Lecture 20 - Respiratory Tract Infections 1 Flashcards Preview

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Flashcards in Lecture 20 - Respiratory Tract Infections 1 Deck (77):
0

What causes LRT infection?

Bacteria

1

What generally causes URT infections?

Viruses

3

Name some LRT infections

• Bronchitis
• Bronchiolitis
• Pneumonia

4

Which viruses commonly cause URT infections?

• Parainfluenza
• Influenza
• Respiratory syncytial virus (RSV)

5

Name some URT infections

• Rhinitis
• Pharyngitis
• Laryngitis
• Croup
• Tracheitis

6

Which groups is commonly affected by pneumonia?

• the young
• the elderly
50% of affected people have a defect with their immune defences

7

Which agents cause pneumonia?

Mainly Strep. pneumoniae

• H. influenzae
• Klebsiella pneumoniae
• M. tuberculosis
• Legionella

8

What are the defences in the URT?

Nose: hairs, turbinates

Epiglottis: cough reflex

Respiratory epithelium: cilia, mucous, lysozyme, lactoferrin, sIgA, mucociliary elevator

9

What are turbinates?

• Bone covered by mucous membrane
• Three on each side of nose
• Warm and humidify air
• Filters dust, pollen, microbes
• Turbulence; expose air to respiratory epithelium for longer

10

What are the defences in the alveoli?

• sIgA
• surfactant
• complement
• alveolar macrophages

11

What are the general defences in the LRT?

• Alveoli
• Blood supply
• MALT

12

Why is a good blood supply protective in the LRT?

Access to:
• neutrophils
• IgG
• complement

13

What is present in the mucous of the URT?

• Lysozyme
• Lactoferrin
• sIgA

14

What components of the innate immune system can be compromised, leading to LRT infection?

Defects in defences
• cough reflex
• phagocytes
• cilia

14

What is aspiration pneumonia ?

Breathe in the bacteria
No cough reflex when comatose
Such as in heavy drinking

16

What is aspiration pneumonia?
When does it happen?

Breathe in contents of URT
• Coma: no cough reflex
• Heavy drinkning

17

Where are most bacteria found in the respiratory tract?

Most to least:
• Saliva
• Gingival scrapings
• Tooth surfaces
• Nose washings

18

Describe the microbiota of the lower respiratory tract

Sterile

18

Which organisms are commonly found in the upper respiratory tract?

G+ cocci
(Streptococci)

19

What are the symptoms of pneumonia?

• Fever
• Cough
• Rapid respiration
• Chest pain
• Cyanosis
• Chest sounds
• Shortness of breath

21

What happens to the chest x ray in pneumonia

May be abnormal
• Lobar: indicates Strep. pneumoniae infection
• Non-lobar: indicates Infleunza infection

21

What do the X rays look like?

Normal: clear

Lobar pneumonia: upper lobe cloudy due to pus. S. pneumoniae

Non-lobar: scatter infiltrate throughout the lungs. Influenza virus

22

Describe the onset of pneumonia

Can be either acute or chronic
(Depends on the cause)

24

Where can pneumonia be acquired?

What is the difference?

• Community
• Hospital

Different organisms and modes of spread

25

How do the microbes get in?

• Inhalation
• Aspiration of URT contents in coma
• Spread along mucous membrane surface
• From blood

25

How is pneumonia diagnosed in a laboratory

1. Specimen collected
2. Microscopy
3. Culture
4. Antigen detection assay using PCR
5. Antibody

26

How do we diagnose pneumoniae?

Clinical: history, examination, predisposing factors

Radiological: chest x ray

Lab

27

What do we look for in the specimen?

Pus cells
Bacteria

Not looking for epithelial cells --> indicates URT

28

What sort of sputum is collected

Sputum

Blood
Serum --> looking for antibodies

29

Why is S. pneumoniae important?

Most common cause of death in <5s world wide

31

Where does S. pneumoniae colonise?

Nasopharynx

32

What is the reservoir of S. pneumoniae?

Humans

33

Does S. pneumoniae normally cause disease

No
Can be part of normal flora

34

When are the generalised outcomes of S. pneumoniae infection

Asymptomatic colonisation

Disease:
• non-invasive
• invasive

35

When does S. pneumoniae cause disease?

When it gains access to normally sterile sites

36

Do children or adults more commonly carry S. pneumoniae?

Children → 60%

37

What is invasive disease of S. pneumoniae?

Spread in blood to sites:

• Septicaemia
• Endocarditis
• Septic arthritis
• Peritonitis
• Meningitis

38

What is non-invasive disease by S. pneuomniae?

Local disease
Spread from nasopharynx to sterile sites

• Conjunctivitis
• Otitis media (middle ear infection)
• Sinusitis
• Pneumonia

39

How many serotyped of S. pneumoniae are there?
How is this bacterium typed?

