Bacterial Pathogenesis Quiz

WIKIQUIZ

Questions reviewed by:

Michael Jones BSc (Hons) MSc PhD Lecturer in Microbiology and Molecular Biology

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What do E. coli release when they die, which can cause disseminated intravascular coagulation? Colonisation factor Alpha-haemolysin Endotoxins Cytotoxic necrotising factors Siderophores Please select an option Incorrect. Colonisation factors are released from bacteria when they are invading and colonising and do not cause disseminated intravascular coagulation.. The correct answer is that endotoxins are released when E. coli die and cause endothelial damage leading to disseminated intravascular coagulation and endotoxic shock. This endotoxin is also pyrogenic. WikiVet Article: E. coli Incorrect.Alpha-haemolysin may increase iron availability for invading organisms but do notdo not cause disseminated intravascular coagulation when bacteria die. The correct answer is endotoxins are released when E. coli die and cause endothelial damage leading to disseminated intravascular coagulation and endotoxic shock. This endotoxin is also pyrogenic.WikiVet Article: E. coli Correct! Endotoxins are released when E. coli die and cause endothelial damage leading to disseminated intravascular coagulation and endotoxic shock. This endotoxin is also pyrogenic.WikiVet Article: E. coli Incorrect. Cytotoxic necrotising factors do not cause disseminated intravascular coagulation. Theyare released by many pathogenic E. coli and produce cell damage at their site of action. The correct answer is endotoxins are released when E. coli die and causesendothelial damage leading to disseminated intravascular coagulation and endotoxic shock. This endotoxin is also pyrogenic. WikiVet Article: E. coli Incorrect. Siderophores are made by certain pathogenic strains, and are responsible for iron aquisition; they include aerobactin and enterobactin. They do not cause disseminated intravascular coagulation. The correct answer is that endotoxins are released when E. coli die and cause endothelial damage leading to disseminated intravascular coagulation and endotoxic shock. This endotoxin is also pyrogenic.WikiVet Article: E. coli

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What is required for Lawsonia intracellularis infection to initiate? Increase in somatostatin Intestinal flora Decrease in mucus secretions Excess gastric acid Anaerobic conditions Please select an option Incorrect. Lawsonia infection can only take place in the presence of intestinal flora. There is a synergistic relationship between L. intracellularis and intestinal flora including E. coli, Clostridium species and Bacteroides species.Somatostatin is growth hormone inhibiting hormone which is secreted in several locations in the gastrointestinal tract. WikiVet Article: Lawsonia Correct! Infection can only take place in the presence of intestinal flora. There is a synergistic relationship between L. intracellularis and intestinal flora including E. coli, Clostridium species and Bacteroides species. WikiVet Article: Lawsonia Incorrect. Lawsonia infection can only take place in the presence of intestinal flora. There is a synergistic relationship between L. intracellularis and intestinal flora including E. coli, Clostridium species and Bacteroides species.WikiVet Article: Lawsonia Incorrect. Lawsonia infection can only take place in the presence of intestinal flora. There is a synergistic relationship between L. intracellularis and intestinal flora including E. coli, Clostridium species and Bacteroides species. Infection occurs in the terminal ilium, caecum and colon where there is not any gastric acid.WikiVet Article: Lawsonia Incorrect. Lawsonia infection can only take place in the presence of intestinal flora. There is a synergistic relationship between L. intracellularis and intestinal flora including E. coli, Clostridium species and Bacteroides species.WikiVet Article: Lawsonia

