Lobar and Bronchopneumonia
Medical Students
Introduction
Exam questions on pneumonia tend to focus on the:
- Aetiology
- Clinical features for and against pneumonia and
- Empiric treatment of pneumonia.
The reason for focussing on this area is because routine clinical practice involves empiric antibiotic therapy as a go-to situation in most patients diagnosed with community acquired pneumonia (CAP). The following two points justify this claim:
- Less than half of patients have an identified microbiological entity when subjected to tests including newer molecular techniques.
- Most guidelines suggest that microbiological testing is only indicated in moderate to high severity CAP since this is where it changes the management.
Hence the context becomes the most important factor that helps in deciding on empiric (best-guess) therapy.
Let’s deal with each of these issues in turn.
1. Aetiology
Clinical context gives you the clue to the microbial aetiology which has been summarised in figure 1.
The contextual factors could be seen as risk factors which we have to elicit in order to guess the likely aetiology. Antibiotics are then chosen to cover the likely micro-organisms. If we have enough clues we go for the narrowest spectrum antibiotic targeted to cover the likely possibilities. If we have no clue and the patient is very ill we go for broad spectrum antibiotics. It’s a bit more complicated than that but let’s keep it simple for now.
When therapy fails to alter the expected outcome i.e. improvement, an extensive search is indicated to identify the aetiologic agent using laboratory tests. In the meantime, in real life, we resort to broad spectrum antibiotics until we know the test results that help us narrow their coverage back down.
Microbiological testing is thus more useful right from the start in the following situations:
- Specific high risk epidemiological conditions like influenza, MERS, SARS etc.
- In the case of severe CAP, to switch to narrow spectrum antibiotics.
- All patients with hospital acquired pneumonia.
- Patients not improving despite seemingly appropriate antibiotics started in the community.
- Immunosuppressed individuals.
2. Clinical diagnosis
Definition
Consolidation is pathologically defined as solidification of air-filled lungs. In lobar pneumonia, the process of consolidation affects the entire lobe (visible on chest radiograph – CXR). This means that the entire lobe goes through all the pathological stages of pneumonia simultaneously. Figure 2a shows a pale, solidified, left upper lobe representing ‘lobar consolidation’.
In bronchopneumonia the infective process starts in the bronchus and spreads peri-bronchially, limiting itself to the lobules. As an extension, the CXR shows patchy consolidation. Figure 2b shows tan-yellow raised lobular areas in the upper lobe representing the bronchopneumonia pattern.
Contrary to popular belief, all bacteria are perfectly capable of producing either a lobar or bronchopneumonia. In exams though, lobar pneumonia is often associated with pneumococcus (Streptococcus pneumoniae).
When do we consider pneumonia?
As usual, it is the combination of history, clinical examination and investigations that increases the likelihood of pneumonia. Acute history of respiratory symptoms, acute confusion in the elderly and gastro-intestinal symptoms in atypical pneumonias is particularly important to elicit. Remember that bacteremic and atypical pneumonia can also cause extra-pulmonary symptoms.
Other contexts when we need to think of pneumonia:
- When we suspect sepsis and then try to detect the source of infection.
- People with chronic lung disease tend to have bacterial colonisation. This can often give rise to episodic infections.
Atypical bacteria
“What are atypical bacteria?” I hear you say. Atypical bacteria are invisible on gram stains, cannot grow in traditional culture techniques and are resistant to beta lactam group of antibiotics. This is largely because they lack a cell wall. (Famous members include Mycoplasma, Chlamydia and Legionella, although the latter is strictly a gram negative genus).
Making the diagnosis
Two points are worth mentioning in the context of diagnosing pneumonia:
- The absence of any abnormal vital signs decreases the probability of pneumonia to < 1% (Gennis et al., 1989).
- Amongst all the clinical signs, the presence of bronchial breathing, fever, dull percussion note and reduced breath sounds increases the probability of pneumonia the most (Metlay, Kapoor and Fine, 1997).
The simple rule of thumb is, the greater the number of abnormal signs of consolidation that you find, the greater is the likelihood of pneumonia. This is true of any diagnosis in medicine!
Table 1 gives the common contextual factors and clinical features that are found in exam questions that give a clue to the aetiologic agent. You have to remember that these contextual factors can sometimes be very different in real life! For example, it is not just the people from the Indian sub-continent who have tuberculosis, but in exams this is true.
