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Bacterial Pathogenesis Quiz (view source)
Revision as of 11:20, 10 November 2009
, 11:20, 10 November 2009New page: {{toplink |linkpage =WikiQuiz |linktext = WikiQuiz |pagetype=Quiz |Review= '''Michael Jones''' BSc (Hons) MSc PhD Lecturer in Microbiology and Molecular Biology }} {{QuizCat|topic=Bugs|...
{{toplink
|linkpage =WikiQuiz
|linktext = WikiQuiz
|pagetype=Quiz
|Review= '''Michael Jones''' BSc (Hons) MSc PhD Lecturer in Microbiology and Molecular Biology
}}
{{QuizCat|topic=Bugs|topicsubcategory=B}}
{{QuizCat|topic=Pathology|topicsubcategory=B}}
<WikiQuiz
questionnumber="1"
question="What do E. coli release when they die, which can cause disseminated intravascular coagulation ?"
choice3="Endotoxins"
choice4="Cytotoxic necrotising factors"
choice2="Alpha-haemolysin"
choice1="Colonisation factor"
choice5="Siderophores"
correctchoice="3"
feedback3="'''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.[[ Escherichia coli |WikiVet Article: E. coli ]]"
feedback4="'''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. [[Escherichia coli |WikiVet Article: E. coli]]"
feedback2="'''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.[[Escherichia coli |WikiVet Article: E. coli]]"
feedback1="'''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. [[Escherichia coli |WikiVet Article: E. coli ]]"
feedback5="'''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.[[Escherichia coli |WikiVet Article: E. coli ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="2"
question="What is required for Lawsonia intracellularis infection to initiate?"
choice2="Intestinal flora"
choice4="Excess gastric acid"
choice5="Anaerobic conditions"
choice3="Decrease in mucus secretions"
choice1="Increase in somatostatin"
correctchoice="2"
feedback2="'''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. [[Lawsonia intracellularis |WikiVet Article: Lawsonia ]]"
feedback4="'''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.[[Lawsonia intracellularis |WikiVet Article: Lawsonia ]]"
feedback5="'''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.[[ Lawsonia intracellularis|WikiVet Article: Lawsonia ]]"
feedback3="'''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.[[Lawsonia intracellularis |WikiVet Article: Lawsonia]]"
feedback1="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Somatostatin |WikiVet Article: LawsoniaLink to Wikipedia: Somatostatin ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="3"
question="What type of cell does Lawsonia intracellularis have affinity for?"
choice3="Enterocytes"
choice4="Paneth cells"
choice5="Parietal cells"
choice1="Enteroendocrine cells"
choice2="Goblet cells"
correctchoice="3"
feedback3="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocyte|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte]]"
feedback4="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocytehttp:/ / en.wikipedia.org/ wiki/ Paneth cell|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Paneth cell.]]"
feedback5="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocytehttp:/ / en.wikipedia.org/ wiki/ Parietal cell|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Parietal cell.]]"
feedback1="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocyte http:/ / en.wikipedia.org/ wiki/ Enteroendocrine cell |WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Enteroendocrine cell.]]"
feedback2="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocytehttp:/ / en.wikipedia.org/ wiki/ Goblet cell|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Goblet cell]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="4"
question="What does Pseudomonas aeruginosa produce that damages the lung parenchyma?"
choice3="Elastase"
choice2="Lipopolysaccharide (LPS)"
choice1="Exotoxin A"
choice5="Phospholipase C"
choice4="Proteases"
correctchoice="3"
feedback3="'''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. [[ Pseudomonas aeruginosa and Burkholderia species|WikiVet Article: Pseudomonas]]"
feedback2="'''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. [[ Pseudomonas aeruginosa and Burkholderia species|WikiVet Article: Pseudomonas]]"
feedback1="'''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. [[ Pseudomonas aeruginosa and Burkholderia species|WikiVet Article: Pseudomonas ]]"
feedback5="'''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. [[Pseudomonas aeruginosa and Burkholderia species |WikiVet Article: Pseudomonas ]]"
feedback4="'''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. [[Pseudomonas aeruginosa and Burkholderia species |WikiVet Article: Pseudomonas ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="5"
question="Which toxin is released by verotoxigenic E. coli into the small intestine in oedema disease?"
