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Vibrio vulnificus infections
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Vibrio vulnificus infections
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Literature review current through: Nov 2017. | This topic last updated: Mar 10, 2017.

INTRODUCTION — Vibrio vulnificus is a gram-negative bacterium that can cause serious wound infections, septicemia, and diarrhea [1-3]. It is the leading cause of shellfish-associated deaths in the United States. Infections due to V. vulnificus are most common in individuals who have chronic, underlying illness; individuals with liver disease or hemochromatosis are at greatest risk.

The pathogenesis, epidemiology, clinical features, diagnosis, and treatment of V. vulnificus infections will be reviewed here. The disease cholera, caused by "epidemic" strains of Vibrio cholerae, infections caused by Vibrio parahaemolyticus, and illnesses associated with other Vibrio strains and species are discussed separately. (See "Overview of cholera" and "Vibrio parahaemolyticus infections" and "Infections due to non-O1/O139 Vibrio cholerae".)

EPIDEMIOLOGY — V. vulnificus exists as a free-living bacterium inhabiting estuarine (eg, saltwater marshes/wetlands, river estuaries) or marine environments. Three biotypes are recognized: biotype 1, which accounts for almost all human infections; biotype 2, which consists primarily of eel pathogens; and biotype 3, an apparent hybrid of biotypes 1 and 2 that has been described in tilapia-associated wound infections in Israel [4].

V. vulnificus accounts for approximately eight percent of the aerobic bacteria in the Chesapeake Bay [5]. Counts peak during summer and late fall, when water temperatures are highest. Reductions in counts have been correlated with drops in salinity of the water, such as occurred in 2011 in Louisiana when opening of the Bonne Carre spillway associated with flooding of the Mississippi river led to fresh water intrusion into estuarine areas [6].

Filter-feeding shellfish such as oysters concentrate bacteria and may have counts of V. vulnificus up to two orders of magnitude greater than those in the surrounding water. V. vulnificus can be isolated from virtually all oysters harvested in the Chesapeake Bay and the United States Gulf Coast when water temperatures exceed 20ºC [5,7]. Over 90 percent of patients with "primary" V. vulnificus septicemia (ie, septicemia without an obvious source such as a wound) report having consumed raw oysters prior to the onset of illness [8].

Wound infections generally result from exposure of a wound to salt or brackish water containing the organism, and most often occur in the setting of handling seafood or in association with recreational water activities [9,10]. As with oyster or other food vehicle associated infections, wound infections are most common during warm summer months. In August and September 2005 after Hurricane Katrina, 14 V. vulnificus wound-associated illnesses were identified; three patients died [11]. Most of these cases occurred among individuals with predisposing medical conditions and wounds exposed to flood waters. In such predisposed individuals (see risk factors below), even minor skin penetrations can result in serious wound infections. In one report, a fish farm hatchery manager with diabetes mellitus and nonalcoholic steatohepatitis developed V. vulnificus necrotizing fasciitis following acupuncture, presumably in the setting of skin contamination [12].

Wound infections and bacteremia have been reported due to biogroup 3 strains associated with injuries sustained while handling live tilapia fish from aquaculture ponds in Israel [4,13,14]. Initial reports of illness were linked with unusually high temperatures in the region [15].

Individuals with the following conditions are at increased risk for serious infection with V. vulnificus [2,9,16]:

Alcoholic cirrhosis (present in 31 to 43 percent of patients with primary septicemia)

Underlying liver disease including cirrhosis and chronic hepatitis (24 to 31 percent of patients)

Alcohol abuse without documented liver disease (12 to 27 percent of patients)

Hereditary hemochromatosis (12 percent of patients)

Chronic diseases such as diabetes mellitus, rheumatoid arthritis, thalassemia major, chronic renal failure, and lymphoma (7 to 8 percent of patients)

Interestingly, men, and particularly older men, appear to be at much greater risk for serious infection than women [17].

