Members of the genus Vibrio are short, curved, rod-shaped organisms. Vibrios are closely related to the family Enterobacteriaceae. They are rapidly motile by means of a single polar flagellum. [Note: This contrasts with the peritrichous flagella (distributed all over the surface) of the motile Enterobacteriaceae.] O and H antigens are both present, but only O antigens are useful in distinguishing strains of vibrios that cause epidemics. Vibrios are facultative anaerobes. The growth of many Vibrio strains either requires or is stimulated by NaCl. Pathogenic vibrios include: 1) Vibrio cholerae, serogroup O1 strains that are associated with epidemic cholera; 2) non-O1 V. cholerae and related strains that cause sporadic cases of cholera like and other illnesses; and 3) Vibrio parahaemolyticus and other halophilic vibrios, which cause gastroenteritis and extraintestinal infections.

A. Epidemiology

  V. cholerae is transmitted to humans by contaminated water and food. In the acquatic environment, a number of reservoirs have been identified, including crustaceans, phytoplankton, and protozoa. Among humans, long-term carriage is considered uncommon. There are two biotypes (subdivisions) of the species V. cholerae: classic and El Tor. In contrast to the classic strain, the El Tor strain is distinguished by the production of hemolysins, higher carriage rates, and the ability to survive in water for longer periods. Outbreaks of both strains have been associated with raw or undercooked seafood harvested from contaminated waters. Natural (and even man-made) disasters are often followed by cholera outbreaks. For example, a severe outbreak of cholera followed the earthquake in Haiti in 2010.

B. Pathogenesis

 Following ingestion, V. cholerae infects the small intestine. Adhesion factor(s) are important for colonization and virulence. Achlorhydria and/or treatments that lessen gastric acidity, greatly reduce the infectious dose. The organism is noninvasive but adheres to the epithelium by expression of pili called Tcp, or toxin-coregulated pili. These pili are coordinately expressed along with cholera toxin, which is an enterotoxin that initiates an outpouring of fluid (Figure 1). Cholera toxin is a multimeric protein composed of an A and a B subunit. The B subunit (consisting of five identical monomers) binds to the GM1 ganglioside receptor of cells lining the intestine. The A subunit has two components: The A2 subunit tethers the A1 subunit to the B pentamer, and the A1 subunit is an adenosine diphosphate (ADP)-ribosyl transferase that ADP-ribosylates the membrane-bound Gs protein.1 Modified Gs protein activates adenylyl cyclase, which produces elevated levels of intracellular cAMP. This, in turn, causes an outflowing of ions and water to the lumen of the intestine.

Fig1. Action of cholera toxin. cAMP = cyclic adenosine monophosphate, PPi = pyrophosphate.

 C. Clinical significance

Full-blown cholera is characterized by massive loss of fluid and electrolytes from the body. After an incubation period ranging from hours to a few days, profuse watery diarrhea (“rice-water” stools) begins. Untreated, death from severe dehydration causing hypovolemic shock may occur in hours to days, and the death rate may exceed 50 percent. Appropriate treatment reduces the death rate to less than 1 percent. [Note: Non-O1 V. cholerae and other non-halophilic vibrios cause sporadic cases of cholera indistinguishable from that caused by V. cholerae, serotype O1. They also cause milder illness, comparable to that caused by enterotoxigenic E. coli.] Patients with suspected cholera need to be treated prior to laboratory confirmation, because death by dehydration can occur within hours.

 D. Laboratory identification

V. cholerae grows on standard media such as blood and MacConkey agars. Thiosulfate-citrate-bile salts–sucrose medium can enhance isolation. The organism is oxidase positive, but further bio chemical testing is necessary for specific identification of V. cholerae.

 E. Treatment and prevention

Replacement of fluids and electrolytes is crucial in preventing shock and does not require bacteriologic diagnosis. Antibiotics (doxycycline is the drug of choice) can shorten the duration of diarrhea and excretion of the organism (Figure 2). Prevention relies primarily on public health measures that reduce fecal contamination of water supplies and food. Adequate cooking of foods can minimize trans mission. Vaccines that are only modestly protective are available in many other countries but not in the United States.

Fig2. Summary of Vibrio disease. 1 Indicates first-line drugs.

F. Vibrio parahaemolyticus and other halophilic, noncholera vibrios

These organisms are characterized by a requirement for higher than-usual concentrations of NaCl and their ability to grow in 10 per cent NaCl. They are common in coastal seawaters. Vibrio parahaemolyticus is associated with outbreaks of GI illness that result from ingestion of contaminated and inadequately cooked seafood, especially shellfish and crustaceans. The disease is self-limiting, and antibiotics do not alter the course of infection. Neither human carriers nor other mammalian reservoirs have been identified. Other halophilic, noncholera vibrios are associated with soft tis sue infections and septicemia resulting either from contact of wounds with contaminated seawater or from ingestion of contaminated seafood. For soft tissue infections, prompt administration of antibiotics, such as tetracycline, fluoroquinolones or cefotaxime, is important, and surgical drainage/debridement may be required. Bacteremia is associated with high mortality, especially when caused by Vibrio vulnificus.

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