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High-Risk Patients


Liver disease (including cirrhosis), alcoholism, hemochromatosis, hemolytic anemia, chronic renal failure, malignancy (including leukemia and lymphoma), diabetes, and HIV can be associated with infection and complications from V. vulnificus. Disorders leading to low gastric acidity may also increase risk. Some of these risk factors have been evaluated in epidemiologic studies. In addition, there are theories of why there is increased infection and complications related to these clinical factors (refer to Pathophysiology section below).



One case series described Vibrio infections in Florida during a 12-year period. Of 626 Vibrio cases with a well-defined illness syndrome, 138 were V. vulnificus. Underlying illnesses in these V. vulnificus cases included liver disease (11.8%), alcoholism (11.1%), diabetes (8.5%), gastrointestinal surgery (6.5%), antacid medication use (8.7%), and various immune disorders, including AIDS (2.4%) (1). These percentages are much higher than in the general population. In another case series of V. vulnificus infections, even higher percentages of high-risk underlying conditions existed: 53% of cases had liver disease, 34% were alcoholics, and 16% had diabetes (2).

Depending on the signs and symptoms (wound infection versus sepsis), risk factors may vary. As the following studies demonstrate, underlying conditions are more commonly associated with sepsis rather than wound infections.  One case control study of V. vulnificus differentiated these two clinical syndromes. Underlying conditions were more common in the sepsis group (89% versus 56%). Liver disease and general chronic illness were significantly associated with sepsis, as was oyster exposure. In the wound group, exposure to saltwater or shellfish was the only significant exposure (3). A similar study found significant association of V. vulnificus sepsis with liver disease, hemochromatosis, chronic renal failure, gastric disease, immunosuppression, and alcohol consumption. In wound infection cases, compared to controls, only injury and saltwater exposure were significantly associated with infection (4).



Cirrhotic patients often have various abnormalities in their immune systems. In addition, if portal hypertension is present, bacteria can bypass the hepatic reticuloendothelial system (5). The virulence of V. vulnificus in humans is associated with the availability of iron. Patients with increased iron stores, such as is seen in hemochromatosis, alcoholic liver disease, or hemolytic anemia, are susceptible to septicemia with V. vulnificus. The organism is unable to use transferrin-bound iron for growth; however, in patients with iron overload and transferrin saturation of 75% or higher, free iron is available for use by the organism (6). Animal studies have also demonstrated that iron can increase the growth of this bacterium (7). Other studies have shown that abnormal phagocytosis activity of neutrophils can impact the survival of this organism in blood (7). Disorders such as diabetes and HIV have been shown to be associated with defects in phagocytosis (8, 9). A laboratory model evaluating the effect of pH on V. vulnificus found that a higher pH led to increased numbers of bacteria and rapid growth of existing bacteria (10).


  1. Hlady W.G. and K.C. Klontz. 1996. The epidemiology of Vibrio infections in Florida, 1981-1993. J Inf Dis 173:1176-83.

  2. Bashin, M. 2004. Vibrio vulnificus Case Analysis 1993-2003. (unpublished report). Interstate Shellfish Sanitation Conference.

  3. Tacket C.O, F. Brenner F. and P.A. Blake. 1984. Clinical features and an epidemiological study of Vibrio vulnificus infections. J Inf Dis 149:558-561

  4. Johnston J.M., S.F. Becker, and L.M. McFarland. 1985. Vibrio vulnificus: man and the sea. JAMA 253:2850-3.

  5. Blake, PA, M.H. Merson, R. E. Weaver, D.G. Hollis and P.C. Heublein. 1979. Disease caused by a marine Vibrio: clinical characteristics and epidemiology. N Engl J Med 300:1-5.

  6. Volberg C.M., and J.L. Herrera. 1997. Vibrio vulnificus infection: an important cause of septicemia in patients with cirrhosis. South Med J. 90(10):1040-2.

  7. Hsueh, P.R., C.Y. Lin, H.J. Tang, H.C. Lee, J.W. Liu, Y.C. Liu, and Y.C. Chuang. 2004 Vibrio vulnificus in Taiwan. Emerg Infect Dis [serial on the Internet]. [cited March 28, 2005].

  8. Marhoffer, W., M. Stein, E. Maeser, and K. Federlin. 1992. Impairment of polymorphonuclear leukocyte function and metabolic control of diabetes. Diabetes Care. 15(2):256-60.

  9. Kedzierska, K., R. Azzam, P. Ellery, J. Mak, A. Jaworowski, and S.M. Crowe. 2003. Defective phagocytosis by human monocyte/macrophages following HIV-1 infection: underlying mechanisms and modulation by adjunctive cytokine therapy. J Clin Virol. 26(2):247-63.

  10. Koo, J., D.L. Marshall, and A. DePaola. 2001. Antacid increases survival of Vibrio vulnificus and Vibrio vulnificus phage in a gastrointestinal model. Appl Envir Microbiol 67:2895-2902

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Page last updated: August 18, 2017

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