In population-based studies in coastal areas in the United States, the estimated incidence of V. vulnificus infections is approximately 0.5/100,000 population per year [18-20]. The estimated national incidence, based on reports to surveillance programs, is substantially lower at 0.04 to 0.05 per 100,000 persons per year [21]. However, this rate has increased dramatically since 1996. In 2014, 124 V. vulnificus cases were reported to the Centers for Disease Control and Prevention; among these individuals, 79 percent were hospitalized and 18 percent died [22].

PATHOGENESIS — Virulence of V. vulnificus has been associated with three major factors: (1) production of an anti-phagocytic polysaccharide capsule [23]; (2) the RtxA toxin [24]; and (3) iron availability and iron acquisition systems [25-27].

Capsule — V. vulnificus produces a capsular polysaccharide that provides protection against phagocytosis and opsonization [23]. Strains are able to undergo phase variation, shifting between encapsulated forms (opaque colony morphology) and unencapsulated forms (translucent colony morphology). Unencapsulated strains are avirulent in mouse models. When these strains are taken up by oysters, there is a high rate of shift to the capsulated phenotype, suggesting that oyster passage selects for the encapsulated, virulent form of the organism [28].

Anticapsular antibodies are protective, but appear to be type-specific rather than cross-reactive [29]. The type-specific nature of protective antibodies is significant since V. vulnificus has great diversity in capsular types. In one study of 120 strains, for example, 96 different capsular types ("carbotypes") were identified [30].

V. vulnificus contains a lipopolysaccharide (LPS) but, in contrast to Escherichia coli and other members of the Enterobacteriaceae, the LPS of V. vulnificus is not a strong trigger for release of tumor necrosis factor (TNF)-alpha and other shock-related cytokines. However, capsular polysaccharide itself may directly trigger some cytokine responses, contributing to the development of the shock syndrome [31]; TNF-alpha was detected in mice up to 12 hours after inoculation of an encapsulated V. vulnificus strain, while an unencapsulated strain was rapidly cleared. Both capsular polysaccharide and LPS provoked cytokine release in vitro from human peripheral blood mononuclear cells.

Toxins — V. vulnificus produces a variety of extracellular toxins, including both a hemolysin and protease, although deletion of these toxins from the bacterium does not affect virulence in mouse models.

Virulence has been linked with RtxA1, a toxin homologous to the pore-forming RTX toxins found in V. cholerae and other gram-negative bacteria. This toxin appears to act via Nox1 to induce significant reactive oxygen species generation in intestinal epithelial cells, leading to cell death and epithelial cell disruption [24,32].

Iron — Growth of V. vulnificus is dependent in part upon the availability of iron [25-27]. Growth of the organism in human serum is related directly to the percentage saturation of transferrin with iron [25]. When transferrin iron saturation exceeds 70 percent, growth of the bacterium is nearly exponential.

The relationship between iron and virulence in V. vulnificus may account for the enhanced susceptibility to serious infections with this organism in patients with hemochromatosis [33,34]. However, most patients with serious V. vulnificus infections have normal iron and iron saturation levels. (See "Clinical manifestations and diagnosis of hereditary hemochromatosis", section on 'Susceptibility to specific infections'.)

Differentiating strains — The number of reported V. vulnificus cases is relatively low, in spite of the frequency with which humans are exposed to V. vulnificus in oysters and in contact with estuarine water (even taking into account differences in host susceptibility). This has led to the hypothesis that certain strain subsets are more likely than others to cause human disease. However, it has not been possible to identify a single V. vulnificus virulence factor that is almost exclusively present in clinical isolates (in contrast to V. parahaemolyticus).

Certain carbotypes of V. vulnificus may be more likely than others to cause human illness [35]. Clustering of human isolates within specific subgroups has also been noted based on ribotyping, pulsed field gel electrophoresis (PFGE), randomly amplified polymorphic DNA (RAPD) PCR techniques, and sequence polymorphism of 16S rRNA [36-39].

CLINICAL MANIFESTATIONS — V. vulnificus causes wound infections and "primary septicemia" (septicemia without a clearly defined source of infection, such as a wound) [1,2,9,16,18,19]. Wound infections may be acquired during handling of shellfish or fish, or after exposure of a preexisting wound to estuarine water. In one case series from Korea, the incubation period for septicemia ranged from three hours to six days [40].

