Immunology Final Exam, Final Section

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Immunology Final Exam, Final Section
2013-04-22 21:24:33
IMIN 200

Final section with Feldman.
Show Answers:

  1. What does Salmonella cause
  2. What does E.Coli Cause
  3. What does C. diff cause
  4. What does Campylobacter Jejuni Cause
    Diarrhea and guillain barre syndrome
  5. What does mycobacteria cause
  6. What does Helicobacter pylori cause
    Ulcer and gastric cancer
  7. What does Yersinia cause
  8. What bacteria causes lime disease
    Borrelia burgdorferi
  9. What bacteria cause meningitis
    Nyceria menengitis and sterptococcus pneumonia
  10. What are two different, basic, strategies that work towards symbiosis
    • 1. recruit neutral/beneficial microbes as defenses
    • 2.Evolve a complex network of defenses to prevent bad microbes from gaining access
  11. What are the steps in infection
    • 1. Exposure to Pathogen
    • 2. Adherence to skin of mucosa
    • 3. Invasion through epithelium
    • 4. Colonization and Growth
    •     -Production of virulence factor
    • 5 a) Toxicity
    •     -Toxin effects are local or systemic
    • 5 b) Invasiveness
    •     - Further growth at original site and       distant sites
    • 6.)  Tissue damage and disease
  12. What is the relation between host and microbe influenced by
    • a) virulence of the microbe
    • b) The defense mechanisms of the host
  13. What are modes of entry of a pathogen into a host
    • Inhalation
    • Ingestion
    • Insect bites
    • Sexual Contact
    • Wound infection
    • Organ transplant
  14. What are defensive barriers of the respiratory tract (4)
    • Mucus
    • Ciliated epithelium
    • Antibody
    • Phagocytes
  15. What are the defensive barriers of the eyes (2)
    • Washing by tears
    • Lysozyme
  16. What are the defensive barriers of the skin (4)
    • Anatomic barrier (sweat)
    • Antimicrobial properites
    • Low pH
    • commensal microbes
  17. What are the defense barriers of the Urinary tract (4)
    • Washing by urine
    • Acidity of urin
    • lysozyme
    • vaginal lactic acid
  18. What are the defensive barriers of the GIT (6)
    • Stomach acidtiy
    • Normal Flora
    • Intestine alkaline pH
    • Mechanical flushing
    • Enzymes
    • Bacteriocines
  19. What are the five body systems where bacteria commonly enter
    • Respiratory Tract
    • Digestive Tract
    • Skin
    • Eyes
    • Gastrourinary tract
  20. What do bacteria need to to once they gain entry to survive
    Resist human defense mechanisms
  21. Would a bacteria want to prevent or promote phagoctyosis inside a host?
    It depends on the bacteria!  The lifestyle of different bacteria varies, therefore both can be beneficial under different situations
  22. What is purpose of modulating the surface of host cells (3)
    • The avoid recognition
    • Inhibit phagocytosis
    • Secretion of Toxins
  23. What type of cells to bacteria adhere too for invasion
    After interactions with mucous membranes, they invade into submucosal epithelial cells
  24. What can Helicobacter alter to achieve molecular mimicry
    • LPS
    • -LPS phage variation
  25. What is a bacteria that persistently colonizes the stomach of 1/2 of the worlds population
    Helicobacter pylori
  26. How is inhibition of phagocytosis achieved
    rearrangement of the cytoskelenton of the
  27. What secretion system are injectisomes of bacteria
    Type 3 secretion system
  28. What does yersinia do once it has binds to a macrophage
    It injects Yops through an injectisome, type 3 secretion system to:

    • -Inhibits phagocytosis
    • -Apoptosis
    • -Inhibits inflammatory response
  29. What is a common way a bacteria gains entry into a cell
    By use of a vacuole
  30. Name virulence factors
    • Siderophore
    • Flaggelum
    • Production of entertoxin
    • Type 3 secretion system (injectisome)
  31. Which bacterial cell wall has more layers, positive of negative?
    Gram Negative Cell Wall
  32. Describe the Gram positive cell wall
    • -Plasma membrane with membrane proteins
    • -Cell wall made out of peptidoglycan
    • -Lipoteichoic acid and teichoic acid extending   through the cell wall
    • -An S layer on the outside of the cell wall
  33. Describe the peptidoglycan structure
    • -polysaccharide chains with alternating Nam NAG
    • -Peptide-cross links between NAM in adjacent chains
  34. What is the function of peptidoglycan
    • Provide stability against osmotic imbalance
    • Permeable barrier
  35. What can prohibit the synthesis of peptidoglycan
  36. Describe the Gram negative cell wall
    • -Cytoplasmic membrane
    • -Peptidoglycan
    • -Outer membrane consisting of Lippolysaccharide (LPS)
  37. What does PAMP stand for
    Pathogen Associate Molecular Pattern
  38. What is a TLR
    • -Toll Like Receptor
    • -Type 1 transmembrane glycoprotein that localize to either plasma membrane or endosomal membrane. 
    • -Bind to PAMP
    • -Following binding they form heterodimers or homodimers and recruit signalling molecules
  39. What is a NLR
    • -Nucleotide-binding domain, Leucine rich repeat containing receptors
    • -Sensors of intracellular PAMPS
    • NOD - Like receptor
    • -Recognize bacterial peptidoglycan and actives NF-kB
  40. What do peptidoglycans produced from bacteria bind to on host cells? What does this do
    • TLR-2 or Nod-2
    • This causes for the production of NF-kB which leads to production of pro-inflammatory cytokines
  41. What Class of bacteria does NOD-1 detect
    Identifies different tetrapeptides/tripeptides products of Gram Negative bacteria
  42. What class of bacteria does NOD-2 ense
    Muramyl dipeptide, a component of bacterial peptidoglycan common to gram positive AND gram negative bacteria
  43. Describe the activation of NLRs
    Also, what does NLR stand for!
    Nod like receptor

