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 taurocholate-tellurite-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 alkaline-peptone 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+ co-transport 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)

Treatment

None or Mild, but Diarrhea 

<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

Stool        

 Adult 135 15 100 45

 Child 100 25 90 30

Ringer's lactate

130 4a  109 28

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 Stool Findings

Examples of Pathogens Involved

Noninflammatory (enterotoxin)

Proximal small bowel

Watery diarrhea

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 small bowel

Dysentery or inflammatory diarrhea

Fecal polymorphonuclear leukocytes; substantial increase in fecal lactoferrin

Shigella spp., Salmonella spp.,

Penetrating Distal small bowel

Enteric fever

Fecal mononuclear leukocytes

Salmonella typhi, Y. 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  Lactase deficiency Small-bowel bacterial overgrowth Malabsorption syndromes (tropical and celiac sprue)

Occurs in 1% of travelers with acute diarrhea     Protozoa account for 1/3 of cases

Initial presentation or exacerbation of inflammatory bowel disease

May be precipitated by traveler's diarrhea

Irritable bowel syndrome Occurs in 10% of travelers with traveler's diarrhea

Reactive arthritis (formerly known as Reiter's syndrome)

Particularly likely after infection with invasive organisms (Shigella, Salmonella, Campylobacter, Yersinia) 

Hemolytic-uremic syndrome (hemolytic anemia, thrombocytopenia, and renal failure)

Follows infection with Shiga toxin–producing bacteria (Shigella dysenteriae type 1 and enterohemorrhagic Escherichia coli) 

Guillain-Barré syndrome Particularly likely after Campylobacter infection 

Bacterial Food Poisoning

Incubation Period, Organism

Symptoms Common Food Sources

1–6 h Staphylococcus aureus 

Nausea, vomiting, diarrhea

Ham, poultry, potato or egg salad, mayonnaise, cream pastries

8–16 h Clostridium perfringens 

Abdominal cramps, diarrhea (vomiting rare)

Beef, poultry, legumes, gravies

>16 h Vibrio cholerae  Watery diarrhea Shellfish, waterEnterohemorrhagic E. coli 

Bloody diarrhea Ground beef, roast beef, salami, raw milk, raw vegetables, apple juice

Salmonella spp.  Inflammatory diarrhea Beef, poultry, eggs, dairy products

Shigella spp.  Dysentery Potato or egg salad, lettuce, raw vegetables

Vibrio parahaemolyticus 

Dysentery Mollusks, crustaceans

The End