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Respiratory System Block > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Normal Defence Mechanisms of Respiratory System (nasopharynx, Oropharynx, Trachea and Bronchi, Terminal Airways and alveoli)

A

1 Nasopharynx: nasal hairs, turbinates, mucociliary apparatus, sIgA secretion.

2 Oropharynx: saliva, sloughing of epithelial cells, pH, bacterial interference, complement production.

3 Trachea and bronchi: cough and epiglottic reflexes, sharp-angled branching of airways, mucociliary apparatus, Ig production (IgG, IgM, IgA).

4 Terminal airways and alveoli: alveolar lining fluid, alveolar macrophages, neutrophils, cell-mediated immunity.

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2
Q

Normal Defence Mechanisms of Nasopharynx

A
  • nasal hairs
  • turbinates
  • mucociliary apparatus
  • sIgA (secretory IgA) secretion.
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3
Q

Normal Defence Mechanisms of Oropharnx

A
  • Saliva
  • Sloughing/shedding of epithelial cells
  • pH
  • Bacterial Interference (colonization resistance by normal flora)
  • Complement Production
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4
Q

Normal Defence Mechanisms of Trachea and Bronchi

A
  • Sharp-angled braching of airways
  • Production of antobodies (IgM, IgA, IgG)
  • mucociliary apparatus
  • Cough and epiglottic reflexes
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5
Q

Normal Defence Mechanisms of Terminal Airways and Alveoli

A
  • Alveolar lining fluid
  • Alveolar macrophage (aka dust cells)
  • Neutrophils
  • Cell-mediated immunity
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6
Q

Route of Connection of Nasophaynx with other parts

A

The nasopharynx is connected to the:

  • middle ear via internal auditory tube
  • the eye via nasolacrimal duct
  • the paranasal sinus via sinus ostium
  • the oropharynx.
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7
Q

colonization resistance

A

Normal flora in our body contribute to colonization resistance -> resistance to colonization by pathogenic organisms

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8
Q

Factors in respiratory tract infection diagnosis

A
  • age of patient
  • time of the year
  • site of infection
  • clinical syndrome
  • underlying disease of the patient (systemic diseases, respiratory diseases)
  • drugs (kill normal flora / suppress immune defense)
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9
Q

Most common cause of pharyngitis (with %)

A

Pharyngitis is mostly due to viral infection (~70%)

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10
Q

Pathogens of viral pharyngitis

A
  • Rhinovirus
  • coronavirus
  • adenovirus
  • Herpes simplex virus (HSV)
  • Epstein–Barr virus (EBV)
  • parainfluenza viruses
  • respiratory syncytial virus (RSV)
  • influenza virus
  • coxsackie A virus
  • Cytomegalovirus
  • HIV
  • etc.
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11
Q

Pathogen for non-viral pharyngitis

A
  • Most common: Group A β-hemolytic streptococcus (GAS, aka Streptococcus pyogenes)
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12
Q

General guideline of antibiotics and sore throat

A

Antibiotics not routinely used for treatment of sore throat as most common pharyngitis pathogens are viral in nature; only used when there is a documented bacterial cause or when bacterial pharyngitis is likely

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13
Q

Group A Streptococcal Pharyngitis (pathogens, carriage and infection, incubation period, onset, treatment, prognosis, symptoms)

A

~ Pathogen: Group A β-hemolytic streptococcus/Streptococcus pyogenes

~ Carriage and infection: Direct person-to-person contact; facilitated by over-crowding. Can have asymptomatic carriage

~ Incubation Period: 2-4 Days

~ Onset: Abrupt

~ Treatment: Penicillin

~ Prognosis: Uncomplicated cases usually subside in about 1 week

~ Symptoms:

1) Sore throat (painful)
2) Hyperaemic tonsils (red, swollen) with greyish white exudates
3) Lymph nodes (cervical nodes) enlarged and tender
4) Redness, lymphoid hyperplasia of posterior pharynx
5) malaise, fever, headache
6) Eye and nose not affected

