Cholera Flashcards
Vibrio cholerae
Facultative anaerobe Gram negative Does not produce spores Can enter a viable but non-culturable state Two serogroups O1 and O139 cause cholera
Vibrio cholerae in the environment
Found in coastal waters and estuaries
Free-living or in association with zooplankton (stuck to side as biofilm) and shellfish
Seasonality of outbreaks follow blooms of zooplankton
V. cholerae and zooplankton
Attached to chitin of zooplankton
Can secrete chitinase for nutrients
Metabolically active at high acidic environment without losing viability/virulence
V. cholerae genome
Chromosome I contains housekeeping genes. VPI gene (attachment pilus) and CTX (enterotoxin).
VPI and CTX inserted by a virus
Chromosome II contains integron island
V. cholerae virulence factors
ACF (accessory colonisation factor). Involved in chemotaxis (intestinal colonisation).
Flagella (adhesion or biofilm formation)
Auto inducer 2 (AI-2) facilitates interspecies communication. LuxPQ receptor responds to AI-2
T6SS. Antibacterial and anti-eukaryotic activities
Cholera A5B toxin
Quorum sensing
Secretion and detection of signalling molecules (autoinducers)
Expression of virulence factors and formation of biofilms at low density
Repression at high cell density and motility switched back on
V. cholerae colonisation
After ingestion, V. cholerae uses motility and mucinases to penetrate mucus gel
GbpA (binding protein) to colonise small intestine epithelium
Expresses vieA, a phosphodiesterase which hydrolyses cyclic di-GMP
Represses chitin-binding mannose-sensitive haemagglutinin pilus
Escape response
Prepares for transmission to another host
Genes for di-GMP synthesis and nutrient scavenging systems
Repression of genes for chemotaxis and ToxR regulon
Motile but non-chemotactic state
Exposure to chitin
V. cholerae induces genes involved in adherence and catabolism of chitin (ChiS regulon)
Genetic competenec (TfoX regulon)
Biofilm formation mediated by induction of Vps regulon
Active but non-culturable state
If V. cholerae not ingested by host or attached to chitin
Adaptation to nutrient-poor conditions
Phosphate and nitrogen starvation genes (phoB and glnB-1)
Repression of translation machinery genes
V. cholerae infection
Secretes enterotoxin which binds intestinal cells
Chloride channels activated
Release of electrolytes and bicarbonates
Fluid hypersecretion out of intestine
Diarrhoea and dehydration (main effect on host)
Action of cholera toxin
5B:1A toxin binds GM1 receptor and taken in by endocytosis
Phagosome transported to ER
A1 subunit detached from B and exported to cytoplasm
Affects G-protein that regulates adenylate cyclase
cAMP levels rise and active ion transport systems
Routes of infection
Faecal-oral
Person to person infection is indirect
Can be carried by houseflies and other insects
Cholera treatment
Main treatment is oral rehydration (or intravenous)
Antibiotics (tetracycline)
Serological anti-vibrio antibodies
Antitoxin antibodies