(See also Chap. 81: Infections Acquired in Health Care Facilities)



Potential etiologic agents of VAP include MDR and non-MDR pathogens; the prominence of the various pathogens depends on the length of hospital stay at the time of infection and the presence of other risk factors.

Epidemiology, Pathogenesis, and Clinical Manifestations

Prevalence estimates of VAP are 6–52 cases per 100 pts, with the highest hazard ratio in the first 5 days of mechanical ventilation.

  • Three factors important in the pathogenesis of VAP are colonization of the oropharynx with pathogenic microorganisms, aspiration of these organisms to the lower respiratory tract, and compromise of normal host defense mechanisms.
  • Clinical manifestations are similar to those in other forms of pneumonia.


Application of clinical criteria consistently results in overdiagnosis of VAP. Use of quantitative cultures to discriminate between colonization and true infection by determining bacterial burden results in less antibiotic use and lower mortality. The more distal in the respiratory tree the diagnostic sampling, the more specific the results.

Treatment: Ventilator-Associated Pneumonia

  • See Table 134-3 for recommended options for empirical therapy for VAP.
    • Higher mortality rates are associated with inappropriate initial empirical treatment.
    • Broad-spectrum treatment should be modified when a pathogen is identified.
    • Clinical improvement, if it occurs, is usually evident within 48–72 h of the initiation of antimicrobial treatment.
  • Treatment failure in VAP is not uncommon, especially when MDR pathogens are involved; MRSA and P. aeruginosa are associated with high failure rates.
  • VAP complications include prolongation of mechanical ventilation, increased length of ICU stay, and necrotizing pneumonia with pulmonary hemorrhage or bronchiectasis. VAP is associated with significant mortality risk.
  • Strategies effective for the prevention of VAP are listed in Table 134-4.
TABLE 134-3: Empirical Antibiotic Treatment of Hospital-Acquired and Ventilator-Associated Pneumonia

Piperacillin-tazobactam (4.5 g IV q6hb)

Cefepime (2 g IV q8h)

Levofloxacin (750 mg IV q24h)

Piperacillin-tazobactam (4.5 g IV q6hb)

Cefepime (2 g IV q8h)

Ceftazidime (2 g IV q8h)

Imipenem (500 mg IV q6hb)

Meropenem (1 g IV q8h)

Amikacin (15–20 mg/kg IV q24h)

Gentamicin (5–7 mg/kg IV q24h)

Tobramycin (5–7 mg/kg IV q24h)

Ciprofloxacin (400 mg IV q8h)

Levofloxacin (750 mg IV q24h)

Colistin (loading dose of 5 mg/kg IV followed by maintenance doses of 2.5 mg × [1.5 × CrCl + 30] IV q12h)

Polymyxin B (2.5–3.0 mg/kg per day IV in 2 divided doses)

Risk factors for MRSAb (add to above)

Linezolid (600 mg IV q12h) or

Adjusted-dose vancomycin (trough level, 15–20 mg/dL)

aPrior antibiotic therapy, prior hospitalization, local antibiogram.
bPrior antibiotic therapy, prior hospitalization, known MRSA colonization, chronic hemodialysis, local documented MRSA pneumonia rate >10% (or local rate unknown).
Abbreviations: CrCl, creatinine clearance rate; MRSA, methicillin-resistant Staphylococcus aureus.
TABLE 134-4: Pathogenic Mechanisms and Corresponding Prevention Strategies for Ventilator-Associated Pneumonia
Oropharyngeal colonization with pathogenic bacteria 
 Elimination of normal floraAvoidance of prolonged antibiotic courses
 Large-volume oropharyngeal aspiration around time of intubationShort course of prophylactic antibiotics for comatose ptsa
 Gastroesophageal refluxPostpyloric enteral feedingb; avoidance of high gastric residuals, prokinetic agents
 Bacterial overgrowth of stomachAvoidance of prophylactic agents that raise gastric pHb; selective decontamination of digestive tract with nonabsorbable antibioticsb
Cross-infection from other colonized ptsHand washing, especially with alcohol-based hand rub; intensive infection control educationa; isolation; proper cleaning of reusable equipment
Large-volume aspirationEndotracheal intubation; rapid-sequence intubation technique; avoidance of sedation; decompression of small-bowel obstruction
Microaspiration around endotracheal tube 
 Endotracheal intubationNoninvasive ventilationa
 Prolonged duration of ventilationDaily awakening from sedation,a weaning protocolsa
 Abnormal swallowing functionEarly percutaneous tracheostomya
 Secretions pooled above endotracheal tubeHead of bed elevateda; continuous aspiration of subglottic secretions with specialized endotracheal tubea; avoidance of reintubation; minimization of sedation and pt transport
Altered lower respiratory host defensesTight glycemic controlb; lowering of hemoglobin transfusion threshold
aStrategies demonstrated to be effective in at least one randomized controlled trial.
bStrategies with negative randomized trials or conflicting results.


