(From Rabbat A, Huchon G: Bacterial pneumonia. In Albert RK, Spiro SG, Jett JR, editors: Clinical respiratory medicine, ed 3, Philadelphia, 2008, Mosby.)

E. coli pneumonia and P. aeruginosa pneumonia typically occur in chronically ill patients; hemoptysis is rare, and the lung infection usually involves the lower lobes. Abscessation and empyema occur frequently. Acinetobacter pneumonia progresses very quickly, with development of severe hypoxemia, shock, bilateral consolidation, and empyema and even death within a few days.

Pseudomonas pseudomallei, which causes melioidosis, is an aerobic, gram-negative bacillus found in soil, vegetation, and water in tropical regions. Infection of the lung occurs more commonly as a result of spread through the bloodstream after cutaneous infection than as a result of inhalation. The clinical presentation may be either acute or chronic. Acute melioidosis manifests with high fever, dyspnea, chest pain, cough with purulent sputum, and hemoptysis. Local cellulitis and lymphangitis may be seen at the place of cutaneous inoculation. The chest radiograph shows diffuse miliary nodules, infiltrates, or cavitation. Chronic melioidosis may occur years after contraction of the infection in an endemic area. Signs and symptoms either are absent or may resemble those of pulmonary tuberculosis: asthenia, anorexia, weight loss, low-grade fever, productive cough, and hemoptysis. Chest radiographs show apical infiltrates, possibly with cavitations.

Anaerobic Bacteria

Anaerobic bacterial pneumonia results from aspiration; therefore, it typically occurs in situations involving alcoholism, coma, seizure, and general anesthesia. Chronic dental infection; head, neck, and lung cancer; and bronchiectasis are additional risk factors. Anaerobic pneumonia begins as a typical pneumonia with pleuritic pain; pulmonary infiltrations preferentially involve the lower lobes, particularly the right lower lobe. If patients aspirate while lying supine, the segments involved typically are the posterior segment of the right upper lobe and the apical segment of the right lower lobe. Necrosis and suppuration follow, and fever with temperatures higher than 39° C (102.2° F), dyspnea, and pleuritic pain persist. Sputum is purulent and fetid, which often is obvious on entering the patient’s room. Leukocytosis is high, and segmental infiltrations with small transparent areas of necrosis are seen. Abscess and empyema occur frequently. The outcome is closely related to treatment—delay in antibiotic treatment or inappropriate antibiotic choice probably will result in necrotizing pneumonia, abscess formation, and empyema, which increases the fatality rate.

Coxiella burnetii

C. burnetii is the causative agent of Q fever and is the most frequent pathogen responsible for pneumonia among the rickettsial organisms. Ticks are vector agents, and various wild and domestic animals (cattle, sheep, goats) are infected with no evidence of disease; C. burnetii multiplies in the placenta of pregnant animals and spreads during parturition. Although C. burnetii is present in numerous species of ticks, the main route of transmission is by inhalation of infectious aerosols. C. burnetii is particularly resistant to chemical and physical agents. The clinical presentation is that of an atypical pneumonia. The onset occurs after a 2- to 4-week incubation period. Patients present with high fever (i.e., body temperature of 40° C [104° F] or more), chills, myalgia, and headache, all of abrupt onset; cough usually is nonproductive. Abdominal and thoracic pain, pharyngitis, and bradycardia also may be features. There usually is no rash, in contrast with other rickettsial infections. Hepatomegaly and splenomegaly may be found on physical examination. The chest radiograph shows dense nodular infiltrates; pleural effusion and linear atelectasis may be seen. Leukocytosis is not a feature, and mild hepatitis may be found. The course usually is benign.

Nocardia Species

Nocardia asteroides and, to a lesser extent, Nocardia brasiliensis are responsible for most cases of Nocardia pneumonia. Nocardiae are aerobic, gram-positive bacilli present mainly in soil. Approximately 50% of patients have no underlying disease. The others tend to have predisposing problems such as immunosuppression, malignancy, or long-term corticosteroid therapy. The onset of the infection is usually subacute, but it can be fulminant; in the latter case, there is a high fatality rate. Symptoms include fever, asthenia, anorexia, productive cough, and chest pain. Multiple subcutaneous abscesses may be present, as well as neurologic signs when there is central nervous system involvement. Chest radiograph abnormalities vary, ranging from infiltration to lobar consolidation; cavitation, nodules, abscesses, and pleural effusion also may be seen. The prognosis depends on whether the infection disseminates, but it is usually good in the case of isolated lung disease. Metastatic infection may occur anywhere but is particularly common in the central nervous system and the skin. Infection also may reach the pleura and the chest wall.

