Lower respiratory tract infections Flashcards
1
Q
What are the common microorganisms of the respiratory tract?
A
- Viridans streptococci
- Neisseria spp
- Anaerobes candida spp
2
Q
What are the less common microorganisms of the respiratory tract?
A
- Streptococcus pneumoniae
- Streptococcus pyogenes
- Haemophilus influenzae
- Others include pseudomonas, Escherichia coli
3
Q
Why are the lungs not sterile?
A
- Normal alveolar microbiota
- Aspiration
- Blood stream spread
- Direct spread
4
Q
What are the defences of the respiratory tract?
A
- Muco-ciliary clearance mechanisms
- Nasal hairs
- Ciliated columnar epithelium of respiratory tract
- Cough and sneezing reflex
- Respiratory mucosal immune system: lymphoid follicles of pharynx and tonsils, alveolar macrophages, secretory IgA and IgG
- Alveolar microbiota
5
Q
What is the course of a typical respiratory infection inside the lungs?
A
- Alveolar macrophage fails to stop pathogen
- Cytokines to recruit more macrophages
- inflammation = increased permeability
- More WBCs/proteins (neutrophils/lymphocytes/antibodies to aid macrophages)
6
Q
What is the course of a typical respiratory infection outside the lungs?
A
- Inflammatory mediators (cytokines/chemokines) into systemic circulation
- This itself is physiological - activates bone marrow/more cardiac output/raised body temp
- Dysregulation - signs of tissue injury/organ injury
7
Q
What causes dysregulation?
A
- Pathogen
- Host factors
- Drugs
8
Q
What is the virulence of chlamydia pneumoniae?
A
- Ciliostatic factor (cilia don’t function properly)
9
Q
What is the virulence of mycoplasma pneumoniae?
A
- Shear off cilia
10
Q
What is the virulence of influenza virus?
A
- Reduces mucus velocity (up to 12 weeks post infection)
11
Q
What is the virulence of strep pneumoniae/Neisseria meningitides?
A
- Split immunoglobin (IgA)
- Immunoglobins can’t destroy pathogens
12
Q
What is the virulence of pneumococcus?
A
- Pneumococcus - capsule inhibits phagocytosis (pneumolysin)
13
Q
What is the virulence factor of mycobacterium/nocardia/legionella?
A
- Resistant to phagocytosis (intracellular survival)
14
Q
Which host factors make people more vulnerable to lower respiratory tract infections?
A
- Age >65
- Lifestyle (smoking, alcohol, drugs)
- Chronic lung diseases (bronchiectasis, cystic fibrosis)
- Aspiration
- Immunocompromised
- Metabolic (malnutrition, hypoxaemia, acidosis)
15
Q
Which drugs make a person more susceptible to lower respiratory tract infections?
A
- Antacids (PPI/H2 antagonists)
- PPI increases risk for pneumonia
- H2 antagonist causes myelosuppression
- Antipsychotics
- ACE-inhibitors
- Glucocorticoids
16
Q
What are some common upper respiratory tract infections?
A
- Rhinitis
- Pharyngitis
- Epiglottitis
- Laryngitis
- Tracheitis
- Sinusitis
- Otitis media
17
Q
Which organisms are most commonly responsible for upper respiratory tract infections?
A
- Viruses
- Rhinovirus, coronavirus, influenza/parainfluenza, RSV
- Bacterial super-infection common with sinusitis and otitis media - can lead to mastoiditis, meningitis, brain abscess
18
Q
What is acute bronchitis?
A
- Inflammation of medium sized airways
- Mainly in smokers
- Cough, fever, increased sputum production, increased shortness of breath
- Normal CXR
19
Q
What organisms cause acute bronchitis?
A
- Viruses
- S. pneumoniae
- H. influenzae
- M. catarrhalis
20
Q
How is acute bronchitis treated?
A
- Bronchodilation
- Physiotherapy
- Antibiotics
21
Q
What is chronic bronchitis?
A
- Not primarily infective
- Exacerbations have been associated with many organisms
- Role of infection remains controversial
22
Q
What are the definitions of LRTI?
A
- Community acquired pneumonia (CAP) - outside healthcare setting
- Hospital acquired pneumonia (HAP) - 48 hours post admission
- Ventilated acquired pneumonia (VAP) - 48 hours post intubation
23
Q
What is the pathology of LRTI?
A
- Acute inflammatory response
- Exudation of fibrin-rich fluid
- Neutrophil infiltration
- Macrophage infiltration
24
Q
Outline the microbiology of community acquired pneumonia?
