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Pneumonia, an infection of the lung parenchyma, is classified as community-acquired (CAP), hospital-acquired (HAP), ventilator-associated (VAP), or health care-associated (HCAP). Although the HCAP category initially referred to CAP caused by a multidrug-resistant (MDR) pathogen, it now describes pts with at least two or three risk factors for infection with MDR pathogens (Table 134-1 Risk Factors for Pathogens Resistant to Usual Therapy for Community-Acquired Pneumoniaa ).

Pathophysiology !!navigator!!

  • Microorganisms gain access to the lower respiratory tract via microaspiration from the oropharynx (the most common route), hematogenous spread, or contiguous extension from an infected pleural or mediastinal space.
  • Many CAP pathogens are components of the normal alveolar microbiota, which is similar to the oropharyngeal microbiota. This observation suggests that alterations in host defenses (e.g., alveolar macrophage activity, surfactant proteins A and D, mucociliary elevator function) allow overgrowth of one or more components of the normal bacterial microbiota. The two most likely sources of an altered alveolar microbiota are viral upper respiratory tract infections for CAP and antibiotic therapy for HAP/VAP.
  • Classic pneumonia (typified by that due to Streptococcus pneumoniae) presents as a lobar pattern and evolves through four phases characterized by changes in the alveoli:
    • Edema: Proteinaceous exudates are present in the alveoli.
    • Red hepatization: Erythrocytes and neutrophils are present in the intra-alveolar exudate.
    • Gray hepatization: Neutrophils and fibrin deposition are abundant.
    • Resolution: Macrophages are the dominant cell type.
  • In VAP, respiratory bronchiolitis can precede a radiologically apparent infiltrate.

Community-Acquired Pneumonia !!navigator!!

Microbiology !!navigator!!

Although many bacteria, viruses, fungi, and protozoa can cause CAP, most cases are caused by relatively few pathogens. In >50% of cases, a specific etiology is never determined.

  • Typical bacterial pathogens include S. pneumoniae, Haemophilus influenzae, Staphylococcus aureus, and gram-negative bacteria such as Klebsiella pneumoniae and Pseudomonas aeruginosa.
    • – The incidence of pneumococcal pneumonia is decreasing because of the increasing use of pneumococcal vaccines.
  • Atypical organisms include Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella spp., and respiratory viruses (e.g., influenza viruses, adenoviruses, human metapneumovirus, respiratory syncytial viruses).
    • A virus may be responsible for a large proportion of CAP cases that require hospital admission, even in adults.
    • Of CAP cases, 10-15% are polymicrobial and involve a combination of typical and atypical organisms.
    • The incidences of cases due to M. pneumoniae and C. pneumoniae are increasing, particularly among young adults.
  • Involvement of anaerobes, which play a significant role in CAP only when aspiration precedes presentation by days or weeks, often results in significant empyemas.

Epidemiology !!navigator!!

CAP affects >5 million adults each year in the United States, 80% of whom are treated on an outpatient basis. CAP causes >55,000 deaths annually and is associated with an overall yearly cost of $17 billion.

  • The incidence of CAP is highest at the extremes of age (i.e., <4 and >60 years).
  • Risk factors for CAP include alcoholism, asthma, immunosuppression, institutionalization, and an age of 70 years (vs 60-69 years).
  • Many factors-e.g., tobacco smoking, chronic obstructive pulmonary disease, colonization with methicillin-resistant S. aureus (MRSA), recent hospitalization or antibiotic therapy-influence the types of pathogens that should be considered in the etiologic diagnosis.

Clinical Manifestations !!navigator!!

Pts frequently have fever, chills, sweats, cough (either nonproductive or productive of mucoid, purulent, or blood-tinged sputum), pleuritic chest pain, and dyspnea.

  • Other common symptoms include nausea, vomiting, diarrhea, fatigue, headache, myalgias, and arthralgias.
  • Elderly pts may present atypically, with confusion but few other manifestations.
  • Physical examination often reveals tachypnea; increased or decreased tactile fremitus; dull or flat percussion reflecting consolidation and pleural fluid, respectively; crackles; bronchial breath sounds; or a pleural friction rub.

Diagnosis !!navigator!!

Both confirmation of the diagnosis and assessment of the likely etiology are required. Although no data have demonstrated that treatment directed at a specific pathogen is superior to empirical treatment, an etiologic diagnosis allows narrowing of the empirical regimen, identification of organisms with public safety implications (e.g., Mycobacterium tuberculosis, influenza virus), and monitoring of antibiotic susceptibility trends.