    • -Peptidoglycan binds to ligand recognition domain of NOD2
    • -LPS binds to ligand recognition domain of NOD1
    • -Nf-kB activation in both cases
    • -secretion of pro-inflammatory cytokines
    • -immune response
  44. Name a bacterial countermeasure to NLR-mediated response of host against bacteria
    • Acetyl group is eliminated in peptidoglycan group
    • -Listeria monocytogenes
  45. What do mutations in NLR cause
    • Disease
    • -Crohns disease with mutation of Nod2
  46. Which TLR detects LPS
  47. What is the essential region of LPS, and what does it interact with
    Lipid A interacts with TLR4
  48. What can bacteria to do avoid recognition by TLR 4
    Modify the lipid A region of LPS to avoid interaction with TLR 4
  49. What is defensin
    Antimicrobial peptides produced by host that kill bacteria by making pores
  50. What are some mechanisms in which bacteria can resist antimicrobial peptides.  Give an example of an antimicrobial peptide.
    An example is defensin

    • -Some species modify their LPS decreasing affinity for cationic peptides
    • -Some species modify teichoic acid on cell wall which decrease negative charge of cell wall, diminishing attractivity of defensins
  51. What are some mechanisms of humoral immunity
    • Opsonization
    • Ingestion by macrophage and digestion inside lysosomes
  52. What is a countermeasure bacteria have to humoral immunity
    -LPS limits access of membrane attack complex (MAC) to the organism surface
  53. Define molecular mimicry
    • Strategy some microbial pathogens use to evade immune recognition by
    • decorating themselves with glycans similar to those of their hosts
  54. Name a bacteria that uses molecular mimicry
    Campylobacter jejuni
  55. What is the first step in the establishment of bacteria disease
  56. Why is adherence important for extracellular bacteria
    Adherence allows bacteria to resist the mechanical clearing mechanisms of the host
  57. What is adherence important for intracellular bacteria
    It is a prerequisite for uptake (invasion)
  58. What is a bacterial component that mediates interaction between bacterium and host cell surface
  59. What are Adhesins
    Bacterial components that mediate interaction between the bacterium and the host cell surface
  60. Do bacteria have only one adhesin?
    No, most bacteria typically contain more than one adhesin
  61. What are some ahesins
    • Bundle-forming pilus (BFP)
    • Flagella
    • Pili (Fimbrae)
  62. What are two bacterial pili found in gram-negative bacteria
    Type 1 pili and Type 4 pili
  63. What are two bacterial pili found in Gram-positive bacteria
    • Fibrils
    • Pili
  64. How many pili proteins are there in a.)Type 1 pili b.) Type 4 pili c.) Fibrils D.)Pili
    • 4-5
    • more than 2
    • 2
    • 2-3
  65. What part of the pilus determines the host specificity
    The tip
  66. What are the four main parts of the P pili
    • PapG adhesin
    • PapeE subunits
    • PapA rod
    • PapH Pilus Anchor
  67. Describe the assembly of a P-Pilus in a gram negative bacteria
    • -Fiber subunits enter the bacterial periplasm
    • -In the absence of a chaperone, subunits misfold
    • -The chaperone (Pap D) forms a soluble complex with each subunit
    • -Chaperone folds and stabilizes the subunits
    • -Chaperone moves subunits to pore-forming outer membrane usher (Pap C)
  68. What is the chaperone of P Pilus in gram negative bacteria
  69. What is the pore-forming outer membrane usher in P Pilus in Gram negative bacteria
    Pap C
  70. What is a large difference in Pili from gram positive and gram negative bacteria
    They are different at the molecular level, gram positive bacteria are connected by covalent linkages of the subunits.
  71. Where does Yersinia grow in an infected host
    Lymphoid tissue outside cells
  72. What are four important molecules at the Yersinia surface, what do they do
    • LPS
    • Injectisomes: inject Yop
    • YadA: Intereacts with integrins through components of the extracellular matrix
    • Invasin: Interacts directly with integrins
  73. What are YadA and Invasin found on together?  What does it mean when it says they are complementary?  Is there a difference?
    • YadA and Invasin are both found on Yersinia surface
    • They can both act as adhesins
    • Invasin is required for internalization
  74. What does invasin interact with for invasion.  What happens?
    Invasion interacts with integrins which leads to cytoskelenton rearrangements
  75. What are the main adhesins of Listeria, and the receptors of the adhesins
    • Internalin A - E-Cadherin
    • Internalin B - Met
  76. What does entry of Listeria into mammalian cells require
    Actin polymerization and membrane remodelling
  77. What is Internalin A
    Where is it found
    • It is a covalently linked bacterial cell-wall protein that binds the host epithelial-cell protein E-Cadherin. 
    • it s an adhesin of Listeria
  78. Describe host specificity of lysteria adhesin Internalin A
    A single change in amino-acid in E-Cadherin at position 16, the host receptor, prevents binding.
  79. Does does enteropathogenic E. Coli induce on the host cell surface
    The formation of a pedestal
  80. Describe the formation of a pedestal of pathogenic e. coli
    • -Bacterium latches onto surface of intestinal cell using tether like pili that adhere to surface of cell
    • -The bacterium injects receptor proteins into intestinal cell using EspA. 
    • -The injected proteins bind to the inside of the membrane, locking the bacteria and cell together
    • -Intestinal cell forms pedestal because of build up of actin filaments pushing membrane up
  81. Why do bacteria secrete toxins (5)
    • Facilitate spread through tissues
    • Damage cell membranes
