatic pressure of up to 150 atm), release of intrinsic tensile forces (up to 375 MPa on the inner capsule wall), or deformation of the wall-induced internal pressure.^86,87,191 The sharp tip of the thread tube enters the victim’s skin (Figures 80-9 and 80-10), and envenomation occurs as toxin is translocated by hydrostatic forces from the surface of the everted and extended tubule through the now helically arranged (Figure 80-11) and extended hollow barbs.^113,114 It has been estimated that the velocity of ejection attains 2 m/sec, which corresponds to an acceleration of 40,000g, with an estimated skin striking force of 2 to 5 psi.⁴⁹ This is one of the most rapid mechanical events found in nature. A human encounter with a large Portuguese man-of-war could conceivably trigger the release of several million stinging cells (Figure 80-12). It has been estimated that more than 2000 sting penetrations can occur within a single square millimeter of skin. The threads penetrate the epidermis and upper dermis, where the venom diffuses into the general circulation. The agitated victim moves about and assists the venom’s distribution by the muscle-pump mechanism. On the basis of mouse studies, it appears that the rapid death of a victim is related to the venom that is discharged directly into capillaries, as opposed to that which must diffuse from the dermis into the bloodstream.

FIGURE 80-8 Nematocyst after discharge.

FIGURE 80-9 Discharged nematocyst that penetrated human skin.

(Scanning electron micrograph by Thomas Heeger, MD.)

FIGURE 80-10 An everted tubule of a nematocyst from a lion’s mane jellyfish (Cyanea capillata) has entered the skin and has lifted an epithelial cell.

(Scanning electron micrograph by Thomas Heeger, MD.)

FIGURE 80-11 Helical arrangement of barbs on the tubule of a nematocyst.

(Courtesy Amit Lotan.)

FIGURE 80-12 Nematocysts of a jellyfish (Versuriga anadyomene, Philippines), mostly discharged as seen by everted tubules.

(Scanning electron micrograph by Thomas Heeger, MD.)

In the case of the Indo-Pacific box-jellyfish C. fleckeri, which may carry up to 59 tentacles bearing millions of nematocysts, it is the cigar-shaped microbasic p-mastigophores that are most important in human envenomation (Figure 80-13). The capsule of the structure holds a hollow coiled tube and granular matrix. The thread tube has a thick butt end that is attached to the operculum. The tube contains three rows of helically arranged spines. When the nematocyst fires into the human victim, the tube everts through the opercular end of the nematocyst, with the butt anchoring first to keep the nematocyst adherent to the victim. The thread then everts through the hollow butt and uncoils, presenting the spines and accompanying toxins to the living tissue. Although the major toxic fractions appear to be present in the nematocysts, there appears to be toxic material present in tentacles denuded of such organelles.²¹ The largest nematocysts of C. fleckeri can penetrate human skin to a depth of 0.9 mm.¹³⁰

FIGURE 80-13 Nematocyst identification guide. A, Microbasic p-mastigophore (undischarged) of Chironex fleckeri. Capsule length, 75 µm. B, Same (discharged and undischarged) of Irukandji. C, Isorhiza (undischarged) of bluebottle—Physalia physalis. D, Clustered isorhizas and euryteles on tentacle of “hair jelly”—Cyanea.

(Courtesy Bob Hartwick.)

Cnidarian venoms are viscous mixtures of proteins, carbohydrates, and other nonproteinaceous components. Although they are heat labile in vitro, this does not seem to apply in the clinical setting. To date, they have been difficult to fractionate. The primary difficulties encountered in jellyfish venom purification have been the lack of stability and the tendency of active toxins to adhere to each other and to support matrices.¹⁴⁷ Lyophilized crude venom can be prepared in water by homogenization, sonication, and rapid freeze-thawing. A second technique consists of grinding samples with a glass mortar and pestle and using phosphate-buffered saline. This has been done to prepare crude venom from isolated nematocysts of the box-jellyfish, the bells of Irukandji jellyfish, and the oral lobes of blubber jellyfish.²¹⁶ Analyses of Western blot tests showed that box-jellyfish antivenom reacted specifically with the venom of each jellyfish, but there is not yet any clinical significance to this observation. Because toxicity was found in the Irukandji jellyfish venom derived by the mortar-and-pestle method, but not by the lyophilization method, the former was deemed the more efficacious method. Within box-jellyfish venom are protein components ranging from 18 to more than 106 kDa.

