Cholera

• Cholera is an acute infection of the small intestine caused by the bacterium Vibrio cholerae, usually caught by drinking water or eating food contaminated by human faeces.
• The cholera toxin forces the gut to pour out water and electrolytes, producing the classic profuse "rice-water" diarrhoea; a severely affected adult can lose up to 1,000 millilitres of stool per hour and die within hours from hypovolaemic shock.^[4]
• Most infection is silent or mild and can be treated with oral rehydration solution (ORS); only patients with severe dehydration need intravenous (IV) fluids, ORS and antibiotics.^[1][3]
• Rehydration is the treatment: sorted promptly, fewer than 1 in 100 patients die, compared with more than half without proper care.^[3][4]
• Prevention rests on safe water, sanitation and hygiene (WASH), early outbreak detection, oral cholera vaccines, and a multisectoral plan under the Global Task Force on Cholera Control (GTFCC).

By the end of this topic you should be able to:

1. Explain how V. cholerae survives, colonises the small intestine, and makes cholera toxin drive secretory diarrhoea.
2. Recognise a cholera case from the history, stool and dehydration signs, and distinguish it from other causes of acute watery diarrhoea.
3. Assess dehydration severity using the WHO signs and select Plan A, Plan B or Plan C correctly, with the right fluid, rate and volume.
4. Choose and dose an antibiotic (including in pregnancy and children) and decide when antibiotics are not indicated.
5. Outline how oral cholera vaccines, WASH and outbreak response work, and what the GTFCC Roadmap to 2030 aims to do.
6. Adapt management for children, pregnant women, severe acute malnutrition, and low-resource settings.

Cholera is an old disease that still kills thousands of people a year. The WHO received reports of 451,499 cases and 7,870 deaths from 47 countries in 2025, the highest annual death count since 1999, while researchers estimate the true burden at 1.3 to 4.0 million cases and 21,000 to 143,000 deaths each year.^[1][4] The gap between reported and estimated numbers reflects weak surveillance and the political disincentive to report.

Two points make cholera essential learning. First, the pathophysiology is a beautifully clear example of a secretory diarrhoea: an intracellular signalling cascade ends in chloride and water pouring into the gut lumen, and the clinical picture follows directly from that mechanism. Second, the management is one of the great successes of clinical medicine and public health. Because the gut mucosa is not damaged, fluid replacement alone, plus ORS that exploits the sodium-glucose co-transporter, reverses the process, and the case fatality rate falls from over 50% to under 1%.^[4]

Cholera is also a marker of inequity. It flourishes where water, sanitation and hygiene are inadequate, and outbreaks follow conflict, displacement, floods, droughts and disasters such as cyclones. A clinician therefore treats the individual patient and, with public health colleagues, addresses the conditions that made them sick.^[4][5]

A cholera case, in the clinical sense, is an illness of acute watery diarrhoea with rapid dehydration; in an outbreak setting, WHO criteria for someone over 5 years old are acute watery diarrhoea more than three times in 24 hours, with or without vomiting.^[4] The infection is caused by V. cholerae, a curved, Gram-negative, motile bacillus that lives in aquatic environments and is spread faeco-orally via contaminated water or food.^[5]

V. cholerae is classified into more than 200 serogroups by the structure of the O antigen of its lipopolysaccharide. Only serogroups O1 and O139 produce cholera toxin and cause cholera and epidemics; non-O1 and non-O139 strains may cause small outbreaks of gastroenteritis, bacteraemia or wound infection but not epidemic cholera.^[4][5] Only O1 has caused recent outbreaks; O139 caused outbreaks in Asia in the 1990s and is now isolated only sporadically.^[1]

O1 strains have three serotypes. Ogawa strains have a methylated terminal perosamine on the O antigen, Inaba strains do not, and Hikojima expresses both and is a rare transitional form. O1 also has two biotypes, classical and El Tor, distinguished by phenotypic and genetic markers.^[5] The classical biotype drove the first six pandemics and is now considered extinct. The ongoing seventh pandemic, which began in Indonesia in 1961, is caused by the El Tor biotype; wave 3 El Tor variants dominate globally today.^[4][5] El Tor strains transmit between people more efficiently, survive better in the environment and in the gut, and produce more asymptomatic than symptomatic carriers compared with classical strains.^[5]

