eMedicine Specialties > Infectious Diseases > Bacterial Infections

Vibrio Infections

Author: Hoi Ho, MD, Associate Dean for Faculty Affairs and Development, Professor, Department of Internal Medicine, Director, Clinical Skills and Clinical Simulation Center, Paul L Foster School of Medicine, Texas Tech University Health Sciences Center; Consulting Staff, Thomason Hospital
Coauthor(s): Thong Huy Do, MD, Staff Physician, Department of Internal Medicine, Thomason Hospital, Texas Tech University; Tony Tran Ho, MS, Texas Tech University School of Medicine
Contributor Information and Disclosures

Updated: Mar 30, 2009

Introduction

Background

Vibrio infections are largely classified into two distinct groups: Vibrio cholera infections and noncholera Vibrio infections. Historically, the noncholera Vibrio species are classified as halophilic or nonhalophilic, depending on their requirement of sodium chloride for growth.

Because most Vibrio infections are associated with the consumption of contaminated food, these infections are often considered a foodborne disease. The prevalence of noncholera Vibrio infections in the United States appears to have increased in recent years. The combination of increased water temperature and salinity where shellfish are harvested may contribute to increased contamination rates of shellfish. Although many foodborne diseases are not reportable in the United States, the Centers for Disease Control and Prevention (CDC) estimates that approximately 76 million cases of foodborne illnesses occur annually, with 5200 deaths.1,2

Since 1988, the CDC has maintained a voluntary surveillance system for culture-confirmed Vibrio infections in Alabama, Florida, Louisiana, Mississippi, and Texas. Cases of culture-confirmed noncholera Vibrio infections from these states accounted for 39% of the 462 cases reported to the CDC in 2003. Noncholera Vibrio species in the United States cause an estimated 8000 illnesses yearly.3

While the estimated incidence of infection with Shiga toxin–producing Escherichia coli O157:H7 (STEC O157) and species of Campylobacter, Cryptosporidium, Listeria, Salmonella, and Yersinia significantly decreased from 1996-1998 to 2004, the incidence of Vibrio infections during this period increased 47% (95% CI, 7%-102%).3,4

Although Vibrio parahaemolyticus is the most common noncholera Vibrio species reported to cause infection, Vibrio vulnificus is associated with 94% of reported deaths. Because clinical laboratories do not routinely use the selective medium thiosulfate-citrate-bile salts-sucrose (TCBS) for stool culture, many cases of Vibrio gastroenteritis are not identified.5,6

In the event of a natural disaster, the disturbance to the environment may increase the risk of infectious diseases such as Vibrio infections. During the 2 weeks following Hurricane Katrina in August 2005, the CDC reported 22 new cases of Vibrio infections in Louisiana and Mississippi. V vulnificus accounted for most (82%) of these wound-associated infections. The increased incidence of Vibrio wound infections in the residents of Gulf Coast states was most likely associated with the exposure of skin and soft-tissue injuries to the contaminated floodwaters.7

Pathophysiology

The Vibrionaceae family includes the genera Vibrio, Plesiomonas, and Aeromonas. Members of the family Vibrionaceae are natural inhabitants of sea water but can also be found in fresh water. Vibrio species are oxidase-positive, gram-negative bacilli. With the exception of nonhalophilic Vibrio species, such as Vibrio cholerae and Vibrio mimicus, all Vibrio species require saline for growth.

Vibrio species can produce multiple extracellular cytotoxins and enzymes that are associated with extensive tissue damage and that may play a major role in the development of sepsis (see Table 1).

