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Questions and Answers
What is the primary effect of increased intracellular cAMP levels in cholera infection?
What is the primary effect of increased intracellular cAMP levels in cholera infection?
- Inhibition of ion reabsorption (correct)
- Reduction of cAMP levels
- Stimulation of sodium absorption
- Decreased fluid secretion
What characterizes the stool in cholera patients?
What characterizes the stool in cholera patients?
- Green and frothy
- Thick and tarry consistency
- Resembles rice water (correct)
- Bright red and bloody
What is NOT a common clinical finding in a cholera case?
What is NOT a common clinical finding in a cholera case?
- Profuse diarrhea with abdominal cramps
- Sudden vomiting
- Rapid weight gain (correct)
- Fluid loss leading to dehydration
Which of the following is an effective treatment for cholera?
Which of the following is an effective treatment for cholera?
What public health measure is least effective in preventing cholera?
What public health measure is least effective in preventing cholera?
What shape are Vibrio cholerae bacteria?
What shape are Vibrio cholerae bacteria?
What is the primary route of transmission for Vibrio cholerae?
What is the primary route of transmission for Vibrio cholerae?
Which of the following statements about cholera toxin is true?
Which of the following statements about cholera toxin is true?
Which component of the cholera toxin dissociates to activate the A1 subunit?
Which component of the cholera toxin dissociates to activate the A1 subunit?
What effect does the activated A1 subunit of cholera toxin have on adenyl cyclase?
What effect does the activated A1 subunit of cholera toxin have on adenyl cyclase?
Which of the following environments is Vibrio cholerae typically found in?
Which of the following environments is Vibrio cholerae typically found in?
What is required for Vibrio cholerae to establish an infection?
What is required for Vibrio cholerae to establish an infection?
What is the incubation period for cholera following the ingestion of Vibrio cholerae?
What is the incubation period for cholera following the ingestion of Vibrio cholerae?
Flashcards
Vibrio cholerae
Vibrio cholerae
A bacterium responsible for causing cholera, a severe diarrheal disease.
Fecal-oral Transmission
Fecal-oral Transmission
The method by which Vibrio cholerae spreads, typically through contaminated food or water.
Incubation Period
Incubation Period
The time period between exposure to Vibrio cholerae and the onset of symptoms.
Adherence and Colonization
Adherence and Colonization
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Cholera Toxin
Cholera Toxin
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B Subunit
B Subunit
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A1 Subunit
A1 Subunit
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Cyclic AMP (cAMP)
Cyclic AMP (cAMP)
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Cholera
Cholera
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Rice water stool
Rice water stool
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Electrolyte imbalance
Electrolyte imbalance
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Rehydration
Rehydration
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Cholera Prevention
Cholera Prevention
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Study Notes
Vibrio Cholerae
- Gram-negative: This bacterium is gram-negative.
- Oxidase-positive: It exhibits a positive oxidase reaction.
- Motile rods: The bacteria are motile and rod-shaped.
- Salt-tolerant: Some strains are tolerant of high salt concentrations.
- Salt-requiring: Some strains require salt for growth.
- Freshwater/brackish water: The bacteria are commonly found in fresh and brackish water environments.
- Comma shape rods: The bacteria's distinctive rod shape is somewhat comma-like.
- Culture: It can be cultured on various media commonly used for stool cultures.
- Cholera Disease: Vibrio cholerae is the causative agent of cholera.
Transmission
- Fecal-oral route: The primary route of transmission is through ingesting contaminated food or water that contains the bacteria's stool.
- Contaminated food/water: Eating contaminated food or drinking contaminated water can lead to infection.
- Large inocula: Relatively high numbers of bacteria are typically needed to establish an infection.
- Person-to-person: Direct contact between people is not a significant mode of transmission.
- Reservoir: Recovered cholera patients can shed the bacteria and act as a reservoir, especially in endemic regions.
Pathogenesis
- Incubation period: The time between ingestion and the onset of symptoms is 6 hours to 3 days.
- Sequence of events: Ingestion -> adherence and colonization -> secretion of toxins -> fluid and electrolyte loss.
- Adherence and colonization: Virulent forms attach to the small intestinal epithelium, specifically microvilli.
- Multiplication: The bacteria multiply after crossing the acid barrier.
- Cholera toxin secretion: The bacteria release a potent toxin, called enterotoxin.
- Specific receptors: The toxin binds to specific GM1 ganglioside receptors on the small intestine cells.
Activation of the A1 Subunit
- B subunit binding: The B subunit binds to the cell membrane receptor.
- A subunit dissociation: The A subunit detaches from the B subunit.
- Membrane penetration: The cell membrane is penetrated during this process.
- A1/A2 subunits: The A subunit is composed of the A1 and A2 subunits linked by a disulfide bond.
- ADP-ribose transfer: Activated A1 subunit transfers part of the NAD molecule to a GTP binding protein.
- Adenyl cyclase activation: This process stimulates adenyl cyclase activity, increasing the cell's cAMP levels.
Pathogenesis...
- Intracellular cAMP increase: The increased cyclic AMP (cAMP) within the cells results from the previous events.
- Inhibition of reabsorption: cAMP inhibits the reabsorption of sodium, potassium and chloride ions.
- Hypersecretion: It increases the secretion of chloride and bicarbonate ions.
- Net loss of electrolytes: The combined effects lead to a significant loss of fluids and electrolytes.
- "Rice water stool": The severe diarrhea which is characteristic of cholera.
Fluid Secretion
- Isotonic with plasma: The secreted fluid has a comparable solute concentration to blood plasma.
- Electrolyte imbalance: High sodium, potassium and bicarbonate but low chloride levels.
- Consequences: The loss of fluids result in dehydration, acidosis, shock, and potential death if not addressed rapidly.
Clinical Findings
- Symptoms: Sudden vomiting and profuse watery diarrhea accompanied by abdominal cramps, mucus-containing stool, rapid electrolyte loss leading to dehydration, circulatory collapse and anuria.
- Complications: Dehydration, circulatory shock and kidney failure (anuria).
- Mortality: The fatality rate is 25-50% without treatment.
Diagnosis
- Stool/vomitus culture: A laboratory test that can identify the bacteria and confirm the infection.
Treatment
- Fluid replacement: Essential for addressing dehydration and electrolyte imbalances.
- Electrolyte replacement: Important to restore the body's lost electrolytes.
- Antimicrobial drugs: Effective antibiotics like oral tetracycline used to reduce the duration and severity of infection.
Prevention
- Public sanitation: Crucial to prevent the contamination of water sources.
- Water purification: Boiling water is an effective method to eliminate the bacteria.
- Food safety: Handling and preparing food safely can also prevent widespread contamination.
- Vaccination: Limited effectiveness and only provides short-term protection.
- Hygiene: Handwashing is a vital step to prevent the spread of the bacteria.
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Description
This quiz covers key characteristics of Vibrio cholerae, including its gram-negative nature, transmission methods, and relationship to cholera disease. Participants will explore the bacterium's morphology, culture requirements, and ecological habitats.