The bacterium needs two things to cause epidemic disease: cholera toxin, carried on the lysogenic bacteriophage CTXphi, and the toxin-coregulated pilus (TCP), which is the phage receptor and the adhesin that forms microcolonies on the gut wall. These are acquired on mobile genetic elements such as the Vibrio pathogenicity islands VPI-1 and VPI-2, which is why environmental non-toxigenic strains can evolve into epidemic strains.^[5]

Cholera is endemic in Asia, Africa, and Latin and Central America and the Caribbean.^[4] A zone is considered endemic when cholera has been confirmed there in 3 of the past 5 years.^[4] Since 2006, more than 50 developing countries have reported increasing numbers of cases. Outbreaks are unpredictable and strike both endemic and non-endemic areas when conditions deteriorate, with refugee camps being particularly susceptible.^[4]

Incidence is highest in children under 5 years, who have little acquired immunity, and lowest, relatively, in adults in endemic areas who have been repeatedly exposed.^[4][5] Cholera follows seasonal patterns: in the Bengal delta, peaks occur in spring and after the monsoon; in Africa, peaks follow the rains.^[4]

Reporting is incomplete. A positive diagnosis is missed because culture, polymerase chain reaction (PCR) or trained staff are often absent, and some countries are slow to declare outbreaks lest trade and tourism suffer. Early reporting actually shortens epidemics, so encouraging countries to notify promptly is itself an intervention.^[4]

The main risk is poverty: inadequate sanitation, contaminated drinking water and unhygienic food handling, especially street food. Handwashing with soap before meals and after defecation reduces risk. Biological risk factors include blood group O, female sex, vitamin A deficiency, hypochlorhydria (from proton-pump inhibitors, antacids or histamine-2 blockers, gastrectomy, or Helicobacter pylori infection), and malnutrition in young children.^[4] Six months of exclusive breastfeeding is recommended for women in endemic communities, because secretory IgA in breast milk protects against severe disease.^[4]

There is no animal reservoir of epidemic cholera. Humans are the principal reservoir during epidemics; the bacteria return to aquatic environments between outbreaks, where they associate with plankton and shellfish. V. cholerae grows best in warm (about 30 degrees C) water of about 15% salinity and pH around 8.5, and it can survive cold winters in a viable but non-culturable state.^[4]

Transmission is faeco-oral through two routes: direct spread when food or water is contaminated by an infected person's faeces, and indirect spread from environmental sources such as ponds, lakes and rivers polluted by human or animal waste. Flies and fomites act as mechanical vectors. Vibrios shed in freshly passed rice-water stool are hyperinfectious for up to 24 hours; prolonged storage or cooking kills the organism.^[4][5]

The infective dose is large. Between 10^3 and 10^8 colony-forming units (CFU) are needed in water, although food reduces gastric acid barrier enough that 10^2 to 10^4 CFU can cause illness, and as few as 10^5 CFU suffice when stomach acid is low.^[4][5] This explains why people taking acid-suppressing drugs and those with hypochlorhydria are at higher risk.

Humans are not just victims. An individual can carry and shed V. cholerae without symptoms. About 80% of infected people remain asymptomatic, yet bacteria appear in their faeces for up to 14 days.^[3] Symptomatic patients shed for 2 days to 2 weeks.^[4] This large hidden reservoir is why outbreaks are hard to control.

The entire illness follows from one molecule.