    • Immunomodulatory
    • Inhibit protein synthesis
    • inhibit release of neurotransmitters
  82. Why do bacteria need to secrete or translocate proteins? (5)
    • -Adhesins need to be exposed at the surface
    • -Bacteria need enzymes in the periplasm to make peptidoglycan
    • -Bacteria may secrete or translocate proteins that mediate antibiotic resistance
    • -Bacteria translocate proteins to sense the environment
    • -Bacteria have channels to transport ions and other substances
  83. Why to bacteria need enzymes in the periplasm
    To make peptidoglycans
  84. Why do bacteria have channels
    To transport ions and other substances
  85. Why do bacteria translocate proteins
    To sense the environment
  86. Where are adhesins exposed in gram negative bacteria? Gram positive?
    • Outer membrane
    • Peptidoglycan
  87. Describe type 3 secretion
    A protein transport mechanism utilized by many Gram-negative bacteria to deliver proteins (effectors) into eukaryotic host cells using injectisomes
  88. What is the function of the type three secretion system in Salmonella? Yersinia? Shigella? Enteropathogenic E. Coli?
    • Uptake and inflammation
    • No phagocytosis and No inflammation
    • Pedestal formation and colonization
  89. What are type three secretion effectors?
    Eukaryotic - like bacterial proteins that interfere with a wide range of cellular processes
  90. What can trigger yop secretion in vitro
    Calcium chelation
  91. What is the virulence plasmid that secretes Yop
    pYV plasmid
  92. How does the type 3 secretion system work in Yersinia
    • Prevent phagocytosis by adding cytochalasin D
    • Infect Cells
    • Lyze and assay cAMP
  93. What does Yop translocation require for injection to occur
    Tight contact between the bacteria and the host cells, mediated by Invasin and YadA adhesins
  94. What are injectisomes related too
  95. What are some factors of type three chaperones
    • Anti-aggregation
    • Anti-folding
  96. What two groups do the type three secretion substrates belong too, and what do they do
    • Translocators: Allow effectors to cross the host cell membrane
    • Effectors: Toxins acting in the cytosol of eukaryotic cells
  97. What are Type three signal substrates secreted via
    Non-cleavable N-terminal signal
  98. What are the functions of the different Yop of Yersinia (5)
    • Yop H: protein tyrosin phosphatase
    • Yop E: GRPase activating protein
    • Top O: Serine/threonine kinase that binds to Rho GTPases
    • YopP: an acetylace that inhibits NF-kB signalling
    • YopM: goes to the nucleous
  99. What are the yersinia effectors that inhibit the cytoskelenton dynamic and prevent phagocytosis
    Yop E, Yop T, Yop H and Yop O
  100. Which yersinia effectors promotes apoptosis
    Yop P and Yop J
  101. define serovar
    Serotype or serovar refers to distinct variations within a subspecies of bacteria or viruses
  102. What do the typhoid serovar of salmonella targer? Non-Typhoid?
    • Human restircted
    • Broad-range
  103. What is a common cause of food borne infections in developed countries
    NonTyphoidal salmonella
  104. What type of cells do salmonella enter
    M cells (Microfold cells --> epithelium of peyers patches), which transport them to T and B cells.
  105. What is the main adhesin of Salmonella to epithelial cells
    Fim H located on the tip of type 1 pili
  106. What type of pili is used in Salmonella for adhesion
    Type 1
  107. Describe the salmonella lifestyle
    • -Presence of salmonella
    • -membrane ruffling
    • -bacteria remain inside vesicle
    • -bacteria multiply in vesicle, cell surface returns to normal
  108. What are the the two ways salmonella can adapt to intracellular life
    • Two-component system
    • Phosphorelay
  109. What does the Phop-Q system do in Salmonella
    • Regulated LPS modification leading to increase survival in the host
    • -LPS is modified by addition of positively charged molecules
    • -Induce uptake by epithelial cells
  110. How many type 3 secretion systems does salmonella use
  111. What does the first type three secretion system in salmonella do
    initiate actin cytoskelenton rearrangements, membrane ruffling and bacteria engulfment
  112. What does the second type three secretion system in salmonella do
    Interact with the host microtubule network, manipulate vesicle trafic
  113. What is the second type three secretion system in salmonella triggered by?
    Acidic vacuolar pH
  114. What does SCV stand for
    Salmonella containing vesicle
  115. What controls the intramacrophage type three secretion system of salmonella
    PhoP/PhoQ system
  116. What do salmonella effectors do
    Promote uptake and help establish Salmonella containing vessicles (SCV)
  117. What are the two salmonella effectors with antagonistic functions
    SopeE and SptP
  118. What is, and what is the function of SptP
    • SptP is an effector of salmonella.  It mediates recovery of cytoskeletal architecture by antagonizing SopE/E2 activity.
    • It targets Cdc42 and Rac1 GTPases from Rho family
  119. What is, and what is the function of SopE/E2
    • SopE is an effector of Salmonella contributing to cytoskeletal remodelling
    • It induced membrane ruffling of host cells to promote entry
  120. What is the secretion system associated with invasion, inflammation and cell death from salmonella?  What about associated with systemic infection/replication in macrophages?
    • Type three secretion system - one
    • type three secretion system - two
  121. What is the archetype of the type three secretion system
  122. What is the archetype of the type four secretion system
  123. Describe type four secretion systems
