Chapter 209. Bites and Stings of Terrestrial and Aquatic Life

Humans are a part of the environment and ideally live peacefully with other animals and plants. However, sometimes the interactions between man and the environment prove harmful to one or the other. The first two sections of this chapter consider the harmful effects of land-borne animal bites, as well as the bacterial and viral infections they may transmit. The last section reviews bites and stings and other forms of injury that may be inflicted by marine life.

Epidemiology

Dog bites account for 80%–90% of all mammalian bites involving humans. Four to five million dog bites are estimated to occur each year in the United States, and, in 2001, it was estimated that 368,245 persons were treated for dog bite-related injuries.1 The human victim is often a 5– 9-year-old boy who may have been teasing or playing with the dog. Sometimes the bite occurs when a person is trying to break up a pair of fighting dogs or trying to aid an animal. In the United States 4%–5% of dog bites are work related and include bites sustained by postal carriers. Overseas, a higher percentage are produced by untamed animals.2–4 Most dog bite injuries involve the upper extremities, especially the hands. Cat bites are the second most common type of mammalian bite after dog bites, but the wounds following a cat's bite are nearly twice as likely to become infected as wounds from dog bites.5

Clinical Approach (Pathogenesis and Treatment)

The evaluation and treatment of all bite wounds should include taking a careful history of the incident, the type of animal, the site of the bite, and the geographic setting. Hand wounds, puncture wounds, and crush injuries are likely to become infected. Specimens from infected bites should be cultured and a Gram-stained smear prepared; the wound should then be washed, well-irrigated, and left open. Most patients with bites on the hands, deep cat bites, deep cat scratches, and sutured wounds should be treated with amoxicillin/clavulanic acid or ceftriaxone because of the risk of Pasteurella multocida infection; if the patient is allergic to these agents a quinolone or a tetracycline should be used. Evidence that the use of prophylactic antibiotics is of benefit exists only for bites of the hand. However, once the patient has an infection, intravenous antibiotics and surgical drainage are often required.4,6–8 Tetanus immune status should be evaluated, and rabies prophylaxis should be considered, depending on the type of animal, local epidemiologic factors, and ability to quarantine the animal for 10 days.9

Human bites and monkey bites deserve special mention, because 30% become infected with aerobic or anaerobic mouth organisms. Infection caused by anaerobes may spread through the metacarpal–phalangeal space and causes severe damage. The same procedure should be followed as for other animal bites; that is, culture and Gram stain, thorough washing, and debridement. Wounds, especially hand wounds, should be left open if possible. Evidence suggests that patients with human bites that penetrate the epidermis should be treated prophylactically with amoxicillin/clavulanic acid for 7–10 days or, if the patient is allergic to penicillins, with a fluoroquinolone plus an antianaerobic agent such as clindamycin.7,10 Clenched-fist injuries should be evaluated by a hand surgeon because of the high likelihood of infectious complications, including septic arthritis and osteomyelitis.2

Specific Bacterial Infections Caused by Animal Bites

Pasteurella Multocida Infection

(See Chapter 183). An organism commonly infecting bite wounds is P. multocida, a bacterium present in the nasopharynx in 50%–66% of dogs and 70%–90% of cats. The most common pattern is that of local infection with adenitis after a dog or cat bite or scratch. P. multocida is the most common pathogen in cat bite infections and may also complicate 26% of dog bite wounds.5 The infection usually presents within 24–48 hours, often within several hours. In patients with a cat bite, the infection may be followed by tenosynovitis or osteomyelitis as a result of inoculation of the organism into the periosteum by the long, sharp tooth of the animal. Pasteurella infections have also been reported after bites of large cats such as lions and tigers.

Systemic infection may also occur as bacteria may enter the respiratory tract through the inspiration of contaminated barn dust, or by inhalation of infectious droplets sprayed by the sneeze of an animal. In such cases, the bacteria probably colonize the respiratory tract and in some patients cause active infection. Bronchiectasis, emphysema, peritonsillar abscess, and sinusitis have all been described with this organism. Finally, systemic infection with bacteremia or meningitis may occur.

P. multocida is a small, Gram-negative, ovoid bacillus that grows well on blood agar but does not grow on selective Gram-negative media such as MacConkey agar. Because of the superficial resemblance of P. multocida to Haemophilus influenzae and Neisseria organisms, infections of the respiratory tract and central nervous system with this bacillus may be misdiagnosed initially.

Treatment of the patient with presumptive P. multocida infection should consist of careful washing of the wound and an attempt to leave it open. The empiric antibiotic of choice is amoxicillin/clavulanic acid orally for 7–10 days, with careful follow-up examination of the wound. P. multocida is susceptible to penicillin alone, and patients may be switched to penicillin if they have a pure infection with this organism. A fluoroquinolone, a tetracycline, and a trimethoprim-sulfamethoxazole are alternatives. In most patients, the antibiotic is aimed at both the patient's skin flora (such as Staphylococcus aureus) and organisms from the animal's mouth. Given the increasing prevalence of community acquired methicillin resistant S. aureus (MRSA), patients should be treated with vancomycin, clindamycin, tetracycline, or trimethoprim-sulfamethoxazole if MRSA is suspected (see Chapters 176 and 177).11

Staphylococcus Intermedius Infection

S. intermedius is an organism associated with dogs weighing more than 40 lb. It is more commonly found in canine gingival flora than is S. aureus (39% vs. 10%).12 It is a Gram-positive, coagulase-positive coccus that can be differentiated from S. aureus in the laboratory by biochemical testing. In comparison with S. aureus, S. intermedius does not produce acetoin from glucose and has β-galactosidase activity. If these tests are not performed (i.e., if only a latex assay is use to identify Staphylococci), the laboratory may incorrectly report an isolate as S. aureus or unspecified Staphylococcus. Antibiotic treatment is the same as that for infections with S. aureus, although resistance to oxacillin is uncommon in S. intermedius and is growing in importance for S. aureus.11

Capnocytophaga Canimorsus Infection

C. canimorsus is a capnophilic (“carbon dioxide-loving”), facultatively anaerobic, slow-growing, Gram-negative rod associated with dog bites.13–16 The organism has been found in the oral cavity of 17% of cats and 24% of dogs. Most infections occur in splenectomized or immunocompromised hosts, although fatal infections including meningitis have been reported in immunocompetent hosts and present as overwhelming sepsis.

Infection by Porphyromonas Species

Porphyromonas sp. are slow-growing anaerobic bacteria found in the deep gingival pockets of animal and humans. The organism is difficult to culture, requiring 4–6 days for colony formation as well as vitamin K and hemin in the media.17,18 Citron and co-workers19 found Porphyromonas sp. in 28% of culture specimens from patients with infected dog and cat bite wounds.

Cat Scratch Disease

Bartonella henselae is the most common etiologic agent of cat scratch disease. Afipia felis and other Bartonella species may cause some cases (see Chapter 182).

Plague

(See Chapter 183).

Tularemia

(See Chapter 183).

Rat-Bite Fever

(See Chapter 183).

Specific Viral Infections Caused by Animal Bites

Rabies

Epidemiology

The most notorious viral disease to occur after an animal bite is rabies, which is caused by a Rhabdovirus. Its epidemiology has changed in the past few years as a result of improved control of rabies in the domestic animal population. Now, nonimmune dogs and domestic animals account for only 8% of cases, whereas sylvatic animals, such as skunks, raccoons, red and gray foxes, and bats, represent the greatest potential danger. Rodents, such as squirrels and hamsters, are probably inconsequential as sources of rabies. However, cases of rabies in cattle are increasing.20 Postexposure prophylaxis, which is nearly 100% effective, has reduced the number of cases of human rabies from more than 100/year a century ago to an average of 1–4 cases a year in the United States today. In 2004, of the eight cases in the 49 states and Puerto Rico, four were acquired as a result of patients’ receiving transplanted organs from an infected donor.20,21 While in the United States death in humans from rabies is rare, WHO estimates that 55,000 deaths occur each year in developing countries, half in children under 15 years.22

Live virus is introduced into nerve tissue at the time of the bite, multiplies at the site, and then spreads to the central nervous system. It replicates in gray matter and then spreads along autonomic nerves to the salivary glands, adrenal glands, and heart. The incubation period varies with the site of the bite from 5 days to as long as several years. Clinical features include a prodromal period of 1–4 days, followed by high fever, headache, and malaise. Paresthesia at the site of inoculation occurs in 80% of patients. The next sequence of events is familiar: agitation, hyperesthesia, dysphagia, excessive thirst, paralysis, and death.

