Description, Causes and Risk Factors:
Vibrio cholerae is a Gram-negative, comma-shaped bacterium. Some strains of V. cholerae cause the disease cholera. V. cholerae is facultatively anaerobic and has a flagellum at one cell pole.
Infection due to V. cholerae begins with the ingestion of contaminated water or food. After passage through the acid barrier of the stomach, the organism colonizes the epithelium of the small intestine by means of the toxin-coregulated pili and possibly other colonization factors such as the different hemagglutinins, accessory colonization factor, and core-encoded pilus, all of which are thought to play a role.
The pathogenesis of Vibrio cholerae infection serves as a paradigm for many classic features of bacterial virulence:
The organism produces a prototypical enterotoxin.
A pilus is required for colonization of the small intestine.
Genes encoding virulence factors are clustered in two regions of the chromosome, on a pathogenicity island and on a filamentous bacteriophage; this suggests that horizontal gene transfer may lead to the development of new epidemic strains.
Multiple virulence genes are coordinately regulated by environmental conditions.
Biofilm formation is important in both infectivity and environmental persistence.
V. cholerae is both an environmental organism and a human intestinal pathogen.
The complete genome of vibrio cholerae consists of two circular chromosomes. The majority of recognizable genes for essential cell functions (e.g., DNA replication, transcription, translation, etc.) and pathogenicity (e.g., toxin, surface antigens, and adhesion) are located on the large chromosome. The small chromosome contains a large percentage of hypothetical genes, more genes that appear to have origins other than the Proteobacteria and a gene capture system (integron island) that suggests this may have been a megaplasmid captured by an ancestral Vibrio species.
The Vibrio cholerae genome sequences provide a starting point for understanding how a free living, environmental microorganism is also a human pathogen.
Symptoms may include:
More severe symptoms may include:
Rapidly lose 10% of body weight.
Dehydration and shock.
Sometime even death.
Rapid loss of body fluid.
The minimum identification of V. cholerae O1 requires only serologic confirmation of the presence of O1 serotype antigens with suspect isolates. However, a more complete characterization of the organism may be necessary and may include various biochemical tests as well as the determination of other characteristics. The laboratory should decide when it is appropriate to perform these additional tests on clinical isolates, since they should not be a routine part of identification of V. cholerae O1. Generally, if the isolate is from a region that is threatened by epidemic cholera or is in the early stages of a cholera outbreak, it is appropriate to confirm the production of cholera toxin and biochemical identification. Other tests that could provide important public health information include hemolysis, biotyping, molecular subtyping, and antimicrobial sensitivity assays. These tests should be performed on only a limited number of isolates.
The use of antisera is one of the most rapid and specific methods of identifying V. cholerae O1. Although identifying the serogroup and serotype of V. cholerae isolates is not necessary for treatment of cholera.
Even before identifying cause of disease, rehydration therapy must being immediately because death can occur within hours.
Sugar and water.
Do not replace potassium, sodium, bicarbonate.
Wash hands frequently.
Boil or treat water with chlorine or iodine.
NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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