V. vulnificus has also been associated with occurrence of watery diarrhea and other symptoms of gastroenteritis [41]. An etiologic role is difficult to establish when the organism is isolated from stool samples since the bacterium is ubiquitous in both water and shellfish, and has been isolated from stool samples of asymptomatic persons.

Wound infections — V. vulnificus may contaminate wounds exposed to estuarine waters, shellfish, or fish. Typical examples include hand injuries related to opening oysters or leg lacerations related to entering, exiting, or launching boats. The cellulitis is usually mild. However, in high-risk individuals, the infection may spread rapidly, producing severe myositis and necrotizing fasciitis reminiscent of gas gangrene (picture 1).

Primary septicemia — Primary V. vulnificus septicemia is associated with ingestion of raw or undercooked shellfish, particularly raw oysters. Patients with primary septicemia generally have underlying liver disease, alcoholism, hereditary hemochromatosis, or a chronic disease as noted above.

Approximately one-third of patients with primary septicemia present in shock or become hypotensive within 12 hours of hospital admission. Three-fourths of patients have distinctive bullous skin lesions (picture 2). Thrombocytopenia is common, and often there is evidence of disseminated intravascular coagulation. Complications such as gastrointestinal bleeding can occur.

Primary V. vulnificus septicemia is a serious illness with a high mortality rate. Among all reported foodborne infections in the United States, V. vulnificus is associated with the highest case fatality rate (39 percent) [42]. Mortality rates exceeding 40 percent have been reported in case series, with a case fatality rate of more than 90 percent among those who are hypotensive when they present for medical care [2,9,16,43]. Advanced liver disease with model for end-stage liver disease (MELD) scores of >20 has also been associated with high mortality (64-fold increased odds of death), as have hypoalbuminemia and severe anemia [44].

Persons who survive the acute shock event often require prolonged hospitalization in intensive care, with complications resulting from multiorgan system failure. While there may be complete recovery from the actual V. vulnificus infection, there may be ongoing morbidity due to associated organ system failure.

DIAGNOSIS — Given the potential severity of the infection, a presumptive diagnosis of V. vulnificus septicemia should be made in any person with fever, hypotension, or symptoms suggestive of septic shock, characteristic bullous skin lesions, and risk factors for acquiring infection as noted above. The infection should also be suspected in persons from these risk groups who have rapidly progressive wound infections associated with exposure to estuarine waters.

The diagnosis is confirmed by culture. V. vulnificus will grow without difficulty in standard blood culture media or on nonselective media (such as blood agar) routinely used for wound cultures; identification and speciation of the organism is possible via any standard, commercially available microbiology identification system.

Isolation of the organism from stool generally requires the use of a specific selective culture media (thiosulfate citrate bile-salts sucrose [TCBS]), on which V. vulnificus, V. parahaemolyticus, and some other Vibrio species produce blue-green colonies, in contrast to the yellow colonies produced by V. cholerae.

THERAPY

Severe infections — Case fatality rates for V. vulnificus septicemia and serious wound infections have been shown to increase with greater delays between onset of illness and initiation of antibiotic treatment [9,18]. Thus, patients with a presumptive diagnosis of V. vulnificus septicemia should be started immediately on antibiotic therapy and managed aggressively in an intensive care unit to minimize the possible consequences of hypotension, septic shock, and the risk of multiorgan system failure.

We favor treatment of patients with septicemia or serious wound infections using combination therapy with either minocycline or doxycycline (100 mg orally twice daily), plus either cefotaxime (2 g intravenously every eight hours) or ceftriaxone (1 g intravenously daily); doses should be appropriately adjusted for underlying renal or hepatic disease. The combination of cefotaxime and ciprofloxacin is also likely effective [45]. Fluoroquinolone monotherapy (ie, levofloxacin 750 mg orally or intravenously once daily) is another alternative.

