Streptococcus pneumoniae characteristics Flashcards

1
Q
Defence mechanisms of the upper respiratory tract
1)
2)
3)
4)
A

1) Nose hairs, tubinates
2) Epiglottis and cough reflex
3) Ciliated respiratory surface of URT, covered with mucus secreting lysozyme, lactoferrin, sIgA
4) Mucocilliary elevator

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2
Q

Defence mechanisms of the lower respiratory tract
1)
2)
3)

A

1) Alveoli contain sIgA, surfactant proteins, alveolar macrophages
2) Well-developed blood supply allows neutrophil, leukocyte, macrophage
3) Abundant MALT, systemic lymphoid tissue

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3
Q

Predisposing factors to LRT infection
1)
2)
3)

A

1) Defect in innate defences, EG: cilia
2) Can occur with influenza infection, smoking, immobility, anaesthetisation, heavy drinking
Immunosuppression, extremes of age, poor nutrition
3)No spleen

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4
Q

Difference in microbiome between URT and LRT

A

URT - Predominantly G+ cocci

LRT - Very few to no organisms

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5
Q

Pneumonia

A

Acute inflammation of the lungs

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6
Q
Symptoms of pneumonia
1)
2)
3)
4)
5)
6)
7)
A

1) Cough
2) Fever
3) Chest pain
4) Shortness of breath
5) Rapid respiration
6) Cyanosis
7) Chest sounds

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7
Q

Type of pneumonia caused by S. pneumoniae

A

Lobar pneumonia

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8
Q

Prevalence of asymptomatic S. pneumoniae infection

A

~60% children carry it

Lower proportion of adults

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9
Q

More common cause of disease in URT

A

Viral

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10
Q

More common cause of disease in LRT

A

Bacterial

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11
Q

Nose turbinates

A

Bone structures with mucus layer in nose
Warm, humidify air passing through nose
Mucus filters microbes, dust, pollen, etc
Three turbinates on each lateral nostril

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12
Q

Role of spleen in bacterial infection

A

Removed capsulated bacteria

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13
Q

Antibody types directed against capsular bacteria

A

IgG, IgM

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14
Q

Difficulty in analyzing sputum sample

A

Sputum coughed up through the mouth –>
Contaminated with normal flora in mouth
Squamous epithelial cells in sample imply contamination from mouth

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15
Q

Diseases caused by S pneumoniae
1)
2)
3)

A

1) Otitis media
2) Bacterial meningitis
3) Pneumonia

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16
Q

Type of hemolysis caused by S pneumoniae

A

Greening

Don’t completely lyse red cells

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17
Q

Anti microbial used to test for S pneumoniae

A

Optochin

18
Q
Lab diagnosis of S pneumoniae
1)
2)
3)
4)
A

1) Gram positive
2) Alpha haemolytic on horse blood agar
3) Optochin resistant
4) Capsule stain

19
Q

Chance of comorbidity with strep pneumoniae

A

50% of people with streptococcal pneumonia have an underlying condition

20
Q
Non-invasive S pneumoniae infections
1)
2)
3)
4)
A

1) Otitis media
2) Conjunctivitis
3) Sinusitis
4) Pneumonia

21
Q
Invasive S pneumoniae infections
1)
2)
3)
4)
5)
A

1) Septicaemia
2) Endocarditis
3) Septic arthritis
4) Peritonitis
5) Meningitis

22
Q

Catalase of S pneumoniae

A

Negative

23
Q

Metabolism of S pneumoniae

A

Facultative anaerobe

24
Q

Role of optochin disc in testing for S pneumoniae

A

Differentiates between pneumoniae and other alpha-haemolytic streptococci of the oral cavity that aren’t associated with LRT infection

25
Q

Appearance of S pneumoniae colonies on HBA

A

Mucoid colonies, greening haemolysis

26
Q

Number of S pneumoniae capsular antigen types

A

91

27
Q

Is S pneumoniae extra- or intracellular?

A

Extracellular

28
Q

Pyogenic

A

Phagocyte-avoiding, therefore pus-forming

29
Q

Specificity of antibodies produced against capsule

A

Very specific

Little cross-reaction

30
Q

S pneumoniae NET evasion mechanisms

A

DNAases break down neutrophil extracellular traps

31
Q

Pathogenesis of S pneumoniae

A

1) Releases hydrogen peroxide
2) Pneumolysin release
3) Autolysin release
4) Inflammation caused by PRR and complement interactions

32
Q

Reason for S pneumoniae being catalase negative

A

Releases H2O2

Would degrade this if it were catalase positive

33
Q

Pneumolysin

A

Released by S pneumoniae in later phase of growth

Triggers the complement cascade (pro-inflammatory)

Forms pores in the membranes of cells with cholesterol in cell membrane (alveolar, endothelial cells)

34
Q

Autolysins

A

Released by bacteria in stationary phase
Initiate bacterial death
Bacterial death leads to cell-wall component release that triggers complement cascade

35
Q

Major component of damage from S pneumoniae infection

A

Inflammatory response

36
Q

How does S pneumoniae induce the inflammatory response?
1)
2)

A

1) Autolyins activate complement

2) C reactive protein binds phosphoryl choline residues on damaged or dying cells –> activates complement cascade

37
Q
Steps in inflammatory response to S pneumoniae
1)
2)
3)
4)
A

1) Endothelial activation leads to fluid influx
2) Neutrophils enter, but bacteria resist phagocytosis
3) Large numbers of neutrophils enter, fever and impaired lung function because of excessive cytokine release
4) Resolution, macrophages scavenge debris

38
Q

Local complication of S pneumoniae infection

A

Pleural effusion

39
Q

Systems that resolve S pneumoniae infection

A

Complement

Antibodies

40
Q

Supportive treatment for S pneumoniae infection

A

Bronchodilators, oxygen, analgesics

41
Q

Antimicrobial agents used against S pneumoniae

A

Penicillin, cephalosporins