Diagnosis

The diagnosis of clinical rabies is difficult and is often not made until after the death of the patient. Viral isolation methods may yield positive results for specimens of saliva or cerebral spinal fluid during the first 2 weeks of the illness, and saliva is infectious, so isolation precautions are needed. Serum antibodies may be detected as early as day 6 and usually by day 13. The fluorescent antibody method for detection of the viral antigen is the most rapid and sensitive means of making the diagnosis, and no matter where the actual bite site is, once patients have central nervous system disease, the diagnosis can be made from a biopsy of skin from the highly innervated hair-covered area of the neck or from brain tissue.

Prevention and Treatment

The most effective prevention for rabies is to avoid contact with any wild animal or any unfamiliar domestic animal. Persons at risk of unavoidable contact with rabies, such as spelunkers, veterinarians, virologists, and travelers spending time in countries where rabies is enzootic, should receive preexposure prophylaxis with the human diploid cell rabies vaccine (HDRV) series (three intramuscular injections on days 0, 7, and 21 or 28) given in the deltoid muscle and repeated every 2 years. In persons vaccinated intradermally (using a lower intradermal dose), the neutralizing antibody titer should be followed, because the immune response may not be fully protective.23

The need for postexposure prophylaxis can be determined by the answers to the following questions: (1) What is the status of animal rabies in the locale where the exposure took place? (2) Was the attack provoked or unprovoked? (3) Of what species and size was the animal? (4) What was the state of health and vaccination record of the animal? (5) Will the brain of the animal be examined within 48 hours? (6) Can the animal be effectively quarantined? Most animals transmit rabies virus in saliva only a few days before becoming ill themselves; bats, however, may harbor the virus for many months.

Bites by Household Pets

If the dog or cat responsible for the bite is healthy and available for observation for 10 days, the patient should not be treated unless the animal develops rabies. At the first sign of rabies in the animal, the patient should be treated with rabies immunoglobulin (RIG) and the vaccine HDRV. The symptomatic animal should be killed and tested as soon as possible. If the animal is rabid or suspected of being rabid, or if it does not have up-to-date vaccination records, the patient should be treated with RIG and HDRV (see Section “Specifics of Treatment”).24

Bites by Wild Animals

All skunks, bats, groundhogs, foxes, coyotes, raccoons, bobcats, and other carnivores should be regarded as rabid unless laboratory test results prove negative. The patient should be treated with RIG and HDRV.

Bites by Other Animals

Bites by other animals (livestock, rodents, lagomorphs such as rabbits and hares, and ferrets) should be considered individually.23 Local and state public health officials should be consulted about the need for prophylaxis. Bites by squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, mice, and other small rodents almost never call for anti-rabies prophylaxis.

Specifics of Treatment

The most important step is to cleanse the wound immediately with a brush and soap to remove as much virus as possible. The wound should be rinsed well and then scrubbed a second time with green soap or 70% alcohol, which is rabicidal. If vaccine treatment is indicated, both RIG and HDRV should be given as soon as possible, regardless of the interval after exposure, unless the patient has been previously vaccinated and a serologic assay shows current immunity. In this case, only HDRV is needed and should be given on day 0 and day 3. For nonimmune hosts, administration of RIG is the most urgent. If HDRV is not immediately available, RIG should be started and HDRV given as soon as it is obtained. RIG (20 IU/kg) should be given immediately—50% around the site of the bite and 50% in the thigh or the arm. This passive immunization will result in the early appearance of antibody but will also inhibit development of the active antibody from HDRV, hence the need for a 28-day series. Active immunization is accomplished using HDRV, given intramuscularly for a total of five doses on days 0, 3, 7, 14, and 28. Serum for rabies antibody testing should be collected 2 weeks after the fifth dose. If there is no antibody response, an additional booster should be given.

Management of the Patient with Clinical Rabies

In the rare cases in which a patient is admitted with the clinical diagnosis of rabies, several steps should be taken immediately. First, the diagnosis must be suspected and the patient placed on isolation precautions while the diagnosis is made rapidly by fluorescent antibody staining of specimens from various tissues, as well as immunofluorescence staining of the source animal's brain tissue. Elevated antibody titers in the absence of immunization are clear evidence of infection. The first signs of clinical rabies are usually nonspecific, such as malaise, anorexia, fatigue, headache, and fever. The acute neurologic illness that follows is most commonly characterized by intermittent episodes of hyperactivity. In some cases, however, a progressive paralysis occurs. The usual period from onset of symptoms to onset of coma is 10 days. Risk of exposure for hospital staff includes contact with open wounds or mucous membranes with saliva or other potentially infectious material such as neurologic tissue, spinal fluid, or urine. Blood, serum, and stool are not considered infectious.

Basic clinical management consists of anticipating and preventing all treatable complications of the rabies infection and induction of coma to manage the patient until the patient generates an immune response.25 Pulmonary hypoxia should be prevented by tracheostomy at the first sign of respiratory difficulty, monitoring of actual partial pressure of oxygen, and use of supplemental oxygen. There are no specific antiviral treatments for rabies, although ribavirin has been tried.25 Anticonvulsant therapy should also be instituted. Extreme increases in intracranial pressure may be prevented by insertion of a cerebrospinal fluid reservoir that allows withdrawal of the intraventricular fluid and measurement of intracranial pressure. Cardiac arrhythmias may be anticipated with careful monitoring. Rabies had been regarded as uniformly fatal, but there have been patients who have survived with prolonged cardiorespiratory support, and there is serologic evidence that some animals have survived. An aggressive approach to treatment of the patient with known rabies infection is worthwhile. In 2004, a 15-year-old girl without a history of prior rabies vaccination survived after her physicians used a treatment based on induced coma as well as other supportive measures and antiviral agents.20,25 The World Health Organization has complied information regarding treatment and prevention accessible on their Web site.22

Herpesvirus Simiae (B Virus) Infection

Herpesvirus simiae (B virus) is enzootic in Old World monkeys, especially rhesus, cynomolgus, and other macaques. The illness in monkeys is similar to that caused by herpes simplex in humans, and asymptomatic monkeys may shed the virus in saliva. Most cases in humans have occurred after direct exposure to macaque monkeys or monkey tissue through bites, scratches, or cuts.26 A vesicular lesion develops at the wound site with progressive lymphadenitis and fever. Over the next few days to weeks patients develop a severe illness, which is characterized by rapidly progressive ascending neuropathy and encephalitis. The illness is rare and before the availability of antiviral therapy, 72% of cases were fatal. A cluster of four cases occurring in 1987 in Pensacola, Florida, were treated with acyclovir. The two patients who received acyclovir when their infections were localized responded well to therapy and were maintained on oral acyclovir. All macaques should be presumed to be shedding B virus and should be handled accordingly. All monkey-inflicted injuries should be cleansed, specimens should be collected for viral culture, and a physician should evaluate the patient. Clinical and serologic monitoring is critical, and high-risk or infected patients should be treated according to established guidelines. The use of acyclovir or ganciclovir initially and acyclovir for years has led to improved survival in infected patients.

Snakebites

In the United States, there are approximately five to six deaths from snakebites and probably 6,000 to 7,000 snakebite envenomations each year.26 The largest number of venomous snakebites occur in the Southwestern States. Worldwide as many as 125,000 fatal snakebites may occur each year.27 Because of regional differences in varieties of snakes, management recommendations including specific antivenom recommendations differ by geographic area. The World Health Organization has published guidelines to help insure the quality and availability of antivenom immunoglobulins worldwide, and has an online database that can be used to explore the global distributions of venomous snake species, and access information on antivenom products and their manufacturers.28

The two major poisonous snakes in the Americas are the pit viper (family Viperidae, subfamily Crotalinae, which includes the rattlesnake, water moccasin, and copperhead) and the coral snake (family Elapidae). Poisonous snakes are found in all states of the United States except Maine, Hawaii, and Alaska.29 The northern copperhead, also called the highland moccasin, is pink or reddish brown and is marked with large chestnut brown barrels resembling dumbbells or hourglasses (Fig. 209-1). The bite is painful but rarely fatal. The timber rattler is dark brown with chevrons of black and brown (Fig. 209-2).