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14
Q

Viral Pharyngitis

A

~ Pathogen: Rhinovirus, coronavirus, adenovirus, Herpes simplex virus (HSV), Epstein–Barr virus (EBV), parainfluenza viruses, respiratory syncytial virus (RSV), influenza virus, coxsackie A virus, Cytomegalovirus, HIV, etc

~ Onset: Gradual

~ Symptoms:

1) Sore throat (uncomfortable)
2) Hyperaemic tonsils (red, swollen) with vesicles and ulcers
3) Lymph nodes (cervical nodes) not enlarged
4) Watery eyes
5) Running nose

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15
Q

Differentiating Streptococcal and viral pharyngitis

A
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16
Q

Suppurative complications of streptococcal pharyngitis

A

• Local abscess formation: swelling of neck/face: may compress airway

 Peritonsillar abscess
 Peritonsillar cellulitis
 Retropharyngeal abscess

  • Streptococcal bacteraemia with metastatic foci of infection
  • Intracranial infection – Head and neck infection: ∵Invade blood vessels => go up brain
  • Acute otitis media, acute sinusitis
  • Penumonia (rarely)
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17
Q

Non-suppurative complications of streptococcal pharyngitis

A
  • Acute Rheumatic Fever (recurrent attacks -> chronic rheumatic heart disease, and even infective endocarditis)
  • Post-streptococcal glomerulonephritis
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18
Q

Acute rheumatic fever (definition, cause, pathogenesis, diagnosis)

A

~ Definition: A delayed non-suppurative complication of upper respiratory infection due to Streptococcus pyogenes (sometimes due to other beta-haemolytic streptococci). A systemic disease affecting the peri-arteriolar connective tissue.

~ Cause: Molecular mimicry - antibody cross-reactivity in a Type II hypersensitivity reaction

~ Pathogenesis: Heart-reactive antibodies (HRA) cross reacts with antigens on heart tissues and group A streptococcal antigens (M protein, group A polysaccharide). During a Streptococcus infection, mature antigen presenting cells such as B cells present the bacterial antigen to CD4-T cells which differentiate into helper T2 cells. Helper T2 cells subsequently activate the B cells to become plasma cells and induce the production of antibodies against the cell wall of Streptococcus. However the antibodies may also cross-react against the myocardium and joints due to similarities between sequences found in microbial proteins and host proteins

~ Diagnosis: Jones criteria

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19
Q

Acute rheumatic fever pathogenesis and prognosis

A

Streptococcal infection

–> may develop acute rheumatic fever (should be treated by penicillin; this may progress to valvular damage)

–> with recurrent attack of streptococcal infection –> more valvular damage (to be treated with long-term prophylaxis, e.g. keep giving low-dose antibiotics)

–> may progress to chronic rheumatic heart disease (Impair the function of the heart –> Predispose the patient to infective endocarditis)

–> tooth extraction / surgical drainage in tooth abscess / other procedures –> a chance of developing into infective endocarditis. Therefore a high-dose antibiotics prophylaxis is given just before such procedures.

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20
Q

Treatment of acute rheumatic fever

A

Antibiotics for Streptococcal infection (*see notes)

  • Penicillin: Treat streptococcal infection, prevent suppurative complications
  • Long-term prophylaxis -> Prevent recurrent attacks of ARF
    • Intra-muscular benzathine penicillin
    • Oral penicillin V
    • Erythromycin
    • Sulphonamides

• Prophylactic antibiotics -> Prevent infective endocarditis

  • Oral amoxicillin (High dose)
  • Intravenous ampicillin + gentamycin
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21
Q

Diphtheria presentation

A
  • ** Formation of White pseudo-membrane (made up of necrotic tissues, inflammatory exudates) in the upper respiratory tract
  • Sore throat
  • Fever
  • airway obstruction
  • myocaridal depression
  • neuropathy
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22
Q

Pathogen causing diphtheria

A

Corynebacterium diphtheriae

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23
Q

Corynebacterium Diphtheriae features

A

1) Gram positive bacillus
2) non-sporulating
3) non-motile
4) unencapsulated
5) **“Chinese character” palisades
6) ** Metachromatic granules in polar regions

