Vibrio cholerae

Gram-negative rods. Facultatively anaerobic Oxidase-positive Polar flagella facilitate rapid motility. Found in water, especially estuaries and coastal waters, because salt is required for growth. Upon ingestion, pathogenic strains cause gastrointestinal disease. Causative agent of cholera. Ingested as free-living cells, micro-colonies, or as biofilms in contaminated foods or water. Sensitive to stomach acids; infection typically requires exposure to a large quantity. However, individuals with impaired stomach acid production are vulnerable to lower infectious doses. Gastroenteritis caused by Vibrio cholerae causes mild to severe vomiting and watery diarrhea. In severe cases, the profuse stool has a characteristic milky-white "rice water" appearance. Proper sanitation and thorough cooking of food can prevent cholera epidemics. Vaccination can help prevent worsening conditions in areas where cholera is endemic. Infected patients should be given antibiotics, such as tetracycline, to avoid dehydration and death. Vibrio cholerae O1 is further subdivided into biotypes and serotypes. Biotypes: Classical and El tor Serotypes: Ogawa and Inaba; Hikojima is thought to be a hybrid transitional state. Severe fluid loss leads to dehydration, which can result in metabolic acidosis, hypokalemia, hypovolemic shock, cardiac arrhythmia, and renal failure. Cholera is endemic in some parts of the world; asymptomatic carriers contribute to its maintained presence. Cholera outbreaks occur in areas where humanitarian and/or environmental crises lead to overcrowding and poor sanitation. We show how Vibrio cholerae O1 and O139 acquire the virulence factors that promote severe gastroenteritis. Horizontal gene transfer is key to this process. First, we draw a couple of small intestine epithelial cells and indicate the intestinal lumen. Then, we draw a non-pathogenic Vibrio cholerae bacterium. Its chromosomal DNA has already acquired Vibrio Pathogenicity Island -1 (VPI-1), which carries genes for Toxin co-regulated pili. Toxin co-regulated pilus is a type of bundle-forming pilus that promotes microcolony formation, which is important for Vibrio cholerae colonization. This pilus is also a receptor for bacteriophage CTX?, which injects DNA into the V. cholerae microbe. Without the pathogenicity island and toxin co-regulated pilus, the bacteriophage would not be able to attach to the microbe and transfer DNA. Next, we show that the CTX prophage has been integrated into the chromosomal DNA. The CTX prophage triggers production of cholera toxin, which interacts with binding sites on the small intestine epithelial cells. Cholera toxin increases cyclic AMP, which leads to water and electrolyte secretion into the lumen. Profuse watery diarrhea ensues. The CTX? prophage also carries genes for two additional toxins: Accessory cholera enterotoxin (ACE) contributes to water and ion secretion; some authors report that this enterotoxin, alone, can induce gastroenteritis. Zona occludens toxin (ZOT) disassembles epithelial tight junctions, which increases intestinal permeability. Neuraminidase increases the availability of cholera toxin binding sites on host cells The nanH gene that codes for this enzyme is carried separately. Virulence factors of these strains vary. Non-O1 strains have polysaccharide capsules that facilitate spread beyond the intestine. Various toxins, including heat-stable enterotoxin, induce diarrheal symptoms.