The degree of toxicity of a snakebite depends on the potency of the venom, the amount injected, the size and condition of the snake, and the size of the person bitten. Pain occurs at the site of the bite (usually within 5 minutes). Signs and symptoms at the bite site include wheal with local edema, numbness, and, within moments, ecchymosis and painful lymphadenopathy (Fig. 209-3).

Nausea, vomiting, sweating, fever, drowsiness, and slurred speech may develop. Bleeding of the gums and hematemesis are common hemorrhagic manifestations. If edema and erythema have not developed within 8 hours after the bite, it can be assumed that significant envenomation did not occur. Estimated mortality rates for victims who receive antivenom in a health care facility are less than 1% and probably less than 0.1%.

For proper treatment, it is extremely important to establish that the bite is from a poisonous snake. Many patients experience symptoms related to fear that may mimic symptoms from venom. The patient should have distinct fang punctures and immediate local pain, followed by edema and discoloration within 30 minutes. It is helpful to inspect the snake, because those that are poisonous may be differentiated from those that are not by the presence of fangs and the shape of the pupils (Fig. 209-4). Availability of a photograph of snakes common to a specific geographic area is important for all hospital emergency wards to aid practitioners in deciding if the patient has been bitten by a poisonous snake.

Although there are still insufficient evidence-based criteria for first aid and out-of-hospital treatment for snakebite envenomations, a rational approach is outlined in Table 209-1.30 In summary, the patient should be stabilized and transported as rapidly as possible to a health care facility capable of administering antivenom, and the affected site should be immobilized below the level of the heart. Constricting bands such as watches or jewelry should be removed; the routine use of venous compression bands is not recommended.29 The patient should be kept as immobilized as possible.29 Venous compression techniques are designed to impede the return of venous and lymphatic flow from the bite site without sacrificing blood flow to the extremity. In cases in which there is likely to be a significant delay in transport and the victim is developing systemic signs of envenomation such as hypotension, these techniques may be of value.30 Arguments against the use of venous compression techniques include the time that it takes to apply the treatments, which may further delay transport time. Additional arguments against the use of these techniques include the potential for concentrating the venom in the affected limb, which may worsen local necrosis, along with the possibility of a bolus effect when the compression is released.30 Another possible disadvantage of the use of these compression techniques is the potential for them to cause arterial compression if the affected limb swells in reaction to the toxin. If a decision is made to use a venous compression band in the field, arterial pulses should be palpable distal to the ligature, and the dressing should be checked frequently to make sure that it is has not become too tight. If a venous compression dressing has been applied in the field and is not causing vascular compromise, it should be left in place until the patient reaches a health care facility and antivenom is at the bedside.30

The role of surgical intervention in the treatment of snakebite envenomations is limited in most cases. Surgery is appropriate only if medical treatment fails. This includes elevation of the bitten body part in conjunction with the administration of four to six vials of Crotalidae polyvalent immune Fab (ovine) (FabAV) over the course of 1 hour, fails.29 Debridement of truly necrotic skin and subcutaneous tissues is recommended 4–5 days after envenomation. In cases of bites to a digit, if there is severe swelling and the finger is tense, blue, or pale, a digit dermotomy may be of use. True compartment syndrome involving an extremity is a rare complication of snakebite envenomation. Fasciotomy should be used only in cases of increased compartment pressure that has not responded to prompt and sufficient treatment with antivenom.31

The primary treatment for crotaline snake venom poisoning is prompt and adequate dosing with antivenom. Antivenom is most effective if given within 4 hours of the snakebite (Box 209-1).

FabAV should be used for all severe American crotaline snakebites, but not those of the coral snake. The dosage should be guided by the severity and progression of local changes and systemic clinical signs. Because some patients develop recurrent manifestations of envenomation after initial treatment, both a loading dose of four to six vials of FabAV and then, once initial control has been achieved, three maintenance doses 6, 12, and 18 hours later are recommended.29

Supportive treatment is indicated, including hospitalization with careful evaluation of baseline hematocrit, platelet count, and prothrombin time. Coagulopathy should be corrected by using antivenin, because fresh frozen plasma is ineffective.29 The wound should be cleansed and covered. Antitetanus therapy and antibiotic prophylaxis with penicillin, ampicillin/sulbactam, or tetracycline should be initiated for severe bites.

Seal Bite

Normally, a seal bite occurs on the finger of a trainer or a seal hunter—thus the term seal finger or spaek finger.32,33 The etiologic agent is unclear and is controversial. One study suggests that a virus similar to that causing Orf may be the culprit,33 although Mycoplasma sp. have been isolated, and some patients respond to tetracycline (see Chapter 183). The incubation period of 4–8 days is followed by throbbing pain, erythema at the site, and swelling of the joint proximal to the bite. Untreated, seal finger progresses to cellulitis, tenosynovitis, and arthritis. Tetracycline, 500 mg orally four times a day for 10 days, remains the antibiotic of choice.30,32 It is also helpful to immobilize and elevate the finger as well as soak it several times a day (see Chapter 183).

Injuries Caused by Jellyfish, Portuguese Man‐of-War, Sea Anemones, and Corals

Stings caused by jellyfish, Portuguese man-of-war, sea anemones, and corals are the most common envenomations experienced by humans in marine environments. All of these creatures are members of the phylum Cnidaria, formerly known as Coelenterata. They are divided into three major classes. The first class, Hydrozoa, includes the Portuguese man-of-war, fire corals, and hydroids. Jellyfish belong to the second class, Scyphozoa. The third class, Anthozoa, encompasses sea anemones and true corals. Approximately 100 of the 9,000 species of Cnidaria that have been identified may cause injury to humans.34

Cnidarians are radially symmetric animals with body walls formed by an inner and outer layer of cells enclosing a jelly-like substance. They may be either free floating in the water like jellyfish or sessile like corals.34 Almost all cnidarians possess nematocysts, or stinging capsules, which are usually concentrated on some form of tentacle. Each nematocyst contains a toxin or group of toxins and a coiled thread-like apparatus with a barbed end that functions like a flexible hypodermic syringe (Fig. 209-5). When the nematocyst comes into contact with a victim, the barbed end is discharged, and the toxin is injected into the skin.

Cnidarian stings range from mild, self-limited irritations to extremely painful and serious injuries, depending on the toxin of the species involved and the magnitude of the envenomation. Stings from certain species such as the cubomedusae, or box jellyfish, can be fatal.

In most cases, jellyfish stings elicit toxic reactions that may be localized and/or systemic. Although immediate-type hypersensitivity reactions, including urticaria, angioedema, and anaphylaxis, occur less frequently, they require prompt medical intervention, because shock and death may ensue in highly sensitized individuals. Allergic contact dermatitis, delayed and persistent hypersensitivity reactions, granuloma annulare, and erythema nodosum are other possible cutaneous reactions to jellyfish stings.35

Injuries Caused by Jellyfish

Sea Nettles

Among the organisms most commonly causing jellyfish stings are the sea nettles, which comprise two different species, both of which inhabit Atlantic as well as Indo-Pacific waters. Cyanea capillata and its relatives are the larger of the two species, with a bell measuring up to 1 m and numerous tentacles reaching 30 m in length (Fig. 209-6).36 Chrysaora fuscescens (Fig. 209-7) is found in the Pacific waters off the coast of California. Chrysaora quinquecirrha is smaller, with a white or rusty bell that may reach 30 cm with four digestive tentacles hanging from it. Although sea nettle stings are seldom lethal, they can be quite painful.37 Initially the victim experiences a sharp burning pain in the area contacted by the tentacles. Within minutes, the sting area develops a zigzag, whip-like pattern of raised red welts 2–3 mm wide (Fig. 209-8). The duration of acute pain may vary, but the pain often begins to abate in 30 minutes. The wheals usually subside by 1 hour, but purplish brown petechial and postinflammatory pigmentation may persist for several days.

