Veterinary World, 2011, Vol.

4(9):423-428 REVIEW

Vibrio cholerae - A Review

Mani Maheshwari1, Krishnaiah Nelapati2, Bindu Kiranmayi
2

1. College of Veterinary Science, Korutla, Karimnagar Dist., A.P., India.

2. College of Veterinary Science, Rajendranagar, Hyderabad-500030, India.
* Corresponding author email: drmani_8@yahoo.co.in
Received: 24-01-2011, Accepted: 02-03-2011, Published Online: 16-07-2011
doi: 10.5455/vetworld.2011.423-428

Abstract
Vibrio cholerae is a facultative anaerobic, Gram negative, non-spore forming curved rod, about 1.04-1.06 µm long. It is
a facultative human pathogen found in coastal waters that causes the acute gastrointestinal disease, cholera, a major
health threat in poor nations. It is widely acknowledged as one of the most important water borne pathogen of
worldwide economic significance. Sea foods and water is the most common vehicle for this infection in humans. It has
been isolated from wide variety of samples such as seawater, sediments, plankton, finfish and shellfishes of coastal and
estuarine environments. Cholera pathogenesis is a complex process and involves synergistic action of several genes.
CT is considered the most important epidemic marker among various toxins produced by V.cholerae. Detection of
V.cholerae from food stuffs is problematic, since they are present at low level together with large number of competing
microflora and also they may be injured by different food processing methods.
Keywords: Diarrhoea, Food, Water borne disease, Sea Food, Aerobic organism.

