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Flashcards

Microbes & Disease - Lecture 3

Afronewtzz Microbes & Disease Degree English 85 cards

Cards in this deck (85)

  1. 1What is Adherence?A mechanism mediated by special molecules or structures called adhesins.
  2. 2What is colonisation?Colonisation is the establishment of a site of microbial reproduction on or within a host.
  3. 3What types of microorganisms utilise colonisation?- Pathogens
    - Commensals
  4. 4What is the name of the bacterial factors which influence disease?Virulence factors
  5. 5What is meant by ID50 and LD50?ID50 = Infectious dose
    LD50 = Lethal dose
  6. 6Define pathogenicity.The ability of a microbe to cause disease.
  7. 7Define virulence.The degree of pathogenicity in a microorganism.
  8. 8Define virulence factors.Microbial products or structural components that contribute to virulence or pathogenicity.
  9. 9What 3 factors influence host-pathogen relationship?- Number of organisms present (ID50 and LD50).
    - Virulence of pathogen
    - Virulence factors
  10. 10What is a reservoir?A place for the microorganism to live, before and after causing infection.
  11. 11What are the 7 stages involved in infection?- Maintain a reservoir
    - Transport to host
    - Adhere/ colonise/ invade host tissue.
    - Multiply or complete life cycle on or in host.
    - Evade host defense.
    - Somtimes damage host.
    - Leave host & return to reservoir OR enter new host.
  12. 12What is chemotaxis?Movement of a motile cell or organism in response to a chemical stimulus.
  13. 13List some virulence factors which influence motility.- Chemotaxis
    - Flagella
    - Pili
  14. 14List some virulence factors which influence adherence and resistance to physical removal of microorganism.- Pili
    - Adhesins
  15. 15Give 2 examples of virulence factors which influence coordination of group behaviour between microorganisms.Biofilms
    Quorum sensing
  16. 16List some virulence factors which influence invasion of host issues and cells.- Enzymes
    - Toxins
    - Invasins
  17. 17List 7 factors which promote host colonisation and disease.- Motility
    - Adherence & resistance to removal.
    - Coordination & communication
    - Invasion of host tissues and cells
    - Scavenging of nutrients
    - Resistance/ modulation of innate immunity.
    - Resistance/ modulation of adaptive immunity.
  18. 18List 4 key facts about Neisseria meningitidis.- Gram negative
    - Diplococci
    - Human-specific
    - Respiratory coloniser/ pathogen.
    - A.k.a. 'Meningococcus' > Can infect the meninges.
  19. 19What is an opportunistic organism?An organism found in healthy individuals but can become pathogenic when possible.
  20. 20When might a microorganism become opportunistic? (3)- Immune deficiency
    - Inflammatory conditions
    - Physical damage to mucosa.
  21. 21List some examples of immune deficiency. (4)- Genetic deficiencies
    - After splenectomy
    - Children & immune deficiency state
    - Certain microbes & viruses inhibit the immune system.
  22. 22Briefly describe how an inflammatory condition might influence an opportunistic organism (6).- Viral infection
    - Cytokine production
    - Cellular production
    - Different/ more receptors
    - Commensals may bind more strongly
    - Invasion
  23. 23What 3 things might lead to physical damage to mucosa?- Dry atmospheric conditions
    - Smoking
    - Infections (i.e. viruses)
  24. 24When is meningococcal disease most common?- Children between 0 and 1 yrs.
    - Late teens (not as high incidence).
  25. 25Who are the most susceptible individuals to N. meningitidis infections?- Children <2 yrs
    - Young adults (15 - 20yrs)
    - Adults
  26. 26Why are children less than 2 years old more prone to developing infections to N. meningitidis?- Natural state of immune deficiency.
    - When babies are born, maternal antibodies slowly decrease and children begin to build up their own immunity.
    - Nm infections peak at 6 months as a result.
  27. 27Why are young adults 15 to 20 yrs more prone to developing infections to N. meningitidis?- Possible change in social behaviour
    - Pre-disposition (stress/ smoking)
  28. 28Why are adults more prone to developing infections to N. meningitidis?- Mucosal damage (viral infections)
    - Immune- deficiency (Complement/ C' deficiency)
  29. 29During what time period is N. mengingitidis most common? Why? Give 2 examples.- During winter months in UK.
    - Following certain viral infections/ influenza virus.
    - Inflammation/ immune modulation & greater spread due to coughing & sneezing.
    - Epidemics in Africa sub sahara:
    - Coincide with dry months
    - The Meningitis Belt
  30. 30What is meant by the 'Meningitis Belt' ?- The region of countries across Africa affected each year by Meningitis.
    - During the winter; rain dries up, Harmattan winds begin to blow south from the sahara across this vast region & swirling sands contribute to the susceptibility of individuals to contract this disease.
