Cholera

Overview

Cholera is an acute secretory diarrhoea caused by the toxin of Vibrio cholerae. It can kill a previously well child within hours through massive fluid loss, shock and acidosis, yet it is cured cheaply by prompt rehydration. It is a disease of poor water supply and sanitation, occurs in outbreaks, and is notifiable. The exam focuses on the organism, the toxin mechanism, the clinical picture, the rehydration plan and prevention.

Organism and epidemiology

The organism

• Vibrio cholerae: a curved, highly motile Gram-negative rod with a single flagellum.
• Epidemic serogroups: O1 and O139 (the "Bengal" strain, first found in Bangladesh). Non-O1/non-O139 strains cause only mild diarrhoea and do not cause epidemics.
• O1 has two biotypes: classical and El Tor. Most cholera today is El Tor or O139.
• El Tor compared with classical: more mild and silent infections, fewer secondary cases in a household, more carriers, and longer survival outside the body.
• Vibrios are acid-sensitive and killed by boiling, drying and sunlight.

Spread

• Humans are the only natural reservoir (cases and carriers).
• Faecal-oral: contaminated water above all, then food, drinks and contaminated hands; bottle feeding is a risk in infants.
• A large dose of organisms is needed in a person with normal stomach acid; low gastric acid increases the risk.
• Incubation: from a few hours to 5 days, usually 1-3 days.
• Breastfeeding protects children in the first 2 years; malnourished children have longer, more severe illness.
• Infection is often silent: asymptomatic infection is commoner than disease, and only about 1-2% of infected people develop severe diarrhoea (Akbar).
• Outbreaks follow floods, crowded camps and breakdown of water and sewage systems.

Pathophysiology of severe dehydration

1. Swallowed vibrios that survive the stomach colonise the small intestine and stick to the mucosa.
2. They produce cholera enterotoxin. The binding subunit attaches the toxin to ganglioside receptors; the active part switches on adenylate cyclase.
3. Cyclic AMP rises in the enterocyte:
   • Crypt cells actively secrete chloride (with sodium and water following).
   • Villous cells absorb less sodium chloride.
4. Large volumes of isotonic fluid enter the lumen, rich in bicarbonate and potassium.
5. The organism does not invade and the mucosa is not inflamed.

Two extra toxins described by Akbar: zonula occludens toxin (loosens tight junctions) and accessory cholera enterotoxin.

What the losses cause

In cholera gravis, purging reaches 500-1,000 mL per hour, so a child can be in shock within hours.

Clinical features

Typical course

• Sudden onset of profuse, painless, watery diarrhoea, soon looking like "rice water" (flecks of mucus) with a fishy smell.
• Vomiting, which may be effortless and projectile, often without nausea.
• Fever is absent or low-grade; there is no tenesmus and no blood.
• Within 2-3 hours signs of severe dehydration appear.

Park describes three stages:

In infants, look for a sunken fontanelle, absent tears, dry mouth and lethargy. Kussmaul breathing signals acidosis.

Complications

• Hypovolaemic shock and death if fluids are delayed.
• Acute renal failure (acute tubular necrosis).
• Hypokalaemia: ileus, arrhythmia.
• Hypoglycaemia, seizures, coma (more in children).
• During treatment: pulmonary oedema from over-rapid fluids, and transient tetany while electrolytes are corrected.

Laboratory findings

Blood

• Metabolic acidosis (low bicarbonate).
• Hypokalaemia.
• Akbar adds hyponatraemia, hypochloraemia and hypoglycaemia in children.
• Raised urea and creatinine with prerenal or established renal failure; raised haematocrit from haemoconcentration.

Stool

• Few white cells or red cells (no inflammation).
• Dark-field or wet-mount microscopy: vibrios with a rapid "darting" (shooting-star) motility.
• Immobilisation test: adding O1 antiserum stops the motility; a rapid, specific presumptive test.
• Culture is the gold standard: collect stool or a rectal swab before antibiotics, carry it in alkaline peptone water or Cary-Blair medium, and plate on alkaline bile-salt media (TCBS agar is the usual selective plate); confirm with O1 or O139 antisera.