Introduction has a specific function. The B subunit serves to bind

the holotoxin to the eukaryotic cell receptor, and the A
Cholera, an enteric diarrheal disease caused by
subunit possesses a specific enzymatic function that
the gram-negative bacterium Vibrio cholerae,
continues to be a worldwide health concern. Two acts intracellular. Recent studies of the aquatic
distinctive epidemiologic features of cholera are its environment have shown that V. cholerae, including
tendency to appear in explosive outbreaks, often strains of O1and O139, are normal inhabitants of
starting in several distinct foci simultaneously, and its surface water, particularly brackish waters, and
propensity to cause true pandemic that progressively survive and multiply in association with zooplankton
affect many countries in multiple continents over the and phytoplankton quite independently of infected
course of many years (Kaper et al., 1995). V. cholerae, human beings (Huq et al., 1983).
the causative agent of cholera in humans, is classified Etiological studies on acute diarrhoeal diseases
into two serotypes: O1 and non O1 (Chatterjee and in gangetic plain areas have shown that gastroenteritis
Maiti, 1984). The O1 serogroup of V. cholerae is caused by V. cholerae ranks first in terms of incidence
further classified into two biotypes, namely, the followed by V. parahaemolyticus in India (Sakazaki et
classical and El Tor biotypes. In 1993, V. cholerae al., 1971) and other developing countries (Albert et
serogroup O139 made an explosive appearance and al., 1993). Cholera has been categorized as one of the
caused a severe epidemic in the Indian continent emerging and re-emerging infections in developing
(Ramamurthy et al., 1993). The major surface antigen countries (Satcher, 1995) and is classified as Category
employed in characterization of V. cholerae is the O B bioterrorism by Centre for Disease Control and
antigen. According to the typing scheme of Sakazaki Prevention (WHO, 2008).
and Shimada, there are 139 different O groups. V. The Centre for Disease Control and Prevention
cholerae O1 and O139 are known to be the dominating (CDC) estimated that 76 million food borne illnesses
and pathogenic strains. occurred in the United States with 325,000
However, the pathogenicity of Vibrio cholerae is hospitalizations and 5,200 deaths (Mead et al., 1999).
chiefly associated with the secretion of the Cholera
History and Epidemiology of the cholera
toxin (CTX), which is a protein complex. CTX is
responsible for the harmful effects of cholera Cholera is one of the oldest and best understood
infection. The structure of CTX is typical of the A-B of the epidemic- prone disease. The ancestral home of
subunit group of toxins in which each of the subunits cholera is thought to be the Ganges delta on the Indian
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 Vibrio cholerae- A Review
subcontinent, where epidemic of cholera like disease Pathogenicity for humans and Virulence
were described as far back as the 16th century factors
(Kindhauser, 2003). John Snows observations on
Infection due to Vibrio cholerae begins with the
cholera during 1848 London epidemic helped to ingestion of contaminated water or food. After passage
establish concept of a living agent, as cause of disease through the acid barrier of the stomach, the organism
and supported the theory of waterborne transmission colonizes the epithelium of the small intestine by
of cholera (Winkelstein, 1995). In 1883, during the means of the toxin-co regulated pili (Taylor et al.,
fifth pandemic Robert Koch, successfully isolated the 1987) and possibly other colonization factors such as
agent of cholera and suggested the existence of CT in the different haemagglutinins, accessory colonization
1884 (Finkelstein, 2000). In 1953, SN De (De and factor and core encoded pilus, all of which are thought
Chatterjee, 1953), bacteriologist in Calcutta discovered to play a role. Cholera enterotoxin produced by the
the crude cholera toxin, responsible for stimulating adherent vibrios is secreted across the bacterial outer
fluid secretion from the small intestine. membrane into the extracellular environment and
There have been seven pandemic of cholera in disrupts ion transport by intestinal epithelial cells. The
recorded history. The classical V. cholerae O1was subsequent loss of water and electrolytes leads to the
responsible for the fifth and sixth pandemic and is severe diarrhea characteristic of cholera.
believed to have been associated with the earlier The major virulence-associated factors are
pandemic as well, although there is no hard evidence present in cluster (Hacker et al., 1997) with at least
(Baruda, 1992). The causative agent of the seventh three regions in V.cholerae chromosome. The first is
pandemic is the E1Tor biotype (Samadi et al., 1983). the CTX genetic element (Mekalanos, 1985) which
In December, 1992, a large epidemic of cholera began has been reported to compromise the genome of a
in Bangladesh. The new serogroup has been filamentous bacteriophage (CTX ? ) (Waldor and
categorized as V. cholerae O139, with synonym Mekalanos, 1996). The second region is a large
Bengal to refer to it first isolation from areas pathogenicity island for V.cholerae (VPI) (Karaolis et
surrounding the Bay of Bengal (Shimada et al., 1993) al., 1998) that encode a toxin regulated pilus (TCP)
possibly working the beginning of the eighth gene cluster, a type IV pilus that function as an
pandemic (Swerdlow and Ries, 1993). essential colonization factor (Taylor et al., 1987) and
Cholera has re-emerged as a major infectious act as CTX ? receptor (Waldor and Mekalanos, 1996).
disease in recent past, with a global increase in its The third gene cluster, the RTX gene cluster in V.
incidence. In 1994, cholera cases were notified from cholerae encodes the presumptive cytotoxin (rtxA), an
94 countries- the highest ever number of countries in acyltransferase (rtxC), and an associated ATP-binding
one year (WHO, 1995). Cholera is one of the three cassette transporter system (rtxB and rtxD, two
