Vibrio Cholerae PDF

Vibrio cholerae Is gramme negative. Oxidase –positive, motile rods and salt tolerant or salt requiring It is comma shape rods grown in freshwater ponds and brackish water. They can be cultured on most media used for stool culture Causes Cholera disease  Transmission...

Vibrio cholerae Is gramme negative. Oxidase –positive, motile rods and salt tolerant or salt requiring It is comma shape rods grown in freshwater ponds and brackish water. They can be cultured on most media used for stool culture Causes Cholera disease  Transmission The bacteria are transmitted between humans through the fecal-oral route; a by eating contaminated food or a drink contaminated water can cause infection. Large inocula are required to establish infection, thus direct contact person to person spread is unlikely. Carries recovered from cholera may shed organism and are an important reservoir of Vibrio cholerae in endemic regions.  Pathogenesis The incubation period varies from 6 hours to 3 days. A well-defined sequence of events occurs following the ingestion of V. cholera. They are as follows: Adherence and colonization Virulent forms of V. cholera attach to the epithelium of microvilli at the brush border no sooner it crosses the acid barrier. After that, they multiply increasing their number  Secretion of cholera toxin As they multiply, they produce a potent exotoxin called enterotoxin. Toxin is produced in close proximity to its specific receptors (GM1 ganglioside) on cell membrane lining the villi and crypts of the small intestines  Activation of the A1 subunit After there is binding of the B unit to the receptor of the cell membrane, the A subunit dissociates from the B subunit. The cell membrane gets penetrated during this dissociation. There are two subunits of A-unit: A1 and A2 which are joined by disulphide bond. The bond between A1 and A2 subunits is broken down and subunit A1 gets activated. The ADP ribose is transferred from a nicotinamide adenine dinucleotide (NAD) to a guanosine triphosphate (GTP)-binding protein by enzymatic action of activated A1 subunit. The adenyl cyclase activity gets regulated by the above event. Adenyl cyclase activity of the cell increases because of the normal GTP “turn off” mechanism is inhibited. Pathogenesis…. This results in an increase and accumulation of intracellular cyclic 3’, 5’-adenosine monophosphate (cAMP). The increased intracellular cAMP level causes various activities like: i)Inhibition of reabsorption of Na+, K+ and Cl– ions by cells lining the villi, together with ii)Hyper-secretion of Cl– and HCO3– The above activities cause a net loss of sodium, potassium and sodium bicarbonate into the intestine, with a corresponding fluid loss to maintain the isotonicity of the intestinal fluid. There is purging diarrhea of “rice water stool” with loss of water and electrolytes.  The fluid secreted is isotonic with plasma with a relatively higher concentration of sodium, potassium and bicarbonate and lower concentration of chloride The result is the outpouring of fluid and electrolytes, with resulting diarrhea, dehydration, acidosis, shock and death.  Clinical findings Sudden vomiting Profuse diarrhea with abdominal cramps The stool resemble rice water and contain mucus. Epithelial cells, and large number of vibrios There is rapid loss of fluids and electrolytes, which lead to dehydration, circulatory collapse and anuria. The death rate without treatment is 25 to 50%  Diagnosis Stool or vomitus culture Treatment Water and electrolytes replacement to correct dehydrationand salt depletion Many antimicrobial are effective e.g oral tetracycline Prevention Good public sanitation measures to reduce contamination of water sources with cholera containing feces Vaccination is largely ineffective , providing only short term protection against cholera. Don’t eat contaminated food Boil drinking water Wash hands