Vibrio Cholerae PDF
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University of Basrah
Prof. Dr. Enas Abdul sahib
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This document provides information on Vibrio cholerae, including its characteristics, pathogenesis, symptoms, and diagnosis. It's a detailed study of the bacterium, providing information to understand infectious diseases.
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Vibrio cholerae Prof. Dr. Enas Abdul sahib ❑ Gram-negative, curved or comma-shaped rod. ❑ On prolonged cultivation, organisms may become straight rods that can resemble other Gram-negative enteric bacteria. ❑ Species of medical importance ❑ Actively motile with a single polar flagellum....
Vibrio cholerae Prof. Dr. Enas Abdul sahib ❑ Gram-negative, curved or comma-shaped rod. ❑ On prolonged cultivation, organisms may become straight rods that can resemble other Gram-negative enteric bacteria. ❑ Species of medical importance ❑ Actively motile with a single polar flagellum. ❑ Aerobic or facultative anaerobic. ❑ Found in fresh water, marine, surface waters, shellfish and other sea food. ❑ Thrive in dirty and unsanitary conditions, especially those which cause raw sewage to become mixed with drinking water. 1 Pathogenesis After ingestion of the V. cholerae by the fecal-oral route of contaminated food or water. V. cholerae serogroups O1 and O139 cause cholera in humans within several hours to 2-3 days of ingestion. Vibrios are sensitive to acid, and most die in the stomach. Surviving virulent organisms may adhere to and colonize the small bowel, where they secrete the potent cholera enterotoxin (also known as choleragen and sometimes abbreviated to CTX, CT, Ctx). This toxin binds to the plasma membrane of intestinal epithelial cells and releases an enzymatically active subunit that causes a rise in cyclic adenosine monophosphate (cAMP) production. The resulting high intracellular cAMP level causes massive secretion of electrolytes and water into the intestinal lumen. Rice water diarrhea occurs and resulting diarrhea containing vibrio's, epithelial cells and mucus. Vibrio cholerae Enterotoxin The heat-labile enterotoxin is inactivated by high temperatures. Ganglioside GM1 serves as the mucosal receptor for subunit B (Ganglioside, receptor- binding domain), which promotes entry of subunit A (toxic domain) into the cell. Activation of subunit A1 yields increased levels of intracellular cyclic adenosine monophosphate (c AMP) from ATP by adenylate cyclase, that changes the ion flow by cystic fibrosis transmembrane conductance regulator (CFTR). The ion channel CFTR allows secretion of chloride ions into the intestinal lumen and results in prolonged hypersecretion of water and electrolytes. There is increased sodium-dependent chloride secretion, and absorption of sodium and chloride by the microvilli is inhibited. 2 A person with normal gastric acidity may have to ingest as many as 1010 or more V. cholerae to become infected. The infectious dose, however, is significantly lower (10^2-10^4) in a person with achlorhydria (absence secretion of hydrochloric acid in the stomach or hypochlorhydria (Low stomach acid). Any medication (e.g., proton-pump inhibitors) or condition that decreases stomach acidity makes a person more susceptible to infection with V. cholerae. The organisms do not reach the bloodstream but remain within the intestinal tract. The spectrum of disease due to V. cholerae ranges from asymptomatic intestinal colonization to mild, moderate, or severe diarrhea. About 50% of infections with classic V. cholerae are asymptomatic. Although the bacteria are present in their feces for 1-10 days after infection, potentially infecting other people. The World Health Organization (WHO) estimates that over 100 000 people die every year from cholera infection. The mortality rate without treatment is 50%. On the contrary, mortality in patients promptly treated with fluid replacement has been reported as 1% or less. 3 Cholera is endemic or epidemic in areas with poor sanitation; it occurs sporadically or as limited outbreaks in developed countries. Endemic disease meaning outbreak of disease that is typically present in a particular region or population. Epidemic is the rapid spread of disease to a large number of hosts in a given population within a short period of time. The incubation period after ingestion of a sufficiently high infectious dose of V. cholerae is 12 hours to 3 days for persons who develop symptoms, depending largely on the size of the inoculum ingested Symptoms of Cholera Watery diarrhea is the hallmark of cholera (Dehydration) Muscle cramps Thirsty and dry tongue Hypotension Vomiting Low blood pH (acidosis) Nausea Coma in your children Hollow and sunken eyes. Very fast heart rate Anuria and the skin become wrinkled. Cholera has been named the "blue death" because a person's skin may turn bluish-gray from extreme loss of fluids Diagnosis 1. Specimen: Stool flecks. 2. Smears: Gram-negative motile curved rods. Motility of vibrios is best seen using dark-field microscopy. 3. Culturing on selective media: Direct cultures of stool on thiosulfate- citrate-bile-sucrose (TCBS) agar and enrichment cultures in alkaline peptone water are appropriate. The incubation period is 12hrs-3days for persons who develop symptoms. 4 V. cholerae produces yellow colonies (sucrose fermented) on TCBS agar that are readily visible against the dark-green background of the agar. Non-sucrose- fermenting vibrios produce green colonies on TCBS agar. V. cholerae grow on MacConkey agar (Non lactose fermenter colonies). On blood agar, V. cholerae produce beta-hemolytic colonies. Characteristically, vibrio’s grow at a very high pH (8.5–9.5) and are rapidly killed by acid. 4. Biochemical tests: Vibrio's are oxidase positive, which differentiates them from enteric Gram-negative bacteria. 5.Serological tests: Slide agglutination tests using anti- O1 and O139 antiserum. 5 Treatment The most important part of treating cholera patients consists of water and electrolyte replacement to correct the severe dehydration and salt depletion. Appropriate antimicrobial therapy can also reduce the duration and amount of shedding of Vibrio organisms in the stool. Tetracycline has shown to be very effective than furazolidone. Erythromycin, azithromycin, doxycycline, trimethoprim–sulfamethoxazole and fluoroquinolones. Prevention A safe and clean supply of water is the key to cholera prevention. Adequate chlorination of public water supplies Distribution of chlorine tablets to households with instructions for their proper use are often effective measures. If chemical disinfection is not possible, people can be instructed to boil water before drinking. Hygienic disposal of human waste. Ensuring the safety of food is yet another important control measure. Oral cholera vaccines are used. 6