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Path Micro FINAL
Review and C. diff
| Question | Answer |
|---|---|
| Which of the following S. pyogenes virulence factors is involved in escaping NETs? M Protein/ Sda1/ SpeA2/ SlaA/ All of the Above | Sda1 |
| The following virulence factor cleaves hyaluronic acid and is involved in the spread of S. pyogenes? M protein/ Steptolysin O/ Streptokinase/ Hyaluronidase/ All of the Above | Hyaluronidase |
| The following virulence factor in S. pyogenes contributes to shock symptoms by activating mast cells Streptokinase/ Hyaluronidase/ Streptolysin O/ Hyaluronic Acid Capsule/ None of the above | Streptolysin O |
| Griffith's experiment proved that this virulence factor was essential for S. pneumoniae: Pneumolysin/ PsaA/ Sialic Acid Capsule/ All of the above/ none of the above | Sialic Acid Capsule |
| How does S. pneumoniae elicit a strong inflammatory response in the lungs? | Peptidoglycan and teichoic acid stimulate inflammatory response - damages endothelial cells and lung tissue. Inflammatory response leads to increase C5a, increased PMN migration and chemotactic signals. Pneumolysin contributes to inflammation |
| How does pneumolysin contribute to inflammation? | causes lysis of pneumocytes, activates complement cascade, binds to Fc portion of antibodies which changes conformation of antibody - activates classical pathway |
| True or False: Helicobacter pylori solely affects the stomach | FALSE |
| Helicobacter pylori is typically found in which portion of the stomach? A. Antrum/ B. Mucosa/ C. Serosa/ D. All of the Above/E. A&B only | E. A&B only |
| True or False: Clostridium difficile can be a component of the normal microbiota for some individuals | True |
| The symptoms of C diff are due to which of the following? Exotoxin A/ ST Toxin/ Urease/ Tir/ All of the above | Exotoxin A |
| Which of the following are involved in the treatment of ulcers caused by H. pylori? Proton pump inhibitors/ bismuth/ antibiotics/ all of the above/ none of the above | ALL OF THE THINGS! |
| Which of the following virulence factors are involved in the pathogenesis of H. pylori? A. Mucinase/ B. Urease/ C. EspB/ D. All of the above/ E. A&B only | E. A&B only |
| Which bacterium causes hemolytic uremic syndrome? | Escherichia coli |
| Vibriobactin is: A. involved in iron uptake/ B. Produced by Vibrio cholerae under low iron conditions C. Produced by V. cholerae under high iron conditions D. all of the above/ E. A&B only | E. A&B only |
| True or False: An infectious does of 10^4 cfu/ml is required for Vibrio cholerae to cause disease in healthy individuals | FALSE (10^8 cfu/ml) |
| The primary virulence factor for Enterohemorrhagic E. coli is: EAST/ Shiga-like toxin/ LT toxin/ All of the above/ none of the above | Shiga-like toxin |
| Enteroinvasive E. coli target which part of the intestine? | Large Intestine |
| Enterotoxigenic E. coli have which virulence factors? | Colonization factor antigen, ST toxin, LT toxin |
| Bundle-forming pilus, intimin, and Tir are associated with which E. coli? | Enteropathogenic |
| True or False: Cholera toxin's B subunit binds to Gs-alpha | False (Gs1) |
| The functions of Tir include: Extracellular domain binds intimin/ N terminal domain extends into host-cell cytoplasm and binds alpha-actin, talin, and vinculin/ C terminal domain when it becomes phosphylated binds to Nck/ All of the Above | ALL OF THE THINGS! |
| The main characteristics of EIEC are: | The ability to adhere to and invade intestinal epithelial cells/ ability to survive and replicate expansively within macrophages without triggering host cell death, and inducing the release of TNFalpha, the lack of known invasive determinant |
| The activities of VacA include: | Membrane channel formation, disruption of endosomal and lysosomal activity, effects on integrin receptor-induced cell signalling, interference with cytoskeleton-dependent cell functions |
| What is the veterinary equivalent strain of Clostridium difficlie? | C. perfringens |
| What color are feces in cases of C. diff infection? | bright green |
| Clostridium difficile characteristics | Gram positive, obligate anaerobe, sporeformer, produces exotoxin - causes CDAD C.diff associated disease or CDI - C. diff infection |
| What percentage of the population are asymptomatic carriers of C. diff? | 5% |
| What are the symptoms of CDI or CDAD (C. diff infection)? | ranges from mild viscus, green diarrhea to lethal pseudomembranous colitis |
| When does C. diff cause infection? | When it produces toxin |
| Spores of C. diff | infection aquired primarily by spores. Spores are able to survive more. The spores pass through stomach into sm. intestine and then become vegetative. Can cause psuedomembrane which causes blockage = MEGACOLON |
| When C. diff is present in the microbiome, what percent of microflora is it? | 1-3% of microbiome |
| What happens when C. diff comes into contact with bile salts? | germination is triggered of flagella (attachment components)which have a resistance to cathelicidin components of MALT |