Both Actinomyces and Arachnia can cause actinomycosis, but Actinomyces israelii is the main responsible organism. These are anaerobic, gram-positive, filamentous, branching bacilli (Figure 24-2) that were incorrectly thought to be fungi for many years. They normally reside in the oropharynx and become invasive pathogens when there is a defect in the anatomic barrier or when they are inhaled, at which time the infection may extend directly from one place to an adjacent area. Bad dentition, bronchiectasis, and COPD are risk factors for pulmonary infection. Men are far more frequently affected than women. The clinical presentation suggests tuberculosis, carcinoma, or chronic fungal infection; asthenia, anorexia, weight loss, and low-grade fever may precede cough and chest pain by months. Cervicofacial and thoracic involvement coexists rarely. When infection progresses to the pleural space and chest wall, the opening of a sinus tract may disclose pus. Radiographic features are variable and include small cavitary nodules confined to one segment; cavitary infiltration; extension of infection to the interlobar fissure, chest wall, bone, or pleura; and empyema.

Figure 24-2 Sputum Gram stain showing Actinomyces organisms (center).

(From Rabbat A, Huchon G: Bacterial pneumonia. In Albert RK, Spiro SG, Jett JR, editors: Clinical respiratory medicine, ed 3, Philadelphia, 2008, Mosby.)

Pasteurella multocida

Pasteurella multocida is a gram-negative coccobacillus present in the oropharynx of mammals. It causes cutaneous infection in humans after animal bites. Pneumonia has been reported in patients with chronic pulmonary diseases. The clinical presentation is nonspecific and includes fever, cough, purulent sputum, and dyspnea. Chest radiographs show lower lobe infiltrates; pleural effusion and empyema may occur.

Francisella tularensis

Francisella tularensis is a gram-negative bacillus found in various mammals and insects of the Northern Hemisphere. Tularemia occurs after the bite of, or contact with, an infected animal. The onset of pneumonia is abrupt; fever, chills, and malaise precede dyspnea, cough, and chest pain. Painful ulceroglandular infection with adenopathy may be found at the site of bacterial inoculation. The chest radiograph shows signs of pneumonia, possibly with hilar adenopathy or pleural effusion.

Yersinia pestis

Yersinia pestis (formerly called Pasteurella pestis) is a short gram-negative rod that causes plague. It is a disease of rodents (squirrels, rabbits, rats) that is transmitted to humans by flea bites or by person-to-person contact through aerosol inhalation. Initial signs and symptoms are chills, fever, prostration, delirium, headache, vomiting, and diarrhea. There are three forms of plague: bubonic, septicemic, and pneumonic. Bubonic plague consists of lymphadenopathy, with palpable masses forming in the cervical, axillary, femoral, and inguinal areas. Signs of septicemia are those of shock and petechial hemorrhages. Plague pneumonia results from either metastatic infection or inhalation of the pathogen. Pneumonia occurs within a week of initial exposure and is characterized by chest pain, productive cough, dyspnea, and hemoptysis. The chest radiograph shows lower lobe infiltrates, possibly nodules, lymphadenopathy, and pleural effusions.

Bacillus anthracis

Bacillus anthracis is a large gram-positive rod that causes anthrax. B. anthracis is found in the soil, water, and vegetation and infects cows, sheep, and horses, which in turn infect humans after contact with contaminated materials. Fever and malaise usually appear progressively. Three forms of anthrax are found: cutaneous, intestinal, and pneumonic. Inoculation of B. anthracis into superficial wounds or skin abrasions causes cutaneous anthrax, which is characterized by a black-crusted pustule on a large area of edema. Intestinal anthrax results from ingestion of contaminated material, and the resulting illness can be severe. Pneumonic anthrax is due to inhalation of the contaminated material. Nonproductive cough and chest pain precede dyspnea, stridor, tachypnea, cyanosis, and edema of the neck and anterior chest. Peribronchovascular edema, enlargement of the mediastinum, and pleural effusions usually are seen on the chest radiograph.