Table 1. Noncholera Vibrio Species and Associated Clinical Presentations

Open table in new window

Table
Infection TypeNoncholera Vibrio SpeciesCytotoxins/Enzymes
GastroenteritisV parahaemolyticus
Non-01 V cholerae
Vibrio fluvialis
V mimicus
Vibrio furnissii
Vibrio hollisae
Vibrio alginolyticus
V vulnificus
Cytotoxin
Hemolysin
Wound infectionV alginolyticus
V vulnificus
Non-01 V cholerae
Vibrio damsela
Vibrio carchariae
V fluvialis
V parahaemolyticus
V mimicus
Protease
Hemolysin
Lipase
DNAase
Cytolysin
SepticemiaV vulnificus
V fluvialis
V damsela
Non-01 V cholerae
Vibrio cincinnatiensis
Proteases
Endotoxic lipopolysaccharide
Infection TypeNoncholera Vibrio SpeciesCytotoxins/Enzymes
GastroenteritisV parahaemolyticus
Non-01 V cholerae
Vibrio fluvialis
V mimicus
Vibrio furnissii
Vibrio hollisae
Vibrio alginolyticus
V vulnificus
Cytotoxin
Hemolysin
Wound infectionV alginolyticus
V vulnificus
Non-01 V cholerae
Vibrio damsela
Vibrio carchariae
V fluvialis
V parahaemolyticus
V mimicus
Protease
Hemolysin
Lipase
DNAase
Cytolysin
SepticemiaV vulnificus
V fluvialis
V damsela
Non-01 V cholerae
Vibrio cincinnatiensis
Proteases
Endotoxic lipopolysaccharide

V vulnificus lives in areas where the temperature exceeds 18°C. In the United States, it is found in the coastal waters of the Gulf of Mexico, New England, and the northern Pacific. Low-to-moderate salinity (15-25 parts per thousand) provides the most favorable growing condition for V vulnificus, and, conversely, high salinity (>25 parts per thousand) adversely affects its survival. Similar to the effect of high salinity, low seawater temperature (<10°C) significantly inhibits the growth of V vulnificus. V vulnificus is ingested by filter-feeding mollusks such as oysters, mussels, clams, and scallops. During the warmer months, the concentration of bacteria can be as high as 1 X 106 bacteria per gram of oyster.8

Several mechanisms contribute to the virulence of V vulnificus. Iron is an important growth factor. However, because free iron is virtually absent in humans, the organism produces siderophores that acquire iron from transferrin or lactoferrin and deliver it to the bacteria. Conversely, the inability to produce siderophores leads to reduction of virulence. Hepcidin, a natural cysteine-rich peptide, has recently been suggested to possess important antibacterial activity. It is possible that inadequate expression of hepcidin in patients with liver disease predisposes them to serious infections, including those caused by Vibrio species.9,10

Clinical conditions associated with increased free iron, such as hemochromatosis or hemolytic anemia, represent a major risk factor for disseminated Vibrio infections. In addition, V vulnificus produces several other virulence factors, including proteases, hemolysins, and cytolysins. One in particular, a thermolysin-like metalloprotease, activates the bradykinin pathway, causing an increase in vascular permeability. This metalloprotease is far more efficient at activating human enzymes than those of other Vibrio species, possibly explaining why V vulnificus causes severe skin damage and necrotizing fasciitis.11

Recently, the gene pyrH has been demonstrated as essential for in vivo survival and growth of V vulnificus in infected mice and is likely associated with its virulence. Clinical isolates of V vulnificus, but not environmental isolates , caused extensive damage to macrophages in animal models, possibly explaining the lethal effects of this infection. One of the major virulence factors in pathogenic V haemolyticus strains is a thermostable direct hemolysin (TDH). This beta-hemolysin has both enterotoxic and cytotoxic effects; it is detoxified at 60-70°C but reactivated at 80°C (Arrhenius effect).

For additional information on cutaneous V vulnificus infections, see the article Vibrio Vulnificus in eMedicine’s Dermatology volume.

Frequency

United States

Between 1996 and 2001, the incidence of Vibrio infections increased by more than 80%. More importantly, despite a significant decline (30-45%) in the incidence of most bacterial foodborne infections in the United States in 2004, the incidence of Vibrio infections increased by 47% over the baseline period of 2001-2002.12 The CDC estimates that 8000 Vibrio infections and approximately 60 deaths related to Vibrio infections may occur annually in the United States. Vibrio infections are acquired through consumption of contaminated raw or undercooked shellfish such as oysters, clams, mussels, or crabs. Exposure of wounds to contaminated sea water, injury caused by contaminated seashells, and shark and alligator bites are potential alternative sources of infection (see Table 2).

