Session 9

Question 1

# Define the term pneumonia distinguish between acute lobar pneumonia & broncho 
pneumonia LO

1. What is pneumonia
2. Presentation
3. What is pneumonitis?
4. Lobar Pneumonia
5. What is bronchopneumonia

Answer 1

1. Infection -> inflammation of the lung parenchyma
2. • malaise, fever
     - cough productive of sputum (rusty, blood stained)
     - pleuritic chest pain
     - breathless
3. Inflammation due to non-infective causes, such as physical or chemical damage

4.

5. Diffuse and patchy pneumonia

Question 2

Outline the distribution and composition of the normal flora of the respiratory tract LO

1. What is the common Flora in the upper respiratory tract
2. What is the less common flora in the upper respiratory tract
3. Other flora that could be present
4. What are the defences of the Respiratory tract (3)

Answer 2

1. Viridans streptococci
   Neisseria spp
   Candida sp
2. Streptococcus pneumoniae
   Streptococcus pyogenes
   Haemophillus influenzae
3. Pseudomonas, Escherichia coli

Outline the natural defences of the respiratory tract against infection LO

4. • Muco-ciliary clearance: nasal hairs, ciliated columnar epithelium of the respiratory
   tract

• Cough & the sneezing reflex
• Respiratory mucosal immune system -> tonsils, secretary IgA and IgG

Question 3

List the main infectious diseases of the upper respiratory tract and state the organisms commonly causing these infections LO

1. What are common upper respiratory tract infections ?
2. What are the common causes of these upper respiratory tract infections

Describe the infectious aetiology of acute community acquired & acute hospital acquired
pneumonias LO

3. What are the 4 ways pneumonia’s can be classified?

Answer 3

1. • Rhinitis (inflammation of the nasal mucosa lining/common cold- virus or allergic rhinitis)
   – Nasal congestion – Sneezing – Nasal irritation – Postnasal drip

• Pharyngitis
• Epiglottis
• Laryngitis
• tracheitis
• Sinusitis - inflammation of lining of sinus (facial pain, blocked nose, pyrexia)
• Otitis media

2. Viruses: rhinovirus, coronavirus, influenza, /parainfluenza, respiratory syncytial virus (RSV)

Bacterial: sinusitis and otitis media –> mastoiditis, meningitis, brain abscess

3. - Community acquired pneumonia
   - Hospital acquired pneumonia
   - Aspiration pneumonia
   - Pneumonia in the immuno-compromised patient

(• By clinical setting (e.g. Community acquired, Hospitals acquired)
• By presentation (acute and chronic)
• By organism (Bacterial, Viral, fungal)
• By lung pathology (lobar pneumonia, bronchopneumonia, interstitial pneumonia))

Question 4

List the aetiological clues for the common respiratory tract pathogens; LO

1. State lower respiratory tract infections

Answer 4

1. Bronchitis ( inflammation -> mucus hypersecretion) -> CXR clear

– viruses – S. pneumoniae – H. influenzae – M. catarrhalis

Pneumonia ( infection -> inflammation of lung parenchyma) -> CXR consolidation

Bronchiolitis empyema (respiratory syncytial virus -> inflammation of bronchioles)

bronchiectasis (chronic dilation, poor mucus secretion, chronic infection, haemoptysis)

lung abscess (liquefactive necrosis)

Question 5

Community acquired Pneumonia (CAP)

1. The commonest causative organism?
2. Pneumonia may also be caused by Atypical organisms. What features? E.g.?
3. Nosocomial Pneumonia:
4. A different range of organisms is usual. Important causative organisms include ?