choice3="Shiga like toxin"
choice1="Alpha-haemolysin"
choice5="Siderophores"
choice4="Endotoxin"
choice2="Enterotoxin"
correctchoice="3"
feedback3="'''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. [[Escherichia coli|WikiVet Article: E. coli ]]"
feedback1="'''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. [[Escherichia coli|WikiVet Article: E. coli ]]"
feedback5="'''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.[[Escherichia coli|WikiVet Article: E.coli]]"
feedback4="'''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.[[Escherichia coli|WikiVet Article: E.coli]]"
feedback2="'''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.[[Escherichia coli|WikiVet Article: E.coli ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="6"
question="How does enteroinvasive E. coli invade epithelial cells?"
choice1="Receptor-mediated endocytosis"
choice4="Pinocytosis"
choice3="Facilitated diffusion"
choice5="Primary active transport"
choice2="Secondary active transport"
correctchoice="1"
feedback1="'''Correct!'''Enteroinvasive E. coli induce receptor-mediated endocytosis in the epithelial cells of the intestine. [[Escherichia colihttp:/ / en.wikipedia.org/ wiki/ Endocytosis|WikiVet Article: E. coliLink to Wikipedia: Endocytosis]]"
feedback4="'''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. [[Escherichia coli http:/ / en.wikipedia.org/ wiki/ Pinocytosis |WikiVet Article: E. coli. Link to Wikipedia: Pinocytosis.]]"
feedback3="'''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. [[Escherichia coli http:/ / en.wikipedia.org/ wiki/ Facilitated diffusion |WikiVet Article: E. coliLink to Wikipedia: Facilitated diffusion ]]"
feedback5="'''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. [[ Escherichia coli http:/ / en.wikipedia.org/ wiki/ Primary active transport|WikiVet Article: E. coliLink to Wikipedia: Primary active transport]]"
feedback2="'''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. [[Escherichia colihttp:/ / en.wikipedia.org/ wiki/ Secondary active transport|WikiVet Article: E. coliLink to Wikipedia: Secondary active transport ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="7"
question="Which of the following is a difference between type A and type B strains of Francisella tularensis?"
choice1="Type A is highly virulent and type B is less virulent."
choice2="Type A is waterborne and type B is terrestrial"
choice3="Type A is found in Eurasia and type B is in North America only"
choice4="Type A causes mild disease and type B severe"
choice5="Type B causes the most infections in domestic animals"
correctchoice="1"
feedback1="'''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."
feedback2="'''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."
feedback3="'''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."
feedback4="'''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."
feedback5="'''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."
image="">
</WikiQuiz>
|linkpage =WikiQuiz
|linktext = WikiQuiz
|pagetype=Quiz
|Review= '''Michael Jones''' BSc (Hons) MSc PhD Lecturer in Microbiology and Molecular Biology
}}
{{QuizCat|topic=Bugs|topicsubcategory=B}}
{{QuizCat|topic=Pathology|topicsubcategory=B}}
<WikiQuiz
questionnumber="1"
question="What do E. coli release when they die, which can cause disseminated intravascular coagulation ?"
choice3="Endotoxins"
choice4="Cytotoxic necrotising factors"
choice2="Alpha-haemolysin"
choice1="Colonisation factor"
choice5="Siderophores"
correctchoice="3"
feedback3="'''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.[[ Escherichia coli |WikiVet Article: E. coli ]]"
feedback4="'''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. [[Escherichia coli |WikiVet Article: E. coli]]"
feedback2="'''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.[[Escherichia coli |WikiVet Article: E. coli]]"
feedback1="'''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. [[Escherichia coli |WikiVet Article: E. coli ]]"
feedback5="'''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.[[Escherichia coli |WikiVet Article: E. coli ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="2"
question="What is required for Lawsonia intracellularis infection to initiate?"
choice2="Intestinal flora"
choice4="Excess gastric acid"
choice5="Anaerobic conditions"
choice3="Decrease in mucus secretions"
choice1="Increase in somatostatin"
correctchoice="2"
feedback2="'''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. [[Lawsonia intracellularis |WikiVet Article: Lawsonia ]]"
feedback4="'''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.[[Lawsonia intracellularis |WikiVet Article: Lawsonia ]]"
feedback5="'''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.[[ Lawsonia intracellularis|WikiVet Article: Lawsonia ]]"
feedback3="'''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.[[Lawsonia intracellularis |WikiVet Article: Lawsonia]]"
feedback1="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Somatostatin |WikiVet Article: LawsoniaLink to Wikipedia: Somatostatin ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="3"
question="What type of cell does Lawsonia intracellularis have affinity for?"