In high-risk patients, more serious wound infections may require aggressive debridement in addition to parenteral antibiotics. In a series of 121 patients in Taiwan who presented with necrotizing fasciitis, surgery within 12 hours of admission resulted in a significant improvement in survival [46]. Among 423 V. vulnificus wound infections reported in the United States, 10 percent of patients required amputation of some type [9].

Clinical data supporting the above antibiotic regimen include a retrospective study involving 93 patients with V. vulnificus septicemia and hemorrhagic bullous cutaneous lesions that suggested combination antibiotic therapy with a third-generation cephalosporin and a tetracycline more effectively reduced mortality than a first- or second-generation cephalosporin plus an aminoglycoside (odds ratio 0.04; 95% CI 0.01-0.19) [43]. Similarly, in a retrospective study of 89 patients with histologically and microbiologically confirmed V. vulnificus necrotizing fasciitis who underwent prompt surgical debridement, those treated with either a third-generation cephalosporin plus minocycline, or ciprofloxacin with or without minocycline had lower mortality rates than those who received a third-generation cephalosporin alone (14, 14, and 61 percent, respectively) [47]. In one case report, the combination of tigecycline and cefpirome was reported to be efficacious as "salvage" therapy in a child with V. vulnificus necrotizing fasciitis who was not responding well clinically to ceftazidime and minocycline [48].

In vitro and in vivo studies in mice have demonstrated an apparent synergism between cefotaxime and minocycline in the treatment of serious V. vulnificus infections [49]. Subsequent mouse studies showed comparable survival with fluoroquinolones [50] and supported the combination of ciprofloxacin and cefotaxime [45].

Mild infections — Mild wound infections in patients who do not have significant underlying diseases generally respond well to local care and oral antibiotics (such as a tetracycline or a fluoroquinolone). Duration of therapy is dictated by severity of the initial infection and clinical response; patients with mild to moderate infections generally respond to five to seven days of antibiotics.

PREVENTION — Given the high mortality associated with V. vulnificus infection, individuals in high-risk groups should avoid eating raw or undercooked shellfish, particularly oysters. Post-harvest treatments (mild heat treatment, freezing, hydrostatic pressure) can reduce V. vulnificus counts in raw oysters, potentially reducing disease risk [51]. Individuals with increased susceptibility to V. vulnificus infections should also avoid situations in which estuarine-associated wounds are likely to occur. Should such a wound occur, there are no specific preventive measures beyond basic wound care. However, immunocompromised patients and those with liver disease, in particular, should be advised that if any signs or symptoms of infection (eg, fever, erythema, tenderness, or drainage) develop, they should contact their clinician or present to medical care immediately for further evaluation and initiation of antibiotics. (See 'Therapy' above.)

SUMMARY AND RECOMMENDATIONS

Vibrio vulnificus is a gram-negative bacterium that can cause serious wound infections, septicemia, and diarrhea. It is the leading cause of shellfish-associated deaths in the United States. Serious infections due to V. vulnificus are most common in individuals who have chronic, underlying illness; those with liver disease or hemochromatosis are at greatest risk. (See 'Introduction' above and 'Clinical manifestations' above.)

V. vulnificus can be isolated from virtually all oysters harvested in the Chesapeake Bay and the United States Gulf Coast when water temperatures exceed 20ºC. Over 90 percent of patients with "primary" V. vulnificus septicemia (ie, septicemia without an obvious source such as a wound) report having consumed raw oysters prior to the onset of illness. (See 'Epidemiology' above.)

Growth of V. vulnificus in human serum is related to the percentage saturation of transferrin with iron. The relationship between iron and virulence in V. vulnificus may account for the enhanced susceptibility to serious infections in patients with hemochromatosis. However, most patients with serious V. vulnificus infections have normal iron and iron saturation levels. (See 'Iron' above.)

Wound infections generally result from exposure of a wound to salt or brackish water containing the organism, and most often occur in the setting of handling seafood or in association with recreational water activities. In high-risk individuals, the infection may spread rapidly, producing severe myositis and necrotizing fasciitis reminiscent of gas gangrene (picture 1). (See 'Epidemiology' above and 'Wound infections' above.)