Differential diagnosis

Watery diarrhoea from enterotoxigenic E. coli or rotavirus. Cholera is suggested by large outbreaks, older children and adults affected, and very rapid dehydration.

Rehydration management

Rehydration is the treatment; everything else is secondary.

Some or no dehydration: oral rehydration

• ORS is the treatment of choice; Akbar notes rice-based ORS is better than standard ORS in cholera.
• Akbar gives about 100 mL/kg over 4 hours, then as much as the child will take to match ongoing losses.
• Vomiting does not stop ORS: give small, frequent sips.
• Reassess every 1-2 hours (more often if purging is heavy), especially in the first 24 hours.

Severe dehydration or shock: IV fluids

• Use Ringer's lactate (or dextrose saline if not available); all fluids should contain glucose or be followed by ORS to prevent hypoglycaemia.
• Shock: 20 mL/kg IV over 10-15 minutes, repeated if the pulse is still weak.
• Then 100 mL/kg in total:

• Start ORS as soon as the child can drink; switch fully to ORS when stable.
• Add potassium once urine is passed.
• Continue feeding (breast milk throughout; food as soon as the deficit is replaced). Small frequent feeds are tolerated better.

Antibiotics

Antibiotics are an adjunct: they shorten the illness, reduce stool volume and fluid needs, and cut the period of vibrio excretion. Give them once the child is rehydrated and vomiting has settled. Options in Akbar:

• Cephalosporins and aminoglycosides are not clinically effective against cholera.
• If diarrhoea continues after 48 hours of treatment, suspect resistance (Park).
• Choice depends on local sensitivity patterns.

Zinc

Give zinc once vomiting stops: 10 mg daily under 6 months and 20 mg daily over 6 months, for 2 weeks. It shortens the episode and reduces later diarrhoea.

Prognosis

• Untreated severe cholera kills over half of those with significant symptoms (Akbar).
• With quick, adequate rehydration, deaths are rare; Akbar quotes a child case fatality of about 1-2% even with early treatment.

Prevention and vaccination

General measures

• Prolonged breastfeeding: the most important protection for infants.
• Safe water: boil or chlorinate; protect water sources; sanitary latrines.
• Hand washing with soap after defecation and before food; protect food from flies; eat food cooked and hot.
• Isolate patients; disinfect stools, vomit and linen.
• Notify: cholera is notifiable nationally and to WHO under the International Health Regulations. Park: an area is considered clear when twice the incubation period (10 days) has passed since the last case.

Chemoprophylaxis

Only for household or closed-community contacts, not the whole community (Park). Park gives doxycycline 6 mg/kg as a single dose for children under 15 (or tetracycline for 3 days).

Oral cholera vaccines

• Protection is partial and short: Akbar quotes about 50% efficacy for 3-6 months.
• Vaccines support but do not replace water, sanitation and hygiene. Use in Pakistan is for outbreaks and high-risk settings as decided by health authorities; check the current national guideline.

Quick revision

• V. cholerae O1 (El Tor, classical) and O139; man the only reservoir; water-borne.
• Toxin → adenylate cyclase → cAMP → chloride secretion; no invasion.
• Painless rice-water stools, vomiting, rapid shock; little or no fever.
• Acidosis, hypokalaemia, hypoglycaemia, renal failure.
• Stool: few white cells; darting motility; culture confirms.
• Severe: Ringer's lactate 100 mL/kg (30 + 70 mL/kg); then ORS; potassium once urine flows.
• Azithromycin 20 mg/kg single dose (or ciprofloxacin, doxycycline); zinc for 2 weeks.
• Prevention: breastfeeding, safe water, sanitation, isolation, notification, oral vaccines.

Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics; Park's Preventive and Social Medicine).

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