Vibrio cholerae
Introduction
The vibrios are found in marine and surface waters , Vibrio cholerae
produces an enterotoxin that causes cholera, a profuse watery diarrhea that can
rapidly lead to dehydration and death.
The Vibrios
Vibrios are among the most common bacteria in surface waters worldwide.
They are curved aerobic rods and are motile, possessing a polar flagellum.
V. cholerae serogroups O1 and O139 cause cholera in humans, while other
vibrios may cause sepsis or enteritis. The medically important vibrios are listed in
Table 1.
Table 1. The Medically Important Vibrios.
Organism
Human Disease
V cholerae serogroups O1 and O139
Epidemic and pandemic cholera
V cholerae serogroups non-O1/non-O139
Cholera-like
diarrhea;
mild
diarrhea; rarely, extraintestinal
infection
V parahaemolyticus
Gastroenteritis,
extraintestinal infection
perhaps
Others
V mimicus, V vulnificus, V hollisae, V Ear, wound, soft tissue, and other
fluvialis, V damsela, V anginolyticus, V extraintestinal
infections,
all
metschnikovii
uncommon
Vibrio cholerae
The epidemiology of cholera closely parallels the recognition of V. cholerae
transmission in water and the development of sanitary water systems.
Morphology & Identification
Typical Organisms
Upon first isolation, V. cholerae is a comma-shaped, curved rod 2–4 mm
long. It is actively motile by means of a polar flagellum. On prolonged
cultivation, vibrios may become straight rods that resemble the gram-negative
enteric bacteria.
Culture
V. cholerae produces convex, smooth, round colonies that are opaque and
granular in transmitted light. V. cholerae and most other vibrios grow well at
37 °C on many kinds of media, including defined media containing mineral salts
and asparagine as sources of carbon and nitrogen. V. cholerae grows well on
thiosulfate-citrate-bile-sucrose (TCBS) agar, on which it produces yellow
colonies that are readily visible against the dark-green background of the agar.
Vibrios are oxidase-positive, which differentiates them from enteric gramnegative bacteria. Characteristically, vibrios grow at a very high pH (8.5–9.5) and
are rapidly killed by acid. Cultures containing fermentable carbohydrates
therefore quickly become sterile.
Growth Characteristics
V. cholerae regularly ferments sucrose and mannose but not arabinose. A
positive oxidase test is a key step in the identification of V. cholerae and other
vibrios. Most Vibrio species are halotolerant, and NaCl often stimulates their
growth. Some vibrios are halophilic, requiring the presence of NaCl to grow.
Antigenic Structure & Biologic Classification
Many vibrios share a single heat-labile flagellar H antigen. Antibodies to the
H antigen are probably not involved in the protection of susceptible hosts.
V. cholerae has O lipopolysaccharides that confer serologic specificity. There
are at least 139 O antigen groups. V. cholerae strains of O group 1 and O group
139 cause classic cholera.
The V. cholerae serogroup O1 antigen has determinants that make possible
further typing; the serotypes are Ogawa, Inaba, and Hikojima. Two biotypes of
epidemic V. cholerae have been defined, classic and El Tor. The El Tor biotype
produces a hemolysin, gives positive results on the Voges-Proskauer test, and is
resistant to polymyxin B. Molecular techniques can also be used to type
V. cholerae. Typing is used for epidemiologic studies.
V. cholerae O139 is very similar to V. cholerae O1 El Tor biotype. V. cholerae
O139 does not produce the O1 lipopolysaccharide and does not have all the genes
necessary to make this antigen. V. cholerae O139 makes a polysaccharide
capsule like other non-O1 V. cholerae strains, while V. cholerae O1 does not
make a capsule.