Primary V. vulnificus septicemia is a serious illness with a high mortality rate. Approximately one third of patients with primary septicemia present in shock or become hypotensive within 12 hours of hospital admission. Three-fourths of patients have distinctive bullous skin lesions (picture 2). Thrombocytopenia is common, and often there is evidence of disseminated intravascular coagulation. (See 'Primary septicemia' above.)

A presumptive diagnosis of V. vulnificus septicemia should be made in any person with fever, hypotension, or symptoms of septic shock, characteristic bullous skin lesions, and risk factors for infection. The diagnosis is confirmed by culture; V. vulnificus will grow without difficulty in standard media. Isolation of the organism from stool generally requires the use of a specific selective culture media (thiosulfate citrate bile-salts sucrose [TCBS]). (See 'Diagnosis' above.)

Patients with a presumptive diagnosis of V. vulnificus septicemia should be started immediately on antibiotic therapy and managed aggressively in an intensive care unit. We suggest treatment with a tetracycline plus a third-generation cephalosporin (Grade 2C). Mild wound infections in patients who do not have significant underlying diseases generally respond well to local care and oral antibiotics; we suggest a tetracycline or fluoroquinolone (Grade 2C). (See 'Therapy' above.)

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REFERENCES

  1. Morris JG Jr, Black RE. Cholera and other vibrioses in the United States. N Engl J Med 1985; 312:343.
  2. Blake PA, Merson MH, Weaver RE, et al. Disease caused by a marine Vibrio. Clinical characteristics and epidemiology. N Engl J Med 1979; 300:1.
  3. Daniels NA. Vibrio vulnificus oysters: pearls and perils. Clin Infect Dis 2011; 52:788.
  4. Bisharat N, Cohen DI, Harding RM, et al. Hybrid Vibrio vulnificus. Emerg Infect Dis 2005; 11:30.
  5. Wright AC, Hill RT, Johnson JA, et al. Distribution of Vibrio vulnificus in the Chesapeake Bay. Appl Environ Microbiol 1996; 62:717.
  6. Griffitt KJ, Grimes DJ. Abundance and distribution of Vibrio cholerae, V. parahaemolyticus, and V. vulnificus following a major freshwater intrusion into the Mississippi Sound. Microb Ecol 2013; 65:578.
  7. Motes ML, DePaola A, Cook DW, et al. Influence of water temperature and salinity on Vibrio vulnificus in Northern Gulf and Atlantic Coast oysters (Crassostrea virginica). Appl Environ Microbiol 1998; 64:1459.
  8. Jones MK, Oliver JD. Vibrio vulnificus: disease and pathogenesis. Infect Immun 2009; 77:1723.
  9. Dechet AM, Yu PA, Koram N, Painter J. Nonfoodborne Vibrio infections: an important cause of morbidity and mortality in the United States, 1997-2006. Clin Infect Dis 2008; 46:970.
  10. Yoder JS, Hlavsa MC, Craun GF, et al. Surveillance for waterborne disease and outbreaks associated with recreational water use and other aquatic facility-associated health events--United States, 2005-2006. MMWR Surveill Summ 2008; 57:1.
  11. Centers for Disease Control and Prevention (CDC). Vibrio illnesses after Hurricane Katrina--multiple states, August-September 2005. MMWR Morb Mortal Wkly Rep 2005; 54:928.
  12. Kotton Y, Soboh S, Bisharat N. Vibrio Vulnificus Necrotizing Fasciitis Associated with Acupuncture. Infect Dis Rep 2015; 7:5901.
  13. Bisharat N, Agmon V, Finkelstein R, et al. Clinical, epidemiological, and microbiological features of Vibrio vulnificus biogroup 3 causing outbreaks of wound infection and bacteraemia in Israel. Israel Vibrio Study Group. Lancet 1999; 354:1421.