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24
Q

Definition of metachromacity

A

The phenomenon bu which different parts of an organism can get stained in two or more different colours with the application of a single dye

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25
Q

Special stains for Corynebacterium Diphtheriae

A

Albert’s stain and **Ponder’s stain **are used to demonstrate metachromatic granules formed in polar regions of Corynebacterium Diphtheriae

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26
Q

Medium for Corynebacterium diphtheriae

A

1) Löffler’s medium - enhance growth of corynebacterium only
2) Hoyle’s medium (blood agar with potassium tellurite) - tellurite helps to differentially select Corynebacterium dophtheria from other URT flora, showing formation of black colonies

3)

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27
Q

Transmission of diphtheria

A

1) Droplet transmission
2) Direct contact with respiratory secretions
3) Asymptomatic carrier state exists

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28
Q

Pathogenesis of diphtheria

A

a) Diphtheria is a exotoxin-mediated disease; tox gene carried by bacteriophage
b) Exotoxin is absorbed into blood; causing inactivation of elongation factor 2
c) Systemic effects of toxin occur (may even cause heart and nerve problems, or skin infection)
d) pseudomembrane may go down to affect lower airway; inflammation of glottic area may obstruct airway -> life threatening in young patients

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29
Q

Treatment of Diphtheria

A

1) Diphtheria antitoxin
2) Penicillin, erythromycin
3) Supportive care

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30
Q

Primary prophylaxis of Diphtheria

A

Vaccination with diphtheria toxoid

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31
Q

Acute epiglottitis (definition)

A

A rapidly progressive cellulitis of the epiglottis and adjacent structures

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32
Q

Infectious and non-infectious causes of acute epiglottitis

A

Infectious: Classically caused by haemophilus influenzae type b (Hib; esp. in children); more diverse etiology in adults, including Haemophilus influenzae, beta-haemolytic streptococci (streptococcus pneumoniae, streptococcus pyogenes), staphylococcus aureus, Klebsiella pneumoniae

non-infectious: trauma, irradiation, caustic ingestion, inhalation injury, etc.

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33
Q

Acute epiglottitis epidemiology

A

Children (2-4 years old) are most commonly affected; can occur in adults

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34
Q

Acute epiglottitis presentation

A

Rapid onset of fever

irritability

dysphonia (children won’t yell as it will be too painful)

dysphagia (drooling may be observed as swallowing will be too paindul)

sore throat

respiratory distress

May progress to complete airway obstruction at any time

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35
Q

Why is acute epiglottitis a medical emergency?

A

May progress to life-threatening complete airway obstruction at any time

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36
Q

Clinical examination for acute epiglottitis

A

1) Laryngoscopy -> cherry red epiglottis (red and swollen)
2) Lateral and frontal neck x-ray -> Narrowed upper-end of trachea (due to oedema)
3) Auscultation -> Stridor sound (can be heard without stethoscope)

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37
Q

Stridor sound explanation

A

Stridor is a high pitched wheezing sound resulting from turbulent air flow in the upper airway. It is primarily inspiratory. It can be indicative of serious airway obstruction from severe conditions such as epiglottitis, a foreign body lodged in the airway, or a laryngeal tumor. Stridor is indicative of a potential medical emergency and should always command attention. (Can be heard without using stethoscope)

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38
Q

Precautions in suspected acute epiglottitis

A

Examine the epiglottis of the patient only when facilities for immediate intubation or tracheostomy are available, as laryngoscope and examination may provoke airway spasm leading to complete airway obstruction

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39
Q

Normal sinus drainage

A

Secretion of sinuses are normally drained into osteomeatal complex and then to pharynx; normal sinus are considered “sterile” with minimal microbes only

