Cholera

Table of Contents

1. Overview
2. Microbiology and Pathophysiology
3. Epidemiology
4. Transmission
5. Clinical Presentation
6. Diagnosis
7. Treatment and Rehydration
8. Antibiotic Therapy
9. Prevention and Vaccines
10. Prognosis and Complications
11. References
12. Featured Videos

Overview

Cholera is an acute secretory diarrheal illness caused by Vibrio cholerae, a comma-shaped Gram-negative bacterium that can produce the most dramatic fluid losses of any infectious diarrheal disease. The pathognomonic "rice-water stool" — copious, pale, nearly odorless watery diarrhea — can reach volumes of up to 1 liter per hour in severe disease, leading to profound dehydration, hypovolemic shock, and death within hours if untreated.

Yet cholera is also one of the most treatable infectious diseases: a patient on the verge of death can be fully resuscitated within hours using oral rehydration solution (ORS) or intravenous fluids. With proper treatment, case fatality rates fall below 1%. Without any treatment, case fatality can exceed 25–50% in outbreak settings.

• Causative agent: Vibrio cholerae serogroups O1 and O139 (O1 is responsible for the current pandemic)
• Mechanism: cholera toxin permanently activates adenylyl cyclase → massive Cl⁻ and water hypersecretion into the intestinal lumen
• Hallmark symptom: sudden-onset painless profuse watery ("rice-water") diarrhea
• Fluid loss rate: up to 1 L/hr in severe cases
• Global burden: 1.3–4 million cases and 21,000–143,000 deaths annually (WHO estimate)
• Endemic regions: Sub-Saharan Africa, South Asia (Bangladesh, India), Haiti, parts of Latin America
• Treatment cornerstone: oral rehydration therapy (ORT) — 90–95% of cases can be managed without IV fluids
• Current pandemic: the 7th pandemic, ongoing since 1961, caused by the El Tor biotype of V. cholerae O1

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Microbiology and Pathophysiology

Understanding how Vibrio cholerae causes such dramatic fluid loss requires tracing a precise molecular cascade from ingestion to secretion.

The Organism

Vibrio cholerae is a facultatively anaerobic, motile, comma-shaped (vibrioid) Gram-negative rod. It is classified by its somatic O antigen into over 200 serogroups, but only O1 and O139 produce the cholera toxin (CT) responsible for epidemic disease. Serogroup O1 is further divided into two biotypes:

• Classical: responsible for the first six pandemics; largely displaced by El Tor
• El Tor: responsible for the current (7th) pandemic; hardier in the environment, capable of longer survival in aquatic reservoirs; produces somewhat less CT per organism but has greater epidemic spread capacity

Within O1, two serotypes exist: Ogawa and Inaba (and rarely Hikojima). These distinctions are used for outbreak tracking rather than clinical management.

Cholera Toxin (CT): The Molecular Mechanism

Cholera toxin is an AB₅ toxin — one A subunit (enzymatically active) + five B subunits (cell binding). After ingestion, V. cholerae colonizes the small intestinal epithelium without invading the mucosa. The bacterium produces CT, which acts via a precisely defined molecular cascade:

1. B subunits bind to GM1 gangliosides on the apical surface of enterocytes — these are abundant on small intestinal epithelium
2. The CT complex is endocytosed and trafficked retrogradely through the Golgi to the endoplasmic reticulum
3. The A subunit is cleaved into A1 and A2 fragments; A1 is released into the cytoplasm
4. A1 ADP-ribosylates the Gsα subunit of adenylyl cyclase — this covalent modification permanently locks Gsα in its active (GTP-bound) conformation, preventing GTP hydrolysis
5. Permanently activated adenylyl cyclase continuously converts ATP to cyclic AMP (cAMP)
6. Elevated intracellular cAMP activates protein kinase A (PKA), which phosphorylates and opens the CFTR chloride channel on the apical membrane
7. Massive Cl⁻ secretion into the intestinal lumen creates an osmotic gradient; water follows passively
8. Simultaneously, sodium-coupled absorption mechanisms (Na⁺/glucose cotransporter SGLT1, Na⁺/H⁺ exchanger) are inhibited

The result is a net secretory state: the gut pours out isotonic fluid that the body cannot reabsorb. Crucially, the Na⁺/glucose cotransporter (SGLT1) remains functional — this is the biological basis for oral rehydration therapy. Glucose-coupled sodium absorption continues even during maximal CT-induced secretion, allowing oral glucose-electrolyte solutions to restore fluid balance from the lumen side.