After ingestion, vibrios must survive gastric acid. Most die, which is why the infective dose is high and why antacids increase susceptibility. Survivors enter the small intestine, their main site of colonisation, and switch on the ToxR regulon in response to bile, bicarbonate, mucin and osmolarity. ToxR upregulates OmpU, an outer membrane porin that confers resistance to bile salts and antimicrobial peptides, and downregulates OmpT. The organism uses its single polar flagellum to swim through the 100 to 400 micrometre mucus layer over the intestinal epithelium, aided by mucinases such as HapA and TagA.^[5]

Attachment is helped by GbpA, which binds N-acetylglucosamine on mucins and epithelial cells. TCP, encoded on VPI-1, then anchors the vibrios and builds microcolonies. Strains lacking TCP cannot colonise animal models or the human intestine.^[5]

Cholera toxin (CT) is an AB5 exotoxin: a catalytic A subunit (CTX-A, a heterodimer of a 22 kDa A1 and a 5 kDa A2 peptide joined by a disulfide bond) and a pentameric B subunit of five identical 11.6 kDa chains.^[5] The B subunit binds GM1 gangliosides on the apical membrane of intestinal epithelial cells; the enzyme neuraminidase (NanH) cleaves sialic acid from higher-order gangliosides to expose more GM1, promoting toxin uptake. CT also binds histo-blood group antigens at a secondary site.^[5]

After binding, the toxin travels by endocytosis to the Golgi and endoplasmic reticulum, where the A1 fragment is freed. Activated by ADP-ribosylation factor 6 (ARF6), A1 catalyses ADP-ribosylation of a G protein-coupled receptor component, activating adenylyl cyclase. Cyclic AMP (cAMP) rises, protein kinase A activates, and the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel is phosphorylated and opened. Chloride and bicarbonate pour into the lumen; sodium and water follow osmotically. The result is a secretory diarrhoea with no mucosal damage. Up to 1,000 mL per hour can be lost in an adult, and 10 to 20 mL per kilogram per hour in a severely affected child.^[4][5]

Accessory toxins contribute but are not the main driver: Zot increases tight-junction permeability, Ace stimulates chloride-bicarbonate transport, MARTX disrupts actin and blocks neutrophil recruitment, HlyA forms pores and kills cells, and VPI-encoded genes and the type VI secretion system help vibrios outcompete the gut microbiota.^[5]

Two more features matter clinically. First, the gut mucosa is intact, so once the toxin is cleared the gut reabsorbs normally and recovery can be rapid. Second, the hyperinfectious state of fresh stool means person-to-person transmission can outpace control efforts in the first 24 hours.^[4][5]

The fluid lost contains sodium, potassium, chloride, bicarbonate and small amounts of protein. Loss of bicarbonate and potassium explains the metabolic acidosis (sometimes severe enough to produce Kussmaul breathing) and hypokalaemia of cholera. Renal hypoperfusion can lead to acute kidney injury. Hypoglycaemia is a particular danger in children, who also develop hypokalaemia and hyponatraemia more easily.^[4]

About 5 to 10% of those infected develop severe dehydration, with tachycardia, hypotension, sunken eyes, dry mouth, loss of skin turgor, and finally cold, clammy skin, oliguria and shock. Without treatment this is "cholera gravis", and death can come within hours.^[4]

Natural infection confers solid protection for at least 3 years in most people who recover, better after symptomatic than subclinical infection. Secretory IgA against O antigen, lipopolysaccharide and cholera toxin is the main effector, with Th17 and Th1 responses and mucosal memory. Blood group O and malnutrition worsen disease, while repeated exposure in endemic areas blunts severity in adults.^{[5] [1]}

The incubation period is 12 hours to 5 days.^[1][4] Vomiting often precedes diarrhoea. The stool is profuse, painless and watery with no fever and little abdominal pain, classically a pale, milky fluid with flecks of mucus and a fishy smell ("rice-water stool"). Dehydration develops rapidly, and the patient may pass many litres in a single day.^[4]

In mild and moderate cases the diarrhoea is troublesome but not dramatic, and the person may not seek care. In severe disease the abdomen may be distended by accumulating fluid, cramps occur, and the patient is prostrate. Fever is absent in typical cholera; fever should make you consider another diagnosis.^[4]

WHO assessment grades dehydration as none, some or severe, using the signs in the table below. Severe dehydration meets at least two signs including one mandatory criterion: lethargic or unconscious, very sunken and dry eyes, absent tears, very dry mouth, drinking poorly or unable to drink, skin pinch going back very slowly, or a weak or absent radial pulse.^[4]

A diagnosis in an outbreak is usually clinical. In resource-limited settings the criteria are: acute watery diarrhoea more than three times in 24 hours with or without vomiting in someone over 5 years.^[4] In non-endemic areas, suspect cholera when acute watery diarrhoea causes severe dehydration or death.

