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PATH30003- Frontiers in Human Disease > Lecture 17-Bacterial infection-pneumococcal disease > Flashcards

Lecture 17-Bacterial infection-pneumococcal disease Flashcards

1
Q

how many serotypes identified so far? what are they based on? challenge for treatment

A

> 90; based on the structural difference in capsule; vaccines that cover all these different types is a challenge

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2
Q

what is pneumococcal disease? (PD)

A

bacterial infection of URT causing pneumonia, meningitis, sepsis and otitis media

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3
Q

where is PD a major burden?

A

in areas where vaccine has not been introduced e.g. sub saharan africa, india, china

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4
Q

reasons for child survival gap between ethiopia and germany?

A

infections left untreated or inadequate prevention/treatment (vaccine)

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5
Q

two types of PD?

A

non-invasive- e.g. otitis media, pneumonia

invasive e.g. meningitis, sepsis

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6
Q

correlation between disease severity and prevalence

A

as disease severity increases, prevalence decreases e.g. meningitis most severe but least prevalent compared to otitis media

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7
Q

indigenous population rates

A

high rates- perhaps genetic factors?

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8
Q

age risk for PD

A

extremes of age
<5 years
>65 yrs

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9
Q

populations at risk

A

children in developing countries, indigenous population of developed countries

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10
Q

how does chronic illness affect your risk of PD?

A

chronic illness (HIV) or the immunocompromised increases your risk

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11
Q

what is the greatest risk factor for getting PD?

A

recent acquisition of a new virulent strain (when immunocompromised or in a high risk population)–>strain disseminates and cause disease

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12
Q

what type of organism is streptococcus pneumoniae?

A

ubiquitous organism, even considered a commensal

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13
Q

nasopharyngeal colonisation

A

prerequisite for disease

  • airborne droplets enter nasopharynx, carriage
  • local spread to ear (otitis media) or sinus (sinusitis)
  • aspiration to alveoli (pneumonia)
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14
Q

what do you want to prevent in disease pathway?

A

prevent carriage to prevent disease dissemination and spread to someone else

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15
Q

colonisation during early life factors

A

first days to weeks- asymptomatic

- within 3 years, 50% people colonised, earlier in some settings

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16
Q

colonisation during adult life

A

relatively stable carriage in older children/adults

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17
Q

streptococcus pneumoniae death rate

A

11% of deaths in children under 5 years of age worlwide

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18
Q

2 main pneumococcal virulence factors

A

polysaccharide capsule

pneumolysin

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19
Q

polysaccharide capsule function

A

inhibits phagocytic clearance and reduce antibiotic exposure (defence mechanisms that enable its survival)

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20
Q

pneumolysin function

A

pore forming cytotoxin, impair respiratory burst (impair neutrophil function)

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21
Q

other pneumococcal virulence factors

A

PspC-pneumococcal surface protein C and other proteins

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22
Q

techniques of pneumococcal capsule

A

level of capsule differs during carriage and invasion
- thick- be away from immune system and protected
-thin- when invading
immune protection based on capsule-specific Ab (IgM, IgG)

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23
Q

what is the basis of current vaccine formulations ?

A

pneumococcal capsule

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24
Q

host response to pneumococcal infection

A
  • pneumococcus releases toxins to promote growth and survival, spreads into tissues
  • Ab deposited, binds to bacteria, facilitates removal through complement mediated phagocytosis
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25
Q

opsonophagocytosis

A

clearance by complement component and phagocytosis by neutrophils

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26
Q

serotype-specific immunity

A

host response to pneumococcal infection

-since colonisation is immunising (memory B cells, CD4T cells)

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27
Q

IL-17A

A

protective against colonisation; helps facilitate removal of bacteria

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28
Q

how is S.pneumoniae detected?

A

invasive disease detected from sterile site (blood, CSF);; other sites (sputum, urine)- gram stain
- capsule swelling by specific antibody-shows what serotype is causing infection

29
Q

3 types of pneumonia

A
  • community acquired acute pneumonia (CAP) e.g. strep pneumoniae, H.influenza
  • community acquired atypical pneumonia e.g. viruses (A and B), chlamydia
  • hospital acquired pneumonia e.g. pseudomonas
30
Q

what is bacterial pneumonia?

A

severe CAP- most common cuase of death from infections in developed countries (low fatality, but most common cuase)

31
Q

what does bacterial pneumonia occur in association with?

A

other causes of infection- viral infection (e.g. influenza)- co infection

32
Q

what happens in bacterial pneumonia?

A

inflammation of lungs accompanied by fluid-filled alveoli and bronchioles- reduce ability to exchange gases and respiratory failure
-described by affected region or organism causing disease e.g. lobar or broncho

33
Q

is pneumonia invasive or non-invasive?

A

non-invasive

34
Q

is meningitis invasive or non-invasive?

A

invasive

35
Q

is sepsis invasive or non-invasive?

A

invasive

36
Q

is otitis media invasive or non-invasive?

A

non-invasive

37
Q

what is the pathogenesis of pneumonia?