Vibrio cholerae Enterotoxin
V. cholerae produce a heat-labile enterotoxin with a molecular weight of about
84,000, consisting of subunits A (MW 28,000) and B Ganglioside GM 1 serves as
the mucosal receptor for subunit B, which promotes entry of subunit A into the
cell. Activation of subunit A1 yields increased levels of intracellular cAMP and
results in prolonged hypersecretion of water and electrolytes. There is increased
sodium-dependent chloride secretion, and absorption of sodium and chloride is
inhibited. Diarrhea occurs—as much as 20–30 L/d—with resulting dehydration,
shock, acidosis, and death. The genes for V. cholerae enterotoxin are on the
bacterial chromosome. Cholera enterotoxin is antigenically related to LT of
Escherichia coli and can stimulate the production of neutralizing antibodies.
Pathogenesis & Pathology
Under natural conditions, V. cholerae is pathogenic only for humans. A
person with normal gastric acidity may have to ingest as many as 10 10 or more
V. cholerae to become infected when the vehicle is water, because the organisms
are susceptible to acid. When the vehicle is food, as few as 10 2–104 organisms are
necessary because of the buffering capacity of food.
Cholera is not an invasive infection. The organisms do not reach the
bloodstream but remain within the intestinal tract. Virulent V. cholerae organisms
attach to the microvilli of the brush border of epithelial cells. There they multiply
and liberate cholera toxin and perhaps mucinases and endotoxin.
Clinical Findings
About 60% of infections with classic V. cholerae are asymptomatic, as are
about 75% of infections with the El Tor biotype. The incubation period is 1–4
days for persons who develop symptoms, depending largely upon the size of the
inoculum ingested. There is a sudden onset of nausea and vomiting and profuse
diarrhea with abdominal cramps. Stools, which resemble "rice water," contain
mucus, epithelial cells, and large numbers of vibrios. There is rapid loss of fluid
and electrolytes, which leads to profound dehydration, circulatory collapse, and
anuria.
Diagnostic Laboratory Tests
Specimens
Specimens for culture consist of mucus flecks from stools.
Smears
The microscopic appearance of smears made from stool samples. Dark-field
or phase contrast microscopy may show the rapidly motile vibrios.
Culture
Growth is rapid in peptone agar, on blood agar with a pH near 9.0, or on
TCBS agar, and typical colonies can be picked in 18 hours.
Specific Tests
V. cholerae organisms are further identified by slide agglutination tests using
anti-O group 1 or group 139 antisera and by biochemical reaction patterns.
Immunity
Gastric acid provides some protection against cholera vibrios. In experimental
animals, specific IgA antibodies occur in the lumen of the intestine.
Treatment
The most important part of therapy consists of water and electrolyte
replacement to correct the severe dehydration and salt depletion. Many
antimicrobial agents are effective against V. cholerae. Oral tetracycline tends to
reduce stool output in cholera and shortens the period of excretion of vibrios.
Epidemiology, Prevention, & Control
Patients should be isolated, their excreta disinfected, and contacts
followed up. Chemoprophylaxis with antimicrobial drugs may have a place.
Repeated injection of a vaccine containing lipopolysaccharides extracted from
vibrios.
Vibrio parahaemolyticus & Other Vibrios
Vibrio parahaemolyticus is a halophilic bacterium that causes acute
gastroenteritis following ingestion of contaminated seafood such as raw fish or
shellfish. After an incubation period of 12–24 hours, nausea and vomiting,
abdominal cramps, fever, and watery to bloody diarrhea occur.
V. parahaemolyticus does not grow well on some of the differential media used
to grow salmonellae and shigellae, but it does grow well on blood agar. It also
grows well on TCBS, where it yields green colonies. V. parahaemolyticus is
usually identified by its oxidase-positive growth on blood agar.
Vibrio vulnificus can cause severe wound infections, bacteremia, and probably
gastroenteritis. Wounds may become infected in normal or immunocompromised
persons who are in contact with water where the bacterium is present.
Tetracycline appears to be the drug of choice for V vulnificus infection;
ciprofloxacin may be effective also based on in vitro activity.