Cytolytic toxins have been characterized from Physalia physalis, Rhizostoma pulmo (Figure 80-14), C. fleckeri, and Carybdea marsupialis. Hemolytic activity, phospholipase A₂, and α-chymotrypsin–like serine protease activity have been noted in the venom of Rhopilema nomadica.⁷⁵ Many jellyfish and marine animal venoms generate autonomic neurotoxicity.³⁴ This may be a result of their ability to affect ion transport (sodium and calcium in particular), induce channels or pores in nerve and muscle cell membranes, alter membrane configurations, and release mediators of inflammation. Cnidarian venoms can target the myocardium, Purkinje fibers, atrioventricular (AV) node, and aortic ring, as well as injure the hepatic P-450 enzyme family.

FIGURE 80-14 Rhizostome medusa, Rhizostoma pulmo (Mediterranean Sea).

(Courtesy Thomas Heeger, MD.)

Freshwater jellyfish, such as the Appalachian mountain jellyfish Craspedacusta sowerbyi, do not appear to pose a hazard to humans.

Clinical Aspects

For clinical purposes, a considerable phylogenetic relationship exists among all stinging species, so that the clinical features of the coelenterate syndrome are fairly constant, with a spectrum of severity. The severity is related to the season and species (venom potency and configuration of the nematocyst), the number of nematocysts triggered and the size of the animal (venom inoculum), the size and age of the victim (the very young and old and the smaller person tend to be more severely affected), the location and surface area of the sting, and the health of the victim. The wise clinician suspects a coelenterate envenomation in all unexplained cases of collapse in the surf, diving accidents, and near-drownings. Any victim in distress pulled from marine waters should be carefully examined for one or more cutaneous lesions that may provide the clue to a coelenterate envenomation.

Mild envenomation may result in only an annoying dermatitis, whereas severe envenomation can progress rapidly to involve virtually every organ system, resulting in significant morbidity and mortality. Clinical envenomation is described here by severity, with the understanding that there is a fair amount of overlap. In the following paragraphs, syndromes associated with specific classes of creatures are discussed in greater detail.

Mild Envenomation

The stings caused by the hydroids and hydroid corals, along with lesser envenomations by Physalia, Velella velella (Figure 80-15), Drymonema dalmatinum (stinging cauliflower), Olindias sambaquiensis (Figure 80-16, online) (known as relojinho in Portuguese; endemic to the Blanca Bay area south of Buenos Aires province and found on the southeastern Brazilian coast) (Figure 80-17), scyphozoans, and anemones, result predominantly in skin irritation.^77,100 Nemopilema nomurai (“echizen kurage”) is a large stinging jellyfish, with a maximum bell size of 2 m and weight of 200 kg, that blooms in the orient.⁹² There is usually an immediate pricking or stinging sensation, accompanied by pruritus, paresthesias, burning, throbbing, and radiation of the pain centrally from the extremities to the groin, abdomen, and axillae. The area involved by the nematocysts becomes red–brown–purple, often in a linear whiplike fashion, corresponding to tentacle prints (Figures 80-18 and 80-19, online). Other features are blistering, local edema, angioedema, and wheal formation (Figures 80-20 and 80-21, online), as well as violaceous petechial hemorrhages. Dyspnea due to upper airway obstruction associated with severe facial swelling is possible.⁵ The papular inflammatory skin rash is strictly confined to the areas of contact and may persist for up to 10 days. Areas of body hair appear to be somewhat more protected from contact than are hairless areas. If the envenomation is slightly more severe, the aforementioned symptoms, which are evident in the first few hours, can progress over a course of days to local necrosis, skin ulceration, and secondary infection. This is particularly true of certain anemone (Sagartia, Actinia, Anemonia, Actinodendron, and Triactis) stings. A painless “jellyfish sting,” in which there is a pattern of hyperpigmented linear streaks, might represent the occurrence of phytophotodermatitis (e.g., from citrus juice spilled on skin and later exposed to light).²⁰

FIGURE 80-15 By-the-wind sailor, Velella velella.

