19. Classification of Vibrio cholerae Ogawa , Inaba , Hikojima Serotypes Classic and El Tor Biotypes Agents of cholera belong to O1 serogroup and O139 serogroup ( a new strain of V.cholerae that appeared in India in late 1992 ) Serogroup cholerae Species Вид Vibrio Genus Vibrionaceae Family
20. Chemogroups of vibrios according to Heiberg classification (1935) V. cholerae belongs to I chemogroup - - - VI - - + V + + - IV + + + ІІІ + - - ІІ + - + І Sucrose Arabinose Mannose Fermentation of carbohydrates Chemogroup
21. Differentiation of biotypes V. cholera classic and El Tor - + Sensitivity to polymyxin + - Susceptibility to group II (El Tor) bacteriophage - + Susceptibility to group IV (C) bacteriophage + - Hemolysis + - Agglutination of chicken erythrocytes V. cholerae El Tor V. cholerae classic Feature
27. Cholera - attachment V. cholerae bacteria, unlike the shigellae, do not penetrate into the intestinal cells
28. Mechanism of infectious diarrhea Intestinal epithelium Secretion of fluids Bacteria Non-blooding diarrhea Blooding diarrhea
29.
30.
31.
32.
Notas do Editor
Shigella causes a dysentery called shigellosis, which is marked by crippling abdominal cramps and frequent defecation of watery stool filled with mucus and blood.
All shigellae have O Ag (polysaccharide) in their cell wall, and this antigen are used to divide the genus into 4 groups:.
All produce a similar disease that can vary in intensity. Sh.dysenteriae causes the severest form of dysentery.
Shigellae can produce an enterotoxins, invasion is the critical factor in pathogenesis. The evidence for this is that mutants that fail to produce enterotoxin but are invasive can still cause disease, whereas noninvasive mutants are nonpathogenic.
1. Shigellosis is only human disease. 3. Shigellae are the most effective pathogens among the enteric bacteria. Ingestion of as few as 10-100 microorganisms cause disease, whereas about 1 million Salmonella bacilli are required to produce symptoms. 6. Shigellosis is different from salmonellosis in that Shigella invades the villus cells of the large intestine, rather than the small intestine. In addition, it is not as invasive as Salmonella and does not perforate the intestine or invade the blood. It enters the intestinal mucosa. Once in the mucosa and causes extensive tissue destruction. As it multiplies, it gives off toxins. Toxins cause bloody diarrhea
Note the patches of blood and mucus, the erosion of the lining, and the absence of perforation.
As you can see from the bacterium’s name V.cholerae causes cholera. Cholera is the classic example of a very severe form of diarrhea. If cholera is left untreated, death can occur in less than 48 hours, and the mortality rate approaches 55%. Cholera is a human disease that originated in Asia but is now distributed worldwide. There have been 7 cholera pandemics since the 19 th century. The last most persistent pandemic, which began in1961 and continues until today, is due to a strain called the El Tor biotype. This pandemic began in Indonesia, spreading to South Asia, the Middle East, and parts of Europe and Africa.
Abilities of V.cholerae to grow in strong alkaline conditions and high salt concentrations allow the use of selective culture media that inhibit other bacteria but not V.cholerae. V.cholerae can live and multiply in soil and water (fresh and salt) in good condition – warm climate, presence of proteins
Showing its characteristic curved shape and single polar flagellum.
V.cholerae, the major pathogen in the vibrio genus, is the cause of cholera.
V.cholerae is divided into 2 groups according to the nature of its O cell wall antigen, agents of cholera belong to O1 serogroup and O139 serogroup. The O1 organisms have 2 biotypes, called cholerae classic and El Tor, and 3 serotypes, called Ogawa, Inaba and Hikojima. These features are used to characterize isolates in epidemiologic investigations.
Therefore organism can live in warm salt water it can contaminate marine shellfish, ingestion of these without adequate cooking can transmit the disease. 3. The pathogenesis of cholera is dependent on colonization of the small intestine by the organism and secretion of enterotoxin. For colonization to occur, large numbers of bacteria must be ingested, because the organism is particularly sensitive to stomach acid and the most quantity of vibrios perish in stomach. Persons with little or no stomach acid are much more susceptible to cholera.
Mechanisms of infectious diarrhea, (a) In a toxigenic infection, the microbe remains on the surface of epithelial cells and secretes toxin into the cells, (b) In an invasive infection, the microbe breaks down epithelial cells and forms ulcerations, loss of the intestinal lining, and bleeding Infectious diarrhea has two basic mechanisms. In the toxigenic type of disease, bacteria release enterotoxins that bind surface receptors of the small intestine. These toxins disrupt the physiology of epithelial cells and cause increased secretion of electrolytes and water loss, a condition called secretory diarrhea. The organism itself does not invade the tissues. Secretory diarrhea is characterized by its large volume, and there is little blood in the stool. This is the mechanism of cholera and some types of Escherichia coli infectious damage. In a more invasive diarrheal disease, the microbe invades the wall of the small or large intestine and disrupts its architecture, leading to gross injury. This form is attended by smaller fecal volume, pain in the rectum, blood in the stool, and ulceration of the inner mucosal lining. Salmonella, Shigella and enteroinvasive strains of E. coli are responsible for this type of intestinal disease.
During epidemics, clinical evidence is usually sufficient to diagnose cholera. But confirmation of the disease is often required for epidemiologic studies and detection of sporadic cases.