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Flashcards

Microbes & Disease - Lecture 12

Afronewtzz Microbes & Disease Degree English 63 cards

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  1. 1When were Streptococcus first recorded?- 1683
    - By van Leeuwenhoek
    - Who vosualised 'animalcules' in plaque.
  2. 2What was significant about Streptococcus in 1879?- Pasteur found chains of 'granules' in women suffering puerperal fever.
    - Contributed to hospital hygiene and aseptic practices.
  3. 3What do we know in the present about Streptococcus ?> 100 recognised species
  4. 4How does Streptococcus appear under the microscope?- Coccus
    - Chains
  5. 5How does Streptococcus react to the catalase test?- Negatively.
    - Streptococcus does not drive this reaction:
    2H202 > 2H2O + O2
    - Streptococcus does not have the catalase enzyme which drives this reaction.
  6. 6What is haemolytic activity?- Lysis of RBCs
  7. 7What is Lancefield typing?- Based upon CHO composition of cell wall antigens.
  8. 8In what 3 ways can Streptococcus be classified?- Haemolytic activitiy
    - Lancefield typing
    - Genome sequencing
  9. 9What is alpha-haemolysis?- Characterised by hydrogen peroxide production by the bacterium.
    - As haemoglobin is oxidised to green haemoglobin (Hb > Met-Hb)
    - A partial zone of clearance.
  10. 10What is beta-haemolysis?- A.k.a Complete haemolysis
    - Complete lysis of RBCs.
    - Complete zone of clearance
    - Area appears lightened/ yellow & transparent.
    - Catalysed by the production of the toxin streptolysin (an exotoxin).
  11. 11What is Gamma haemolysis?- No heamolysis
    - Agar under/ around colony is unchanged.
    - No clearance zone.
  12. 12Categorise the following pyogenic Streptococcus (Type of Hameolysis & Lancefield Group): - S. pyogenes - S. agalactiae - S. dysgalalctiae- Beta haemolysis, Lancefield Group A
    - B- haemolysis, LG B
    - B- haemolysis, LG C
  13. 13Categorise the following viridian Streptococcus (Hameolysis type & Lancefield Group): - S. sanguinis - S. mitis - S. gordonii - S. salivarius- Alpha haemolysis, Lancefield Group H
    - Alpha haemolysis, LG O
    - Alpha haemolysis, LG H
    - Gamma haemolysis, LG H, K
  14. 14What is the only Pyogenic, Streptococcus species which is alpha haemolysis?- S. pneumoniae
  15. 15Name 4 pyogenic species of Streptococcus.- S. pyogenes
    - S. agalactiae
    - S. dysgalactiae
    - S. pneumoniae
  16. 16Name 4 viridan species of Streptococcus.- S. sanguinis
    - S. mitis
    - S. gordonii
    - S. salivarius
  17. 17What species of viridan Streptococcus is not haemolytic (gamma haemolytic)?S. salivarius
  18. 18Name 3 pathogenic Streptococci.- S. pyogenes
    - S. agalactiae
    - S. pneumoniae
  19. 19Name 4 viridan Streptococci.- S. sanguinis
    - S. mitis
    - S. gordonii
    - S. salivarius
  20. 20Streptococcus is a commensal bacterium of what area of the human body?- Oropharynx
    - Skin
  21. 21What superficial infections are caused by S. pyogenes?- Tonsilitis
    - Pharyngitis
    - Otitis media
    - Impetigo
    - Cellulitis (inflammation of sub-cutaneous connective tissue)
  22. 22What invasive infections are caused by S. pyogenes?- Necrotising fasciitis (inflammation of the fasciae of muscles/ other organs > destruction of tissue).
