Pulmonology 5 Lung Infections

Pulmonology
LOWER RESPIRATORY TRACT INFECTIONS

I. GENERAL PRINCIPLES
A. Pathogenesis: aerosolised pathogen  travel down to alveoli  enter
type 2 pneumocytes  multiply in alveoli  invade alveolar epithelial
cells  pass through one alveoli to next (through pores of Cohn) 
inflammation (& can spread to other lobe or involve entire lung
eventually).
B. General complications: abscess, empyema, sepsis, chronic  secondary
amyloidosis, clubbing. Antibiotics harder to access in abscess and
empyema. Drain them.
II. LOBAR PNEUMONIA

A. Characterised by consolidation of an entire lope.
B. Usually bacterial – MCC is Streptococcus pneumoniae (95%), followed
by Klebsiella pneumoniae (Table 1)
C. Classic gross phases
1. Congestion – due to congested vessels & oedema
2. Red hepatitisation – due to exudate, neutrophils, and haemorrhage
filling alveolar airspaces, giving lung normally spongy lung a solid
consistency.
3. Grey hepatitisation – due to degradation of RBCs within exudate;
penumococci die.
4. Resolution (type 2 pneumocytes regenerate); or death (usually multi-
lobar)
D. Histological features: neutrophils & infilitrates in airway + capillary
dilatation
Organism High-yield associations

Streptococcus MCC of CAP, and 2o PNA (bacterial PNA superimposed on viral
pneumoniae URTI). Usually seen in middle-aged adults and elderly.
Pneumococcal vaccines are given to high-risk groups (elderly > 65

y.o. – 1X pneumoccocal polysaccharide vaccine jab = 23-valent;
chronic disease, splenic problems, immunocompromised etc. 
either single jab or q5y jabs). Also children < 2 y.o. schedule (3 X:
week 8, 16, and year 1  pneumococcal conjugate vaccine, called
Prevenar 13).
Check urinary Ag. Other clinical features: herpes labialis.
Klebsiella pneumoniae Enteric flora that is aspirated; often affects malnourished and
debilitated individuals esp. elderly in nursing homes, alcoholics,
and diabetics. Thick mucoid capsule results in currant jelly
(gelatinous) sputum. Often complicated by abscess.
 Aspirate upright  basal RLL
 Aspirate supine  posterior RUL, superior RLL
Legend: gram positive & gram negative
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Pulmonology
III. BRONCHOPNEUMONIA
A. Characterised by scattered patchy consolidation (diffused shadowing)
centred around bronchioles. Often multi-focal and bilateral.
1. Caused by variety of bacterial organisms (Table 2)
B. Scarring is more common than lobar pneumonia (as usually very
chronic)

Staphylococcus aureus 2nd MCC of 2o PNA. Often associated with abscess or empyema. Can cause a
bilateral cavitating bronchoPNA.
Haemophilus influenzae Common cause of 2o PNA and PNA super-imposed on COPD  infective
exacerbation of COPD.
Pseudomonas PNA in CF patient. Also cause HAP, particularly in post-op or ITU patients.
aeuroginosa
Moraxella catarrhalis CAP and PNA super-imposed on COPD  infective exacerbation of COPD.
Legionella pneumophilia CAP, PNA super-imposed on COPD  infective exacerbation of COPD, or

(also atypical) PNA in immunocompromised states.
Transmitted via water source (water tanks kept < 60 oC e.g. air conditioners
or hot water systems). Intracellular form best visualised by silver stain.
Causes extra-pulmonary features: hyponatraemia, renal failure,

lymphopenia, hepatitis (deranged LFTs), D+V, anorexia, coma/confusion,
haematuria, & bilateral basal consolidation.
Urine antigen or culture. 10% mortality.
Strept can also cause bronchopneumonia.
IV. ATYPICAL (INTERSTITIAL) PNEUMONIA

A. Characterised by diffuse interstitial infiltrates
B. Presents with relatively mild upper respiratory Sx (minimal sputum and
low fever): “walking” PNA.
C. Inflammatory infiltrate in the interstitium (c.f. lobar and bronchoPNA)
D. Caused by bacterial or viruses (Table 3)

Mycoplasma pneumoniae MCC of atypical PNA. Usually affects young adults (classically
military recruits or college students in dorm). Complications
include AIHA (IgM vs I antigen on RBCs – causing cold haemolytic
anaemia) & erythema multiforme. Not visible on Gram stain due
to lack of cell wall.
Chylamydophilia 2nd MCC of atypical PNA in young adults. Is intracellular (obligate

pneumoniae intracellular bacteria).
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Pulmonology
Chylamydophilia psittaci An ornithosis acquired from infected birds esp. parrots