    • Membrane-associate transporter complexes used to deliver substrate molecules to a wide range of target cells
    • -involved in horizontal DNA transfer
    • -Involved in DNA uptake from extracellular mileu
    • -Toxic secretion
    • -Injection of virulence factors
  124. What type of secretion system is involved in horizontal DNA transfer
    Type four secretion system
  125. What are the four mechanisms of DNA exchange associated with the type four secretion system
    • Effector molecule translocation
    • Conjugation
    • DNA uptake
    • DNA release
  126. What is the target cell of H. Pylori
    • Human gastric epithelial cells
    • Phagocytes
  127. Describe the lifecycle of Legionella.
    • Environment
    • -biofilm communities in the environment
    • -planktonic form in environment
    • -Exposure of humans to aerosolized contaminated water can result in infection of alveolar macrophages
    • Intracellular life
    • -Internalized within macrophages
    • -once within host cells, evades delivery to lysosome
    • -prevent host cell death in infected macrophages
    • -Infected vacuole undergoes remodelling by intercepting host traffic from ER to Golgi
    • -Vacuole fuses with ER and turns into a specialized compartment
    • -Replication and leaves cell and reinfects
  128. What type of secretion system is referred to as the autotransporters
    Type 5
  129. What are the two types of autotransporters
    • Autotransporter (AT)
    • two-partner secretion (TPS)
  130. What is the protein associated with the autotransporters of Yersinia, Bordetella, Helicobacter and Shigella.  What is the function of each
    • -YadA: oligomeric coiled coil adhesion
    • -BrkA: Resistance to complement
    • BacA: Toxin
    • IcsA/VirG: Actin based motility
  131. What is the major cause of urinary tract infections
    Uropathogenic E Coli (UPEC)
  132. What type of secretion system is haemolysin
    Type 1 secretion system
  133. What is the outer membrane protein of type 1 secretion systems
  134. What is a component of multidrug resistant efflux pumps and type 1 secretion system
    ToIC, the outer membrane protein of type 1 secretion systems
  135. What is involved in the secretion of siderophores that is also present in the type 1 secretion system
    ToIC, the outer membrane protein of type 1 secretion system
  136. What is ToIC and what is it involved with?
    • ToIC is the outer membrane protein of the type one secretion system
    • -It is also a component of multi drug efflux pumps
    • -It is also involved in the secretion of siderophores
  137. What is one of the major virulence factors of bordetella pertussis
    Adenylate cyclase toxin-haemolysin (CyaA)
  138. What does Bordatella pertussis cause.  What type of bacteria is it?
    It is a gram negative pathogen causing whooping cough.
  139. What is the role of Vibrio cholerae neuraminidase (VCNA)
    Plays a significant role in the pathogenesis of cholera by removing sialic acid residues
  140. What does the type 2 secretion system do
    Assembly and secretion of toxins ??????
  141. What is the type 6 secretion system similar to
    The cell-puncturing device of bacteriophages
  142. What are the distinctive features of all type six secretion system
    • -Required set of 15 conserved genes
    • -phage-related extracellular structural components
    • -Effects are contact dependent
  143. What are exotoxins
    Soluble proteins secreted by living bacteria
  144. What type of bacteria produce exotoxins
    Both Gram positive and gram negative bacteria
  145. Are toxins specific?
    Yes, a specific toxin is generally specific to a particular bacterial species
  146. Do non-virulent strains produce toxins?
    Not usually. Usually only virulent strains product the toxin
  147. What is considered to be a novel class of toxins
    Effector proteins
  148. What is an enterotoxin
    A toxin that acts on the GIT producing food poisoning symptoms
  149. What is endotoxin
    A name that immunologists use for LPS
  150. How are toxins named?
    • -Named for host cell attacked
    • -Named for producer or disease
    • -Named for activity
  151. What are most bacterial diseases caused by?
    The production of bacterial toxins, proteins secreted by the bacteria
  152. What is the A-B toxin concept
    • The toxin is made of two elements
    • -one having enzymatic activity (A for activity)
    • -one binding at the cell surface, which leads to internalization (called B for binding)
  153. What are the three mechanisms of toxin entry into target cells
    • -Direct entry
    • -Receptor-mediated endocytosis
    • -Inject toxins (effectors) mediated by type 3, 4 or 6 secretion systems
  154. Describe direct toxin entry into target cells
    The B (binding) subunit of the A/B toxin bind to a specific receptor on the target cell and induced the formation of a pore in the membrane through which the A subunit (Activity) is transferred into the cell
  155. Describe receptor-mediated endocytosis (RME) of toxins into target cells.
    • The A and B structure toxin is internalized in the cell in a membrane-enclosed vesicle called an endosome.
    • H+ ions enter the endosome lowering the internal pH which causes the A and b subunits to seperate
  156. What is required in both direct entry and receptor mediated endocytosis of a toxin into a target cell
    A large protein molecule must insert into and cross a membrane lipid bilayer
  157. Can toxins use more than one mechanism of entry to get into a target cell
    Yes.  A few toxins are known to utilize both direct entry and receptor mediated endocytosis
  158. What are the two subcategories of receptor mediated endocytosis of toxins into a target cell?
    What is the difference
    • -short intracellular pathway
    • -Long intracellular pathway