  • CXR is often required to differentiate CAP from other conditions, particularly since the sensitivity and specificity of physical examination findings for CAP are only 58% and 67%, respectively.
    • CT of the chest may be helpful for pts with suspected postobstructive pneumonia or suspected cavitary disease.
    • Some radiographic patterns suggest an etiology; e.g., pneumatoceles suggest S. aureus.
  • Sputum samples must have >25 WBCs and <10 squamous epithelial cells per high-power field to be appropriate for culture. The sensitivity of sputum cultures is highly variable; in cases of proven bacteremic pneumococcal pneumonia, the yield of positive cultures from sputum samples is 50%.
  • Blood cultures are positive in 5-14% of cases, most commonly yielding S. pneumoniae. Blood cultures are optional for most CAP pts but should be performed for high-risk pts (e.g., pts with chronic liver disease or asplenia).
  • Urine antigen tests for S. pneumoniae and Legionella pneumophila type 1 can be helpful.
  • PCR of nasopharyngeal swabs has become the standard for diagnosis of respiratory viral infection and is also useful for detection of many atypical bacteria.
  • Serology: A fourfold rise in titer of specific IgM antibody can assist in the diagnosis of pneumonia due to some pathogens; however, the time required to obtain a final result and difficulty of interpretation limits the clinical utility of serology.
  • Biomarkers: Serial measurements of C-reactive protein (CRP) levels in serum may help identify worsening disease or treatment failure. Measurement of serum procalcitonin (PCT) levels can help distinguish bacterial from viral infection, determine the need for antibacterial therapy, or determine when to discontinue treatment.
TREATMENT

Community-Acquired Pneumonia

DECIDING WHETHER TO HOSPITALIZE PTS

  • Two sets of criteria identify pts who will benefit from hospital care. It is not clear which set is superior, and application of each tool should be tempered by a consideration of factors relevant to the individual pt.
    • Pneumonia Severity Index (PSI): Points are given for 20 variables, including age, coexisting illness, and abnormal physical and laboratory findings. On this basis, pts are assigned to one of five classes of mortality risk.
    • CURB-65: Five variables are included: confusion (C); urea >7 mmol/L (U); respiratory rate 30/min (R); blood pressure, systolic 90 mmHg or diastolic 60 mmHg (B); and age 65 years (65). Pts with a score of 0 can be treated at home, pts with a score of 1 or 2 (not counting any point given for age 65 years) should be hospitalized, and pts with a score of 3 may require management in the ICU.

SELECTING ANTIBIOTIC THERAPY

  • For recommendations on empirical antibiotic treatment of CAP, see Table 134-2 Empirical Antibiotic Treatment of Community-Acquired Pneumonia. U.S. guidelines always target S. pneumoniae and atypical pathogens. Retrospective data suggest that this approach lowers the mortality rate.
  • Pts initially treated with IV antibiotics can be switched to oral agents when they can ingest and absorb drugs, are hemodynamically stable, and are improving clinically.
  • A 5-day course of a fluoroquinolone is sufficient for cases of uncomplicated CAP, but a longer course may be required for pts with bacteremia, metastatic infection, or infection with a particularly virulent pathogen (e.g., P. aeruginosa, community-acquired MRSA).
  • Fever and leukocytosis usually resolve within 2-4 days. Pts who have not responded to therapy by day 3 should be reevaluated, with consideration of alternative diagnoses, antibiotic resistance in the pathogen, and the possibility that the wrong drug is being given.

Complications

Common complications of severe CAP include respiratory failure, shock and multiorgan failure, coagulopathy, cardiac complications (e.g., MI, CHF, arrhythmias), and exacerbation of comorbid disease. Metastatic infection (e.g., brain abscess, endocarditis) occurs rarely and requires immediate attention.

  • Lung abscess (see below) may occur in association with aspiration or infection caused by single CAP pathogens (e.g., community-acquired MRSA or P. aeruginosa). Drainage should be established and proper antibiotics administered.
  • Any significant pleural effusion should be tapped for diagnostic and therapeutic purposes. If the fluid has a pH <7, a glucose level <2.2 mmol/L, and an LDH content >1000 U or if bacteria are seen or cultured, fluid should be drained; a chest tube is usually required.

Follow-Up

CXR abnormalities may require 4-12 weeks to clear. Pts should receive influenza and pneumococcal vaccines, as appropriate.

Outline

Section 9. Pulmonology