Why the Stool Looks Like Rice Water

The secreted fluid is nearly isotonic with plasma — containing sodium (~130 mEq/L), chloride (~100 mEq/L), bicarbonate (~44 mEq/L), and potassium (~20 mEq/L). Because the fluid is secreted faster than intestinal mucus and epithelial debris can mix with it, the stool appears pale, turbid, and odorless — classically described as resembling "rice water" because flecks of mucus and epithelial cells float in the clear fluid. This appearance is nearly pathognomonic for cholera in epidemic settings.

Electrolyte Consequences

The massive bicarbonate losses cause metabolic acidosis. Large potassium losses cause hypokalemia, which can be severe enough to cause cardiac arrhythmias. Sodium losses drive hypovolemia and hypotension. This triad — acidosis, hypokalemia, and hypovolemia — accounts for the life-threatening physiology of severe cholera.

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Epidemiology

Cholera has caused seven recorded pandemics. The current 7th pandemic, driven by V. cholerae O1 El Tor biotype, began in the Celebes Islands of Indonesia in 1961 and has spread globally, reaching Africa, Europe, and the Americas. It has never ended.

Global Burden

WHO estimates that cholera causes 1.3 to 4 million cases and 21,000 to 143,000 deaths annually. The enormous range reflects severe underreporting — most endemic countries lack the diagnostic infrastructure to confirm cases, and governments sometimes suppress cholera notifications for economic (trade and tourism) reasons.

Endemic Regions

• Bangladesh and India (Ganges Delta): The most persistent endemic reservoir, with cholera present year-round and large seasonal epidemics. Bangladesh has been the epicenter of cholera research (icddr,b in Dhaka is the world's leading cholera research institution)
• Sub-Saharan Africa: Accounts for roughly 60% of reported cases globally; endemic in Democratic Republic of Congo, Mozambique, Somalia, Ethiopia, Tanzania, Cameroon, and other countries; severely amplified by conflict and displacement
• Haiti: Cholera was absent from Haiti for at least 100 years until it was introduced in October 2010 by UN peacekeepers after the earthquake — a stark demonstration of how cholera travels with human movement; over 800,000 cases and 9,000 deaths in Haiti 2010–2019
• Yemen: The world's largest active cholera outbreak (2016–ongoing) driven by conflict, collapse of water and sanitation infrastructure, and displacement; over 2.5 million suspected cases as of 2020

The El Tor Variant and Climate Factors

El Tor V. cholerae survives in aquatic environments — particularly coastal brackish estuaries — in association with zooplankton (copepods) and biofilms. Sea surface temperature elevation associated with El Niño events and climate change has been linked to increased cholera outbreaks in coastal Bangladesh, as warmer water promotes zooplankton blooms. This ecological connection means cholera is partly a climate-sensitive disease, and climate projections suggest expanding geographic risk areas.

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Transmission

Cholera is transmitted almost exclusively by the fecal-oral route through contaminated water or food. V. cholerae does not spread by respiratory droplets, person-to-person casual contact, or insect vectors.

