The Chief Resident Presenting with a Coral Cut Injury

Case Report

By Marc A. Ciampi, MD, and Andre N. Sofair, MD, MPH

A 30-year-old previously healthy male presented with pain in his left knee and left groin. Five days prior to presentation, he had scraped his exposed left knee against a large brain coral while snorkeling in the Caribbean, near the island of Aruba. He noted local erythema, slight pruritus, and a small abrasion. After irrigating the wound, the patient used topical antibacterial cream daily. He remained afebrile with no evidence of local or systemic complaints. He denied significant pain, increasing erythema, or wound drainage. On the day of presentation, the patient developed notable groin tenderness and mild left-sided lumbar pain along with increasing knee pain. He denied fever, chills, night sweats, or fatigue. He had no significant past medical history and was taking no medications. He had no known allergies and denied recent ingestion of shellfish.

The patient was afebrile with normal vital signs and general appearance. Physical examination of his knee was notable for the presence of a raised, slightly erythematous rash showing a dermatograph of brain coral, and a 2 mm abrasion with no significant drainage or fluctuance. The joint was normal with no evidence of effusion or inflammation. The left leg revealed tender inguinal lymphadenopathy without lymphangitis. Abdominal examination showed mild left upper quadrant and left costovertebral angle tenderness; a spleen tip was not palpated.

He was empirically started on an oral fluoroquinolone antibiotic, levofloxacin, to treat his soft tissue infection. Oral doxycycline was added one day later to ensure adequate coverage of various marine microorganisms. He was treated for 10 days with resolution of his groin tenderness and back pain after two days of therapy. Over three weeks, the rash resolved completely without complications.

Discussion

Contact with coral or "coral cuts" may produce significant and sometimes dramatic cutaneous reactions.1,2 Manifestations include localized erythema, urticara, and occasional pruritus.3 The local reaction can be a response to coral nematocysts, contamination of the wound site with microparticulate coral and calcium carbonate, possible bacterial infection, or toxin effects.

Although on a worldwide basis staphylococci and streptococci remain the most common causes of soft tissue infections, vibrios, and some Aeromonas spp. are virulent waterborne organisms that may infect wounds sustained in a marine environment.1-8 Erysipelothrix rhusiopathiae, coliforms such as Escherichia coli, and Mycobacterium marinum, M. balnei, or Pseudomonas spp. are also capable of producing localized infections after exposure to salt water.6 Wound infections acquired in this environment may also be polymicrobial.7,9

Ecology and Epidemiology

The halophilic Vibrio spp. are naturally free-living aerobic inhabitants of marine environments. These organisms have been found in Europe, Asia, Australia, South America, and North America.10 In North America, they have been recovered from the waters of the Gulf coast, the entire East Coast from Florida to Maine, the California and Washington State coasts, and from the waters around Hawaii. Halophilic vibrios have been found in both water and marine sediments, adherent to plankton, or absorbed onto mollusks and crustaceans.11 Vibrio spp. are taken up by filter-feeding molluscs such as oysters, clams, mussels, and scallops achieving concentrations as high as 106 bacteria per gram of oyster during periods of warm water temperatures. Bacteria are also found in the intestines of some estuarine fish, which may transport them between oyster beds or serve as a source of wound infections.12

Vibrio spp. reside in ocean water or marine estuaries within a wide range of salinity (1-34 parts per thousand). Organisms have been isolated from brackish lakes and even from the Great Salt Lake.13 A salinity greater than 25 parts per thousand has adverse effects on their survival.

Intolerant of cold conditions, Vibrio spp. thrive during the summer and fall months, but they may also survive the winter months in marine sediment.5,14-18 Vibrio spp. are found in zones where there is decreased dissolved oxygen concentrations, possibly reflecting increased nutrient concentrations in such areas. Vibrios are rarely found in the open ocean, likely due to colder water temperatures, the absence of nutrients, the higher hydrostatic pressures, and the relatively higher salinity.18

Vibrio infections are acquired either by the consumption of contaminated food and water or through skin and soft tissue injuries.4 The primary food sources for acquisition are raw/undercooked oysters or other seafoods.4,19 In those with skin and soft-tissue infections, nearly all report prior recreational or occupational exposure to sea water or marine organisms.9

Clinical Presentations

Three major presenting clinical syndromes have been described for vibrios including gastroenteritis, soft tissue infection, and septicemia. There have been additional case reports of vibrio-associated otitis media, pneumonitis, keratitis, meningitis, and endometritis.4,13

