Bacterial and Fungal Respiratory Tract Infections Flashcards

1
Q

Microbiome of respiratory tract

A

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

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2
Q

Transmission (3 routes)

A

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
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3
Q

Classification of Infections

A

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
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4
Q

Sore Throat: Common cold vs Acute pharyngitis (onset, age, aetiology, symptoms, signs, treatment, complications)

A

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
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5
Q

Streptococcal Pharyngitis: organism, diagnosis (2), treatment

A

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
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6
Q

Post-streptococcal diseases: age, incubation period, pathogenesis, symptoms, diagnosis

A

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)
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7
Q

Lower respiratory tract infections aetiologies

A

Acute bronchitis

  • viruses
  • mycoplasma and chlamydophila pneumoniae

Bronchiolitis
- RSV

Pneumonia
- S. pneumoniae, viruses, MTB

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8
Q

Pneumonia: definitions, clinical manifestations (signs and symptoms), radiological changes, classifications (4)

A
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

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9
Q

Community Acquired Pneumonia: typical vs atypical (aetiology, onset, signs/ symptoms (5), CXR, WBC)

A

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
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10
Q

Streptococcus pneumoniae: normal site, virulence factor, pathogenesis

A

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)
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11
Q

Mycoplasma pneumoniae: symptoms and manifestations, CXR

A

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)

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12
Q

Laboratory Diagnosis: samples and methods

A

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

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13
Q

Management of CAP: empirical drugs (mild, severe, structural lung disease, pseudomonas, aspiration, HAP), pneumococcal pneumonia, MSSA, MRSA, Mycoplasma

A

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
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14
Q

Prevention of CAP: vaccines available, efficacy, recommendation in HK (3)

A

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
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15
Q

Infection Control

A

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)
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16
Q

Healthcare associated pneumonia: aetiologies, risk factors (7)

A

= 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
17
Q

Aspiration Pneumonia: aetiologies, risk factors (4)

A

Aetiology:

  • anaerobes from URT
  • s. aureus
  • gram -ve aerobes e.g. enterbacteriaceae, p. aeruginosa

Risk factors:
- unconscious patients, alcoholics, elderly, head injury

18
Q

Pneumonia in immunocompromised host

A

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
19
Q

Pneumocystis jirovecii pneumonia: presentations (4), diagnosis, treatment

A

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

20
Q

Opportunistic Mycoses (fungal infections) - aspergillosis manifestations (4), diagnosis, treatment

A

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

21
Q

Chronic pulmonary sepsis: definition, diseases, risk factors

A

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

22
Q

Bronchiectasis: definition, pathogenesis, causes, organisms, manifestations, complications, management (5)

A

= 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
23
Q

Chronic bronchitis/ COPD: definition, pathogenesis, clinical manifestations (chronic and acute exacerbation), organisms, management

A

= 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)
24
Q

Empyema: definition, causes, manifestations, diagnosis, organisms, treatment

A

= 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
25
Q

Lung abscess: risk factors (4), aetiologies, manifestations, complications, diagnosis (3), treatment

A

= 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