Cholera Gastroenteritis and
Food Poisoning
Dr. Ravi Kant
Assistant Professor,
Department of medicine

Definition

Cholera is an acute diarrheal disease that can, in a
matter of hours, result in profound, rapidly
progressive dehydration and death.

The term cholera has occasionally been applied to
any severely dehydrating secretory diarrheal
illness, whether infectious in etiology or not, it now
refers to disease caused by V. cholerae serogroup
O1 or O139—i.e., the serogroups with epidemic
potential.

The natural habitat of V. cholerae is coastal salt
water and brackish estuaries, where the organism
lives in close relation to plankton.

Humans become infected incidentally but, once
infected, can act as vehicles for spread.

Ingestion of water contaminated by human feces
is the most common means of acquisition of V.
cholerae.

There is no known animal reservoir.
Pathogenesis

Cholera is a toxin-mediated disease.

The watery diarrhea characteristic of cholera is
due to the action of cholera toxin, a potent
protein enterotoxin elaborated by the organism
in the small intestine.

The toxin-coregulated pilus (TCP), so named
because its synthesis is regulated in parallel with
that of cholera toxin, is essential for V. cholerae
to survive and multiply in (colonize) the small
intestine.

Cholera toxin, TCP, and several other virulence
factors are coordinately regulated by ToxR.

This protein modulates the expression of genes
coding for virulence factors in response to
environmental signals via a cascade of
regulatory proteins.

Additional regulatory processes, including
bacterial responses to the density of the bacterial
population (in a phenomenon known as quorum
sensing), control the virulence of V. cholerae.
Clinical Manifestations

In a nonimmune individual, after a 24- to 48-h
incubation period, cholera characteristically
begins with the sudden onset of painless watery
diarrhea that may quickly become voluminous.

Patients often vomit. In severe cases, volume loss
can exceed 250 mL/kg in the first 24 h.

If fluids and electrolytes are not replaced,
hypovolemic shock and death may ensue.

Fever is usually absent. Muscle cramps due to
electrolyte disturbances are common.

The stool has a characteristic appearance: a
nonbilious, gray, slightly cloudy fluid with
flecks of mucus, no blood, and a somewhat
fishy, inoffensive odor.
Rice water cholera stool

It has been called "rice-water" stool because of
its resemblance to the water in which rice has
been washed.

Clinical symptoms parallel volume contraction:
At losses of <5% of normal body weight, thirst
develops; at 5–10%, postural hypotension,
weakness, tachycardia, and decreased skin turgor
are documented; and at >10%, oliguria, weak or
absent pulses, sunken eyes (and, in infants,
sunken fontanelles), wrinkled ("washerwoman")
skin, somnolence, and coma are characteristic.

Complications derive exclusively from the
effects of volume and electrolyte depletion and
include renal failure due to acute tubular
necrosis.

Thus, if the patient is adequately treated with
fluid and electrolytes, complications are averted
and the process is self-limited, resolving in a
few days.

Elevated levels of blood urea nitrogen and
creatinine consistent with prerenal azotemia;
normal sodium, potassium, and chloride levels.

A markedly reduced bicarbonate level (<15
mmol/L); and an elevated anion gap (due to
increases in serum lactate, protein, and
phosphate).

Arterial pH is usually low (7.2).
Diagnosis

The clinical suspicion of cholera can be
confirmed by the identification of V. cholerae in
stool.

It can be detected directly by dark-field
microscopy on a wet mount of fresh stool, and
its serotype can be discerned by immobilization
with specific antiserum.

Laboratory isolation of the organism requires the
use of a selective medium such as taurocholatetellurite-gelatin (TTG) agar or thiosulfate–
citrate–bile salts–sucrose (TCBS) agar.

If a delay in sample processing is expected,
Carey-Blair transport medium and/or alkalinepeptone water-enrichment medium may be used
as well.

Standard microbiologic biochemical testing
for Enterobacteriaceae will suffice for
identification of V. cholerae.

All vibrios are oxidase-positive.
Treatment: Cholera

Death from cholera is due to hypovolemic shock.

In light of the level of dehydration and the
patient's age and weight, euvolemia should first
be rapidly restored, and adequate hydration
should then be maintained to replace ongoing
fluid losses.

Administration of oral rehydration solution
(ORS) takes advantage of the hexose-Na+ cotransport mechanism to move Na+ across the
gut mucosa together with an actively
transported molecule such as glucose (or
galactose).

This transport mechanism remains intact even
when cholera toxin is active.

ORS may be made by adding safe water to
prepackaged sachets containing salts and sugar or
by adding 0.5 teaspoon of table salt (NaCl; 3.5 g)
and 4 tablespoons of table sugar (glucose; 40 g)
to 1 L of safe water.

The WHO now recommends "low-osmolarity"
ORS for treatment of individuals with
dehydrating diarrhea of any cause.

Rice-based ORS is considered superior to
standard ORS in the treatment of cholera.

ORS can be administered via a nasogastric tube
to individuals who cannot ingest fluid.