Brucella Species

Brucella organisms are gram-negative coccobacilli found in the genitourinary tract of cows, pigs, goats, and dogs. Brucellosis results from contact with infected animals or from ingestion of unpasteurized milk products. The pathogen then spreads through the body by way of the bloodstream. General symptoms include fever, malaise, and headache. Hepatic enlargement and splenomegaly are common, as is lower back pain. Respiratory symptoms are less frequent than abnormalities on the chest radiograph, which include nodules, miliary infiltrates, and lymphadenopathy.

Moraxella catarrhalis

Moraxella catarrhalis, formerly named Branhamella catarrhalis, is a gram-negative diplococcus that commonly is found in the oropharynx of normal persons. M. catarrhalis pneumonia is seen in patients with underlying chronic diseases such as COPD, congestive heart disease, or malignancy. Symptoms and radiographic findings are nonspecific. Leukocytosis is common, and the course usually is favorable.

Treatment

Site of Care Decision

A crucial decision in the treatment of CAP is whether or not the patient’s condition warrants hospital admission. Numerous factors contribute to such decision making, including risk of death from the pneumonia, disease severity, presence of comorbid conditions, need for advanced diagnostics, ability to take oral medications, and the degree of social support. In the past, hospital admission was an instinctive “knee jerk” response to the diagnosis of CAP. However, hospitalization is associated with an increased risk of acquiring multidrug-resistant nosocomial bacterial strains, increased risk for thromboembolic events, up to a 75-fold increase in cost, and less patient satisfaction. Informed practitioners have therefore mounted a vigorous effort to reduce unnecessary admissions for CAP, primarily by better identification of patients who can be safely treated at home.

Several outcome tools have been developed to predict prognosis in CAP, and these are now being used to identify patients at low risk of mortality and appropriate for treatment at home rather than in hospital. Among the well-validated ones are the Pneumonia Severity Index (PSI) and the CURB-65 and CRB-65 indices. These are summarized in Chapter 23, Figures 23-5 and 23-6.

CURB-65 or CRB-65 (which is CURB-65 without the blood urea nitrogen level) indices are significantly more user-friendly scoring systems requiring consideration of four or five readily assessed variables (see Chapter 23, Figure 23-6).

Another sometimes challenging decision is whether and when to admit the patient to an ICU. Generally, patients with high scores on mortality prediction indices (such as class V PSI or group 3 CURB-65) are likely to benefit from early ICU admission. Emerging data suggest that early admission to the ICU in appropriate patients can improve outcomes. The challenge is identifying these patients among the larger group of patients at risk for higher mortality. Latest ATS/IDSA guidelines defined need for ICU admission as the presence of one of the major criteria (need for invasive mechanical ventilation or hemodynamic instability requiring vasopressor use) or three of nine minor criteria listed in Box 24-1. Several scoring systems (CURXO, SMART-COP, and CAP-PIRO) tested criteria similar to the ATS minor criteria set and found them to be similar in terms of predicting need for admission to intensive care. All of the aforementioned scoring systems, however, are not without limitations, especially when applied in younger populations. Development and validation of a dedicated scoring system to predict need for ICU treatment will be useful.

Box 24-1

American Thoracic Society Criteria for Admission of Patients with Community-Acquired Pneumonia to an Intensive Care Unit

Major Criteria

Invasive mechanical ventilation

Vasopressor use

Modified from Mandell LA, Wunderink RG, Anzueto A, et al: Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults, Clin Infect Dis 44(Suppl 2):S27–S72, 2007.

These scoring systems have contributed significantly to the objective assessment of the severity and prognosis prediction of CAP. Such systems, however, should not be used as the sole parameter for determining the need for hospital admission. In practice, as many as 40% of patients with CAP who are at low risk for dying as assessed by these scores get admitted for management of the pneumonia. In many of these patients, comorbid conditions requiring inpatient management or social factors that make home treatment unsafe necessitate hospital care. A combination of a prognostic scoring system and assessment for comorbidity and risk factors related to the patient’s social situation should guide decisions about site of care for CAP.