    -Long intracellular has assembled multicomponent toxins, while short has free multicomponent toxins or single chain toxins.
  159. What is the mechanism of entry of the pertussis toxin
    Direct entry, using ADP ribosylation of regulatory proteins of the eukaryotic adenylate cyclase complex
  160. Which toxins take advantage of ADP ribosylation of target proteins
    • Pertussis toxin
    • Diptheria toxin
    • Cholera toxin

    It is also the activity of several type three secretion system effectors like Exo T from pseudomonas and some type four secretion systems like RalF from Legionella
  161. What is the effector of Legionella
  162. Which organism produces tetanus toxin, and what are its effects
    • Clostridium Tetani
    • Blocks inhibitory neuron action leading to chronic muscle contraction
  163. Which organism causes Diptheria toxin, and what are its effect
    • Corynebacterium diptheriae
    • Inhibits protein synthesis leading to epithelial cell damage
  164. What organism produces clostridial toxin, and what are its effects
    • Clostridium perfringens
    • Phospholipases activation, leading to cell death
  165. What organism produces the cholera toxin, and what are its effects?
    • Vibrio cholerae
    • Activates adenylate cyclase, elevates cAMP in cells, leading to changes in intestinal epithelial cells that cause loss of water and electrolytes
  166. What is the toxin that often causes food poisoning
    Staphylococcal enterotoxin
  167. What is the organism that produces botuilnum toxin, and what are the effects
    • Clostridum botulinum
    • Blocks release of acetylcholine leading to paralysis
  168. What are two toxins that are use receptor mediated endocytosis to enter the cell.
    • C. diphtheriae Diptheria toxin
    • aeruginosa exotoxin A
  169. Which secretion system is cholera toxin excreted by
    Type 2 secretion system
  170. What is secreted from type 2 secretion system that is secreted with cholera and eliminates sialic acid on glycolipid.
  171. What is the function of Neuraminidas when injected from a type 2 secretion system with cholera
    Eliminates sialic acid from glycolipd making it accessible for binding
  172. What to bacterial toxins do to gain entry into host cytosol
    Bacterial toxins subvert transport pathways and endoplasmic reticulum
  173. How does the cholera toxin enter the host cytosol
    • -The KDEL sequence at the carboxyl terminus of the cholera toxin A subunit binds to Erd2 in Golgi
    • -Cholera toxin is packaged in retrograde transport vesicles and delivered to ER
    • -Unfolded by protein disulfide isomerase in ER lumen
    • -Dissociated A subunit is delivered into cytosol by reverse translocation
  174. What produces shiga toxin.  What does it cause
    • Shiga toxin-producing E.Coli (STEC)
    • -watery diarrhea, bloody diarrhea and hemolytic uremic syndrome
  175. How many non toxic proteins are in anthrax.  What are they.

    • Lethal Factor (LF)
    • Edema Factor (EF)
    • -both act on cytosolic substrates

    • Protective Antigen (PA)
    • -deliver LF and EF into host cells
  176. What forms of botulism affect humans.  What types are responsible for waterfowl die offs
    • Type A and B affect humans
    • C and E waterfowl
  177. Describe the mechanism of action of botulinum toxin
    A component of synaptobrevin is cleaved, there by preventing the release of acetyl choline across synaptic cleft ->  Flaccid paralysis!
  178. Name two types of membrane disrupting toxins
    Large pores induced by PFO, an example of cholesterol-dependent cytolysins