Portuguese Man‐of-War

Physalia physalis is the species name for the Portuguese man-of-war, which is a member of the class Hydrozoa and is therefore not a true jellyfish. P. physalis is encountered in both Atlantic and Mediterranean waters, and is easily recognized by its translucent blue to pink or purple bladder-like float with multiple tentacles (Fig. 209-9). P. physalis is distinguished from its Pacific ocean relative Physalia utriculus, commonly known as the blue bottle, by its larger bell, which ranges in size from 10 to 30 cm, and multiple fishing tentacles extending up to 30 m; in contrast, P. utriculus has only a single tentacle that rarely exceeds 5 m.38 These tentacles are armed along their entire length with hundreds of thousands of nematocysts arranged in stinging batteries, with each battery containing hundreds of nematocysts. The nematocysts remain active even after portions of the tentacles are broken off in storms or when these animals are stranded on the shoreline by high winds or waves. A beached Portuguese man-of-war can cause a severe sting when stepped on or touched. Children who are stung after handling these animals and then cry and rub their eyes may develop an acute conjunctivitis.

Stings of P. physalis are more painful and severe than those caused by sea nettles and are more extensive and serious than those caused by P. utriculus. At the moment of contact with the tentacles of P. physalis, the victim experiences a sharp, shock-like, burning pain. There may be painful paresthesias or numbness in the sting area. Initially, the sting area appears as an irregular single line or multiple lines composed of red papules, beaded streaks, or erythematous welts that correspond to the areas of tentacle contact. The wheals resolve in hours but may progress to vesicular, hemorrhagic, necrotic, or ulcerative stages before healing (Fig. 209-10).39

Postinflammatory striae may persist for weeks to months. Severe localized complications of P. physalis stings may also include arterial spasm in the sting site that can result in distal digital gangrene.40,41

Within 10–15 minutes of a Physalia sting, the victim may develop symptoms of an envenomation reaction characterized by nausea, abdominal cramps, muscular pains, backache, irritability, dyspnea, and chest tightness. Intravascular hemolysis and acute renal failure were reported in a 4-year-old girl after a severe sting by P. physalis.42 Most reports of death due to stings of P. physalis are not well-documented, but well-substantiated case reports of human fatalities do exist.43–45

Cubomedusae (Class Cubozoa): Box Jellyfish

Of all the species of jellyfish that cause painful stings and distress to swimmers, the species with the most established record of lethality are the cubozoans. Chironex fleckeri or box jellyfish causes at least one death each year in Australia.46 The fatality is usually a child, presumably because the size of the victim and the total area of the sting determine the likelihood of death. Until recently, most of the published cases of C. fleckeri stings involved fatal or nearly fatal envenomations, but less serious stings do occur in endemic areas.47–49

C. fleckeri (commonly known as the sea wasp) is an advanced species of jellyfish, with a semitransparent cubic bell that may grow to a volume of 9 L and weigh more than 6 kg (Fig. 209-11).46 Trailing from the bell are up to 60 stinging tentacles, which may reach 2–3 m in length. When a human comes into contact with a box jellyfish, some of the tentacles are torn off and adhere to the skin. Rescuers of C. fleckeri sting victims must exercise caution, because they also are at risk of envenomation until the tentacles have been neutralized and removed.

The stings appear initially as linear welts that give the patient the appearance of having been whipped.46 Fresh stings of C. fleckeri are easily recognized because they have a diagnostic, frosted, cross-hatched, or ladder-like appearance (Fig. 209-12). Microscopic diagnosis is also possible from blade scrapings or tape-strippings from the sting site. The intense pain may persist for many hours. Severely stung areas of skin take on a dusky cyanotic appearance and blister formation and necrosis may occur. The healing process is slow and may be complicated by bacterial superinfection and scarring.

Death may ensue within minutes due to cardiotoxic and neurotoxic agents in the venom that can produce ventricular arrhythmias and cardiac arrest, and respiratory failure, respectively.48 Intravascular hemolysis caused by the toxin can precipitate acute renal failure. First aid for these victims frequently involves cardiopulmonary resuscitation. Intravenous verapamil has been proposed for both treatment and prophylaxis of ventricular arrhythmias.50,51 Antivenom is available for C. fleckeri stings, and its early use in severe envenomations may be lifesaving and significantly reduces the pain and inflammation at the sting site.47

Irukandji syndrome is a severe and delayed response (usually 30 minutes but between 5 and 40 minutes) to the sting of a small box jellyfish, termed the Irukandji jellyfish, that has resulted in the death of two tourists in the Cairns–Port Douglas region of Australia.52 The classic syndrome consists of local signs of inflammation together with severe back pain, excruciating muscle cramps, piloerection, sweating, nausea, vomiting, headache, and palpitations. The most severe cases may progress to include extreme hypertension and cardiac failure. Only one species, Carukia barnesi, has been clearly linked to this syndrome, but it is thought that at least six different species of small jellyfish, each with only one tentacle arising from each corner of the bell (carybdeids), may be etiologic agents. The stings most often occur in deep water. Treatment includes application of vinegar to discharge nematocysts and victim transport for medical attention including pain control and α-blockade, because the venom is thought to act as a presynaptic neuronal sodium agonist and to stimulate norepinephrine release.

Prevention and Treatment of Jellyfish Stings

Tables 209-2, 209-3, 209-4 give details on the prevention of jellyfish stings and first aid for and treatment of the stings. Systemic reactions may occur, and the treatment for these includes support of vital functions with cardiopulmonary resuscitation, oxygen, and intravenous fluids.53,54 Application of a venous-lymphatic constriction bandage proximal to the wound site should be considered in the case of severe stings when systemic reactions are present or likely to occur, when topical deactivation of tentacles is not possible, and when transport to receive specific antivenin for C. fleckeri stings is available. The antivenin is prepared from sheep serum and may therefore pose a risk of allergic reaction in sensitive individuals.35,37 The preferred route of administration is intravenous, but the antivenin may be given intramuscularly. In severe stinging, it has proved lifesaving. It is also the only treatment that can alleviate the intense pain and may reduce inflammation at the sting site and decrease the chance of scarring. Intravenous administration of verapamil has been advocated for both treatment and prophylaxis of arrhythmias.50,51 For pain in severe stinging, parenteral narcotic analgesics and ice packs, as well as antivenin, should be considered. Local reactions may be treated with topical anesthetic ointments, creams, lotions, or sprays to relieve itching or burning pain.34 For delayed-type hypersensitivity reactions, which may occur days to weeks after the stinging (see Fig. 209-13), topical glucocorticoids, topical tacrolimus, antihistamines, and systemic glucocorticoids should be used as necessary.36

Secondary infections should be treated with the appropriate parenteral antibiotics, and antitetanus therapy should be considered. Application of ice or cold packs can relieve the pain of mild to moderate stings of many types of jellyfish, and aspirin or acetaminophen, alone or in combination with codeine, can be used to relieve persistent pain.

Sea Anemone Dermatitis

Sea anemones are members of the phylum Cnidaria, class Anthozoa. They are sessile creatures with flowery tentacles armed with nematocysts (Fig. 209-14). The stings of sea anemones may cause dermatitis in sponge fishermen, sponge divers, and beachcombers who gather snails and crabs from rocky hollows along the shore. Their toxicity to humans depends on the species. After the immediate reaction has subsided, delayed-type hypersensitivity reactions can develop at the site of a sting from a sea anemone (Fig. 209-15).

The genus Sagartia is the cause of sponge fisherman's disease.34 This anemone lives at the base of sponges sought by commercial fishermen. When they harvest or sort the sponges with their bare hands or forearms, they are likely to come into contact with the tentacles of Sagartia. Itching and burning occur at the sting site within minutes, accompanied by erythema, edema, and vesicles.34

Treatment of sea anemone stings is similar to that of jellyfish envenomations (see Section “Prevention and Treatment of Jellyfish Stings”).56 The tentacles should be removed carefully.34 Both vinegar and Stingose (an aqueous solution of 20% aluminum sulfate and 11% surfactant) have been suggested for application to neutralize the sites of anemone stings.57 Sea anemone sting sites often heal slowly and may require treatment with antibiotics.

