CHAPTER 286  CHOLERA AND OTHER VIBRIO Infections 1917

286
CHOLERA AND OTHER
VIBRIO INFECTIONS
EDUARDO GOTUZZO AND CARLOS SEAS

CHOLERA
DEFINITION
Cholera is a feared epidemic diarrheal disease caused by Vibrio cholerae sero-
group O1 and, since 1992, by the new serogroup O139. The disease is char-
acterized by acute watery diarrhea. In its more severe form, a person may be
severely dehydrated and in hypovolemic shock; the patient may die in a matter
of a few hours after contracting the infection if treatment is not provided.
Cholera is endemic today in Africa, Asia, and Latin America. Seven pandemics
have been registered in history since 1817; the most recent has lasted more
than five decades since its recognition in Indonesia in 1961.1

The Pathogen
V. cholerae is a curved gram-negative bacillus that belongs to the family
Vibrionaceae and shares common characteristics with the family
Enterobacteriaceae. V. cholerae O1 can be classified into three serotypes accord-
ing to the presence of somatic antigens and into two biotypes, classic and El Tor,
according to specific phenotypic characteristics. There is no evidence of differ-
ent clinical spectra among the three serotypes of V. cholerae. The classic biotype,
responsible for the first six pandemics of cholera, causes an approximately equal
number of symptomatic and asymptomatic cases, whereas the El Tor biotype
causes more asymptomatic infections. The classic biotype is confined to the
south of Bangladesh, and the El Tor biotype is responsible for the current
pandemic. Variants of El Tor biotype, that share phenotypic features of both
biotypes, are responsible for the current epidemics in Asia, Africa, and Latin
America and may cause more severe disease. The O139 serogroup is composed
of a variety of genetically diverse strains, both toxigenic and nontoxigenic; it
is genetically closer to El Tor V. cholerae. 

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 CHAPTER 286  CHOLERA AND OTHER VIBRIO Infections 1917.e3

ABSTRACT KEYWORDS
Cholera is a feared epidemic diarrheal disease caused by Vibrio cholerae cholera
serogroup O1 and, since 1992, by the new serogroup O139. The disease is vibrio
characterized by acute watery diarrhea. In its more severe form, a person may diarrhea
be severely dehydrated and in hypovolemic shock; the patient may die in a dehydration
matter of a few hours after contracting the infection if treatment is not provided. epidemics
Cholera is endemic today in Africa, Asia, and Latin America. Seven pandemics
have been registered in history since 1817; the most recent has lasted more
than five decades since its recognition in Indonesia in 1961. Changes in the
environment and in the pathogen have promoted transmission to humans.
Diagnosis is suspected based on clinical presentation and confirmed by isolation
of Vibrio in culture or by molecular methods. Treatment is based on replacing
intestinal losses with rehydration solutions and providing antimicrobials for
severe cases. Prevention includes implementing sanitation and hygiene and
using licensed oral vaccines in endemic and epidemic settings.

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1918 CHAPTER 286  CHOLERA AND OTHER VIBRIO Infections
EPIDEMIOLOGY
Cholera has both a predisposition to cause epidemics with pandemic potential
and an ability to remain endemic in all affected areas. People of all ages are
at risk to contract the infection in epidemic settings, whereas children older
than 2 years are mainly affected in endemic areas. V. cholerae lives in riverine,
brackish, and estuarine ecosystems, where both O1 and non-O1 strains coexist,
with non-O1 and nontoxigenic O1 strains predominating over toxigenic O1
strains. In its natural environment, V. cholerae lives attached to algae or to
crustacean shells and copepods, with which it coexists in a symbiotic manner.
Several conditions, such as temperature, salinity, and availability of nutrients,
determine the survival of V. cholerae; when these conditions are adverse, vibrios
survive in a viable but nonculturable state. More recent data suggest that
cholera phages modulate the abundance of V. cholerae in the environment and
determine the beginning and end of epidemics. Phages may also play a role in
the emergence of new V. cholerae serogroups by transferring genetic material
to nontoxigenic strains.
