PathogenesisVibrio Cholerae Vibrio Cholerae enterotoxin activates the stimulatory Gs protein via ADP-ribosylation. This stimulates secretion of chloride ions and water from enterocytes into the small intestines, and causing watery diarrhea.
Epidemiology Major pandemics since 1817 V. cholerae O1 biotype el tor Began in Asia in 1961, spread to Africa and Europe In 1991, the pandemic strain spread to Peru V. cholerae O139 Bengal emerged in 1992 in India History of travel (S. America, India, Asia)
Etiology Drinking contaminated and inadequately sterilized water or eating undercooked seafood Risk Factor: antacids and achlorhydria Gastric acid production is reduced will allow easier entrance of the bacteria to the small interstines Based on agglutination of antiserum against O1 (LPS) antigen O1 and non-O1 strains V. cholerae O1 and O139 associated with epidemics Produce cholera toxin Non-O1, non-O139 serotypes Cause diarrheal disease identical to classical cholera but does not cause large outbreaks of disease. Due to being a nonadherent strain.
Risk Factors Ingestion of contaminated water Replicates in fresh and low-salt-containing water Drinking unsterile water and ice in developing countries Ingestion of comtaminated food sources Shelfish, clams, oysters and crabs and its products or food handlers High poverty Urban slums, refugee camps, conflict zones, naterual disasters and prisons where sanitation facilities may not exist Periods of flooding Peope using tube-wells that become contaminated with fecal contents from the poo-quality sanitation. Blood Group O at a risk of more severe disease, but may actually be protective against initial infection.
Key Diagnostic Factors Onset begins 2-3 days after ingestion of bacteria Copious Watery Diarrhea Diarrhea >1 liter/hour is most likely cholera if sustained. >20 mL/kg during a 4-hour observation period Evidence of Volume Depletion (WHO Criteria) Mild (<5% volume depletion) = alert, but increased HR, dry mucous membranes and small postural BP drop (<20 mmHg) Moderate (5% to 10%) = irritability, sunken eyes, dry mouth, decreased skin turgor significant (>20 mmHg) postural BP drop. Severe (>10% volume depletion) = lethargy or coma, circulatory collapse (systolic BP< 80 mmHg Family History of recent, severe cholera outbreak Family clusters due to secondary cases or due to a common source
Key Diagnostic Factors ContinuedGreater than 20 Liters Rice Water Stoollost per day
Diagnostic Tests CBC Elevated Hct / Neutrophil CT. Serum Electrolyes K+ (low normal or high) and anion gap acidosis ECG Assess severtiy of volume depletion Serogroup confirmation Antisera Either O1 or O139 Darkfield Phase contrast Large quantity of curved microscopy of stool bacteria
Diagnostic Tests ContinuedVibrio Cholerae Microscopy: Small, rarely seen on stool Gram stain Darkfield microscopy can be used Culture: Next Slide
Question What media does V. Cholerae grow on? A. Mannitol salt agar B. Eosin methylene blue C. Thiosulfate citrate bile salts sucrose D. Buffered charcoal yeast extract agar E. Don’t care, hurry up I want to leave.
C.Thiosulfatecitrate bilesalts sucrose(TCBS) agar
World Health Organization Diagnosis Criteria[WHO: Standard clinical case definition] WHO Standard case definition:A case of cholera suspected when: An area where the disease is not known to be present, a patient aged 5 years or more develops severe dehydration or dies from acute watery diarrhoea; In an area where there is a cholera epidemic, a patient aged 5 years or more develops acute watery diarrhoea, with or without vomiting. A case of cholera is confirmed when Vibrio cholerae O1 or O139 is isolated from any patient with diarrhoea.
Treatment No need for a a formal diagnosis of cholera to initiate treatment Urgent rehydration is the most important feature of treatment. IV rehydration is usually started for severely volume-depleted patients, but oral replacement solution (ORS) is the mainstay of therapy for mild-to-moderate disease and should be added to IV therapy as soon as is clinically possible. Antibiotics (based on local resistances) reduce both the severity and length of disease and should be used where possible Vitamin and micronutrient supplements in specific cases. Antisecretory agents have NOT been shown to be useful
The standardWorld HealthOrganizationOralRehydrationSalts (ORS)comesprepacked andcontains: Na+ 75, K+ 20, Cl- 65, citrate 10, and glucose 75, with an osmolality of 245 mosmol/L (all in mmol/L)
Treatment of Severe Volume Depleted Precisely calculating volume depletion is difficult. The equations provided in WHO document may be used in balance with clinical judgment. [WHO/UNICEF: Clinical mgmt of acute diarrhea] Secretory diarrhea is high in Sodium, Potassium and Bicarbonate therefore Ringer lactate should be used. With the loss of Bicarbonate and Potassium in the stool, cholera patients have a profound metabolic acidosis and total body K+ depletion. K+ should be replaced through inclusion of K+ in the IV or oral fluids regardless of initial K+ level.
Treatment of Moderate - Mild Volume Depleted Oral Rehydration is usually preferred as this avoids the complications of IV fluids Aggressive catch-up rehydration for 2-4 hours, followed by maintenance fluids until diarrhea stops, which takes 2 to 5 days later.
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Cholera CotDeath can occurs within hours if untreated60% mortality rate in untreated patients and <1% in treated The use of the cholera Cot enables health care providers to measure the enteric loss and replace losses with an equal volume of oral or IV fluids.
Prevention Water treatment and sanitation with chlorination of municipal water supplies. Boiling or filtration of water locally Health education Attention to careful handwashing with soap and water Disinfection of the dead and their belongings with simple burial procedures 2 oral vaccines available Composed of Killed, whole-cell bateria Contains the B-toxin subunit