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40
Q

Acute sinusitis pathogenesis

A

1 Obstruction of normal sinus drainage.

2 The commonest antecedent condition is an upper respiratory tract viral infection.

3 Other predisposing conditions: allergy; rarely, dental root infection (maxillary sinusitis).

4 Swelling of inflamed mucosal lining further impairs sinus drainage.

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41
Q

Acute sinusitis pathogens

A

1 Streptococcus pneumoniae (∼40%), Haemophilus influenzae (∼20%), Moraxella catarrhalis (∼20%).

2 Respiratory viruses (rhinovirus, parainfluenza virus, adenovirus, influenza virus): ∼10%.

3 Sterile cultures in ~25%.

4 May be fungal infection in fungal sinusitis (e.g. bone marrow transplant recipient)

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42
Q

Acute sinusitis clinical presentation

A

1 Persistent and severe symptoms after upper respiratory tract infection.

2 Purulent nasal and postnasal discharge (yellowish/greenish)

3 Facial pain, headache (frontal sinusitis), fever.

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43
Q

Acute sinusitis complications

A

intra-orbital extension

intracranial extension of infection: brain abscess, meningitis

osteomyelitis of frontal bone (frontal or ethmoid sinus).

44
Q

Acute sinusitis diagnosis

A

1 Clinical symptomatology

2 physical examination

3 Imaging:

  • sinus X ray: sinus opaque, no normal black air shadow
  • CT Scan: swollen mucosa in sinus

4 Culture: culture of nasal pus or sinus exudates not reliable. Sinus puncture and aspiration of sinus contents is preferred. Routine sinus puncture not necessary.

45
Q

Types of sinusitis

A

1) Acute community-acquired sinusitis
2) Nosocomial (hospital-acquired) sinusitis [e.g. nasogastric tube can cause irritation to nasal mucosa, causing it to be swollen -> occlude osteomeatal complex -> sinus secretion cannot be drained to nasopharynx]
3) chronic sinusitis
4) fungal sinusitis

46
Q

Sinusitis managements

A

1 Empirical antibiotic coverage (e.g. amoxicillin, amoxicillin-clavulanate, cefuroxime) against Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis, taking into account the local pattern of antibiotic resistance.

2 Surgical therapy for severe sinusitis, suspected intra-orbital or intracranial involvement, correction of sinus drainage in chronic sinusitis.

47
Q

Otitis Externa (definition, pathogens, presentation, treatment)

A

Defintion: Infection of the external auditory meatus

Pathogens: Staphylocaccus aureus (acute localized otitis media), pseudomonas aeruginosa (Malignant otitis media, especially in elderly, diabetics, and immunocompromised hosts), normal flora similar to that on the skin

Presentation: Red swollen ear; may have pus in the ear canal

Treatment: Systemic antibiotics; surgical drainage of abscess and debridement may be necessary

48
Q

acute otitis media epidemiology

A

Primarily affecting children; peak incidence between 6 to 24 months

49
Q

acute otitis media Predisposing factors

A

1 Anatomical defects, e.g. cleft palate, cleft uvula.

2 Physiological abnormalities of Eustachian tube.

3 Congenital or acquired immunodeficiencies.

4 Colonization of the nasopharynx by potential bacterial pathogens at the time of viral upper respiratory tract infection.

50
Q

acute otitis media Presentation

A

1) Ear Pain, ear drainage, hearing loss
2) Fever, lethargy, irritability
3) Erythema of tympanic membrane (red, bulging outwards); fluid (pus) in middle ear

51
Q

acute otitis media pathogenesis

A

1 Anatomical or physiological dysfunction of the Eustachian tube.

2 Obstruction of Eustachian tube → accumulation of fluids and secretions in the middle ear → increased risk of infection.

3 Often preceded by a viral upper respiratory tract infection. Up to 37% of the episodes of upper respiratory tract infection may be complicated by the development of acute otitis media.

52
Q

acute otitis media pathogen

A

1 Bacteria: Streptococcus pneumoniae (35–40%), Haemophilus influenzae (30– 35%), Moraxella catarrhalis (15–18%). Uncommon: Streptococcus pyogenes (2– 4%), Staphylococcus aureus.

2 Viruses: less common.

3 Sterile culture in ~20%.

53
Q

acute otitis media diagnosis

A

1) Clinical symptomology and examination
2) culture of the external auditory meatus not useful in predicting the pathogens.