From its aquatic environment, V. cholerae is introduced to humans through
contamination of water sources and food.2 Once humans are infected, very
high attack rates may take place, particularly in previously naïve populations.
Acquisition of the disease by drinking contaminated water from rivers, ponds,
lakes, and even tube well sources has been documented.2b Drinking unboiled
water, introducing hands into containers used to store drinking water, drinking
beverages from street vendors, drinking beverages to which contaminated ice
has been added, and drinking water outside the home are risk factors; these
factors contributed to the acquisition of cholera during the large Peruvian
epidemic of 1991. Drinking boiled water, acidic beverages, and carbonated
water and using narrow-necked vessels for storing water are protective measures.
Epidemics of cholera associated with the ingestion of leftover rice, raw fish,
cooked crabs, seafood, raw oysters, and fresh vegetables and fruits have been
documented. Person-to-person transmission is less likely to occur because
a large inoculum is necessary to transmit disease. High transmission rates
(approximately 50%) are reported among household contacts of patients with
cholera in endemic areas.
Epidemics of cholera tend to occur during the hot season. Factors affect-
ing climate change and climate variability have an impact on the incidence of
cholera. The El Niño–southern oscillation (ENSO), a periodic phenomenon
representative of global climate variability, affects the transmission of cholera
and vector-borne diseases. ENSO causes the warming of normally cool waters
in the Pacific coastline of Peru, thereby promoting phytoplankton bloom,
zooplankton bloom, and V. cholerae proliferation.3
Some host factors are important in the transmission of cholera. The chronic
gastritis associated with Helicobacter pylori predisposes to cholera by induc-
ing hypochlorhydria, which reduces the ability of the stomach to contain the
Number of cholera cases per continent
450
400
350
Number of cases per 1000
300
250
200
150
100
50
0
1990 1992 1994 1996
  FIGURE 286-1.     World distribution of cholera from 1989 to 2015 based on reports to the World Health Organization. (Reprinted with permission from the World Health Organiza-
tion. Cholera, 2016. Wkly Epidemiol Rec. 2017;92:521-530.)
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infection. An unexplained predisposition to severe disease due to El Tor biotype
in persons with the O blood group has been observed in Asia and more recently
in Latin America. Innate predisposition has also been reported in endemic areas.
Thus, complex associations among climatic, seasonal, bacterial, and human
factors affect cholera transmission. Although for the most part cholera affects
developing countries, several developed countries, such as the United States,
Canada, and Australia, have reported indigenous and imported cases.4 The
most recent epidemics occurred in Haiti in 2010 and Yemen in 2016 and
2017.5 Figure 286-1 shows the distribution of cholera in the world from 1989
to 2015.6 
PATHOBIOLOGY
V. cholerae O1 and O139 cause clinical disease by secreting an enterotoxin that
promotes the secretion of fluids and electrolytes by the small intestine. The
infectious dose of bacteria varies with the vehicle. When water is the vehicle,
more bacteria are needed to cause disease (103 to 108), but when the vehicle
is food, lower amounts are needed (102 to 104). The incubation period varies
from 12 to 72 hours; the median is 1.4 days. Cholera toxin (CTX) has two
subunits, a pentamer B subunit and a monomer A subunit. The B subunit
allows binding of the toxin to a specific receptor, a ganglioside (GM1) located
on the surface of cells lining the mucosa along the intestine of humans and
certain suckling mammals. The active, or A, subunit has two components,
A1 and A2, linked by a disulfide bond. Activation of adenylate cyclase by the
A1 component results in an increase in cyclic adenosine monophosphate in
intestinal epithelial cells, which blocks the absorption of sodium and chloride
by microvilli and promotes the secretion of chloride and water by crypt cells.
These events lead to the production of watery diarrhea with electrolyte con-
centrations similar to those of plasma, as shown in Table 286-1. A few other
toxins have been isolated from pathogenic V. cholerae, but their roles in genesis
of the disease are less clear. 
