Vibrio Cholerae Virulency

PATHOLOGY:
  • Cholera is not an invasive infection
  • Organisms do not reach blood, only act locally
  • Virulent V.cholrae organism attach to the microvillus of the brush border of epithelial cells
  • They multiply and liberate cholera toxin and perhaps Mucinase and Endotoxin.
  • Pathogencity of 0-139 vibrio is due to 0 antigen
  • Any medication or conditions that decreases stomach acidity makes a person more susceptible to infection with V.cholrae
  • But a person with normal gastric acidity has to consume 1010 or more V.cholrae are when ingested with water
TOXINS OF VIBRIO CHOLERA:
  • ENTEROTOXIN
  • V.cholrae produce heat labile enterotoxin with a Moll wt. of about 84,000 consisting of sub units A ( MW 28,000 ) and B
  • The genes for V.cholrae Enterotoxin are on the bacterial chromosome
  • Cholera toxin production is determined by a filamentous phage integrated with bacterial chromosome.
  1. Cholerae Enterotoxin is antigenically related to heat labile toxin of Escherichia
  • MECHANISM OF ACTION:
  1. Cholera toxin consists of 2 subunits
  2. Monomeric enzymatic moiety (A subunit)
  3. Pentameric binding moiety (B subunit)
  4. Ganglioside GM1 serves as a mucosal receptor for subunit B, which promotes entry of subunit A into the cell
  5. Activation of subunit Ai which interacts with cytosolic proteins called ADP-ribosylation factors (ARF)
  6. ARF-A1 complexes catalyze ADP-ribosylation of a G-protein called GSa.
  • ADP-ribosylated Gsa in turn binds to and stimulates adenylate cyclase that causes increased levels of intracellular cAMP 
  • cAMP inhibits the absorptive sodium transport system & activates the secretory chloride transport system
  • Results in prolonged hyper secretion of water and electrolytes
OTHER KNOWN VIRULENCE FACTORS:
  • Integrons
  • Toxins
  1. CT
  2. HA Protease
  3. RTX Toxin
  4. ACE and Zot
  5. Adherence/Adhesins
  • Accessory Colonization Factors (ACF)
  1. OmpU & other Omp Proteins - outer membrane proteins
  2. Mannose-fucose-resistant cell hemagglutinin & Mannose sensitivevhemagglutinin (Faruque, 2002)
  3. Toxin Co-regulated Pilus (TCP)
Exam Question
  • ADP-ribosylation of the G regulatory protein is the mechanism of action of cholera toxin in the small intestine
  • Cholera toxin Causes continued activation of adenylate cyclase
  • Cholera toxin prevents absorption of salts from intestine leading to watery diarrhoea and loss of water from body.
  • Toxin action of cholera is c-AMP mediated
  • Cholera toxin production is determined by a filamentous bacteriophage integrated with bacterial chromosome.
  • Pathogencity of 0-139 vibrio is due to 0 antigen
  • The function of B subunit of cholera toxin is to bind GM1 ganglioside receptor
  • Cholerae Enterotoxin is antigenically related to heat labile toxin of Escherichia

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