Tympanocentesis (aspiration of the middle ear content) is the method of choice but is not routinely needed unless patient is critically ill, not responsive to antibiotics, or has altered host defence.

54
Q

acute otitis media management

A

1 Empirical antibiotic coverage (e.g. amoxicillin, amoxicillin-clavulanate, cefuroxime) against Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, taking into account the local pattern of antibiotic resistance.

2 In neonates or immunosuppressed individuals, the possibility of infection due to more resistant or unusual organisms should be considered.

55
Q

acute otitis media complications

A

If it is not adequately treated, it may develop into chronic suppurative otitis media.

Can go to other surrounding areas like

  • Mastoid cortex
  • Epidural abscess
  • Subdural abscess
56
Q

Wheezing sound explanation

A

Abnormal breathing sound (high-pitched, whistling sound) due to lower airway obstruction (e.g. asthma, croup)

57
Q

Stridor

A

Stridor is a high pitched wheezing sound resulting from turbulent air flow in the upper airway. It is primarily inspiratory. It can be indicative of serious airway obstruction from severe conditions such as epiglottitis, a foreign body lodged in the airway, or a laryngeal tumor. Stridor is indicative of a potential medical emergency and should always command attention. (Can be heard without using stethoscope)

58
Q

tracheolaryngobronchitis (definition)

A

Also known as croup; inflammation in the subglottic area resulting in dyspnoea and inspiratory stridor

59
Q

tracheolaryngobronchitis (epidemiology)

A

relatively common in children (3 months to 3 years); peak incidence at 2 years of age

60
Q

tracheolaryngobronchitis (pathogen)

A

Mainly viruses such as parainfluenza virus, influenza virus, respiratory syncytial virus

Mycoplasma pneumoniae

61
Q

tracheolaryngobronchitis presentation

A

1) Fever
2) laryngitis
3) Insiratory stridor with or without respiratory distress
4) wheezing sound
5) tachypnoea or dyspnoea
6) rales
7) Hypoxaemia

62
Q

tracheolaryngobronchitis diagnosis

A

Clinical diagnosis. Aetiological diagnosis by viral culture or antigen detection if necessary.

63
Q

Croup treatment

A

oxygen, nebulized bronchodilators.

64
Q

Pertussis alternate name

A

whooping cough

65
Q

Pertussis pathogen

A

Bordetella pertussis, a Gram negative coccobacillus

66
Q

pertussis epidemiology

A

1) Epidemic in most populations; transmitted via respiratory droplets
2) Not just a disease of childhood. In developed countries, overall disease burden shifting to adolescents and adults. Pertussis is a common but under-recognized cause of chronic cough in adolescents and adults.
3) In many western countries, nosocomial outbreaks of pertussis have been described.

67
Q

Pertussis pathogenesis and 3 phases of disease

A

1) Filamentous haemagluttinin, helps in attachment to ciliated respiratory epithelium
2) Production of a number of toxins:
- pertussis toxin (PT), adenylate cyclase toxin (ACT), tracheal cytotoxin, dermonecrotic toxin (DNT), pertactin (PTN)
3) Incubation period from less than 1 week to more than 3 weeks
4) 3 phases of disease
a) Catarrhal phase: rhinorrhoea, conjunctival injection, malaise, low grade fever, dry cough
b) Paraoxysmal phase: short expiratory bursts followed by an inspiraory gap (whoop)
c) Convalescent phase

68
Q

Pertussis presentation

A

a) Catarrhal phase: rhinorrhoea, conjunctival injection, malaise, low grade fever, dry cough
b) Paraoxysmal phase: short expiratory bursts followed by an inspiraory gap (whoop)

Chronic cough in general; symptomatology in adolescents and adults differ from that in children

69
Q

Pertussis complications

A 
pneumonia; haemorrhage; pneumothorax; central nervous
 system abnormalities (convulsion, encephalopathy).
70
Q

Pertussis diagnosis

A

culture of nasopharyngeal aspirate or swab on special medium (Bordet-Gengou medium).