Antimicrobial Treatment

Eradication of the offending pathogen from the lower respiratory tract is the goal of antimicrobial CAP therapy. Ideally, the identity and the antimicrobial susceptibility of the pathogen should be known before initiation of treatment, so that an antibiotic that has the narrowest antimicrobial spectrum, least side effects, and the lowest cost can be prescribed. However, diagnostic testing able to identify causative organisms so rapidly that the results would be available before initiation of antimicrobial therapy are still lacking. The lack of sensitivity and specificity of current diagnostic testing is also a concern. Biomarkers and molecular detection may ultimately provide the necessary diagnostic tools to support pathogen directed treatment, but are not adequately validated for clinical use at present. Furthermore, there is evidence that earlier administration of appropriate antimicrobial therapy (with one or more antibiotics effective in vitro against the causative pathogen and given in adequate doses) improves outcomes in CAP. Therefore, delay in initiation of antimicrobial therapy while awaiting the results of microbiologic studies, or even for obtaining such studies (e.g., waiting for the patient to produce an adequate sputum sample) could have deleterious effects on patient outcome.

These considerations have prompted the current emphasis on broad-spectrum empirical therapy, with or without subsequent adjustment of antimicrobial spectrum once diagnostic results become available. Empirical choice of antimicrobials depends on factors such as severity of illness, knowledge of the most common pathogens associated with the patient’s condition, local resistance patterns, and the growing understanding that CAP frequently can be a polymicrobial infection, most commonly consisting of a combination of a virus or an atypical pathogen with a typical bacterial pathogen. In view of the lack of sensitivity of current diagnostic testing, hesitation to adjust the antibiotic regimen is common if the patient is responding to therapy, even if diagnostic data support narrowing of the antimicrobial spectrum. Current recommendations also emphasize rapid administration of antibiotics in CAP, with retraction of previous guidelines on specific time intervals at which antibiotics should be administered. Therefore, current guidelines do not include specific timing for administration of antibiotics for CAP, except that antibiotics should be started in the emergency department if that is the facility admitting the patient to the hospital.

A major consideration determining empirical antibiotic choice in the current ATS/IDSA guidelines is the site of care, which serves as a surrogate marker for disease severity (outpatient, inpatient, and ICU settings) (Box 24-2 and Table 24-2). In the outpatient setting, choice of antibiotics is influenced primarily by presence of comorbid conditions and by recent antibiotic use. These two risk factors portend poor outcomes and infection by drug-resistant pathogens. Recent antibiotic use (within 3 months) should prompt choice of an agent from an antibiotic class other than the one to which the patient has already been exposed. Local resistance patterns also should be kept in mind in choosing agents for empirical antimicrobial therapy; for example, high-level macrolide resistance (minimum inhibitory concentration [MIC] of 16 µg/mL or higher) at a prevalence of 25% or more should discourage macrolide use as a single agent. Of the multitude of potential causative agents, five or six pathogens typically account for a majority of cases of CAP; nevertheless, the possibility of unusual pathogens should always be kept in mind. A thorough recent travel or exposure history and an awareness of specific pathogen association with certain epidemiologic settings are necessary to consider these unusual pathogens in CAP.

Box 24-2

Most Common Etiologic Agents of Community-Acquired Pneumonia *

Outpatient

Streptococcus pneumoniae

Mycoplasma pneumoniae

Haemophilus influenzae

Chlamydophila pneumoniae

Respiratory viruses; influenza A and B viruses, adenovirus, respiratory syncytial virus, parainfluenza virus

Inpatient Non-ICU

Respiratory viruses (see above)

Inpatient ICU

S. pneumoniae

S. aureus

Legionella

Gram-negative organisms

H. influenzae

ICU, intensive care unit.

^* As designated by the American Thoracic Society and the Infectious Diseases Society of America.