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What type of cell does Lawsonia intracellularis have affinity for? Enteroendocrine cells Goblet cells Enterocytes Paneth cells Parietal cells Please select an option Incorrect. Lawsonia intracellularis is not known to have an affinity for enteroendocrine cells. Enteroendocrine cells are specialized endocrine cell of the GI tract. The correct answer is that Lawsonia intracellularis has an affinity for enterocytes. Enterocytes are simple columnar epithelium cells of the small intestine and colon. They are thought to have a a secretory role. WikiVet Article: Lawsonia intracellularis Incorrect. Lawsonia intracellularis is not known to have an affinity for goblet cells. Goblet cells are glandular simple columnar epithelial cells that secrete mucus. The correct answer is that Lawsonia intracellularis has an affinity for enterocytes. Enterocytes are simple columnar epithelium cells of the small intestine and colon. They are thought to have a a secretory role. WikiVet Article: Lawsonia intracellularis Correct! Lawsonia intracellularis has an affinity for enterocytes. Enterocytes are simple columnar epithelium cells of the small intestine and colon. They are thought to have a a secretory role. WikiVet Article: Lawsonia intracellularis Incorrect. Lawsonia intracellularis is not known to have an affinity for paneth cells. Paneth cells are also found in the intestinal tract and contain zinc and lysoyme. The correct answer is that Lawsonia intracellularis has an affinity for enterocytes. Enterocytes are simple columnar epithelium cells of the small intestine and colon. They are thought to have a a secretory role. WikiVet Article: Lawsonia intracellularis Incorrect. Lawsonia intracellularis is not known to have an affinity for parietal cells. Parietal are part of the stomach epithelium and secrete gastric acid and intrinsic factor. The correct answer is that Lawsonia intracellularis has an affinity for enterocytes. Enterocytes are simple columnar epithelium cells of the small intestine and colon. They are thought to have a a secretory role. WikiVet Article: Lawsonia intracellularis

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What does Pseudomonas aeruginosa produce that damages the lung parenchyma? Exotoxin A Lipopolysaccharide (LPS) Elastase Proteases Phospholipase C Please select an option Incorrect. Exotoxin A, phospholipase C and proteases, produced by Pseudomonas, allow tissue invasion and damage, but not of the lung parenchyma.The correct answer is elastase which is produced by Pseudomonas aeruginosa and damages elastin in lung parenchyma and blood vessel walls. This aids in the disease process which in many circumstances leads to pneumonia. WikiVet Article: Pseudomonas Incorrect. LPS is a component of the outer membrane of bacteria and is not released by bacteria until death. Pseudomonas resists phagocytosis and complement via its LPS. The correct answer is elastase which is produced by Pseudomonas aeruginosa and damages elastin in lung parenchyma and blood vessel walls. This aids in the disease process which in many circumstances leads to pneumonia. WikiVet Article: Pseudomonas Correct! Elastase is produced by Pseudomonas aeruginosa and damages elastin in lung parenchyma and blood vessel walls. This aids in the disease process which in many circumstances leads to pneumonia. WikiVet Article: Pseudomonas Incorrect. Exotoxin A, phospholipase C and proteases, produced by Pseudomonas, allow tissue invasion and damage, but not of the lung parenchyma. The correct answer is elastase which is produced by Pseudomonas aeruginosa and damages elastin in lung parenchyma and blood vessel walls. This aids in the disease process which in many circumstances leads to pneumonia. WikiVet Article: Pseudomonas Incorrect. Exotoxin A, phospholipase C and proteases, produced by Pseudomonas, allow tissue invasion and damage, but not of the lung parenchyma. The correct answer is elastase which is produced by Pseudomonas aeruginosa and damages elastin in lung parenchyma and blood vessel walls. This aids in the disease process which in many circumstances leads to pneumonia. WikiVet Article: Pseudomonas