Injuries Caused by Fire Coral and Coral Cuts

Corals are colonial organisms belonging to the phylum Cnidaria. Coral injuries may be caused by nematocyst stings or lacerations. Both injuries may occur at the same time and may be complicated by foreign-body reactions, bacterial infections, and localized eczematous reactions. For most true corals nematocyst envenomation is a relatively innocuous experience, resulting in mild pruritic erythema that requires little if any treatment. Calamine lotion or antipruritic lotions may bring relief.58

In contrast to the stings of true corals, the sting of the fire coral, Millepora alcicornis, is quite painful, as many scuba divers and snorkelers from the Florida Keys to the Caribbean will attest (Fig. 209-16). The wet mucous membrane or slime surrounding the organism contains numerous nematocysts that readily discharge on contact with the skin, causing immediate burning and stinging pain. Within 1 to several hours a pruritic erythematous papular eruption appears, which in severe cases may become pustular and, in rare cases, may progress to necrosis and eschar formation.58 Lesions heal in 1–2 weeks, often with postinflammatory hyperpigmentation. A delayed and persistent allergic contact dermatitis has also been reported to occur from a fire coral sting in the Red Sea.59

Fire coral stings should be rinsed with seawater to remove undischarged nematocysts. The sting area can then be compressed with either 5% acetic acid (vinegar) or 40%–70% isopropyl alcohol for 15–30 minutes or until the pain is relieved.37,60 Seawater compresses, hot to the point of tolerance, are also reported to inactivate the toxin. A topical steroid cream or ointment may relieve pruritus and promote healing.

Coral cuts, lacerations caused by the razor-sharp exoskeletons of coral, are notorious for their slow-healing and propensity for secondary infection. Factors that complicate healing include the following: (1) wounds often involve the lower extremities and these generally heal more slowly because of decreased tissue blood supply; (2) wound edges are often irregular, contused, crushed, and abraded; (3) contamination of wounds is likely because of pathogenic bacteria in shore waters; and (4) foreign bodies, including marine algae growing on the coral or portions of the coral itself, may be implanted in the wound.

Treatment of coral cuts should begin with vigorous cleansing of the wound with soap and water with a soft brush or rough towel, followed by copious irrigation with saline to remove foreign bodies. If the wound is extensive, local anesthesia may be required to allow adequate cleansing, exploration, and debridement and to achieve good hemostasis. Hydrogen peroxide washing of the wound before dressing it is recommended.

The decision whether to perform primary closure of a coral cut wound or to allow it to heal by secondary intention depends on the location of the wound, the degree of tissue trauma at the wound margins, and the likelihood of subsequent infection. Tape-stripping is preferable to suturing of leg wounds, because sutured leg wounds have a high chance of abscess formation. Once the wound is closed, antibiotic ointment and rest are advisable. Tetanus prophylaxis should be given according to immunization history.

Dermatitis from Sponges

Sponges are members of the phylum Porifera, class Desmospongiae. They are simple multicellular animals that live attached to the sea bottom. Sponges grow by forming a series of hollow-centered branching tubes composed of a fibrous material called spongin, which contains spicules of calcium carbonate or silica.34,61,62 Spicules of certain species of sponges are capable of penetrating the skin, causing a localized irritant or foreign-body reaction. Treatment of sponge spicule dermatitis involves tape-stripping of the affected area.

At least 13 species of sponges can cause a toxic dermatitis. Of these, the most commonly encountered are the West Indian and Hawaiian fire sponge, Tedania ignis; the poison bun sponge, Fibula nolitangere (Fig. 209-17); and the red sponge, Microciona prolifera, found in the Northeastern United States.63 These creatures are covered by a surface secretion, or slime, that produces an irritant or toxin-induced dermatitis when contacted by bare skin.62

Symptoms of itching, prickling, stinging, or burning appear within minutes of exposure and are followed within a few hours by pain, swelling, and stiffness. If the fingers are involved, they often become immobile within 24 hours. The first cutaneous sign of sponge poisoning is local erythema, which progresses to a papular, vesicular, or bullous eruption with weeping of a serous or purulent fluid.62,63 Desquamation of the site occurs within several days. Erythema multiforme and anaphylactoid reactions have been reported in highly sensitized individuals. Treatment of sponge dermatitis is similar to that of severe poison ivy.63

Injuries Caused by Echinoderms: Sea Urchins, Starfish, and Sea Cucumbers

Sea Urchins

Sea urchins are spiny creatures that belong to the phylum Echinodermata, class Echinoidea. They are encased in a fragile, roughly spherical, calcareous shell, which is protected by a formidable array of mobile spines and pincer-like organs known as pedicellariae (Fig. 209-18).64,65

Bathers, surfers, divers, and fishermen are all at risk for sea urchin injuries. These creatures, such as the purple sea urchin, hide in rocks in low tide zones along the Pacific coast between Alaska and Mexico (Fig. 209-19). Injuries may occur when the victim steps on an urchin, driving the spines into an unprotected foot, or as a result of loss of balance or wave action, in which case the hands or other body parts may be impaled. Sea urchin spines are composed of calcium carbonate and are covered with a proteinaceous membrane.62 Injuries from sea urchins may be inflicted either by penetrating wounds from the animals’ spines, which often break off and become imbedded in the wound, or by bites from the pedicellaria. In certain species, the spines or pedicellaria are venomous. This fact may explain why the pain of some sea urchin wounds is so excruciating and out of proportion to the apparent injury.

Encounters with sea urchins can result in both immediate and delayed reactions. Immediate reactions are usually localized and are initially manifested by a severe burning pain at the wound site, which quickly becomes red and swollen and may bleed profusely. There may be a black or purple discoloration at the site of the spine penetration due to either retained spines in the wound or to a tattoo-like effect from dye released by spines that have exited intact, but this discoloration will likely disappear within 48–72 hours.60 Paresthesias may develop at the wound area. Systemic symptoms are not common but can occur in injuries due to particularly venomous species. Symptoms may include nausea, syncope, paresthesias, ataxia, muscle cramps, paralysis, and respiratory distress.63

Delayed-type hypersensitivity reactions may occur with erythema and intense pruritus days after the initial injury.66 In one of these cases, the diagnosis was confirmed by patch testing with extracts of the ground sea urchin spines.67 Nodular reactions are localized to the area of spine penetration and are not usually painful. Nodules may take on colors from the dye in the spines64 and may have a central umbilication or a keratotic surface64 (Fig. 209-20).

The diffuse form more commonly involves the fingers or toes and is manifested by a fusiform swelling of the affected digit with accompanying pain and loss of function.63,64 In addition to joint synovitis and arthritis, osteoarticular complications of sea urchin spine penetration may include tenosynovitis with or without destruction of the underlying bone, fasciitis, and bursitis.68 Sea urchin spine wounds may also cause direct mechanical injuries to nerves and may be complicated by secondary infection.69

Initial first aid for the pain from immediate reactions is to soak the affected area in hot water [43°C to 46°C (110°F to 115°F)] for 30–90 minutes until maximal relief is obtained. Infiltration of the wound site with 1%–2% lidocaine without epinephrine may be required in some cases to produce significant pain relief.70 Spines protruding from the wound may be carefully removed. They are very fragile; therefore, it is difficult to extract the entire spine intact. Tumescence of the skin with a local anesthetic may allow superficially imbedded spines to be extracted when radiographs demonstrate no evidence of joint or bony impingement.65 More invasive attempts at spine removal should not be made without the benefit of aseptic surgical facilities and radiographs to confirm the spine locations. Removal of the spines may be aided by the use of an operating microscope. Antibiotics are indicated for secondary infections, and tetanus prophylaxis should be given if indicated.

Starfish

Certain species of starfish may produce puncture wound injuries similar to those caused by sea urchins. The crown-of-thorns starfish, Acanthaster planci, accounts for most severe starfish envenomations.63 The ice pick-like spines of A. planci, which may reach 4–6 cm in length, are covered with a thin skin and glandular tissue that produce a poisonous slime.70 The resulting wound is quite painful and may be accompanied by numbness and paresthesias. Systemic symptoms including nausea, vomiting, and muscle weakness are infrequent and short lived.63 Fragments of spines and their surrounding integument may become imbedded in the wounded area, resulting in granulomatous reactions.

