Community-Acquired Pneumonia (CAP)

A 68-year-old man with a history of diabetes mellitus, COPD, and chronic smoking presents with 4 days of fever, productive cough, pleuritic chest pain, and progressive shortness of breath. His family reports new-onset confusion since this morning. He has had no recent hospitalizations or antibiotic use. On examination, his temperature is 38.8°C, heart rate 112/min, respiratory rate 32/min, blood pressure 92/58 mm Hg, and oxygen saturation 88% on room air. Chest examination reveals dullness to percussion, bronchial breath sounds, and crackles over the right lower lung field. Laboratory studies show leukocytosis, elevated CRP, mild hyponatremia, and elevated blood urea nitrogen. A chest X-ray demonstrates right lower lobe consolidation. Diagnosis?

Diagnosis is community-acquired pneumonia (CAP).

1. Definition

Community-acquired pneumonia is an acute infection of the lung parenchyma acquired outside hospital settings, characterized by:

1.1 Diagnostic Criteria

1. Symptoms and/or signs of lower respiratory tract infection
2. New pulmonary infiltrate on imaging
3. Supportive systemic or laboratory features of inflammation

There is no single gold-standard diagnostic test, and clinical examination alone cannot confirm the diagnosis. Imaging is a key step in securing it.

2. Etiology

2.1 Common Bacterial Causes

1. Streptococcus pneumoniae most frequently detected bacterial cause worldwide
2. Haemophilus influenzae
3. Staphylococcus aureus
4. Enterobacteriaceae spp.

2.2 Atypical Pathogens

1. Mycoplasma pneumoniae
2. Chlamydophila pneumoniae
3. Legionella pneumophila

2.3 Viral Causes

1. Influenza A and B
2. Rhinovirus
3. RSV
4. Human metapneumovirus
5. Parainfluenza viruses
6. Coronaviruses, including SARS-CoV-2 in the right context

Respiratory viruses are detectable in about one-third of adults with CAP, and viral–bacterial co-infection is important clinically.

2.4 Special Clinical Settings

1. Alcohol misuse, aspiration risk, or neurologic depressants increase susceptibility
2. Profound immunocompromise raises concern for opportunistic pathogens
3. Risk factors for MRSA or Pseudomonas aeruginosa should guide broader empiric therapy rather than severity alone

3. Pathophysiology

3.1 Route of Infection

1. Most bacterial CAP arises via microaspiration of pharyngeal secretions
2. Inhalation of infectious particles also contributes, especially in viral CAP

3.2 Core Process

1. Pathogens proliferate in the lower respiratory tract
2. Macrophages initiate cytokine and chemokine release
3. Neutrophils and inflammatory monocytes are recruited
4. Alveolar epithelial injury leads to edema, exudate, and impaired gas exchange

3.3 Consequences

1. Breathlessness, fever, hypoxia, and sometimes hypercarbia
2. Severe disease may progress to sepsis, shock, and extrapulmonary organ failure

4. Physiological Consequences

1. Ventilation–perfusion mismatch
2. Hypoxemia
3. Increased work of breathing
4. In severe disease: acute respiratory failure, septic shock, and multiorgan dysfunction

5. Classification and Severity

5.1 By Setting

1. Community-acquired pneumonia
2. Hospital-acquired pneumonia
3. Ventilator-associated pneumonia

5.2 CURB-65

1. Confusion
2. Urea >7 mmol/L or BUN >19 mg/dL
3. Respiratory rate ≥30/min
4. Blood pressure <90 systolic or ≤60 diastolic
5. Age ≥65 years

5.2.1 Interpretation

1. 0–1 low risk, outpatient usually appropriate
2. 2 consider admission
3. ≥3 severe CAP, consider ICU

5.3 IDSA/ATS Severe CAP Criteria

5.3.1 Major criteria

1. Need for invasive mechanical ventilation
2. Septic shock requiring vasopressors

5.3.2 Minor criteria

1. Respiratory rate >30/min
2. PaO₂/FiO₂ <250
3. Multilobar infiltrates
4. Confusion or disorientation
5. BUN ≥20 mg/dL
6. Leukocyte count <4000/μL
7. Platelets <100000/μL
8. Core temperature <36°C
9. Hypotension requiring aggressive fluid resuscitation

Severe CAP is diagnosed by 1 major or 3 or more minor criteria.

6. Clinical Features

6.1 Symptoms

1. Cough, often productive
2. Dyspnea
3. Pleuritic chest pain
4. Fever

6.2 Signs

1. Tachypnea
2. Rales or rhonchi
3. Dullness to percussion
4. Egophony
5. Bronchial breathing may indicate consolidation

6.3 Atypical Presentation

1. Older adults may have confusion or functional decline rather than classic symptoms
2. Immunocompromised patients may have mild respiratory symptoms despite significant disease

7. Diagnosis

7.1 Laboratory Features

1. Leukocyte count <4000/μL or >10000/μL can support the diagnosis
2. Neutrophilia or bandemia may be present
3. CRP and procalcitonin may be elevated

Important correction: CRP and procalcitonin have only modest diagnostic performance and should not be used to decide whether to start antibiotics. Procalcitonin may assist antibiotic discontinuation in selected patients.