(psittacosis). Clinical features: flu-like + extra-pulmonary (rare) e.g.
meningo-encephalitis, infective endocarditis, hepatitis, nephritis,
rash, splenomegaly.
Coxiella burnetii Atypical PNA with high fever (Q fever); seen in farmers and vets
(Coxiella spores are deposited on cattle/sheep by ticks, or present
in cattle/sheep placenta). Coxiella is a rickettsial organism
(intracellular) that is distinct from other rickettsiae because: (1)
causes PNA; (2) do not require arthropod vector for transmission
(survives as highly heat-resistant endospores); and (3) doesn’t
produce skin rash.
Respiratory syncytial virus MCC atypical PNA in infants.

(RSV)
Cytomegalovirus (CMV) Atypical PNA associated with post-TXP immunosuppression.
Influenza virus Atypical PNA in the elderly, immunocompromised, and those with
pre-existing lung disease. Commonest viral infection.
Avian influenza (H5N1) A very serious infection (high To, sick as shit) with > 50% mortality.
From a mutant virus from an avian and human viruses through
genetic reassortment.
Hx: contact with poultry; human-to-human spread is unusual.

Dx: H5 and N1 RT-PCR + viral cultures.
Tx: contain the outbreak, contact trace, start empirical antivirals

and support. Oseltamivir may reduce Sx 1-2 days but resistant
strains reported. Post-exposure PPx with oseltamivir in close
contacts (check for Sx in 1 week).
SARS-COV coronavirus Another very serious infection; similar picture as H5N1.

Respiratory failure most feared complication, with progression to
ARDS. Mortality = 1-50%  highly dependent on age.
Tx: supportive; drugs don’t do anything… start early, isolate, and

control.
Neonates Infants Child Older child Adults Elderly

Group B Strep RSV Mycoplasma H. Flu (other
strains than Hib,
due to vaccine)
E. coli C. Para- Influenza A Pneumococci
trachomatis influenza
Listeria
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Pulmonology
V. ASPIRATION PNEUMONIA
A. Seen in patients at risk for aspiration e.g. oesophageal disease
(achalasia, reflux), alcoholics, stroke, post-ictal and comatose patients.
B. Most often due to anaerobic bacteria in oropharynx e.g. Bacteriodes,
Fusobacterium, and Peptococcus.
C. Classically results in RLL abscess.
1. Since, right main stem bronchus branch at less acute angle than left.
VI. CLINICAL APPROACH Immunocompromised: atypical

A. Community acquired PNA – G(+) > G(-). Viruses are rare (15%). bugs…
B. Hospital acquired PNA (HAP) – defined as > 48 h after hospital
admission. Most commonly G(-) enterobacteria or S. aureus.
C. C(U)RB-65 score and general management of CAP (NICE 2014)

1. Only applicable to CAP. Each criteria gets +1. NICE 2014 recommends using
CRB-65 rather than CURB-65 in
a. Confusion (AMTS < 8) primary care.
b. Urea (BUN) > 7 N.B. in hospital: CURB-65 is used
c. Respiratory rate > 30
d. BP < 90/60
e. Age > 65
2. It calculates the mortality at 30 days.
3. Risk stratification Mild – pneumococcal (amoxicillin
a. 0-1  outpatient covers G (+)), Hib (cephalosporin
 Score of 0: PO amoxicillin 500 mg TDS, 5 days (allergy: covers G(-)).
clarithromycin 500 mg BD, 5 days; or doxycycline 200 mg 1 st Moderate – pneumococcal, Hib,
day then 100 mg OD for 4 more days). mycoplasma (macrolides like
clarithromycin covers this weirdo)
b. 2  short-stay
 Score of 1 or 2: amoxicillin and clarithromycin for 7-10 days Severe includes PVL- staph (may
need clindamycin); MRSA (may
(doses as above). Alternative: doxycycline monotherapy 7-10
need vancomycin); Legionella
days. (may need clindamycin).
 Support.
c. >3)  urgent hospitalisation + ITU Anti-pseudo e.g. tazocin,

ciprofloxacin, ceftazidime,
 Co-amoxiclav 1.2 g IV AND clarithromycin 500 mg IV for 7-10 carbapenems (e.g. meropenem),
days. (Pen allergy: use cephalosporin; macrolide intolerance: gentamicin.
use ciprofloxacin)
 Support.
4. Follow-up: 3 days (response to Abx), then 6 weeks for patients with

slow/persistent signs despite Tx, who smoke and are > 60.
5. Advise smoking cessation.
D. General management of HAP NICE 2014: Abx accordance to