V parahaemolyticus is the leading cause of seafood-associated gastroenteritis in the United States. During a large outbreak of gastroenteritis in July 2004 in the Gulf of Alaska, V parahaemolyticus caused illness in almost one third of cruise ship passengers who consumed Vibrio -contaminated oysters. From May to July 2006, health departments of New York City, New York state, Oregon, and Washington state reported a total of 177 cases of V parahaemolyticus gastroenteritis. Of these reported cases, 113 (64%) involved residents of Washington state.13

Table 2. Clinical Presentation Rates of Pathogenic Vibrio Infections

Open table in new window

Table
Vibrio SpeciesGastroenteritis
(%)
Wound Infection
(%)
Septicemia
(%)
Miscellaneous
(%)
V parahaemolyticus593452
V vulnificus545437
Non-01 V cholerae 67915
V alginolyticus5-1271110-15
V mimicus8533
V fluvialis73106
V damselaRare>95Rare
V furnissii>90RareRare
Vibrio metschnikoviiCommonRareRare
V hollisae8575
V cincinnatiensisRareRareRareMeningitis
Vibrio SpeciesGastroenteritis
(%)
Wound Infection
(%)
Septicemia
(%)
Miscellaneous
(%)
V parahaemolyticus593452
V vulnificus545437
Non-01 V cholerae 67915
V alginolyticus5-1271110-15
V mimicus8533
V fluvialis73106
V damselaRare>95Rare
V furnissii>90RareRare
Vibrio metschnikoviiCommonRareRare
V hollisae8575
V cincinnatiensisRareRareRareMeningitis

International

Noncholera Vibrio infections are commonly reported in areas such as Japan, Taiwan, China, Hong Kong, Korea, Italy, and Israel. The high prevalence of hepatitis B infections in areas such as China and Taiwan may also contribute to the high incidence of severe noncholera Vibrio infections.

Contrary to epidemiologic patterns of Vibrio infections, only sporadic cases were reported among survivors and injured individuals following the tsunami that devastated Thailand, Indonesia, and India in December 2004.

Despite a high annual estimated incidence of V vulnificus septicemia in Japan (425 cases; 95% CI, 238-752), a survey of registered emergency physicians in Japan surprisingly revealed that only 15.7% (95% CI, 11.3-21.0) of responding physicians had a basic knowledge of this frequently fatal infection.14

Mortality/Morbidity

According to CDC estimates, foodborne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5200 deaths annually in the United States.14

  • Foodborne noncholera Vibrio infections may occur at rate of 0.2-0.3 per 100,000 population. Three thousand cases of V parahaemolyticus infection are estimated to occur annually, resulting in 40 hospitalizations and 7 deaths. Ninety-five cases of V vulnificus infection are estimated to occur annually, resulting in 85 hospitalizations and 35 deaths.
  • Although Vibrio infections are not as common as Campylobacter, Salmonella, or Listeria infections, more patients with Vibrio infections die because of the high mortality rate associated with V vulnificus septicemia.
  • Among all foodborne diseases, V vulnificus infection is associated with the highest case fatality rate (39%).
  • Patients with cirrhosis who consumed raw oysters were 80 times more likely to develop V vulnificus infection and 200 times more likely to die of the infection than those without liver disease who consumed raw oysters.15
  • Regardless of pre-existing conditions, the mortality risk increases in patients with V vulnificus infection who are hospitalized more than two days after symptoms develop (OR, 2.9; 95% CI, 1.8-4.8).16
  • A delay in performing the first fasciotomy (>24 h) after development of clinical symptoms in patients with V vulnificus necrotizing fasciitis was associated with 5-fold increase in the mortality risk.

