Bacterial and Fungal Respiratory Tract Infections Flashcards
Microbiome of respiratory tract
Upper respiratory tract
- normal flora protect tract from more pathogenic organisms e.g. viridans strep
- anaerobes, spirochetes
- NP carriage of s. pneumoniae
- neisseria species
Lungs
- not sterile!!
- oral flora, anaerobes from subclinical micro-aspiration of pharyngeal secretions
In chronic diseases, conditions of the lung may create niches for selective bacterial growth
Transmission (3 routes)
Aspiration
- of oropharyngeal secretions
Inhalation
- infectious aerosols or droplet nuclei 3-5 micrometers in diameter
Haematogenous dissemination
- bloodstream and seeding in organs
- e.g. staph aureus/epidermidis in IVDA
Classification of Infections
Upper resp tract
- sinusitis, pharyngitis, epiglottitis, laryngitis, tracheitis
- infection often confined to particular site, can manage in community
Lower respiratory tract
- bronchitis, bronchiolitis, pneumonia, pleuritis/ empyema
- may need hospitalisation with O2 supplement
Sore Throat: Common cold vs Acute pharyngitis (onset, age, aetiology, symptoms, signs, treatment, complications)
Common cold
- acute onset, all ages
- aetiology: respiratory viruses e.g. rhinovirus, coronavirus, parainfluenza virus
- symptoms: rhinorrhea, nasal congestion, sneezing, cough, sore throat
- signs: fever, erythematous pharynx
- treatment: self-limiting
- complications – occasionally secondary bacterial infections
Acute pharyngitis
- acute onset, older school children
- aetiology: group A streptococcus
- symptoms: headache, sore throat
- signs: fever, purulent erythematous swollen tonsils (exudates), tender enlarged anterior cervival nodes, scarlet fever rash
- treatment: antibiotics e.g. penicillin
- complications – rheumatic fever, acute GN
Streptococcal Pharyngitis: organism, diagnosis (2), treatment
Group A Strep (gram +ve cocci in chains)/ S. pyogenes
- more than 200 M serotypes e.g. M1. M12
- usually infect children due to crowded playing and droplet spread
Diagnosis:
- rapid POCT by Ag detection (poor sensitivity and specificity)
- THROAT SWAB for CULTURE (contraindicated in suspected epiglottitis)
Treatment;
- penicillin or 1st gen cephalosporin for 10 days
- aim to eradicate to prevent complications
Post-streptococcal diseases: age, incubation period, pathogenesis, symptoms, diagnosis
Rheumatic fever
- 6-15 yrs old
- 2-4 weeks post-streptococcal pharyngitis (org no longer present)
- Ab against M protein of strep cross-reacts with sarcolemma of heart and other tissues
- symptoms: pancarditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules
- diagnosis: Anti-streptolysin O titre (ASOT) >200 IU/ml (indicating previous exposure)
Acute glomerulonephritis
- children and adults
- 10 days post-streptococcal pharyngitis or pyoderma
- due to “nephritogenic” strains e.g. M1, M12, M25 (don’t cause rheumatic fever)
- circulating immune complexes deposit in glomerulus causing inflammation
- signs/ symptoms: nephritic syndrome (oedema, proteinuria, HT, oliguria/ AKI, haematuria etc)
- diagnosis: raised ASOT (not for pyoderma)
Lower respiratory tract infections aetiologies
Acute bronchitis
- viruses
- mycoplasma and chlamydophila pneumoniae
Bronchiolitis
- RSV
Pneumonia
- S. pneumoniae, viruses, MTB
Pneumonia: definitions, clinical manifestations (signs and symptoms), radiological changes, classifications (4)
pathological = infection of pulmonary parenchyma clinical = consolidation (radiological/PE) + microbiological proof
Clinical manifestations:
- symptoms: fever, chills, rigors, coughing, SOB, tachypnea, pleuritis
- signs: fever, tachycardia, tachypnea, dull on percussion, bronchial breathing, friction rub
- other systemic upset e.g. delirium, circulatory collapse
Radiological changes
- new lobar or multilobar infiltrates
- consolidation
Classifications:
- community acquired –> atypical and typical
- hospital acquired (nosocomial)