Less well studied than VAP, HAP more commonly involves non-MDR pathogens. Anaerobes may also be more commonly involved in non-VAP pts because of the increased risk of macroaspiration in pts who are not intubated.


Etiology and Epidemiology

Bronchiectasis is an irreversible airway dilation that involves the lung in either a focal (due to obstruction) or a diffuse (due to a systemic or infectious process) manner. Bronchiectasis can arise from infectious or noninfectious causes.

  • The epidemiology varies greatly with the underlying etiology; in general, the incidence of bronchiectasis increases with age and is higher among women than among men.
  • Of pts with bronchiectasis, 25–50% have idiopathic disease.


The most widely cited mechanism of infectious bronchiectasis is the “vicious cycle hypothesis,” in which susceptibility to infection and poor mucociliary clearance result in microbial colonization of the bronchial tree. Proposed mechanisms for noninfectious bronchiectasis include immune-mediated reactions that damage the bronchial wall and parenchymal distortion as a result of lung fibrosis (e.g., postradiation fibrosis or idiopathic pulmonary fibrosis).

Clinical Manifestations

Presenting pts typically have a persistent productive cough with ongoing production of thick, tenacious sputum.

  • Physical examination usually reveals crackles and wheezing on lung auscultation and occasionally reveals digital clubbing.
  • Acute exacerbations are associated with increased production of purulent sputum.


The diagnosis of bronchiectasis is based on clinical presentation with consistent CXR findings, such as parallel “tram tracks,” a “signet-ring sign” (a cross-sectional area of the airway with a diameter at least 1.5 times that of the adjacent vessel), lack of bronchial tapering, bronchial wall thickening, or cysts emanating from the bronchial wall.

Treatment: Bronchiectasis

Treatment of infectious bronchiectasis is directed at the control of active infection and at improvements in secretion clearance and bronchial hygiene.

  • Acute exacerbations should be treated with a 7- to 10-day course of antibiotics targeting the causative or presumptive pathogen; H. influenzae and P. aeruginosa are isolated commonly.
  • Hydration and mucolytic administration, aerosolization of bronchodilators and hyperosmolar agents (e.g., hypertonic saline), and chest physiotherapy can be used to enhance secretion clearance.
  • For pts with three or more recurrences per year, suppressive antibiotic treatment to minimize the microbial load and reduce the frequency of exacerbations has been proposed.
  • In select cases, surgery (including lung transplantation) should be considered.



Lung abscess—necrosis and cavitation of the lung following microbial infection—can be categorized as primary (∼80% of cases) or secondary; alternatively, it can be categorized as acute (<4–6 weeks in duration) or chronic (∼40% of cases).

  • Primary lung abscesses usually arise from aspiration in the absence of an underlying pulmonary or systemic condition, are often polymicrobial (primarily including anaerobic organisms and microaerophilic streptococci), and occur preferentially in dependent segments (posterior upper and superior lower lobes) of the right lung.
  • Secondary lung abscesses arise in the setting of an underlying condition (e.g., a postobstructive process, an immunocompromising condition) and can be due to a number of different organisms, among which P. aeruginosa and other gram-negative rods are most common.

Clinical Manifestations

Initial presentation of lung abscess may be similar to that of pneumonia.

  • Anaerobic lung abscesses may have a more chronic and indolent presentation, with night sweats, fatigue, and anemia; in addition, pts may have discolored phlegm and foul-tasting or foul-smelling sputum.
  • Pts with lung abscesses due to non-anaerobic organisms (e.g., S. aureus) may present with a more fulminant course characterized by high fevers and rapid progression.


Chest CT is the preferred radiographic study for precise delineation of the lesion.

  • It is not clear whether invasive diagnostics (e.g., transtracheal aspiration) to identify an etiologic agent in primary lung abscesses is helpful.
  • Sputum and blood cultures, serologic studies for opportunistic pathogens, and—if needed—more invasive methods of sample collection (e.g., bronchoalveolar lavage, CT-guided percutaneous aspiration) are recommended for secondary lung abscesses or when empirical therapy fails.

Treatment: Lung Abscess

Treatment depends on the presumed or established etiology.

  • For primary lung abscesses, the recommended regimens are clindamycin (600 mg IV tid) or an IV-administered β-lactam/β-lactamase combination. After clinical improvement, the pt can be transitioned to an oral regimen (clindamycin, 300 mg qid; or amoxicillin/clavulanate).
  • In secondary lung abscesses, antibiotic coverage should be directed at the identified pathogen.
  • Continuation of oral treatment is recommended until imaging shows that the lung abscess has cleared or regressed to a small scar.
  • Pts who continue to have fever ≥7 days after antibiotic initiation and whose additional diagnostic studies fail to identify another treatable pathogen may require surgical resection or percutaneous drainage of the abscess.