Soft tissue infections caused by noncholera vibrios may present as one of two distinct clinical entities, primary vibrio cellulitis, or secondary cellulitis following primary bacteremia.4 Direct cutaneous inoculation from abrasions, lacerations, or puncture wounds may result in primary vibrio cellulitis. With the exception of V. cholerae O1, primary vibrio cellulitis has been associated with all known Vibrio spp.1,5,20-23 In hospitalized patients with vibrio wound infections, the majority are caused by V. vulnificus (43%), followed by V. parahaemolyticus (29%) and V. alginolyticus (18%). The case fatality for V. vulnificus was 11%, and for V. parahaemolyticus it was 5%.9

Wound infections range from mild, limited disease to rapidly progressive, necrotizing infections.9,10,13,19 Virulence may be related to the organisms’ capsular polysaccharide and lipopolysaccharide. Many vibrios also produce degradative toxins and enzymes. These include chitinases, which allow vibrios to colonize the exoskeletons of marine zooplankton, as well as hemolysins and metalloproteases, which break down tissues at the site of colonization. Vibrios also produce siderophores that scavenge iron from host transport proteins, transferrin and lactoferrin. This may account for the increased virulence of Vibrio spp. in patients with iron overload states.12

Cellulitis usually occurs within 24-48 hours but can occur as early as four hours, or as late as 12 days after exposure.20,24,25 Fever occurs in 45-80% of primary cellulitis cases.4 Infected wounds are usually erythematous or ecchymotic, swollen and notably tender with little to no purulent discharge.4,24 Vesicles or bullae with secondary necrotic centers and necrotizing fasciitis have also been described.9,12,16,24,26

Patients with a history of liver disease, renal disease, chronic illness or immunodeficient states are at considerably increased risk of generalized sepsis following cellulitis.4,9,19,20,27-30 In cirrhosis, it has been suggested that porto-systemic shunting may allow vibrios to bypass the hepatic reticuloendothelial system. Additionally, liver disease predisposes such patients to complement deficiencies, impaired chemotaxis, and phagocytosis.31 Iron overload states also contribute to fulminant vibrio infection. Increased bioavailability of free iron, found in patients with hemochromatosis, may stimulate bacterial growth and metabolism. In addition, iron overload may impair normal host phagocytic activity, increasing susceptibility to infections.12,31,32 Septicemia occurs in 15% of patients with primary soft tissue infections and contributes to the high case-fatality rates. In those with bacteremia, the rate is 32%; without hematogenous involvement, the case fatality rate is only 1%.9

Secondary cellulitis in the setting of primary septicemia associated with Vibrio spp. carries a 32-50% mortality rate.4,9,10,19,33 In these cases, there is usually a preceding history of having eaten raw/undercooked oysters or other seafood ingestion.4,19 These individuals develop generalized, metastatic, macular, or papular lesions in the setting of primary bacteremia. Culture-positive cutaneous lesions have been reported with bacteremia caused by V. vulnificus, V. cholerae non-O1, V. parahaemolyticus, and rarely V. alginolyticus.4,34

Treatment of Coral-related Soft Tissue Infection

Local wound care should include soap and water, followed by aggressive irrigation and debridement with saline solution and hydrogen peroxide to remove foreign material from the site and prevent secondary infection or granuloma formation.35

Given the potential polymicrobial nature of coral-related infections, broad-spectrum antibiotics should be considered. For those with obvious cellulitis, or as a prophylactic measure in those with abnormal immune systems, antibiotics with a spectrum of activity against staphylococci and streptococci should be used. In addition, antibiotics that are effective against halophilic Vibrio spp. should be administered.

Vibrio spp. frequently produce beta-lactamases and are often resistant to various beta-lactam antibiotics. The beta-lactam inhibitor, sulbactam, does not completely render these organisms susceptible to ampicillin. They are often resistant to cephalothin, cefuroxime, and cefoperazone, but sensitive to cefotaxime, ceftazidime, aztreonam, and imipenem.

Although the fluoroquinolones, ofloxacin and norfloxacin, are effective against these organisms, ciprofloxacin appears to have the greatest activity with an MIC90 of approximately 0.25 mg/L. Trimethoprim/sulfamethoxazole is effective, as are the tetracyclines and chloramphenicol.36 For those with devitalized tissue or fasciitis, surgical intervention is indicated. This may be particularly important when dealing with infections caused by Vibrio damsela, which were reviewed in the July/August issue of TMA Update for our readers.16,21,37 (Dr. Ciampi is a Clinical Instructor in Medicine at Yale University and Dr. Sofair is an Assistant Clinical Professor of Medicine at Yale University with the Emerging Pathogens Program, New Haven, Conn.) 

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