diseases requiring notification to WHO under the proteins for toxin transportation) (Lin et al., 1999).
International Health Regulation. It is endemic V. cholerae virulence cassette or CTX element
throughout much of the African continent, where it corresponds to genome of CTX ? , a lysogenic
thrives under conditions of poor sanitation and waste filamentous bacteriophage has given a way for
disposal. In 2006, the total number of cases reported in emergence of new clones of toxigenic V. cholerae
Africa accounted for 99% of the global total. Africa strains (Waldor and Mekalanos, 1996).
has been the continent with the highest number of CT is clearly the most important causative factor
officially reported cholera cases since 1996 in the disease cholera, CT deficient isolates of V.
(Kindhauser, 2003). Cholera remains a global threat to cholerae also elicit mild to severe diarrhea and other
public health, especially in developing countries reactogenic symptoms in human indicating that other
(WHO, 2008). toxins are likely to contribute to pathogenesis of the
The World Health Organization (WHO) disease (Coster et al., 1995). The signs and symptoms
(http://www.who.int/wer/2007) reported a 30% of cholera are caused by cholera toxin (CT) or
increase in cases of cholera worldwide between 2004 choleragen, a protein enterotoxin (Kaper et al., 1995
(101,383 cases) and 2005 (131,943 cases), and a and Albert and Morris, 1999) produced by pathogenic
further 79% increase between 2005 and 2006 (236,860 V. cholerae (Herrignton et al., 1988). The structure of
cases), whereas the number of countries reporting CT is typical of A-B subunit group toxins. An active,
cases has remained constant. At the same time, the (A1) subunit of 23500 Da and a bridging piece (A2) of
global case fatality rate rose from 1.72% in 2005 to 5500 Da that links A1 to the 5B subunits (Guidolin and
2.66% in 2006. Manning, 1987). The A subunit functions for adenylate
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 Vibrio cholerae- A Review
cyclase activation in small intestinal epithelial cells, associated with extraintestinal infection with
leading to the loss of fluid and electrolytes. The 5 septicemia, wound infection, ear infection, cellulitis,
binding (B) subunits of 11500 Da each serves to bind peritonitis, necrotizing fascitis, cholecystitis,
the toxin to the epithelial cell surface receptor, GM1. endophthalmitis and meningitis (Yang et al., 2008).
The genes expressing A and B subunits are designated These symptoms are seen in patients with diabetes
ctxA and ctxB, respectively, and are expressed as a mellitus, chronic renal failure and dialysis,
single transcriptional unit (Mekalanos et al., 1983). immunocompromized patient and post splenectomy.
Toxin production does not correlate with serotype
Water borne infection
(Kaper et al., 1981). The effect is dependent on a
specific receptor, monosialosyl ganglioside (GM1 Cholera is usually transmitted by ingestion of
ganglioside) present on the surface intestinal mucosal contaminated water and sewage contaminated water
cells (Guidolin and Manning, 1987). remains the primary vehicle for cholera outbreaks
Although not fully characterized, other toxins (Tauxe and Blake 1992). Sewage contamination of
produced by V.cholerae include the shiga-like toxin ground water in Delhi was responsible for the
(OBrien et al., 1984), a heat-stable enterotoxin epidemic of V.cholerae (Pathak et al., 1993). The
(Takeda et al., 1991), new cholera toxin (Sanyal et al., presence of critical virulence genes in environmental
1983), sodium channel inhibitor (Tamplin et al., strains of V. cholerae cultured from three different
1987), thermostable direct haemolysin-like toxin freshwater lakes and ponds in Eastern part of Calcutta,
(Nlishibuchi et al., 1992), and a cell-rounding India (Chakraborty et al., 2000). Seawater and
cytotoxic enterotoxin known as the non-membrane- plankton samples from Peru were positive for V.
damaging cytotoxin (Saha and Nair, 1997). cholerae O1 and found to contain ctx toxin. Mourino-
Clinical Manifestations Perez et al. (2003) found that dissolved organic matter
during intense phytoplankton blooms has supported
Infection due to V.cholerae begins with the growth of V. cholerae in seawater. The toxigenic V.
ingestion of food or water contaminated directly or cholerae is a native flora of the aquatic environment
indirectly with faeces or vomitus of infected person which is transmitted through drinking water and still
(CDC, 2003). remains the leading cause of morbidity and mortality
Infection of approximately 104-106 V.cholerae in many developing countries including Thailand
O1 organisms is likely to produce clinical (Chomvarin et al., 2007).
cholera (Cash et al., 1974). A dose of V.cholerae O1
(106 cells) was normally needed to cause diarrhea Food borne infection
(Levine et al., 1981). a. Fruits and vegetables: In many countries, the
The incubation period for cholera ranges from a practice of fertilizing gardens with untreated night soil
few hours to five days, usually two to three days and the habit of consuming uncooked vegetables have
followed by acute watery diarrhoea, often associated often resulted in cholera outbreaks. Vegetables may be
with vomiting, muscle cramps and complications contaminated during washing with polluted water.
related to severe dehydration. The water diarrhoea is This can also occur when contaminated water is
speckled with flakes of mucus and epithelial cells injected into fruits, such as watermelons, to preserve
(rice-water stool). Cardiac complications and their weight and taste (Feachem, 1981). The pH of a
circulatory failure occur due to loss of potassium. In specific fruit is an important factor that influences
severe cases, fluid loss of 500-1000 ml, an hour can contamination by V. cholerae. Sour fruits such as
occur, which may result in death in less than 24 hrs lemons and oranges, with lower pH (below 4.5) do not
(Weinke et al., 2008) if untreated, with high (50- 60%) support the growth of V. cholerae, and, thus, do not