Primary Transmission Routes

• Contaminated water: The dominant route in most outbreaks. Untreated surface water (rivers, ponds, wells) contaminated by feces from cholera patients. During outbreaks, municipal water systems can become contaminated if water treatment breaks down
• Contaminated food: Raw or undercooked shellfish (oysters, crabs, shrimp) harvested from contaminated coastal waters; raw vegetables irrigated with sewage-contaminated water; food prepared with contaminated water; food handled by infected food handlers with poor hand hygiene
• Direct contact at funerals and ritual washing: Traditional funeral practices involving contact with or washing of the body of a cholera victim are a documented transmission route in parts of Africa, accounting for a significant proportion of cases in some outbreaks

Infective Dose and Inoculum

The infective dose of V. cholerae is relatively high compared to other enteric pathogens — approximately 10⁶–10⁸ organisms are typically required to cause illness in a healthy adult with normal gastric acid. Gastric acid is a critical defense, as it kills the organism efficiently at physiological pH (1.5–3.5). Conditions that reduce gastric acidity dramatically lower the infective dose:

• Achlorhydria (absent gastric acid, e.g., in elderly or malnourished individuals)
• Proton pump inhibitor or H₂ blocker use
• Gastrectomy
• Blood type O (for poorly understood reasons, individuals with blood type O are 2–3× more likely to develop severe cholera than those with blood types A, B, or AB)

Household Transmission During Outbreaks

During epidemic settings, household members of a cholera patient have a markedly elevated risk of developing cholera — estimated at 100-fold higher than community baseline. This is driven by shared contaminated water sources, food preparation, and secondary contamination of household water storage containers. Household contacts should be given prophylactic antibiotics in high-risk settings and educated about ORS preparation and water treatment.

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Clinical Presentation

The clinical spectrum of cholera ranges from asymptomatic carriage (most common) through mild self-limited diarrhea to the full "cholera gravis" presentation that is one of medicine's most dramatic emergencies.

Incubation Period

Symptoms typically begin 12 hours to 5 days after ingestion (most commonly 1–3 days). The short incubation reflects the organism's rapid proliferation in the small intestinal lumen after the gastric acid barrier is breached.

Spectrum of Disease

• Asymptomatic infection: 75–80% of infected individuals — the large majority carry and shed V. cholerae without symptoms, acting as silent transmission reservoirs
• Mild to moderate diarrhea: 15–20% — indistinguishable from other gastroenteritis; loose stools, no dramatic fluid losses; self-limited
• Cholera gravis (severe cholera): 5% of infected individuals — the explosive syndrome that defines the disease

Cholera Gravis: Clinical Course

The onset of cholera gravis is sudden and without warning — there is typically no prodrome of fever, nausea, or abdominal cramping before the diarrhea begins. The classic sequence is:

1. Abrupt onset of profuse watery diarrhea: Unlike most infectious diarrheas, cholera stool is essentially painless. There are no tenesmus, cramps, or urgency — the fluid simply pours out. Volume can reach 10–20 liters in the first 24 hours.
2. Rice-water appearance: As described above — pale, slightly turbid, with floating mucus flecks, nearly odorless.
3. Vomiting: Often accompanies severe diarrhea in early disease, further accelerating fluid and electrolyte losses. Vomiting is typically effortless (not forceful) and bilious or watery.
4. Dehydration progresses rapidly: Over hours, if untreated, the patient develops the classic signs of severe dehydration.

Signs of Dehydration — WHO Classification

WHO classifies cholera dehydration severity for treatment guidance:

• No dehydration (<5% fluid deficit): Alert; normal pulse, eyes, skin turgor; drinks normally
• Some dehydration (5–9% fluid deficit): Restless/irritable; sunken eyes; thirsty, drinks eagerly; skin pinch recoils slowly (>2 seconds)
• Severe dehydration (≥10% fluid deficit): Lethargic or unconscious; very sunken eyes; unable to drink or drinks poorly; skin pinch recoils very slowly (>3 seconds); weak/absent radial pulse; hypotension

Physical Findings in Severe Cholera

• "Washerwoman's hands": severe wrinkling of the palmar skin from dehydration
• "Sunken eyes" with loss of periorbital fat pads from fluid loss
• Hypotension and tachycardia from hypovolemia
• Muscle cramps (particularly in calves) from hypokalemia and hyponatremia
• Hoarse voice or aphonia ("vox choleraica") from dehydration
• Absent fever — cholera is characteristically afebrile; fever suggests co-infection or another diagnosis
• Oliguria or anuria from hypovolemia

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Diagnosis

In epidemic settings, the clinical diagnosis of cholera gravis is straightforward: a patient from an endemic or outbreak area presenting with sudden-onset profuse rice-water diarrhea has cholera until proven otherwise and should be treated immediately without waiting for laboratory confirmation. Laboratory testing is valuable for surveillance, outbreak investigation, and antibiotic resistance monitoring.

