Vibrio vulnificus

Vibrio vulnificus is a species of Gram-negative, motile, curved, rod-shaped bacteria of the genus Vibrio. Present in marine environments such as estuaries, brackish ponds, or coastal areas, V. vulnificus is related to V. cholerae, the causative agent of cholera.[3],[4] Infection with V. vulnificus leads to rapidly expanding cellulitis or septicemia.[5]:279 It was first isolated in 1976.[6] The capsule, made of polysaccharides, is thought to protect against phagocytosis. The observed association of the infection with liver disease (associated with increased serum iron) might be due to the capability of more virulent strains to capture iron bound to transferrin. Toxin production plays a relevant role in pathogenicity.[7]

Signs and symptoms[edit]

V. vulnificus causes an infection often incurred after eating seafood, especially raw or undercooked oysters. It does not alter the appearance, taste, or odor of oysters.[8] The bacteria can also enter the body through open wounds when swimming or wading in infected waters,[4] or by puncture wounds from the spines of fish such as tilapia or stingrays.[9]

Symptoms include vomiting, diarrhea, abdominal pain, and a blistering dermatitis sometimes mistaken for pemphigus or pemphigoid.

V. vulnificus is 80 times more likely to spread into the bloodstream in people with compromised immune systems, especially those with chronic liver disease. When this happens, severe symptoms including blistering skin lesions, septic shock, and even death can occur.[10][11] This severe infection may occur regardless of whether the infection began from contaminated food or an open wound.[11]


V. vulnificus wound infections have a mortality rate around 25%. In patients in whom the infection worsens into septicemia, typically following ingestion, the mortality rate rises to 50%. The majority of these patients die within the first 48 hours of infection. The optimal treatment is not known, but, in one retrospective study of 93 patients in Taiwan, use of a third-generation cephalosporin and a tetracycline (e.g., ceftriaxone and doxycycline, respectively) were associated with an improved outcome.[12] Prospective clinical trials are needed to confirm this finding, but in vitro data support the supposition this combination is synergistic against V. vulnificus. Likewise, the American Medical Association and the Centers for Disease Control and Prevention (CDC) recommend treating the patient with a quinolone or intravenous doxycycline with ceftazidime; this treatment regimen was first proposed and used successfully by Dr. William Abernathy of Destin, Florida. The first successful documented treatment of fulminant V. vulnificus sepsis by the CDC was patient V. B., who was diagnosed and treated in 1995 by Dr. William Abernathy at Twin Cities Hospital in Niceville, Florida. Treatment was Fortaz and intravenous Cipro and IV doxycycline, which proved successful. Prevention of secondary infections from respiratory failure and acute renal failure are crucial. Key to the diagnosis and treatment was early recognition of bullae in an immunocompromised patient with liver cirrhosis and oyster ingestion within the previous 48 hours, and request by the physician for STAT Gram stain and blood cultures for V. vulnificus.[13]

V. vulnificus often causes large, disfiguring ulcers that require extensive debridement or even amputation.

V. vulnificus is commonly found in the Gulf of Mexico, where more than dozen people have died from the infection since 1990.[14] Most deaths at that time were occurring due to fulminant sepsis either in the area of oyster harvest and ingestion or in tourists returning home. Lack of disease recognition and the risk factors, presentation, and cause were and are major obstacles to good outcome and recovery.

After the successful treatment of patient V.B. by Dr. Abernathy, the CDC and the Florida Department of Health were able to trace back the origin of the outbreak to Apalachicola Bay oysters and their harvesting in water prone to excessive growth of the organism due to warmth of the water and lack of fresh water dilution by reduced flow of the Chattahoochee River into the Apalachicola River into Apalachicola Bay. A similar situation occurred after Hurricane Katrina in New Orleans.


The worst prognosis is in those patients arriving at hospital in a state of shock. Total mortality in treated patients (ingestion and wound) is around 33%.[12]

Patients especially vulnerable are those with liver disease (especially cirrhosis and hepatitis) or immunocompromised states (cancer, bone marrow suppression, HIV, diabetes, etc.). With these cases, V. vulnificus usually enters the bloodstream, wherein it may cause fever and chills, septic shock (with sharply decreased blood pressure), and blistering skin lesions.[15] According to the CDC, about half of those who contract blood infections die.