    - Streptococcal Toxic Shock Syndrome
  23. 23What post-infective complications are caused by S. pyogenes?- Rheumatic fever (acute fever marked by inflammation & pain in the joints)
    - Post- streptococcal glomerulonephritis (inflammation of the kidney)
  24. 24How many Superficial infections of S. pyogenes are recorded each year?700 million cases
  25. 25How many invasive infections of S. pyogenes are recorded each year?650,000 cases
  26. 26What % of invasive S. pyogene infections result in mortality each year?- 10 - 35 % of 650,000
  27. 27What is Pharyngitis?- 'Strep throat'
    - Localised infection
    - Sore throat
    - High temperature
    - Inflamed pharynx (with or without pus)
    - Caused by S. pyogenes
  28. 28What is cellulitis?- Skin & soft tissue infection
    - Skin becomes red, swollen, hot & painful
    - Caused by S. pyogenes
  29. 29What is Impetigo?- Caused by S. pyogenes in some cases
    - Bullous/ primary impetigo = Painless blisters on trunk
    - Non-bullous/ secondary impetigo = Sores around nose/ mouth that rupture to leave yellow-brown crust (most contagious).
    - No symptoms until several days after infection.
  30. 30What is Toxic Shock Syndrome?- Caused by Group A Strep, typically S. pyogenes.
    - Follows prior skin infections/ necrotising fasciitis.
    - High temp.
    - Low blood pressure
    - Diffuse rash
    - Possible additional symptoms: Vomiting; diarrhea; renal failure; hepatitis and confusion.
    - Mediated by Superantigen exotoxin causing a cytokine storm.
    - Causes production of 150 pro-inflammatory mediators.
  31. 31What is necrotising fasciitis?- Caused by S. pyogenes.
    - Bacteria introduced through trauma (minor or severe)
    - Rapidly progressive, invasive infection
    - Damage to fat & connective (subcutaneous) tissue.
    - Mediated by exotoxins.
    - Radical surgery recquired to prevent spread.
  32. 32What is Rheumatic Fever?- Caused by S. pyogenes.
    - Follows S. pyogenes (GA Strep.) pharyngitis 2-5 weeks later.
    - Driven by inflammation in the joints (arthritis), brain (uncontrolled movements), skin (rash) & heart (carditis/ shortness of breath & chest pain).
    - Antibodies generated by host against S. pyogenes can cross react with human tissue > autoimmunity.
  33. 33Where are Step. agalactiae found in the human body?- Form part of the Gastro-intestinal & Geniitiurinary Tract flora.
    - In 15 - 30% of the healthy female population.
  34. 34What 3 invasive diseases are S. agalactiae responsible for?- Neonatal sepsis
    - Pneumonia
    - Meningitis
  35. 35What 2 ways can S. agalactiae cause neonatal sepsis?- Bacterium crosses placenta from UT into amniotic fluid.
    - The foetus ingests invaginal fluids during birth process from colonised mother.
  36. 36How many days accounts for both the early onset & the late onset of Streptococcus agalactiae disease?- Early onset = < or equal to 6 days.
    - Late onset = 7 - 89 days
  37. 37What is the % mortality of somebody suffering from S. agalactiae diseases?5%
  38. 38What is the % mortality if the person suffering from invasive S. agalactiae diseases is elderly (65+ yrs)?15 - 25 %
  39. 39What are 4 pathogenic strategies of Streptococcus agalactiae?- Adhesion
    - Evasion of host defences
    - Tissue damage & spread
    - The conentration of systemic toxicity
  40. 40How do pathogenic Streptococcus colonise the host?- Initial weak interaction with epithelium using lipotechoic acids (LTA) and pili.
    - Stronger binding can follow using protein- CHO or protein- protein interactions.
  41. 41What fatal illnesses can S. agalactiae cause in the elderly?- Skin & soft tissue infections
    - UTIs
    - Sepsis
    - Pneumoniae
  42. 42How do Streptococcus evade the host defences? 4 key things. (determine the differences between Group A and Group B Strep.)- Disguise surface - appear as 'self' using PS capsule (GAS = Hyaluronic acid capsule, GBS = Sialic acid capsule).
    - Impair phagocytosis - GAS = Binds & blocks phagocyte receptor CR3 using Mac, GBS = Lyses phagocytes & induces apoptosis using Haemolysin CyIE.