- others: aspiration pneumonia, pneumonia in immunocompromised host
Outcome depends on: virulence, inoculum size, host susceptibility, treatment efficacy
Community Acquired Pneumonia: typical vs atypical (aetiology, onset, signs/ symptoms (5), CXR, WBC)
30-40% unknown, 10-30% bacteria, 10-20% atypical, 5-10% viruses (50% if in season)
Typical Pneumonia
- aetiology: S. pneumoniae, H. influenzae, Moraxella catarrhalis
- abrupt onset
- high fever, rigors, productive cough with purulent sputum, pleurisy
- CXR: consolidation (unilobar, may spread to multilobar)
- WBC: raised neutrophils
Atypical Pneumonia
- aetiology: mycoplasma pneumoniae and chlamoydophila pneumoniae, legionella pneumophilia (rare)
- gradual onset (3-4 days)
- low grade fever, no rigors, non-productive cough with non-purulent sputum, pleurisy uncommon
- CXR: patchy infiltrates (multilobar)
- WBC: normal
Streptococcus pneumoniae: normal site, virulence factor, pathogenesis
Reside in human nasopharynx in 20% (carriers)
Polysaccharide capsule – 98 serotypes, virulence factor (evade phagocytosis)
- 10-15 serotypes account for >80% paediatric infections
- type specific Ab are protective (vaccine made against capsule)
Pathogenesis:
- enter bloodstream via nasopharyngeal epithelium
(NanA cleaves mucin, IgA1 protease degrades host IgA1, CbpA binds to host polymeric IgR, hyaluronate lyase degrades hyaluronan - to enter, capsule evade phagocytosis and Spa prevent C3b activation)
- evade host immunity and further multiply and invade –> spectrum of disease (otitis media, pneumonia, bacteriaemia, meningitis)
Mycoplasma pneumoniae: symptoms and manifestations, CXR
Atypical pneumonia
- malaise and headache 1-5 days before chest symptoms
- extra pulmonary manifestations
- –> myocarditis, erythema multiforme, hepatitis, myalgia/arthalgia, encephalitis, GBS
- cold agglutinin production: clumping of blood at 4 degrees (obsolete diagnostic method; now use PCR on NPA)
CXR: patchy infiltrates (not correlating with severity of illness)
Laboratory Diagnosis: samples and methods
SPUTUM
- MICROSCOPY for WBC and bacteria
- GRAM STAIN and CULTURE
- early morning sputum most purulent (especially for ZN stain and TB culture)
- –> minimise salivary contamination (rinse mouth) – reject sample if >10 squamous epithelial cells in low power field or few WBCs
- TB should be considered in all cases of productive cough
NPA
- for PCR
- atypical organisms and viruses
BLOOD
- CULTURE
- bacterial pneumonia +ve
BAL/ Bronchial aspirate
- via bronchoscopy (inject saline and draw)
- distinguish infection from contamination by quantitative culture (>10^4 org/mL)
TRACHEAL ASPIRATE
- patients intubated or with tracheostomy
- but tube rapidly develops its own flora of gram-ve rods
Serology (older method)
- rising Ab titres in acute and convalescent
- resp viruses, atypical infections
Urine
- streptococcus Ag, legionella Ag
Management of CAP: empirical drugs (mild, severe, structural lung disease, pseudomonas, aspiration, HAP), pneumococcal pneumonia, MSSA, MRSA, Mycoplasma
Antibiotics (org cultured and susceptibility testing)
Hospitalisation in severe cases
Empirical:
- mild to moderate - Augmentin IV/PO
- severe - IV Ceftriaxone + Macrolide
- structural lung disease - Tazocin
- pseudomonas suspected - + Gentamicin
- aspiration - IV Cefuroxime + metronidazole
- healthcare associated - Tazocin
Pneumococcal Pneumonia
- Penicillin (low or high dose) if MIC of penicillin <4 microgram/mL
- Ceftriaxone if MIC >8 microgram/mL (i.e. high level of resistance)
(avoid fluoroquinolone as need for TB and don’t want to increase resistance)
Other specific aetiologies:
- MSSA - Cloxacillin
- MRSA - Vancomycin, Linezolid
- Mycoplasma - Doxycycline (macrolide if susceptible)
- Q fever, psittacosis - Doxycycline
- Aspiration - BL + BLI/ Metronidazole
Prevention of CAP: vaccines available, efficacy, recommendation in HK (3)
Vaccines
PCV13: protein conjugate vaccine covering 13 serotypes