A
- No microbiological ID made in most cases
- True prevalence difficult to establish due to use of indirect methods/mixed infections
- Typical and atypical organisms
25
What are the typical organisms that cause community acquired pneumonia?
- Strep. pneumoniae
- Haemophilus influenzae
- Moraxella catarrhalis
- RSV
- Rhinovirus
- Influenza
26
What are the atypical organisms that cause community acquired pneumonia?
- Mycoplasma (commonest)
- Legionella - contaminated water sources
- Chlamydophila pneumoniae
27
How is CAP diagnosed?
- Cough +/- sputum/ dyspnoea/ pleurisy/ fever/ tachycardia/ crackles/ bronchial breathing
- Imaging - consolidations/ infiltrates/ cavitations
28
When do you admit a patient with CAP?
- CURB-65
- Confusion
- Urea >7 mmol/l
- Resp rate >30
- BP <90 systolic <60 diastolic
- >65 years
29
What investigations should be carried out if a patient has CAP?
- FBC
- Urea and electrolytes
- CRP
- ABG
- CXR
30
Which microbiological investigations should be done in a patient with CAP?
- Sputum/induced sputum
- Blood culture
- Broncho Alveolar Lavage fluid
- Nose and throat swabs
- Urine antigen test (legionella/pneumococcus)
- Serum antibody test
31
How is a patient with mild CAP managed?
- Treat empirically
32
How is a patient with moderate CAP managed?
- Blood cultures/sputum culture
- Urinary streptococcal antigen
- Legionella
- PCR/viral screen
33
How is a patient with severe CAP managed?
- Moderate + bronchoscopic specimens
34
What are some differential diagnoses for CAP?
Heart failure + pulmonary oedema
- Pulmonary embolism
- Atelectasis
- Aspiration/chemical pneumonitis
- Drug reactions
- Lung cancer
35
How is CAP treated?
- Principles of antibiotic treatment
- Empirical regimes can differ depending on hospital/allergy status/comorbidities
- General approach 5-7 days for mild CAP
- 7-10 days for severe CAP
36
How is mild-moderate CAP treated in UHL?
- Amoxicillin
- Or doxycycline or erythromycin/clarithromycin
37
How is moderate-severe CAP treated in UHL?
- Needing hospital admission
- Co-amoxiclav and clarithromycin/doxycycline
38
What are the complications of CAP?
- Initial infection progression - empyema/ lung abscess/ bacteraemia
39
What might lead to non-resolving CAP?
- Delayed clinical response
- Closed space infections
- Bronchial obstruction e.g. tumour
- Subacute, chronic CAP (TB/fungal)
- Incorrect initial diagnosis
- All these factors delay progression of treatment
40
What is the aetiology of hospital acquired pneumonia?
- Staphylococcus aureus
- MRSA
- Enterobacteriaceae (E.coli and Klebsiella spp)
- Pseudomonas SPP
- Fungi (Candida)
41
How is hospital acquired pneumonia managed?
- Cover Staph aureus and gram negative enteric bacilli (e.g. Klebsiella) + typical/atypical pathogens - give co-amoxiclav
- If pseudomonas risk give antipseudomonal beta lactam (meropenem) or anti-pseudomonal fluoroquinolone (ciprofloxacin)
- If MRSA risk give Vancomycin/Linezolid
42
What is the first line treatment for hospital-acquired pneumonia?
- Co-amoxiclav
43
What is the second-line treatment for hospital-acquired pneumonia?
- Piperacillin/tazobactam
- Meropenem
44
What causes aspiration pneumonia?
- Aspiration of exogenous material or endogenous secretions into respiratory tract
45
Which patients are susceptible to aspiration pneumonia?
- Patients with neurological dysphagia (strokes)
- Epilepsy
- Alcoholics
- Drowning
- Nursing home residents
- Drug overdose
46
How is aspiration pneumonia treated?
- Moderate to severe is treated with co-amoxiclav
47
Which organisms can cause LRTI in patients with HIV?
- Pneumocystis jirovecci
- TB
- Atypical mycobacteria
48
Which organisms can cause LRTI in patients with neutropenia?
- Aspergillus spp
49
Which organisms can cause LRTI in patients with bone marrow transplant?
- Cytomegalovirus
50
Which organisms can cause LRTI in patients with splenectomy?
- Encapsulated organisms e.g. S. pneumoniae, H. influenzae
51
How do we prevent LRTI?
- Immunisation - flu vaccine annually, pneumococcal vaccine every 5 years
- Chemoprophylaxis - oral abx, smoking advice
