Respiratory Tract Infections Flashcards

1
Q

What are the sterile areas of the respiratory tract?

A
  • Sinuses
  • Middle ear
  • Lower respiratory tract (below larynx)
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2
Q

What are the frequent aetiological agents and aetiological therapy in the following URTI conditions:

  1. Common cold
  2. Pharyngitis/tonsilitis (with nasal involvement)
  3. Pharyngitis/tonsilitis (without nasal involvement)
  4. Sinusitis
  5. Epiglottis
  6. Otitis media
  7. Epiglottitis
  8. Croup (LTB)
A
  1. Common cold:
    - Rhinovirus
    - Parainfluenza virus
    - RSV
    - Enterovirus
    - Coronavirus
  2. Pharyngitis/tonsilitis (with nasal involvement):
    - more likely to be viral
    - Adenovirus
    - Enterovirus
    - Reovirus
    - Influenza
  3. Pharyngitis/tonsilitis (without nasal involvement):
    - Adenovirus
    - Enterovirus
    - Reovirus
    - Influenza
    - Group A strep
    - Group C and G strep
    - Only antimicrobials if bacterial
  4. Sinusitis:
    - Viral (common cold syndrome)
    - Secondary: H. influenzae, Strep pneumoniae
    - Only antimicrobials if bacterial and severe
  5. Epiglottis:
    - H. influenzae b
    - Always conduct diagnosis of aetiological agent 5
    - Needs antimicrobial
  6. Otitis media:
    - Pneumococci
    - H. influenzae
    - Moraxella
    - Viruses (flu, RSV)
  7. Croup (LTB):
    - Parainfluenza virus
    - Influenza A
    - RSV
    - Inhaled GCs if severe
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3
Q

What are the frequent aetiological agents for the following LRTIs?

A
  1. Acute bronchitis:
    - Usually part of viral URTI
  2. Acute exacerbation of chronic bronchitis:
    - Usually Strep. pneumoniae or H. influenzae
  3. Bronchiolitis:
    - RSV
4. Pneumonia: 
Typical (acute onset, severe): 
- Strep. pneumoniae (80%)
- H. influenzae
- Klebsiella pneumoniae 
- Moraxella catarrhalis 
Atypical (gradual onset): 
- Mycoplasma pneumoniae, - Legionella
- Chalmydophila
- Viruses (influenza, adenovirus, RSV, parainfluenza, VZV)
- Fungi (histoplasma, aspergillus, pneumocystitis jirovecii)
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4
Q

Pathogenesis of pneumonia:

A
  • Lungs are constantly exposed to microbes (especially from URT) and sterility is maintained by innate and adaptive immunity
  • Pneumonia occurs when there is a defect in host defence, microbe is highly virulent or the infective dose is large
  • The route of infection is microaspiration of URT microbiota, direct inhilation and spread to lungs from blood
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5
Q

What is the standard emperical treatment for CAP?

A
  1. PenG/amoxycillin (B-lactam)
    +
  2. Any doxycline/any macrolide e.g. erythromycin
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6
Q

How is influenza spread?

A
  • Droplet infection from coughing and sneezing

- Virus binds sialic acid-containing receptors (SA a2,6 in humans) on the respiratory tract

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7
Q

Describe the structure of influenza A?

A
  • Viral envelope: hemagglutinins (HA) and neuraminidase (NA) and M2 proteins on surface
  • Matrix proteins under envelope
  • 8 ribonucleoproteins inside that contain -ve ssRNA and RNA dependent RNA polymerase subunits
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8
Q

Describe the replication cycle of influenza A?

A
  1. Viral HA binds to a sialic acid 2,6 on the surface of respiratory epithelial cells
  2. Binding induces receptor-mediated endocytosis
  3. As endosome migrates into the cell it becomes more acidic and the HA undergoes a confirmational change so it can fuse with the endosome membrane
  4. Viral HA opens the endosome and the 8 RNPs escape the endosome and enter the nucleus
  5. The RNPs use their viral RNA polyemerase to generate +ssRNA (mRNA) and replicate their genome
  6. The viral mRNA is used for viral protein synthesis
  7. HA and NA are trafficked through the Golgi and onto the cell membrane
  8. Viral RNPs package together under the cell membrane where HA and NA are expressed
  9. The RNPs bud out of the cell acquiring an envelope and glycoproteins from the host membrane
  10. To prevent the new viruses from binding back to the dying cell- the NA cleaves the sialic acid molecules from the dying host cell surface
  11. Newly formed viruses shed into respiratory lumen and their NA is cleaved by trypase Clara in order to be infectious
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9
Q

What is antigenic drift?

A
  • The acquisition of mutations within a virus (especially in RNA viruses where polymerase has no proof reading capacity)
  • If these mutations are advantageous (e.g. are in the site where neutralising antibodies bind NA or HA) they may be selected for
  • Leads to the development of new strains within a flu subtype
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10
Q

What is antigenic shift?