    Small pores resulting from heptamerization of staphylococcus alpha-toxin
  179. What is heamolysin
    A pore forming toxin secreted by many different species
  180. What is a gram positive bacterium responsible for listeriosis
    LIsteria monocytogenes
  181. describe Listeria monocytogenes
    • A gram positive bacterium responsible for listeriosis.
    • -causes gastroenteritis, mother to child infections, CNS infections.
    • -Can cross intestinal, blood-brain and placental barrier
    • -Facultative intracellular pathogen and can invade and replicate in epithelial cells and macrophages
  182. What are the two types of related Listeria.  Which one is pathogenic, which one isnt?
    • Listeria monocytogenes --> pathogenic
    • Listeria Innocua --> is non-pathogenic
  183. What is the life cycle of Listeria monocytogenes
    • -Able to induce entry into target cells mainly by activity of two invasion proteins, Internalin A and Internalin B
    • -Initially trapped within phagocytic vacuole
    • -Use hamolysin and LLO (listeriolysin O) to lyse compartment
    • -once in cytoplasm, multiply and polymerize cellular actin
    • -Bacteria move inside cytosol of infected cell and invaginates membrane of neighboring cell, invading it
    • -bacteria are then found in a double membrane bound compartment in new cell
    • -lyse the membrane again with LLO
    • -Ready to start new infection cycle
  184. What is the result of interaction of Met with soluble Internalin B
    Clathrin dependent endocytosis of Met, and internalization of bacteria
  185. What is Met
    Receptors on host cell that bind pathogens/molecules
  186. What is Listeriolysin O
    It is secreted during the invasion phase and eases the entry of Listeria monocytogenes
  187. What is the acidic pH optimum of Listeriolysin O (LLO)
  188. What family does LLO (Listerolysin O) belong to
    Cholesterol dependent pore-forming cytolysins CDCs
  189. What part of the host must be avoided when Lysteria monocytogenes enters the cytosol
    How is this done
    • Nod like receptors
    • By the modification of peptidoglycan
  190. Describe the process in which listerlolysin O LLO forms pores
    • 1. Soluble monomer
    • 2. (IN LOW PH) Membrane bound monomers
    • 3. Pre-pore oligomer
    • 4.Formation of the pre-insertion Beta-sheet
    • 5. Pore oligomer
  191. What is ActA
    • It is a polarized surface protein anchored noncovalently to the Listeria monocytogenes cell wall
    • -Responsible for polymerizion of actin-enriched structures that enable listeria to move in host cell cytoplasm after lysis of phagocytic vacuole
  192. What is InIC
    It is abundantly secreted in cells infected with listeria, preventing NfkB activation, impairing cytokine expression and neutrophil recruitment. 

    Dampens innate immune response
  193. What is an essential cofactor of many enzymes
  194. Why is Iron important for living organisms
    • Essential cofactor of many enzymes
    • necessary for DNA synthesis
    • Glycolosis
    • Electron transport
    • etc
  195. Why is Iron dangerous
    It is highly insoluble at physiological pH in aerobic environments and can react with oxygen intermediates to produce free radicals
  196. Why is iron limiting in the host
    lactoferrin, transferrin, ferritin and hemoglobin bind most of the available iron
  197. Which bacteria can live without iron. How?
    Borrelia burgdorferi: the bacterium that causes lyme disease

    Substite Mn for Fe in reactions by changing genes that encode enzymes
  198. Define siderophore
    • Iron binding compound secreted
    • -small molecules that scavenge iron
  199. What as more siderophores, humans or bacteria
    Bacteria! Allowing them to steal iron from eukaryotic binding proteins
  200. What is the suffix often used to indicated that a molecule is a siderophoer
    Bactin and chelin
  201. Name a bacteria that is a siderophore
    How do hosts prevent iron loss from this
    Next how to bacteria respond?

    Secretion of the protein siderocalin to sequester Enterobacter

    Addition of two sugars to scaffold periphery blocks sequesteration by siderocalin
  202. How is iron taken up by gram positive bacteria
    What is it mediated by
    • Peptidoglycan-bound proteins
    • Mediated by sortase
  203. What are some factors contributing to antibiotic resistance in mycobacteria
    What disease does mycobacteria cause
    Mycobacterium tuberculosis

    • -Cell wall impermeability
    • -Efflux pumps
    • -Antibiotic modifying enzymes
    • -Antibiotic degrading enzymes
    • -Target-modifying enzymes
    • -mimicking drug targets
  204. What system does tuberculosis affect
    The respiratory system
  205. Where does Mycobacterium tuberculosis invade and replicate
  206. What is a good place to get iron
    In vacuoles

    • -Iron-saturated form of transferrin, holotransferring binds to the transferring receptor (TFR) on the surface of the macrophage
    • -TFR delivers iron into early endosome
  207. What is the iron saturated form of transferrin
  208. What are the six bacterial species responsible for over two thirds of all healthcare associated infections?
    ESKAPE Pathogens

    • Enteroccus faecalis (VRE)
    • Staphylococcus aureus (MRSA)
    • Klebsiella pneumoniae
    • Pseudomonas aeruginosa
    • Acinetobacter baumanni (MDRAB)
    • Enterbacter sp
  209. Describe Acinietobacter baumanni (class, oxygen use, motility, natural habitat, secretion system, quorum sensing and iron siderophores)
    • Gram negative
    • non fermentative
    • aerobic coccobacilli
    • non-motile (no flagella)
    • It is a superbug with multidrug resistance) MDRAB
    • Natural habitat not known! Aliens maybe :)
    • Type 6 secretion system
    • 3 different iron siderophores
    • 4 different molecules involved with quorum sensing
  210. How long can Acinetobacter baumannii survive desiccation
    27 days because of biofilm formation, capsule and exopolysaccharides
  211. What is often correlated with outbreaks of bacterial disease
    Natural disaster
  212. What does O-linked glycosylation do to bacteria
    It leads to loss of motility, thereby decreasing adherence and invasion of host cells
  213. Is O-linked glycosylation present in A. baumannii
    Of course.  I wouldn't write this question if it wasn't.  FML. So screwed for this test. 