    - Impair complement- mediated killing = Bind factor H to negatively regulate the pathway.
    - Impair neutrophil recruitment = Degrade chemotactic C5a peptide (C5a peptidase).
  43. 43How do Streptococcus damage tissue and spread? 3 key actions. (determine the differences between Group A and Group B Strep.)- Lyse host (GAS = Streptolysin O & S, GBS = CyIE)
    - Break down connective tissue (hyaluronidase > breaks down hyaluronic acid)
    - Break down ECM proteins (GAS = Streptokinase/ protease which promotes plasmin production, GBS = Collagenase/ protease which causes placental membrane rupture)
  44. 44What does Streptokinase do? (released from GA Strep.)- Protease
    - Tissue damage & spread in host
    - Breaks down ECM proteins
    - Promotes plasmin production
  45. 45What does Collagenase do? (released from GB Strep.)- Protease
    - Promotes host tissue damage & spread.
    - ECM degradation
    - Placental membrane rupture
  46. 46What toxins of Group A pathogenic Strep. (i.e. Strep. pyogenes) cause systemic toxicity?- Streptococcal pyogenic toxins / SPEs.
  47. 47What is associated with the release od pyogenic exotoxins by Group A Strep?Fever
  48. 48What protein family do Streptococcal Pyogenic exotoxins belong to?Superantigenic protein family
  49. 49Where do Streptococcal pyogenic toxins bind when released by GAS? What does this initiate?- Bind simultaneously to MHC Class II complexes on APC & TCRs.
    - Activate many cells within T cell subset, causing proinflammatory cytokine release i.e. TNF-alpha; IL-8- beta).
  50. 50Name 4 different Viridan Strep.- S. mutans
    - S. mitis
    - S. gordonii
    - S. sanguinis
  51. 51How can you remember that most of Viridan Strep. are alpha- heamolytic?- Virids = Green
    - Green zones associated with alpha-haemolytic.
  52. 52Where are virdian Streptococci found in the human body? What is their function in healthy individuals?- Members of resident oral microflora.
    - Colonisation resistance > Protects us from colonisation of other pathogens.
    - They are however, opportunistic.
  53. 53What disorder can be caused by viridan S. mutans?- Dental caries
    - Affects 60 - 90% of school children & most adults.
  54. 54What systemic diseases can be caused by viridan Strep?- Atherosclerosis
    - Infective endocarditis
  55. 55What is Bacteraemia? Why is this common in a lot of viridan Strep?- Entry of bacteria into bloodstream
    - First step for most systemic diseases of oral origin > and these bacteria are members of resident oral microflora.
  56. 56What is root scaling?The removal of bacteria- impregnated later from the surface of a tooth root to prevent bacteraemia.
  57. 57How can bacteraemia by viridan Strep. be prevented?- Chewing
    - Flossing
    - Tooth brushing
  58. 58What is infective endocarditis?- Infection of lining of the heart chambers (endocardium) > usually involves heart valves.
  59. 59How many cases of Infective Endocarditis are there normally per 100,00 individuals?2 - 6
  60. 60What % of Infective Endocarditis cases result in death?Up to 30%
  61. 61Describe how damaged heart valves are normally resolves with platelets?- Damaged endothelium
    - Platelets in the blood roles over damaged endothelial and can easily adhere.
    - Firm adhesion
    - Platelets change morphology > pseudopodia with filaments.
    - Aggregation of platelets creates a platelet plug over area of damage.
  62. 62Why do viridan Strep such as S. gordonii increase your risk of thrombosis?- First, catch adhesin, Hsa, on S. gondii, slows platelets in the blood.
    - Using PadA, S. gondii then firmly adhere to & activate platelet.
    - Aggregation - S. gondii can bind to other paltelets/ bacteria, host cells and cause thrombus in the heart valve.
  63. 63What is a Parallel Perfusion Chamber?- Used to investigate thrombus formation.
    - Glass slide > Bacteria lie on the slide > Platelets adhere to bacteria as whole blood is passed over.
    - All of this is viewed under a microscope.

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Streptococcus bacteria
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