Race

Vibrio infections have no racial predilection.

  • Because Vibrio species are natural inhabitants of sea water, Vibrio infections are more commonly reported in states or countries bordered by large bodies of sea water.
  • Persons with underlying medical conditions, such as alcoholism, cirrhosis, or malignancy, and recipients of organ transplants are at increased risk of Vibrio infections and serious complications.
  • Patients with end-stage renal failure who are on continuous ambulatory peritoneal dialysis (CAPD) may develop peritonitis after eating or handling raw sea fish.

Sex

Vibrio infections can occur in all persons, regardless of sex. V vulnificus infections were reported in women who engaged in sexual intercourse in brackish water of the Gulf of Mexico. In general, V vulnificus infections are more common in males (82%), according to most reports.

Age

  • Persons of any age who consume or are exposed to Vibrio- contaminated food or water are at risk of developing Vibrio infection, especially if they have underlying medical conditions such as advanced liver disease.
  • Most patients with Vibrio wound infections and septicemia are aged 50-60 years.

Clinical

History

Most patients with noncholera Vibrio infections report having recently consumed raw seafood such as oysters, clams, crabs, or mussels. With the exception of a dramatic clinical progression in wound infection and septicemia, no characteristic signs and symptoms of early-stage noncholera Vibrio infections exist (see Table 3).

Table 3. Clinical Signs and Symptoms of Vibrio Infections

Open table in new window

Table
Clinical PresentationSymptoms (Frequency)
GastroenteritisDiarrhea (100%)
Abdominal cramps (89%)
Nausea (76%)
Vomiting (55%)
Fever (47%)
Bloody stools (29%)
Headache (24%)
Myalgia (24%)
Wound infectionSwelling (100%)
Pain (100%)
Erythema (100%)
Bullae (30-50%)
Necrosis (30-50%)
Gangrene (<10%)
SepticemiaFever (>90%)
Hypothermia (<10%)
Hypotension (100%)
Tachycardia (80-90%)
Shock (50-70%)
Bullae (80-100%)
Acute respiratory distress syndrome (<5%)
Multiple organ dysfunction (30-50%)
Clinical PresentationSymptoms (Frequency)
GastroenteritisDiarrhea (100%)
Abdominal cramps (89%)
Nausea (76%)
Vomiting (55%)
Fever (47%)
Bloody stools (29%)
Headache (24%)
Myalgia (24%)
Wound infectionSwelling (100%)
Pain (100%)
Erythema (100%)
Bullae (30-50%)
Necrosis (30-50%)
Gangrene (<10%)
SepticemiaFever (>90%)
Hypothermia (<10%)
Hypotension (100%)
Tachycardia (80-90%)
Shock (50-70%)
Bullae (80-100%)
Acute respiratory distress syndrome (<5%)
Multiple organ dysfunction (30-50%)
  • Vibrio gastroenteritis: After an average incubation period of 19 hours (12-52 h), patients with Vibrio gastroenteritis report diarrhea, abdominal cramps, nausea, and vomiting.17,5
    • Patients frequently pass several watery stools (10-15/d).
    • The occurrence of bloody diarrhea varies. It is reported in 25% of patients with V parahaemolyticus infection but may develop in up to 75% of patients with V fluvialis infection.
    • Low-grade fever may be observed in patients with Vibrio gastroenteritis.
    • Most patients remain alert upon admission. However, elderly patients may have decreased mental status due to dehydration or sepsis.
  • Noncholera Vibrio wound infection: Patients frequently report injury caused by fish hooks; preparation of St Peter's fish (Tilapia zillii); preparation of crabs, lobsters, or mussels; or stepping on seashells.18
    • Initially, patients with such infections almost always report severe pain of the involved limb or body part.
    • Numbness of the wound and the surrounding area may predominate if the patient has delayed seeking medical attention.
  • Noncholera Vibrio septicemia: Patients frequently exhibit a dramatic clinical presentation characterized by the following:
    • High fever
    • Shaking chills
    • Generalized myalgia
    • Exquisite pain in the lower extremities (most characteristic) or, rarely, pain in the lower trunk19

Physical

The physical findings of Vibrio infections vary according to clinical presentations.