Because profound acidosis (pH < 7.2) is
common in this group, Ringer's lactate is the
best choice among commercial products.
Assessing the Degree of
Dehydration in Patients with
Cholera
Degree of Dehydration
Clinical Findings
None or mild,
but diarrhea
Thirst in some cases; <5% loss of total body
weight
Moderate
Thirst,
postural
hypotension,
weakness,
tachycardia, decreased
skin
turgor, dry
mouth/tongue, no tears; 5–10% loss of total body
weight
Severe
Unconsciousness, lethargy, or "floppiness"; weak
or absent pulse; inability to drink; sunken eyes
(and, in infants, sunken fontanelles); >10% loss of
total body weight
Degree of Dehydration, Patient's Age
(Weight)
None or Mild, but Diarrhea
Treatment
<2 years
1/4–1/2 cup (50–100 mL) of ORS, to a
maximum of 0.5 L/d
2–9 years
1/2–1 cup (100–200 mL) of ORS, to a
maximum of 1 L/d
10 years
As much ORS as desired, to a maximum of
2 L/d
Moderate
<4 months (<5 kg)
200–400 mL of ORS
4–11 months (5–<8 kg)
400–600 mL of ORS
12–23 months (8–<11 kg)
600–800 mL of ORS
2–4 years (11–<16 kg)
800–1200 mL of ORS
5–14 years (16–<30 kg)
1200–2200 mL of ORS
15 years (30 kg)
2200–4000 mL of ORS
Composition of World Health
Organization Reduced-Osmolarity
Oral Rehydration Solution (ORS)
Constituent
Concentration, mmol/L
Na+
75
K+
20
Cl–
65
Citrate
10
Glucose
75
Total osmolarity
245
Electrolyte Composition of
Cholera Stool and of Intravenous
Rehydration Solution
Concentration, mmol/L
Substance
Na+
K+
Cl–
Base
Adult
135
15
100
45
Child
100
25
90
30
Ringer's
lactate
130
4a
109
28
Stool
Prevention

Provisionof safe water and facilities for sanitary
disposal of feces, improved nutrition, and
attention to food preparation and storage in the
household can significantly reduce the incidence
of cholera.

Much effort has been devoted to the
development of an effective cholera vaccine
over the past few decades, with a particular
focus on oral vaccine strains.

Traditional killed cholera vaccine given
intramuscularly provides little protection to
nonimmune subjects and predictably causes
adverse effects, including pain at the injection
site, malaise, and fever.

The vaccine's limited efficacy is due, at least in
part, to its failure to induce a local immune
response at the intestinal mucosal surface.

Two types of oral cholera vaccines have been
developed.

The first is a killed whole-cell (WC) vaccine.

Two formulations of the killed WC vaccine have
been prepared: one that also contains the nontoxic
B subunit of cholera toxin (WC/BS) and one
composed solely of killed bacteria.

Protective efficacy rates for both vaccines
declined to 50% by 3 years after vaccine
administration.
Gastrointestinal Pathogens Causing
Acute Diarrhea
Mechanism
Location
Illness
Noninflammatory Proximal small Watery
(enterotoxin)
bowel
diarrhea
Stool Findings
Examples of
Pathogens
Involved
No fecal
leukocytes; mild or
no increase in fecal
lactoferrin
Vibrio cholerae,
enterotoxigenic
Escherichia coli
(LT and/or ST),
Inflammatory
(invasion or
cytotoxin)
Colon or distal Dysentery or Fecal
Shigella spp.,
small bowel
inflammatory polymorphonuclear Salmonella spp.,
diarrhea
leukocytes;
substantial increase
in fecal lactoferrin
Penetrating
Distal small
bowel
Enteric fever Fecal mononuclear Salmonella typhi,Y.
leukocytes
enterocolitica
Approach to the Patient: Infectious
Diarrhea or Bacterial Food Poisoning
Physical Examination

The examination of patients for signs of
dehydration provides essential information
about the severity of the diarrheal illness and the
need for rapid therapy.

Mild dehydration is indicated by thirst, dry
mouth, decreased axillary sweat, decreased
urine output, and slight weight loss.

Signs of moderate dehydration include an
orthostatic fall in blood pressure, skin
tenting, and sunken eyes (or, in infants, a
sunken fontanelle).

Signs of severe dehydration include
lethargy, obtundation, feeble pulse,
hypotension, and frank shock.
Post-Diarrhea Complications of
Acute Infectious Diarrheal Illness
Complication
Comments
Chronic diarrhea
Occurs in 1% of travelers with acute
Lactase deficiency
diarrhea
Small-bowel bacterial overgrowth
Protozoa account for 1/3 of cases
Malabsorption syndromes (tropical and
celiac sprue)
Initial presentation or exacerbation of May be precipitated by traveler's diarrhea
inflammatory bowel disease
Irritable bowel syndrome
Occurs in 10% of travelers with traveler's
diarrhea
Reactive arthritis (formerly known as Particularly likely after infection with
Reiter's syndrome)
invasive organisms (Shigella, Salmonella,
Campylobacter, Yersinia)
Hemolytic-uremic syndrome (hemolytic Follows infection with Shiga toxin–
anemia, thrombocytopenia, and renal producing bacteria (Shigella dysenteriae
failure)
type 1 and enterohemorrhagic Escherichia
coli)
Guillain-Barré syndrome
Particularly likely after Campylobacter
infection
Bacterial Food Poisoning
Incubation Period,
Organism
1–6 h
Staphylococcus aureus
8–16 h
Clostridium perfringens
Symptoms
Common Food Sources
Nausea, vomiting, diarrhea
Ham, poultry, potato or egg
salad, mayonnaise, cream
pastries
Abdominal cramps, diarrhea Beef, poultry, legumes,
(vomiting rare)
gravies
>16 h
Vibrio cholerae
Enterohemorrhagic E. coli
Watery diarrhea
Bloody diarrhea
Salmonella spp.
Inflammatory diarrhea
Shigella spp.
Dysentery
Vibrio parahaemolyticus
Dysentery
Shellfish, water
Ground beef, roast beef,
salami, raw milk, raw
vegetables, apple juice
Beef, poultry, eggs, dairy
products
Potato or egg salad, lettuce,
raw vegetables
Mollusks, crustaceans
The End