- weak Ag attached to strong Ag
- more powerful immune response, longer memory
- part of CIP
PPSV23: polysaccharide vaccine covering 23 serotypes
- polysaccharide from capsule
- weaker immune response and poorer memory
HK
- Child <2yrs old –> PCV13 at 2-4-6-12 mths
- at risk groups from 2-64 e.g. DM, asplenia –> PCV13 then PPSV23 at least 8 wks later
- elderly >65
- -> same as at risk grps if never received PPSV23
- -> PPSV23 Q5y if received before or mop-up PPV13 for high risk grps
Infection Control
Droplet precautions
- transmission within 1-2 metres
- large resp droplet 5-10 micrometres
- mask, face shield, goggles, limit transport and movement
Airborne precautions
- droplet nuclei <5 micrometres
- suspension in air over long distances and time
- single room isolation with negative pressure, N95 respirator, PPE, restrict movement, immunise susceptible (TB, avian influenza)
Healthcare associated pneumonia: aetiologies, risk factors (7)
= Hospital acquired (after 48 hrs of admission) or resident in nursing home
Aetiology:
- Gram -ve aerobes: enterobacteriaceae (Klebsiella), pseudomonas aeruginosa
- Gram -ve anaerobes: e.g. bacteroides
MORE LIKELY RESISTANT STRAINS
Risk factors:
Host
- old age
- underlying disease e.g. COPD, DM
Hospitalisation
- instrumentation: mechanical ventilators, humidifiers (colonised)
- broad spectrum antibiotics
- immobility and reduced consciousness
Nasopharyngeal aspiration
- decreased cough reflex e.g. opioids
- direct access to LRT via tracheostomy
- decreased mucociliary clearance
Aspiration Pneumonia: aetiologies, risk factors (4)
Aetiology:
- anaerobes from URT
- s. aureus
- gram -ve aerobes e.g. enterbacteriaceae, p. aeruginosa
Risk factors:
- unconscious patients, alcoholics, elderly, head injury
Pneumonia in immunocompromised host
defect in host defence
- B and T cell defects e.g. HIV and AIDS
- neutrophil defect e.g. neutropenia from chemotherapy, neutrophil dysfunction
Aetiology
- usual primary pathogens
- opportunistic infections by pneumocystis jirovecii, TB, aspergillum, candida, nocardia, strongyloidiasis
Pneumocystis jirovecii pneumonia: presentations (4), diagnosis, treatment
underlying cellular mediated immunodeficiency e.g. AIDS, SCIDS
Dyspnea, non-productive cough, fever, hypoxaemia
Diagnosis:
- BAL/ induced sputum –> toluidine blue O stain showing numerous cysts
- or calcofluor white or Grocott’s stain
- culture not available
Treatment:
- high dose co-trimoxazole or nebulised pentamidine
Opportunistic Mycoses (fungal infections) - aspergillosis manifestations (4), diagnosis, treatment
Candidiasis, aspergillosis, cryptococcosis, penicillosis, zygomyocosis
Aspergillosis
- Aspergillus fumigatus
- inhalation of spores into alveoli
- allergic aspergillosis, non-invasive local colonisation e.g. aspergilloma (prev lung disease and can’t clear; no symptoms), invasive aspergillosis (pulmonary or disseminated; immunodeficiency)
- invasion of blood vessels by mycelia (haemoptysis)
- histology of tissues with vascular invasion shows invasive disease and thrombus/infarct/bleeding (but usually biopsy is risky since patient likely have BM problems and low platelets)
Diagnosis:
- septated hyphae, dichotomous acute angle branching (but biopsy risk is high in most cases)
Treatment: will need to embolism or resect part of lung if haemoptysis or other symptoms
Chronic pulmonary sepsis: definition, diseases, risk factors
Chronic chest damage with repeated infections
Bronchiectasis, Chronic Bronchitis/ COPD, Empyema, Lung abscess
Risk factors:
- impaired mucociliary clearance e.g. cystic fibrosis. chronic inflammation, pollutants, smoking, viral infection e.g. measles
Bronchiectasis: definition, pathogenesis, causes, organisms, manifestations, complications, management (5)
= permanent damage with dilation of one or more bronchi leading to chronic suppuration with regular production of large amounts of purulent sputum
Pathogenesis:
- initial damage + inflammation –> permanent fibrosis and scarring bronchial tree –> non-elastic –> lumen dilated –> static mucous ==> bacterial growth and infection
- localised –> spread to other parts with persistent inflammation and bacterial growth
Causes:
- Congenital e.g. cystic fibrosis, Kartagener’s syndrome (ciliary dysmotility)
- Acquired e.g. post-infection (measles, pertussis), post-viral (influenza), TB (necrotising effect)
Organisms:
- typicals, atypical, MTB, aspergillus
- Multiple use of antibiotics selects for more drug resistant organisms e.g. pseudomonas
Clinical manifestations:
- recurrent cough with haemoptypsis and purulent sputum
- crackles, rhonchi, wheezes
- clubbing
- chronic hypoxaemia
- CXR: “tramtracks” or signet rings
Complications - recurrent LRTI with lung abscess, cerebral abscess (bacteria seed into blood and spread), cor pulmonale (increased resistance –> RVH –> RHF and hepatic congestion –> type II resp. failure)
Management:
- clear secretions (postural drainage)
- reverse airflow obstruction
- antibiotics for acute exacerbations
- DNAase gene therapy
- arterial embolisation
Chronic bronchitis/ COPD: definition, pathogenesis, clinical manifestations (chronic and acute exacerbation), organisms, management
= Chronic cough with production of sputum for at least 3 mths/yr in 2 consecutive years
Pathogenesis:
- abnormal inflammatory responses to noxious particles/ gases e.g. smoke, dust, pollution –> elasticity of alveoli alters with recurrent inflammation
- mixture of small airway disease and parenchymal destruction
==> airflow limitation that is not fully reversible by bronchodilators
Mild-moderate-severe-very severe (assess by FEV1)
Clinical manifestations:
- dyspnea (progressive, worse with exertion, persistent)
- chronic cough (may be unproductive)
- chronic production of sputum
- Hx of risk factors e.g. smoking, occupational dust, pollution
Acute exacerbations: - increased shortness of breath - sputum (mucopurulent, increased) - +/- cough - increased chest tightness and fatigue == usually H. influenzae, S. pneumoniae
Management of acute exacerbation
- bronchodilators, anti-inflammatory agents
- antibiotics 7-10 days
- physiotherapy (postural drainage)
Empyema: definition, causes, manifestations, diagnosis, organisms, treatment
= infection with accumulation of pus in pleural space
Causes:
- 60% secondary to pneumonia
- 20% thoracic surgery
- Others: trauma, oesophageal perforation, contiguous infected sites
May spread to other sites e.g. contiguous pericardium or remote e.g. brain
Manifestations:
- constitutive symptoms (weight loss)
- pleural effusion on PE
Lab Dx:
- pleural aspirate –> gram stain and culture, ZN stain and TB culture
Aetiologies:
- typical pneumonia organisms
- surgery and trauma: s. aureus, GN bacilli
- sub diaphragmatic source: polymicrobial, anaerobes
- TB
Treatment:
- drainage of pus (thoracocentesis)
- antibiotics (org cultured + anaerobic cover with BLBLI; 2-4 wks with good drainage)
- prolong in longstanding cases and actinomycosis
Lung abscess: risk factors (4), aetiologies, manifestations, complications, diagnosis (3), treatment
= destruction of lung parenchyma to produce one more large cavities with air fluid level (pus)
Risk factors:
- aspiration
- periodontal disease, gingivitis (larger load of bacteria in aspiration)
- underlying lung disease e.g. bronchiectasis
- immunosuppression
- blood stream infection
Aetiologies:
- oropharyngeal flora
- nosocomial e.g. s. aureus, klebsiella
- ANAEROBES (bacteroides, clostridium, fusobacterium, actinomyces)
Manifestations:
- constitutional symptoms (weight loss), anaemia for weeks
- productive cough
Complications:
- accompanying empyema, brain abscess, bronchopleural fistula
Diagnosis:
- BAL for gram stain and culture
- Empyema fluid
- Blood culture
Treatment:
- 2-4 mths therapy to prevent relapse
- anaerobic coverage e.g. metronidazole + penicillin, BLBLI
- +/- postural drainage
