CLINICAL CASE

A 35-year-old woman presents to the emergency room with a 2-day history of

severe diarrhea and vomiting. Her symptoms started shortly after returning from a
mission trip that she took with her church to a rural area in central Africa. She
recalls eating shrimp that seemed undercooked.
Her symptoms started abruptly, with watery diarrhea followed by vomiting. She has
not had a fever and denies abdominal pain. On examination, her temperature is
C (98.9F), pulse is 115 beats per minute, and blood pressure is 80/50 mm Hg. Her
Her mucous membranes are dry, and her eyes appear sunken. Her skin is dry and
tents when lightly pinched. Her abdomen has hyperactive bowel sounds but is soft
and nontender. Her stool is watery and tests negative for blood.
A complete blood count shows an elevated white blood cell count and an elevated
hematocrit. A metabolic panel shows hypokalemia, low serum bicarbonate, and
prerenal azotemia. You assess this patient to be in hypovolemic shock and metabolic
acidosis, and institute appropriate therapy.

What organism is most likely to be identified on stool culture?

What is the cause of this patients diarrhea?
ANSWERS TO CASE 23: Vibrio cholerae
Summary: A 35-year-old woman recently traveled to Africa and developed diarrhea
causing hypovolemic shock and metabolic acidosis. She remembers eating
undercooked shrimp.

Most likely etiologic agent: Vibrio cholerae

Cause of the diarrhea: Hypersecretion of water and electrolytes into the

intestinal lumen caused by cholera toxin

CLINICAL CORRELATION
The first priorities as with any patient are the ABCs: airway, breathing, circulation.
This patient is in hypovolemic shock, meaning insufficient circulation to maintain
tissue perfusion needs. The most important step in intervention is volume repletion,
usually with intravenous isotonic saline solution. A likely therapy would be 3 L of
normal saline intravenously.

Vibrio species are found in saltwater and infections usually occur in the spring and
summer. Transmission is by either consumption of contaminated shellfish or
traumatic injury associated with infected water. The disease cholera is caused by
toxigenic strains of V. cholerae (01 and 0139 serotypes). Vibrio cholerae is spread
by ingestion of contaminated water or food. The organism is sensitive to gastric
acid; therefore, the dose required to cause an infection is high. Conditions that
reduce gastric acid, such as antacid medica- tions or achlorhydria, increase the risk
of infection.
The hallmark of cholera is severe watery diarrhea with mild to severe
dehydration because of production of toxin by the organism. In cases of severe
dehydration, patients have a nonpalpable pulse and very low blood pressure. Fever
is usually not present. Patients may become obtunded with sunken eyes and dry
mucous membranes.
Vibrio parahaemolyticus is associated with gastroenteritis that is self- limited even
though patients present with explosive watery diarrhea, with abdominal pain and
fever. The disease rarely progressed to the severity of dehydration of V. cholerae.
Vibrio vulnificus is more often associated with wound infections, that is, cellulitis,
rather than gastroenteritis. In alcoholic patients or those with other underlying liver
disease, the organism can become disseminated and be associated with a high
mortality rate.

APPROACH TO SUSPECTED Vibrio INFECTION Objectives

Know the structure, physiology, and virulence factors of V. cholerae. 
Know the reservoirs and mechanisms of spread of V. cholerae and
the mechanism of action of the cholera toxin in causing disease.

Definitions
Azotemia: Buildup in the blood of nitrogenous end-products of protein
metabolism.
Obtunded: Loss or dulling of sensations.

DISCUSSION
Characteristics of Vibrio
Vibrio species are motile, curved, gram-negative bacilli with a single polar
flagellum. They are facultative anaerobic organisms. Their natural environ- ment
is saltwater, where they can multiply freely, and it has been found in shellfish and

plankton. The major human pathogens are V. parahaemolyticus, V. vulnificus, and

Vibrio cholerae.
Over 200 serotypes of V. cholerae have been identified, based on their O antigen
serogroup. Serotype O1 has been responsible for the major cholera pandemics of the
past 200 years, but serotype O139 has been identified as con- tributing to disease
since 1992.
The major virulence of this organism is its enterotoxin. The toxin consists of five B
subunits, which bind to mucosal cell receptors and allow for release of the single A
subunit into the cell. The A subunit activates adenyl cyclase, resulting in the
hypersecretion of water, sodium, potassium, chloride, and bicarbonate into the
intestinal lumen.
Bacteria that survive transit through the stomach can colonize the upper small
intestine. Colonization pili facilitate attachment to the intestinal mucosa. The
volume of the secreted fluid and electrolytes can overwhelm the gastrointestinal
tracts ability to reabsorb them, resulting in large volumes of watery diarrhea. The
loss of an isotonic, bicarbonate-containing fluid results in dehydration,
hypovolemia, metabolic acidosis, hemoconcentration, and hypokalemia.

Diagnosis
The presumptive diagnosis of Vibrio disease can be made after history of association with saltwater, either involving trauma or consumption of raw shell- fish.
The watery diarrhea associated with V. parahaemolyticus cannot be easily
distinguished clinically from other forms of bacterial gastroenteritis. Cellulitis
caused by V. vulnificus should be diagnosed rapidly to avoid mortality. History of
recent exposure to seawater is helpful in making a presumptive diagnosis.
The diagnosis of cholera should be suspected in those with severe diarrheal illness
who live in or have traveled to an endemic area. Diagnosis of Vibrio infection can be
confirmed by culturing stool or wound samples. Gram stain of wound or blood
cultures may demonstrate a characteristic curved appearance to the gramnegative bacilli.
Most of the Vibrio species require salt for growth and therefore specialized media,
such as thiosulfate citrate bile salts sucrose (TCBS) agar. Most of the Vibrio species
will grow on blood agar and may appear -hemolytic, but poor growth is seen on
MacConkey agar. Vibrio cholerae appear as yellow colonies, and V.
parahaemolyticus and V. vulnificus appear as green colonies on TCBS agar.

Treatment and Prevention

The treatment of cholera involves volume replacement with isotonic,

bicarbonate-containing fluids, either using oral rehydration solutions in mild to
moderate dehydration or IV fluids, such as Ringer lactate, in the profoundly
dehydrated or those unable to tolerate oral intake. Oral antibiotics can be given to
kill the bacteria and decrease the duration of the illness, but do not take away the
need for appropriate rehydration therapy. Most commonly administered
antimicrobial is doxycycline.
Treatment with antimicrobials is not usually needed for gastroenteritis caused by V.
parahaemolyticus. Wound infections or bacteremia caused by V. vulnificus
require rapid administration of antimicrobials such as tetra- cycline or a
quinolones. Prevention of cholera includes improvement of hygienic practices
including treatment of the potable water supply with either heat or chlorine and
ensuring thorough cooking of seafood. Research is ongo- ing to perfect a vaccine to
prevent cholera.

MICROBIOLOGY PEARLS

The A subunit of the Vibrio enterotoxin activates adenyl cyclase, resulting in

the hypersecretion of water, sodium, potassium, chlo- ride, and bicarbonate
into the intestinal lumen.
The predominant clinical presentation of Vibrio gastroenteritis is watery
diarrhea.
The Vibrio organism appears as gram-negative, curved, motile bacilli. Vibrio
gastroenteritis or cholera is associated with con- sumption of contaminated
seafood or water.
Vibrio vulnificus is associated with cellulitis caused by trauma incurred in a
seawater environment and carries a high mortality rate if not treated rapidly.
Vibrio species require salt for growth and can be differentiated from other
organisms by growth on TCBS agar.