Pneumonia¶
Chapter 131 | Part 5: Infectious Diseases
KEY CLINICAL POINTS¶
- Pneumonia is classified as community-acquired (CAP), hospital-acquired (HAP), ventilator-associated (VAP), or healthcare-associated, with CAP being the most common and associated with significant morbidity/mortality.
- Key pathogens include Streptococcus pneumoniae, Haemophilus influenzae, Legionella spp., and MRSA, with increasing prevalence of drug-resistant organisms like Pseudomonas aeruginosa and Acinetobacter.
- Diagnosis relies on clinical criteria (e.g., CURB-65, PSI), imaging, and microbiological tests (sputum cultures, PCR, urinary antigens), with empirical therapy guided by local resistance patterns.
- Treatment involves de-escalation of antibiotics based on culture results, with ICU admission required for severe cases (e.g., respiratory failure, septic shock).
- Prevention strategies include minimizing intubation duration, elevating head of bed, and strict infection control to reduce VAP incidence.
1. DEFINITION & OVERVIEW¶
Pneumonia is an infection of the pulmonary parenchyma, often misdiagnosed and under-treated. It is classified as community-acquired (CAP), hospital-acquired (HAP), ventilator-associated (VAP), or healthcare-associated. Aspiration pneumonia is a subset of CAP/HAP, with risk factors including poor dentition, structural lung disease, and impaired consciousness.
Table 131-1: Microbial Causes of Community-Acquired Pneumonia¶
| Site of Care | Outpatients | Hospitalized Patients (Non-ICU) | Hospitalized Patients (ICU) |
|---|---|---|---|
| Streptococcus pneumoniae | Streptococcus pneumoniae | Streptococcus pneumoniae | Streptococcus pneumoniae |
| Mycoplasma pneumoniae | Mycoplasma pneumoniae | Mycoplasma pneumoniae | Mycoplasma pneumoniae |
| Haemophilus influenzae | Haemophilus influenzae | Haemophilus influenzae | Haemophilus influenzae |
| Chlamydia pneumoniae | Chlamydia pneumoniae | Chlamydia pneumoniae | Chlamydia pneumoniae |
| Respiratory viruses | Respiratory viruses | Respiratory viruses | Respiratory viruses |
Table 131-2: Epidemiologic Factors Suggesting Possible Causes of Community-Acquired Pneumonia¶
| Factor | Possible Pathogen(s) |
|---|---|
| Alcoholism | Streptococcus pneumoniae, oral anaerobes, Klebsiella pneumoniae, Acinetobacter spp., Mycobacterium tuberculosis |
| Factor | Possible Pathogen(s) |
|---|---|
| COPD and/or smoking | Haemophilus influenzae, Pseudomonas aeruginosa, Legionella spp. |
| Chronic lung disease | Pseudomonas aeruginosa, Burkholderia cepacia, Staphylococcus aureus |
| Recent hospitalization | Respiratory viruses, S. pneumoniae, S. aureus, Gram-negative bacilli |
| Immunosuppression | Pneumocystis jirovecii, Mycobacterium tuberculosis, Cytomegalovirus |
1.1 Pathophysiology¶
Pneumonia results from microbial proliferation in the alveoli and host immune response. Inflammation, cytokine release, and microbial toxins drive disease progression. Aspiration of oropharyngeal contents is a key trigger, with positive feedback loops exacerbating inflammation and bacterial growth.
1.2 Clinical Spectrum¶
Ranges from mild (e.g., viral pneumonia) to severe (e.g., necrotizing pneumonia). Aspiration pneumonia often presents with localized infiltrates, while CAP typically involves lobar patterns. VAP is associated with higher mortality due to multidrug-resistant pathogens.
2. EPIDEMIOLOGY¶
CAP affects ~7 million annually in the U.S., with 16–23/1000 incidence in adults. Mortality ranges from <5% in outpatients to 40% in hospitalized patients. VAP occurs in 6–52/100 ventilated ICU patients, with 70% of HAP cases acquired outside the ICU. Risk factors include advanced age, immunosuppression, and prior antibiotic use.