Table 1
| History | Examination | Laboratory tests | Aetiology |
|---|---|---|---|
|
Brown, rusty phlegm |
Classic signs of lobar, or broncho-pneumonia, sepsis |
Neutrophilia, elevated CRP, positive urine pneumococcal antigen |
Streptococcus pneumoniae
(Gram positive) |
|
Red currant jelly like sputum (from intense inflammation and necrosis of lung parenchyma), alcoholism, diabetes mellitus, COPD |
Classic signs of lobar or bronchopneumonia |
Neutrophilia, elevated CRP, bulging fissure sign on CXR |
Klebsiella pneumoniae
(Gram negative)
|
|
COPD |
Bronchopneumonia |
Neutrophilia, elevated CRP |
Haemophilus influenzae (Gram negative)
Moraxella catarrhalis (Gram negative) |
|
Neurological disorders e.g. stroke, Parkinson’s are accompanied by swallowing disorders which predispose to aspiration pneumonia |
Signs of pneumonia in right lower lobe if aspirated in sitting position. If aspirated in sleeping position signs found in posterior segment of upper lobe and apical segment of lower lobe.
i.e. think of most dependent segment. |
Inflammatory marker rise. CXR may show cavitation as usually secondary to anaerobes. |
Oral anaerobes, gram negative enteric pathogens. |
|
Post-influenza secondary bacterial infection |
Classic signs of CAP. Subpleural pneumatocoeles can rupture causing pneumothorax if due to Staphylococus aureus. |
Inflammatory marker rise. CXR may show cavitation if due to Staphylococcus aureus
Lung abscess if due to community acquired MRSA |
Streptococcus pneumoniae, Staphylococcus aureus (Gram positive), Haemophilus influenzae |
|
Chronic structural lung disease e.g. COPD, bronchiectasis predisposing to colonisation |
Episodic infectious illnesses with or without pulmonary infiltrates on CXR. |
Sputum cultures positive for colonising organism including previous cultures. |
Pseudomonas aeroginosa (Gram negative), Burkholderia cepacia (Gram negative), Staphylococcus aureus, the latter two more commonly in bronchiectasis. |
|
IV drug abuse often associated with social overcrowding and risky behaviour |
Signs of CAP +/-right sided valvular infective endocarditis e.g. tricuspid regurgitiation. |
Blood cultures and IV injection site swabs of underlying abscesses usually yield positive microbial growth |
Staphylococcus aureus, anaerobes, Mycobacterium tuberculosis, Streptococcus pneumoniae |
|
Recent hotel or cruise ship stay in last two weeks |
Clinical features similar to typical CAP + GI symptoms of nausea, vomiting and diarrhea |
Hyponatremia, elevated hepatic transaminases, raised inflammatory markers
CXR – unilobar infiltrates
Positive urine legionella antigen
|
Legionella pneumophila (Gram negative) |
|
‘Walking’ pneumonia – Mild symptoms but CXR shows infiltrates
Usually affects young adults, smokers
|
Predominant upper respiratory tract symptoms and extra-pulmonary manifestations like CNS e.g. encephalitis, hemolysis, skin signs |
Hyponatremia, elevated hepatic transaminases and inflammatory markers.
CXR – bronchopneumonia
Nasopharyngeal swab PCR positive.
Cold agglutinins.
|
Mycoplasma pneumoniae (No cell wall) |
If you are interested in learning why certain bacteria cause infections in certain pre-existing disease states like COPD, you can read more in my blog on the lung microbiome.
Pneumonia severity
There are various scoring systems to help us predict the prognosis or outcome, often defined as 30 day mortality. Like all scoring systems we must learn to understand their limitations which primarily stem from the populations from which these scoring systems were derived.
For instance, CURB-65 has not been validated in pregnant and immunocompromised patients. CURB-65 also over-estimates disease severity in the elderly and under-estimates it in younger patients because it has an age cut-off of 65. We must use severity scores as a second opinion to our clinical judgement but not replace it. (Read more on CURB-65 here)
3. Antibiotic therapy
There are two ways of deciding on which antibiotic to use in a given patient with CAP: pneumonia severity scores (like CURB-65 used in UK or pneumonia severity index) or site of care i.e. out-patients, in-patients or ICU (used in US).
Ultimately it is clinical judgement including recognition of an ill patient that helps in selecting the right antibiotic. We can use severity scores as a second opinion to our clinical judgement but not replace it.
From an exam perspective the choice of antibiotic is based on the suspected aetiology and the co-morbidities like drug allergy, immunosuppressed state etc. Study fugure 3 for a few minutes to understand the antibiotic spectrum in CAP.
Figure 3
Now use this to understand the antibiotic choices superimposed on table 1 in table 2. For a complete discussion on the rationale behind choosing antibiotics in CAP please read my blog here.