Serology (not widely available and may not be useful in acute infection).

PCR of nasopharyngeal specimens.

71
Q

Pertussis treatment

A

Specific antibiotic therapy: macrolides (e.g. erythromycin, clarithromycin, azithromycin).

72
Q

Pertussis vaccination

A

1) Killed whole-cell vaccine
- protection not life long
- adults have partial or little immunity
- lots of side effects (pain, swelling, high fever)
2) Acellular vaccine (aP)
- A subunit vaccine presents an antigen to the immune system without introducing viral particles. It is the combination of different pathogenic mechanisms (e.g. filamentous haemagglutinin) instead of using whole cell
- fewer side effects
- From 2007, HK childhood immunization programme replaced killed whole-cell vaccine with aP vaccine delivered in combined formula DTaP-IPV. (D=diphtheria toxoid, T=tetanus toxoid, aP= acellular purtussis, IPV=inactivated poliomyelitis vaccine)
- **[IPV replaved oral poliomyelitis vaccine which is live attenuated)

73
Q

Pneumonia Definition

A

Inflammation affecting the parenchyma of the lung (respiratory bronchioles and alveolar units).

74
Q

Common causes of community-acquired pneumonia

A

a) Bacteria: Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae;

in some clinical or epidemiological settings, Staphylococcus aureus, Enterobacteriaceae (especially Klebsiella pneumoniae), Legionella pneumophilia, and Burkholderia pseudomallei (melioidosis), and Mycobacterium tuberculosis (tuberculosis) are also important considerations.

b) Viruses: respiratory syncytial virus (especially in infants, children), influenza virus, parainfluenza viruses, coronaviruses, etc.

75
Q

Pneumonia - Route of infection

A

1 Direct inhalation of infectious particles from ambient air.

2 Aspiration of secretions from the mouth and nasopharynx.

3 Rarely: haematogenous spread from another focus of infection in the body.

76
Q

Approach to Pneumonia

A

1 History.

a) Clinical setting: acute or chronic; age, underlying illness, occupation, travel history, animal
contacts, etc; community- or hospital-acquired.

b) Patient characteristics - e.g. age, any defect in host resistance (opportunistic pathogens)? Exposure history - Possible exposure to specific pathogens (human, animals, environment)?

2 Physical examination.

3 Investigations.

a) Blood counts, blood gas.
b) Cultures: respiratory tract specimens, blood, pleural fluid.
c) Radiological examinations: plain X ray; CT scan in selected cases.
d) Sputum examination.
i) Macroscopic examination: colour, amount, consistency, (odour); e.g. ‘rusty’ sputum (Streptococcus pneumoniae), ‘currant-jelly’ sputum (Klebsiella pneumoniae). Not sensitive or specific, though.
ii) Gram stain: leukocytes (neutrophils, mononuclear cells), epithelial cells (quality of specimen), predominant flora.
iii) Culture: blood agar, chocolate agar, selective media (e.g. Legionella) when indicated.
e) Viral investigations on respiratory specimens: antigen detection (e.g. by direct immunofluorescent staining, immunochromatographic tests), viral culture, PCR/RT-PCR.
f) Other respiratory tract specimens.

i) More invasive procedure generally have a higher yield for the true
pathogens. However, one needs to balance between risk of procedure
and the anticipated pathogens and yields.

ii) Transtracheal aspiration (seldom performed nowadays).
iii) Endotracheal aspiration.
iv) Fibre optic bronchoscopy + bronchoalveolar lavage (BAL).
v) Transbronchial biopsy, open lung biopsy.
vi) Pleural effusion, pleural biopsy.
vii) Nasopharyngeal aspirate: mainly for respiratory viruses.
g) Serology: mainly for ‘atypical’ pneumonia pathogens (e.g. Mycoplasma, Chlamydia, Chlamydophila, Legionella, viruses). Not always useful in the acute stage.
h) Urine antigen detection assays: Streptococcus pneumoniae, Legionella pneumophila serogroup 1.

