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Cholera

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    • Cholera is a dreaded diarrheal illness known for its severity and potential to cause outbreaks.
    • The disease continues to be a burden in resource-poor countries lacking access to safe water supply and sanitation.
    • The term "cholera" likely originates from the Greek word for the 'gutter of a roof,' likening the deluge of water after a rainstorm to the flow from the anus of an infected person.
    • Cholera is an ancient disease caused by Vibrio cholerae.
    • Endemic: Common in resource-poor areas.
    • Epidemic: Occurs during natural disasters and emergencies, affecting displaced people, slums, and institutionalized populations.
    • Pandemic disease: Affects a wide geographic area.
    • Despite significant advances in research, cholera remains a challenge for developing countries.

    • Cholera is rare in developed countries.
    • Statistics on cholera worldwide are uncertain.

    Contributory Factors

    • Most cases occur in remote areas where definitive diagnosis is not possible.
    • Reporting systems are often non-existent in such areas.
    • The stigma of reporting cholera has direct consequences on commercial trade and tourism.
    • Many countries with endemic cholera do not report at all.

    • Vibrio cholerae is a saltwater organism and its primary habitat is the marine ecosystem.
    • There are about 140 known serogroups of V. cholerae, only serogroups 01 and 0139 cause epidemics.
    • Other serotypes cause non-cholera gastroenteritis with occasional extra-intestinal manifestations.
    • Cholera has 2 main reservoirs: humans and water. V. cholerae is rarely isolated from animals, and animals do not play a role in disease transmission.
    • Vibrio cholerae belongs to the family Vibronaceae.
    • It is a non-spore forming organism, slightly curved, gram-negative, aerobic bacillus, with flagellum.
    • It has antigenic structures:
      • Flagella H antigen
      • Somatic O antigen
    • It produces a potent enterotoxin known as CTX.

    • Cholera toxin (CTX) is a potent protein enterotoxin elaborated by the organism in the small intestine.
    • The organism has to negotiate the normal defense mechanisms of the gastrointestinal (GI) tract.
    • A large inoculum of bacteria (≥∼108 viable units) is required.
    • The organisms produce CTX that consists of subunits A and B.
    • The B subunits bind to the GM1 ganglioside receptors in the small intestinal mucosa, allowing the A subunit to enter into the cell.
    • Activation of adenylate cyclase, leading to an increase in cyclic adenosine monophosphate (AMP).
    • Cyclic AMP blocks the absorption of sodium chloride by the microvilli and promotes the secretion of chloride and water by the crypt cells.
    • The result is massive outpouring of electrolyte-rich isotonic fluid into the small intestine (about 10-12L).
    • The large volume of fluid produced in the upper intestine overwhelms the absorptive capacity of the lower bowel (daily absorption by the large intestine is between 5-8L), resulting in severe diarrhea.
    • The diarrheal fluid contains large amounts of sodium, chloride, bicarbonate, and potassium.
    • Since the enterotoxin acts locally and does not invade the intestinal wall, few red blood cells and neutrophils are found in the stool.
    • The loss of electrolyte-rich isotonic fluid leads to blood volume depletion with resulting low blood pressure and shock.
    • Loss of bicarbonate and potassium leads to metabolic acidosis and hypokalemia.

    • Primary infection in humans is acquired incidentally.
    • Risk of primary infection is facilitated by seasonal increases in the number of organisms from changes in water temperature and algal blooms.
    • Secondary transmission occurs through fecal-oral spread of the organism through person-to-person contact or through contaminated water and food.