Treatment is similar to that of sea urchin wounds.

Sea Cucumbers

Sea cucumbers are sausage-shaped, bottom-feeding echinoderms that can produce a papular contact dermatitis by means of a toxic liquid substance, known as holothurin, that is secreted from their body walls.34 Conjunctivitis, even blindness, can result from corneal involvement if the toxin comes in contact with the eyes.63 Prevention of sea cucumber dermatitis involves protecting the skin and eyes from contact with these creatures and educating children and curious divers about the risk of handling them. Treatment consists of washing the affected area with soap and water to remove the toxin and then treating as for a mild contact dermatitis.

Dermatitis and Bites from Marine Worms

Bristleworm Dermatitis

Bristleworms are multisegmented marine worms of the phylum Annelida, class Polychaeta (which means “many bristles”; Fig. 209-21). Each segment of the worm is armed with rows of silky or bristle-like, hollow, venom-filled setae that can easily penetrate and break off in the unprotected skin of a victim as do cactus spines.70 Contact with the bristleworm results in an erythematous papular or urticarial eruption at the site, accompanied by symptoms of paresthesias, intense itching, or burning pain.34,70 The bristles are too small and fragile in most cases to be removed with a forceps; however, tape-stripping with cellophane adhesive tape can be effective. After the setae have been removed, the application of ammonia soaks or alcohol or water compresses may bring symptomatic relief.

Leech Bites

Leeches are another class of segmental worms whose bites may be encountered in freshwater or saltwater as well as on land. Although freshwater leeches are capable of attaching painlessly to their human hosts, saltwater leeches produce bites with pain similar to that of a bee sting. Leeches inject a powerful anticoagulant, hirudin, into the wound, as well as other antigenic substances that are capable of eliciting allergic reactions (including anaphylaxis) in sensitized individuals. Local symptoms of leech bites include bleeding from the puncture marks, pain, swelling, redness, and severe pruritus; urticarial, bullous, or necrotic reactions may occur in sensitized persons.34

Severe ulcerations may result if the leech is removed forcibly and its mouth parts are left behind in the bite site. Leeches must be induced to fall off by applying a noxious agent (such as alcohol, vinegar, brine, or a match flame) to their site of attachment.

Cercarial Dermatitis (Clam Digger's Itch)

Cercarial dermatitis, also known as schistosome dermatitis or swimmer's or clam digger's itch, is an acute pruritic eruption resulting from penetration of the skin by the cercarial forms of certain parasitic flatworms of the family Schistosomatidae.

Symptoms of cercarial dermatitis begin with urticaria-like lesions and a prickling sensation of the skin, which lasts about half an hour after exposure to cercaria-infested waters. Severe pruritus of the affected area occurs 10–12 hours later. Within 24 hours, erythematous papules appear that may progress to vesicles and later to pustules. Pain and swelling of the area accompanies the intense itching, which usually peaks in 48–72 hours. Headache, fever, and superinfection with lymphangitis are occasionally present.

In the Great Lakes region, several species of Schistosoma cercariae that cause swimmer's itch have been reported, and many other such species have been discovered throughout the world in both freshwater and saltwater.71,72 A severely disabling form of cercarial dermatitis affects the paddy workers and rice farmers of the Far East. Cercarial dermatitis has also been described in individuals exposed to shallow coastal waters, notably on Long Island Sound where the condition affects clam diggers, giving rise to the name, clam digger's itch (Fig. 209-22). There is one reported case of cercarial dermatitis occurring on the hands and arms of a patient after he cleaned the aquarium in which he kept native water snails.73

Humans are accidental hosts in the life cycle of dermatitis-producing schistosomes. The cycle begins when the primary host, a waterfowl, marsh bird, finch, muskrat, mouse, or deer, passes schistosomal eggs in its feces into a body of water. Each egg hatches in 10–15 minutes, releasing a secondary stage miracidium. The miracidia are free-swimming and must locate and infect their definitive snail host within 12 hours or they will die. The miracidia migrate to the snail's digestive gland, where they develop into multiple sporocysts. In about 5 weeks, the sporocysts give rise to hundreds of fork-tailed cercariae that measure 0.75 mm in length. The cercariae are released from the snail under favorable conditions of light and heat, and are carried toward the shore by prevailing winds and currents.72 When an appropriate host is encountered, the cercaria attach to the skin with their oral suckers and penetrate the epidermis and dermis by means of histolytic enzymes. They lose their tails in this process and are now called schistosomula. The schistosomula migrate via the blood vessels through the heart and lungs to the intrahepatic veins, where they mature into adult male and female trematode flukes. When the worms mate, they pass in pairs through the mesenteric venules of the intestinal wall where the female lays hundreds of eggs.72 The eggs then penetrate the gut wall and are discharged in the feces, and the cycle is repeated.

When cercariae that do not cause schistosomiasis in humans accidentally attach to the skin, they may penetrate the epidermis but are unable to reach the bloodstream. The organisms die in the superficial papillary dermis and undergo total histolysis within 3–4 days. The cercarial protein residua stimulate a delayed-type hypersensitivity response, which may increase in severity with repeated exposures. Skin biopsies taken at 3–4 days reveal an amorphous eosinophilic mass at the site of the dissolved cercaria, with an intense lymphocytic infiltrate. Later, histiocytes appear in the middle and deep papillary dermis.

The differential diagnosis of cercarial dermatitis includes insect bites from chiggers, mosquitoes, and fleas; contact dermatitis from poison ivy; and the stings of other marine coelenterates. In Africa, Asia, South America, and Puerto Rico, swimmer's itch must be distinguished from the dermatitis associated with human schistosomiasis, which produces an eruption with very similar but milder and more transient symptoms.74 Swimmer's itch must also be distinguished from sea bather's eruption (SE), which is discussed in the next section.

Prevention of cercarial dermatitis in waters where swimmer's itch is known to be a problem is difficult. Coating the skin with petrolatum and various chemical repellents has been tried, but the effectiveness of these methods remains unproven. Clothing barriers may be of some help.

Treatment of cercarial dermatitis is largely symptomatic. In mild cases, antipruritic or drying lotions, oatmeal or starch baths, and antihistamines may alleviate pruritus. Aspirin may be helpful for the pain and swelling, and a bedtime sedative may be required to allow the patient much-needed sleep. Proper washing and hygiene should be maintained to prevent bacterial superinfection. In severe cases, potent topical glucocorticoids and occasionally systemic glucocorticoids may be required.

Sea Bather's Eruption

SE, also known as marine dermatitis and often misnamed sea lice infestation, is an acute dermatitis that begins shortly after bathing in seawater. SE is often confused with swimmer's itch (cercarial dermatitis, see previous section), not only because they both occur after exposure to water but also because the common names of these two conditions are easily confused. For many years, the cause of SE remained a mystery, but it is now known that the responsible agents in at least two types of SE are the larval forms of marine coelenterates. In waters off the coast of Florida and in the Caribbean, the tiny larvae of the thimble jellyfish, Linuche unguiculata, are to blame.75 Off the coast of Long Island, New York, researchers found that the larval forms of the sea anemone Edwardsiella lineata were responsible for the eruption.

In addition to having a different etiology, SE can be distinguished from cercarial dermatitis by several other characteristics: SE primarily involves areas of the body covered by bathing suits from which water evaporates slowly, as opposed to uncovered areas as is typical of swimmer's itch. Most symptoms are not noted until the bather has left the water (although some of those affected have complained of a prickling sensation while still in the water).

The eruption is caused by minute stings from the nematocysts of the coelenterate larvae, which become trapped underneath swimwear or may adhere to hairy areas of the body. In addition to SE after contact with the larvae, which are most abundant in May and June, swimmers and bathers may also develop SE after contact with the other two free-swimming stages of L. unguiculata, the ephyrae and medusae stages.76

The lesions begin within 4–24 hours after exposure as erythematous macules, papules, or wheals that may itch or burn (Fig. 209-23).34 These lesions may progress to vesiculopapules, which crust over and heal in 7–10 days. Associated systemic symptoms may include chills and a low-grade fever as well as nausea, vomiting, diarrhea, headache, weakness, muscle spasms, and malaise. Febrile and systemic symptoms are more common in children and adolescents.77 In the presence of such constitutional symptoms, caregivers who fail to recognize the pattern of the eruption or who fail to take a history of exposure to saltwater may mistakenly make the diagnosis of a viral syndrome.