  31. 31What is localised infection?Restricted to a specific location or region within the body of the host.
  32. 32What is a systemic infection?An infection that has spread to several regions or areas in the body of the host.
  33. 33How does N. meningitis enter the body?- Acquired through inhalation of respiratory droplets.
  34. 34List the 4 stages of the infectious cycle of N. meningitidis leading to meningitis.- Enter through respiratory droplets.
    - Adhere to non-ciliated, mucosal, epithelial cells of the Upper respiratory tract.
    - Cross epithelial layer via transcytosis, phagocytosis or due to damage to the monolayer.
    - In the blood: Can survive, multiply rapidly & disseminate throughout the body & brain.
  35. 35What happens in healthy adults when N. meningitidis is inhaled through respiratory droplets?- Asymptomatic carriage - bacteria are normally eliminated before crossing the epithelial barrier.
  36. 36Why is the Human nasopharynx/ NP a sufficient example of a niche for N. epidermidis?Because microbes usually colonise host tissues that are in contact with the external environment.
  37. 37What might microorganisms encounter when inhaled into the Human Nasopharynx/ NP? (4)- Muco-ciliary activity.
    - Secretory IgA (mucosal antibodies to clear microbes).
    - Policing phagocytes.
    - Lysozyme in saliva/ tears.
  38. 38How might Neisseria. meningitidis anchor to the substrata in the human Nasopharynx/ NP? (4)- Different epithelial cells cells of NP - ciliated, non ciliated.
    - Mucus itself
    - Phagocytes
    - Via specific surface structures
  39. 39If bacteria are successful in a chosen niche, what do they become?Commensals.
  40. 40How might Neisseria. meningitidis overcome host defences? (3)- Invasion of epithelia (entry = escape)
    - Reduce complement/ phagocyte toxicity
    - Change the surface
  41. 41What 2 ways can Neisseria meningitidis alter the surface of host cells in order to overcome host defences? - Briefly explain both types.- Phase variation = On & off expression of certain genes in order to select for the best phenotype.
    - Antigenic variation = Structural variation/ modification of the gene in order to alter the structure of the surface antigen i.e. a change in DNA sequence.
  42. 42How might Neisseria meningitidis evade the effects of IgA antibodies in the Nasopharynx?Using IgA proteases (cleavage)
  43. 43What is a capsule?A hydrated polysaccharide structure protecting bacteria during airborne transmission between hosts.
  44. 44Do meningococci have a capsule during air borne tranmission?Yes
  45. 45Apart from during air borne transmission, when else is N. meningitidis capsulated?Cap+ are found in the blood/ CNS since capsule is essential for evasion of the host during systemic infection.
  46. 46Why is the capsule effective in evading the host's immune system?Because it masks outer membrane antigens of the bacteria so the host doesn't recognise it as foreign.
  47. 47How many different capsular structures do N. meningitidis have?13 variations, giving them different serogroups.
  48. 48What is significant about N. meningitidis serogroups B, C, Y and W?- All contain sialic acid
    - Results in a negative surface charge
    - Prevents antibody/ C' action (anti-opsonic)
    - Causes repulsion (anti-phagocytic)
  49. 49What is meant by anti-opsonic?Anti-opsonic means that the bacteria has the ability to prevent complement binding due to the inability of the antibody to bind to the surface of the pathogen (thus, no opsonisation).
  50. 50What is it about N. meningitidis serogroup B that allows it to escape recognition as a foreign antigen?- It mimics glycans from Neuronal Cell Adhesion Molecules/ NCAM, a.k.a. CD56.
  51. 51What 2 ways do capsulate (cap+) bacteria utilise to adhere to host cells?- Adhesins
    - Long polymeric 'pili' or fimbriae traverse the capsule.
  52. 52What 2 features of pili make them effective virulence factors of N. meningitidis?- Thousands of monomers called pilins increase the surface area for adherence.
    - Pili are subject to antigenic and phase variation.
  53. 53What does it sometimes mean when capsulated bacteria rid themselves of their capsule (cap-)?They expose a lot of their outer membrane proteins which can now function as adhesins to the host cell.
  54. 54List 4 major adhesins of N. meningitidis.- OMPs
    - Opa
    - Opc
    - Pili
  55. 55Are the adhesins of N. meningitidis subject to phase and antigenic varation?- All = phase
    - Some = antigenic
  56. 56In what 2 ways does antigenic variation alter the structure of pathogens?- Genes recombine = novel structures
    - Multiple genes = variant forms of adhesins
  57. 57What are 2 positive effects of antigenic variation in pathogens?- Leads to avoidance of antibodies
    - Changes in receptor binding
  58. 58What is host/ tissue tropism?The tissue of a host which supports growth of a bacterium.
  59. 59How does the Opa protein of Neisseria species reflect atigenic variation?- Has 4 structural variants
    - Can bind to the same receptors on host cells