A
  • The sudden appearance of a influenza A virus with new HA (and sometimes NA) within the human population
  • Results in rapid spread and mortality (pandemic) as there is no Ab immunity in the population
  • Can occur due to mixing of influenza viruses in a “mixing vessel” such as a pig- the new virus will have avian HA and NA and human internal genes
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11
Q

What factors predispose a person to developing a LRI?

A
  1. Smoking (impairs cilia and alveolar macrophages)
  2. Viral infection (impairs cilia)
  3. Cystic fibrosis
  4. Anaesthetic (impairs cilia)
  5. Genetic factors
  6. Oedema in the lungs (impairs alveolar macrophages)
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12
Q

What are the 3 types of inflammation that can occur in pneumonia and their likely pathogens?

A
  1. Acute (typical):
    - Strep. pneumoniae
    - H. influenzae
    - Klebsiella pneumoniae
    - Strep. pyogenes
    - Staph. aureus
    - Other gram -ves
  2. Chronic (atypical):
    - Mycoplasma pneumoniae
    - Chlamydophila pneumoniae
    - Legionella
  3. Granulomatous:
    - Mycoplasma tuberculosis
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13
Q

What is seen histologically in typical pneumonia?

A
  • Acute inflammatory exudate (many neutrophils)
  • Fibrin exudate
  • Vasodilation
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14
Q

What are the 2 patterns of typical pneumonia?

A
  1. Bronchopneumonia:
    - Primary spread along airways with patchy involvement of alveoli
    - Dull to percussion + bronchial breath sounds
  2. Lobar pneumonia:
    - Spread from alveolus to alveolus
    - Pale consolidations seen on CXR + dull to percussion + brochial breath sounds
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15
Q

What are the main complications of typical pneumonia?

A
  1. Hypoxaemia/respiratory failure:
    - Severe gas exchange and ventilatory defect leads to decrease in O2
    - Hyperventilation occurs to try and correct this
    - Respiratory muscles fatigue
  2. Local necrosis and ongoing inflammation:
    - Forming a mass lesion in parenchyma: abscess
    - Creating a hole: bronchopleural fistula
    - Distension and destruction of airways (bronchiectasis)
  3. Spread into pleural space
    - Empyema
  4. Spread into blood:
    - Bacteremia
    - Septic shock
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16
Q

Describe aspiration pneumonia:

A
  • Occurs when a person has inspired a foreign substance e.g. food/vomit
  • Typically occurs below the R bronchus
  • Macrophages can create giant cells to attempt to wall off foriegn bodies e.g. food
  • Typical pathogens are the same as normal pneumonia
17
Q

What is seen typically in atypical pneumonia?

A
  • Interstitial inflammation + oedema
  • Chronic inflammatory infiltrate: lymphocytes, macrophages, plasma cells
  • Caused by intracellular bacteria so no neutrophils and purulent exudate
  • Very difficult to see on CXR
  • Generally appear well
18
Q

What are the complications of atypical pneumonia?

A
  1. Progression to typical pneumonia:
    - Secondary purulent bacterial infection
  2. Acute respiratory distress syndrome:
    - Massive inflammation in lungs
    - Pulmonary capillaries become much more leaky and leads to massive pulmonary oedema
19
Q

What is typically seen with tuberculosis infection in the lung?

A
  • Granulomatous inflammation:
    1. Epithelioid macrophages
    2. Multinucleate giant cell formation from macrophages
    3. Chronic inflammatory infiltrate (Th1 cells and macrophages)
    4. Granuloma- caseous necrotic core surrounded by epitheloid macropahges and Th1 cells
20
Q

Describe the process of tuberculosis granuloma formation:

A
  1. Mycobacterium recognised by PRRs on macrophages
  2. Macrophages phagocytose mycobacterium
  3. Mycobacterium resists killing via maturation, impaired lysosomes etc.
  4. Mycobacterium replicate and proliferate within the macrophages
  5. CD4+ T helper cells bind tuberculosis antigen in the groove of MHC II on macrophages (IL-12 also secreted)
  6. CD4+ T cells activate and differentiate into Th1 cells
  7. Th1 cells secrete lots of IFNy which stimulates macrophages to become supreme killers of intracellular bacteria (phagolysosome activation, production of NO and ROS)
  8. IFNy also drives macrophages to form epitheloid macrophage cells to wall off the necrotic core + multinucleate giant cells which scattered T-cells (granuloma formation)
  9. Activated macrophages + also secrete TNFa which leads to weight loss, night sweats etc.
21
Q

What is the pattern of primary tuberculosis infection?

A
  1. Infection completely cleared:
    - Small scar in lung
  2. Latent infection:
    - Ghon focus (mid-zone peripheral opacity due to granuloma)
    - Hilar lymphadenopathy
  3. Primary progressive:
    - TB bronchopneumonia
    - Miliary TB
22
Q

Describe the pattern of secondary tuberculosis infection?

A
  • Reactivated lesions tend to be in apex of lung
    1. Secondary progressive:
  • TB bronchopneumonia: consolidation and cavitation due to caseous necrosis
  • Presents with cough, haemoptysis, night sweats, fever, weight loss, fatigue
  • Miliary spread: immune system unable to control infection and haematogenous dissemination