    There is a homologogue in A. Baumannii as well to the oligosaccharyltransferase (OTase) and type 4 pili subunit PilE.
  214. What is required for glycosylation and capsule formation of A baumanni
    pgIC (same glycan)
  215. What are the roles of bacterial biofilms
    • Virulence
    • Defense
    • Persistence
  216. Describe Heliobacter pylori
    • -Colonizes the stomach of half the worlds population
    • -gram negative bacteria
  217. What are factors important for virulence
    • LPS
    • Flagella
    • Urease
    • Collagenease
    • Peptidoglycan
    • DNA transformation
    • Neutrophil-activating protein (NAP)
    • Adhesins
    • Phase variability
    • Molecular mimicry
    • VacA toxin
    • Cag Pathogenecity Island
    • Type 4 secretion
  218. Describe how H. Pylori survives the gastric environment of the stomach
    H.pylori has a pH neutral microenvironment around the bacteria because of the exogenous shedding of urease, converting urea to ammonia ions

    ammonia ions neutralize the gastric acid
  219. What is a multifunctional type four effected in H. Pylori
  220. What do all strains of H. Pylori that are isolated from humans enconde (hint:autotransporter secreted toxin)
  221. How does VacA, a multifunctional autotransporter secreted toxin of H. pylori, contribute to the colonization of H. Pylori of the stomach
    • -Alterations in mitochondrial membrane permeability and apoptosis
    • -Stimulation of pro-inflammatory signalling
    • -increased permeability of the plasma membrane
  222. What is the presence of lewis blood-group antigens on H. Pylori LPS associated with?
    More severe gastric diseases

    Through molecular mimicry, enable H. Pylori to evade the host immune system to persist longer
  223. Describe campylobacter spp
    • -Causes campylobacteriosis
    • -Most common cause of bacterial gastroenteritis
    • -commensal in chickens, cattle and pigs
    • -Gram negative
  224. Describe the function of the type three secretion system in Campylobacter
    Hasn't been detected!  Trick question :)
  225. What is cytolethal distending toxin
    It is present in most campylobacter strains (97%) and causes apoptosis by cellular arrest
  226. What is another term for germ free? What does it mean?
    • Gnotobiotic
    • It means that the animal has no microbes inside of it!
    • Free from detectable viruses, bacteria and other organisms
  227. Which of these sentences regarding Pertussis toxin is correct:
    • a)     
    • Uses the direct
    • entry mechanism to access to the cell

    • b)     
    • It activates
    • Adenylate cyclase

    • c)     
    • Exerts its toxic
    • effect by ADP-ribosylation

    • d)     
    • It is secreted
    • using a type IV secretion system

    • e)     
    • All the above is correct
  228. Which of these sentences regarding Cholera toxin is
    • a)     
    • It is secreted by
    • a type II secretion system

    • b)     
    • Uses
    • receptor-mediated endocytosis to enter into the host cell

    • c)     
    • Uses retrograde
    • transport to be directed to the endoplasmic reticulum

    • d)     
    • Binds to
    • E-cadherin

    • e)     
    • Exerts its toxic
    • effect by ADP-ribosylation
  229. Which of these bacterial components is a virulence
    factor but not a toxin
    • a)     
    • YopH

    • b)     
    • Botox

    • c)     
    • Internalin A

    • d)     
    • Listeriolysin O

    • e)     
    • LPS
  230. Which of the following sentences about Salmonella is correct:
    • a)           
    • Replicates in the
    • cytosol after escaping the SVC

    • b)           
    • Induces
    • phagocytosis mainly using the TTSS-2 (SPI2) secretion system

    • c)           
    • Induces
    • phagocytosis mainly using the TTSS-1 (SPI1) secretion system

    • d)           
    • Survives and
    • replicates  in the SVC mainly using the
    • TTSS-1 (SPI1) secretion      system

    • e)           
    • Avoids  phagocytosis mainly using the TTSS-1 (SPI1)
    • secretion system
  231. Which of these sentences regarding Listeriolysin O is
    • a)     
    • It is secreted by
    • the type III secretion system

    • b)     
    • It is activated
    • by low pH

    • c)     
    • It requires
    • cholesterol for activity

    • d)     
    • It is rapidly
    • degraded in the cytoplasm

    • e)     
    • Belongs to the
    • pore forming toxin family
  232. of these organisms decorate the lipidA-core mimicking
    human antigens
    • a) Helicobacter
    • pylori

    • b) Campylobacter
    • jejuni

    • c) Listeria
    • monocytogenes

    • d) Campylobacter
    • jejuni and Helicobater pylori

    • e) Campylobacter
    • jejuni and Gretzkyrinia oileriensis
  233. Gretzkyrinia oileriensis
    has a type III secretion system. A mutant in the gene GadA resulted in lack of
    injection of the effectors inside the host cell.
    • a)     
    • GadA could be a
    • translocator

    • b)     
    • GadA could be an
    • ATPase

    • c)     
    • GadA could be an
    • adhesin

    • d)     
    • a and c are
    • correct

    • e)     
    • a, b and c are
    • correct
  234. Gretzkyrinia oileriensis
    has a type III secretion system. A mutant in the gene RadA resulted in lack of
    injection of the effectors inside the host cell. However, secretion is normal
    in vitro upon calcium chelation:
    • a)     
    • RadA could be a
    • translocator

    • b)     
    • RadA could be an
    • ATPase

    • c)     
    • RadA could be an
    • adhesin

    • d)     
    • a and c are
    • correct

    • e)     
    • a, b and c are
    • correct.
  235. Gretzkyrinia
    oileriensis has a type III
    secretion system. A mutant in the gene OadA resulted in lack of injection of
    the effectors inside the host cell. Secretion is also abolished  in vitro upon calcium chelation
    • a)     
    • OadA could be a
    • translocator

    • b)     
    • OadA could be an
    • ATPase

    • c)     
    • OadA could be an
    • adhesin

    • d)     
    • a and c are
    • correct

    a, b and c are correct
  236. Which of these proteins is not a Listeria virulence factor.
    • a)     
    • ActA

    • b)     
    • Listeriolysin O

    • c)     
    • InlA

    • d)     
    • InlB

    • e)     
    • E-cadherin
  237. ) Which of these sentences is not true about Campylobacter jejuni
    • a) Possesses a short oligosaccharide instead
    • the "regular" O-antigen

    b) Secretes proteins using the flagella.

