Updated: Feb 20, 2009
Exposure to aquatic life encompasses a variety of clinical situations. Dermatologists usually encounter patients with erythema, blisters, wheals, edema, scars, pigmentary changes, and paresthesias. Whereas the circumstances under which they occur and the distribution of these injuries can be characteristic, most of these lesions are not specific.
Cutaneous exposure to marine life occurs not only in the water but also when encountering living or dead marine animals on the beach. Commercial and recreational activities (eg, commercial or recreational fishing, beach combing, snorkeling, scuba diving, fish processing) have their specific concerns. Note that exposure to aquatic life can accompany various hobbies (eg, the keeping of saltwater fish tanks) or merchandising activities (eg, sellers of fish tank equipment of tropical fish).1,2 Exposure to freshwater life can also cause cutaneous injuries, sometimes manifesting with skin lesions similar to those caused by saltwater life.
Treatment of the severe acute sequelae of exposure to hazardous marine animals (eg, cardiorespiratory arrest, anaphylactic shock, bleeding) is in the realm of emergency medicine. This article focuses only on the cutaneous sequelae of exposure to aquatic life. Some first-aid measures are briefly mentioned. For further details, see the eMedicine Emergency Medicine section, for example, the following articles:
The injuries can be grouped into several general categories. Overlap can also occur (such as when an abrasion also allows a toxin into injured skin or when microbes are inoculated into a puncture wound). Some of the injuries may be accompanied by bleeding and/or functional impairment of the affected area (eg, after extensive exposure to jellyfish tentacles). Others, such as injuries followed by the exposure to venoms, can be very mild and self-limited but may also lead to fatal consequences.
Geographic area, season, and type of activity affect the prevalence of these injuries. With the increase of worldwide traveling, dermatologists may encounter lesions that would otherwise be unknown in their local area.
Mortality or morbidity depends on the nature and severity of the injury. Infection with Vibrio vulnificus in an immunocompromised host can lead to septicemia and death. Morbidity observed in dermatologic practice includes infection, pigmentary changes, scarring, severe deformities, and loss of function.
Persons of any race can be affected.
Both sexes can be affected.
People of any age can be affected.
| Contact Dermatitis, Allergic | Insect Bites |
| Contact Dermatitis, Irritant | Urticaria, Acute |
| Erythema Nodosum | Urticaria, Contact Syndrome |
| Folliculitis | Urticaria, Dermographism |
| Granuloma Annulare |
Granuloma annulare11
Histologic findings generally are nonspecific.
In seabather's eruption, superficial and deep perivascular and interstitial infiltrate consisting of lymphocytes, neutrophils, and eosinophils are described.
Biopsy of tissues infected with M marinum shows a mixed suppurative and granulomatous reaction with sparse-to-absent acid-fast bacilli.
Delayed skin reaction can be characterized by liquefaction degeneration of the basal layer.
Polarized light can reveal symmetric structures, corresponding to cross-sections of sea urchin spines.
Infections with V vulnificus show a nonspecific, yet characteristic, picture. Destruction extends into the dermis without an inflammatory cell infiltrate. Vasculitis may be present. Subepidermal noninflammatory bullae can be noted. Multiple organisms are observed.
Patients are usually seen in the dermatologist's office several hours or days after the initial injury. By the time of this encounter, the patient might already have undergone emergency treatment, including the use of specific measures such as the use of antivenins.
Evaluate the nature of the initial lesion and ask patients to describe any first aid measures that have been applied.
Consult specialists as required by the type of injury or complication (eg, orthopedic surgeon in case of joint or bone involvement, plastic surgeon in cases of extensive scars, infectious diseases specialist for complicated primary or secondary infections).
Activity is determined by the nature of the injury.
Medical therapy in the dermatologist's office includes topical treatment of hypersensitivity reactions, systemic corticosteroid treatment of severe hypersensitivity reactions, and topical or systemic antibiotics for the prevention or treatment of infections.
Treatment with antibiotics either is initiated empirically because culture and sensitivity results are not yet available or is tailored according to the laboratory results.
Generally, the use of a first-generation cephalosporin is appropriate for empirical therapy. For mycobacterial infections, rifampin, isoniazid, or ethambutol can be used, often in combination therapy. Some authors recommend sulfonamide alone or in combination with trimethoprim; others used minocycline, doxycycline, tetracycline, or cefoxitin. Culturing and sensitivity testing of the organisms in these situations is strongly advisable to initiate specific therapy. Antibiotic therapy of some infections (especially those caused by Mycobacteria) can be lengthy.13,14
Used to alleviate local inflammation and accompanying pruritus or pain. Several topical steroids are available. Select the product according to the severity and location of the lesions (see Precautions in triamcinolone table). Triamcinolone is discussed only as a prototype.
Systemic steroids are used for the treatment of severe hypersensitivity reactions. They have anti-inflammatory effects and modify the immunologic responses. Exercise caution because of their metabolic effects. Prednisone is discussed as a prototype.
Treats inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Apply a thin film bid/tid until a favorable response is obtained
Apply as in adults
None reported
Documented hypersensitivity; fungal, viral, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use causes striae and atrophy; do not use in areas of decreased skin circulation; prolonged use, applications over large areas, and use of potent steroids and occlusive dressings may result in systemic absorption; systemic absorption may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria
Has anti-inflammatory properties. Must be metabolized to active metabolite prednisolone for effect, and thus, its conversion may be impaired in liver disease.