In waters along the coast of South Florida, the season for SE is between March and August with a peak in May. The incidence among bathers during May and June 1993 in Palm Beach County was reported to be 16%.77 The strongest risk factor for developing SE is a previous history of the condition, which is consistent with the theory that SE represents a hypersensitivity response to the nematocyst stings. Other risk factors include age younger than 16 years and surfing. Showering with swimwear removed was found to be a protective measure.77

Prevention of SE includes the measures listed in Table 209-5. Treatment of SE is symptomatic and includes the use of antipruritic lotions, colloidal baths with starch or oatmeal, antihistamines, and topical glucocorticoids. Severe unremitting cases may warrant systemic glucocorticoid therapy.75 Secondary bacterial infections may complicate the condition and should be diagnosed and treated appropriately.

Injuries Caused by Mollusks

Cone Shell Envenomations

Cone shells are univalvular gastropods whose ornate cone-shaped shells are highly prized by shell collectors and divers. A number of species have a highly developed venom apparatus that can inflict a lethal sting. Most of the dangerous cone shell species are found in the shallow waters of the Indo-Pacific. Cone shells are carnivorous. They live on the ocean bottom and, depending on the species, may hunt worms, other mollusks, or fish. Cone shells kill their prey by means of a spear-like venomous radular tooth that is thrust out from the animal's proboscis. Cone shell venom contains several different kinds of neurotoxins, and death may result from respiratory paralysis. There is so far no antivenin for cone shell toxin, and mortality rates after envenomations from the more dangerous species (Conus geographicus and C. magus) may be as high as 15%–20%.34

Injuries from cone shells are of the puncture wound variety. The degree of pain is variable, ranging from a mild stinging sensation, similar to that of an insect bite, to excruciating pain. Early symptoms may include edema, ischemia, numbness, and paresthesias of the wound site. Paresthesias may become widespread, with the lips and mouth commonly affected.34,63 Localized muscular paralysis may progress to generalized weakness or paralysis with eventual respiratory distress and cardiopulmonary failure.78 Neurotoxic symptoms that indicate severe envenomation include diplopia, blurred vision, aphonia, dysphagia, and coma. Rare cases of disseminated intravascular coagulation have been reported after cone shell envenomation.

Great care must be exercised in handling live cone shells. Thick protective gloves should be worn, and the soft under portion of the animal should be avoided. Cone shells should never be placed in pockets of clothing or swimwear, because they have been known to sting through clothing.55

Treatment of cone shell envenomations is supportive. The victim should be kept at rest and the sting area kept dependent and immobilized. A compression dressing should be applied to occlude lymphatic-venous, but not arterial, flow.55 Local suction may be helpful if it can be applied immediately to the wound site with a plunger device, such as the Extractor Vacuum Pump (Sawyer Products, Safety Harbor, Florida).

Octopus Bites

Octopuses are an advanced group of mollusks belonging to the class Cephalopoda. The octopus bites with a parrot-like chitinous beak located on the ventral side of the head in the middle of its eight tentacles (Fig. 209-24). Species of octopi range in size from a few centimeters to 1–2 m in diameter.79 They are shy and reclusive creatures that tend to avoid encounters with humans; however, bites can occur when curious divers, fishermen, or beachgoers encounter these animals and handle them carelessly. Most octopus bites are not life threatening to humans. The bite site may be immediately painful, as after a bee sting, and is recognized by the presence of two small puncture wounds, which may bleed profusely.55 Symptoms from octopus bites are usually mild and transient and consist of redness, swelling, and itching.79

The most dangerous species of octopus, the Australian blue-ringed octopus, Hapalochlaena maculosa, is found in Australian coastal waters. Mortality rates after bites from H. maculosa may be as high as 25%. H. maculosa produces a toxin in its salivary glands that is introduced into the bite site by the animal's powerful beak and contains a fraction identical to tetrodotoxin; this toxin blocks peripheral nerve conduction and results in paralysis of the victim with subsequent respiratory failure. The bite of the blue-ringed octopus may or may not be painful, so that victims may not realize they have been bitten until neurologic symptoms develop.63

There is no antivenin for bites of H. maculosa. Treatment is supportive and similar to that recommended in the previous section for severe cone shell envenomations.

Injuries Caused by Venomous Fish Spines

Ichthyoacanthotoxicosis is the proper term for envenomations as a result of puncture wounds or lacerations inflicted by the spines of venomous fish. There are more than 200 species of venomous fish in the world that can cause injury to humans.63 The most notorious of these species are the stingrays, catfish, lionfish, scorpionfish, stonefish, weevers, toadfish, and spiny dogfish. All of these fish have in common a venom apparatus consisting of a single spine or multiple spines, in various locations, which are covered by an integumentary sheath enclosing various forms of venom glands. When the spine of the animal penetrates the victim, the sheath is torn and the venom glands release their toxins into the wound. The toxins from some of these fish may remain potent for 24–48 hours after the death of the fish.80

Stingrays

Stingrays are one of the most common causes of venomous fish stings confronting humans, with as many as 1,500 to 2,000 stingray attacks reported each year in the United States alone.70,81 Rays are grouped into one of four categories: (1) gymnurid (butterfly rays), (2) urolophid (round stingrays), (3) myliobatid (bat or eagle rays), and (4) dasyatid (proper stingrays). The groupings are based on their relative stinging ability, which depends on the size, number, and location of the caudal stinging appendages. The most dangerous group, the dasyatid or true stingrays, have the largest spines located further out on their tails, which makes them the most potent striking weapons. The spines have retroserrated teeth, so that removal is difficult (Fig. 209-25).

Most stingray injuries occur when bathers, waders, or fishermen accidentally step on rays as they lie partially covered with sand in shallow waters.82,83 Severe lacerations and puncture wounds are inflicted by the ray as it defensively whips its tail upward and forward when stepped on or threatened (Fig. 209-26).82,83 The majority of wounds, therefore, are located on the dorsum of the foot or lower leg. Penetrating wounds to other locations have occurred to fishermen stung while attempting to remove rays from their lines or nets. Rarely these injuries are fatal. Soaking in warm water relieves the pain.

Catfish

Both freshwater and saltwater catfish are armed with stout, sharp spines located immediately in front of the soft rays of their dorsal and pectoral fins. Catfish defensively lock these spines into an extended position when they are handled or threatened. Bathers may sustain stings on their feet or legs if they step on a catfish, but most catfish stings involve the hand or upper extremity of fishermen or seafood processors.84 To prevent these injuries, it has been suggested that the offending spines be removed with a pair of pliers before cleaning of the fish is attempted.

Swimmers and bathers in the Amazon River are at risk for urologic injuries if they encounter a very small species of catfish called the candiru, which has the ability to enter the human urethra. Barbs on the head of this fish prevent it from swimming backward out of the orifice, and surgical intervention is often required to extract the fish.

Scorpionfish

Scorpionfish, family Scorpaenidae, are divided into three main groups on the basis of their stinging apparatus. All have venomous spines of varying sizes and toxicity, which may be found in dorsal, pelvic, and anal locations, depending on the species.

Scorpionfish, genus Scorpaena, have stings that are of intermediate severity. They are bottom dwellers with superior camouflage abilities that allow them to blend in almost invisibly with their surroundings (Fig. 209-27). Their spines are long and heavy and have moderate-sized venom glands.

Stonefish, genus Synanceja, are the most dangerous members of the scorpionfish family. They live in shallow waters, sometimes partially buried in sand or mud, or in holes of rocky shoals, reef areas, or tidal pools.70 Injuries occur when a wader steps on the erect venomous dorsal spine that the stonefish raises in defense. Stonefish spines are short and thick and have very large and well-developed venom glands. The wounds caused by stonefish are quite severe and may be fatal. A stonefish antivenin is available.