(From Norbert Wu, with permission. http://www.norbertwu.com.)

FIGURE 80-17 Skin irritation from sting of Olindias species.

(Courtesy Vidal Haddad, Jr.)

FIGURE 80-16 Tamoya and Olindias species jellyfishes.

(Courtesy Vidal Haddad Jr.)

FIGURE 80-18 Telltale Physalia species sting pattern.

(Courtesy Vidal Haddad Jr.)

FIGURE 80-19 Man-of-war sting.

(Courtesy Paul S. Auerbach, MD.)

FIGURE 80-20 Jellyfish sting around the lips.

FIGURE 80-21 Jellyfish sting.

(Courtesy Paul S. Auerbach, MD.)

Untreated, the minor to moderate skin disorder resolves over 1 to 2 weeks, with occasional residual hyperpigmentation for 1 to 2 months. Rubbing can cause lichenification. Local hyperhidrosis, fat atrophy, and contracture may occur.²⁵ Mondor’s disease of the breast has been reported following jellyfish stings.⁸⁸ Facial swelling with sterile abscess formation has been reported.¹⁹² Permanent scarring or keloids may result. Persistent papules or plaques at the sites of contact may demonstrate a predominantly mononuclear cell inflammatory infiltrate, which may represent a delayed hypersensitivity response to an antigenic component of the coelenterate nematocyst or venom. This may be accompanied by localized arthritis and joint effusion. It has been suggested that sensitization may occur without a definite history of a previous sting, because coelenterates may release antigenic and allergenic venom components into the water. Granuloma annulare, which is usually both a sporadic and a familial inflammatory dermatosis, has been associated with a Physalia utriculus envenomation.¹¹⁹ Gangrene has been observed.

Moderate and Severe Envenomation

The prime offenders in this group are the anemones, Physalia species, and scyphozoans. The skin manifestations are similar or intensified (as with Chironex) and are compounded by the onset of systemic symptoms, which may appear immediately or be delayed by several hours:

• Neurologic: Malaise, headache, aphonia, diminished touch and temperature sensation, vertigo, ataxia, spastic or flaccid paralysis, mononeuritis multiplex, Guillain-Barré syndrome, parasympathetic dysautonomia, plexopathy, radial–ulnar–median nerve palsies, brainstem infarction (not a confirmed relationship), delirium, loss of consciousness, convulsions, coma, and death^{26,37,60,131,151}

• Cardiovascular: Anaphylaxis, hemolysis, hypotension, small artery spasm, bradyarrhythmias (including electromechanical dissociation and asystole), tachyarrhythmias, elevated serum troponin I level in the absence of myocardial injury, vascular spasm, deep venous thrombosis, thrombophlebitis, acute myocardial infarction, congestive heart failure, and ventricular fibrillation^81,124,167

• Respiratory: Rhinitis, bronchospasm, laryngeal edema, dyspnea, cyanosis, pulmonary edema, and respiratory failure

• Musculoskeletal or rheumatologic: Abdominal rigidity, diffuse myalgia and muscle cramps, muscle spasm, fat atrophy, arthralgias, reactive arthritis (seronegative symmetric synovitis with pitting edema),²⁰⁷ and thoracolumbar pain

• Gastrointestinal: Nausea, vomiting, diarrhea, paralytic ileus,¹⁵⁴ dysphagia, hypersalivation, and thirst

• Ocular: Conjunctivitis, chemosis, corneal ulcers, corneal epithelial edema, keratitis, iridocyclitis, elevated intraocular pressure, synechiae, iris depigmentation, chronic unilateral glaucoma, and lacrimation^70,71,218