40-80 mg qd or divided bid/qid; taper slowly over 4-6 wk as symptoms resolve to decrease chances of adverse reactions
0.5-1.5 mg/kg/d, qd, or divided bid/qid; taper over 4-6 wk, as symptoms resolve
Coadministration with estrogens may decrease prednisone clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; hypertension; diabetes mellitus; fungal or tubercular skin infections; administration of vaccinations for immunization during treatment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Exclude underlying infection before starting prednisone; monitor for hyperglycemia should long-term use be necessary; abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur
For the prevention of infection (eg, patient experienced a penetrating injury, foreign body was inoculated into the wound) or for the treatment of a clinically apparent infection.
Initially, a broad-spectrum antibiotic should be selected. Penicillin G was once the drug of choice; however, it has fallen out of favor because of inactivity against penicillinase-producing bacteria, including many strains of staphylococci. Ideally, antibiotics should be selected after establishing the sensitivity of the microorganism.
For mycobacterial infections, the antibiotic treatment may be lengthy.
Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.
Uncomplicated infections: 250 mg IM once
Severe infections: 1-2 g IV qd or divided bid; not to exceed 4 g/d
>7 days: 25-50 mg/kg/d IV/IM; not to exceed 125 mg/d
Infants and children: 50-75 mg/kg/d IV/IM divided q12h; not to exceed 2 g/d
Probenecid may increase levels; coadministration with ethacrynic acid, furosemide, or aminoglycosides may increase nephrotoxicity; may increase risk of cyclosporine toxicity
Documented hypersensitivity; hyperbilirubinemic neonates; increased risk of bilirubin encephalopathy (kernicterus)
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy; caution in breastfeeding women
Primarily for the treatment of tuberculosis. Inhibits DNA-dependent bacterial but not mammalian RNA polymerase. May be effective against aquatic M marinum. Additional medications can include co-trimoxazole, alone or combined with minocycline, clarithromycin, doxycycline, and ethambutol. Minocycline, doxycycline, or tetracycline as single agents have been used successfully to treat localized M marinum infections.
10 mg/kg/d PO; not to exceed 600 mg qd as single dose
Administer as in adults
Induces microsomal enzymes, which may decrease effects of acetaminophen, PO anticoagulants, barbiturates, benzodiazepines, beta-blockers, chloramphenicol, PO contraceptives, corticosteroids, mexiletine, cyclosporine, digitoxin, disopyramide, estrogens, hydantoins, methadone, clofibrate, quinidine, dapsone, tazobactam, sulfonylureas, theophyllines, tocainide, and digoxin; blood pressure may increase with coadministration of enalapril; coadministration with isoniazid may result in higher rate of hepatotoxicity than with either agent alone (discontinue one or both agents if alterations in LFTs occur)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Obtain CBC counts and baseline clinical chemistries prior to and throughout therapy; in liver disease, weigh benefits against risk of further liver damage; interruption of therapy and high-dose intermittent therapy are associated with thrombocytopenia that is reversible if therapy is discontinued as soon as purpura occurs; if treatment is continued or resumed after appearance of purpura, cerebral hemorrhage or death may occur
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa. Was found to be effective in some nontuberculotic mycobacterial infections.
160 mg TMP/800 mg SMZ PO q12h for 10-14 d
<2 months: Do not administer
>2 months: 10-20 mg TMP/kg/d PO/IV divided tid/qid for 14 d
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly patients; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine; coadministration of pyrimethamine with cotrimoxazole, an antifolic drug, may increase risk of bone marrow suppression; severe hyperkalemia has been reported with the concurrent use of ACE inhibitors and trimethoprim; cotrimoxazole and lamivudine may cause elevated lamivudine serum concentrations
Documented hypersensitivity; megaloblastic anemia due to folate deficiency; <2 mo of age; pregnant patients at term, nursing mothers
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of skin rash or sign of adverse reaction, immune hypersensitivity reaction (severe), Stevens-Johnson syndrome, or toxic epidermal necrolysis; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, people with long-term alcoholism, elderly people, those receiving anticonvulsant therapy, those with malabsorption syndrome); hemolysis may occur in people with G-6-PD deficiency; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation
Treats infections caused by susceptible gram-negative and gram-positive organisms, in addition to infections caused by susceptible Chlamydia, Rickettsia, and Mycoplasma. Was found to be effective in some nontuberculotic mycobacterial infections.
100 mg PO bid for 5-7 d
<8 years: Not recommended
>8 years: 4 mg/kg PO initially, followed by 2 mg/kg q12h
Alternatively, 200 mg PO/IV initially
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; concomitant use of vitamin A supplementation or oral retinoids (eg, isotretinoin) not recommended; additive risk of pseudotumor cerebri; simultaneous administration of cinnamon and tetracycline may slow tetracycline absorption; bacteriostatic drugs (eg, tetracyclines) may interfere with bactericidal effect of penicillin
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines; hepatitis or lupuslike syndromes may occur; autoimmune syndromes; drug-induced lupus – like syndrome, hepatitis, and vasculitis reported with long-term use; caution in preexisting renal impairment; risk of azotemia, hyperphosphatemia, and acidosis due to drug accumulation; minocycline use may result in false elevations of urinary catecholamine levels due to interference with the fluorescence test
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marine envenomations, saltwater injury, marine creature injury, exposure to saltwater life, exposure to freshwater life
Zoltan Trizna, MD, PhD, Private Practice
Zoltan Trizna, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
James J Nordlund, MD, Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine
James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.
Jeffrey Meffert, MD, Assistant Clinical Professor of Dermatology, University of Texas Health Science Center-San Antonio
Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society
Disclosure: Nothing to disclose.
Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.
William D James, MD, Paul R Gross Professor of Dermatology, University of Pennsylvania School of Medicine; Vice-Chair, Program Director, Department of Dermatology, University of Pennsylvania Health System
William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology
Disclosure: elsevier Royalty Other; american college of physicians Honoraria Other
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