Weeverfish

In European coastal waters, the weeverfish is one of the most common and serious causes of venomous fish spine injuries.85 These fish are equipped with between five and eight venomous dorsal spines and two venomous opercular spines (one on each side of the head near the gill plate).86 Waders and bathers are at risk when they step on weeverfish that lie partly buried in mud or sand in shallow waters.

Local and Systemic Symptoms of Fish Spine Envenomations

The toxicity of a given venomous fish sting depends on a number of factors, including the species of fish involved, the location and severity of the wound, the amount of venom released, and the first aid and subsequent medical care provided to the victim. In general, these wounds produce pain out of proportion to the apparent severity of the injury. The pain is immediate and intense. In the case of scorpionfish stings, the pain may be so severe as to cause the victim to thrash about wildly, scream, and finally lose consciousness.

Initially, the sting site may appear pale or cyanotic. The area around the wound may be anesthetic or hyperesthetic. Erythema and edema soon develop, giving the appearance of a cellulitis. Vesicles may form. In severe stinging, especially those caused by stonefish, the wounded area may become indurated and develop areas of ischemic necrosis with subsequent sloughing and ulcer formation.

Systemic effects from toxic fish spine envenomations may range from mild to severe, depending on the species involved and the amount of venom entering the wound. They can include headache, nausea, vomiting, diarrhea, abdominal cramps and pain, fever, local lymphangitis and lymphadenitis, joint aches, muscle weakness, diaphoresis, peripheral neuropathy, limb paralysis, restlessness, delirium, seizures, cardiac arrhythmias, myocardial ischemia, pericarditis, hypotension, and respiratory distress, and can lead to death.78,84,87,88

Prevention

Prevention of toxic fish spine wounds begins with knowledge of and appreciation for the various venomous species that may be encountered in a given area. Waders and bathers should shuffle their feet to scare away and avoid stepping on rays or scorpionfish. Fishermen must exercise care when removing rays or catfish from their fishing lines or when cleaning fish with venomous spines. Fish hobbyists and divers should wear protective clothing and avoid handling venomous species.

Treatment

Puncture wounds and lacerations from venomous fish spines should be irrigated immediately with sterile saline or water, if available, and with seawater as a last resort.55 The wounded area should then be soaked as quickly as possible in hot (not scalding) water of approximately 43°C to 46°C (110°F to 115°F) for 30–90 minutes or until maximal pain relief is achieved. Hot soaks may be repeated if the pain returns. Because the wound or extremity may be partially anesthetic, the person administering first aid must test the water's temperature for the victim.54,89 One source of hot water that is often overlooked and may be useful in an emergency is hot seawater from a boat motor's cooling system.

Local infiltration of the wound with 1%–2% lidocaine without epinephrine may bring about significant pain relief and allow exploration of the wound after radiographs have been obtained to locate retained portions of spines.60,70 Longer-acting anesthetics such as procaine and bupivacaine may be chosen to provide a longer period of pain relief. The wound should be thoroughly cleaned to remove any remnants of integumentary sheath. Abdominal and thoracic wounds and deep wounds to the hands, feet, or fascial compartments of the legs should be explored in the operating room.70 Debridement of necrotic tissues may be required at the time of exploration, and sequential debridement may be necessary. In general, these wounds should be left open or closed loosely with tape or suture to allow for adequate drainage and to prevent abscess formation.

Tetanus prophylaxis should be administered if indicated, and antibiotics are recommended if the wound is more than 6-hours-old, is extensive, or involves deep puncture injuries to the hand or foot. The choice of antibiotic should be based on the bacteriology of the marine environment in which the wound occurred and, subsequently, on results of deep wound or tissue cultures. Empiric antibiotic therapy for infections of wounds occurring in saltwater should include coverage for Vibrio species. Before final wound culture results are known, initial choices of parenteral antibiotics include intravenous ciprofloxacin, imipenem-cilastatin, a third-generation cephalosporin, gentamicin, tobramycin, or trimethoprim-sulfamethoxazole.

Stonefish stings complicated by severe reactions may be treated with antivenin by slow intravenous infusion. Antivenom is not usually required for the stings of lionfish and other species of scorpionfish except for stonefish.70 Stonefish antivenom is available from the Australian Commonwealth Serum Laboratory, Melbourne, Australia.

Fish Bites

There are many species of fish whose bites are dangerous to humans. Among the best known are the sharks and barracudas, whose bites may cause severe injuries.

Although they are well-publicized by the news media, shark attacks are relatively rare events. The average number of shark attacks worldwide is between 50 and 100 annually.90 Only 32 of the 400 known species of sharks have been reported to attack humans. Most shark attacks involve surfers, scuba divers, and swimmers. Because sharks are attracted to bright or shiny objects, as well as to those with contrasting colors, these items should not be worn in the water. Sharks are also attracted by any sort of blood in the water; therefore, women who are menstruating should refrain from water sports in areas in which sharks may be prevalent, and no one should swim with an open bleeding wound. Spear fishermen should never tie their catch to themselves, and they should place their catch in the dive boat as soon as possible. Although most shark bites are not life-threatening, more severe attacks may cause extensive soft-tissue loss with massive hemorrhage, which, in the worst cases, can result in amputation of a limb or death.91,92

Barracuda attacks are even rarer than shark bites. They tend to occur in turbid waters where these predators may mistake jewelry or other brightly colored objects worn by bathers for the baitfish on which they feed. Barracuda bites typically produce straight or V-shaped lacerations.

Divers and aquarium hobbyists must be careful when feeding or handling moray eels, which have powerful jaws and knife-like teeth. Although they are not considered venomous by most sources, they can produce deep puncture wounds and lacerations (Fig. 209-28).55 When biting, moray eels tend to lock onto their prey; decapitation of the eel or disarticulation of its jaw may be required to release the victim.93 As with all deep puncture wounds or lacerations, victims of moray eel bites should receive tetanus prophylaxis. Empiric antibiotic therapy for prophylaxis or treatment can include ciprofloxacin or cefuroxime for coverage of Vibrio or Pseudomonas species.93

A variety of infections may result from exposures to aquatic environments. Pathogenic organisms may be actively introduced into the bite, sting, or laceration wounds caused by marine life; preexisting wounds may be passively infected when exposed to contaminated waters. V. carchariae, a halophilic (saltwater-loving) Gram-negative bacillus, was reported as the cause of a wound infection after a shark bite.94 Table 209-6 lists those organisms commonly associated with waterborne infections (see also Chapter 183). A host of other agents, such as Streptococcus and Staphylococcus sp., Bacteroides fragilis, Clostridium perfringens, Escherichia coli, Salmonella enteritidis, marine Vibrio sp., Chromobacterium violaceum, and Chlorella, also require consideration when dealing with infections associated with aquatic settings.70

Dermatologic reactions may appear after the ingestion of seafood. Urticaria, angioedema, and, rarely, leukocytoclastic vasculitis may occur in individuals sensitized to fish or shellfish. Many seafoods, such as kelp, contain large amounts of iodine, which may cause acneiform eruptions.

Scombroid food poisoning involves the ingestion of spoiled fish from the Scombridae family of fish, such as tuna, mackerel, and Bonita. If these fish are not kept cold enough after being caught, their flesh develops scombrotoxins as a consequence of the bacterial breakdown of histidine into histamine, saurine, and possibly other toxic by-products. These can cause striking erythema and flushing of the face, neck, and upper trunk, as well as pruritus and urticarial and angioedematous eruptions. Antihistamines can provide symptomatic relief in severe cases.

Ciguatera toxin, which is produced during blooms of toxic dinoflagellates, is incorporated into the marine food chain and concentrated in the flesh of a variety of fish. It is heat stable, and symptoms may occur after eating cooked or raw fish containing the toxin. Dermatologic symptoms of ingesting these fish may include generalized pruritus and diffuse erythematous macular and papular exanthems, which may progress to blister formation and desquamation.

The authors wish to thank Dr. Bruce Halstead of the World Life Research Institute, Colton, California, for allowing us to reprint the photographs from the first and second editions of Poisonous and Venomous Marine Animals of the World.