CLINICAL MANIFESTATIONS
Cholera is characterized by watery diarrhea and dehydration, which ranges from
mild to severe and life-threatening.7 Patients with mild dehydration cannot be
differentiated from those infected by other enteric pathogens causing watery
diarrhea. In contrast, patients with severe dehydration secondary to cholera are
easy to identify in that their stools have the appearance of rice water, and no
other clinical illness produces such severe dehydration as quickly (in a matter
of a few hours) as cholera. Onset of the disease is abrupt and characterized by
watery diarrhea, vomiting, generalized cramps, and oliguria. Physical exami-
nation shows a feeble pulse, fever is rarely present, patients look anxious and
restless, the eyes are very sunken, mucous membranes are dry, the skin has
lost its elasticity and when pinched retracts very slowly, the voice is almost
nonaudible, and intestinal sounds are prominent. Although watery diarrhea
Asia
Africa
America
1998 2000 2002 2004 2006 2008 2010
 CHAPTER 286  CHOLERA AND OTHER VIBRIO Infections 1918.e1
The genetic material of El Tor V. cholerae O1 is included in two circular
chromosomes, the larger containing 3 megabases and the smaller containing
1.07 megabases. The main virulence genes are ctxA and ctxB, which encode
CTX subunits A and B, respectively, and tcpA, which codes for toxin coregu-
lated pilus. Regulation of expression of these genes is complex. Recent data
suggest that vibrios are able to upregulate the expression of CTX in response to
intestinal fluid components as well as in the presence of certain environmental
factors. Genes unique to El Niño–southern oscillation (ENSO) V. cholerae
may encode specific features that allow this biotype to better survive in the
environment as well as to be more infectious to humans.

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 CHAPTER 286  CHOLERA AND OTHER VIBRIO Infections
TABLE 286-1 ELECTROLYTE COMPOSITION OF CHOLERA STOOLS AND SOLUTIONS RECOMMENDED FOR TREATMENT
Na+
Stools of adults with severe cholera 130
Intravenous lactated Ringer solution 130
Intravenous normal saline 154
Standard oral rehydration solution promoted by the WHO 90
Reduced-osmolarity oral rehydration solution promoted by the WHO 75
Rice-based oral rehydration solution 90
*Lactated Ringer solution contains citrate instead of bicarbonate.
†
Bicarbonate is replaced by trisodium citrate.
Glucose concentration is in mg/dL, electrolyte concentrations are in mEq/L, and osmolarity is in mOsm/L.
Cl− = chloride; K+ = potassium; Na+ = sodium; WHO = Word Health Organization.
Modified with permission from Seas C, DuPont HL, Valdez LM, et al. Practical guidelines for the treatment of cholera. Drugs. 1996;51:966-973.
is the hallmark of cholera, some patients do not have diarrhea but instead
have abdominal distention and ileus, a relatively rare type of cholera called
cholera sicca.
Laboratory findings in patients with severe dehydration consist of an increase
in hematocrit, urine specific gravity, and total serum protein; azotemia; meta-
bolic acidosis with a high anion gap; normal or low serum potassium levels; and
normal or slightly low sodium and chloride levels. The calcium and magnesium
content in plasma is high as a result of hemoconcentration. Leukocytosis
is observed in patients with severe cholera. Hyperglycemia, caused by high
concentrations of epinephrine, glucagon, and cortisol stimulated by hypov-
olemia, is more commonly seen than hypoglycemia. Acute renal failure is the
most severe complication of cholera. Incidence rates of 10.6 cases per 1000
were reported in Peru during the first months of the 1991 epidemic. Patients
with acute renal failure almost always have a history of improper rehydration.
Cholera in pregnant women carries a poor prognosis. Pregnant women have
more severe clinical illness, especially when the disease is acquired at the end
of the pregnancy. Fetal loss occurs in as many as 50% of these pregnancies.
Cholera in the elderly also carries a poor prognosis because of an increase in
complications, particularly acute renal failure, severe metabolic acidosis, and
pulmonary edema.  Start an oral antimicrobial agent in patients with severe cholera when full rehydra-
DIAGNOSIS
Chaotic movement under dark-field microscopy and a high number of bacteria
in a stool sample from patients with diarrhea are characteristic of V. cholerae
infection. Specific antisera against the serotype block the movement of vibrios
and allow confirmation of the diagnosis. Under epidemic conditions, observ-
ing bacteria with a darting movement in a stool sample from a patient with
suspected infection under dark-field microscopy is adequate to make the diag-
nosis. Definitive confirmation requires isolation of the bacterium in culture.