What does this mean?

91

By its capsule

This means someone can be infected multiple times

40

What is the morphology of S. pneumoniae?

Gram + coccus

Diplococci: in pairs

41

What does naturally transform able mean?

Readily pick up DNA from the environment
→ resistance genes

42

What are the features of S. pneumoniae?

Catalase negative

Facultative anaerobe

43

How do we differentiate S. pneumoniae from other alpha haemolytic streptococci?

S. pneumoniae is susceptible to Optochin

44

Which medium do we grow S. pneumoniae on?

Describe the colonies

Horse blood agar

Alpha haemolysis: Greening colonies

45

Does S. pneumonia have a capsule?

The virulent ones do have a capsule

Unencapsulated S. pneumoniae can't cause disease

46

Why are the colonies of S. pneumoniae wet and shiny?

What is this called?

Due to the capsule

Mucoid colonies

47

What are the different serotypes of S. pneumoniae?

The capsular polysaccharide antigens

47

What is the role of the capsule

Masks underlying structures
Blocks complement binding

48

How do we classify S. pneumoniae?

Serotyping

50

What is the major virulence determinant of S. pneumoniae?

The capsule

50

What does pyogenic mean?

Pus forming
An extracellular bacterium that evades phagocyte action

52

What does pyogenic mean?

Pus forming
Induces phagocytes but avoids their action

53

Give an overview of the Pathogenesis of S. pneumoniae

Colonisation
Penetration
Replication
Evasion of immune system
Damage
Recovery / immunity

53

How does the bacterium colonise?

Cell wall adhesins
Attach to nasopharyngeal and lung mucosa (pneumocytes)

54

Are capsular antigens cross reactive?

No

55

How does the bacterium colonise?

Cell wall adhesins (loads of them)
Attach to nasopharyngeal and lung mucosa (pneumocytes)

57

What are NETS?

Neutrophil extracellular traps
Mainly made of DNA
Meshes extruded from neutrophils that trap microbes

58

How does S. pneumoniae evade NETS?

Releases pneumococcal DNAases that break down NETS

59

How does S. pneumoniae cause damage?

1. Hydrogen peroxide → local tissue damage

2. Pneumolysin

3. Autolysins: self lyse the bacteria → more inflammation

4. Inflammation

60

What are the stages of the inflammatory response?

1. Activation of endothelium → exudate

2. Entrance of neutrophils. Ineffective, bacteria persist

3. Neutrophils → impaired lung function, fever

4. Resolution: macrophage action

61

How do we recover?

• Complement activation → phagocytosis
• Antibodies

62

What are the complications of S. pneumoniae infection?

1. Pleural effusion: fluid in the pleural space

2. Dissemination:
• Into blood and lymphatics
• Heart
• Meningitis

63

How is complement effective against the bacterium?

CRP (c reactive protein) eventually triggers the cascade by binding to the cell wall

64

How do we detect s. pneumoniae in the lab?

Growth on HBA
• greening, alpha haemolysis
• sensitivity to optochin

Serotyping

Gram stain

Capsule stain

65

How is S. pneumoniae infection treated?

Supportive treatment:
• Bronchodilators
• Oxygen
• Analgesics

Antimicrobials:
• Cephalosporins
• Penicillins
→ however resistance

Vaccination

66

Does S. pneumoniae cause pharyngtis?

Not normally
It is part of the normal flora and is kept in check

67

What is the connection of S. pneumoniae with Australian Indigneous populations?

Very high incidence of invasive disease

68

Describe how pneumolysin causes damage to the host

Released later in growth
Cytotoxic to endothelial cells (with cholesterol)
Triggers complement

69

Describe how autolysins cause damage to the host

Induce bacterial cell death
Release cell wall components
→ Trigger complement cascade

70

Describe how inflammation leads to host tissue damage

Inflammation sparked by pneumolysin and CRP binding to dying cells

Big inflammatory response

71

Describe how inflammation leads to host tissue damage

Inflammation sparked by pneumolysin and CRP binding to dying cells

Big inflammatory response

72

How does pneumolysin cause damage?

When is it released?

• Puts pores in cells with cholesterol in the membrane (endothelium and alveolar cells)
• Triggers complement cascade

Produced later on

73

Which proinflamamatory compounds does S. pneumoniae produce?

• Pneumolysin
• Autolysin

74

What is pneumonia?

Acute inflammation of the lungs, typically, the alveoli

75

What things decrease the function of the defences in the respiratory tract?

• pre-existing disease (influenza)
• smoking
• drinking
• anaesthesia
• immobilisation
• immunosuppression
• extremes of age

76

How can heavy drinking put a person a risk of LRT infection?

Aspiration pneumonia
• unconscious, cough reflex isn't working

77

Is Strep. pneumoniae intra- or extracellular?

Extracellular