77
Q

Therapy of pneumonia: general considerations

A

1) General supportive measures: oxygen, cardiovascular support, etc.
2) Treat as outpatients or inpatients?
3) Oral or parenteral antibiotics?
4) Empirical therapy or known-pathogen therapy?
5) Empirical therapy: usually a beta lactam antibiotic (e.g. penicillins or cephalosporins) ± a macrolide (e.g. erythromycin, clarithromycin, azithromycin) or a tetracycline.

Different antibiotics have been used for the treatment of pneumonia in different clinical settings. However, antibiotics must be chosen carefully: a balance between clinical efficacy, antibiotic resistance, and cost is essential. Guidelines on the treatment of community-acquired pneumonia may be obtained from various authorities like British Thoracic Society

78
Q

Acute community acquired pneumonia (CAP) presentation

A

Fever, chills, pleuritic chest pain, cough, mucopurulent sputum. Mortality 6– 24%.

79
Q

Acute CAP Pathogens

A

1) Streptococcus pneumoniae: commonest; average ~20% -> pneumococcal pneumonia
2) Haemophilus influenzae: average ~7%.
3) Staphylococcus aureus (elderly; post-influenza pneumonia); average ~3%.

Although S. aureus is often quoted as a typical pathogen seen in secondary bacterial pneumonia in patients with influenza, it is not necessarily the commonest one. In most epidemics or pandemics of influenza, Streptococcus pneumoniae is the commoner bacterial pathogen involved.

5) Other bacteria such as Klebsiella pneumoniae.
6) Viruses: especially in children (RSV, parainfluenza), primary influenza pneumonia.

80
Q

Pneumococcal Pneumonia pathogen and epidemiology

A

Pathogen: Streptococcus pneumoniae (pneumococcus)

Epidemiology: Accounts for 16–60% of acute community-acquired pneumonia.

81
Q

Pneumococcal pneumonia risk and predisposing factor

A

Risk: Increasing problem of antibiotic resistance.

Predisposing factors: old age, smoking, institutionalization, COAD, chronic liver and renal diseases, congestive heart failure, splenectomy.

82
Q

Pneumococcal pneumonia Vaccines

A

Pneumococcal vaccines are available for the prevention of invasive pneumococcal diseases and pneumonia.

There are 2 types of pneumococcal vaccine currently available, the polysaccharide vaccine (23-valent) and the conjugate vaccines (7- and 13-valent vaccines are registered in Hong Kong at the moment). Since 2009, the vaccine is made available to at-risk populations in Hong Kong.

83
Q

Atypical pneumonia characteristics

A

a) Routine culture of sputum does not reveal significant pathogens.
b) Not responding to beta lactam antibiotics commonly used for the treatment of pneumonia.
c) Sometimes may have a more prolonged course of illness.
d) May not appear very ill clinically (“walking pneumonia”)

84
Q

Atypical pneumonia pathogens

A

a) Bacteria: e.g. Mycoplasma pneumoniae, Chlamydia and Chlamydophila, Legionella pneumophila.
b) Viruses: e.g. influenza virus, adenovirus, parainfluenza virus, respiratory syncytial virus, coronaviruses.

85
Q

Atypical pneumonia epidemiology

A

Can affect any age group but often more severe in the elderly.

86
Q

Legionella characteristics

A

Aerobic

Gram negative

non-spore-forming

bacilli

Occurs in natural and artificial fresh water environments.

87
Q

Legionella pneumophila characteristics

A

a) Aerobic, Gram negative, non-spore-forming bacilli
b) Colonizes artificial water sources, such as cooling towers and other water distribution systems, such as potable water.
c) Aerosolization and aspiration are the commonest routes of transmission.

88
Q

Clinical diseases caused by legionella

A

a) Pontiac fever: an acute, self-limiting, flu-like illness without pneumonia.
b) Legionnaires’ disease: pneumonia; diarrhoea, nausea, vomiting, abdominal pain, extrapulmonary diseases.

89
Q

Route of transmission of legionella diseases

A

Aerosolization and aspiration are the commonest routes of transmission.