| spores of C. diff are commonly ingested from what material? | fecal matter. yum. |
| What treatment is C. diff infection usually associated with? | Antibiotic treatment. Typically clindamycin, cephalosporins, and ampicillin reduce the number of normal microbiota (anaerobes). C. diff resistant to cephalosporins, can grow to large numbers. |
| What toxins does C. diff produce? What does C. diff toxins do? | A (TcdA) and B (TcdB) toxin. Toxins kill epithelial cells which create an immune response (lesions, layers of dead cells, mucin and fibrin) = diarrhea, ulceration of colon, maybe death |
| Infection with what strain can lead to immunity to C. diff? By what mechanism is this happening? | Clostridium sondelli by cross-reactivity |
| C. diff Exotoxin A: (TcdA) toxin A | produces chemotaxis; induces cytokine production with hypersecretion of fluid; produces hemorrhagic necrosis |
| C. diff cytotoxin: (TcdB) toxin B | Induces depolymerization of actin with loss of cellular cytoskeleton |
| C. diff adhesin factors | mediates binding to human colonic cells |
| C. diff hylauronidase | produces hyaluronic acid |
| C. diff spore formation | permits organism's survival for months in hospital environment |
| True or False: a person can get C. diff infections over and over by the same strain | True: phase different cell wall |
| Where are C. diff virulence factors found? | on pathogenicity island |
| What does C. diff transferase (CDT) do? | causes ADP ribosylation - adds ADP ribosyl to stop glycosylation |
| The use of what antibiotics leads to C. diff infection? and why? | Cephalosporins, clindamycin and ampicillin - knocks out normal flora but C. diff is resistant |
| What antibiotics are C.diff infections treated with and when? | Vancomycin and Metronidazole in cases with pseudomembrane |
| What other treatments are possible for C. diff? | treatment with antisera for ToxinA and ToxinB. Also fecal slurry bacterial enemas = bacteriotherapy and probiotics to restore normal microbiota |
| What is C. diff pseudomembranous colitis buildup composed of? | inflammation, lesions, layers of dead cells, mucin and fibrin - C. diff pizza. |
| What are things that can happen due to C. diff infection? | Diarrhea, ulceration of colon, pseudomembranous colitis, even death! |
| What is the association between antibiotics and C. diff? | Typically patient is treated with antibiotic that knocks out normal microbiota and C. diff is resistant to. C. diff then can grow |
| What are the virulence factors that C. diff possesses? | TcdA, TcdB, CDT |
| What kills epithelial cells in C. diff infection | toxins A & B |
| C. Diff Toxin A: | causes viscous bloody appearance - affects motility of intestinal content -attracts and activates PMNs by stimulating mucosal cells to produce cytokines - damage mucosal cells/underlying tissue - PMNs break tight junctions in mucosa allowing ToxB through |
| C. Diff Toxin B: | cytotoxic by altering cytoskeleton |
| What is the mode of action for C. diff toxins? | Glyosylate threonine residue on G protein targets Rho, Rac, and Cdc42 (regulatory proteins that control polymerization and depolymerization of actin) Glycosylation reduces G protein activity - disrupts G protein control of cell process |
| What do C. diff toxins cause on a cellular level? and what does this do for the bacterium? | actin cytoskeletal rearrangement, cytokine release, and apoptosis - this allows C. diff to adhere and invade cells |
| Binary toxin CDT: | ADP-ribosylating actin proteins, resulting in cytoskeletal rearrangement and enhances C. diff adhesion by creating actin protrusions |
| Patients with antibiotic associated diarrhea are tested for the presence of what in their feces? | Toxin A & B |
| What triggers the germination of C. diff from spore form into vegetative form? | Bile salts. - also triggers the formation of flagella! |
| What component of MALT are C. diff flagella resistant to? | cathelicidin |
| In what form is C. diff infection usually acquired? | spore form (from feces) |
| What can happen when blockage is caused by psueudomembrane in C. diff infection? | MEGACOLON! |
| What kind of IgG response is a predictor for infection by C. diff? | poor IgG response |
| Virulence factors of C. diff (from table) | pilus, capsule, flagella. collagen and fibronectin and von-Willebrand factor binding proteins, sortase, major surface layer protein, adhesin, hemagglutinin/Adhesin, phase-variable cell wall, cell lysis, collagen-specific protease |
| what does a capsule do for C. diff? | evades immune response |
| What does IL-1(beta)do? | stimulates fever |
| What does IL-8 do? | attract more immune components |
| What does TNF-(alpha) do? | causes enteritis |
| What type of toxin is the C. diff toxin? | AB toxin - GTPase |
| What organisms are being examined for this final? | Clostridium Difficile, Streptococcus pyogenes, Streptococcus pneumoniae, Helicobacter pylori, Vibrio cholerae, Escherichia coli (EPEC, EIEC, ETEC, EHEC, EAggEC, DAEC) |
Created by:
arsenicgerbil
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