  • Acute gastroenteritis
    • Patients with acute Vibrio gastroenteritis are typically acutely ill with diarrhea, nausea, vomiting, abdominal pain, and fever (50%).
    • The vital signs, such as blood pressure and heart rate, vary depending on the level of dehydration.
    • Unless the patient has underlying disease, no physical findings are specific for acute Vibrio gastroenteritis.5
  • Wound infection
    • After a short incubation period (3-24 h), patients with Vibrio wound infections frequently present with rapidly progressing wound swelling and severe pain.
    • The majority of such wounds involve the fingers, palms, or soles of the feet.
    • In milder cases, erythema, edema, and pain are localized to the initial wound, without signs of compartment syndrome, necrosis, gangrene, or necrotizing fasciitis.
    • In patients with medical conditions such as cirrhosis or malignancies, the wound infection may progress very rapidly, with formation of hemorrhagic bullae and extensive soft-tissue necrosis.18
  • Septicemia
    • After a short incubation period (12-48 h) following the consumption of raw seafood or exposure of broken skin to warm seawater, patients with Vibrio septicemia frequently develop fever, shaking chills, generalized myalgia, edema, and severe pain in the lower extremities.19
    • Within 3-24 hours, edema of the lower extremities worsens.
    • Multiple hemorrhagic bullae and extensive ecchymoses distributed predominantly over the lower extremities form rapidly (see Images 1-3).

      <EM>Vibrio</EM> infections. Early bullous lesions...

      Vibrio infections. Early bullous lesions appear over the dorsum of the foot of a patient with cirrhosis.

      <EM>Vibrio</EM> infections. Early bullous lesions...

      Vibrio infections. Early bullous lesions appear over the dorsum of the foot of a patient with cirrhosis.


      <EM>Vibrio</EM> infections. In a patient with cir...

      Vibrio infections. In a patient with cirrhosis, skin lesion rapidly becomes necrotic.

      <EM>Vibrio</EM> infections. In a patient with cir...

      Vibrio infections. In a patient with cirrhosis, skin lesion rapidly becomes necrotic.


      <EM>Vibrio</EM> infections. Bullous lesions in a ...

      Vibrio infections. Bullous lesions in a patient with cirrhosis continue to progress, and the patient rapidly develops hypotension and shock despite aggressive medical therapy.

      <EM>Vibrio</EM> infections. Bullous lesions in a ...

      Vibrio infections. Bullous lesions in a patient with cirrhosis continue to progress, and the patient rapidly develops hypotension and shock despite aggressive medical therapy.

    • Patients frequently become hypotensive despite aggressive intravenous fluid therapy.
    • Patients become lethargic, obtunded, and, finally, unconscious as the disease progresses.
    • Oliguria may develop.
    • Noncardiogenic pulmonary edema may develop.
  • Ocular infection -Conjunctivitis, keratitis, endophthalmitis
  • Peritonitis - Abdominal pain and cloudy peritoneal fluid in patients receiving CAPD

Causes

  • Noncholera Vibrio infections are foodborne diseases that are largely associated with the following:
    • Consumption of raw or undercooked seafood such as oysters, clams, crabs, or mussels
    • Exposure of wound to contaminated water
  • Acute gastroenteritis associated with noncholera Vibrio infection is frequently self-limited, although persons with certain underlying medical conditions may develop fulminant infections. These underlying medical conditions include the following:
    • Advanced liver diseases, such as cirrhosis, hepatitis B virus (HBV) infection, hepatitis C virus (HCV) infection, alcoholism, hemochromatosis, and liver transplantation
    • Hematologic diseases, such as acute leukemia, aplastic anemia, hemolytic anemia, and thalassemia
    • Immunosuppressive therapy, including cytotoxic chemotherapy, corticosteroids, and tacrolimus
    • Kidney disease involving kidney transplantation or hemodialysis
    • Miscellaneous procedures and conditions, including splenectomy and diabetes mellitus