Table 24-2 ATS/IDSA Recommendations for Empirical Antibiotic Treatment of Community-Acquired Pneumonia

In-Hospital Setting	Antibiotic Regimen
In-Hospital Setting	Outpatient	Inpatient
Non-ICU setting
Absence of risk factors	Macrolide (preferred) OR Doxycycline

Respiratory fluoroquinolone (moxifloxacin, gemifloxacin, or levofloxacin 750 mg)

Beta-lactam + macrolide

Presence of risk factors: chronic heart, lung, liver, or renal disease; diabetes mellitus; alcoholism; malignancy; asplenia; immunosuppressive condition/medications; use of antimicrobials in past 3 months

Respiratory fluoroquinolone (moxifloxacin, gemifloxacin, or levofloxacin 750 mg)

Beta-lactam + macrolide

ICU setting Beta-lactam + either azithromycin or respiratory fluoroquinolone (aztreonam + respiratory fluoroquinolone in penicillin-allergic patients)

ATS/IDSA, American Thoracic Society/Infectious Diseases Society of America; ICU, intensive care unit.

Data from Mandell LA, Wunderink RG, Anzueto A, et al: Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults, Clin Infect Dis 44(Suppl 2):S27–S72, 2007.

With respect to management, inpatients with CAP treated in the non-ICU setting are quite similar to the outpatients with equivalent risk factors. Pathogen spectra for these patient groups also are similar, except that Legionella and aspiration are more common in inpatients. Parenteral therapy is the preferred mode in the hospitalized patients.

With CAP severe enough to warrant admission to an ICU, an expanded list of likely pathogens has been reported. Although S. pneumoniae remains the most common, Legionella, S. aureus, and gram-negative bacilli including P. aeruginosa are identified with increasing frequency and warrant consideration for empirical coverage (Table 24-3). Those patients with CAP admitted to the ICU are by definition severely ill, and available data point to improved outcomes with use of antibiotic combinations in these patients; thus, monotherapy with fluoroquinolones or beta-lactams is not indicated. All patients should receive antibiotic combinations active against the most likely offending organisms. Presence of certain comorbid conditions such as bronchiectasis and severe COPD and other factors such as frequent antibiotic and systemic corticosteroid use are associated with increased probability of infection with P. aeruginosa; in such instances, empirical treatment effective against this pathogen is warranted. If S. aureus infection is suspected, coverage for community-acquired MRSA with agents such as vancomycin or linezolid should be provided. If necrotizing pneumonia is evident, clindamycin should be added to the regimen.

Table 24-3 Empirical Coverage for Uncommon Pathogens Causing Community-Acquired Pneumonia

Suspected Pathogen	Special Considerations
Pseudomonas	Piperacillin-tazobactam, cefepime, imipenem, or meropenem PLUS either ciprofloxacin or levofloxacin (750 mg) OR Aminoglycoside and azithromycin OR Aminoglycoside and antipneumococcal fluoroquinolone OR Substitute beta-lactam (piperacillin-tazobactam, cefepime, imipenem, or meropenem) with aztreonam in patients allergic to penicillin
Community-acquired methicillin-resistant Staphylococcus aureus	Vancomycin (+ clindamycin in patients with necrotizing pneumonia) OR Linezolid

Route and Duration of Therapy; Hospital Discharge

Most patients with CAP severe enough to warrant hospital admission are treated with intravenous antibiotics. Switching to oral therapy should be considered once the patient has achieved clinical stability (Box 24-3), is able to tolerate oral medications, and has a functioning gastrointestinal tract. In general, either the same agent or same class of antimicrobials should be used for the oral therapy regimen. Early initiation of oral therapy leads to earlier hospital discharge and overall decreased number of adverse events. In-hospital observation before discharge is unnecessary after the switch to oral medications if the patient meets at least four of the five stability criteria (see Box 24-3), is free from comorbid conditions of clinical significance, and has adequate social supports in place.

Box 24-3

Criteria for Clinical Stability in Management of Community-Acquired Pneumonia

Temperature ≤37.8° C

Heart rate ≤100 beats/minute

Systolic blood pressure ≥90 mm Hg

Respiratory rate ≤24 breaths/minute

Oxyhemoglobin saturation ≥90% or PO₂ ≥60 mm Hg on preadmission level of oxygen supplementation

In an effort to decrease the rate of adverse events of antibiotic therapy along with cost optimization, shorter durations of antimicrobial therapy have been considered, with current ATS/IDSA guideline recommendations denoting 5 days as minimal duration of therapy. Antibiotics can be discontinued once clinical stability has been achieved and maintained for 48 to 72 hours. Biomarker-guided determination of therapy duration has been attempted, suggesting that even 3-day therapy may be a viable option; however, further studies are needed to validate such an approach.