2.1 CAP Statistics¶
CAP is the 8th leading cause of death in the U.S., with ~60,000 annual deaths. 30% of patients are hospitalized, costing ~$17 billion yearly. 18% of hospitalized patients are readmitted within 1 month.
2.2 VAP Trends¶
VAP incidence peaks in the first 5 days of ventilation, with ~1% per day thereafter. 70% of HAP cases occur outside the ICU. VAP is associated with 50–70% crude mortality but 5–10% attributable mortality in non-COVID cases.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
CAP is caused by bacteria (S. pneumoniae, H. influenzae), viruses (influenza, RSV), and atypical pathogens (Mycoplasma, Chlamydia). VAP is driven by oropharyngeal colonization, aspiration, and immune compromise. Aspiration pneumonia often involves anaerobes and gram-negative rods. MRSA and P. aeruginosa are increasingly common in ICU settings.
3.1 Microbial Resistance¶
Pneumococcal resistance to penicillin (MIC ≥ 0.1 µ g/mL) is 58.9% in the U.S. Macrolide resistance in S. pneumoniae is 40–60% in some regions. P. aeruginosa resistance to β -lactams and fluoroquinolones is common, with 25–40% resistance in some countries.
3.2 Pathogenesis¶
Inflammation, cytokine release, and microbial toxins drive pneumonia. Aspiration of oropharyngeal contents leads to alveolar damage, neutrophil infiltration, and capillary leak. Positive feedback loops amplify inflammation and bacterial growth.
4. CLINICAL FEATURES¶
Symptoms include fever, cough, dyspnea, and pleuritic chest pain. Physical findings may include crackles, tactile fremitus, and decreased breath sounds. Severe cases present with hypoxemia, respiratory failure, or septic shock. Aspiration pneumonia often has localized infiltrates, while CAP typically involves lobar patterns.
4.1 Aspiration Pneumonia¶
Often presents with localized infiltrates, often in dependent lung regions. May have a history of dysphagia, stroke, or alcoholism. Risk factors include poor dentition, lung abscess, and empyema.
4.2 Viral Pneumonia¶
Common in elderly and immunocompromised. Presents with nonproductive cough, low-grade fever, and interstitial infiltrates. Often associated with influenza or RSV.
5. DIFFERENTIAL DIAGNOSIS¶
Acute bronchitis, heart failure, pulmonary embolism, and interstitial lung disease must be considered. Viral pneumonia (e.g., influenza) and atypical pathogens (e.g., Mycoplasma) may mimic bacterial CAP. Pulmonary embolism and pleural effusion can mimic pneumonia on imaging.
5.1 Noninfectious Mimics¶
Pulmonary edema, interstitial lung disease, and malignancy can mimic pneumonia. Cardiac decompensation and drug-induced lung injury may present with similar findings.
5.2 Atypical Pathogens¶
Mycoplasma and Chlamydia infections may present with nonproductive cough and interstitial infiltrates. Legionella is associated with waterborne outbreaks and hyponatremia.
6. INVESTIGATIONS & DIAGNOSIS¶
Chest radiography is the primary diagnostic tool, with infiltrates in dependent lung regions. Blood cultures have low yield (<15% positive). Urinary antigens for S. pneumoniae and Legionella are sensitive (70–99%). PCR detects viral and atypical pathogens. CURB-65 and PSI scores guide severity assessment.
Table 131-3: Criteria for Severe Community-Acquired Pneumonia¶
| Minor Criteria | Major Criteria |
|---|---|
| Respiratory rate ‡30/min | Respiratory failure requiring invasive ventilation |
| PaO2/FiO2 £250 | Septic shock requiring vasopressors |
| Multilobar infiltrates | |
| Confusion/disorientation |
| Minor Criteria | Major Criteria |
|---|---|
| Uremia (BUN ‡20 mg/dL) | |
| Leukopenia (WBC <4000/mL) | |
| Thrombocytopenia (platelets <100,000/mL) | |
| Hypothermia (core temp <36°C) | |
| Hypotension requiring fluid resuscitation |
6.1 Diagnostic Criteria¶
CURB-65: Confusion, urea >7 mmol/L, respiratory rate ≥ 30, blood pressure ≤ 90/60, age ≥ 65. PSI: 20 variables (age, comorbidities, lab findings) with mortality rates 0.1–29.2% across 5 classes.