More on Vibrio Infections

Overview: Vibrio Infections
Differential Diagnoses & Workup: Vibrio Infections
Treatment & Medication: Vibrio Infections
Follow-up: Vibrio Infections
Multimedia: Vibrio Infections
References

References

  1. Mead PS, Slutsker L, Dietz V, McCaig LF, Bresee JS, Shapiro C, et al. Food-related illness and death in the United States. Emerg Infect Dis. Sep-Oct 1999;5(5):607-25. [Medline].

  2. Morris JG, Black RE. Cholera and other vibrioses in the United States. N Engl J Med. Feb 7 1985;312(6):343-50. [Medline].

  3. Olsen SJ, MacKinnon LC, Goulding JS, Bean NH, Slutsker L. Surveillance for foodborne-disease outbreaks--United States, 1993-1997. MMWR CDC Surveill Summ. Mar 17 2000;49(1):1-62. [Medline].

  4. Preliminary FoodNet data on the incidence of infection with pathogens transmitted commonly through food--10 sites, United States, 2004. MMWR Morb Mortal Wkly Rep. Apr 15 2005;54(14):352-6. [Medline].

  5. Daniels NA, MacKinnon L, Bishop R. Vibrio parahaemolyticus infections in the United States, 1973-1998. J Infect Dis. May 2000;181(5):1661-6. [Medline].

  6. Marano NN, Daniels NA, Easton AN, McShan A, Ray B, Wells JG. A survey of stool culturing practices for vibrio species at clinical laboratories in Gulf Coast states. J Clin Microbiol. Jun 2000;38(6):2267-70. [Medline].

  7. Centers for Disease Control and Prevention (CDC). Vibrio illnesses after Hurricane Katrina--multiple states, August-September 2005. MMWR Morb Mortal Wkly Rep. Sep 23 2005;54(37):928-31. [Medline].

  8. Shapiro RL, Altekruse S, Hutwagner L. The role of Gulf Coast oysters harvested in warmer months in Vibrio vulnificus infections in the United States, 1988-1996. Vibrio Working Group. J Infect Dis. Sep 1998;178(3):752-9. [Medline].

  9. Brennt CE, Wright AC, Dutta SK. Growth of Vibrio vulnificus in serum from alcoholics: association with high transferrin iron saturation. J Infect Dis. Nov 1991;164(5):1030-2. [Medline].

  10. Hor LI, Chang TT, Wang ST. Survival of Vibrio vulnificus in whole blood from patients with chronic liver diseases: association with phagocytosis by neutrophils and serum ferritin levels. J Infect Dis. Jan 1999;179(1):275-8. [Medline].

  11. Miyoshi S, Nakazawa H, Kawata K, Tomochika K, Tobe K, Shinoda S. Characterization of the hemorrhagic reaction caused by Vibrio vulnificus metalloprotease, a member of the thermolysin family. Infect Immun. Oct 1998;66(10):4851-5. [Medline].

  12. Centers for Disease Control and Prevention (CDC). Preliminary FoodNet data on the incidence of infection with pathogens transmitted commonly through food--selected sites, United States, 2003. MMWR Morb Mortal Wkly Rep. Apr 30 2004;53(16):338-43. [Medline].

  13. Vibrio parahaemolyticus infections associated with consumption of raw shellfish--three states, 2006. MMWR Morb Mortal Wkly Rep. Aug 11 2006;55(31):854-6. [Medline].

  14. Osaka K, Komatsuzaki M, Takahashi H, Sakano S, Okabe N. Vibrio vulnificus septicaemia in Japan: an estimated number of infections and physicians' knowledge of the syndrome. Epidemiol Infect. Oct 2004;132(5):993-6. [Medline].