Table 2
| History | Examination | Laboratory tests | Aetiology | Antibiotic choice |
|---|---|---|---|---|
|
Brown, rusty phlegm |
Classic signs of lobar, or broncho-pneumonia, sepsis |
Neutrophilia, elevated CRP, positive urine pneumococcal antigen |
Streptococcus pneumoniae
(Gram positive) |
Amoxycillin/ Co-Amoxiclav or Clarithromycin (note resistance) |
|
Red currant jelly like sputum (from intense inflammation and necrosis of lung parenchyma), alcoholism, diabetes mellitus, COPD |
Classic signs of lobar or bronchopneumonia |
Neutrophilia, elevated CRP, bulging fissure sign on CXR |
Klebsiella pneumoniae
(Gram negative)
|
Co-Amoxiclav or newer macrolides
|
|
COPD |
Bronchopneumonia |
Neutrophilia, elevated CRP |
Haemophilus influenzae (Gram negative)
Moraxella catarrhalis (Gram negative) |
Co-Amoxiclav or Doxycycline |
|
Neurological disorders e.g. stroke, Parkinson’s are accompanied by swallowing disorders which predispose to aspiration pneumonia |
Signs of pneumonia in right lower lobe if aspirated in sitting position. If aspirated in sleeping position signs found in posterior segment of upper lobe and apical segment of lower lobe.
i.e. think of most dependent segment. |
Inflammatory marker rise. CXR may show cavitation as usually secondary to anaerobes. |
Oral anaerobes, gram negative enteric pathogens. |
Co-Amoxiclav |
|
Post-influenza secondary bacterial infection |
Classic signs of CAP. Subpleural pneumatocoeles can rupture causing pneumothorax if due to Staphylococus aureus. |
Inflammatory marker rise. CXR may show cavitation if due to Staphylococcus aureus
Lung abscess if due to community acquired MRSA
|
Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae
|
Co-Amoxiclav. If Community acquired MRSA is suspected – consider Vancomycin
|
|
Chronic structural lung disease e.g. COPD, bronchiectasis predisposing to colonisation |
Episodic infectious illnesses with or without pulmonary infiltrates on CXR. |
Sputum cultures positive for colonising organism including previous cultures. |
Pseudomonas aeroginosa (Gram negative), Burkholderia cepacia (Gram negative), Staphylococcus aureus, the latter two more commonly in bronchiectasis. |
Piperacillin-tazobactam or ciprofloxacin for Pseudomonas. Burkholderia – seek microbiology advice. |
|
IV drug abuse often associated with social overcrowding and risky behaviour |
Signs of CAP +/-right sided valvular infective endocarditis e.g. tricuspid regurgitiation. |
Blood cultures and IV injection site swabs of underlying abscesses usually yield positive microbial growth |
Staphylococcus aureus, anaerobes, Mycobacterium tuberculosis, Streptococcus pneumoniae |
MSSA – Nafcillin.
MRSA – see above. Tuberculosis – refer to specialist.
|
|
Recent hotel or cruise ship stay in last two weeks |
Clinical features similar to typical CAP + GI symptoms of nausea, vomiting and diarrhea |
Hyponatremia, elevated hepatic transaminases, raised inflammatory markers
CXR – unilobar infiltrates
Positive urine legionella antigen
|
Legionella pneumophila (Gram negative) |
Newer macrolides and respiratory fluoroquinolones |
|
‘Walking’ pneumonia – Mild symptoms but CXR shows infiltrates
Usually affects young adults, smokers
|
Predominant upper respiratory tract symptoms and extra-pulmonary manifestations like CNS e.g. encephalitis, hemolysis, skin signs |
Hyponatremia, elevated hepatic transaminases and inflammatory markers.
CXR – bronchopneumonia
Nasopharyngeal swab PCR positive.
Cold agglutinins.
|
Mycoplasma pneumoniae (No cell wall) |
Newer macrolides and respiratory fluoroquinolones |
References
Gennis, P. et al. (1989) ‘Clinical criteria for the detection of pneumonia in adults: guidelines for ordering chest roentgenograms in the emergency department.’, The Journal of emergency medicine, 7(3), pp. 263–8.
Jain, S. et al. (2015) ‘Community-Acquired Pneumonia Requiring Hospitalization among U.S. Adults.’, The New England journal of medicine, 373(5), pp. 415–27. doi: 10.1056/NEJMoa1500245.
Metlay, J. P., Kapoor, W. N. and Fine, M. J. (1997) ‘Does this patient have community-acquired pneumonia? Diagnosing pneumonia by history and physical examination.’, JAMA, 278(17), pp. 1440–5.
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