Laboratory Methods

• Stool culture (gold standard): V. cholerae grows well on thiosulfate-citrate-bile salts-sucrose (TCBS) agar, forming yellow colonies (sucrose-fermenting). Sensitivity is highest in the first 2–3 days of illness before antibiotics are given. Requires a microbiology laboratory with TCBS media.
• Rapid diagnostic tests (RDTs): Lateral flow immunoassays targeting V. cholerae O1/O139 are now available (e.g., Crystal VC, SD Bioline Cholera Ag O1/O139). Sensitivity 80–95%, specificity 75–90%. WHO-prequalified RDTs are useful for field diagnosis in outbreak settings lacking culture capacity.
• Dark-field microscopy: Characteristic "shooting star" motility of comma-shaped vibrios visible on dark-field microscopy of fresh stool — useful in settings with microscopes but no culture media
• String test (classical): Addition of specific O1 antiserum to a stool suspension causes immediate immobilization of the organisms — a rapid agglutination test used historically; still used in some reference laboratories
• PCR: Highly sensitive; used for outbreak investigation and CT gene confirmation; not routinely available at the point of care
• Antimicrobial susceptibility testing: Critical because V. cholerae O1 El Tor has developed resistance to multiple antibiotics in many endemic regions; guides empiric antibiotic selection

Differential Diagnosis

In the appropriate clinical and geographic context, the differential is narrow. Key considerations:

• Enterotoxigenic E. coli (ETEC): Also causes watery diarrhea via a similar LT/ST toxin mechanism, but usually less severe and associated with travel diarrhea
• Rotavirus and norovirus: Profuse watery diarrhea, especially in children; often with vomiting; seasonal clustering
• Cryptosporidium: Voluminous watery diarrhea; important in HIV/immunocompromised patients
• Other Vibrio species: V. parahaemolyticus (seafood-associated gastroenteritis; usually self-limited) and V. vulnificus (wound infections and septicemia, not primarily diarrheal)

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Treatment and Rehydration

The primary treatment for cholera is replacement of fluid and electrolyte losses. This is straightforward in concept but requires precise execution in severe cases. Approximately 80–90% of cholera patients — including those with moderate dehydration — can be managed with oral rehydration alone.

Oral Rehydration Therapy (ORT) — The Cornerstone

The development of oral rehydration solution in the 1960s–1970s, largely through research at icddr,b in Bangladesh, is considered one of the greatest medical advances of the 20th century. It exploits the preserved SGLT1 glucose-sodium cotransporter in the intestine — even during maximal cholera toxin-driven secretion, glucose-coupled sodium absorption continues, dragging water along.

WHO/UNICEF ORS formula (low-osmolarity, 2002 reformulation):

• Sodium chloride: 2.6 g/L
• Trisodium citrate dihydrate: 2.9 g/L
• Potassium chloride: 1.5 g/L
• Anhydrous glucose: 13.5 g/L
• Total osmolarity: 245 mOsm/L (reduced from 311 in earlier formula; lower osmolarity reduces stool output and vomiting without compromising efficacy)

Practical ORS preparation when packets unavailable: 1 liter of clean water + 6 level teaspoons of sugar + ½ teaspoon of salt. This home formula is imprecise but adequate for mild-moderate dehydration when commercial packets are unavailable.