    • Poor sanitary conditions
    • Household exposures
    • Age
    • Non-breastfed infants
    • Hydrochlorhydria or Achlorhydria
    • Malnutrition
    • Raw or undercooked shellfish and vegetables
    • O blood group
    • Previous exposure and acquired immunity
    • Asymptomatic carriers

    • Diarrhea:
      • Profuse watery diarrhea is a hallmark of cholera.
      • V cholerae does not elicit an inflammatory response, and cholera stool contains few leukocytes and no erythrocytes.
      • High stool volume >250 mL/kg body weight in a 24-hour period.
      • The characteristic cholera stool is an opaque white liquid that is not malodorous and often is described as having a rice water appearance.
    • Frequent and often uncontrolled bowel movements.
    • Abdominal cramps
    • Vomiting
    • Decreased gastric and intestinal motility
    • Acidaemia
    • Isotonic dehydration which could lead to vascular collapse, shock, and death.
    • Dehydration can develop with remarkable rapidity, within hours after the onset of symptoms.
    • Water loss is proportional between 3 body compartments: intracellular, intravascular, and interstitial.
    • Signs of Dehydration
    • Tachypnea and hypercapnia attributable to the metabolic acidosis.
    • Metabolic and systemic manifestations:
      • Hypoglycemia is the most common lethal complication of cholera in children.
      • Metabolic acidosis:
        • Tachypnea and tachycardia.
      • Hypokalemia.
      • Hyponatremia.
      • Hypocalcemia.
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    • Direct microscopic examination:
      • Gram stain.
      • Dark field organism.
    • Culture:
      • Routine differential media.
      • Alkaline enrichment media.
    • Serotyping and biotyping.
    • Hematological tests:
      • Hematocrit, serum-specific gravity, and serum protein are elevated.
      • Leucocytosis without a left shift.
    • Serum electrolytes.
    • Renal profile:
      • Blood urea nitrogen and serum creatinine are elevated.

    Causes of Gastroenteritis

    • Rotavirus: A highly contagious virus that primarily affects infants and young children, causing severe diarrhea, vomiting, and fever.
    • Escherichia coli (E. coli): Various strains of E. coli, such as enterotoxigenic E. coli (ETEC) and enteropathogenic E. coli (EPEC), are responsible for traveler's diarrhea and endemic cases of gastroenteritis.
    • Salmonella: Different species of Salmonella bacteria can lead to foodborne illnesses and gastroenteritis with symptoms like diarrhea, abdominal cramps, and fever.
    • Shigella: Shigella species cause bacillary dysentery, characterized by bloody diarrhea, abdominal pain, and fever.
    • Entamoeba histolytica: This parasite causes amoebic dysentery, leading to bloody diarrhea and potential systemic complications.
    • Giardia lamblia: A protozoan parasite that causes giardiasis, often resulting in diarrhea, abdominal pain, and other gastrointestinal symptoms.
    • Norovirus: A highly contagious virus that causes outbreaks of gastroenteritis, with symptoms like nausea, vomiting, diarrhea, and stomach cramps.
    • Cryptosporidium: A parasite responsible for cryptosporidiosis, leading to watery diarrhea and other gastrointestinal symptoms.
    • Helminthic Infections: Parasitic worms like Ascaris lumbricoides, Trichuris trichiura, and hookworms can cause chronic gastrointestinal issues in tropical areas.
    • Typhoid Fever: Caused by Salmonella typhi bacteria, typhoid fever leads to high fever, abdominal pain, and gastrointestinal complications.

    • The disease:
      • Dehydration
      • Hypovolemic shock
      • Renal failure
      • Electrolyte imbalances
      • Hypoglycemia
    • Therapy:
      • Over-hydration
      • Pulmonary edema

    1. Assess for dehydration
    2. Rehydrate the patient and monitor frequently. Maintain hydration
    3. Administer an antibiotic to patients with severe dehydration*.
    4. Feed the patient.

    *Doxycycline, tetracycline, ampicillin, ciprofloxacin, erythromycin, trimethoprim and sulfamethoxazole*

    • Maintain high level of hygiene
    • Scrupulous hand wash
    • Proper disposal of faeces
    • Proper handling of faeces
    • Use of disposable gloves
    • Ensure frequent disinfection of designated room(s)

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