• Other: Acute renal failure, lymphadenopathy, chills, fever, and nightmares

The extreme example of envenomation occurs with C. fleckeri, the dreaded box jellyfish. Physalia and anemone stings, although extremely painful, are rarely fatal. Death after Physalia stings has been attributed to primary respiratory failure or cardiac arrhythmia, which may have reflected an element of anaphylaxis.^30,185 Confirmed deaths after coelenterate envenomation have been attributed to C. fleckeri, Chiropsalmus quadrigatus, and Chiropsalmus quadrumanus (Figure 80-22).¹³⁰ Stomolophus nomurai (the sand jellyfish) has caused at least eight deaths in the South China Sea.⁵³ Although there have been other deaths, the animals have not been definitively identified.

FIGURE 80-22 Skin biopsy from a child after fatal sting from Chironex fleckeri. Nematocysts are seen on the skin.

(Courtesy Jamie Seymour, MD.)

Clinical reports and studies on the serologic response to jellyfish envenomation suggest that allergic reactions may play a significant pathophysiologic role in humans. When crude or partially purified nematocyst venom and an antigen are used in an enzyme-linked immunosorbent assay (ELISA), both IgG and IgE can be detected.^69,165 Elevated specific anti–jellyfish IgG and IgE may persist for several years, recurrence of the clinical cutaneous reaction to jellyfish stings may occur within a few weeks without additional contact with the tentacles, and serologic cross-reactivity between the sea nettle (Chrysaora quinquecirrha) and P. physalis occurs. In a case of significant envenomation by the moon jellyfish Aurelia aurita (Figure 80-23), the victim developed significant cross-reacting antibodies to C. quinquecirrha antigens.²⁹

FIGURE 80-23 Moon jellyfish, Aurelia aurita.

(From Norbert Wu, with permission. http://www.norbertwu.com.)

Persons with extracutaneous or anaphylactoid responses to a coelenterate sting have been noted to have higher specific IgG and IgE antibody levels.¹⁶⁵ However, elevated persistent specific anti-jellyfish serum IgG concentrations are not protective against the cutaneous pain resulting from a natural sting.²⁸ A false-positive ELISA serologic test to venom may occur, as demonstrated by negative skin testing.

A person stung by P. physalis may have recurrent cutaneous eruptions for 2 to 3 weeks after the initial episode, without repeated exposure to the animal. This may take the forms of lichenification, hyperhidrosis, angioedema, vesicles, large bullae, nodules that resemble erythema nodosum, granuloma annulare, or a more classic linear urticarial eruption.^8,27,120 Recurrent eruptions have also followed a solitary envenomation by the cnidarian Stomolophus meleagris.²⁴ In a histologic study of delayed reaction to a Mediterranean Sea coelenterate, skin biopsy demonstrated grouping of human leukocyte antigen–DR-positive cells with Langerhans cells and helper/inducer T lymphocytes, which indicates the possibility of a type IV immunoreaction.¹⁵³

Venom-specific IgG antibodies appear to persist for longer periods than IgM antibodies. The binding of brown recluse spider venom and purified cholera toxin to anti-Chrysaora and anti-Physalia monoclonal antibodies indicates that there may be a common or cross-reacting antigenic site or sites between these toxic substances and certain coelenterate venoms.¹⁴⁵

Acute regional vascular insufficiency of the upper extremity has been reported after jellyfish envenomation. It can be manifested by acral ischemia, signs and symptoms of compartment syndrome, and massive edema.²¹¹

Treatment

Therapy is directed at stabilizing major systemic decompensation, opposing the venom’s multiple effects, and alleviating pain.