Dehydration-Specific Rehydration Plans

• No dehydration (Plan A): Give ORS at home after each loose stool. Adults: 200–400 mL per stool. Continue until diarrhea stops. Return to health facility if worsening signs.
• Some dehydration (Plan B): Supervised ORS therapy at health facility. Give 75 mL/kg over 4 hours, then reassess. Continue if improving.
• Severe dehydration (Plan C): Intravenous rehydration immediately. WHO recommends Ringer's lactate (preferred) or normal saline as the IV fluid of choice. Protocol: 100 mL/kg Ringer's lactate over 3 hours for adults (30 mL/kg in first 30 minutes, then 70 mL/kg over the next 2.5 hours). Reassess frequently and switch to ORS as soon as the patient can drink.

Why Ringer's Lactate is Preferred Over Normal Saline

Cholera stool is rich in bicarbonate (~44 mEq/L), leading to metabolic acidosis. Normal saline (0.9% NaCl) contains no buffer and provides excess chloride, worsening hyperchloremic acidosis. Ringer's lactate contains lactate (metabolized to bicarbonate), potassium, and calcium, more closely matching cholera stool losses and correcting the acidosis.

What NOT to Do

• Do not use antidiarrheal agents (loperamide, diphenoxylate, bismuth subsalicylate) — they do not address the underlying hypersecretion and may retain toxins in the intestinal lumen; not recommended in cholera
• Do not use hypertonic or high-sodium IV fluids — hypernatremia worsens outcomes
• Do not delay ORS while waiting for IV access — even patients with moderate dehydration should start drinking ORS immediately
• Do not restrict feeding — breastfeeding should continue throughout; age-appropriate food should resume as soon as vomiting ceases (usually within 4–6 hours of rehydration)

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Antibiotic Therapy

Antibiotics are an adjunct to rehydration — not a replacement. They shorten the duration of illness by approximately 50%, reduce stool volume by approximately 50%, and reduce the duration of V. cholerae fecal shedding (reducing transmission). Antibiotics should be given to patients with moderate-to-severe dehydration after initial rehydration, and to all hospitalized cholera patients. They are NOT recommended for mild disease or contacts (except in specific household chemoprophylaxis scenarios).

First-Line Antibiotics

• Doxycycline (adults, non-pregnant): Single 300 mg oral dose. Most effective when susceptible; simple regimen maximizes compliance. First-line in most settings where susceptibility is known or likely.
• Azithromycin (children, pregnant women): 20 mg/kg as a single oral dose (max 1 g). Preferred for pediatric patients and pregnancy because tetracyclines are contraindicated in these groups. Also the preferred agent in areas with doxycycline-resistant strains.
• Ciprofloxacin: 1 g single oral dose (adults) or 20 mg/kg in children. Alternative first-line, particularly where doxycycline-resistant strains are prevalent; however, fluoroquinolone-resistant V. cholerae is increasingly reported from South Asia and Africa.

Antimicrobial Resistance

Resistance patterns vary significantly by region and are evolving rapidly. Key trends:

• Tetracycline resistance: Widespread in Bangladesh, Sub-Saharan Africa; transmitted on integrating conjugative elements (ICE) and self-transmissible plasmids; limits doxycycline utility in these regions
• Fluoroquinolone resistance: Increasing in South Asia (India, Bangladesh); isolates with reduced susceptibility to ciprofloxacin are common
• Azithromycin resistance: Emerging; high-level azithromycin-resistant O1 El Tor strains first detected in Bangladesh ~2016; spreading
• Practical recommendation: Always culture and test susceptibility when possible; empiric treatment should be guided by local resistance surveillance data

Prophylactic Antibiotics for Household Contacts

The WHO and CDC advise against mass antibiotic prophylaxis during outbreaks (promotes resistance, insufficient evidence for population-level benefit). However, for household contacts of a confirmed severe cholera case, a single dose of doxycycline (300 mg adult) or azithromycin is sometimes given — evidence is limited but supported by plausibility given the 100-fold increased household risk.

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Prevention and Vaccines

Cholera prevention operates at three levels: environmental (water and sanitation), behavioral (hygiene), and immunological (vaccines). No single intervention is sufficient; the most durable cholera control comes from improvements in water, sanitation, and hygiene (WASH) infrastructure.