    • c) It is able to glycosylate proteins,
    • including the flagellins.

    • d) Campylobacter LOS can mimic human
    • glycolipids.

    • e) Can provoke the Guillain-Barre syndrome
    • by adhering to human glycolipids.
  238. It has been proposed that YopP is an acetylase that
    adds an acetyl group to IKK. Which of the following pathways better describes
    the events following IKK acetylation?
    • a) Acetylated IKK cannot be phosphorylated.
    • If this happens, IKK cannot phosphorylate IkB. Then IkB is not degraded,
    • preventing migration of NF-kB to the nucleus.


    • b) Acetylated IKK cannot be phosphorylated.
    • If this happens, IKK phosphorylates IkB. Then IkB is degraded, preventing
    • migration of NF-kB to the nucleus.


    • c) Acetylated IKK cannot be phosphorylated.
    • If this happens, IKK phosphorylates IkB. Then IkB is not degraded, which
    • results is increased migration of NF-kB to the nucleus.


    • d) Acetylated IKK is highly phosphorylated.
    • If this happens, IKK cannot phosphorylate IkB. Then IkB is not degraded,
    • preventing migration of NF-kB to the nucleus.


    • e) Acetylated IKK is highly phosphorylated.
    • If this happens, IKK phosphorylates IkB. Then IkB is not degraded, preventing
    • migration of NF-kB to the nucleus.
  239. 13)
    Choose the right sentence regarding siderophores:
    • a) Siderophores have lower affinity for
    • iron than eukaryotic proteins. Some siderophores can be covalently modified to
    • avoid sequestration by siderocalin.


    • b) 
    • Siderophores have lower affinity for iron than eukaryotic proteins. Some
    • siderophores can be covalently modified to avoid sequestration by haemoglobin.


    • c) Siderophores have higher affinity for
    • iron than eukaryotic proteins. Some siderophores can be covalently modified to
    • avoid sequestration by haemoglobin.


    • d) Siderophores have higher affinity for
    • iron than eukaryotic proteins. Some siderophores can be covalently modified to
    • avoid sequestration by siderocalin.


    • e) Siderophores have higher affinity for
    • iron than eukaryotic proteins. Some siderophores can be covalently modified to
    • promote sequestration by siderocalin.
  240. 14) Choose the right sentence
    regarding Legionella.
    • a) Contains a type III secretion that
    • secretes many effectors, and replicates in specialized vacuoles..

    • b) Contains a type IV secretion that
    • secretes many effectors, and replicates in specialized vacuoles

    • c) Contains a type IV secretion that
    • secretes a single effector, and replicates in specialized vacuoles.

    • d) Contains a type IV secretion that
    • secretes many effectors, and replicates in the cytosol after escaping from the
    • vacuole.

    • e) Contains a type IV secretion that
    • secretes a single effector, and replicates in the cytosol after escaping from
    • the vacuole.
  241. 15)
    Which of these groups of bacteria contain species that replicate inside
    vacuoles or vesicles:
    a) Listeria, Legionella and Mycobacteria

    b) Legionella, Salmonella and Mycobacteria

    c) Listeria, Salmonella and Legionella

    d) Salmonella, Yersinia and Mycobacteria

    e) Gretzkyrinia oileriensis, Legionella and Yersinia
  242. 16) Listeria's host specificity is dictated
    • a) Interaction between InlA and E-cadherin
    • only

    • b) Interaction between InlB and E-cadherin
    • only

    c) Interaction between InlB and Met only

    • d) Interaction between InlA and E-cadherin
    • and InlB with Met

    • b) Interaction between InlA and Met and
    • InlB with E-cadherin
  243. 17)
    Which of these virulence factors is not an adhesin.
    a) Intimin

    b) Internalin A

    c) CagA

    d) YadA

    e) pilus
  244. 18)
    Two bacterial effectors get phosphorylated by eukaryotic kinases once they are
    delivered by a type III and a type IV secretion system. These are:
    a) Tir and CagA

    b) YopE and Tir

    c) YopE and YopH

    d) YopH and CagA

    e) Tir and YopH
  245. 19) Which of these toxins uses retrograde transport
    before reaching the cytosol:
    a) VacA

    b) Cholera toxin

    c) Diphteria toxin

    e) Anthrax toxin

    d) Pertussis toxin
  246. 20) Which
    of these phenotypes would you expect to find for a sortase mutant in Gram
    positive bacteria
    a) Absence of pili

    b) Reduced adhesion

    • c) Reduced growth in a media containing
    • limited iron amounts.

    • d) Absence of pili and reduced growth in a
    • media containing limited iron amounts.
    • e) Absence of pili, reduced adhesion, and reduced growth in a media containing
    • limited iron amounts.
  247. What is the answer to life, the universe and everything