When laboratories exist, stool or rectal swab culture is the gold standard. Specimens are enriched in alkaline peptone water and subcultured on thiosulfate citrate bile salt (TCBS) or taurocholate tellurite gelatin (TTGA) agar. Dark-field microscopy gives a rapid presumptive result, but more than half of dark-field-negative samples turn positive on culture. PCR is highly sensitive but needs equipment. Rapid diagnostic tests (RDTs) such as Crystal VC have reported 97% sensitivity and 76% specificity; Cholkit has 76% sensitivity and 90% specificity and detects only O1.^[4] RDTs are useful for early warning, but confirmation requires culture, seroagglutination or PCR, and any outbreak should have samples sent for antimicrobial susceptibility testing.^[3][4]

The main distinction is between cholera and other acute watery diarrhoeas. Cholera is typically painless, afebrile, and produces very large volumes of clear fluid. Viral gastroenteritis tends to cause smaller volumes with prominent vomiting; enterotoxigenic Escherichia coli causes traveller's diarrhoea, usually less severe and self-limiting; giardiasis is slower and steatorrhoeic; Clostridioides difficile follows antibiotics and may be bloody; cryptosporidiosis matters in immunocompromised patients. Dysentery from Shigella, Campylobacter or amoebiasis presents with fever, blood and mucus and colonic symptoms. Non-infectious causes include osmotic diarrhoea, pancreatic cholera (VIPoma), and coeliac disease or inflammatory bowel disease with prolonged history.

The guiding principle is to replace what was lost, and to do it fast, because dehydration is the killer. Antibiotics are secondary; rehydration comes first.^[2]

The patient has no signs of dehydration. They can be treated at home, at an oral rehydration point, or as an outpatient. Give ORS after each loose stool and keep them under observation for 2 to 4 hours before sending them home, with clear instructions to return immediately if vomiting is repeated, stool frequency increases, or drinking and eating become poor.^[3]

Admit the patient to a cholera treatment facility and give 75 mL of ORS per kilogram over the first 4 hours, plus additional ORS to replace ongoing stool and vomit losses. Monitor closely throughout; if severe vomiting prevents drinking or signs of severe dehydration appear, move immediately to Plan C. Reassess after 4 hours: if still some dehydration, repeat Plan B; if no signs, discharge with advice to continue ORS after each stool and to return if deterioration occurs.^[3]

If the patient vomits the ORS, slow the rate down and increase again as vomiting settles.

Severe dehydration is a medical emergency; seconds count. Start IV fluid immediately, preferably Ringer's lactate, which contains more potassium and bicarbonate than normal saline. Give a total of 100 mL per kilogram, split so that one third is infused in the first 30 minutes and the rest over the next 2.5 hours; for patients 1 year and older this means 30 mL per kilogram in 30 minutes and 70 mL per kilogram over the next 2.5 hours. Children under 1 year need the full course over 6 hours.^[3][4]

If Ringer's lactate is unavailable, use normal saline, 5% glucose in normal saline, or cholera saline (the Dhaka solution). Plain 5% glucose (dextrose) alone is not recommended. As soon as the patient can drink, give ORS as well. If IV access is impossible and the patient cannot drink, ORS can be given by nasogastric tube, switching to IV as soon as possible; nasogastric tubes should not be used in vomiting patients.^[3][4] More than one IV line may be needed for the initial bolus; intraosseous or femoral access may be used by trained staff with appropriate equipment.^[3]

Monitor every 15 to 30 minutes. Reassess fully after 3 hours in older children and adults, 6 hours in infants under 1 year; if hydration has improved and the patient can drink, step down to Plan B if some dehydration remains, or Plan A if none.^[3][4] A cholera cot, with a hole and a collecting bucket, helps track ongoing stool loss so fluid replacement matches output.^[4]