Water, Sanitation, and Hygiene (WASH)

• Safe water supply: Piped treated municipal water eliminates cholera; point-of-use water treatment (chlorination, boiling, solar disinfection) reduces risk in settings without piped water
• Sanitation: Open defecation-free environments prevent fecal contamination of water sources; access to latrines/toilets is fundamental
• Hand hygiene: Handwashing with soap, especially after defecation and before food preparation, dramatically reduces transmission
• Food safety: Cooking food thoroughly; avoiding raw shellfish in endemic areas; using safe water for food preparation
• Safe burial practices: Gloves, gowns, and limiting direct contact with bodies during funerals in outbreak settings

WHO-Prequalified Oral Cholera Vaccines (OCVs)

Two oral killed whole-cell vaccines are WHO prequalified and used in endemic and outbreak settings:

• Shanchol (Shantha Biotechnics/Sanofi): Contains killed whole cells of V. cholerae O1 (both biotypes, both serotypes) and O139. No B subunit component. 2-dose regimen, 2 weeks apart. Efficacy: ~65% for 2 years in endemic populations. Storage: 2–8°C. Lower cost than Dukoral; used in mass vaccination campaigns by GAVI/WHO/MSF.
• Dukoral (Crucell/Janssen): Killed whole cells of V. cholerae O1 plus recombinant B subunit of CT. 2-dose regimen. Provides short-term (3 months) additional protection against ETEC diarrhea (cross-reactive B subunit). Storage: 2–8°C. Higher cost; primarily used for travelers from high-income countries.

Global OCV Stockpile (ICG)

The International Coordinating Group (ICG) on Vaccine Provision maintains a global emergency OCV stockpile (pre-positioned doses funded by Gavi, UNICEF, MSF) for rapid deployment to outbreak settings. This stockpile has been used in Yemen, Haiti, Bangladesh, and multiple African outbreak responses. Reactive vaccination campaigns targeting outbreak epicenters with at least one dose of Shanchol are now standard WHO outbreak response practice.

Travel Advice

For travelers to cholera-endemic areas: the most protective measures are safe food and water practices, not vaccination. Dukoral is available for travelers and provides 2 years of protection. The risk for typical short-stay travelers staying in hotels with treated water is very low; OCVs are most indicated for travelers to remote/rural areas, humanitarian workers, and healthcare workers in outbreak settings.

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Prognosis and Complications

The prognosis of cholera is almost entirely determined by the timeliness and adequacy of rehydration. This makes cholera unusual among severe infectious diseases: the treatment is straightforward, inexpensive, and highly effective, yet the disease continues to kill tens of thousands per year because access to care is insufficient.

Case Fatality Rates

• Untreated severe cholera: Case fatality rate (CFR) 25–50%; death occurs within hours from hypovolemic shock, metabolic acidosis, and cardiac arrhythmias from hypokalemia
• With oral rehydration only (moderate dehydration): CFR <1%
• With proper IV rehydration + ORS + antibiotics (severe dehydration): CFR <1% in well-resourced settings
• During large-scale outbreaks with overwhelmed health systems: CFR 1–3% (Haiti 2010: ~1.1%; Yemen ongoing: ~0.2% at peak of response improvement)

Complications

• Hypovolemic shock: The primary cause of death; results from uncompensated massive fluid losses exceeding cardiac output
• Acute kidney injury: From hypovolemia and renal hypoperfusion; largely reversible with rehydration if caught before irreversible tubular necrosis develops
• Hypokalemia and cardiac arrhythmias: Severe potassium depletion in stool can cause ventricular arrhythmias; potassium replacement (preferably oral, via ORS/foods) is essential in all but mild cases
• Metabolic acidosis: Bicarbonate loss in stool; corrected by Ringer's lactate in severe IV-treated cases and by the citrate in WHO ORS formulation
• Hypoglycemia: Particularly in malnourished children; blood glucose should be monitored and glucose supplementation provided
• Aspiration pneumonia: Can occur during copious vomiting, particularly in obtunded severely dehydrated patients
• Pregnancy complications: Cholera in pregnancy carries high risk of fetal loss and maternal mortality; pregnant women should be treated aggressively

Long-Term Outlook

Patients who survive cholera and receive adequate rehydration typically recover completely without long-term sequelae. Prior cholera infection provides partial immunity — individuals with prior exposure have lower risk of subsequent severe disease — but this immunity is incomplete and wanes over years. The immune response to V. cholerae O-antigen is the basis for natural immunity and vaccine-induced protection.