Answer 5

1. • Streptococcus Pneumoniae
     - Haemophilus influenzae

Moraxella catarhalis, Klebsiella pneumoniae and Staphylococcus aureus

In the community you want to keep a good REP to influence the KLEBS

2. • Lack a cell wall

• Mycoplasma pneumoniae (the commonest cause of the atypical pneumonia), Chlamydia
  pneumoniae, & Legionella pneumophila

3. An infection of the lower respiratory tract in hospitalised patients, occurring > 48 hours after admission and was not incubating at the time of admission
4. Gram negative bacteria and Staphylococcus aureus, including MRSA

Hospital are underSTAFFED that’s why they get pneumonia

Question 6

1. Aspiration is likely in which individuals?
2. Causative organisms
3. Treatment?

Answer 6

1. V -> stroke, M- Alcohol, I- parkinsons
2. oral flora & anaerobes, Mixed infection - viridans streptococci & anaerobes
3. Treat with Co-amoxiclav

Question 7

Pneumonia in the immunocompromised patient

1. Organisms, e.g?

Understand the spectrum of clinical features of acute community acquired and acute hospital acquired pneumonias and how to assess severity LO + Describe the infectious aetiology of acute community acquired and acute hospital acquired pneumonias LO

2. How do you assess the severity of pneumonia? Explain iT.
3. Give examples of viruses which can cause pneumonia

Answer 7

1. Pneumocystis jiroveci (HIV)

Aspergillus spp (chronic granulomatious disease - neutrophils can’t release radicals)

Cytomegalovirus

2. CURB 65

2 or more for hospital treatment, & patients with high scores may require ICU treatment:

C – New mental confusion

U – Urea > 7 mmol/L

R – Respiratory rate > 30 per minute

B – blood pressure (systolic BP < 90 or DBP <60 mmHg)

Age > 65 years

3. Viruses – (10%) Influenza, Parainfluenza, Respiratory Syncytial virus (RSV) Adeno virus,

• Severe viral pneumonia necrosis / haemorrhage into the lung parenchyma – picture similar to adult respiratory distress syndrome (ARDS)
• Patchy or diffuse ground glass opacity on chest X ray

4.

Question 8

Answer 8

Question 9

Answer 9

Question 10

1. Understand the principles of collection of specimens for laboratory diagnosis of pneumonias LO
2. List the common opportunistic pathogens causing pneumonias in immunosuppressed hosts LO

Answer 10

Microbiological – samples/ investigations
• Sputum / Induced sputum
• Blood culture
• Broncho Alveolar Lavage fluid (BAL)
• Nose & Throat swabs or NPAs (viruses)
• Urine (antigen test for legionella / pneumococcus)
• Serum (antibody test) acute & convalescent sera (usually collected at presentation and 10-14 days later)

2. • HIV: PCP, TB, atypical mycobacteria
   • Neutropenia: fungi e.g. Aspergillus spp
   • Bone marrow transplant: CMV
   • Splenectomy: encapsulated organisms – e.g. S. pneumoniae, H. influenzae, malaria

Question 11

Describe the microbiology of mycobacterium tuberculosis LO

1. Describe what type of pathogen TB is?
2. How can you confirm a diagnosis of TB?
3. Spread?

Answer 11

1. • obligate aerobic, acid & alcohol fast bacilli
     - Long-chain fatty (mycolic) acids, complex waxes & glycolipids in cell wall
2. • On smears (e.g. sputum smears) stained by the Ziehl-Nielsen method
     - Grow slowly on culture (on media such as the Lowenstein-Jensen Medium) taking 2-6 weeks to form colonies
3. Droplets <10 um e.g. sneezing coughing

infectious dose < 10 bacilli

not infective after 2wks of treatment

Question 12

1. Describe the structure of tubercles formed in TB

Explain what is meant by the terms primary infection, primary TB, post primary TB, extra
pulmonary TB and Miliary TB LO

2. Explain what is meant by the primary infection?
3. What is the result of most primary infections?

Answer 12

1. • necrotic core (caseous necrosis)
     - surrounded by epithelioid macrophages,
     - Langerhans giant cells, and lymphocytes

E= epitheliod cells, Ly =Lymphocytes L = multinucleated Langerhans giant cells

2. – 1st exposure to MTB
   - Deposition of TB bacilli in the alveoli -> Ghons focus
   - drain into Hilar lymph nodes
   - Primary complex = Hilar lymph nodes + Ghons focus

(complex as its become more complex!)