1. Depends on the bug – but you still start empirical Tx 1 st ASAP (within local guidelines (local sensitivities)
4 h) then tailor according to MCS. This is a 5- 10 day course.
a. G (-) bacilli
 Pseudomonas  gentamicin AND anti-pseudomonals
 Anaerobes  gentamicin AND 3rd-generation cephalosporin
b. Aspiration  metronidazole AND cephalosporin
c. Neutropenic patients  gentamicin AND anti-pseudomonals;
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Pulmonology
consider anti-fungals after 2 days.
E. Emergency management
1. ABCDE Ensure it is not an infective
2. CURB-65 & order other relevant investigations: CRP, FBC, U&Es, LFTs, exacerbation (see asthma &
culture (initiate sepsis-6 if pyrexial) COPD) – different management.
a. Urinary antigen e.g. legionella, and other serology may be useful May be worth doing BAL or
3. Use Abx to treat “severe” PNA in CAP aspirate pleural fluid if
a. If suspect Legionella: add levofloxacin + rifampicin immunocompromised or in ICU
b. If suspect Chlamyodphila: add doxycycline
c. If suspect PCP: add TMP-SMX (co-trimoxazole).
4. If HAP or neutropenic: gentamicin AND anti-pseudomonals.
5. No improvement with O2 = may need NIPPV (CPAP); if hypercapnic =
may need intubation.
6. Discuss with ICU early if rising PaCO2 or remain hypoxic.
VII. COMPLICATIONS
A. Death (CURB-65 prognosis + co-morbidity + extent of lung involvement
+ ABGs). Septic shock; ARDS; type 1 respiratory failure.
B. Heart: pericarditis, pericardial effusion, tamponade, myocarditis, atrial
fibrillation
C. Post-pneumonic lung abscess
1. May be multiple in IVDU.
2. Swinging fever + constitutional Sx
3. CXR shows air-fluid level; CT to R/O obstruction; bronchoscopy to
obtain sample.
4. Tx: long-term Abx (tailored to sensitivity) – but may need drainage,
repeated aspiration, or surgical excision (since Abx poorly penetrates
fibrin wall)
D. Bronchiectasis
E. Pleural effusions, empyema, PTX.
F. Meningitis and brain abscess.
G. Cholestatic jaundice (2o to sepsis, or Abx treatment esp. flucloxacillin
and co-amoxiclav)
H. Biochemical derangement – hypoNa+ (Legionella); hepatitis
I. Haematological: DIC, haemolysis (e.g. AIHA from Mycoplasma); WCC
derangement (either way); thrombocytosis (common).
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Pulmonology
TUBERCULOSIS
I. PATHOLOGY
centre
II. DIAGNOSIS
centre
III. MANAGEMENT
centre
FUNGI AND THE LUNGS

I. PATHOLOGY
A. Characterise
B.
BRONCHIECTASIS
I. PATHOLOGY
A. Characterise
B.
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Pulmonology 5 Lung Infections

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Pulmonology

LOWER RESPIRATORY TRACT INFECTIONS

II. LOBAR PNEUMONIA

Organism High-yield associations

Pneumococcal vaccines are given to high-risk groups (elderly > 65

Check urinary Ag. Other clinical features: herpes labialis.

Legend: gram positive & gram negative

Organism High-yield associations

Legionella pneumophilia CAP, PNA super-imposed on COPD  infective exacerbation of COPD, or

Causes extra-pulmonary features: hyponatraemia, renal failure,

Urine antigen or culture. 10% mortality.

Strept can also cause bronchopneumonia.

IV. ATYPICAL (INTERSTITIAL) PNEUMONIA

Organism High-yield associations

Chylamydophilia 2nd MCC of atypical PNA in young adults. Is intracellular (obligate

Chylamydophilia psittaci An ornithosis acquired from infected birds esp. parrots

Respiratory syncytial virus MCC atypical PNA in infants.

Hx: contact with poultry; human-to-human spread is unusual.

Tx: contain the outbreak, contact trace, start empirical antivirals

SARS-COV coronavirus Another very serious infection; similar picture as H5N1.

Tx: supportive; drugs don’t do anything… start early, isolate, and

Neonates Infants Child Older child Adults Elderly

VI. CLINICAL APPROACH Immunocompromised: atypical

C. C(U)RB-65 score and general management of CAP (NICE 2014)

c. >3)  urgent hospitalisation + ITU Anti-pseudo e.g. tazocin,

4. Follow-up: 3 days (response to Abx), then 6 weeks for patients with

D. General management of HAP NICE 2014: Abx accordance to

consider anti-fungals after 2 days.

FUNGI AND THE LUNGS

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