7.2 Imaging

1. Chest radiography is standard first-line imaging
2. CT is more sensitive and is advised for uncertain or inconclusive cases
3. Lung ultrasound can be a valid alternative where expertise is available
4. Dynamic air bronchograms are a highly specific sonographic sign
5. Lung ultrasound is helpful but does not have enough sensitivity to rule out pneumonia

7.3 Microbiology

1. Low-severity community-managed CAP usually does not require routine microbiological sampling
2. Hospitalized patients often have sputum and blood cultures, though yield is low
3. Urinary antigen tests are available for S pneumoniae and L pneumophila
4. Antigen tests have good positive predictive value, but false negatives are common and they do not exclude co-infection

7.4 Molecular Testing

1. NAATs improve pathogen detection, especially for viruses and atypicals
2. Influenza and SARS-CoV-2 testing is recommended when exposure is suspected or circulating
3. Expanded viral testing may be useful in severe CAP
4. Evidence that syndromic NAATs reliably change antibiotic prescribing remains uncertain

8. Management

8.1 Empirical Antimicrobial Therapy

8.1.1 Outpatient

1. Amoxicillin or doxycycline
2. If chronic lung disease or asplenia: amoxicillin-clavulanate or oral cephalosporin plus macrolide or doxycycline
3. If allergic: respiratory fluoroquinolone
4. If respiratory viral PCR positive and no comorbidity and no suspicion of bacterial co-infection, empiric antibacterials may be avoided; with comorbidity, consider empiric antibacterials

8.1.2 Hospital ward

1. Beta-lactam plus macrolide is standard
2. Respiratory fluoroquinolone is an alternative in selected cases

8.1.3 ICU / severe CAP

1. Broad treatment is guided by risk factors and likely pathogens
2. If prior MRSA or Pseudomonas infection or recent hospitalization with IV antibiotics, use MRSA plus antipseudomonal coverage
3. In severe influenza, oseltamivir is recommended

8.2 Key Stewardship Principles

1. Severity alone is not a reason to add antipseudomonal or anti-MRSA agents
2. Known carriage, prior colonization, or recent IV antibiotics are important risk factors
3. If empiric MDR coverage is started, de-escalate rapidly when screening is negative

8.3 Anaerobic Coverage

Routine anaerobic coverage is not recommended, even when aspiration is present, unless there is a specific complication such as abscess or another clear indication.

8.4 Adjunctive Therapy

1. Corticosteroids are not recommended for non-severe CAP
2. For severe CAP, corticosteroids are suggested, except in influenza pneumonia
3. Guidelines are more supportive when septic shock coexists

8.5 Duration of Therapy

1. Minimum 5 days AND until clinical stability is achieved
2. Outpatient: 3–5 days
3. Inpatient without ICU: 5–7 days
4. ICU: 7–10 days, tailored to response and microbiology
5. Prolonged courses should be avoided unless specific indications (necrotizing pneumonia, empyema, bacteremia, S aureus, Pseudomonas, Legionella, or slow response)

9. Acute Severe CAP

1. Early antibiotics should not be delayed by testing
2. Oxygen and ventilatory support as needed
3. Vasopressors for septic shock
4. ICU admission based on severity criteria and organ support needs

10. Prognosis and Monitoring

1. Hospitalized CAP 30-day mortality: 4.1% to 9.6%
2. ICU CAP 30-day mortality up to 49.4%
3. Clinical stability guides transition to oral therapy and discharge
4. Stability criteria include afebrile, HR <100, RR <24, adequate oxygenation, and SBP >90 mm Hg

11. Long-Term Follow-Up

1. CAP has important post-acute sequelae
2. Persistent respiratory dysfunction, bronchiectasis risk, and COPD exacerbations can occur
3. Follow-up imaging not required if symptoms resolve
4. Imaging at 4–6 weeks if persistent symptoms or lung cancer risk factors
5. Cardiovascular complications: MI, arrhythmias, heart failure, stroke
6. Rehabilitation, vaccination, smoking cessation, cardiovascular risk management

12. Key Clinical Insight

Fever + cough + dyspnea + new infiltrate on imaging strongly indicates CAP. Early severity assessment (CURB-65) determines the site of care and guides initial management.

13. Exam Level Pearls

1. Streptococcus pneumoniae is the most common cause
2. Viral CAP common (~30%)
3. Imaging required for diagnosis
4. Procalcitonin → de-escalation, not initiation
5. Dynamic air bronchograms support diagnosis
6. Do not add MRSA/Pseudomonas coverage without risk factors
7. Do not routinely add anaerobic coverage
8. Steroids: no in non-severe, yes in severe non-influenza CAP