Specific medium is needed to isolate V. cholerae from stool. Higher sensitivity
and specificity have been reported with DNA amplification by polymerase
chain reaction (PCR) for detection of vibrios in stool and environmental
samples. A number of rapid tests have been developed, but few are suitable
for public health purposes.  with simple solutions containing glucose and electrolytes. The World Health
TREATMENT 
The objectives of therapy are to restore the fluid losses caused by diarrhea and
vomiting, to correct the metabolic acidosis, to restore potassium deficits, and
to replace continuous fluid losses. Treatment of patients with milder forms of
dehydration is easy, but treatment of patients with severe dehydration requires
experience and proper training. The intravenous route should be restricted
to patients with some dehydration who do not tolerate the oral route, those
who purge more than 10 to 20 mL/kg/hour, and all patients with severe dehy-
dration. Rehydration should be accomplished in two phases: the rehydration
phase and the maintenance phase. The purpose of the rehydration phase is to
restore normal intravascular volume, and it should last no longer than 4 hours.
Intravenous fluids should be infused at a total volume of 100 mL/kg during the
rehydration phase in severely dehydrated patients. Lactated Ringer solution is
preferred, but other solutions may be used as well (see Table 286-1). All signs
of dehydration should have disappeared and the patient should pass urine at
a rate of 0.5 mL/kg/hour or greater after the rehydration phase is finished. The
maintenance phase follows immediately. During this phase, the objective is to
maintain normal hydration status by replacement of ongoing losses. The oral
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1919
Cl− K+ HCO3− GLUCOSE OSMOLARITY
100 20 44
109 4 28* 0 271
154 0 0 0 308
†
80 20 10 111 311
65 20 10† 75 245
80 20 10† 270
TABLE 286-2 RECOMMENDATIONS FOR TREATMENT OF
CHOLERA PATIENTS
Determine the degree of dehydration on arrival.
Rehydrate the patient in two phases:
• Rehydration phase—lasts 2 to 4 hours
• Maintenance phase—lasts until the end of the diarrheal episode
Register and periodically review input and output in predesigned charts.
Use the intravenous route in the following situations:
• In all severely dehydrated patients, in whom the total volume to be infused
during the rehydration phase is 100 mL/kg. For patients older than 1 year,
30 mL/kg should be infused in the first 30 minutes, the remaining 70 mL/kg
should be infused in 2.5 hours. For children younger than 1 year, the first
30 mL/kg should be infused in 1 hour.
• Patients with some dehydration who are unable to tolerate the oral route
• Patients with high stool output (>10 mL/kg/hour) during the maintenance
phase
Use oral rehydration solutions, glucose or rice based, during the maintenance phase
to match ongoing losses. Volumes of 800 to 1000 mL/hour are usually required.
Low-osmolarity solutions are not recommended.
tion has been achieved and oral tolerance is confirmed. Single-dose doxycycline,
300 mg, is the preferred regimen. Erythromycin or a quinolone is a suitable alter-
native.
Discharge patients only if oral tolerance is adequate (≥1000 mL/hour), urine output
is satisfactory (≥40 mL/hour), and stool volume is low (≤400 mL/hour).
Modified with permission from Seas C, DuPont HL, Valdez LM, et al. Practical guidelines for the
treatment of cholera. Drugs. 1996;51:966-973.
route is preferred during this phase, and the use of oral rehydration solutions
is highly recommended. Oral rehydration therapy uses the principle of common
transportation of solutes, electrolytes, and water by the intestine not affected
by cholera toxin. People with diarrhea can undergo successful rehydration
Organization recommends an oral rehydration solution with reduced osmolar-
ity (245 mOsm/L) to treat all diarrheal diseases. This solution contains lower
sodium than the standard oral rehydration solution promoted since 1975 (75 vs.