Ingestion of contaminated water source

90
Q

Legionellosis diagnosis

A

bacterial culture, urine antigen detection, serology (antibody detection), direct immunofluorescent staining of clinical specimens.

91
Q

Legionellosis treatment

A

macrolide or fluoroquinolone antibiotics. Beta lactam antibiotics are generally not effective for legionellosis.

92
Q

Nosocomial pneumonia epidemiology

A

Hospital-acquired pneumonia. Accounts for 10% to 20% of all nosocomial infections.

93
Q

Nosocomial pneumonia risk factors

A

a Advanced age.

b Underlying diseases.

c Altered mental status.

d Intubation and use of respiratory equipment.

e Use of antacids and H2-antagonists with reduction of gastric acidity.

94
Q

Nosocomial pneumonia pathogens

A

Often caused by aerobic Gram negative bacilli, e.g. Enterobacteriacae such as Escherichia coli, Klebsiella pneumoniae, or non-fermenters like Pseudomonas aeruginosa, Acinetobacter baumannii; or other multi-resistant bacteria such as meticillin-resistant Staphylococcus aureus.

95
Q

Aspiration pneumonia Pathogenesis

A

Can occur in any condition in which consciousness is altered and the normal gag and swallowing reflexes are impaired; e.g. alcoholism, cerebrovascular disorders, convulsion.

Three important pathogenic mechanisms:

1) chemical pneumonitis (acute, e.g. due to gastric acid)
2) bronchial obstruction with particulate matter (acute)
3) bacterial aspiration pneumonia (insidious, need incubation period, 2-4 days after aspiration episode)

96
Q

Aspiration pneumonia presentation

A

1) acute
2) insidious: fever, weight loss, productive cough, putrid sputum

97
Q

Aspiration Pneumonia Pathogens

A

Predominantly the oral flora: anaerobes (Bacteroides, Porphyromonas, Prevotella, Fusobacterium, anaerobic cocci), Streptococcus (community- acquired); Gram negative bacilli, Staphylococcus aureus (community- acquired or nosocomial).

98
Q

Aspiration pneumonia treatment

A

Often needs broad spectrum coverage against aerobic and anaerobic organisms.

99
Q

Which lung is more commonly affected by Aspiration Pneumonia

A

Right lung, because the right bronchi is more vertical

100
Q

Lung abscess predisposing conditions

A

a Aspiration due to impaired conscious level, e.g. alcoholism, stroke,
general anaesthesia, drug overdose, seizures, etc.

b Poor dental hygiene with periodontal disease, gingivitis.

c Bronchiectasis, bronchial obstruction, cavitating pulmonary infection.

d Septic embolization (e.g. infective endocarditis), bacteraemia.

e Amoebic lung abscess (Entamoeba histolytica; very rare).

101
Q

Lung abscess pathogen

A

Usually due to mixed oral flora if the predisposing cause is aspiration -

i.e. [anaerobes (Bacteroides, Porphyromonas, Prevotella, Fusobacterium, anaerobic cocci), Streptococcus (community- acquired); Gram negative bacilli, Staphylococcus aureus (community- acquired or nosocomial).]

102
Q

Empyema thoracis definition

A

Abscess in the pleural cavity.

103
Q

Empyema thoracis causes

A

a) Complication of pneumonia (50% to 60%).
b) Complication of intrathoracic surgery or trauma: oesophagus, mediastinum, cardiac surgery (25%).
c) Secondary to subdiaphragmatic sepsis.

104
Q

Empyema thoracis pathogens

A

a) Secondary to pneumonia: Staphylococcus aureus, Streptococcus pneumoniae, etc.
b) Secondary to surgery or perforation of oesophagus: anaerobes; aerobic Gram negative bacilli, Staphylococcus aureus, Actinomyces, etc.

105
Q

empyema thoracis treatment

A

a) Adequate drainage of collections: percutaneous catheters, chest drains, surgery if necessary.
b) Antibiotics: according to pathogen(s) involved; often requires a prolonged course of antibiotic.
c) Decortication may be necessary in some patients.

106
Q
A

Respiratory System Block (33 decks)

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