V. vulnificus infections also disproportionately affect males; 85% of those developing endotoxic shock from the bacteria are male. Females having had an oophorectomy experienced increased mortality rates, as estrogen has been shown experimentally to have a protective effect against V. vulnificus.[16]


The pathogen was first isolated in 1976 from a series of blood culture samples submitted to the CDC in Atlanta.[6] It was described as a "lactose-positive vibrio".[6] It was subsequently given the name Beneckea vulnifica,[1] and finally Vibrio vulnificus by Farmer in 1979.[2]

Health officials clearly identified strains of V. vulnificus infections among evacuees from New Orleans due to the flooding there caused by Hurricane Katrina.[17]


  1. ^ a b Reichelt JL, Baumann P, Baumann L (October 1976). "Study of genetic relationships among marine species of the genera Beneckea and Photobacterium by means of in vitro DNA/DNA hybridization". Arch. Microbiol. 110 (1): 101–20. doi:10.1007/bf00416975. PMID 1015934. 
  2. ^ a b Farmer JJ (October 1979). "Vibrio ("Beneckea") vulnificus, the bacterium associated with sepsis, septicaemia, and the sea". Lancet 2 (8148): 903. doi:10.1016/S0140-6736(79)92715-6. PMID 90993. 
  3. ^ Oliver JD, Kaper J (2001). Vibrio species. pp. 263-300 In: Food Microbiology: Fundamentals and Frontiers. (Doyle MP et al., editors) (2nd ed.). ASM Press. ISBN 1-55581-117-5. 
  4. ^ a b Oliver JD (2005). "Wound infections caused by Vibrio vulnificus and other marine bacteria". Epidemiol Infect 133 (3): 383–91. doi:10.1017/S0950268805003894. PMC 2870261. PMID 15962544. 
  5. ^ James, William D.; Berger, Timothy G. (2006). Andrews' Diseases of the Skin: Clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0. 
  6. ^ a b c Hollis DG, Weaver RE, Baker CN, Thornsberry C (April 1976). "Halophilic Vibrio species isolated from blood cultures" (PDF). J. Clin. Microbiol. 3 (4): 425–31. PMC 274318. PMID 1262454. 
  7. ^ Oxford handbook of Infect Dis and Microbiol, 2009
  8. ^ "Vibrio vulnificus General Information Frequently Asked Questions". Centers for Disease Control. Retrieved April 19, 2013. 
  9. ^
  10. ^ "Vibrio vulnificus". NCBI Genome Project. Retrieved 2005-09-01. 
  11. ^ a b "Vibrio vulnificus General Information Frequently Asked Questions What type of illness does V. vulnificus cause?". Centers for Disease Control. Retrieved April 19, 2013. 
  12. ^ a b Liu JW, Lee IK, Tang HJ et al. (2006). "Prognostic factors and antibiotics in Vibrio vulnificus septicemia". Archives of Internal Medicine 166 (19): 2117–23. doi:10.1001/archinte.166.19.2117. PMID 17060542. 
  13. ^
  14. ^
  15. ^ Oliver JD, Kaper J (2005). Vibrio vulnificus. In: Oceans and Health: Pathogens in the Marine Environment. (Belken SS, Colwell RR, editors) (2nd ed.). Springer Science. ISBN 0-387-23708-9. 
  16. ^ Merkel SM, Alexander S, Zufall E, Oliver JD, Huet-Hudson YM (2001). "Essential Role for Estrogen in Protection against Vibrio vulnificus-Induced Endotoxic Shock". Infection and Immunity 69 (10): 6119–22. doi:10.1128/IAI.69.10.6119-6122.2001. PMC 98741. PMID 11553550. 
  17. ^ Gold, Scott (September 6, 2005). "Newest Peril from Flooding Is Disease". Los Angeles Times. 
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