Prevention

A topical jellyfish sting inhibitor has been commercialized. Safe Sea (“jellyfish-safe sunblock”) by Nidaria Technology, Ltd, Zemah, Jordan Valley, Israel (http://www.nidaria.com) was compared in a blinded fashion with conventional sunscreen for protection against Chrysaora fuscescens (sea nettle) and Chiropsalmus quadrumanus jellyfish. Subjects were stung with jellyfish tentacles on each forearm for up to 60 seconds, and erythema and pain were assessed at 15-minute intervals over a 2-hour period. The jellyfish sting inhibitor prevented sting symptoms of C. fuscescens in 10 of 12 subjects and diminished the pain of the jellyfish sting in the remaining two subjects.⁹⁷ It was equally impressive with C. quadrumanus. The inhibitor is formulated to inactivate jellyfish stinging in several ways: (1) it is hydrophobic and thus prevents tentacles from making sufficient skin contact to induce a sting; (2) glycosaminoglycans in the inhibitor mimic the same compounds found in the jellyfish bell, thus causing self-recognition; (3) the inhibitor contains a competitive antagonist to nonselective receptors on the jellyfish that bind to amino acids and sugar secretions from prey; and (4) calcium and magnesium within the inhibitor block transmembrane signaling channels of the jellyfish, thereby altering the osmotic forces required to generate the firing pressure within the nematocyst capsule.⁹⁷ The product has not yet been tested prospectively against Physalia, Carukia, or Chironex species, to name a few.

Derma Shield is a topical formulation that contains lanolin, aloe vera, and vitamin E. According to the manufacturer, this chemically inert (1-vinyl-2-pyrrolidione) barrier protectant is hydrophobic (dimethicone and stearic acid) and does not wash off but is shed as the epithelium sloughs naturally. It has been reported anecdotally by ocean bathers to protect against the agents of seabather’s eruption. To this author’s knowledge, no prospective evaluation of the use of Derma Shield to protect against any coelenterate has been published.

Smerbeck and co-workers were assigned a U.S. patent in 1999 for a method and composition of polymeric quaternary ammonium salts for protecting the skin from jellyfish stings.

A protocol has been developed to establish the effectiveness of topical agents to block firing of nematocysts.³³ Unreliable topical barriers include petrolatum, mineral oil, silicone ointment, cocoa butter, and mechanic’s grease.

If jellyfish are sighted, they should be given a wide berth because the tentacles may trail great distances from the body. All swimmers and divers in hazardous areas should be on constant alert. Persons should not dive headfirst into jellyfish-infested waters; it is far safer to walk in. Bathers should wear protective clothing in infested areas. This includes Lycra “stinger suits” or a double thickness of panty hose. In hot weather, it is possible to cause human heat storage while stinger suits are being worn during beach activities, so one should be cognizant of the potential for heat-related illness when out of the water.¹⁸¹ If “stinger enclosures” are present, bathers should stay within the netted barriers, although it should be noted that the small (2 cm) Irukandji jellyfish will pass with ease through the mesh of a stinger net. Many bathers suffering from Irukandji envenomations in northern Queensland, Australia were swimming in a “stinger enclosure” at the time of their envenomation.

Divers concerned about jellyfish tentacles dangling from the surface or congregations of creatures at the surface should remain deeper than 20 feet and should always check snorkel and regulator mouthpieces for tentacle fragments before entering the water in endemic areas. In areas inhabited by anemones and hydroid corals, protective gloves should be worn when handling specimens. Beached dead jellyfish or tentacle fragments washed up after a storm can still inflict serious stings. Any person stung by a jellyfish should leave or be assisted from the water because of the risk of drowning.

The Consortium of Jellyfish Stings publishes a newsletter (http://medschool.umaryland.edu/dermatology/jellyfish.asp).

Class Hydrozoa

The hydrozoans range in configuration from the feather hydroids and sedentary Millepora hydroid coral to the free-floating siphonophore Physalia (Portuguese man-of-war).

Hydroids

Hydroids are the most numerous of the hydrozoans. The feather hydroids of the order Leptomedusae, typified by Lytocarpus philippinus (fire weed or fire fern), are feather-like or plumelike (Figure 80-24) animals that sting the victim who brushes against or handles them.¹⁶⁰ After a storm, the branches may be fragmented and dispersed through the water, so that merely diving or swimming in the vicinity causes itching and may induce visible skin irritation.

FIGURE 80-24 Coelenterate hydroid.