Home-made ORS in an emergency: half a teaspoon of salt and six teaspoons of sugar dissolved in 1 litre of safe water; it is not the ideal composition but saves lives when sachets run out.^[4] Plain 5% glucose (dextrose) should not be used for IV replacement, although oral fluids without too much sugar (water, broth, soup) are acceptable when ORS is unavailable; drinks with high sugar content make diarrhoea worse.^[2][3]

Antibiotics are a useful adjunct but never a substitute for fluid. They shorten the course of diarrhoea (from about 5 days to 1 or 2 days) and reduce stool volume by up to 50%, and they reduce the period of shedding V. cholerae.^[4] WHO recommends antibiotics for patients with severe dehydration requiring hospitalisation, and for patients with high purging (one stool or more per hour in the first 4 hours) or treatment failure (still dehydrated after 4 hours of rehydration) regardless of degree of dehydration, and for anyone with coexisting conditions such as pregnancy, severe acute malnutrition, HIV, or other comorbidities.^[3][4]

Give antibiotics as soon as the patient can take oral medication, once vomiting has stopped. Doxycycline is the antibiotic of choice for all patients, including pregnant women and children, as a single oral dose.^[3][4]

Where multidrug resistance is a concern, choice follows local susceptibility, and first-line agents should change if the laboratory reports resistance.^[3][4] Resistance patterns have shifted over decades: resistance to co-trimoxazole, tetracyclines, fluoroquinolones and third-generation cephalosporins has been reported in recent years, and resistance to the agents of first choice is emerging.^[4]

Mass antibiotic chemoprophylaxis for the community is not recommended: it has no proven effect on spread and drives antimicrobial resistance.^[1][3][4] Selective chemoprophylaxis may be considered for close contacts in high-risk settings, such as prisons or outbreaks in institutions.^[3][4]

In children from 6 months to 5 years, zinc supplementation reduces the volume and duration of diarrhoea. Give 20 mg of zinc sulphate by mouth daily for 10 days, starting immediately. Zinc may reduce the absorption of some antibiotics, including ciprofloxacin; give antibiotics 2 hours before or 4 to 6 hours after zinc for best effect. Children receiving therapeutic feeding for severe acute malnutrition do not need extra zinc, as therapeutic foods contain enough.^[3][4]

Vitamin A is also suggested for children 6 months to 5 years to protect against further diarrhoeal episodes, and a high-calorie diet during illness helps prevent hypoglycaemia and hypokalaemia.^[4]

Children with severe acute malnutrition should be referred to a cholera treatment facility. Assess their dehydration and nutritional status separately. For oral rehydration give standard ORS, not ReSoMal (the rehydration solution for malnutrition), and rehydrate cautiously with close monitoring, because overhydration is a serious risk; IV rehydration follows malnutrition protocols.^[3]

Pregnant women should receive antibiotic treatment for cholera regardless of the degree of dehydration, because the risk of fetal loss is much higher than in other pregnant women and rises with dehydration and vomiting. Dehydration is harder to assess late in pregnancy, so systolic blood pressure and hydration should be monitored carefully to maintain uterine blood flow. Oral cholera vaccine is considered safe and is recommended in pregnancy.^{[3][5] [1]}

Immunocompromised patients (including those with HIV) and people with co-morbidities should be treated as higher risk and given antibiotics regardless of dehydration degree.^[3]

Consider discharge when the patient has no signs of dehydration, can take ORS without vomiting, has had no watery stools for 4 hours, can walk without assistance, and is passing urine. Before discharge, give clear instructions on when to return and on household prevention, provide ORS and confirm the patient or carer can prepare and give it correctly, and review hygiene measures.^[3]

Return criteria include repeated vomiting, increasing stool frequency, or poor drinking and eating. Teach handwashing, safe water use, and proper handling of bedding and clothing soiled by diarrhoeal stool (disinfection with 0.2% chlorine, or boiling and drying in sunlight).^[3]

Every patient with severe dehydration, any patient with vomiting that prevents oral rehydration, babies under 6 months, pregnant women, patients with malnutrition, immunocompromise, diabetes, heart, liver or kidney disease, and anyone with altered consciousness or who is getting worse should be referred or admitted promptly. Severe dehydration requires IV fluids and monitoring that community settings cannot provide. Non-cholera differential diagnoses, persistent fever, or a suspected outbreak also warrant referral and public health notification.