3. • heal with/ without calcification of the primary complex
     - Before healing, haematogenous spread (lymph - venous) of Tb bacilli
     - Tubercle bacilli to other parts of the lung as well as other organs (extra pulmonary sites)

Question 13

1. What is primary TB?
2. What is post primary TB
3. Reactivation of latent TB and occurs most upper lung lobes
4. The higher alveolar pO2 in upper zones of the lungs relative to the rest of the lung is believed to predispose to reactivation of TB bacilli at these sites. The following are some of the sequelae:

Answer 13

1. 1. • primary complex does not heal but progresses to cause active TB.

2.Cavity formation: Softening and liquefaction of the caseous material which is discharged into a bronchus results in cavity formation. Fibrous tissue forms around the periphery of such lesions but is usually unable to limit extension of the tuberculous process.
Haemorrhage resulting from extension of the of the caseous process into vessels in the cavity walls -> causes haemoptysis
Spread to involve rest of the lung - caseous and liquefied material spread the infection through the bronchial tree to other lung zones.
Pleural Effusion: Seeding of TB bacilli in the pleura, or hypersensitivity can result in a pleural effusion.
Miliary TB: Rupture of a caseous pulmonary focus into a blood vessel may result in widespread dissemination of bacilli throughout the body, resulting in miliary tuberculosis with the formation of multiple miliary (millet seed like) 0.5 – 2mm tuberculous foci in the lung and in other organs.

(The pathological changes in primary TB are similar to those seen in reactivation TB)

Question 14

Difference between active & primary

Answer 14

Question 15

Risk factors for TB

Answer 15

Answer 16

Q. How do you test if a patient is susceptible to a latent infection? (I.e. latent infection is
characterised by?)

A.- positive ͚Quantiferon͛ test (UHL)
- Positive tuberculin skin test

Q. Explain how the quantiferon test works

A. - Some MTB antigens can stimulate host production of interferon gamma
- Lymphocytes from the patient͛s blood are cultured with these antigens. If the patient has been exposed to TB before, T lymphocytes produce interferon gamma in response. Because the antigens used in the test are not present in non TB mycobacteria (atypical mycobacteria) or in the bacilli used in the BCG vaccine, the test can distinguish Latent TB from previous BCG or exposure to atypical mycobacteria

Q. Describe how you would perform the skin test

A. Tuberculin, a protein derived from mycobacteria, is injected intra-dermally. The presence of a skin reaction (induration) 48 – 72 hours later at the site indicates previous exposure to TB and is due to a type IV hypersensitivity reaction to proteins derived from Mycobacteria. In the naturally infected host, immunity and hypersensitivity usually develop simultaneously.

Q. Those infected with TB have about a 10% life time risk of developing active disease:

A. 5% develop primary TB at the time of the initial infection, while another 5% develop post primary
TB due to reactivation of latent TB after a variable period of time (up to 60 years) following the primary infection.

Question 17

1. What would you see in a CXR ?
2. Symptoms/signs of TB

Answer 17

1. Pulmonary shadowing, which may be patchy solid lesions, cavitated solid lesions, streaky fibrosis flecks of calcification.

Question 18

Describe how the diagnosis of TB is established LO
Q. Investigations:

Q. What can we do to the sputum?

Answer 18

A. • Chest X Ray - > Apex, patchy consolidation, cavitation usually develops within consolidation, healing results in fibrosis

• Sputum –3 early morning samples minimum volume 5ml (First thing in the mourning lying down sputum build up in the lung (Night secretions))
• Induced Sputum
• Bronchoscopy (patients with a dry cough)

Interferon Gamma Releasing Assays (IGRAs)
•Detection of antigen- specific IFN-gamma production

Question 19

Tb symptoms

Answer 19

Question 20

1. TB treatment

Answer 20

First line medications:

• Rifampicin (R) (6m) ->Raised transaminases & induces cytochrome P450, Orange secretions

•Isoniazid (H) (6m) -> Peripheral neuropathy (pyridoxine 10mg od), Hepatotoxicity

•Pyrazinamide (Z) (2m) -> hepatotoxicity

•Ethambutol (E) (2m) -> visual disturbance

Second line medications

•Quinolones (Moxifloxacin)

Adherence
– Directly observed therapy (DOT)
– Video observed therapy (VOT) was

Pyridoxone prevent peripheral nerve damage