(Courtesy Paul S. Auerbach, MD.)

Clinical Aspects

Contact with the nematocysts of a feather hydroid induces a mild reaction, which consists of instantaneous burning, itching, and urticaria. If the exposure is brief, the skin rash may not be noticeable or it may consist of a faint erythematous and miliary irritation (Figure 80-25). A second variety of envenomation consists of a delayed papular, hemorrhagic, or zosteriform reaction (Figure 80-26) with onset 4 to 12 hours after contact. Rarely, erythema multiforme or a desquamative eruption may develop. In turbulent waters or in a strong current, fragments may be washed into a diver’s mask or regulator mouthpiece; this will be evident as a burning sensation in the conjunctivae or oral mucous membranes. Systemic manifestations (such as abdominal pain, nausea, vomiting, diarrhea, muscle cramps, and fever) are rarely reported and are associated with large areas of surface involvement. Allergic sensitization and subsequent anaphylaxis have been proposed.

FIGURE 80-25 Hydroid sting on the arm of a diver.

(Courtesy Neville Coleman.)

FIGURE 80-26 Fernlike hydroid print on the knee of a diver.

(Courtesy Paul S. Auerbach, MD.)

Treatment

The skin should be rinsed with seawater and gently dried without abrasive activity. Application of freshwater and brisk rubbing are strictly prohibited because they encourage any nematocysts remaining on the skin to discharge and thus worsen the envenomation. An application of 5% acetic acid (vinegar) or isopropyl alcohol (40% to 70%) to the skin for 15 to 30 minutes has traditionally been recommended to relieve the cutaneous reaction. In an in vitro evaluation, vinegar and urine caused discharge of a few nematocysts in 10% to 15% of defensive tentacle polyps; methylated spirits were found to cause gross discharge of microbasic mastigophores in all defensive polyps.¹⁶⁰ Freshwater did not cause discharge. On the basis of this study, the authors recommended that freshwater irrigation and the application of ice be used to treat acute stings. However, the clinical correlation remains to be described.

Alternative topical agents are addressed in the larger discussion on therapy for coelenterate stings. After pain relief is achieved, a mild steroid cream (hydrocortisone, 1%) or moisturizing lotion may be applied.

Fire Coral

The stony, hydroid, and coral-like Millepora species (e.g., Millepora alcicornis), or fire corals, are not true corals. They are widely distributed in shallow tropical waters. Sessile creatures, they are found attached to the bottom in depths of up to 1000 m (3281 feet). They are often mistaken for seaweed because they attach to pilings, rocks, shells, or coral. Although smaller segments resemble Christmas trees or bushes 7.6 to 10.2 cm (3 to 4 inches) in height, they may attain heights of 2 m (6.6 feet). The color ranges from white to yellow-green, with pale yellow (Figure 80-27) most common. Rare purple fire corals exist. Fire coral is structured on a razor-sharp calcium carbonate (calcic limestone) exoskeleton, which is an important component in the development of coral reefs. The outcroppings assume upright, clavate, blade-like, honeycomb, or branching calcareous growth structures that form encrustations over coral and objects such as sunken vessels. From numerous minute surface gastropores protrude tiny nematocyst-bearing tentacles, wherein lies the stinging apparatus. M. alcicornis probably accounts for more coelenterate envenomations than any other species. Unprotected and unwary recreational scuba enthusiasts handle, kneel on, or lean on this marine stinger.

FIGURE 80-27 Fire coral.

(Courtesy Paul S. Auerbach, MD.)