  14. Broza YY, Danin-Poleg Y, Lerner L, et al. Epidemiologic study of Vibrio vulnificus infections by using variable number tandem repeats. Emerg Infect Dis 2009; 15:1282.
  15. Paz S, Bisharat N, Paz E, et al. Climate change and the emergence of Vibrio vulnificus disease in Israel. Environ Res 2007; 103:390.
  16. Tacket CO, Brenner F, Blake PA. Clinical features and an epidemiological study of Vibrio vulnificus infections. J Infect Dis 1984; 149:558.
  17. Lee SH, Chung BH, Lee WC. Retrospective analysis of epidemiological aspects of Vibrio vulnificus infections in Korea in 2001-2010. Jpn J Infect Dis 2013; 66:331.
  18. Klontz KC, Lieb S, Schreiber M, et al. Syndromes of Vibrio vulnificus infections. Clinical and epidemiologic features in Florida cases, 1981-1987. Ann Intern Med 1988; 109:318.
  19. Johnston JM, Becker SF, McFarland LM. Vibrio vulnificus. Man and the sea. JAMA 1985; 253:2850.
  20. Hoge CW, Watsky D, Peeler RN, et al. Epidemiology and spectrum of Vibrio infections in a Chesapeake Bay community. J Infect Dis 1989; 160:985.
  21. Newton A, Kendall M, Vugia DJ, et al. Increasing rates of vibriosis in the United States, 1996-2010: review of surveillance data from 2 systems. Clin Infect Dis 2012; 54 Suppl 5:S391.
  22. CDC. National Enteric Disease Surveillance: COVIS Annual Summary, 2014. www.cdc.gov/nationalsurveillance/pdfs/covis-annual-summary-2014-508c.pdf (Accessed on February 22, 2017).
  23. Wright AC, Simpson LM, Oliver JD, Morris JG Jr. Phenotypic evaluation of acapsular transposon mutants of Vibrio vulnificus. Infect Immun 1990; 58:1769.
  24. Chung KJ, Cho EJ, Kim MK, et al. RtxA1-induced expression of the small GTPase Rac2 plays a key role in the pathogenicity of Vibrio vulnificus. J Infect Dis 2010; 201:97.
  25. Brennt CE, Wright AC, Dutta SK, Morris JG Jr. Growth of Vibrio vulnificus in serum from alcoholics: association with high transferrin iron saturation. J Infect Dis 1991; 164:1030.
  26. Kim CM, Park RY, Choi MH, et al. Ferrophilic characteristics of Vibrio vulnificus and potential usefulness of iron chelation therapy. J Infect Dis 2007; 195:90.
  27. Kim CM, Park YJ, Shin SH. A widespread deferoxamine-mediated iron-uptake system in Vibrio vulnificus. J Infect Dis 2007; 196:1537.
  28. Srivastava M, Tucker MS, Gulig PA, Wright AC. Phase variation, capsular polysaccharide, pilus and flagella contribute to uptake of Vibrio vulnificus by the Eastern oyster (Crassostrea virginica). Environ Microbiol 2009; 11:1934.
  29. Devi SJ, Hayat U, Powell JL, Morris JG Jr. Preclinical immunoprophylactic and immunotherapeutic efficacy of antisera to capsular polysaccharide-tetanus toxoid conjugate vaccines of Vibrio vulnificus. Infect Immun 1996; 64:2220.
  30. Bush CA, Patel P, Gunawardena S, et al. Classification of Vibrio vulnificus strains by the carbohydrate composition of their capsular polysaccharides. Anal Biochem 1997; 250:186.
  31. Powell JL, Wright AC, Wasserman SS, et al. Release of tumor necrosis factor alpha in response to Vibrio vulnificus capsular polysaccharide in in vivo and in vitro models. Infect Immun 1997; 65:3713.
  32. Gavin HE, Beubier NT, Satchell KJ. The Effector Domain Region of the Vibrio vulnificus MARTX Toxin Confers Biphasic Epithelial Barrier Disruption and Is Essential for Systemic Spread from the Intestine. PLoS Pathog 2017; 13:e1006119.