90 mEq/L). No more symptomatic hyponatremia is observed with the reduced-
osmolarity solution than with the standard solution. The addition of l-histidine
to rice-based oral rehydration solutions has been shown to reduce the volume
and duration of diarrhea and the unscheduled use of intravenous therapy in
adult cholera patients. Patients without severe dehydration who tolerate the
oral route can be rehydrated with oral rehydration solutions exclusively and
discharged promptly from the health center. Recommendations for treatment
of cholera patients are shown in Table 286-2. Treatment of cholera caused by
V. cholerae O139 is the same as described earlier.
Antimicrobial agents are not life-saving and always need to be accompa-
nied by fluid therapy. Effective antibiotics in patients with severe dehydration
decrease the duration of diarrhea and the volume of stool by nearly half.A1 Oral
tetracycline and doxycycline are the agents of choice in areas of the globe where
sensitive strains predominate. A single dose of doxycycline (300 mg) is the
preferred regimen. Pregnant women can be treated with erythromycin or fura-
zolidone. Because of the emergence of resistance to tetracyclines and other
antimicrobials in many endemic areas, the quinolones and, more recently,
azithromycin have been tested in clinical trials. A single-dose regimen of azithro-
mycin (20 mg/kg) showed clinical and bacteriologic results that were compa-
rable to a 3-day regimen with erythromycin and to a single-dose regimen of

ciprofloxacin in children and comparable to a single-dose regimen of ciprofloxa-
cin (1 g) in adults, and 1 g azithromycin is equivalent to 3 days of norfloxacin
(400 mg twice daily).A2  The addition of oral zinc (30 mg/day) to an erythromycin
regimen in children reduced the duration of diarrhea by 12%, with an additional
11% reduction in the volume of diarrhea in comparison to placebo. Antimotility
agents such as loperamide or diphenoxylate, adsorbents, analgesics, and anti-
emetics are not recommended. Antisecretory drugs, including racecadotril, an
enkephalinase inhibitor, are not useful in patients with severe cholera.
PREVENTION
Access to potable water and ensuring proper management of excreta to avoid
contamination of other water sources are important measures to reduce trans-
mission of cholera. Alternative ways to prevent cholera transmission are nec-
essary in developing countries. Water can be made safer to drink by boiling,
adding chlorine, or filtering it with cloth made of cotton. Chemoprophylaxis
of household contacts of cholera cases is not routinely recommended.
An ideal vaccine against cholera should elicit a fast and long-lasting immune
response with minimal side effects. Parenteral vaccines are no longer recom-
mended. Two oral vaccines, the two-dose regimen of the inactivated vaccine
WC-BS (whole cell plus B subunit) and a single dose of the live attenuated
CVD 103-HgR vaccine, have been tested extensively in epidemic settings
and in field trials in endemic areas, where they have safely elicited excellent
immunogenicity.A3,A4 Although the WC-BS vaccine showed good short-term
protective efficacy (85% at 6 months), the results at 3 and 5 years were less
impressive (40% or less).A5,A6 A large effectiveness study in Mozambique con-
firmed the high short-term protection against cholera (80%) by this vaccine,
especially against severe dehydration (90%). In Guinea, oral vaccine was 87%
protective. In addition, reanalysis of data on this vaccine in field trials and in
Zanzibar has shown that it may also confer herd protection in the unvacci-
nated population. Cost-effectiveness of interventions like this require prices of
the oral vaccine below 1.3 USD. More recently, a single dose of the whole cell
oral killed vaccine achieved 89.7% effectiveness during a cholera outbreak.8
Complementary use of oral cholera vaccination, water sanitation, and hygiene
interventions may have additive impact in endemic areas. A large field trial of the
live attenuated vaccine in an endemic country showed no protective efficacy.
However, this vaccine is immunogenic and effective in adult travelers and has
been recently licensed in the United States.9 Indications for use of the cur-
rently available cholera vaccines include travel to endemic areas and situations
in which high attack rates of cholera are expected, such as after environmen-
tal disasters, in refugee camps, and in urban slums in highly endemic areas.
