Vibrio Cholera. Michelle Ross, Kristin Roman, Risa Siegel. Vibrio Cholera. Micro and Molecular biology. Vibrio Cholera. Gram-negative Curved rod .5-.8 μ m width 1.4-2.6 μ m length Facultative anaerobe Single polar flagellum Chemoorganotroph Optimal growth 20-30 degrees. V. Cholera.
Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.
Michelle Ross, Kristin Roman, Risa Siegel
Micro and Molecular biology
different strains of the same bacterial species
distinguished by a group of phenotypic or genetic traits
bacteria of the same species with different antigenic
determinants on the cell surface
V. Cholera has more than 150 different serogroups, only two of which cause epidemic disease
genome: 3.2-3.6 Mb
El Tor (El)
genome: 4 Mb
01 antigen is divided into 3 types: A,B,C
made of 3-deoxy-L-glycerotetronic acid
not been characterized
1. acquisition of VPI
2. lysogenic conversion by phage
3. exchange of genes leads to expression of O-antigen and capsule
the change in structure is thought to have arisen from a recombination event.V. Cholera
two circular chromosomes
Chromosome 1 is larger (2.96
million base pairs) and carries
many genes for essential cell
functions and housekeeping
Chromosome 2 is smaller (about
1.07 million base pairs and
carries the integron island
ONE VIRUS is called the V. cholera pathogenicity island phage
(VPI), which infects and inserts its DNA into the bacterial
chromosome and allows the synthesis of a pilus which
the bacteria uses to attach to the host intestine
SECOND VIRUS is called the cholera-toxin phage (CTX).
The CTX phage inserts itself into chromosome
one and the bacterium is then capable of secreting
a powerful enterotoxin
The integron region is often found on plasmids and serves as a "gene capture system." This region may contain antibiotic resistance genes.
Cholera disease begins with ingestion of contaminated water or food. The bacteria that survive the acidic conditions of the stomach colonize in the small intestine.
The cholera toxin (CT) is responsible for the severe diarrhea characteristic of the disease.
CT is a proteinaceous enterotoxin secreted by
The A1 subunit contains a ADP-ribosyltransferase which covalently modifies the G protein, which regulates adenylate cyclase. Adenylate cyclase mediates the formation of cAMP
The increase in cAMP levels bring about the secretion of chloride and bicarbonate from the mucosal cells into the intestinal lumen
The change in ion concentrations leads to the secretion of large amounts of water into the lumen, known as diarrhea
Genes encoding CT
ctxAB - recognized to be the genome of a filamentous phage CTXΦ (ctxA and ctxB)
Transcription of ctxAB is regulated by several proteins
CTXΦ genome can integrate into the host genome at a specific site, attRS
The CTX genetic element also has a “core” region carrying several phage morphogenesis genes
These entire CTX gene set is flanked repeated sequences, the attRS1 site
The entire genetic element is 6.9kb
The receptor for CTXΦ is Toxin-Coregulated Pili (TCP)
Efficient colonization of V. cholera in the small intestine requires the expression of TCP’s
The major pilin subunit is TcpA
Genes for TCP production are clustered on the pathogenicity island located on chromosome 2
Expression of CT & TCP have been shown in vitro to be strongly influenced by changes in cultural conditions
ie. temperature, pH, osmolarity, &
growth medium composition
CT & TCP are regulated via a cascade in
which ToxR and TcpP control expression
of ToxT, which is a transcriptional activator
directly controlling several virulence genes
ToxR & TcpP are inner-membrane proteins
which interact with other transmembrane
ToxR/S proteins are required for transcription of toxT gene and are also important for ctx transcription and regulation other outer membrane proteins
V. cholerae did not always cause disease. Infection with the CTX phage gives the bacterium its toxinogenicity. The phage recognizes a pilus on the surface of the bacterium and uses it to enter the cell. Once inside the cell, the CTX phage integrates into the chromosome and the lysogen expresses cholera toxin.
The CTX phage has received special attention because it is the first filamentous phage found to transfer toxin genes to its host. The important lesson from this discovery is that many different types of phage may carry virulence factors, and transfer of virulence genes by phage may be a major mechanism of evolution of new bacterial diseases.