More than 7 to 10 days of total antibiotic administration is rarely required, unless extrapulmonary infections such as endocarditis or meningitis are present, initial therapy was not active against a subsequently identified offending pathogen, or P. aeruginosa infection, S. aureus bacteremia, or tissue necrosis was present.

Complications/Failure to Respond to Therapy

A lack of response to empirical therapy is observed in up to 10% of outpatients and 15% of patients hospitalized with CAP. Challenges remain in the definition of nonresponse and treatment failure; however, the general consensus is that treatment adjustments probably should be withheld in the first 72 hours unless the patient’s condition is deteriorating. Failure to achieve clinical stability using the aforementioned criteria within the first 3 days is suggestive of nonresponse to therapy, although in up to 25% of patients (especially those of advanced age and with multiple comorbid conditions), 6 days or longer may be needed to meet these criteria.

Several factors may potentially lead to lack of response to empirical therapy, including misdiagnosis of CAP, infection or superinfection with resistant organisms, infection dissemination with or without abscess formation, and others (Figure 24-3). However, no apparent cause for lack of response can be identified in up to 30% to 44% of such cases, with suggested reasons including comorbidity and possibly variations in inflammatory response.

Figure 24-3 Common causes of lack of response to treatment in patients with community-acquired pneumonia (CAP).

Failure of empirical antimicrobial therapy usually results in a combination of further diagnostic testing, broadening of the antibiotic treatment regimen and/or transfer to higher-level care. An aggressive and complete reevaluation is still required in nonresponding and especially deteriorating patients. Exhaustive review of the findings on the history and physical examination, with increased attention to risk factors including personal habits and environmental, occupational, social, and travel history, is indicated. Reevaluation of patient’s immune status could be helpful if compromise of any sort is suspected (e.g., HIV infection, common variable immunodeficiency). Valuable information occasionally can be obtained from the patient’s social contacts, rather than directly from the patient.

Obtaining repeat microbiologic studies with evaluation for less common pathogens might be of benefit, although one must be aware of decreased sensitivity of bacterial studies obtained during antimicrobial therapy. Abscesses (if present) and pleural effusions should be drained, acquired fluid sent for microbiologic studies. Alternative sources of infection should be excluded. If no explanation emerges from these measures, bronchoalveolar lavage (BAL) could be considered, with differential cell count often providing important clues to the possible cause of nonresponse. For example, neutrophil-predominant BAL fluid is suggestive of bacterial infection and possibly bronchiolitis obliterans; lymphocyte-predominant BAL fluid is common in tuberculosis, sarcoidosis, and hypersensitivity pneumonitis; hemosiderin-laden macrophages are seen in alveolar hemorrhage; and a predominance of eosinophils is suggestive of fungal, Pneumocystis, or drug-induced diseases and eosinophilic pneumonia. In intubated patients, tracheal aspirates should be carefully examined. Absence of multidrug-resistant pathogens in the aspirate suggests that such organisms are less likely to be responsible for the lack of clinical improvement; however, the reverse is not true because of high rates of colonization by such pathogens in intubated patients.

Radiologic evaluation with a computed tomography (CT) scan of the chest with contrast simultaneously assess the lung parenchyma, pulmonary vasculature, and the pleural space and could provide valuable clues for the reason for nonresponse. For example, presence of nodules with a halo sign may suggest invasive aspergillosis complicating CAP in a patient with COPD on systemic corticosteroids.

Empirical escalation of antibiotic therapy could be considered, especially in patients with risk factors for potentially untreated pathogens; however, little evidence points to better outcomes with this approach. Severity of illness at presentation and comorbid conditions seem to be responsible for the failure to respond to guidelines-based therapy in a majority of such cases of CAP.

Specific Complications

Aspiration Pneumonia

Mendelson originally described the syndrome of aspiration of gastric contents in 1946 in 61 obstetric patients in whom aspiration pneumonia developed after ether anesthesia. Manifestations appear very rapidly after the event and include cough (dry or productive of pink sputum from bronchoalveolar hemorrhage), tachypnea, tachycardia, fever, diffuse crackles, cyanosis, and bronchospasm in some cases. The chest radiograph shows extensive atelectasis and infiltrates, and arterial blood gas analysis reveals hypoxemia and normocapnia or hypocapnia. In the most severe cases, the PaCO₂ may be elevated, and a metabolic acidosis may be present.