6.2 Microbiological Tests¶
Sputum Gram stain and culture ( ≥ 25 neutrophils/HPF) identify pathogens. Urinary antigens for S. pneumoniae and Legionella are sensitive. PCR detects viral and atypical pathogens in respiratory secretions.
7. MANAGEMENT & TREATMENT¶
Empirical therapy covers S. pneumoniae, atypical pathogens, and MRSA. Outpatient treatment: amoxicillin/clavulanate or doxycycline. Inpatient: β -lactam + macrolide or fluoroquinolone. De-escalation based on culture results. ICU admission for respiratory failure, septic shock, or severe comorbidities.
Table 131-4: Initial Treatment Strategies for Outpatients¶
| Status | Standard Regimen |
|---|---|
| No comorbidities or resistance risk factors | Amoxicillin (1 g tid) + macrolide or doxycycline |
| Monotherapy | Doxycycline (100 mg bid) or macrolide |
| With comorbidities | Amoxicillin/clavulanate + macrolide or cephalosporin |
Table 131-5: Initial Treatment for Inpatients¶
| Disease Severity/Risk Status | Regimen |
|---|---|
| Nonsevere, no risk factors | b-lactam + macrolide or respiratory fluoroquinolone |
| Severe, no risk factors | b-lactam + macrolide or fluoroquinolone |
| Nonsevere with MRSA/P. aeruginosa risk | Piperacillin-tazobactam or ceftazidime |
7.1 Antibiotic Selection¶
For CAP: amoxicillin/clavulanate, doxycycline, or respiratory fluoroquinolone. For VAP: piperacillin-tazobactam, ceftazidime, or meropenem. MRSA: vancomycin or linezolid. P. aeruginosa: carbapenem or ceftazidime-avibactam.
7.2 Duration of Therapy¶
Uncomplicated CAP: 5–7 days. Severe CAP or bacteremia: 7–14 days. VAP: 7–14 days, with de-escalation based on culture results. Prolonged courses increase MDR risk.
8. PROGNOSIS & COMPLICATIONS¶
Mortality varies from <5% in outpatients to 40% in hospitalized patients. Complications include respiratory failure, septic shock, and metastatic infection. VAP is associated with prolonged ICU stays and higher mortality. Recurrent VAP is common due to biofilm formation on endotracheal tubes.
8.1 Mortality Rates¶
CAP: 5–10% mortality. VAP: 50–70% crude mortality, but 5–10% attributable mortality. MRSA pneumonia: 40% failure rate with standard vancomycin.
8.2 Long-Term Effects¶
Chronic lung disease, bronchiectasis, and recurrent pneumonia may develop. Elderly patients may experience prolonged disability or nursing home placement.
9. SPECIAL CONSIDERATIONS¶
Pregnancy: Avoid fluoroquinolones; use amoxicillin/clavulanate. Pediatrics: Atypical pathogens (Mycoplasma, Chlamydia) are common. Elderly: Higher risk of aspiration and drug interactions. Immunocompromised: Risk of fungal or viral pneumonia (e.g., Pneumocystis).
9.1 Antimicrobial Stewardship¶
Avoid prolonged antibiotic courses to reduce MDR risk. De-escalate therapy based on culture results. Use biomarkers (procalcitonin) to guide duration.
9.2 Prevention Strategies¶
Minimize intubation duration, elevate head of bed, and use chlorhexidine for oral care. Implement strict infection control to prevent cross-transmission.
10. KEY POINTS & CLINICAL PEARLS¶
- Use CURB-65 and PSI to assess severity and guide ICU admission.
- Empirical therapy should cover S. pneumoniae, atypical pathogens, and MRSA.
- De-escalate antibiotics based on culture results and clinical response.
- Prevent VAP with early extubation, head-of-bed elevation, and infection control.
- Monitor for treatment failure (e.g., worsening oxygenation, new infiltrates) and adjust therapy accordingly.