  15. Haq SM, Dayal HH. Chronic liver disease and consumption of raw oysters: a potentially lethal combination--a review of Vibrio vulnificus septicemia. Am J Gastroenterol. May 2005;100(5):1195-9. [Medline].

  16. Liu JW, Lee IK, Tang HJ, Ko WC, Lee HC, Liu YC. Prognostic Factors and Antibiotics in Vibrio vulnificus Septicemia. Arch Intern Med. Oct 23 2006;166(19):2117-23. [Medline].

  17. Dadisman TA Jr, Nelson R, Molenda JR. Vibrio parahaemolyticus gastroenteritis in Maryland. I. Clinical and epidemiologic aspects. Am J Epidemiol. Dec 1972;96(6):414-26. [Medline].

  18. Howard RJ, Lieb S. Soft-tissue infections caused by halophilic marine vibrios. Arch Surg. Feb 1988;123(2):245-9. [Medline].

  19. Klontz KC, Lieb S, Schreiber M. Syndromes of Vibrio vulnificus infections. Clinical and epidemiologic features in Florida cases, 1981-1987. Ann Intern Med. Aug 15 1988;109(4):318-23. [Medline].

  20. Anand RG, Lopez FA, deBoisblanc B. Vibrio vulnificus sepsis successfully treated with antibiotics, surgical debridement, and recombinant human activated protein C. J La State Med Soc. May-Jun 2004;156(3):130-3; quiz 133. [Medline].

  21. Mouzin E, Mascola L, Tormey MP. Prevention of Vibrio vulnificus infections. Assessment of regulatory educational strategies. JAMA. Aug 20 1997;278(7):576-8. [Medline].

  22. Hlady WG, Klontz KC. The epidemiology of Vibrio infections in Florida, 1981-1993. J Infect Dis. May 1996;173(5):1176-83. [Medline].

  23. Hollis DG, Weaver RE, Baker CN. Halophilic Vibrio species isolated from blood cultures. J Clin Microbiol. Apr 1976;3(4):425-31. [Medline].

Further Reading

Keywords

Vibrio infections, Vibrio cholera infections, noncholera Vibrio infections, halophilic Vibrio species, nonhalophilic Vibrio species, Vibrio parahaemolyticus, Vibrio vulnificus, V parahaemolyticus, V vulnificus, Vibrionaceae family, vibriosis, vibrioses, Vibrio gastroenteritis, Vibrio wound infection, Vibrio septicemia, Vibrio sepsis, Vibrio cholerae, Vibrio mimicus, Vibrio fluvialis, Vibrio furnissii, Vibrio hollisae, Vibrio alginolyticus, Vibrio damsela, Vibrio carchariae, Vibrio cincinnatiensis, Vibrio metschnikovii, V cholerae, V mimicus, V fluvialis, V furnissii, V hollisae, V alginolyticus, V damsela, V carchariae, V cincinnatiensis, V metschnikovii

Contributor Information and Disclosures

Author

Hoi Ho, MD, Associate Dean for Faculty Affairs and Development, Professor, Department of Internal Medicine, Director, Clinical Skills and Clinical Simulation Center, Paul L Foster School of Medicine, Texas Tech University Health Sciences Center; Consulting Staff, Thomason Hospital
Hoi Ho, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Forensic Examiners, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Coauthor(s)

Thong Huy Do, MD, Staff Physician, Department of Internal Medicine, Thomason Hospital, Texas Tech University
Thong Huy Do, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Tony Tran Ho, MS, Texas Tech University School of Medicine
Tony Tran Ho, MS is a member of the following medical societies: American Medical Association and Texas Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Mary Nettleman, MD, MS, Chair, Department of Medicine, Michigan State University
Mary Nettleman, MD, MS is a member of the following medical societies: American College of Physicians, Association of Professors of Medicine, Central Society for Clinical Research, Infectious Diseases Society of America, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Richard B Brown, MD, FACP, Chief, Division of Infectious Diseases, Baystate Medical Center; Professor, Department of Internal Medicine, Tufts University School of Medicine
Richard B Brown, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.