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Which toxin is released by verotoxigenic E. coli into the small intestine in oedema disease? Alpha-haemolysin Enterotoxin Shiga like toxin Endotoxin Siderophores Please select an option Incorrect. Alpha-haemolysin are released by E. coli but increase the avaliability of iron for invading organism, they do not cause the pathogenesis that results in oedema disease. In oedema disease of pigs, verotoxin, or shiga like toxin is released from verotoxigenic E. coli (VTEC) in the small intestine and carried in the bloodstream. This leads to acute, frequently fatal enterotoxaemia of weaned pigs. WikiVet Article: E. coli Incorrect. Enterotoxins are released by enterotoxigenic E. coli (ETEC). In oedema disease of pigs, verotoxin, or shiga like toxin is released from verotoxigenic E. coli (VTEC) in the small intestine and carried in the bloodstream. This leads to acute, frequently fatal enterotoxaemia of weaned pigs.WikiVet Article: E.coli Correct! Verotoxin (Shiga like toxin) is released by verotoxigenic E. coli (VTEC) in the small intestine and carried in the bloodstream.This leads to acute, frequently fatal enterotoxaemia of weaned pigs. WikiVet Article: E. coli Incorrect. Endotoxin is not released by E. coli as they are a structural component of the live bacteria and so only act when the bacteria die. In oedema disease of pigs, verotoxin, or shiga like toxin is released from verotoxigenic E. coli (VTEC) in the small intestine and carried in the bloodstream. This leads to acute, frequently fatal enterotoxaemia of weaned pigs.WikiVet Article: E.coli Incorrect. Siderophores are made by certain pathogenic strains, and are responsible for iron acquisition; they include aerobactin and enterobactin. In oedema disease of pigs, verotoxin, or shiga like toxin is released from verotoxigenic E. coli (VTEC) in the small intestine and carried in the bloodstream. This leads to acute, frequently fatal enterotoxaemia of weaned pigs.WikiVet Article: E.coli

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How does enteroinvasive E. coli invade epithelial cells? Receptor-mediated endocytosis Secondary active transport Facilitated diffusion Pinocytosis Primary active transport Please select an option Correct! Enteroinvasive E. coli induce receptor-mediated endocytosis in the epithelial cells of the intestine. WikiVet Article: E. coli Incorrect. In secondary active transport the electrochemical potential difference created by pumping ions out of the cell is used for movement. Enteroinvasive E. coli induce receptor-mediated endocytosis in the epithelial cells of the intestine. WikiVet Article: E. coli Incorrect. Facilitated diffusion is a form of passive transport facilitated by transport proteins. Enteroinvasive E. coli induce receptor-mediated endocytosis in the epithelial cells of the intestine. WikiVet Article: E. coli Incorrect. Pinocytosis is concerned with the uptake of solutes and single molecules such as proteins. Enteroinvasive E. coli induce receptor-mediated endocytosis in the epithelial cells of the intestine. WikiVet Article: E. coli Incorrect. Primary active transport uses energy (ATP) to transport molecules across a membrane. Enteroinvasive E. coli induce receptor-mediated endocytosis in the epithelial cells of the intestine. WikiVet Article: E. coli

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Which of the following is a difference between type A and type B strains of Francisella tularensis? Type A is highly virulent and type B is less virulent. Type A is waterborne and type B is terrestrial Type A is found in Eurasia and type B is in North America only Type A causes mild disease and type B severe Type B causes the most infections in domestic animals Please select an option Correct! Francisella tularensis causes a lymphadenitis and septicaemia in wildlife, domestic animals and humans, known as Tularaemia. Type A is highly virulent where as type B is less virulent. WikiVet Article: Francisella tularensis Incorrect. Francisella tularensis causes a lymphadenitis and septicaemia in wildlife, domestic animals and humans, known as Tularaemia. Type A is a terrestrial strain with reservoirs in lagomorphs, rodents, galliforms and birds.Type B is waterborne with reservoirs in water, mud and affects aquatic animals. The correct answer is that type A is highly virulent and type B is less virulent. WikiVet Article: Francisella tularensis Incorrect. Francisella tularensis causes a lymphadenitis and septicaemia in wildlife, domestic animals and humans, known as Tularaemia. Type A is confined to North America, whereas type B is found in both Eurasia AND North America. The correct answer is that type A is highly virulent and type B is less virulent. WikiVet Article: Francisella tularensis Incorrect. Francisella tularensis causes a lymphadenitis and septicaemia in wildlife, domestic animals and humans, known as Tularaemia.Type A causes severe disease and type B causes mild disease. The correct answer is type A is highly virulent and type B is less virulent. WikiVet Article: Francisella tularensis Incorrect. Francisella tularensis causes a lymphadenitis and septicaemia in wildlife, domestic animals and humans, known as Tularaemia. Type A causes the most infections in domestic animals. The correct answer is type A is highly virulent and type B is less virulent. WikiVet Article: Francisella tularensis