Preemptive and reactive vaccination approaches should be thoroughly evaluated
in epidemic settings. New oral vaccines, including both killed and live Vibrio,
are being evaluated in endemic areas, with promising preliminary reports.  A5. Bi Q, Ferreras E, Pezzoli L, et al. Protection against cholera from killed whole-cell oral cholera vac-
PROGNOSIS
Patients with severe cholera left untreated or improperly treated carry a poor
prognosis, with mortality rates higher than 50%. However, case-fatality rates
during epidemics may be reduced to values below 1% even in disaster situ-
ations, provided adequate access to health care centers and proper manage-
ment of patients can be ensured. For example, mortality rates were extremely
low during the Latin America epidemic in the 1990s, but rates of 19 to 35
deaths/1000 person-years were estimated during the epidemic in Haiti.10
Lack of treatment, delay in treatment, and not being managed in an estab-
lished treatment center were factors associated with mortality in a study in
Cameroon.11 
OTHER VIBRIO INFECTIONS
Noncholera vibrios have worldwide distribution and coexist in environments in
which V. cholerae lives. They cause a spectrum of clinical syndromes, including
acute diarrhea, soft tissue infections, and sepsis,12 especially in immunocom-
promised hosts. The CDC estimates about 80,000 cases of vibriosis annu-
ally in the United States, about two thirds of which are food borne.13 Vibrio
parahaemolyticus predominates (about 45% of isolates) but is associated with
a case-fatality rate below 1%. In contrast, Vibrio vulnificus accounts for about
20% of the isolates but is associated with a case-fatality rate of about 30%.
Vibrio illnesses in the United States are seasonal and peak during the summer.
The incubation period for noncholeragenic Vibrio infection is usually 12 to
72 hours but can be as long as 1 week.
Nontoxigenic V. cholerae causes gastroenteritis, but unlike toxigenic V. chol-
erae O1 or O139, nontoxigenic V. cholerae does not cause epidemics. Illness
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ranges in severity from mild diarrhea to severe watery diarrhea. Fever and
bloody diarrhea are unusual, but immunocompromised persons and those
with liver disease can experience more severe illness, including fever, chills,
and septic shock.
V. parahaemolyticus lives in marine environments and is a source of intestinal
illness associated with the ingestion of contaminated shellfish. Certain serovars
have shown pandemic spread (O3:K6 and O4:K68). It is not well known
how this Vibrio causes infection in humans, but the clinical illness may mimic
cholera, although most cases are milder and self-limited forms of acute watery
diarrhea. Acute dysentery is reported rarely. Oral antibiotics, as used for trave-
ler’s diarrhea (Chapter 270), are usually efficacious, although local resistance
patterns vary.
V. vulnificus is associated with wound infections in persons in contact with
contaminated water as well as with primary sepsis in immunocompromised
hosts. This pathogen is responsible for 95% of seafood related mortality in
the United States. Wound infections follow trauma and are characterized by
rapid progression of skin and soft tissue involvement, with necrosis and bulla
formation occurring in more severe cases. Fever, chills, and sepsis syndrome
may ensue rapidly. Primary sepsis with bacteremia and metastatic lesions on
the skin, characterized by disseminated erythematous lesions that may evolve to
necrotic lesions, is a distinctive clinical manifestation in patients with chronic
liver illnesses or alcohol dependence and in patients with blood disorders such
as thalassemia. A history of seafood ingestion, usually oysters, is typical. Patients
are acutely ill with high fever and need to be managed aggressively with fluid
resuscitation, surgical débridement, general supportive care, and antibiotic
coverage. V. parahaemolyticus wound infections are generally less severe than
those caused by V. vulnificus. However, in persons with liver disease or those
who are immunocompromised, fatal infections can occur.
The recommended antibiotic approach is an intravenous combination of
cefotaxime, 2 g four times a day, plus doxycycline, 100 mg two times a day.
This combination is synergistic in vitro. Alternative antimicrobials are cef-
tazidime and ciprofloxacin.
Grade A References
A1. Leibovici-Weissman Y, Neuberger A, Bitterman R, et al. Antimicrobial drugs for treating cholera.