A number of clinical features help distinguish aspiration pneumonia from other CAPs. Aspiration pneumonia tends to have a more insidious course, such that the patient may have an empyema, lung abscess, or necrotizing pneumonia at the time medical care is first sought. The sputum may be putrid because of anaerobic bacteria, and weight loss is common. Chest imaging commonly shows necrotizing infiltrates or multiple abscesses, typically located in dependent regions of the lung (Figure 24-4).

Figure 24-4 Necrotizing aspiration pneumonia. Chest computed tomography scan demonstrates involvement of the entire right middle lobe (which suggests pulmonary gangrene) and an effusion, which was found to represent an empyema.

(From Rabbat A, Huchon G: Bacterial pneumonia. In Albert RK, Spiro SG, Jett JR, editors: Clinical respiratory medicine, ed 3, Philadelphia, 2008, Mosby.)

Lung Abscess

The incidence of pulmonary abscess has decreased over the past decade. Lung abscess is associated with several conditions, including poor dental status or periodontal disease, chronic alcoholism, intravenous drug use, and head and neck cancer. Lung abscess may complicate bronchiectasis (Figure 24-5) and the course of aspiration pneumonia in persons with impaired consciousness, dysphagia and gastroesophageal reflux, or acute or chronic neurologic diseases, but it also may occur with bronchial obstruction by a foreign body or bronchial carcinoma.

Figure 24-5 Radiographic appearance in left lower lobe pneumonia. A, Lung abscess associated with lower lobe pneumonia. B, At 3 months after resolution of the lung abscess, widened airways with thickened walls are apparent in the left lower lobe (arrow). These bronchiectatic changes were consequent to the pneumonia. C, Fiberoptic bronchoscopic bronchogram of the left lower lobe confirms gross dilatation of the airways, typical of postinfective bronchiectasis.

(From Rabbat A, Huchon G: Bacterial pneumonia. In Albert RK, Spiro SG, Jett JR, editors: Clinical respiratory medicine, ed 3, Philadelphia, 2008, Mosby.)

Pulmonary abscesses usually are polymicrobial, with a predominant anaerobic flora, such as Streptococcus intermedius, Streptococcus salivarius, Streptococcus constellatus, Fusobacterium spp., Prevotella spp., or Bacteroides spp.

Clinical manifestations usually develop insidiously, particularly before onset of frank necrosis. This period may last several weeks after an initial aspiration. By the time of diagnosis of the lung abscess, patients may have lost weight and have a high fever, chills, putrid expectoration, and chest pain. Pleural involvement with an empyema is a frequent complication of lung abscess. Laboratory findings include a very high white cell count and considerable elevation of inflammatory and catabolic markers.

Radiologic features of lung abscess typically consist of a peripheral cavity more than 2 cm in diameter in the dependent lung regions. CT is useful to distinguish empyema with bronchopleural fistula from lung abscess.

Appearance of the sputum Gram stain often is misleading. Bronchoscopic sampling such as bronchial aspiration, protected specimen brush procedures, or BAL should be performed with inoculation onto anaerobic media. Percutaneous fluoroscopic or ultrasound or CT-guided fine needle aspiration may be a useful diagnostic technique. Aspirates should be grown on anaerobic media, and samples should be sent promptly to the laboratory for specific anaerobic cultures.

Parapneumonic Effusion and Empyema

The signs and symptoms suggestive of a parapneumonic collection are increased breathlessness, swinging pyrexia, and raised levels of inflammatory markers. The chest radiograph usually demonstrates the collection of fluid. A lateral radiographic view or an ultrasound scan is useful to confirm the presence of fluid.

All pleural fluid specimens should be submitted for Gram stain and culture, because the identification of significant bacterial cultures confirms the diagnosis of infection and aids in antibiotic choice. Unfortunately, approximately 40% of infected pleural effusions are culture negative, and in this situation, biochemical pleural fluid markers (pH, lactate dehydrogenase, white blood cell count, and glucose) are central to establishing a diagnosis. Fluid drainage by means of a chest tube and prolonged antibiotic therapy is necessary in all cases of complicated parapneumonic pleural effusion and empyema. (See Chapter 69 for a more detailed description of these two clinical entities.)