Complications stem from fluid and electrolyte disturbance and from treatment itself.

• Dehydration leading to hypovolaemic shock, acute kidney injury, and death if untreated.
• Metabolic acidosis from bicarbonate loss; hypokalaemia; hyponatraemia or hypernatraemia; hypocalcaemia.^[4]
• Hypoglycaemia, especially in children and malnourished patients.^[4]
• Pulmonary oedema from over-aggressive IV fluid, and renal failure from under-replacement.^[3]
• Aspiration pneumonia, particularly in children and the elderly.^[4]
• Fetal loss in pregnancy.

With prompt rehydration and antibiotics the case fatality rate is under 1% (and deaths from dehydration should be avoidable altogether); without proper management over half of patients with severe disease die.^[3][4] Survivors recover without long-term sequelae once gut function returns. Natural infection protects most people for at least 3 years.^[5] Children under 5 carry the highest burden of severe disease and of post-cholera malnutrition and enteropathy. ^[1]

Prevention is everyone's job, but the clinician's role is to recognise cases early, treat them, and notify public health authorities promptly.

The long-term solution is universal access to safe drinking water, basic sanitation and hygiene, together with food safety and health education. During outbreaks, emergency measures include improving WASH in health facilities, monitoring water quality, distributing WASH kits, promoting handwashing with soap and safe water, boiling or chlorinating water, and safe food storage and preparation. Community engagement is central: involving communities in locating oral rehydration points, adapting funeral practices, and spreading messages on safe water and handwashing.^[1][4]

Oral cholera vaccines (OCVs) are a key component of integrated control in endemic and outbreak settings. WHO currently prequalifies three products: Dukoral, Euvichol-Plus and Euvichol-S. All require two doses for full protection in adults, lasting at least 3 years; one dose of Euvichol-Plus or Euvichol-S provides good shorter-term protection. Euvichol-Plus and Euvichol-S need no buffer and can be given from 1 year of age; Dukoral needs a buffer and is given from 2 years. All are considered safe in pregnancy. The Shancol vaccine is no longer produced.^{[1] [4]}

Introducing vaccination early in an outbreak offers about 79% protection, and even a single dose significantly reduces risk.^[4] A single-dose strategy has been used since October 2022 because of a global supply shortage, with SAGE endorsement; preventive campaigns resumed in 2026 after supply improved (from around 30 million doses in 2022 to about 80 million in 2025), and an allocation of 20 million doses for preventive campaigns was made in February 2026.^[1]

Key elements of cholera outbreak response:

• Early detection through integrated surveillance and case definitions; RDTs for early warning, culture, PCR or seroagglutination for confirmation.
• Laboratory capacity for V. cholerae isolation on TCBS agar and antimicrobial susceptibility testing, run in parallel from the start of the outbreak.
• Establishment of cholera treatment units or centres with Plan A, B and C and infection prevention (chlorine disinfection, safe water, safe burial practices).
• Case management training and ORS distribution points in communities.
• WASH interventions and risk communication/community engagement.
• Reactive vaccination campaigns, prioritising affected and at-risk populations.
• Reporting to WHO and notification under the International Health Regulations.