choice3="Enterocytes"
choice4="Paneth cells"
choice5="Parietal cells"
choice1="Enteroendocrine cells"
choice2="Goblet cells"
correctchoice="3"
feedback3="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocyte|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte]]"
feedback4="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocytehttp:/ / en.wikipedia.org/ wiki/ Paneth cell|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Paneth cell.]]"
feedback5="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocytehttp:/ / en.wikipedia.org/ wiki/ Parietal cell|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Parietal cell.]]"
feedback1="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocyte http:/ / en.wikipedia.org/ wiki/ Enteroendocrine cell |WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Enteroendocrine cell.]]"
feedback2="'''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. [[Lawsonia intracellularis http:/ / en.wikipedia.org/ wiki/ Enterocytehttp:/ / en.wikipedia.org/ wiki/ Goblet cell|WikiVet Article: Lawsonia intracellularis. Link to Wikipedia: Enterocyte, Goblet cell]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="4"
question="What does Pseudomonas aeruginosa produce that damages the lung parenchyma?"
choice3="Elastase"
choice2="Lipopolysaccharide (LPS)"
choice1="Exotoxin A"
choice5="Phospholipase C"
choice4="Proteases"
correctchoice="3"
feedback3="'''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. [[ Pseudomonas aeruginosa and Burkholderia species|WikiVet Article: Pseudomonas]]"
feedback2="'''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. [[ Pseudomonas aeruginosa and Burkholderia species|WikiVet Article: Pseudomonas]]"
feedback1="'''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. [[ Pseudomonas aeruginosa and Burkholderia species|WikiVet Article: Pseudomonas ]]"
feedback5="'''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. [[Pseudomonas aeruginosa and Burkholderia species |WikiVet Article: Pseudomonas ]]"
feedback4="'''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. [[Pseudomonas aeruginosa and Burkholderia species |WikiVet Article: Pseudomonas ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="5"
question="Which toxin is released by verotoxigenic E. coli into the small intestine in oedema disease?"
choice3="Shiga like toxin"
choice1="Alpha-haemolysin"
choice5="Siderophores"
choice4="Endotoxin"
choice2="Enterotoxin"
correctchoice="3"
feedback3="'''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. [[Escherichia coli|WikiVet Article: E. coli ]]"
feedback1="'''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. [[Escherichia coli|WikiVet Article: E. coli ]]"
feedback5="'''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.[[Escherichia coli|WikiVet Article: E.coli]]"
feedback4="'''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.[[Escherichia coli|WikiVet Article: E.coli]]"
feedback2="'''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.[[Escherichia coli|WikiVet Article: E.coli ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="6"
question="How does enteroinvasive E. coli invade epithelial cells?"
choice1="Receptor-mediated endocytosis"
choice4="Pinocytosis"
choice3="Facilitated diffusion"
choice5="Primary active transport"
choice2="Secondary active transport"
correctchoice="1"
feedback1="'''Correct!'''Enteroinvasive E. coli induce receptor-mediated endocytosis in the epithelial cells of the intestine. [[Escherichia colihttp:/ / en.wikipedia.org/ wiki/ Endocytosis|WikiVet Article: E. coliLink to Wikipedia: Endocytosis]]"
feedback4="'''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. [[Escherichia coli http:/ / en.wikipedia.org/ wiki/ Pinocytosis |WikiVet Article: E. coli. Link to Wikipedia: Pinocytosis.]]"
feedback3="'''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. [[Escherichia coli http:/ / en.wikipedia.org/ wiki/ Facilitated diffusion |WikiVet Article: E. coliLink to Wikipedia: Facilitated diffusion ]]"
feedback5="'''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. [[ Escherichia coli http:/ / en.wikipedia.org/ wiki/ Primary active transport|WikiVet Article: E. coliLink to Wikipedia: Primary active transport]]"
feedback2="'''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. [[Escherichia colihttp:/ / en.wikipedia.org/ wiki/ Secondary active transport|WikiVet Article: E. coliLink to Wikipedia: Secondary active transport ]]"
image="">
</WikiQuiz>
<WikiQuiz
questionnumber="7"
question="Which of the following is a difference between type A and type B strains of Francisella tularensis?"
choice1="Type A is highly virulent and type B is less virulent."
choice2="Type A is waterborne and type B is terrestrial"
choice3="Type A is found in Eurasia and type B is in North America only"
choice4="Type A causes mild disease and type B severe"
choice5="Type B causes the most infections in domestic animals"
correctchoice="1"
feedback1="'''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."
feedback2="'''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."
feedback3="'''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."
feedback4="'''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."
feedback5="'''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."
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