Clinical Aspects

Immediately after contact with fire coral, the victim suffers burning or stinging pain, rarely with central radiation. Intense and painful pruritus follows within seconds, which frequently induces the victim to rub the affected area vigorously, worsening the envenomation. Over the course of 5 to 30 minutes, urticarial wheals develop, marked by redness, warmth, and pruritus (Figure 80-28). The wheals become moderately edematous and reach a maximal size in 30 to 60 minutes. Untreated, they flatten over 14 to 24 hours and resolve entirely over 3 to 7 days, occasionally leaving an area of hyperpigmentation (Figure 80-29) that may require 4 to 8 weeks to disappear. The pain generally resolves without treatment in 30 to 90 minutes. A hemorrhagic or ulcerative lesion(s) may occur acutely. In the case of multiple stings, regional lymph nodes may become inflamed and painful. This does not necessarily indicate a secondary infection. The skin may take on the appearance of leukocytoclastic vasculitis.¹⁴⁸ Long thoracic mononeuritis with serratus anterior muscle paralysis has been described after Millepora sting, confirmed by demonstrated presence of immune-specific IgG.¹³³ Delayed skin reaction after Red Sea fire coral injury was characterized by superficial granulomas and atypical CD30+ lymphocytes (Figure 80-30).¹³² In another series, contact with fire coral resulted in a typical pruritic urticarial lesion and blister formation, followed by a lichenoid stage that developed 3 weeks after the initial injury; resolution, with residual hyperpigmented macules, required 15 weeks.² A persistent cutaneous reaction characterized by eczematous dermatitis lasting more than 18 months is possible.¹⁴⁸ Grouped or linear papulonodular lesions, round or oval in shape, may follow as a delayed reaction to jellyfish sting.²⁰¹ In a rare case, a full-thickness skin burn may occur.¹⁶⁶

FIGURE 80-28 Fire coral sting of the author.

(Courtesy Kenneth Kizer, MD.)

FIGURE 80-29 Hyperpigmentation of forearm depicted in Figure 80-22 after a fire coral sting.

(Courtesy Kenneth Kizer, MD.)

FIGURE 80-30 A, Streaks of red papules on the knee of a victim stung by a Red Sea fire coral. B, Wedge-shaped inflammatory infiltrate with edema of the papillary dermis and an epithelioid granuloma (hematoxylin and eosin, ×100). C, CD30+ atypical lymphoid cells (alkaline phosphatase–antialkaline phosphatase, ×400).

(Courtesy Dr. Clelia Miracco.)

Renal minimal change disease (nephrotic syndrome, renal failure) responsive to corticosteroid therapy has been associated with fire coral exposure.¹⁵⁵

Treatment

The skin should be rinsed liberally with seawater and then immediately soaked with acetic acid 5% (vinegar) or isopropyl alcohol (40% to 70%) until pain is relieved. Alternative topical agents are discussed in the larger coelenterate treatment section, earlier. Residual dermatitis is generally not very severe and can be managed in a fashion similar to that used after a feather hydroid sting. If the rash becomes eczematous and indolent, it may respond to a course of systemic corticosteroids (prednisone, 60 to 100 mg, tapered over 2 weeks). Divers should avoid touching with bare skin anything resembling coral. For example, the underwater statue of Jesus at John Pennycamp Park in Key Largo, Florida, is encrusted with fire coral, so posing divers have been envenomed.

Physalia (Man-of-War)

The Atlantic Portuguese man-of-war (Physalia physalis) of the phylum Coelenterata, order Siphonophora, is a pelagic (open sea) polymorphic colonial siphonophore that inhabits the surface of the ocean. It is constructed of a blue or pink-violet and iridescent floating sail (pneumatophore) that is filled with nitrogen and carbon monoxide and up to 30 cm (11.8 inches) in length, from which are suspended multiple nematocyst-bearing tentacles, which may measure up to 30 m (98 feet) in length (Figure 80-31). It has recently been reported that an Australian version of P. physalis is present in northern Australian waters.⁵⁸ This jellyfish is characterized by float lengths of up to 15 cm (5.9 inches), up to five thick, dark blue “main” tentacles, and up to 10 other long, thin, and pale-colored tentacles. The smaller Pacific bluebottle (Physalia utriculus) usually has a single fishing tentacle, which attains lengths of up to 15 m (49.2 feet). In some species, the sail can be deflated to allow the animal to submerge in rough weather.

FIGURE 80-31 Atlantic Portuguese man-of-war.

(From Norbert Wu, with permission. http://www.norbertwu.com.)

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