    - Different Opas means different affinities
  60. 60How can phase variation have an effect on the bacteria invading the host?Switching off the ligand means NO host immune recognition, HOWEVER, also no bacterial adhesion.
  61. 61If meningococci are non-piliated and capsulate, what does this mean?They cannot adhere.
    Anti-phagocytic
    Adhesion-inhibitory
  62. 62What is meant by natural 'competence' in N. meningitidis?- They undergo phase variation (on & off) at a high frequency.
  63. 63What is meant when we have 'intra strain variants' ?Clones
  64. 64How does it work when mixtures of phenotypes of a bacteria are present in a population at any one time?One will always prevail, but revertants are always present.
  65. 65Do intra strains of a particular bacteria have different morphologies? Give an example.Yes - N. meningitidis Pili, Opa and Opc expression statuses give rise to different colony appearances.
  66. 66Describe the morphologies of the following phenotypes of N. meningitidis (cap-) on agar-grown colonies: - Opc+, Pili+ - Opc+, Pili- - Opc-Opc+, Pili+ = High-lighted & small colonies
    Opc+, Pili- = Opaque & large colonies
    Opc- = Transparent
  67. 67Describe the morphologies of the following phenotypes of N. meningitidis (cap-) on mirror image immunoblot colonies: - Opc+, Pili+ - Opc+, Pili- - Opc-- Opc+, Pili+ = Dark & small colonies
    - Opc+, Pili- = Dark & large colonies
    - Opc- = Transparent
  68. 68What virulence factor is responsible for mediating deadly inflammation during sepsis of N. meningitidis?Lipopolysaccharide/ LPS (endotoxin)
  69. 69What is an endotoxin?A toxin that is present inside a bacterial cell and is released when the cell disintegrates.
  70. 70What species mediates sialylation of LPS on N. meningitidis?Lst
  71. 71How many immunotypes of N. meningitidis are there dependent on the sialic acid addition to LPS (sialyation)?12 immunotypes - identified on a serological basis - L1 - L12
  72. 72Aside from the immunotype assigned to N. meningitidis, what other impact can the sialic acid addition to the LPS side chain have?Can impart capsule-like properties
  73. 73What are the 2 mechanisms brought about by the deposition of C3b on N. meningitidis' bacterial surface by the Alternative Complement pathway?- Lysis - 'Membrance Attack Complex'
    - Phagocytosis
  74. 74What is the main host regulator in the cleavage of C3 to C3b, and what enzyme does it regulate?- Host regulator = fH (an abundant glycoprotein in human plasma)
    - C3 convertase
  75. 75In what way does the fH host regulator protect the host from the complement attack?- fH binds to specific host polyanions, such as heparin-like glycosaminoglycans (GAGs) and protects the host from attack.
  76. 76In what way have some pathogens (i.e. N. meningitidis) evolved to evade ACP (Alternative Complement Pathway) killing?Binding fH on their surface (fH interacts with fH binding protein on the surface of the pathogen) and convincing the host's immune system that it is a healthy cell.
  77. 77What type of vaccine could you synthesise to prevent pathogens evading ACP killing?Blocking fH - fH protein (on surface of pathogen) interaction.
  78. 78What is an RNA thermosensor?- A temperature sensitive non-coding RNA molecule, found in pathogens, which regulates gene expression, so that they translate at a temp. which suits them.
  79. 79What is an RNA thermosensor's role in coordinating translation?- At low temperatures, it prevents translation.
    - At increasing temperatures, their structure melts away and liberates the ribosome binding site so that protein synthesis of effective virulence factors are permitted.
  80. 80During immune evasion, what 3 virulence factors are expressed through translation of the following genes: - Nm cssA - Nm 1st gene - Complement binding- Nm cssA = Capsule synthesis
    - Nm 1st gene = LPS modification
    - Nm fHbp gene = Complement binding
  81. 81What is a cardinal feature of inflammation?Increase in temperature
  82. 82What is the role of neuraminidase?Cleaves sialic acid
  83. 83What 3 effects does influenza have on our bodies?- Complement activation
    - Rise in core body temp. (from inflammation)
    - Elaborates Neuroamindiase (which cleaves sialic acid on the surface of N. meningitidis) capsule.
  84. 84In what way does the Influenza virus' effects stimulate the expression of certain factors of microbes in the Nasopharynx in order for immune evasion?- N. meningitidis senses local inflammation and thermal co-regulationof immune defense, and stimulates changes in the Nasopharynx during infections with other respiratory pathogens.
    - Thermoregulation by N. meningitidis also provides an advantage to bacteria entering the bloodstream; higher temp. than Nasopharynx.
  85. 85What can sometimes happen as a result of bacterial colonisation during co-infection and inflammation?Promotion of virulence of otherwise commensal microbes.

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Bacterial Colonisation & Virulence Factors
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