Household contacts of cases gained protection from prophylactic antibiotics in some trials, but mass chemoprophylaxis is not recommended because of antimicrobial resistance; selective prophylaxis (for example in prisons) may be considered. Additional information is given in the GTFCC technical notes.^[3][4]

The GTFCC, hosted by WHO, drives strategy. In 2017 it published "Ending Cholera: A Global Roadmap to 2030", aiming to reduce cholera deaths by 90% and to eliminate cholera in as many as 20 countries by 2030, through early detection and containment, targeting the relatively small cholera-affected areas, and coordinated technical support. The roadmap was endorsed at the Seventy-first World Health Assembly in 2018.^[1][4]

Pregnancy, children and severe acute malnutrition have been covered above. Two more notes:

• Blood group O increases severity, so in an outbreak, identifying blood group is not clinical management but helps risk stratification at population level.
• Immunocompromised patients, people with liver disease or diabetes, and older adults dehydrate faster and have higher mortality; manage aggressively and early.

In low-resource settings, the same principles apply with simpler tools.

• A transthoracic echocardiogram is irrelevant here: the diagnosis is clinical, confirmed if possible by RDT or culture. Teach staff to recognise rice-water stool and severe dehydration.
• Prepare ORS at home with half a teaspoon of salt and six teaspoons of sugar in one litre of safe water when sachets are unavailable; make it fresh daily. Boil or chlorinate water; store safely.
• Rice-based ORS, made with rice powder instead of glucose, is an acceptable alternative for patients over 6 months and reduces stool volume.^[4]
• Zinc and vitamin A for young children; continue breastfeeding.
• If IV fluid or trained staff are not available, ORS by nasogastric tube is an alternative until referral. Intraosseous or femoral access may be used by trained staff with equipment.
• Refer severe cases early; cholera treatment centres with IV fluid, cholera cots, and trained staff save lives. Delay is the main cause of death.
• Antibiotics only according to local patterns; watch for resistance. Avoid mass chemoprophylaxis.
• Engage the community: safe water storage, handwashing stations with soap or ash, and rapid treatment-seeking are high-impact, low-cost.

• Cholera is a secretory diarrhoea caused by cholera toxin of V. cholerae serogroups O1 and O139; only O1 causes recent outbreaks.
• The organism colonises the small intestine and activates an AB5 toxin that raises intracellular cAMP, opens CFTR, and pours chloride, bicarbonate and water into the lumen; the mucosa itself is not damaged.
• About 80% of infections are asymptomatic; 5 to 10% become severe "cholera gravis" and can kill within hours. ^[5]
• Incubation 12 hours to 5 days; stool is profuse, painless, clear "rice-water"; fever is unusual.
• Rehydration is the treatment. Plan A (none), Plan B (some, 75 mL/kg ORS over 4 hours), Plan C (severe, IV 100 mL/kg). Step down as hydration improves.
• Ringer's lactate is first-choice IV fluid; total 100 mL/kg, one third in 30 minutes. Avoid plain 5% glucose IV.
• Low-osmolarity WHO ORS (75/20/65/10/75 mmol/L) is the current standard; home-made salt-and-sugar solution is a fallback.
• Antibiotics are adjunctive: doxycycline 300 mg (adults) or 2 to 4 mg/kg (children under 12), single dose; alternatives azithromycin or ciprofloxacin in documented resistance. Mass chemoprophylaxis is not recommended.
• Treat pregnant women, severely malnourished patients, the immunocompromised, and those with comorbidity as high-risk, with antibiotics regardless of dehydration degree.
• Zinc 20 mg daily for 10 days in children 6 months to 5 years; separate from certain antibiotics.
• Prevention combines WASH, surveillance, early treatment, safe burials, and oral cholera vaccines. Three WHO-prequalified products exist; all two-dose courses protect adults for at least 3 years; one dose of the bivalent vaccines gives shorter protection; all safe in pregnancy. ^[1]
• The GTFCC Roadmap to 2030 aims for a 90% reduction in cholera deaths and elimination in up to 20 countries.

• Infectious diarrhoea and the approach to acute diarrhoea in children.
• Enteric fever (typhoid and paratyphoid).
• Infection prevention and control in healthcare settings.
• Oral rehydration and paediatric fluid calculations.
• Antimicrobial resistance and stewardship.
• Travel medicine and pre-travel vaccination advice.
• Nutrition in childhood: zinc, vitamin A and therapeutic feeding.