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References

1. Ali M, Nelson AR, Lopez AL, Sack DA. Updated global burden of cholera in endemic countries. PLoS Negl Trop Dis. 2015;9(6):e0003832. PMID: 26043000. PubMed
2. Bhatt S, Ali M, Sack DA. Cholera vaccines: a solution to the continuing global challenge. Curr Opin Infect Dis. 2019;32(5):411-419. PMID: 31274544. PubMed
3. Sack DA, Sack RB, Nair GB, Siddique AK. Cholera. Lancet. 2004;363(9404):223-233. PMID: 14738797. PubMed
4. Harris JB, LaRocque RC, Qadri F, Ryan ET, Calderwood SB. Cholera. Lancet. 2012;379(9835):2466-2476. PMID: 22748592. PubMed
5. Waldor MK, Mekalanos JJ. Lysogenic conversion by a filamentous phage encoding cholera toxin. Science. 1996;272(5270):1910-1914. PMID: 8658163. PubMed
6. Levine MM. Immunological Adjuvants for Enteric Vaccines: Lessons from Cholera. Vaccine. 2003;21(Suppl 2):S24-S26. PMID: 12763003. PubMed
7. Bhattacharya SK, Sur D, Ali M, et al. 5 year efficacy of a bivalent killed whole-cell oral cholera vaccine in Kolkata, India: a cluster-randomised, double-blind, placebo-controlled trial. Lancet Infect Dis. 2013;13(12):1050-1056. PMID: 24157105. PubMed
8. Bart KJ, Huq Z, Khan M, Mosley WH. Seroepidemiologic studies during a simultaneous epidemic of infection with El Tor Ogawa and classical Inaba Vibrio cholerae. J Infect Dis. 1970;121(Suppl):S17-S24. PMID: 5424764. PubMed
9. Reyburn R, Kim DR, Emch M, et al. Climate variability and the outbreaks of cholera in Zanzibar, East Africa: a time series analysis. Am J Trop Med Hyg. 2011;84(6):862-869. PMID: 21633019. PubMed
10. Legros D, Paquet C, Perea W, et al. Mass vaccination with a two-dose oral cholera vaccine in a refugee camp. Bull World Health Organ. 1999;77(10):837-842. PMID: 10593035. PubMed
11. Alam M, Hasan NA, Sultana M, et al. Genes of multidrug resistance and toxin-coregulated pili in environmental Vibrio cholerae. Appl Environ Microbiol. 2010;76(15):5019-5028. PMID: 20543045. PubMed
12. Mukhopadhyay AK, Basu I, Bhattacharya SK, et al. Emergence of fluoroquinolone resistance in strains of Vibrio cholerae isolated from hospitalized patients with acute diarrhea. Antimicrob Agents Chemother. 1998;42(9):2443-2445. PMID: 9736581. PubMed

Research Papers

The following PubMed topic searches retrieve current peer-reviewed literature on Cholera.

1. Cholera toxin mechanism cAMP
2. Vibrio cholerae O1 El Tor pandemic
3. Oral rehydration therapy cholera efficacy
4. Cholera vaccine oral killed whole cell
5. Cholera global burden endemic mortality
6. Cholera doxycycline azithromycin treatment
7. Vibrio cholerae antimicrobial resistance
8. Cholera WASH water sanitation prevention
9. Haiti cholera 2010 outbreak epidemiology
10. Yemen cholera outbreak humanitarian
11. Cholera rice water stool diagnosis
12. Cholera climate change ecology

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