A
  • pneumococcus invades airspace–>interactions between bug and receptors (TLRs on alveolar macrophages)
  • response–>cytokine production (in most conditions enough to clear infection)
  • chronic doses–>infiltrates of neutrophils doesnt actually clear infection–>accumulation in air space–>overwhelmed, leakage–>invasion into bloodstream (due to increased permeability)–>severe
38
Q

histopathology of pneumonia

A
  • alveoli filled with inflammatory cells
  • thickened alveolar wall
  • congested blood vessels (RBCs)
  • infected part of lung doesnt function if not treated within time
39
Q

clinical features of pneumonia

A

onset of severe illness is abrupt (fever, cough, chest pain, chills, productive sputum, dyspnoea)

40
Q

untreated pneumonia–>

A

acute respiratory failure, septic shock, multi-organ failure

41
Q

two major signs for pneumonia in children

A

fast breathing

chest in drawing

42
Q

diagnosis of pneumonia

A

chest x-ray- determine consolidation
pleural effusion
systemic features (fever)

43
Q

what is meningitis?

A

infection of the subarachnoid space with meningeal involvement (leptomeningeal inflammation surrounding brain and spinal cord)

44
Q

bacterial causes of meningitis?

A

most common (S.pneumoniae, N.meningitidis)

45
Q

other infectious causes of meningitis?

A

viral, fungal, malaria, mycoplasma, rickettsiae

46
Q

non infectious causes of meningitis

A

malignancy, SLE, lead/mercury poisoning

47
Q

what is the pathogenesis of meningitis?

A
  • translocation across BBB- facilitated by upregulation of receptors on endothelial cells during infection
  • bacteria multiply–>engage with APCs–>produce cytokines (TNF-alpha, IL-1, IL-6)–>causes inflammation and recruitment of neutrophils–>increase BBB permeability–>intracranial pressure, oedema
48
Q

pathological features of meningitis

A

inflammatory infiltrate (lymphocytic blood vessels due to increase BBB permeability), oedema

49
Q

clinical signs and symptoms of meningitis

A
  • common- severe headache, high fever, stiff neck, nausea, vomiting
  • clearer indications- numbness, loss of feelings, light sensitivity, confusion, seizures, rash
50
Q

what is otitis media?

A

inflammation of the middle ear cavity

51
Q

clinical types of otitis media

A

many

  • acute
  • recurrent
  • OM with effusion (glue ear)
  • chronic suppurative OM
52
Q

major consequences of otitis media

A

hearing loss, developmental problems

53
Q

pathogenesis of otitis media

A

nasopharyngeal carriage (prerequisite)

  • accumulation of fluid in eustachian tube (links nasopharynx to middle ear)
  • leads to otorrhoea (fluid drainage), tympanic membrane perforation, hearing loss
54
Q

acute OM

A

follows a cold–>leading to active infection and pain

- ear drum can rupture, pus discharge, inflammation, swelling (self-limiting within 2-4 weeks)

55
Q

chronic suppurative OM

A

initial episode of AOM–> becomes persistent

- usually up to 3 months duration, can spread to brain causing meningitis, hearing loss

56
Q

first line treatment

A

antibiotics esp penicillin (as we enter resistance, need to find new drugs)

57
Q

two major types of vaccines

A 
conjugate vaccines (PCVs)
polysaccharide vaccine (PPV)
58
Q

conjugate vaccines (PCVs)

A

in infancy, up to 13 serotypes
- take polysaccharide structure from different serotypes, conjugate into protein, makes them immunogenic and long-lasting

59
Q

polysaccharide vaccine (PPV)

A

older children and adults. 23 serotypes

60
Q

probiotics

A

alternative strategy to prevent/reduce colonisation

61
Q

what do PCVs produce?

A

highly functional serotype-specific IgG- protects against IPD, less effective for mucosal disease

62
Q

what impacts efficacy of PCV?

A

geographic differences in serotype distribution

63
Q

what is serotype replacement?

A

introduce vaccine —>severe decline in serotype e.g. 7–>rise in non7 type (replacement)–>e.g. 19A increased –>therefore make vaccine for that serotype
*vaccine efficacy against IPD

64
Q

19A

A

most common serotype replacement disease in australia

65
Q

vaccine efficacy of PCV against pneumonia

A
  • non-invasive
  • correlates of protection less understood
  • immune response generated by these vaccines may not provide same protection as for invasive
66
Q

nutrition role in disease

A

undernourished children at increased risk of death

  • maternal and child nutrition important
  • zinc, vitamins A/D important (prevent respiratory infections); weakened respiratory muscles, reduce ability to clear infection
67
Q

breastfeeding role in disease

A

highly protective

  • exclusive breastfeeding until 6 months until 2 years (developed countries)
  • developing countries- low rates
68
Q

indoor air pollution role in disease

A

open stove (high risk), smoke for heating enters child’s lungs (increase susceptibility to pneumococcal infection and transmission)

PATH30003- Frontiers in Human Disease (20 decks)

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