mortality rate (Guidolin and Manning, 1987). pose risk of cholera transmission. Fruit pulp and
Cholera enterotoxin is major virulence factor concentrate preserved in cans are also less likely to be
responsible for profuse diarrhoea, typically known as contaminated if they have an acidic pH. Spices,
cholera gravis, characterized by profuse watery including raw onions and garlic, can support the
diarrhoea, vomiting and dehydration, often associated survival of V. cholerae for 2-3 days at ambient
with leg cramps due to electrolyte imbalance leading temperature (Felsenfeld, 1967).
to severe dehydration and death (Choopun et al., 2002). b. Seafoods: The importance of fish and shellfish as a
V. cholerae is non invasive enterotoxigenic vehicle of cholera has been recognized by early
organism causing gastroenteritis, whereas non O1 is observers. Fishes are likely to be contaminated by V.
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 Vibrio cholerae- A Review
cholerae when the surrounding water is contaminated weeks during storage under refrigeration (Depaola,
by the sewage or other environmental sources of V. 1981). Huq et al. (1983) reported that oysters get the
cholerae O1. It has been shown that V. cholerae can infection of V. cholerae due to feeding on plankton to
survive in seawater in association with zooplankton which V. cholerae organisms are attached due to
(copepods). Zooplankton secretes a self-protective production of chitinase. Consumption of raw oysters
coat of chitin that can be dissolved by chitinase, an correlated strongly with gastrointestinal infections in
enzyme produced by V. cholerae O1. Seafoods, which V. cholerae has been implicated as causative
including mollusks, crustaceans, crabs, and oysters, agent (Rippey, 1994). It has been reported that V.
feed on plankton and can become infected with V. cholerae exist in water with a salinity of 3-8% only
cholerae. Once infected, particularly clams, and (Sousa et al., 2004).
oysters can harbour V. cholerae for weeks, even if g. Dairy Products: V. cholerae O1 can survive for
refrigerated (Depaola, 1981). In crabs, the organisms more than two weeks in different dairy products,
can rapidly multiply at ambient temperature, and including milk, milk products, soft deserts, and cakes.
boiling for less than 10 minutes or steaming for less Addition of sugar and eggs enhances bacterial
than 30 minutes does not completely kill V. cholerae survival. Although V. cholerae is killed by
(Huq et al., 1983). pasteurization of milk, the organisms can persist in
c. Fish: Raw fish consumption was the cause for raw milk as long as four weeks, even if refrigerated
cholera outbreaks in Japan as early as 1886 (Felsenfeld, 1967).
(Donitz, 1892) and in Philippines in 1908 (Heiser, h. Poultry and meat: Contamination of meat of
1908). V. cholerae was isolated from salted fish animal origin occurs exogenously during processing,
responsible for cholera outbreaks in Guan during 1974 cooking, storage or consumption. It has been shown
(Kuberski et al., 1979). Feldhusen (2000) reported that that V. cholerae can live and grow on cooked chicken,
raw fish was initially implicated epidemiologically as an increase in numbers of V. cholerae from 103 to 106
a source of transmission of V. cholerae in the South within 16 hours has been demonstrated (Kolvin and
American epidemic in 1991. V.cholerae O1 was Roberts, 1982). An early observation by Seligmann
present in 0.2% of raw fishery products, whereas V. indicates that consumption of improperly cooked
cholerae non O1 was present in 26.3% of raw and horsemeat was incriminated in a small outbreak of
12.14% of frozen products in Kerala and Tamil Nadu cholera in Berlin in 1918 (Seligman, 1918). The meat
coasts during 1986-87 (Verma et al., 1989). Fish had been prepared by an infected butcher who
samples from fresh as well as marine waters carry succumbed to cholera the next day. There are many
V.cholerae and it has been reported that fish intestine other types of food that may be contaminated with V.
contained 5 X 103 V. cholerae cfu/g (Senderovich et cholerae. V. cholerae can survive on cooked rice,
al., 2010) potato, eggs, and pasta for up to 5 days, and can also
d. Shellfish: Ingestion of aquatic vegetation or survive in spices, including pepper and cinnamon, for
sewage contamination of water are the main up to several days (PAHO, 1991).
contamination sources of V. cholerae in shellfish
Diagnosis
(Colwell, 1990). Garate Lizarranga et al. (2006)
reported that V. cholerae adhere strongly to shellfishs The conventional isolation procedure includes
digestive tract and cannot be removed efficiently by growth in enrichment broth like Alkaline Peptone
rinsing the shellfish or depuration. Gholami et al. water or Luria broth (LB) at 37 oC for 18-24 hr to increase
(1998) studied the risk factor of V. cholerae among the ratio of V. cholerae to competitor organisms and
renal diseased patients and reported that the infections plating on selective medium, TCBS i.e. Thiosulfate-
were usually acquired by raw shellfish which has Citrate-Bile salts-Sucrose agar (Finkelstein, 1988) for
damaged the kidney. 24-48 hr at 37 oC. V. cholerae ferment sucrose and
e. Crabs: Inadequately steamed crabs infected with V. produce yellow colonies. So, this medium is widely
cholerae were responsible for outbreaks of cholera in used for isolation of V. cholerae. These colonies are
Louisiana, USA (Blake et al., 1980). In crabs, the submitted to the oxidase test for the identification of V.
organisms can rapidly multiply at ambient cholerae complemented by biochemical and serological
temperature and boiling for less than 10 minutes or tests (Sack et al., 1980).
steaming for less than 30 minutes does not completely
Prevention and Control
kill V. cholerae (Depaola, 1981).
f. Oysters: V. cholerae in oysters can survive for Since the infection primarily occurs via faeco-
www.veterinaryworld.org Veterinary World, Vol.4 No.9 September 2011 426
 Vibrio cholerae- A Review
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