  33. Bullen JJ, Spalding PB, Ward CG, Gutteridge JM. Hemochromatosis, iron and septicemia caused by Vibrio vulnificus. Arch Intern Med 1991; 151:1606.
  34. Gerhard GS, Levin KA, Price Goldstein J, et al. Vibrio vulnificus septicemia in a patient with the hemochromatosis HFE C282Y mutation. Arch Pathol Lab Med 2001; 125:1107.
  35. Hayat U, Reddy GP, Bush CA, et al. Capsular types of Vibrio vulnificus: an analysis of strains from clinical and environmental sources. J Infect Dis 1993; 168:758.
  36. Tamplin ML, Jackson JK, Buchrieser C, et al. Pulsed-field gel electrophoresis and ribotype profiles of clinical and environmental Vibrio vulnificus isolates. Appl Environ Microbiol 1996; 62:3572.
  37. Jackson JK, Murphree RL, Tamplin ML. Evidence that mortality from Vibrio vulnificus infection results from single strains among heterogeneous populations in shellfish. J Clin Microbiol 1997; 35:2098.
  38. Nilsson WB, Paranjype RN, DePaola A, Strom MS. Sequence polymorphism of the 16S rRNA gene of Vibrio vulnificus is a possible indicator of strain virulence. J Clin Microbiol 2003; 41:442.
  39. Rosche TM, Yano Y, Oliver JD. A rapid and simple PCR analysis indicates there are two subgroups of Vibrio vulnificus which correlate with clinical or environmental isolation. Microbiol Immunol 2005; 49:381.
  40. Park SD, Shon HS, Joh NJ. Vibrio vulnificus septicemia in Korea: clinical and epidemiologic findings in seventy patients. J Am Acad Dermatol 1991; 24:397.
  41. Johnston JM, Becker SF, McFarland LM. Gastroenteritis in patients with stool isolates of Vibrio vulnificus. Am J Med 1986; 80:336.
  42. Mead PS, Slutsker L, Dietz V, et al. Food-related illness and death in the United States. Emerg Infect Dis 1999; 5:607.
  43. Liu JW, Lee IK, Tang HJ, et al. Prognostic factors and antibiotics in Vibrio vulnificus septicemia. Arch Intern Med 2006; 166:2117.
  44. Huang KC, Tsai YH, Huang KC, Lee MS. Model for end-stage liver disease (MELD) score as a predictor and monitor of mortality in patients with Vibrio vulnificus necrotizing skin and soft tissue infections. PLoS Negl Trop Dis 2015; 9:e0003720.
  45. Jang HC, Choi SM, Kim HK, et al. In vivo efficacy of the combination of ciprofloxacin and cefotaxime against Vibrio vulnificus sepsis. PLoS One 2014; 9:e101118.
  46. Chao WN, Tsai CF, Chang HR, et al. Impact of timing of surgery on outcome of Vibrio vulnificus-related necrotizing fasciitis. Am J Surg 2013; 206:32.
  47. Chen SC, Lee YT, Tsai SJ, et al. Antibiotic therapy for necrotizing fasciitis caused by Vibrio vulnificus: retrospective analysis of an 8 year period. J Antimicrob Chemother 2012; 67:488.
  48. Lin YS, Hung MH, Chen CC, et al. Tigecycline salvage therapy for necrotizing fasciitis caused by Vibrio vulnificus: Case report in a child. J Microbiol Immunol Infect 2016; 49:138.
  49. Chuang YC, Ko WC, Wang ST, et al. Minocycline and cefotaxime in the treatment of experimental murine Vibrio vulnificus infection. Antimicrob Agents Chemother 1998; 42:1319.
  50. Tang HJ, Chang MC, Ko WC, et al. In vitro and in vivo activities of newer fluoroquinolones against Vibrio vulnificus. Antimicrob Agents Chemother 2002; 46:3580.
  51. Depaola A, Jones JL, Noe KE, et al. Survey of postharvest-processed oysters in the United States for levels of Vibrio vulnificus and Vibrio parahaemolyticus. J Food Prot 2009; 72:2110.
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