Cochrane Database Syst Rev. 2014;6:CD008625.
A2. Bhattacharya MK, Kanungo S, Ramamurthy T, et al. Comparison between single dose azithromycin
and six doses, 3 day norfloxacin for treatment of cholera in adult. Int J Biomed Sci. 2014;10:248-251.
A3. Lopez AL, Deen J, Azman AS, et al. Immunogenicity and protection from a single dose of interna-
tionally available killed oral cholera vaccine: a systematic review and metaanalysis. Clin Infect Dis.
2018;66:1960-1971.
A4. Desai SN, Akalu Z, Teshome S, et al. A randomized, placebo-controlled trial evaluating safety and
immunogenicity of the killed, bivalent, whole-cell oral cholera vaccine in Ethiopia. Am J Trop Med
Hyg. 2015;93:527-533.
cines: a systematic review and meta-analysis. Lancet Infect Dis. 2017;17:1080-1088.
A6. Qadri F, Wierzba TF, Ali M, et  al. Efficacy of a single-dose, inactivated oral cholera vaccine in
Bangladesh. N Engl J Med. 2016;374:1723-1732.
GENERAL REFERENCES
For the General References and other additional features, please visit Expert Consult
at https://expertconsult.inkling.com.
 CHAPTER 286  CHOLERA AND OTHER VIBRIO Infections 1920.e1

GENERAL REFERENCES
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8. Azman AS, Parker LA, Rumunu J, et al. Effectiveness of one dose of oral cholera vaccine in response
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9. Wong KK, Burdette E, Mahon BE, et al. Recommendations of the Advisory Committee on Immu-
nization Practices for use of cholera vaccine. MMWR Morb Mortal Wkly Rep. 2017;66:482-485.
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1920.e2 CHAPTER 286  CHOLERA AND OTHER VIBRIO Infections
REVIEW QUESTIONS 4. Intravenous fluids are indicated in patients with cholera under the follow-
ing conditions:
1. Cholera is an acute diarrheal disease caused by:
A . In every patient with cholera irrespective of the degree of dehydra-
A . Vibrio cholerae O1 and Vibrio cholerae O139 tion
B. Vibrio cholerae O1 only B. In patients with some degree of dehydration
C. Vibrio cholerae O139 only C. In patients with severe dehydration, in those who cannot tolerate the
D. Non-O1 Vibrio cholerae oral route, and in those with high stool output
E. Vibrio vulnificus D. In patients who do not respond to antimicrobials
Answer: A  Cholera is the disease caused by both O1 V. cholerae and, since E. In those thought to be infected by resistant pathogens
1992, O139 V. cholerae. These two pathogens have the potential to cause local Answer: C  Intravenous fluids should be restricted to those with severe dehy-
epidemics with pandemic potential. dration, to those with lesser degrees of dehydration who cannot tolerate the
oral route, and to those with high stool output.
2. The typical solute concentration of cholera stools, compared with
plasma, is: 5. A patient with chronic liver disease presents to the emergency depart-
A . Hypertonic ment with the acute onset of fever after ingestion of oysters. The physical
B. Hypotonic examination reveals a patient in shock with multiple erythematous lesions
C. Isotonic on the extremities. The most likely pathogen involved is:
D. Hyperosmolar A . Vibrio cholerae O1
E. Hypo-osmolar B. Vibrio cholerae O139
Answer: C  Typical diarrhea of cholera is isotonic compared with plasma, C. Vibrio vulnificus
having almost the same concentration of sodium. D. Salmonella enterica
E. Shigella dysenteriae type 1
3. The benefit of using effective antimicrobials in patients with severe Answer: C  Vibrio vulnificus is the most likely pathogen. It causes severe sepsis
cholera is: with soft tissue involvement in patients with chronic liver disease.
A . To reduce the excretion of Vibrio
B. To reduce the duration of diarrhea and volume of stool by half
C. To reduce the duration of hospitalization by half
D. To reduce the need for intravenous treatment
E. To reduce the need for oral rehydration solutions
Answer: B  Effective antimicrobials reduce the duration of diarrhea and the
volume of stools by almost half compared with controls.

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