Bronchopleural Fistula

A bronchopleural fistula is caused by a connection between the pleural space and the consolidated lung; it can complicate either an empyema or a lung abscess. The bronchopleural fistula causes a pyopneumothorax (i.e., air-fluid level in the pleural space), so that, on drainage of an empyema, not only pus but also air comes out through the chest drain. A bronchopleural fistula will not seal unless infection is controlled. Initial treatment is conservative, with antibiotics and tube drainage, to allow healing of the fistula. If this approach fails, surgery may be necessary to attempt primary closure of the fistula or closure of the potential space with other living tissues, such as muscle flaps. The management of bronchopleural fistulas that do not close with conservative treatment requires the surgical skills of a thoracic specialist.

Organizing Pneumonia

Organizing pneumonia, sometimes known as cryptogenic organizing pneumonia (now the preferred designation for bronchiolitis obliterans organizing pneumonia [BOOP]), is a condition in which an organizing inflammatory exudate with fibroblast proliferation occurs after an episode of pneumonia. The consolidation often is patchy and may be fleeting. Organizing pneumonia subsequent to a bacterial infection is suggested when a residual consolidation (often fleeting) is observed despite adequate antibiotic treatment. Investigation includes examination of sputum or bronchial washings to exclude infection. CT may help to visualize the consolidation and exclude other causes. The definitive investigation is an open lung biopsy showing the typical histologic changes, which along with highly suggestive clinical findings constitute sufficient evidence for a confident diagnosis. A course of steroids usually leads to resolution. When the steroids are stopped, however, relapse may occur; in such cases, treatment for several months may be necessary (see Chapter 50).

Bronchiectasis

Permanent dilatation of the bronchus can be a sequela of severe pneumonia, causing localized bronchiectasis. CT scanning during or after an episode of acute pneumonia may show bronchial dilatation, so the diagnosis cannot be made with confidence until after the pneumonia has completely resolved. The presence of bronchiectasis is suggested by continual cough productive of sputum or recurrent infections in one part of the lung. Investigation consists of sputum examination, when organisms associated with bronchiectasis such as H. influenzae or P. aeruginosa may be isolated. The diagnostic test of choice is a thin-section, high-resolution CT scan. Management consists of postural drainage of the infected lobe and antibiotic treatment for any acute infection. In patients who have coexisting airflow obstruction, treatment with bronchodilators or inhaled steroids may be helpful. (See Chapter 45 for a full description of this clinical entity.)

Prevention

Administration of vaccines targeting S. pneumoniae and influenza viruses and risk factor modification such as smoking cessation, aspiration precautions, and cessation of alcohol abuse constitute the main preventive measures for CAP (Table 24-4). Vaccination status should be assessed at the beginning of the hospitalization, and vaccination may be performed either at discharge or during outpatient follow-up if needed. Vaccination at discharge is preferred in patients in whom compliance with outpatient follow-up care is likely to be unreliable.

Table 24-4 Recommendations for Vaccine Prevention of Community-Acquired Pneumonia

Controversies and Pitfalls

Whether empirical treatment of atypical pathogens, specifically C. pneumoniae and M. pneumoniae, is essential and clearly beneficial in all patients with CAP is an area of controversy. This is reflected in American guidelines recommending coverage for atypical pathogens in all patients, in contrast with European recommendations making such coverage optional at the discretion of the treating physician.

Health care–associated pneumonia (HCAP) is a more recent designation for a form of pneumonia acquired in the community but warranting treatment more like that for nosocomial pneumonia, because of risk factors that predispose affected patients to infections by pathogens that usually are found in the local hospital setting (see Chapter 27). Current criteria used to distinguish HCAP from CAP are in question as being too broad in scope, potentially leading to excessive use of broad-spectrum antibiotics. It is likely that refinement of these criteria in the near future will redefine the boundaries between HCAP and CAP.

Acknowledgment

In preparation of this chapter, we retained some material from Chapter 27 on bacterial pneumonias, by Antoine Rabbat and Gérard J. Huchon, in the third edition of this book. The contribution of these authors is gratefully acknowledged.

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